Index to this page

The Pathway Breathing Central Control of Breathing Local Control of Breathing Diseases of the Lungs o Pneumonia o Asthma o Emphysema o Chronic Bronchitis o Chronic Obstructive Pulmonary Disease o Lung Cancer

This photo (courtesy of the Anatomical Institute, Bern) shows a rubber cast of human lungs.

The Human Respiratory System

The Pathway

Air enters the nostrils passes through the nasophar ynx, the oral pharynx through the glottis into the trachea into the right and left bronchi, which branches and rebranches into

bronchioles, each of which terminates in a cluster of alveoli

Only in the alveoli does actual gas exchange takes place. There are some 300 million alveoli in two adult lungs. These provide a surface area of some 160 m2 (almost equal to the singles area of a tennis court and 80 times the area of our skin!).

Breathing
In mammals, the diaphragm divides the body cavity into the

abdominal cavity, which contains the viscera (e.g., stomach and intestines) and the thoracic cavity, which contains the heart and lungs.

The inner surface of the thoracic cavity and the outer surface of the lungs are lined with pleural membranes which adhere to each other. If air is introduced between them, the adhesion is broken and the natural elasticity of the lung causes it to collapse. This can occur from trauma. And it is sometimes induced deliberately to allow the lung to rest. In either case, reinflation occurs as the air is gradually absorbed by the tissues. Because of this adhesion, any action that increases the volume of the thoracic cavity causes the lungs to expand, drawing air into them.

During inspiration (inhaling), o The external intercostal muscles contract, lifting the ribs up and out. o The diaphragm contracts, drawing it down . During expiration (exhaling), these processes are reversed and the natural elasticity of the lungs returns them to their normal volume. At rest, we breath 1518 times a minute exchanging about 500 ml of air. In more vigorous expiration, o The internal intercostal muscles draw the ribs down and inward o The wall of the abdomen contracts pushing the stomach and liver upward. Under these conditions, an average adult male can flush his lungs with about 4 liters of air at each breath. This is called the vital capacity. Even with maximum expiration, about 1200 ml of residual air remain.

The table shows what happens to the composition of air when it reaches the alveoli. Some of the oxygen dissolves in the film of moisture covering the epithelium of the alveoli. From here it diffuses into the blood in a nearby capillary. It enters a red blood cell and combines with the hemoglobin therein. At the same time, some of the carbon dioxide in the blood diffuses into the alveoli from which it can be exhaled.

Link to discussion of gas transport in the blood. Composition of atmospheric air and expired air in a typical subject. Note that only a fraction of the oxygen inhaled is taken up by the lungs. Component N2 (plus inert gases) O2 CO2 H2O Atmospheric Air (%) Expired Air (%) 78.62 74.9 20.85 0.03 0.5 100.0% 15.3 3.6 6.2 100.0%

The ease with which oxygen and carbon dioxide can pass between air and blood is clear from this electron micrograph of two alveoli (Air) and an adjacent capillary from the lung of a laboratory mouse. Note the thinness of the epithelial cells (EP) that line the alveoli and capillary (except where the nucleus is located). At the closest point, the surface of the red blood cell is only 0.7 m away from the air in the alveolus. (Reproduced with permission from Keith R. Porter and Mary A. Bonneville, An Introduction to the Fine Structure of Cells and Tissues, 4th. ed., Lea & Febiger, 1973.)

Central Control of Breathing

The rate of cellular respiration (and hence oxygen consumption and carbon dioxide production) varies with level of activity. Vigorous exercise can increase by 2025 times the demand of the tissues for oxygen. This is met by increasing the rate and depth of breathing. It is a rising concentration of carbon dioxide not a declining concentration of oxygen that plays the major role in regulating the ventilation of the lungs. Certain cells in the medulla oblongata are very sensitive to a drop in pH. As the CO2 content of the blood rises above normal levels, the pH drops [CO2 + H2O HCO3 + H+], and the medulla oblongata responds by increasing the number and rate of nerve impulses that control the action of the intercostal muscles and diaphragm. This produces an increase in the rate of lung ventilation, which quickly brings the CO2 concentration of the alveolar air, and then of the blood, back to normal levels.

Link to a description of experiments that demonstrate this. However, the carotid body in the carotid arteries does have receptors that respond to a drop in oxygen. Their activation is important in situations (e.g., at high altitude in the unpressurized cabin of an aircraft) where oxygen supply is inadequate but there has been no increase in the production of CO2.

Local Control of Breathing

The smooth muscle in the walls of the bronchioles is very sensitive to the concentration of carbon dioxide. A rising level of CO2 causes the bronchioles to dilate. This lowers the resistance in the airways and thus increases the flow of air in and out.

Diseases of the Lungs

Pneumonia
Pneumonia is an infection of the alveoli. It can be caused by many kinds of both bacteria (e.g., Streptococcus pneumoniae) and viruses. Tissue fluids accumulate in the alveoli reducing the surface area exposed to air. If enough alveoli are affected, the patient may need supplemental oxygen.

Asthma
In asthma, periodic constriction of the bronchi and bronchioles makes it more difficult to breathe in and, especially, out. Attacks of asthma can be

triggered by airborne irritants such as chemical fumes and cigarette smoke airborne particles to which the patient is allergic. Link to discussion of allergic asthma.

Emphysema
In this disorder, the delicate walls of the alveoli break down, reducing the gas-exchange area of the lungs. The condition develops slowly and is seldom a direct cause of death. However, the gradual loss of gas-exchange area forces the heart to pump ever-larger volumes of blood to the lungs in order to satisfy the body's needs. The added strain can lead to heart failure. The immediate cause of emphysema seems to be the release of proteolytic enzymes as part of the inflammatory process that follows irritation of the lungs. Most people avoid this kind of damage during infections, etc. by producing an enzyme inhibitor (a serpin) called alpha-1 antitrypsin.

Those rare people who inherit two defective genes for alpha-1 antitrypsin are particularly susceptible to developing emphysema.

Chronic Bronchitis
Any irritant reaching the bronchi and bronchioles will stimulate an increased secretion of mucus. In chronic bronchitis the air passages become clogged with mucus, and this leads to a persistent cough. Chronic bronchitis is usually associated with cigarette smoking.

Chronic Obstructive Pulmonary Disease (COPD)

Irritation of the lungs can lead to asthma, emphysema, and chronic bronchitis. And, in fact, many people develop two or three of these together. This constellation is known as chronic obstructive pulmonary disease (COPD). Among the causes of COPD are

cigarette smoke (often) cystic fibrosis (rare)

Cystic fibrosis is a genetic disorder caused by inheriting two defective genes for the cystic fibrosis transmembrane conductance regulator (CFTR), a transmembrane protein needed for the transport of Cl and HCO3 ions through the plasma membrane of epithelial cells. Defective ion transport in the lung reduces the water content of the fluid in the lungs making it more viscous and difficult for the ciliated cells to move it up out of the lungs. Precisely how defective CFTR function produces this effect is still under investigation. In any case, the accumulation of mucus plugs the airways and provides a fertile breeding ground for pathogenic fungi and bacteria. All of this damages the airways interfering with breathing and causing a persistent cough. Cystic fibrosis is the most common inherited disease in the U.S. white population. Some mutations that cause cystic fibrosis.

Lung Cancer
Lung cancer is the most common cancer and the most common cause of cancer deaths in U.S. males. Although more women develop breast cancer than lung cancer, since 1987 U.S. women have been dying in larger numbers from lung cancer than from breast cancer. Link to lung cancer data. Lung cancer, like all cancer, is an uncontrolled proliferation of cells. There are several forms of lung cancer, but the most common (and most rapidly increasing) types are those involving the epithelial cells lining the bronchi and bronchioles.

Ordinarily, the lining of these airways consists of two layers of cells. Chronic exposure to irritants

causes the number of layers to increase. This is especially apt to happen at forks where the bronchioles branch. The ciliated and mucus-secreting cells disappear and are replaced by a disorganized mass of cells with abnormal nuclei. If the process continues, the growing mass penetrates the underlying basement membrane. Link to illustrations of the cellular changes in developing lung cancer.

At this point, malignant cells can break away and be carried in lymph and blood to other parts of the body where they may lodge and continue to proliferate. It is this metastasis of the primary tumor that eventually kills the patient.

Respiration (physiology)

Respiratory tract
In humans the respiratory tract is the part of the anatomy that has to do with the process of respiration. The respiratory tract is divided into 3 segments:

Upper respiratory tract: nose and nasal passages, paranasal sinuses, and throat or pharynx Respiratory airways: voice box or larynx, trachea, bronchi, and bronchioles

Lungs: respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli

The respiratory tract is a common site for infections. Upper respiratory tract infections are probably the most common infections in the world. Most of the respiratory tract exists merely as a piping system for air to travel in the lungs, and alveoli are the only part of the lung that exchanges oxygen and carbon dioxide with the blood. Moving down the respiratory tract starting at the trachea, the tubes get smaller and divide more and more. There are estimated to be about 20 to 23 divisions, ending up at an alveolus. Even though the cross-sectional area of each bronchus or bronchiole is smaller, because there are so many, the total surface area is larger. This means there is less resistance at the terminal bronchioles. (Most resistance is around the 3-4 division from the trachea due to turbulence.)

General histology
The respiratory tract is covered in an epithelium, the type of which varies down the tract. There are glands and mucus produced by goblet cells in parts, as well as smooth muscle, elastin or cartilage. Most of the epithelium (from the nose to the bronchi) is covered in pseudostratified columnar ciliated epithelial cells, commonly called respiratory epithelium. The cilia beat in one direction, moving mucus towards the throat where it is swallowed. Moving down the bronchioles, the cells get more cuboidal in shape but are still ciliated. Cartilage is present until the small bronchi. In the trachea they are C-shaped rings, whereas in the bronchi they are interspersed plates. Glands are abundant in the upper respiratory tract, but there are fewer lower down and they are absent from the bronchioles onwards. The same goes for goblet cells, although there are scattered ones in the first bronchioles. Smooth muscle starts in the trachea, where it joins the C-shaped rings of cartilage. It continues down the bronchi and bronchioles which it completely encircles. Instead of hard cartilage, the bronchi and bronchioles have a lot of elastic tissue. Summary: Upper respiratory tract - nose, pharynx & asscociates structures Lower respiratory tract - larynx, trachea, bronchi & lungs

In physiology, respiration (often mistaken with breathing) is defined as the transport of oxygen from the outside air to the cells within tissues, and the transport of carbon dioxide in the opposite

direction. This is in contrast to the biochemical definition of respiration, which refers to cellular respiration: the metabolic process by which an organism obtains energy by reacting oxygen with glucose to give water, carbon dioxide and ATP (energy). Although physiologic respiration is necessary to sustain cellular respiration and thus life in animals, the processes are distinct: cellular respiration takes place in individual cells of the animal, while physiologic respiration concerns the bulk flow and transport of metabolites between the organism and the external environment. In unicellular organisms, simple diffusion is sufficient for gas exchange: every cell is constantly bathed in the external environment, with only a short distance for gases to flow across. In contrast, complex multicellular animals such as humans have a much greater distance between the environment and their innermost cells, thus, a respiratory system is needed for effective gas exchange. The respiratory system works in concert with a circulatory system to carry gases to and from the tissues. In air-breathing vertebrates such as humans, respiration of oxygen includes four stages:

Ventilation, moving of the ambient air into and out of the alveoli of the lungs. Pulmonary gas exchange, exchange of gases between the alveoli and the pulmonary capillaries. Gas transport, movement of gases within the pulmonary capillaries through the circulation to the peripheral capillaries in the organs, and then a movement of gases back to the lungs along the same circulatory route.

Peripheral gas exchange, exchange of Oxygen consumption Organ gases between the tissue capillaries and (ml O2/min per 100g)[1] the tissues or organs, impacting the Heart (rest) 8 cells composing these and Heart (heavy exercise) 70 mitochondria within the cells. Brain 3 Kidney 5 Note that ventilation and gas transport require energy to power a mechanical Skin 0.2 pump (the heart) and the muscles of Resting skeletal muscle 1 respiration, mainly the diaphragm. In 50 heavy breathing, energy is also required to Contracting skeletal muscle power additional respiratory muscles such as the intercostal muscles. The energy requirement for ventilation and gas transport is in contrast to the passive diffusion taking place in the gas exchange steps. Respiratory behavior is correlated to the cardiovascular behavior to control the gaseous exchange between cells and blood. Both behaviors are intensified by exercise of the body. However, respiratory is highly voluntary compared to cardiovascular activity which is totally involuntary.

Classifications of respiration
There are several ways to classify the physiology of respiration:
By species

Aquatic respiration Aquatic respiration

From Wikipedia, the free encyclopedia Jump to: navigation, search

Sea slugs breath through a gill (or ctenidium)

Aquatic respiration is the process whereby an aquatic animal obtains oxygen from water.

Contents
[hide]

1 Respiratory systems o 1.1 Fish o 1.2 Molluscs o 1.3 Aquatic reptiles o 1.4 Amphibians o 1.5 Aquatic birds 2 Gills 3 Control of respiration

4 See also 5 Notes

Respiratory systems
Fish

In most fish respiration takes place through gills. Lungfish, however, possess one or two lungs. The labyrinth fish have developed a special organ that allows them to take advantage of the oxygen of the air, but is not a true lung.
Molluscs

Mollusks generally possess gills that allow exchange of oxygen from an aqueous environment into the circulatory system. These animals also possess a heart that pumps blood which contains hemocyaninine as its oxygen-capturing molecule. Hence, this respiratory system is similar to that of vertebrate fish. The respiratory system of gastropods can include either gills or a lung.
Aquatic reptiles

The anatomical structure of the lungs is less complex in reptiles than in mammals, with reptiles lacking the very extensive airway tree structure found in mammalian lungs. Gas exchange in reptiles still occurs in alveoli however, reptiles do not possess a diaphragm. Thus, breathing occurs via a change in the volume of the body cavity which is controlled by contraction of intercostal muscles in all reptiles except turtles. In turtles, contraction of specific pairs of flank muscles governs inspiration or expiration.[1] See also reptiles for more detailed descriptions of the respiratory system in these animals.
Amphibians

Both the lungs and the skin serve as respiratory organs in amphibians. The skin of these animals is highly vascularized and moist, with moisture maintained via secretion of mucus from specialized cells. While the lungs are of primary importance to breathing control, the skin's unique properties aid rapid gas exchange when amphibians are submerged in oxygen-rich water.[2]
Aquatic birds

The respiratory system of birds differs significantly from that found in mammals, containing unique anatomical features such as air sacs. The lungs of birds also do not have the capacity to inflate as birds lack a diaphragm and a pleural cavity. Gas exchange in birds occurs between air capillaries and blood capillaries, rather than in alveoli. See Avian respiratory system for a detailed description of these and other features.

Gills

Posterior view of the gills of a tuna

Large aquatic animals have developed gills for respiration which are specifically adapted to their function, for example, they have:

A large surface area to allow as much oxygen to enter the gills as possible due to the fact that more of the gas comes into contact with the membrane Good blood supply to maintain the concentration gradient needed Thin membrane to allow for a short diffusion pathway each gill arch has two rows (hemibranchs) of gill filaments each gill filament has many lamellae

In osteichthyes, the gills contain 4 gill arches on each side of the head, two on each side for chondrichthyes or 7 gill baskets on each side of the fish's head in Lampreys In fish, the long bony cover for the gill (the operculum) can be used for pushing water. Some fish pump water using the operculum. Without an operculum, other methods, such as ventilation, are required. Some species of sharks use this system. When they swim, water flows into the mouth and across the gills. Because these sharks rely on this technique, they must keep swimming in order to respire. Bony fish use countercurrent flow to maximize the intake of oxygen that can diffuse through the gill. Countercurrent flow occurs when deoxygenated blood moves through the gill in one direction while oxygenated water moves through the gill in the opposite direction. This mechanism maintains the concentration gradient thus increasing the efficiency of the respiration process as well and prevents the oxygen levels from reachin an equilibrium. Cartilaginous fish do not have a countercurrent flow system as they lack bones which are needed to have the opened out gill that bony fish have.

Control of respiration

Scientists have investigated what part of the body is responsible for maintaining the respiratory rhythm. They found that neurons located in the brainstem of fish are responsible for the genesis of the respiratory rhythm[3]. The position of these neurons is slightly different from the centers of respiratory genesis in mammals but they are located in the same brain compartment, which has caused debates about the homology of respiratory centers between aquatic and terrestrial species. In both aquatic and terrestrial respiration, the exact mechanisms by which neurons can generate this involuntary rhythm are still not completely understood (see Involuntary control of respiration). Another important feature of the respiratory rhythm is that it is modulated to adapt to the oxygen consumption of the body. As observed in mammals, fish breathe faster and heavier when they do physical exercise. The mechanisms by which these changes occur have been strongly debated over more than 100 years between scientists.[4] The authors can be classified in 2 schools: 1. Those who think that the major part of the respiratory changes are pre-programmed in the brain, which would imply that neurons from locomotion centers of the brain connect to respiratory centers in anticipation of movements. 2. Those who think that the major part of the respiratory changes result from the detection of muscle contraction, and that respiration is adapted as a consequence of muscular contraction and oxygen consumption. This would imply that the brain possesses some kind of detection mechanisms that would trigger a respiratory response when muscular contraction occurs. Many now agree that both mechanisms are probably present and complementary, or working alongside a mechanism that can detect changes in oxygen and/or carbon dioxide blood saturation.

Buccal pumping

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Buccal pumping
From Wikipedia, the free encyclopedia

Jump to: navigation, search Buccal pumping is a method of respiration in which the animal moves the floor of the mouth in a rhythmic manner that is externally apparent. This method has several stages. These will be described for an animal starting with lungs in a deflated state: First, the glottis (opening to the lungs) is closed, and the nostrils are opened. The floor of the mouth is then depressed (lowered), drawing air in. The nostrils are then closed, the

glottis opened, and the floor of mouth raised, forcing the air into the lungs for gas exchange. To deflate the lungs, the process is reversed. Gular pumping refers to the same process, but accomplished by expanding and contracting the entire throat to pump air, rather than just relying upon the mouth. This method of ventilation is inefficient, but is nonetheless used by all air-breathing amphibians and gular pumping is utilized to a varying extent by various reptile species[1]. Mammals, in contrast, use the thoracic diaphragm to inflate and deflate the lungs more directly.

References
1. ^ Owerkowicz, Tomasz; Colleen G. Farmer, James W. Hicks, Elizabeth L. Brainerd (4 June 1999). "Contribution of Gular Pumping to Lung Ventilation in Monitor Lizards". Science (www.sciencemag.org) 284 (5420): 16611663. doi:10.1126/science.284.5420.1661. PMID 10356394.

By mechanism

Respiratory organs (or breathing organs)

are used by most, or all, animals to exchange the gases necessary for their life function known as respiration. These organs come in many forms, some of them apparently having independently evolved:

skin some aquatic and small terrestrial animals (including some of the smallest spiders, earthworms and mites) can breathe simply by exchanging gas through the surface of their body gill many aquatic like fish, and a few smaller terrestrial, animals use gills to breathe. Even land animals can do this, as with isopods like the woodlice that probably can be found living under rocks in a yard. Gills are simply layers of tissue adapted specifically to gas exchange.

book lung Some spiders, scorpions, and other arthropods still use primitive book lungs, essentially gills adapted for land use, in their respiration. These are simply tissue with many wrinkles to increase their surface area. Branchiostegal lung - some crabs, coconut crabs in particular, use this gill-like lung Labyrinth organ A secondary breathing organ specific to the labyrinth fish, essentially an enclosed maze of tissue, evolved from a niche in their gill structure. Invertebrate trachea tubes evolved by many arthropods, possibly from book lungs, which simply lead directly into their bodies through holes called spiracles, where their internal organs generally absorb their own air. These can be very primitive, as with some spiders, or more complex, ending with specialized air sacs, as with many insects. lung The lung is made up of muscle tissues, the cells inside the lung which collect the oxygen in the air and pass it into the blood stream via veins and carbon dioxide passes out and that is breathing respiratory. diaphragm a layer of muscular membrane located at the bottom of the thoracic cavity which in responsible in adjusting the volume of the thoracic cavity.

by gas exchange
Gas exchange takes place at a respiratory surfacea boundary between the external environment and the interior of the organism. For unicellular organisms the respiratory surface is governed by Fick's law, which determines that respiratory surfaces must have:

a large surface area a thin permeable surface a moist exchange surface.

Many also have a mechanism to maximise the diffusion gradient by replenishing the source and/or sink. Control of respiration is due to rhythmical breathing generated by the phrenic nerve in order to stimulate contraction and relaxation of the diaphragm during inspiration and expiration. Ventilation is controlled by partial pressures of oxygen and carbon dioxide and the concentration of hydrogen ions. The control of respiration can vary in certain circumstances such as during exercise.

Gas exchange in humans and other mammals

In humans and mammals, respiratory gas exchange is carried out by mechanisms of the heart and lungs. Ventilation is the process of air movement into and out of the lungs. Once air enters the lungs, diffusion of O2 and CO2 occurs in the alveoli. The oxygenated blood is then perfused throughout the body where gas exchange occurs in the capillary beds.[1] The blood is subjected to a transient electric field (QRS waves of the EKG) in the heart, which dissociates molecules of

different charge. The blood, being a polar fluid, aligns dipoles with the electric field, is released, a then oscillates in a damped driven oscillation to form Y or Osborn Waves, V, U, and Y waves. The electric field exposure and subsequent damped driven oscillation dissociate gas from hemoglobin, primarily CO2, but more important, BPG, which has a higher affinity for hemoglobin than does oxygen, due in part to its opposite charge. Completely dissociated hemoglobin (which will even effervesce if the electric field is too strong the reason defibrillation joules are limited, to avoid bubble emboli that may clog vessels in the lung) enters the lung in red blood cells ready to be oxygenated. The primary force applied in the respiratory tract is supplied by atmospheric pressure. Total atmospheric pressure at sea level is 760 mmHg (101 kPa), with oxygen (O2) providing a partial pressure (pO2) of 160 mmHg (21 kPa), 21% by volume, at the entrance of the nares, a partial pressure of 150 mmHg (20 kPa) in the trachea due to the effect of partial pressure of water vapor, and an estimated pO2 of 100 mmHg (13 kPa) in the alveoli sac, pressure drop due to conduction loss as oxygen travels along the transport passageway. Atmospheric pressure decreases as altitude increases, making effective breathing more difficult at higher altitudes. Higher BPG levels in the blood are also seen at higher elevations, as well. In similar manner, CO2, which is a result of tissue cellular respiration, is also exchanged. The pCO2 changes from 45 to 40 mmHg (6.0 to 5.3 kPa) in the alveoli. The concentration of this gas in the breath can be measured using a capnograph. As a secondary measurement, respiration rate can be derived from a CO2 breath waveform. Gas exchange occurs only at pulmonary and systemic capillary beds, but anyone can perform simple experiments with electrodes in blood on the bench-top to observe electric field-stimulated effervescence. Trace gases present in breath at levels lower than a part per million are ammonia, acetone, isoprene. These can be measured using selected ion flow tube mass spectrometry.

Diffusion
Blood carries oxygen, carbon dioxide, and hydrogen ions between tissues and the lungs. The majority of CO2 transported in the blood is dissolved in plasma (primarily as dissolved bicarbonate; 60%). A smaller fraction is transported in red blood cells combined with the globin portion of haemoglobin as carbaminohaemoglobin. This is the chemical portion of the red blood cell that aids in the transport of oxygen and nutrients around the body, but, this time, it is carbon dioxide that is transported back to the lung. As CO2 diffuses into the blood stream, it is absorbed by red blood cells before the majority is converted into H2CO3 by carbonic anhydrase, an enzyme that is not present in the plasma. The H2CO3 dissociates into H+ and HCO 3. The HCO 3 moves out of the red blood cells in exchange for Cl (chloride shift). The hydrogen ions are removed by buffers in the blood (Hb).

By Arterial blood gas

An arterial blood gas (ABG) is a blood test that is performed using blood from an artery. It involves puncturing an artery with a thin needle and syringe and drawing a small volume of blood. The most common puncture site is the radial artery at the wrist, but sometimes the femoral artery in the groin or other sites are used. The blood can also be drawn from an arterial catheter. Pulse oximetry plus transcutaneous carbon dioxide measurement is an alternative method of obtaining similar information as well. An ABG is a test that measures the arterial oxygen tension (PaO2), carbon dioxide tension (PaCO2), and acidity (pH). In addition, arterial oxyhemoglobin saturation (SaO2) can be determined. Such information is vital when caring for patients with critical illness or respiratory disease. As a result, the ABG is one of the most common tests performed on patients in intensive care units (ICUs). The test is used to determine the pH of the blood, the partial pressure of carbon dioxide and oxygen, and the bicarbonate level. Many blood gas analyzers will also report concentrations of lactate, hemoglobin, several electrolytes, oxyhemoglobin, carboxyhemoglobin and methemoglobin. ABG testing is mainly used in pulmonology and critical care medicine, to determine gas exchange which reflect gas exchange across the alveolar-capillary membrane. ABG testing also has a variety of applications in other areas of medicine. Combinations of disorders can be complex and difficult to interpret, so calculators,[1] nomograms, and rules of thumb[2] are commonly used.

Sampling and analysis

Arterial blood for blood gas analysis is usually drawn by a respiratory therapist and sometimes a phlebotomist or nurse.[3] Blood is most commonly drawn from the radial artery because it is easily accessible, can be compressed to control bleeding, and has less risk for occlusion, the selection of which radial artery to draw from is based on the outcome of an Allen's test. The femoral artery (or less often, the brachial artery) is also used, especially during emergency situations or with children. Blood can also be taken from an arterial catheter already placed in one of these arteries. The syringe is pre-packaged and contains a small amount of heparin, to prevent coagulation or needs to be heparinised, by drawing up a small amount of heparin and squirting it out again. Once the sample is obtained, care is taken to eliminate visible gas bubbles, as these bubbles can dissolve into the sample and cause inaccurate results. The sealed syringe is taken to a blood gas analyzer. If the sample cannot be analyzed within 10-15 minutes, it must be placed on ice for valid results. Even when placed on ice, samples should still be analyzed within 1 hour. [4] Standard blood tests can also be performed on arterial blood, such as measuring glucose, lactate, hemoglobins, dys-haemoglobins, bilirubin and electrolytes.

Calculations

Blood gas analyzer

The machine used for analysis aspirates this blood from the syringe and measures the pH and the partial pressures of oxygen and carbon dioxide. The bicarbonate concentration is also calculated. These results are usually available for interpretation within five minutes. Two methods have been used in medicine in the management of blood gases of patients in hypothermia: pH-stat method and alpha-stat method. Recent studies suggest that the -stat method is superior.

pH-stat: the arterial carbon dioxide tension (paCO2) is maintained at 5.3 kPa (40 mmHg) and the pH is maintained at 7.40 when measured at the actual patient temperature. It is then necessary to add CO2 to the sample to calculate results. -stat (alpha-stat): the arterial carbon dioxide tension and the pH are maintained at 5.3 kPa (40mmHg) and 7.40 when measured at +37C. When a patient is cooled down, the pH-value will increase and the pCO2-value and the pO2-value will decrease with lowering of the temperature if measured at the patients temperature.

Both the pH-stat and alpha-stat strategies have theoretical disadvantages. -stat method is the method of choice for optimal myocardial function. The pH-stat method may result in loss of autoregulation in the brain (coupling of the cerebral blood flow with the metabolic rate in the brain). By increasing the cerebral blood flow beyond the metabolic requirements, the pH-stat method may lead to cerebral microembolisation and intracranial hypertension.[5]
Helpful Guidelines 1. A 1mmHg change in PaCO2 above or below 40 mmHg results in 0.008 unit change in pH in the opposite direction.[6] 2. The PaCO2 will decrease by about 1 mmHg for every 1 mEq/L reduction in [HCO3-] below 24 mEq/L 3. A change in [HCO3-] of 10 mEq/L will result in a change in pH of approximately 0.15 pH units in the same direction.

Reference ranges
These are typical reference ranges, although various analysers and laboratories may employ different ranges.
Analyte pH Range 7.357.45 Interpretation The pH or H+ indicates if a patient is acidemic (pH < 7.35; H+ >45) or alkalemic (pH > 7.45; H+ < 35).

H+

3545 nmol/L See above. (nM) A low PaO2 indicates that the patient is not oxygenating properly, and is 9.313.3 kPa hypoxemic. (Note that a low PaO2 is not required for the patient to have or 80100 hypoxemia.) At a PaO2 of less than 60 mm Hg, supplemental oxygen should be administered. At a PaO2 of less than 26 mmHg, the patient is at risk of mmHg death and must be oxygenated immediately.[citation needed] The carbon dioxide partial pressure (PaCO2) is an indicator of CO2 production and elimination: for a constant metabolic rate, the PaCO2 is determined entirely by its elimination through ventilation.[7] A high PaCO2 (respiratory acidosis, alternatively hypercapnia) indicates underventilation (or, more rarely, a hypermetabolic disorder), a low PaCO2 (respiratory alkalosis, alternatively hypocapnia) hyper- or overventilation. The HCO3 ion indicates whether a metabolic problem is present (such as ketoacidosis). A low HCO3 indicates metabolic acidosis, a high HCO3 indicates metabolic alkalosis. As this value when given with blood gas results is often calculated by the analyzer, correlation should be checked with total CO2 levels as directly measured (see below). the bicarbonate concentration in the blood at a CO2 of 5.33 kPa, full oxygen saturation and 37 Celsius.[8] The base excess is used for the assessment of the metabolic component of acid-base disorders, and indicates whether the patient has metabolic acidosis or metabolic alkalosis. Contrasted with the bicarbonate levels, the base excess is a calculated value intended to completely isolate the nonrespiratory portion of the pH change.[9] This is the total amount of CO2, and is the sum of HCO3 and PCO2 by the formula:

PaO2

PaCO2

4.76.0 kPa or 3545 mmHg

HCO3

2226 mmol/L

SBCe

21 to 27 mmol/L

Base excess

2 to +2 mmol/L

total CO2

25 to 30

(tCO2 (P)c) mmol/L

tCO2 = [HCO3] + *PCO2, where =0.226 mM/kPa, HCO3 is expressed in millimolar concentration (mM) (mmol/l) and PCO2 is expressed in kPa [10] This is the sum of oxygen dissolved in plasma and chemically bound to hemoglobin as determined by the calculation: CaO2 = (PaO2 * 0.003) + (SaO2 * 1.34 * Hgb) where hemoglobin concentration is expressed in g/dL.[11]

O2 Content vol% (mL (CaO2, CvO2, oxygen/dL CcO2) blood)

Contamination of the sample with room air will result in abnormally low carbon dioxide and possibly elevated oxygen levels, and a concurrent elevation in pH. Delaying analysis (without chilling the sample) may result in inaccurately low oxygen and high carbon dioxide levels as a result of ongoing cellular respiration.

By Control of respiration
Control of ventilation refers to the physiological mechanisms involved in the control of physiologic ventilation. Gas exchange primarily controls the rate of respiration. The most important function of breathing is gas exchange (of oxygen and carbon dioxide). Thus the control of respiration is centered primarily on how well this is achieved by the lungs. There are four main centers in the brain to regulate the respiration: 1. Inspiratory center 2. Expiratory center 3. Pneumotaxic center 4. Apneustic center The first two centers are present on the medulla oblongata whereas the last two centers on the pons region of brain.

Ventilatory Pattern
The pattern of motor stimuli during breathing can be divided into inspiratory and expiratory phases. Inspiration shows a sudden, ramped increase in motor discharge to the inspiratory muscles (including pharyngeal dilator muscles). Before the end of inspiration, there is a decline in motor discharge. Exhalation is usually silent, except at high minute ventilation rates. The mechanism of generation of the ventilatory pattern is not completely understood, but involves the integration of neural signals by respiratory control centers in the medulla and pons. The nuclei known to be involved are divided into regions known as the following:

medulla (reticular formation) o ventral respiratory group (nucleus retroambigualis, nucleus ambigus, nucleus parambigualis and the pre-Botzinger complex). The ventral respiratory group controls voluntary forced exhalation and acts to increase the force of inspiration.

dorsal respiratory group (nucleus tractus solitarius). The dorsal respiratory group controls mostly inspiratory movements and their timing. pons o pneumotaxic center. Coordinates transition between inhalation and exhalation Sends inhibitory impulses to the inspiratory area The pneumotaxic center is involved in fine tuning of respiration rate. o apneustic center Coordinates transition between inhalation and exhalation Sends stimulatory impulses to the inspiratory area activates and prolongs inhalation (long deep breaths) overridden by pneumotaxic control from the apneustic area to end inspiration

There is further integration in the anterior horn cells of the spinal cord.

Control of ventilatory pattern

Ventilation is normally controlled by the autonomic nervous system, with only limited voluntary override. An exception to this is Ondine's curse, where autonomic control is lost.

Determinants of ventilatory rate

Ventilatory rate (minute volume) is tightly controlled and determined primarily by blood levels of carbon dioxide as determined by metabolic rate. Blood levels of oxygen become important in hypoxia. These levels are sensed by chemoreceptors in the medulla oblongata for pH, and the carotid and aortic bodies for oxygen and carbon dioxide. Afferent neurons from the carotid bodies and aortic bodies are via the glossopharyngeal nerve (CN IX) and the vagus nerve (CN X), respectively. Levels of CO2 rise in the blood when the metabolic use of O2 is increased beyond the capacity of the lungs to expel CO2. CO2 is stored largely in the blood as bicarbonate (HCO3-) ions, by conversion first to carbonic acid (H2CO3), by the enzyme carbonic anhydrase, and then by disassociation of this acid to H+ and HCO3-. Build-up of CO2 therefore causes an equivalent build-up of the disassociated hydrogen ion, which, by definition, decreases the pH of the blood. During moderate exercise, ventilation increases in proportion to metabolic production of carbon dioxide. During strenuous exercise, ventilation increases more than needed to compensate for carbon dioxide production. Lactate produced during anaerobic metabolism lowers pH and thus increases breathing. In aerobic metabolism, one molecule of acid (CO2) is produced in order to produce 6 molecules of the energy carrier ATP, whereas in anaerobic metabolism, 6 molecules of lactate are produced to provide the same amount of energy. Mechanical stimulation of the lungs can trigger certain reflexes as discovered in animal studies. In humans, these seem to be more important in neonates and ventilated patients, but of little

relevance in health. The tone of respiratory muscle is believed to be modulated by muscle spindles via a reflex arc involving the spinal cord. Drugs can greatly influence the control of respiration. Opioids and anaesthetic drugs tend to depress ventilation, especially with regards to Carbon Dioxide response. Stimulants such as Amphetamines can cause hyperventilation. Pregnancy tends to increase ventilation (lowering plasma carbon dioxide tension below normal values). This is due to increased progesterone levels and results in enhanced gas exchange in the placenta. Ventilation is temporarily modified by voluntary acts and complex reflexes such as sneezing, coughing and vomiting.

Feedback control
Receptors play important roles in the regulation of respiration; central and peripheral chemoreceptors, and mechanoreceptors.

Central chemoreceptors of the central nervous system, located on the ventrolateral medullary surface, are sensitive to the pH of their environment.[1][2] Peripheral chemoreceptors act most importantly to detect variation of the oxygen in the arterial blood, in addition to detecting arterial carbon dioxide and pH. Mechanoreceptors are located in the airways and parenchyma, and are responsible for a variety of reflex responses. These include: o The Hering-Breuer reflex that terminates inspiration to prevent over inflation of the lungs, and the reflex responses of coughing, airway constriction, and hyperventilation. o The upper airway receptors are responsible for reflex responses such as, sneezing, coughing, closure of glottis, and hiccups. o The spinal cord reflex responses include the activation of additional respiratory muscles as compensation, gasping response, hypoventilation, and an increase in breathing frequency and volume. o The nasopulmonary and nasothoracic reflexes regulate the mechanism of breathing through deepening the inhale. Triggered by the flow of the air, the pressure of the air in the nose, and the quality of the air, impulses from the nasal mucosa are transmitted by the trigeminal nerve to the breathing centres in the brainstem, and the generated response is transmitted to the bronchi, the intercostal muscles and the diaphragm.

In addition to involuntary control of respiration by the respiratory center, respiration can be affected by conditions such as emotional state, via input from the limbic system, or temperature, via the hypothalamus. Voluntary control of respiration is provided via the cerebral cortex, although chemoreceptor reflex is capable of overriding conscious control

By apnea
Apnea, apnoea, or apna (Greek: , from -, privative, , to breathe) is a term for suspension of external breathing. During apnea there is no movement of the muscles of respiration and the volume of the lungs initially remains unchanged. Depending on the patency of the airways there may or may not be a flow of gas between the lungs and the environment; gas exchange within the lungs and cellular respiration is not affected.

Causes
Apnea can be voluntarily achieved (e.g., "holding one's breath"), drug-induced (e.g., opiate toxicity), mechanically induced (e.g., strangulation or choking), or it can occur as a consequence of neurological disease or trauma. Voluntary apnea can be achieved by closing the vocal cords, simultaneously keeping the mouth closed and blocking the nasal vestibule, or constantly activating expiratory muscles.

Complications
Under normal conditions, humans cannot store much oxygen in the body. Prolonged apnea leads to severe lack of oxygen in the blood circulation. Permanent brain damage can occur after as little as three minutes and death will inevitably ensue after a few more minutes unless ventilation is restored. However, under special circumstances such as hypothermia, hyperbaric oxygenation, apneic oxygenation (see below), or extracorporeal membrane oxygenation, much longer periods of apnea may be tolerated without severe consequences. Untrained humans cannot sustain voluntary apnea for more than one or two minutes[citation needed]. The reason for the time limit of voluntary apnea is that the rate of breathing and the volume of each breath are tightly regulated to maintain constant values of CO2 tension and pH of the blood. In apnea, CO2 is not removed through the lungs and accumulates in the blood. The consequent rise in CO2 tension and drop in pH result in stimulation of the respiratory centre in the brain which eventually cannot be overcome voluntarily. When a person is immersed in water, physiological changes due to the mammalian diving reflex enable somewhat longer tolerance of apnea even in untrained persons. Tolerance can in addition be trained. The ancient technique of free-diving requires breath-holding, and world-class freedivers can hold their breath underwater up to depths of 214 metres and for more than four minutes.[1] Apneists, in this context, are people who can hold their breath for a long time.

Hyperventilation

Voluntary hyperventilation before beginning voluntary apnea is commonly (and falsely) believed to allow the person involved to hold their breath for a longer period. Some have incorrectly attributed this effect to increased oxygen in the blood, not realizing that it is actually due to a decrease in CO2 in the blood and lungs. Blood leaving the lungs is normally fully saturated with oxygen, so hyperventilation of normal air cannot increase the amount of oxygen available. Lowering the CO2 concentration increases the time before the respiratory center becomes stimulated, as described above. This error has led some people to use hyperventilation as a means to increase their diving time, not realizing that there is a danger that their body may exhaust its oxygen while underwater, before they feel any urge to breathe, and that they can suddenly lose consciousnessa shallow water blackoutas a result. If a person loses consciousness underwater, especially in fresh water, there is a considerable danger that they will drown. An alert diving partner would be in the best position to rescue such a person.

Apneic oxygenation
Because the exchange of gases between the blood and airspace of the lungs is independent of the movement of gas to and from the lungs, enough oxygen can be delivered to the circulation even if a person is apneic. This phenomenon (apneic oxygenation) is explained as follows: With the onset of apnea, an underpressure develops in the airspace of the lungs, because more oxygen is absorbed than CO2 is released. With the airways closed or obstructed, this will lead to a gradual collapse of the lungs. However, if the airways are patent (open), any gas supplied to the upper airways will follow the pressure gradient and flow into the lungs to replace the oxygen consumed. If pure oxygen is supplied, this process will serve to replenish the oxygen stores in the lungs. The uptake of oxygen into the blood will then remain at the usual level and the normal functioning of the organs will not be affected. However, no CO2 is removed during apnea. The partial pressure of CO2 in the airspace of the lungs will quickly equilibrate with that of the blood. As the blood is loaded with CO2 from the metabolism, more and more CO2 will accumulate and eventually displace oxygen and other gases from the airspace. CO2 will also accumulate in the tissues of the body, resulting in respiratory acidosis. Under ideal conditions (i.e., if pure oxygen is breathed before onset of apnea to remove all nitrogen from the lungs, and pure oxygen is insufflated), apneic oxygenation could theoretically be sufficient to provide enough oxygen for survival of more than one hour's duration in a healthy adult.[citation needed] However, accumulation of carbon dioxide (described above) would remain the limiting factor. Apneic oxygenation is more than a physiologic curiosity. It can be employed to provide a sufficient amount of oxygen in thoracic surgery when apnea cannot be avoided, and during manipulations of the airways such as bronchoscopy, intubation, and surgery of the upper airways. However, because of the limitations described above, apneic oxygenation is inferior to

extracorporal circulation using a heart-lung machine and is therefore used only in emergencies and for short procedures. In 1959, Frumin described the use of apneic oxygenation during anesthesia and surgery. Of the eight test subjects in this landmark study, the highest recorded PaCO2 was 250 millimeters of mercury, and the lowest arterial pH was 6.72 after 53 minutes of apnea.[2]

Apnea test in determining brain death

A recommended practice for the clinical diagnosis of brain death formulated by the American Academy of Neurology hinges on the conjunction of three diagnostic criteria: coma, absence of brainstem reflexes, and apnea (defined as the inability of the patient to breathe unaided, that is, with no life support systems). The apnea test follows a delineated protocol.[3]

By experiments

Huff and puff apparatus The huff and puff apparatus is used in school biology labs to demonstrate that carbon dioxide is a product of respiration. A pupil breathes in and out of the middle tube. The glass tubing is arranged in such a way that one flask bubbles as the pupils breathes in, the other as the pupil breathes out. A suitable carbon dioxide indicator, such as lime water or bicarbonate indicator shows the increased presence of carbon dioxide in the outgoing breath.This turns the bicarbonate into milky white

substance Spirometry

Selected ion flow tube mass spectrometry

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Selected-ion flow-tube mass spectrometry

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Picture of SIFT-MS profile 3.

Selected ion flow tube mass spectrometry, SIFT-MS, is a quantitative mass spectrometry technique for trace gas analysis which involves the chemical ionization of trace volatile compounds by selected positive precursor ions during a well-defined time period along a flow tube. Absolute concentrations of trace compounds present in air, breath or the headspace of bottled liquid samples can be calculated in real time from ratio of the precursor and product ion signal ratios, without the need for sample preparation or calibration with standard mixtures. The instrument is an extension of the selected ion flow tube, SIFT, technique, which was first described in 1976 by Adams and Smith[1]. It is a fast flow tube/ion swarm method to react positive or negative ions with atoms and molecules under truly thermalised conditions over a wide range of temperatures. It has been used extensively to study ionmolecule reaction kinetics. Its application to ionospheric and interstellar ion chemistry over a 20-year period has been crucial to the advancement and understanding of these interesting topics. SIFT-MS was initially developed for use in human breath analysis, and has shown great promise as a non-invasive tool for physiological monitoring and disease diagnosis. It has

since shown potential for use across a wide variety of fields, particularly in the life sciences, such as agriculture and animal husbandry, environmental research and food technology.

[edit] Instrumentation
In the selected ion flow tube mass spectrometer, SIFT-MS, ions are generated in a microwave plasma ion source, usually from a mixture of laboratory air and water vapor. From the formed plasma, a single ionic species is selected using a quadrupole mass filter to act as "precursor ions" (also frequently referred to as primary or reagent ions in SIFTMS and other processes involving chemical ionization). In SIFT-MS analyses, H3O+, NO+ and O2+ are used as precursor ions, and these have been chosen because they are known not to react significantly with the major components of air (nitrogen, oxygen etc.), but can react with many of the very low level (trace) gases. The selected precursor ions are injected into a flowing carrier gas (usually helium at a pressure of 1 Torr) via a Venturi orifice (~1 mm diameter) where they travel along the reaction flow tube by convection. Concurrently, the neutral analyte molecules of a sample vapor enter the flow tube, via a heated sampling tube, where they meet the precursor ions and may undergo chemical ionization, depending on their chemical properties, such as their proton affinity or ionization energy. The newly formed "product ions" flow into the mass spectrometer chamber, which contains a second quadrupole mass filter, and an electron multiplier detector, which are used to separate the ions by their mass-to-charge ratios, m/z, and measure the count rates of the ions in the desired m/z range.

[edit] Analysis
The concentrations of individual compounds can be derived largely using the count rates of the precursor and product ions, and the reaction rate coefficients, k. Exothermic proton transfer reactions with H3O+ are assumed to proceed at the collisional rate (see Collision Theory), the coefficient for which, kc, is calculable using the method described by Su and Chesnavich[2], providing the polarizability and dipole moment are known for the reactant molecule. NO+ and O2+ reactions proceed at kc less frequently, and thus the reaction rates of the reactant molecule with these precursor ions must often be derived experimentally by comparing the decline in the count rates of each of the NO+ and O2+ precursor precursor ions to that of H3O+ as the sample flow of reactant molecules is increased[3]. The product ions and rate coefficients have been derived in this way for well over 200 volatile compounds, which can be found in the scientific literature. The instrument can be programmed either to scan across a range of masses to produce a mass spectrum (Full Scan, FS, mode), or to rapidly switch between only the m/z values of interest (Multiple Ion Monitoring, MIM, mode). Due to the different chemical properties of the aforementioned precursor ions (H3O+, NO+, and O2+), different FS mode spectra can be produced for a vapor sample, and these can give different information relating to the composition of the sample. Using this information, it is often possible to identify the trace compound(s) that are present. The MIM mode, on the other hand will usually employ a much longer dwell time on each ion, and as a result, accurate quantification is possible to the parts-per-billion, ppb, level[3]. It is an important point that the reactions of the chosen precursor ions, H3O+, NO+, and O2+, with the trace analyte molecules occur at relatively low energies (compared to hard

forms of ionization, such as electron bombardment), and therefore tend to cause relatively little fragmentation. This greatly simplifies the resulting spectra and thereby facilitates the analysis of complex mixtures of gases, such as human breath. Another key feature of SIFT-MS is the upstream mass quadrupole, which allows the use of multiple precursor ions. On the one hand, this means that the precursor ion counts can be limited, compared to say PTR-MS, which has no upstream quadrupole, and as a result is capable of sensitivities to parts-per-trillion, ppt, levels, as opposed to the ppb levels that are possible with SIFT-MS. However, the ability to use three precursor ions, H3O+, NO+ and O2+, to obtain three different spectra is extremely valuable because it allows the operator to analyse a much wider variety of compounds. An example of this is methane, which cannot be analysed using H3O+ as a precursor ion (because it has a proton affinity of 543.5kJ/mol, somewhat less than that of H2O), but can be analysed using O2+[4]. Furthermore, the parallel use of three precursor ions may allow the operator to distinguish between two or more compounds that react to produce ions of the same mass-to-charge ratio in certain spectra. For example, dimethyl sulphide (C2H6S, 62amu) accepts a proton when it reacts with H3O+ to generate C2H7S+ product ions which appear at m/z 63 in the resulting spectrum. This may conflict with other product ions, such as the association product from the reaction with carbon dioxide, H3O+CO2, and the single hydrate of the protonated acetaldehyde ion, C2H5O+(H2O), which also appear at m/z 63, and so it may be unidentifiable in certain samples. However dimethyl sulfide reacts with NO+ by charge transfer, to produce the ion C2H6S+, which appears at m/z 62 in resulting spectra, whereas carbon dioxide does not react with NO+, and acetaldehyde donates a hydride ion, giving a single product ion at m/z 43, C2H3O+, and so dimethyl sulfide can be easily distinguished.

Bell Jar Model Lung School Science/Bell jar model lung

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Bell jar model lung

This simple Bell jar model lung can be used to demonstrate the basic principles of breathing. The model should be assembled as in the diagram. A swimming cap makes a suitable diaphragm. The cap can be attached to the bottom of the bell jar, and the balloons can be attached to the Y shaped tube, with elastic bands or plastic coated wire.

Contents
[hide]

1 How the Model Works 2 More Advanced Models 3 References 4 See Also

[edit] How the Model Works

The cavity inside the bell jar is airtight

As the diaphragm is pulled down, the volume of the cavity increases. This causes the pressure to fall. Air rushes in to equalise the pressure causing the balloons to inflate:). As the diaphragm is pushed up, the volume of the cavity decreases, the pressure rises, and the air rushes out of the balloons causing them to deflate. This is a great project for classes studying health or for those students learning fluids in science.

[edit] More Advanced Models

To more accurately render the anatomical and physiological properties of the lung, where the intrapleural space is filled with aqueous fluid you might want to replace the air in the bell jar with water. By filling the intrapleural space with water the model becomes a little bit more responsive, because of the incompressibility of water in contrast to air. Additionally preloading the balloons by removing water also better assures their automatic return to the exhaled position. A good introduction and overview is given by an article by T. Sherman in Advances in Physiological Education. [1]

Sudden Infant Death Syndrome infant death syndrome

From Wikipedia, the free encyclopedia (Redirected from Sudden Infant Death Syndrome) Jump to: navigation, search

Sudden

This article's lead section may not adequately summarize its contents. Please consider expanding the lead to provide an accessible overview of the article's key points. (July 2011)

Sudden infant death syndrome

Classification and external resources

ICD-10

R95.

ICD-9

798.0

OMIM

272120

DiseasesDB

12633

eMedicine

emerg/406 ped/2171

MeSH

D013398

Sudden infant death syndrome (SIDS) is marked by the sudden death of an infant that is unexpected by medical history, and remains unexplained after a thorough forensic autopsy and a detailed death scene investigation. An infant is at the highest risk for SIDS during sleep, which is why it is sometimes referred to by the terms cot death or crib death. The cause of SIDS is unknown, but characteristics associated with the syndrome have been identified. One of these characteristics is sleeping in the prone position. There are many risk factors and medical causal relationships associated with SIDS. Infants exposed to tobacco smoke are at risk. Infanticide and child abuse cases are misdiagnosed as SIDS due to lack of evidence.[1][2] Accidental suffocations are sometimes misdiagnosed as SIDS.[citation needed] Genetics play a role, as SIDS is more prevalent in males.[3][4] Safe sleep environments that reduce the risk of SIDS include proper ventilation, and putting infants on their back to sleep.[5] Pacifiers and tummy time can help reduce known risk factors.[6]

Contents
[hide]

1 Definition 2 Risk factors o 2.1 Before birth o 2.2 After birth 3 Hypotheses o 3.1 Bacterial Infections o 3.2 Bed Sharing o 3.3 Brain disorders o 3.4 Central respiratory pattern deficiency o 3.5 Cervical spinal injury from birth trauma o 3.6 Child abuse o 3.7 Genetics o 3.8 Inner ear damage o 3.9 Nitrogen dioxide o 3.10 Toxic gases o 3.11 Vaccination o 3.12 Vitamin C 4 Differential diagnosis 5 Prevention o 5.1 Air circulation with fan use o 5.2 Bedding o 5.3 Breastfeeding o 5.4 Bumper pads o 5.5 Concerns regarding recommendations o 5.6 Pacifiers

5.7 Secondhand smoke reduction 5.8 Sleep positioning 5.9 Sleep sacks 6 Epidemiology 7 References 8 Further reading 9 External links

o o o

[edit] Definition
Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.[7] SIDS is a diagnosis of exclusion. It should only be applied to an infant whose death is sudden and unexpected and remains unexplained after the performance of an adequate postmortem investigation including:
1. an autopsy (by an experienced pediatric pathologist, if possible); 2. investigation of the death scene and circumstances of the death; 3. exploration of the medical history of the infant and family.

Australia and New Zealand are shifting to the term "sudden unexplained death in infancy" (SUDI) for professional, scientific and coronial clarity. The term SUDI is now often used instead of sudden infant death syndrome (SIDS) because some coroners prefer to use the term 'undetermined' for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data.[8] In addition, the U.S. Centers for Disease Control and Prevention (CDC) has recently suggested that such deaths be called "sudden unexpected infant deaths" (SUID) and that SIDS is a subset of SUID.[9]

[edit] Risk factors

The cause of SIDS is unknown. Although studies have identified risk factors for SIDS, such as putting infants to bed on their stomachs, there has been little understanding of the syndrome's biological cause or potential causes. The frequency of SIDS appears to be a strong function of the infant's sex, age and ethnicity, and the education and socio-economic-status of the infant's parents. Listed below are several risk factors associated with increased probability of the syndrome.

[edit] Before birth

teenage mother (SIDS rates decrease with increasing maternal age)[10] lack of prenatal care (SIDS rates increase with increasing delay in starting pre-natal care)[10] exposure to nicotine by maternal smoking (SIDS rates are higher for infants of mothers who smoke during pregnancy)[10][11]

[edit] After birth

mold (can cause bleeding lungs plus a variety of other uncommon conditions leading to a misdiagnosis and death). It is often misdiagnosed as a virus, flu, and/or asthma-like conditions.[12] low birth weight (in the US from 1995-1998 the rate for 1000-1499 g was 2.89/1000 and for 35003999 g it was 0.51/1000)[13][14] exposure to tobacco smoke[15] prone sleep position (lying on the stomach, see sleep positioning below)[16][17] not breastfeeding[18] elevated or reduced room temperature[19] excess bedding, clothing, soft sleep surface and stuffed animals[20] co-sleeping with parents or other siblings may increase risk for SIDS, but the mechanism remains unclear[21] infant's age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)[22] premature birth (increases risk of SIDS death by about 4 times.[10][13] In 1995-1998 the US SIDS rate for 3739 weeks of gestation was 0.73/1000; The SIDS rate for 2831 weeks of gestation was 2.39/1000)[13] anemia[23] [NB: per item 6 in the list of epidemiologic characteristics below, extent of anemia cannot be evaluated at autopsy because "total hemoglobin can only be measured in living infants.[24]"

[edit] Hypotheses
[edit] Bacterial Infections

In a British study released May 29, 2008 researchers discovered that the common bacterial infections Staphylococcus aureus (staph) and Escherichia coli (E. coli) appear to be a risk factor in some cases of SIDS. Both bacteria were present at greater-than-usual concentrations in infants who died from SIDS.[25] SIDS cases peak between eight and ten weeks after birth, which is also the time frame in which the antibodies that were passed along from mother to child are starting to disappear and babies have not yet made their own antibodies.
[edit] Bed Sharing

A 2005 policy statement by the American Academy of Pediatrics on sleep environment and the risk of SIDS deemed co-sleeping and bed sharing unsafe.[26] One article reports that co-sleeping infants have a greater risk of airway covering than when the same infant sleeps alone in a cot, but came to the conclusion that "Although numerous authors have suggested that bed-sharing infants

face risks because of airway covering by bed-clothes or parental bodies, the present trial does not lend support to this hypothesis".[27]
[edit] Brain disorders

According to a JAMA 2006 study some babies who die of SIDS have abnormalities in the brain stem (the medulla oblongata) of underdevelopment of receptors for serotonin, which help control functions like breathing, blood pressure and arousal, and abnormalities in serotonin signaling. According to the National Institutes of Health, this finding was the strongest evidence at that time that structural differences in a specific part of the brain may contribute to the risk of SIDS.[28] This abnormality can continue postpartum until the end of the first year. This could account for there being few SIDS deaths after the first year of infancy and the reason the risk is greater for premature infants. The authors noted that males have fewer serotonin receptors than females, perhaps contributing to the increased incidence of SIDS in males, but their follow-up 2010 paper failed to reconfirm that gender difference.[29] Another 2006 study showed that a possible cause of SIDS is because parents leave their infants in a position known as the Trendelenburg position.[30] This position can cause the brain stem to fall, and in a result, the brain becomes "crushed". The proper position for an infant is either Fowler's position or Sims'.[citation needed] A 2010 study suggests Interleukin-2, a neuromodulator, as the potential mechanism. Intense neuronal IL-2 immune-reactivity in the SIDS brainstem was found, which could be responsible for decreased cardiorespiratory and arousal responses.[31]
[edit] Central respiratory pattern deficiency

There is ongoing research in the pediatric/neonatal community that has begun to associate apnealike breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits including the pre-Btzinger complex.[32]
[edit] Cervical spinal injury from birth trauma

During birth, if the infant's head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brain-stem injury.[33] When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomach for sleep, they are forced to turn their head to the side to breathe.
[edit] Child abuse

Several instances of infanticide have been uncovered where the diagnosis was originally SIDS.[34][35] This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides.[36][37][38][39] In 1997 The New York Times, covering a book called The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:

The misdiagnosis of infanticide as SIDS "happens all over," Ms. Talan, a medical reporter at Newsday, said. "A lot of doctors and police don't know how to handle it. They don't take it as seriously as they should." As a result of the book's revelations, people are starting to scrutinize possible cases of this "perfect crime," which involves no physical evidence and no witnesses.[40] A pediatrician, Roy Meadow, from the UK believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent. During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of homicide to various extents, on the basis of Meadow's opinion. In 2003 a number of high-profile acquittals brought Meadow's theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being re-opened and convictions overturned. Meadow was struck off in 2005.[41]Meadow appealed to the High Court, which ruled in his favour in February 2006. The GMC appealed to the Court of Appeal and in October 2006 by a majority decision, with the Master of the Rolls, Sir Anthony Clarke, dissenting, the Court of Appeal upheld the decision of the High Court in part ruling that Meadow's misconduct was not sufficiently serious to merit the punishment which he had received. The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.[42]
[edit] Genetics

There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate (105 male to 100 female live births) there appear to be 3.15 male SIDS per 2 female SIDS for a male fraction of 0.61.[43][44] This value of 61% in the US is an average of 57% black male SIDS, 62.2% white male SIDS and 59.4% for all other races combined. Note that when multiracial parentage is involved, infant "race" is arbitrarily assigned to one category or the other; most often it is chosen by the mother. The X-linkage hypothesis for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele that occurs with a frequency of 13 that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of 23 and an unprotected XX female would occur with a frequency of 49. The ratio of 23 to 49 is 1.5 to 1 which matches the observed male 50% excess rate of SIDS. Although many authors have found autosomal and mitochondrial genetic risk factors for SIDS they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence for an X-linkage is found by examination of other causes of infant respiratory death, such as suffocation by inhalation of food and other foreign objects. Although food is prepared identically for male and female infants, there is a similar 50% male excess of death from such causes indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS.[45][original
research?]

The JAMA 2006 study which indicated that there was a relationship between fewer serotonin binding sites and SIDS noted that the boys "had significantly fewer serotonin binding sites than girls",[28] but the authors could not reproduce it in their 2010 paper.[29] However, such

neurological prematurity decreases with age, but the male fraction of approximately 0.61 persists each month throughout the first year of life.[46] Furthermore, this cannot explain the identical male fraction of 0.61 in other respiratory mortality causes such as respiratory distress syndrome or suffocation from inhalation of food or foreign objects cited above, that also exists for all ages 1 to 14 years in the US from 1979 to 2005.[13][original research?]
[edit] Inner ear damage

Records of hearing tests (oto-acoustic emissions, OAEs) administered to certain infants show that those who later died of SIDS had differences in the pattern of these tests compared with normal babies. To be specific the OAE signal to noise ratio was reduced in the right ear in the SIDS babies (Rubens DD et al. Early Human Development 84, 225-9 (2008)).[47] It should be noted this was a small study (n=31 cases and 31 controls), had serious limitations (several significant factors were not controlled), and has been criticised from various perspectives.[48] The authors' suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (other than suffocation). The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep. It is speculated that this inner ear damage could be linked to SIDS. It is speculated that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the "line of fire" for blood entering the fetus from the placenta, and thus could be most susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.[49]
[edit] Nitrogen dioxide

A 2005 study by researchers at the University of California, San Diego found that "SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life."[50] While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.
[edit] Toxic gases

In 1989, a controversial piece of research by UK Scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.[citation needed] Support for this hypothesis was based on the observation that the risk of cot death rises from one sibling to the next.[citation needed] Richardson claimed that parents are more likely to buy new bedding for their first child, and to re-use that bedding for later children. The more frequently used the bedding is, the more chance there will be that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair[51] references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing and suggests that this is still inconclusive.

Dr. Jim Sprott recommends new parents either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.[52] However, a final report of "The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis", published in May 1998, concluded that "there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants."[53] The report also states that "in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses" and "babies have also been found to die on wrapped mattresses." According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed: In February 2000 Dr Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.[54]
[edit] Vaccination

Vaccination does not increase the risk of SIDS, and may reduce the risk slightly.[55][56] According to the US Centers for Disease Control and Prevention: From 2 to 4 months old, babies begin their primary course of routine vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.[56]
[edit] Vitamin C

In the 1970s, high doses of vitamin C were touted as a preventive measure for SIDS,[57] although the claim was controversial even then.[58][59] Subsequent studies failed to support a preventive role for vitamin C in SIDS.[60] To the contrary, a 2009 study found that high levels of vitamin C were strongly associated with SIDS, possibly through a pro-oxidant interaction with iron.[61]

[edit] Differential diagnosis

Some conditions that may be undiagnosed and thus could be alternative diagnoses to SIDS include:

medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency)[62]

infant botulism[63] long QT syndrome (accounting for less than 2% of cases)[64] infections with the bacterium Helicobacter pylori[65] shaken baby syndrome and other forms of child abuse[66][67] overlying[68]

For example an infant with MCAD deficiency could have died by "classical SIDS" if found swaddled and prone with head covered in an overheated room where parents were smoking. Genes of susceptibility to MCAD and Long QT syndrome do not protect an infant from dying of classical SIDS. Therefore presence of a susceptibility gene, such as for MCAD, means the infant may have died either from SIDS or from MCAD deficiency. It is impossible for the pathologist to distinguish between them. A 2010 study looked at 554 autopsies of infants in North Carolina that listed SIDS as the cause of death and suggested that many of these deaths may have been due to accidental suffocation. The study found that 69% of autopsies listed other possible risk factors that could lead to death such us unsafe bedding or sleeping with adults.[69]

[edit] Prevention
[edit] Air circulation with fan use See also: Fan death

According to a study of nearly 500 babies published in the October 2008 Archives of Pediatrics & Adolescent Medicine, using a fan to circulate air correlates with a lower risk of sudden infant death syndrome. This is plausible because a prone sleeping baby with nose to the sleeping surface could rebreathe some of its exhaled breath which is enriched in CO2 and depleted in oxygen. A fan could increase the mixing of the exhalation into the room air and lessen the risk of SIDS related to infant hypoxia. Researchers took into account other risk factors and found that fan use was associated with a 72% lower risk of SIDS. Only 3% of the babies who died had a fan on in the room during their last sleep, the mothers reported. That compared to 12% of the babies who lived. Using a fan reduced risk most for babies in poor sleeping environments.[70] Author De-Kun li said that "the baby's sleeping environment really matters" and that "this seems to suggest that by improving room ventilation we can further reduce risk."[71] However, Dr. John Olssen at East Carolina University has pointed out that this study had a number of methodological flaws, such as selection and recall bias, low enrollment numbers, and dissimilar study groups. Olssen argues that although fan use is probably not harmful, it should not be recommended as a means to reduce the risk of SIDS.[72]
[edit] Bedding

Product safety experts advise against using pillows, sleep positioners, bumper pads, stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib "naked."[73][74]

Blankets should not be placed over an infant's head.[75] It has been recommended that infants should be covered only up to their chest with their arms exposed. This reduces the chance of the infant shifting the blanket over his or her head.
[edit] Breastfeeding

A 2003 study published in Pediatrics, which investigated racial disparities in infant mortality in Chicago, found that previously or currently breastfeeding infants in the study had 1/5 the rate of SIDS compared with non-breastfed infants, but that "it became nonsignificant in the multivariate model that included the other environmental factors". These results are consistent with most published reports and suggest that other factors associated with breastfeeding, rather than breastfeeding itself, are protective."[76] A single more recent study claims to show a significantly reduced incidence of SIDS in breastfed infants.[77]
[edit] Bumper pads

Bumper pads may be a contributing factor in SIDS deaths and should be removed. Health Canada, the Canadian government's health department, issued an advisory[78] recommending against the use of bumper pads, stating: The presence of bumper pads in a crib may also be a contributing factor for Sudden Infant Death Syndrome (SIDS). These products may reduce the flow of oxygen rich air to the infant in the crib. Furthermore, proposed theories indicate that the rebreathing of carbon dioxide plays a role in the occurrence of SIDS.
[edit] Concerns regarding recommendations

Dr. Rafael Pelayo from Stanford University and a number of other pediatric sleep researchers in the US have stated that they believe that the American Academy of Pediatrics' recommendations regarding cosleeping and pacifier use may have unintended consequences. They have stated that the SIDS prevention strategy of the American Academy of Pediatrics which keeps infants at a low arousal threshold and reduces the time in quiet sleep may be unhealthy for children. They state that slow wave sleep is the most restorative form of sleep and limiting this sleep in the first 12 months of life may have unintended consequences to both the sleep and the infant.[79] According to a 1998 study by British researchers that compared back sleeping infants to stomach sleeping infants there were developmental differences at 6 months of age between the two groups. At 6 months of age the stomach sleeping infants had higher gross motor scores, social skills scores, and total development skills scores than the back sleeping infants. The differences were apparent at the 5% statistical significant level. But, at 18 months the differences were no longer apparent. The researchers deemed the lower development scores of back sleeping infants at 6 months of age to be transient and stated that they do not believe the back sleeping recommendations should be changed.[80] Other scientists have stated that the conclusion that the negative effects of back sleep at 18 months of age is transient is based upon very little evidence and that no long-term randomized trials have been completed.[81]

Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis.[82] Some scientists dispute that plagiocephaly is a negative side effect. Dr. Peter Fleming, who is co-author of the study that deemed delays at 6 months of age to be transient, has stated that he does not think plagiocephaly is a negative side effect of back sleep. In an interview with the Guardian Dr. Fleming stated "I do not think it is a medical problemit is more of a cosmetic one. Mothers may feel it is a syndrome and a problem when it really is nonsense."[83] A research study on children with plagiocephaly plus a confounding condition such as premature birth or failure to thrive, found that 26% had mild to severe psychomotor delay. This study also showed that 10% of infants with plagiocephaly had mild to severe mental development delay.[84] Because of the delays caused by back sleep some medical professionals have suggested that the "normal" ages at which children had previously attained developmental milestones should be pushed back. This would enable medical professionals to consider "normal" children who previously were considered developmentally delayed.[85] Additional studies have reported that the following negative conditions are associated with the back sleep position: increase in sleep apnea, decrease in sleep duration, strabismus, social skills delays, deformational plagiocephaly, and temporomandibular jaw difficulties.[82] In addition, the following are symptoms that are associated with sleep apnea: growth abnormalities, failure to thrive syndrome in infants, neurocognitive abnormalities, daytime sleepiness, emotional problems, decrease in memory, decrease in learning, and a delay in nonverbal skills. The conditions associated with deformational plagiocephaly include visual impairments, cerebral dysfunction, delays in psychomotor development and decreases in mental functioning. The conditions associated with gross motor milestone delays include speech and language disorders. In addition, it has been hypothesized that delays in motor skills can have a negative impact on the development of social skills.[86][87] In addition, other studies have reported that the prone position prevents subluxation of the hips, increases psychomotor development, prevents scoliosis, lessens the risk of gastroesophageal reflux, decreases infant screaming periods, causes less fatigue in infants, and increases the relief of infant colic.[88] In addition, prior to the "Back to Sleep" campaign many babies self-treated their own torticollis by turning their heads from one side to the other while sleeping in the prone position.[89] Supine sleeping infants cannot self-treat their own torticollis. jm
[edit] Pacifiers

According to a 2005 meta-analysis, most studies favor pacifier use.[90] According to the American Academy of Pediatrics, pacifier use seems to reduce the risk of SIDS, although the mechanism by which this happens is unclear.[91] SIDS experts and policy makers haven't recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated with pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species.[91] A 2005 study indicated that use of a pacifier is associated with up to a 90% reduction in the risk of SIDS depending on the ambient factors, and it reduced the effect of other risk factors.[92] It has been speculated that the raised surface of the pacifier holds the infant's face away from the mattress, reducing the risk of suffocation. If a postmortem

investigation does not occur or is insufficient, a suffocated baby may be misdiagnosed with SIDS. A 2010 study at Monash University suggests pacifiers can prevent SIDS by changing sleep patterns. They believe a pacifier ensures the baby remains in a light sleep and is more easily aroused if they feel uncomfortable.[93] The most recent 2011 study confirms that pacifier usage also reduces SIDS risks from other known SIDS risk factors [94]
[edit] Secondhand smoke reduction

According to the US Surgeon General's Report, secondhand smoke is connected to SIDS.[95] Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their body fluids than those who die from other causes.[96] Parents who smoke can significantly reduce their children's risk of SIDS by either quitting or smoking only outside and leaving their house completely smoke-free. The maternal pregnancy smoking rate decreased by 38% between 1990 and 2002.[97]
[edit] Sleep positioning Main article: Back to Sleep

A plot of SIDS rate from 1988 to 2006

Sleeping on the back has been recommended by (among others) the American Academy of Pediatrics (starting in 1992) to avoid SIDS, with the catchphrases "Back To Bed" and "Back to Sleep". The incidence of SIDS has fallen sharply in a number of countries in which the back to bed recommendation has been widely adopted, such as the US and New Zealand.[98] However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already dropping in the US, from 1.511 per 1000 in 1979 to 1.301 per 1000 in 1991.[13][original research?] Among the theories supporting the Back to Sleep recommendation is the idea that small infants with little or no control of their heads may, while face down, inhale their exhaled breath (high in carbon dioxide) or smother themselves on their beddingthe brain-stem anomaly research (above) suggests that babies with that particular genetic makeup do not react "normally" by moving away from the pooled CO2, and thus smother. Another theory[99] is that babies sleep

more soundly when placed on their stomachs, and are unable to rouse themselves when they have an incidence of sleep apnea, which is thought to be common in infants. Hospital neonatal-intensive-care-unit (NICU) staff commonly place preterm newborns on their stomach, although they advise parents to place their infants on their backs after going home from the hospital.[100]
[edit] Sleep sacks

In colder environments where bedding is required to maintain a baby's body temperature, the use of a "baby sleep bag" or "sleep sack" is becoming more popular. This is a soft bag with holes for the baby's arms and head. A zipper allows the bag to be closed around the baby. A study published in the European Journal of Pediatrics in August 1998[101] has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study "The use of a sleeping-sack should be particularly promoted for infants with a low birth weight." The American Academy of Pediatrics also recommends them as a type of bedding that warms the baby without covering its head.[102]

[edit] Epidemiology
SIDS was responsible for 0.543 deaths per 1,000 live births in the US in 2005.[13][original research?] It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in healthy infants after one month of age. SIDS deaths in the US decreased from 4,895 in 1992 to 2,247 in 2004.[103] But, during a similar time period, 1989 to 2004, SIDS being listed as the cause of death for sudden infant death (SID) decreased from 80% to 55%.[103] According to Dr. John Kattwinkel, chairman of the Centers for Disease Control and Prevention (CDC) Special Task Force on SIDS "A lot of us are concerned that the rate (of SIDS) isn't decreasing significantly, but that a lot of it is just code shifting".[103] A set of 14 epidemiologic characteristics associated with SIDS have been identified:[104][105]
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. A characteristic 4-parameter lognormal age distribution; Increased risk associated with prone sleep position; Prone and supine SIDS have same age and gender distributions; Male and female SIDS have same age distribution; Total sudden respiratory deaths at home have same age and gender distributions;[106] No evidence of cause of death at forensic autopsy and death scene investigation; SIDS spares infants at birth[?]; Seasonality: winter maximum, summer minimum; Increasing SIDS rate with Live Birth Order; Consistent male excess of approximately 50%; Low increased risk of SIDS in subsequent siblings of SIDS; Parental smoking is a risk factor for SIDS;

13. Acute Life Threatening Events (ALTE) are not a risk factor for subsequent SIDS; 14. SIDS risk is greatest during sleep.

Myasthenia gravis Myasthenia gravis

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Myasthenia gravis
Classification and external resources

Detailed view of a neuromuscular junction: 1. Axon 2. Sarcolemma 3. Synaptic vesicle 4. Nicotinic acetylcholine receptor 5. Mitochondrion

ICD-10

G70.0

ICD-9

358.0

OMIM

254200

DiseasesDB

8460

MedlinePlus 000712

eMedicine

neuro/232 emerg/325 (emergency), med/3260 (pregnancy), oph/263 (eye)

MeSH

D009157

Myasthenia gravis (from Greek "muscle", "weakness", and Latin: gravis "serious"; abbreviated MG) is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction,[1] inhibiting the excitatory effects of the neurotransmitter acetylcholine on muscarinic receptors throughout neuromuscular junctions. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. The disease incidence is 330 cases per million per year and rising as a result of increased awareness.[2] MG must be distinguished from congenital myasthenic syndromes that can present similar symptoms but offer no response to immunosuppressive treatments.

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Pathophysiology o 3.1 Associated condition o 3.2 In pregnancy 4 Diagnosis o 4.1 Physical examination o 4.2 Blood tests o 4.3 Electrodiagnostics o 4.4 Edrophonium test o 4.5 Imaging o 4.6 Pulmonary function test o 4.7 Pathological findings 5 Treatment o 5.1 Medication o 5.2 Plasmapheresis and IVIG

o 5.3 Surgery 6 Prognosis 7 Epidemiology 8 Notable patients 9 References 10 External links

[edit] Classification
The most widely accepted classification of myasthenia gravis is the Myasthenia Gravis Foundation of America Clinical Classification:[3]

Class I: Any eye muscle weakness, possible ptosis, no other evidence of muscle weakness elsewhere Class II: Eye muscle weakness of any severity, mild weakness of other muscles o Class IIa: Predominantly limb or axial muscles o Class IIb: Predominantly bulbar and/or respiratory muscles Class III: Eye muscle weakness of any severity, moderate weakness of other muscles o Class IIIa: Predominantly limb or axial muscles o Class IIIb: Predominantly bulbar and/or respiratory muscles Class IV: Eye muscle weakness of any severity, severe weakness of other muscles o Class IVa: Predominantly limb or axial muscles o Class IVb: Predominantly bulbar and/or respiratory muscles (Can also include feeding tube without intubation) Class V: Intubation needed to maintain airway

[edit] Signs and symptoms

Blepharoptosis of the left eye

The hallmark of myasthenia gravis is fatigability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expressions, chewing, talking, and swallowing are especially susceptible. The muscles that control breathing and neck and limb movements can also be affected. Often, the physical examination yields results within normal limits.[4]

The onset of the disorder can be sudden. Often symptoms are intermittent. The diagnosis of myasthenia gravis may be delayed if the symptoms are subtle or variable. In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in MG varies greatly among patients, ranging from a localized form that is limited to eye muscles (ocular myasthenia), to a severe and generalized form in which many muscles sometimes including those that control breathing - are affected. Symptoms, which vary in type and severity, may include asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision) due to weakness of the muscles that control eye movements, an unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia (difficulty in swallowing), shortness of breath and dysarthria (impaired speech, often nasal due to weakness of the velar muscles). In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life. In patients whose respiratory muscles are already weak, crises may be triggered by infection, fever, an adverse reaction to medication, or emotional stress.[5] Since the heart muscle is only regulated by the autonomic nervous system, it is generally unaffected by MG.

[edit] Pathophysiology

A juvenile thymus shrinks with age.

Myasthenia gravis is an autoimmune channelopathy: it features antibodies directed against the body's own proteins. While various similar diseases have been linked to immunologic crossreaction with an infective agent, there is no known causative pathogen that could account for myasthenia. There is a slight genetic predisposition: particular HLA types seem to predispose for MG (B8 and DR3 with DR1 more specific for ocular myasthenia). Up to 75% of patients have an abnormality of the thymus; 10% have a thymoma, a tumor (either benign or malignant) of the thymus, and other abnormalities are frequently found. The disease process generally remains stationary after thymectomy (removal of the thymus).

The nicotinic acetylcholine receptor

In MG, the autoantibodies most commonly act against the nicotinic acetylcholine receptor (nAChR),[6] the receptor in the motor end plate for the neurotransmitter acetylcholine that stimulates muscular contractions. Some forms of the antibody impair the ability of acetylcholine to bind to receptors. Others lead to the destruction of receptors, either by complement fixation or by inducing the muscle cell to eliminate the receptors through endocytosis. The antibodies are produced by plasma cells, derived from B-cells. B-cells convert into plasma cells by T-helper cell stimulation. To carry out this activation, T-helpers must first be activated themselves, which is done by binding of the T-cell receptor (TCR) to the acetylcholine receptor antigenic peptide fragment (epitope) resting within the major histocompatibility complex of antigen presenting cells. Since the thymus plays an important role in the development of T-cells and the selection of TCR, myasthenia gravis is closely associated with thymoma. The exact mechanisms are, however, not convincingly clarified, although resection of the thymus (thymectomy) in MG patients without a thymus neoplasm often have positive results. In normal muscle contraction, cumulative activation of the nAChR leads to influx of sodium ions, which in turn causes the depolarization of muscle cell and subsequent opening of voltagegated sodium channels. This ion influx then travels down the cell membranes via T-tubules and, via calcium channel complexes, leads to the release of calcium from the sarcoplasmic reticulum. Only when the levels of calcium inside the muscle cell are high enough will it contract. Decreased numbers of functioning nAChRs therefore impairs muscular contraction by limiting depolarization. In fact, MG causes the motor neuron action potential to muscular twitch ratio to vary from the nonpathological one to one ratio. A second category of gravis is due to autoantibodies against the MuSK protein (muscle specific kinase), a tyrosine kinase receptor which is required for the formation of the neuromuscular junction. Antibodies against MuSK inhibit the signaling of MuSK normally induced by its nervederived ligand, agrin. The result is a decrease in patency of the neuromuscular junction, and the consequent symptoms of MG. People treated with penicillamine can develop MG symptoms. Their antibody titer is usually similar to that of MG, but both the symptoms and the titer disappear when drug administration is discontinued.

MG is more common in families with other autoimmune diseases. A familial predisposition found in 5% of the cases is associated with certain genetic variations, such as an increased frequency of HLA-B8 and DR3. People with MG suffer from coexisting autoimmune diseases at a higher frequency than members of the general population. Of particular mention is coexisting thyroid disease, where episodes of hypothyroidism may precipitate a severe exacerbation. The acetylcholine receptor is clustered and anchored by the Rapsyn protein, research into which might eventually lead to new treatment options.[7]
[edit] Associated condition

Myasthenia gravis is associated with various autoimmune diseases,[8] including:

Thyroid diseases, including Hashimoto's thyroiditis and Graves' disease Diabetes mellitus type 1 Rheumatoid arthritis Lupus, and Demyelinating CNS diseases

Seropositive and "double-seronegative" patients often have thymoma or thymic hyperplasia. However, anti-MuSK positive patients do not have evidence of thymus pathology.
[edit] In pregnancy

In the long term, pregnancy does not affect myasthenia gravis. The mothers themselves suffer from exacerbated myasthenia in a third of cases, and in those for whom it does worsen, it usually occurs in the first trimester of pregnancy. Signs and symptoms in pregnant mothers tend to improve during the second and third trimesters. Complete remission can occur in some mothers.[9] Immunosuppressive therapy should be maintained throughout pregnancy, as this reduces the chance of neonatal muscle weakness, as well as controls the mother's myasthenia.[10] Up to 10% of infants with parents affected by the condition are born with transient (periodic) neonatal myasthenia (TNM), which generally produces feeding and respiratory difficulties.[10] TNM usually presents as poor suckling and generalized hypotonia (low muscle tone). Other reported symptoms include a weak cry, facial diplegia (paralysis of one part of the body) or paresis (impaired or lack of movement) and mild respiratory distress. A child with TNM typically responds very well to acetylcholinesterase inhibitors. Very rarely, an infant can be born with arthrogryposis multiplex congenita, secondary to profound intrauterine weakness. This is due to maternal antibodies that target an infant's acetylcholine receptors. In some cases, the mother remains asymptomatic.[10]

[edit] Diagnosis
MG can be a difficult diagnosis, as the symptoms can be subtle and hard to distinguish from both normal variants and other neurological disorders.[4] A thorough physical examination can reveal easy fatiguability, with the weakness improving after rest and worsening again on repeat of the

exertion testing. Applying ice to weak muscle groups characteristically leads to improvement in strength of those muscles. Additional tests are often performed, as mentioned below. Furthermore, a good response to medication can also be considered a sign of autoimmune pathology.
[edit] Physical examination

Muscle fatigability can be tested for many muscles.[11] A thorough investigation includes:

looking upward and sidewards for 30 seconds: ptosis and diplopia looking at the feet while lying on the back for 60 seconds keeping the arms stretched forward for 60 seconds ten deep knee bends walking 30 steps on both the toes and the heels five situps, lying down and sitting up completely "Peek sign": after complete initial apposition of the lid margins, they quickly (within 30 seconds) start to separate and the sclera starts to show[4]

[edit] Blood tests

If the diagnosis is suspected, serology can be performed in a blood test to identify certain antibodies:

One test is for antibodies against the acetylcholine receptor.[4] The test has a reasonable sensitivity of 8096%, but in MG limited to the eye muscles (ocular myasthenia) the test may be negative in up to 50% of the cases. A proportion of the patients without antibodies against the acetylcholine receptor have antibodies against the MuSK protein.[12] In specific situations (decreased reflexes which increase on facilitation, coexisting autonomic features, suspected presence of neoplasm, especially of the lung, presence of increment or facilitation on repetitive EMG testing) testing is performed for Lambert-Eaton syndrome, in which other antibodies (against a voltage-gated calcium channel) can be found.

[edit] Electrodiagnostics

Muscle fibers of patients with MG are easily fatigued, and thus do not respond as well as muscles in healthy individuals to repeated stimulation. By stimulating a nerve-muscle motor unit with short sequences of rapid, regular electrical impulses, before and after exercising the motor unit, the fatiguability of the muscle can be measured. This is called the repetitive nerve stimulation test. In single fiber electromyography (SFEMG), which is considered to be the most sensitive (although not the most specific) test for MG,[4] a thin needle electrode is inserted into different areas of a particular muscle to record the action potentials from several samplings of different individual muscle fibers. Two muscle fibers belonging to the same motor unit are identified and the temporal variability in their firing patterns are measured. Frequency and proportion of particular abnormal action potential patterns, "jitter" and "blocking," are

diagnostic. Jitter refers to the abnormal variation in the time interval between action potentials of adjacent muscle fibers in the same motor unit. Blocking refers to the failure of nerve impulses to elicit action potentials in adjacent muscle fibers of the same motor unit.[13]
[edit] Edrophonium test

Photograph of a patient showing right partial ptosis (left picture), the left lid shows compensatory pseudo lid retraction because of equal innervation of the levator palpabrae superioris (Hering's law of equal innervation). Right picture: after an edrophonium test, note the improvement in ptosis.

The "edrophonium test" is infrequently performed to identify MG; its application is limited to the situation when other investigations do not yield a conclusive diagnosis. This test requires the intravenous administration of edrophonium chloride (Tensilon, Reversol) or neostigmine (Prostigmin), drugs that block the breakdown of acetylcholine by cholinesterase (cholinesterase inhibitors) and temporarily increases the levels of acetylcholine at the neuromuscular junction. In people with myasthenia gravis involving the eye muscles, edrophonium chloride will briefly relieve weakness.[14]
[edit] Imaging

A chest CT-scan showing a thymoma (red circle)

A chest X-ray is frequently performed; it may point towards alternative diagnoses (e.g. LambertEaton syndrome due to a lung tumor) and comorbidity. It may also identify widening of the mediastinum suggestive of thymoma, but computed tomography (CT) or magnetic resonance imaging (MRI) are more sensitive ways to identify thymomas, and are generally done for this reason.[15]
[edit] Pulmonary function test

Spirometry (lung function testing) may be performed for the assessing of respiratory function if there are concerns about a patient's ability to breathe adequately. The forced vital capacity may

be monitored at intervals so as not to miss a gradual worsening of muscular weakness. Acutely, negative inspiratory force may be used to determine adequacy of ventilation. Severe myasthenia may cause respiratory failure due to exhaustion of the respiratory muscles.[16]
[edit] Pathological findings

Muscle biopsy is only performed if the diagnosis is in doubt and a muscular condition is suspected. Immunofluorescence shows IgG antibodies on the neuromuscular junction. (The antibody which causes myasthenia gravis does not fluoresce, but rather a secondary antibody directed against it.) Muscle electron microscopy shows receptor infolding and loss of the tips of the folds, together with widening of the synaptic clefts. Both these techniques are currently used for research rather than diagnostically.[7]

[edit] Treatment
Treatment is by medication and/or surgery. Medication consists mainly of cholinesterase inhibitors to directly improve muscle function and immunosuppressant drugs to reduce the autoimmune process. Thymectomy is a surgical method to treat MG. For emergency treatment, plasmapheresis or IVIG can be used as a temporary measure to remove antibodies from the blood circulation.
[edit] Medication

Neostigmine, chemical structure.

Acetylcholinesterase inhibitors: neostigmine and pyridostigmine can improve muscle function by slowing the natural enzyme cholinesterase that degrades acetylcholine in the motor end plate; the neurotransmitter is therefore around longer to stimulate its receptor. Usually, doctors will start with a low dose, e.g. 3x20mg pyridostigmine, and increase until the desired result is achieved. If taken 30 minutes before a meal, symptoms will be mild during eating. Side effects, such as perspiration and diarrhea, can be countered by adding atropine. Pyridostigmine is a short-lived drug, with a half-life of about four hours.

Azathioprine, chemical structure

Immunosuppressive drugs: prednisone, cyclosporine, mycophenolate mofetil and azathioprine may be used. Patients are commonly treated with a combination of these drugs with a cholinesterase inhibitor. Treatments with some immunosuppressives take weeks to months before effects are noticed. Other immunomodulating substances, such as drugs that prevent acetylcholine receptor modulation by the immune system, are currently being researched.[17]

[edit] Plasmapheresis and IVIG

If the myasthenia is serious (myasthenic crisis), plasmapheresis can be used to remove the putative antibodies from the circulation. Also, intravenous immunoglobulins (IVIGs) can be used to bind the circulating antibodies. Both of these treatments have relatively short-lived benefits, typically measured in weeks.[18]
[edit] Surgery Main article: thymectomy

Thymectomy, the surgical removal of the thymus, is essential in cases of thymoma in view of the potential neoplastic effects of the tumor. However, the procedure is more controversial in patients who do not show thymic abnormalities. Although some of these patients improve following thymectomy, some patients experience severe exacerbations and the highly controversial concept of "therapeutic thymectomy" for patients with thymus hyperplasia is disputed by many experts, and efforts are underway to unequivocally answer this important question.

There are a number of surgical approaches to the removal of the thymus gland: transsternal (through the sternum, or breast bone), transcervical (through a small neck incision), and transthoracic (through one or both sides of the chest). The transsternal approach is most common and uses the same length-wise incision through the sternum (breast bone)used for most openheart surgery. The transcervical approach, a less invasive procedure, allows for removal of the entire thymus gland through a small neck incision. There has been no difference in success in symptom improvement between the transsternal approach and the minimally invasive transcervical approach.[19] For patients with a thymoma, though, complete tissue removal is important, as thymic tissue can regrow. Thymomas can be malignant and are thought to be the onset of other diseases, as well, so many surgeons will only recommend the full sternotomy approach to a thymectomy. Thymoma is relatively rare in younger (<40) patients, but especially younger patients with generalized MG without thymoma benefit, paradoxically, from thymectomy. Resection is also indicated for those with a thymoma, but it is less likely to improve the MG symptoms.

[edit] Prognosis
With treatment, patients have a normal life expectancy, except for those with a malignant thymoma (whose lesser life expectancy is on account of the thymoma itself and is otherwise unrelated to the myasthenia). Quality of life can vary depending on the severity and the cause. The drugs used to control MG either diminish in effectiveness over time (cholinesterase inhibitors) or cause severe side effects of their own (immunosuppressants). About 10% of MG patients are found to have tumors in their thymus glands, in which case a thymectomy is a very effective treatment with long-term remission. However, most patients need treatment for the remainder of their lives, and their abilities vary greatly. MG is not usually a progressive disease; the symptoms may come and go, but do not always get worse as the patient ages. For some, the symptoms decrease after a span of three to five years.

[edit] Epidemiology
Myasthenia gravis occurs in all ethnic groups and both genders. It most commonly affects women under 40 and people from 50 to 70 years old of either sex, but it has been known to occur at any age. Younger patients rarely have thymoma. The prevalence in the United States is estimated at 20 cases per 100,000.[20] Risk factors are the female gender with ages 20 40, familial myasthenia gravis, D-penicillamine ingestion (drug-induced myasthenia), and having other autoimmune diseases. Three types of myasthenic symptoms in children can be distinguished:[11]
1. Neonatal: In 12% of the pregnancies with a mother with MG, she passes the antibodies to the infant through the placenta, causing neonatal myasthenia gravis. The symptoms will start in the first two days and disappear within a few weeks after birth. With the mother, it is not uncommon for the symptoms to even improve during pregnancy, but they might worsen after labor.

2. Congenital: Children of a healthy mother can, very rarely, develop myasthenic symptoms beginning at birth, congenital myasthenic syndrome or CMS. Other than myasthenia gravis, CMS is not caused by an autoimmune process, but due to synaptic malformation, which in turn is caused by genetic mutations. Thus, CMS is a hereditary disease. More than 11 different mutations have been identified, and the inheritance pattern is typically autosomal recessive. 3. Juvenile myasthenia gravis: myasthenia occurring in childhood, but after the peripartum period

The congenital myasthenias cause muscle weakness and fatigability similar to those of MG. The symptoms of CMS usually begin within the first two years of life, although in a few forms, patients can develop their first symptoms as late as the seventh decade of life. A diagnosis of CMS is suggested by the following:

Onset of symptoms in infancy or childhood Weakness which increases as muscles tire A decremental EMG response, on low frequency, of the compound muscle action potential (CMAP) No anti-AChR or MuSK antibodies No response to immunosuppressant therapy Family history of symptoms which resemble CMS

The symptoms of CMS can vary from mild to severe. It is also common for patients with the same form, even members of the same family, to be affected to differing degrees. In most forms of CMS, weakness does not progress, and in some forms, the symptoms may diminish as the patient gets older. Only rarely do symptoms of CMS become worse with time.

Asthma Asthma
From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Asthma (disambiguation).

Asthma
Classification and external resources

Peak flow meters are used to measure one's peak expiratory flow rate

ICD-10

J45.

ICD-9

493

OMIM

600807

DiseasesDB

1006

MedlinePlus

000141

eMedicine

article/806890

MeSH

D001249

Asthma (from the Greek , sthma, "panting") is the common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm.[1] Symptoms include wheezing, coughing, chest tightness, and shortness of breath.[2] Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate.[3] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic).[4] It is thought to be caused by a combination of genetic and environmental factors.[5] Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol).[6] Symptoms can be prevented by avoiding triggers, such as allergens[7] and irritants, and by

inhaling corticosteroids.[8] Leukotriene antagonists are less effective than corticosteroids and thus less preferred.[9] Its diagnosis is usually made based on the pattern of symptoms and/or response to therapy over time.[10] The prevalence of asthma has increased significantly since the 1970s. As of 2010, 300 million people were affected worldwide.[11] In 2009 asthma caused 250,000 deaths globally.[12] Despite this, with proper control of asthma with step down therapy, prognosis is generally good.[13]

Contents
[hide]

1 Classification o 1.1 Brittle asthma o 1.2 Asthma attack o 1.3 Status asthmaticus o 1.4 Exercise induced o 1.5 Occupational 2 Signs and symptoms o 2.1 Gastro-esophageal reflux disease o 2.2 Sleep disorders 3 Causes o 3.1 Environmental 3.1.1 Tobacco 3.1.2 Hygiene hypothesis 3.1.3 Volatile organic compounds 3.1.4 Phthalates o 3.2 Genetic o 3.3 Geneenvironment interactions o 3.4 Exacerbation o 3.5 Hygiene hypothesis o 3.6 Socioeconomic factors 4 Diagnosis o 4.1 Differential diagnosis 4.1.1 Chronic obstructive pulmonary disease 4.1.2 Others 5 Prevention 6 Management o 6.1 Lifestyle modification o 6.2 Medications o 6.3 Other o 6.4 Complementary medicine 7 Prognosis 8 Epidemiology o 8.1 Increasing frequency

o 8.2 Variability 9 History 10 References 11 External links

[edit] Classification
Asthma is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread, but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment".[14]
Clinical classification of severity[3] Use of shortacting beta2 FEV1 agonist for Variability symptom control (not for prevention of EIB) <20% 2030% 2 days per week >2 days/week but not daily Daily Several times per day

Severity in patients 12 years of age [15]

Symptom frequency

Night time symptoms

%FEV1 of predicted

Intermittent Mild persistent Moderate persistent Severe persistent

2 per week >2 per week but not daily Daily

2 per month 3-4 per month >1 per week but not nightly

80% 80%

6080%

>30%

Throughout the Frequent (often day 7x/week)

<60%

>30%

Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate.[3] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic).[4] While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system.[16] Within the classifications described above, although the cases of asthma respond to the same treatment differs, thus it is

clear that the cases within a classification have significant differences.[16] Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.[16] Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema.[15] Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation of the lungs during asthma can become irreversible obstruction due to airway remodeling.[17] In contrast to emphysema, asthma affects the bronchi, not the alveoli.[18]
[edit] Brittle asthma Main article: Brittle asthma

Brittle asthma is a term used to describe two types of asthma, distinguishable by recurrent, severe attacks.[19] Type 1 brittle asthma refers to disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma describes background well-controlled asthma, with sudden severe exacerbations.[19]
[edit] Asthma attack

An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness.[20] While these are the primary symptoms of asthma,[21] some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.[19] Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.[22] A blue color of the skin and nails may occur from lack of oxygen.[23] In a mild exacerbation the peak expiratory flow rate (PEFR) is 200 L/min or 50% of the predicted best.[24] Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as 80 L/min or 25% of the predicted best.[24] Insufficient levels of vitamin D are linked with severe asthma attacks.[25]
[edit] Status asthmaticus Main article: Status asthmaticus

Status asthmaticus is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and steroids. Nonselective beta blockers (such as Timolol) have caused fatal status asthmaticus.[26]
[edit] Exercise induced Main article: Exercise-induced asthma

A diagnosis of asthma is common among top athletes. One survey of participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15% had been diagnosed with asthma, and that 10% were on asthma medication.[27] There appears to be a relatively high incidence of asthma in sports such as cycling, mountain biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It is unclear how much of these disparities are from the effects of training in the sport.[27][28] Exercise induced asthma can be treated with the use of a short-acting beta2 agonist.[15]
[edit] Occupational Main article: Occupational asthma

Asthma as a result of (or worsened by) workplace exposures is a commonly reported occupational respiratory disease. Still most cases of occupational asthma are not reported or are not recognized as such. Estimates by the American Thoracic Society (2004) suggest that 1523% of new-onset asthma cases in adults are work related.[29] In one study monitoring workplace asthma by occupation, the highest percentage of cases occurred among operators, fabricators, and laborers (32.9%), followed by managerial and professional specialists (20.2%), and in technical, sales, and administrative support jobs (19.2%). Most cases were associated with the manufacturing (41.4%) and services (34.2%) industries.[29] Animal proteins, enzymes, flour, natural rubber latex, and certain reactive chemicals are commonly associated with work-related asthma. When recognized, these hazards can be mitigated, dropping the risk of disease.[30]

[edit] Signs and symptoms

Wheezing

The sound of wheezing as heard with a stethoscope.

Problems listening to this file? See media help.

Common symptoms of asthma include wheezing, shortness of breath, chest tightness and coughing, and use of accessory muscle. Symptoms are often worse at night or in the early morning, or in response to exercise or cold air.[31] Some people with asthma only rarely experience symptoms, usually in response to triggers, whereas other may have marked persistent airflow obstruction.[32]

[edit] Gastro-esophageal reflux disease

Gastro-esophageal reflux disease coexists with asthma in 80% of people with asthma, with similar symptoms. Various theories say that asthma could facilitate GERD and/or viceversa. The first case could be due to the effect of change in thoracic pressures, use of antiasthma drugs, could facilitate the passage of the gastric content back into the oesophagus by increasing abdominal pressure or decreasing the lower esophageal sphincter. The second by promoting bronchoconstriction and irritation by chronic acid aspiration, vagally mediated reflexes and others factors that increase bronchial responsiveness and irritation.[33]
[edit] Sleep disorders

Due to altered anatomy of the respiratory tract: increased upper airway adipose deposition, altered pharynx skeletal morphology, and extension of the pharyngeal airway; leading to upper airway collapse.[34]

[edit] Causes
Asthma is caused by environmental and genetic factors.[5] These factors influence how severe asthma is and how well it responds to medication.[35] The interaction is complex and not fully understood.[36] Studying the prevalence of asthma and related diseases such as eczema and hay fever have yielded important clues about some key risk factors.[37] The strongest risk factor for developing asthma is a history of atopic disease;[38] this increases one's risk of hay fever by up to 5x and the risk of asthma by 3-4x.[39] In children between the ages of 3-14, a positive skin test for allergies and an increase in immunoglobulin E increases the chance of having asthma.[40] In adults, the more allergens one reacts positively to in a skin test, the higher the odds of having asthma.[41] Because much allergic asthma is associated with sensitivity to indoor allergens and because Western styles of housing favor greater exposure to indoor allergens, much attention has focused on increased exposure to these allergens in infancy and early childhood as a primary cause of the rise in asthma.[42][43] Primary prevention studies aimed at the aggressive reduction of airborne allergens in a home with infants have shown mixed findings. Strict reduction of dust mite allergens, for example, reduces the risk of allergic sensitization to dust mites, and modestly reduces the risk of developing asthma up until the age of 8 years old.[44][45][46][47] However, studies also showed that the effects of exposure to cat and dog allergens worked in the converse fashion; exposure during the first year of life was found to reduce the risk of allergic sensitization and of developing asthma later in life.[48][49][50] The inconsistency of this data has inspired research into other facets of Western society and their impact upon the prevalence of asthma. One subject that appears to show a strong correlation is the development of asthma and obesity. In the United Kingdom and United States, the rise in asthma prevalence has echoed an almost epidemic rise in the prevalence of obesity.[51][52][53][54] In Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each 20% increase in body-mass index.[55] Several factors associated with obesity may play a role in

the pathogenesis of asthma, including decreased respiratory function due to a buildup of adipose tissue (fat) and the fact that adipose tissue leads to a pro-inflammatory state, which has been associated with non-eosinophilic asthma.[56] Asthma has been associated with ChurgStrauss syndrome, and individuals with immunologically mediated urticaria may also experience systemic symptoms with generalized urticaria, rhino-conjunctivitis, orolaryngeal and gastrointestinal symptoms, asthma, and, at worst, anaphylaxis.[57] Additionally, adult-onset asthma has been associated with periocular xanthogranulomas.[58]
[edit] Environmental

Many environmental risk factors have been associated with asthma development and morbidity in children. Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and childhood asthma.[59] This research finds that both the occurrence of the disease and exacerbation of childhood asthma are affected by outdoor air pollutants. High levels of endotoxin exposure may contribute to asthma risk.[60] Viral respiratory infections are not only one of the leading triggers of an exacerbation but may increase one's risk of developing asthma especially in young children.[15][38] Respiratory infections such as rhinovirus, Chlamydia pneumoniae and Bordetella pertussis are correlated with asthma exacerbations.[61] Psychological stress has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.[62][63] Beta blocker medications such as metoprolol may trigger asthma in those who are susceptible.[64] [edit] Tobacco Maternal tobacco smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms, wheezing, and respiratory infections during childhood.[65] Low air quality, from traffic pollution or high ozone levels,[66] has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[62][67] [edit] Hygiene hypothesis Antibiotic use early in life has been linked to development of asthma[68] in several examples; it is thought that antibiotics make children who are predisposed to atopic immune responses susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[69] The hygiene hypothesis (see below) is a hypothesis about the cause of asthma and other allergic disease, and is supported by

epidemiologic data for asthma.[70] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause an increased risk for asthma and allergy. Caesarean sections have been associated with asthma, possibly because of modifications to the immune system (as described by the hygiene hypothesis).[71] [edit] Volatile organic compounds Observational studies have found that indoor exposure to volatile organic compounds (VOCs) may be one of the triggers of asthma, however experimental studies have not confirmed these observations.[72] Even VOC exposure at low levels has been associated with an increase in the risk of pediatric asthma. Because there are so many VOCs in the air, measuring total VOC concentrations in the indoor environment may not represent the exposure of individual compounds.[73][74] Exposure to VOCs is associated with an increase in the IL-4 producing Th2 cells and a reduction in IFN- producing Th1 cells. Thus the mechanism of action of VOC exposure may be allergic sensitization mediated by a Th2 cell phenotype.[75] Different individual variations in discomfort, from no response to excessive response, were seen in one of the studies. These variations may be due to the development of tolerance during exposure.[76] Another study has concluded that formaldehyde may cause asthma-like symptoms. Low VOC emitting materials should be used while doing repairs or renovations which decreases the symptoms related to asthma caused by VOCs and formaldehyde.[77] In another study "the indoor concentration of aliphatic compounds (C8-C11), butanols, and 2,2,4-trimethyl 1,3-pentanediol diisobutyrate (TXIB) was significantly elevated in newly painted dwellings. The total indoor VOC was about 100 micrograms/m3 higher in dwellings painted in the last year". The author concluded that some VOCs may cause inflammatory reactions in the airways and may be the reason for asthmatic symptoms.[78][79] [edit] Phthalates There is a significant association between asthma-like symptoms (wheezing) among preschool children and the concentration of DEHP (phthalates) in indoor environment.[80] DEHP (diethylhexyl phthalate) is a plasticizer that is commonly used in building material. The hydrolysis product of DEHP (di-ethylhexyl phthalate) is MEHP (Mono-ethylhexyl phthalate) which mimics the prostaglandins and thromboxanes in the airway leading to symptoms related to asthma.[81] Another mechanism that has been studied regarding phthalates causation of asthma is that high phthalates level can "modulate the murine immune response to a coallergen". Asthma can develop in the adults who come in contact with heated PVC fumes.[82] Two main type of phthalates, namely n-butyl benzyl phthalate (BBzP) and di(2-ethylhexyl) phthalate (DEHP), have been associated between the concentration of polyvinyl chloride (PVC) used as flooring and the dust concentrations. Water leakage were associated more with BBzP, and buildings construction were associated with high concentrations of DEHP.[83] Asthma has been shown to have a relationship with plaster wall materials and wall-to wall carpeting. The onset of asthma was also related to the floorleveling plaster at home. Therefore, it is important to understand the health aspect of these materials in the indoor surfaces.[84]

[edit] Genetic

Over 100 genes have been associated with asthma in at least one genetic association study.[85] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[85]
GSTM1 IL10 CTLA-4 SPINK5 LTC4S LTA GRPA NOD1 CC16 GSTP1 STAT6 NOS1 CCL5 TBXA2R TGFB1 IL4 IL13 CD14 ADRB2 (-2 adrenergic receptor) HLA-DRB1 HLA-DQB1 TNF FCER1B IL4R ADAM33

Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[85] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma.[citation needed] For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[86]
[edit] Geneenvironment interactions CD14-endotoxin interaction based on CD14 SNP C-159T[87] Endotoxin levels High exposure Low exposure CC genotype Low risk High risk TT genotype High risk Low risk

Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.[5] The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person's genotype at CD14 C159T and level of endotoxin exposure.[87]

[edit] Exacerbation

Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different asthmatic individuals react differently to various factors.[88] However, most individuals can develop severe exacerbation of asthma from several triggering agents.[88][89] Home factors that can lead to exacerbation include dust, house mites, animal dander (especially cat and dog hair), cockroach allergens and molds at any given home.[88] Perfumes are a common cause of acute attacks in females and children. Both virus and bacterial infections of the upper respiratory tract infection can worsen asthma.[88]
[edit] Hygiene hypothesis Main article: Hygiene hypothesis

One theory for the cause of the increase in asthma prevalence worldwide is the "hygiene hypothesis"[15] that the rise in the prevalence of allergies and asthma is a direct and unintended result of reduced exposure to a wide variety of different bacteria and virus types in modern societies, or modern hygienic practices preventing childhood infections.[90] Children living in less hygienic environments (East Germany vs. West Germany,[91] families with many children,[92][93][94] day care environments[95]) tend to have lower incidences of asthma and allergic diseases. This seems to run counter to the logic that viruses are often causative agents in exacerbation of asthma.[96][97][98] Additionally, other studies have shown that viral infections of the lower airway may in some cases induce asthma, as a history of bronchiolitis or croup in early childhood is a predictor of asthma risk in later life.[99] Studies which show that upper respiratory tract infections are protective against asthma risk also tend to show that lower respiratory tract infections conversely tend to increase the risk of asthma.[100]
[edit] Socioeconomic factors

The incidence of asthma is highest among low-income populations worldwide[specify]. Asthma deaths are most common in low and middle income countries,[101] and in the Western world, it is found in those low-income neighborhoods whose populations consist of large percentages of ethnic minorities.[102] Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters; these insects are more likely to be found in those same neighborhoods.[103] Most likely due to income and geography, the incidence of and treatment quality for asthma varies among different racial groups.[104] The prevalence of "severe persistent" asthma is also greater in low-income communities than those with better access to treatment.[104][105]

[edit] Diagnosis
Severity of acute asthma exacerbations[19]

Near-fatal asthma

High PaCO2 and/or requiring mechanical ventilation Any one of the following in a person with severe asthma:Clinical signs Measurements

Altered level of consciousness Peak flow < 33% Exhaustion Life threatening asthma Arrhythmia Low blood pressure Cyanosis Silent chest Poor respiratory effort Any one of:Peak flow 33-50% Acute severe asthma Respiratory rate 25 breaths per minute Heart rate 110 beats per minute Unable to complete sentences in one breath Worsening symptoms Moderate asthma exacerbation Peak flow 80%-50% best or predicted Oxygen saturation < 92% PaO2 < 8 kPa "Normal" PaCO2

No features of acute severe asthma

Obstruction of the lumen of the bronchiole by mucoid exudate, goblet cell metaplasia, epithelial basement membrane thickening and severe inflammation of bronchiole in a patient with asthma.

There is currently not a precise physiologic, immunologic, or histologic test for diagnosing asthma. The diagnosis is usually made based on the pattern of symptoms (airways obstruction and hyperresponsiveness) and/or response to therapy (partial or complete reversibility) over time.[10] The British Thoracic Society determines a diagnosis of asthma using a response to therapy approach. If the patient responds to treatment, then this is considered to be a confirmation of the diagnosis of asthma. The response measured is the reversibility of airway obstruction after treatment. Airflow in the airways is measured with a peak flow meter or spirometer, and the following diagnostic criteria are used by the British Thoracic Society:[106]

20% difference on at least three days in a week for at least two weeks; 20% improvement of peak flow following treatment, for example: o 10 minutes of inhaled -agonist (e.g., salbutamol); o six weeks of inhaled corticosteroid (e.g., beclometasone); o 14 days of 30 mg prednisolone. 20% decrease in peak flow following exposure to a trigger (e.g., exercise).

In contrast, the US National Asthma Education and Prevention Program (NAEPP) uses a symptom patterns approach.[107] Their guidelines for the diagnosis and management of asthma state that a diagnosis of asthma begins by assessing if any of the following list of indicators is present.[107][13] While the indicators are not sufficient to support a diagnosis of asthma, the presence of multiple key indicators increases the probability of a diagnosis of asthma.[107] Spirometry is needed to establish a diagnosis of asthma.[107]

Wheezinghigh-pitched whistling sounds when breathing outespecially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.) history of any of the following: o Cough, worse particularly at night o Recurrent wheeze

Recurrent difficulty in breathing Recurrent chest tightness Symptoms occur or worsen in the presence of: o Exercise o Viral infection o Animals with fur or hair o House-dust mites (in mattresses, pillows, upholstered furniture, carpets) o Mold o Smoke (tobacco, wood) o Pollen o Changes in weather o Strong emotional expression (laughing or crying hard) o Airborne chemicals or dusts o Menstrual cycles Symptoms occur or worsen at night, awakening the patient

o o

The latest guidelines from the U.S. National Asthma Education and Prevention Program (NAEPP) recommend spirometry at the time of initial diagnosis, after treatment is initiated and symptoms are stabilized, whenever control of symptoms deteriorates, and every 1 or 2 years on a regular basis.[108] The NAEPP guidelines do not recommend testing peak expiratory flow as a regular screening method because it is more variable than spirometry. However, testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young patients who may experience only exercise-induced asthma. It may also be useful for daily self-monitoring and for checking the effects of new medications.[108] Peak flow readings can be charted together with a record of symptoms or use peak flow charting software. This allows patients to track their peak flow readings and pass information back to their doctor or respiratory therapist.[109]
[edit] Differential diagnosis

Differential diagnoses include:[107]

Infants and Children o Upper airway diseases Allergic rhinitis and allergic sinusitis o Obstructions involving large airways Foreign body in trachea or bronchus Vocal cord dysfunction Vascular rings or laryngeal webs Laryngotracheomalacia, tracheal stenosis, or bronchostenosis Enlarged lymph nodes or tumor o Obstructions involving small airways Viral bronchiolitis or obliterative bronchiolitis Cystic fibrosis Bronchopulmonary dysplasia Heart disease o Other causes Recurrent cough not due to asthma

Aspiration from swallowing mechanism dysfunction or gastroesophageal reflux Medication induced

Adults o COPD (e.g., chronic bronchitis or emphysema) o Congestive heart failure o Pulmonary embolism o Mechanical obstruction of the airways (benign and malignant tumors) o Pulmonary infiltration with eosinophilia o Cough secondary to drugs (e.g., angiotensin-converting enzyme (ACE) inhibitors) o Vocal cord dysfunction

Before diagnosing asthma, alternative possibilities should be considered such as the use of known bronchoconstrictors (substances that cause narrowing of the airways, e.g. certain antiinflammatory agents or beta-blockers). Among elderly people, the presenting symptom may be fatigue, cough, or difficulty breathing, all of which may be erroneously attributed to Chronic obstructive pulmonary disease(COPD), congestive heart failure, or simple aging.[110] [edit] Chronic obstructive pulmonary disease Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smoking cessation.[111] It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy.[112][113] [edit] Others The term "atopy" was coined to describe this triad of atopic eczema, allergic rhinitis and asthma.[57] Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a modified barium swallow test. If the aspiration is indirect (from acid reflux), then treatment is directed at this is indicated.[citation needed]

[edit] Prevention
The evidence for the effectiveness of measures to prevent the development of asthma is weak.[114] Ones which show some promise include limiting smoke exposure both in utero and after delivery, breastfeeding, increased exposure to respiratory infection per the hygiene hypothesis (such as in those who attend daycare or are from large families).[114]

[edit] Management
A specific, customized plan for proactively monitoring and managing symptoms should be created. Someone who has asthma should understand the importance of reducing exposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment plan should be written down and adjusted according to changes in symptoms.[115] The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, medical treatment is recommended. Medical treatments used depend on the severity of illness and the frequency of symptoms. Specific medications for asthma are broadly classified into fast-acting and longacting categories.[116][117] Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who suffer daily attacks, a higher dose of inhaled glucocorticoid is used. In a severe asthma exacerbation, oral glucocorticoids are added to these treatments.[107]
[edit] Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective betablockers, and sulfite-containing foods.[107][118]
[edit] Medications

Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.[119]
Fast acting

Salbutamol metered dose inhaler commonly used to treat asthma attacks.

Short acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN) are the first line treatment for asthma symptoms.[6] Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms.[6] Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA.[15] Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy to SABAs.[120] They are however not recommended due to concerns regarding excessive cardiac stimulation.[121]

Long term control

Fluticasone propionate metered dose inhaler commonly used for long term control.

Glucocorticoids are the most effective treatment available for long term control.[122] Inhaled forms are usually used except in the case of severe persistent disease, in which oral steroids may be needed.[122] Inhaled formulations may be used once or twice daily, depending on the severity of symptoms.[123] Long acting beta-adrenoceptor agonists (LABA) have at least a 12-hour effect. They are however not to be used without a steroid due to an increased risk of severe symptoms.[124][125][126] In December 2008, members of the FDA's drug-safety office recommended withdrawing approval for these medications in children. Discussion is ongoing about their use in adults.[127] Leukotriene antagonists (such as zafirlukast) are an alternative to inhaled glucocorticoids, but are not preferred. They may also be used in addition to inhaled glucocorticoids but in this role are second line to LABA.[122] Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to glucocorticoids.[122]

Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms however insufficient evidence is available to determine whether or not a difference exists in those severe symptomatology.[128]
Safety and adverse effects

Long-term use of glucocorticoids carries a significant potential for adverse effects. The incidence of cataracts is increased in people undergoing treatment for asthma with corticosteroids, due to altered regulation of lens epithelial cells.[129] The incidence of osteoporosis is also increased, due to changes in bone remodeling.[130][131]
[edit] Other

When asthma is unresponsive to usual medications, other options are available for both emergency management and prevention of flairs. For emergency management other options include:

Oxygen is used to alleviate hypoxia if saturations fall below 92%.[132] Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.[133][134] Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.[134] Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.[132] Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the effects of inhaled beta-agonists.[132] The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation is needed in people who are approaching respiratory arrest; however, there is no evidence from clinical trials to support this.[135]

For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs bronchial thermoplasty can lead to clinical improvements.[136] It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies and result in a prolonged reduction in airway smooth muscle mass.[136]
[edit] Complementary medicine

Many people with asthma, like those who suffer from other chronic disorders, use alternative treatments; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.[137][138] There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C.[139] Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use.[140][141] Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[142] Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms.[143] However, a review of 30 studies found that "bedding encasement might be an effective asthma treatment under some conditions" (when the patient is highly allergic to dust mite and the intervention reduces the dust mite exposure level from high levels to low levels).[144] Washing laundry/rugs in hot water was also found to improve control of allergens.[15]

A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres, found there is insufficient evidence to support their use in treating.[145] The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function.[146] Thus an expert panel felt that evidence was insufficient to support its use.[140]

[edit] Prognosis
The prognosis for asthma is good, especially for children with mild disease.[13][not in citation given] Of asthma diagnosed during childhood, 54% of cases will no longer carry the diagnosis after a decade.[citation needed] The extent of permanent lung damage in people with asthma is unclear. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes.[147] Although conclusions from studies are mixed, most studies show that early treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by several parameters.[148] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities. It is more likely to consider immediate medication of inhaled corticosteroids as soon as asthma attacks occur. According to studies conducted, patients with relatively mild asthma who have received inhaled corticosteroids within 12 months of their first asthma symptoms achieved good functional control of asthma after 10 years of individualized therapy as compared to patients who received this medication after 2 years (or more) from their first attacks.[citation needed] Though they (delayed) also had good functional control of asthma, they were observed to exhibit slightly less optimal disease control and more signs of airway inflammation.[citation needed] Asthma mortality has decreased over the last few decades due to better recognition and improvement in care.[149]

[edit] Epidemiology

Disability-adjusted life year for asthma per 100,000 inhabitants in 2004.[150] no data <100 100150 150200

200250 250300 300350 350400 400450 450500 500550 550600 >600

The prevalence of childhood asthma in the United States has increased since 1980, especially in younger children.

As of 2009, 300 million people worldwide were affected by asthma leading to approximately 250,000 deaths per year.[12][124][151][152] It is estimated that asthma has a 7-10% prevalence worldwide.[153] As of 1998, there was a great disparity in the prevalence of asthma across the world, with a trend toward more developed and westernized countries having higher rates of asthma[154], with as high as a 20 to 60-fold difference. Westernization however does not explain the entire difference in asthma prevalence between countries, and the disparities may also be affected by differences in genetic, social and environmental risk factors.[62] Mortality however is most common in low to middle income countries,[155] while symptoms were most prevalent (as much as 20%) in the United Kingdom, Australia, New Zealand, and Republic of Ireland; they were lowest (as low as 23%) in Eastern Europe, Indonesia, Greece, Uzbekistan, India, and Ethiopia.[154][dated info] While asthma is more common in affluent countries, it is by no means a restricted problem; the WHO estimate that there are between 15 and 20 million people with asthma in India.[citation needed] In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole.[citation needed] Striking increases in asthma prevalence have been observed in

populations migrating from a rural environment to an urban one,[156][dated info] or from a thirdworld country to Westernized one.[157][dated info] Asthma affects approximately 7% of the population of the United States[124] and 5% of people in the United Kingdom.[158] Asthma causes 4,210 deaths per year in the United States.[153][159] In 2005 in the United States asthma affected more than 22 million people including 6 million children.[160] It accounted for nearly 1/2 million hospitalizations that same year.[160] More boys have asthma than girls, but more women have it than men.[161] Of all children, African Americans and Latinos who live in cities are more at risk for developing asthma.[citation needed] African American children in the U.S. are four times more likely to die of asthma and three times more likely to be hospitalized, compared to their white counterparts.[citation needed] In some Latino neighborhoods, as many as one in three children has been found to have asthma.[162] In England, an estimated 261,400 people were newly diagnosed with asthma in 2005; 5.7 million people had an asthma diagnosis and were prescribed 32.6 million asthma-related prescriptions.[163] The frequency of atopic dermatitis, asthma, urticaria and allergic contact dermatitis has been found to be lower in psoriatic patients.[57]
[edit] Increasing frequency

Rates of asthma have increased significantly between the 1960s and 2008.[164][165] Some 9% of US children had asthma in 2001, compared with just 3.6% in 1980. The World Health Organization (WHO) reports that some 10% of the Swiss population suffers from asthma today,[166] compared with just 2% some 2530 years ago. In the United States specifically data from several national surveys in the United States reveal the age-adjusted prevalence of asthma increased from 7.3 to 8.2 percent during the years 2001 through 2009 [167]. Previous analysis of data from 2001 to 2007 had suggested the prevalence of asthma was stable.[168]
[edit] Variability

Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.[62] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in Mexicans and Koreans.[169][170][171] Mortality rates follow similar trends, and response to salbutamol is lower in Puerto Ricans than in African Americans or Mexicans.[172][173] As with worldwide asthma disparities, differences in asthma prevalence, mortality, and drug response in the US may be explained by differences in genetic, social and environmental risk factors. Asthma prevalence also differs between populations of the same ethnicity who are born and live in different places.[174] US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.[175]

There is no correlation between asthma and gender in children. More adult women are diagnosed with asthma than adult men, but this does not necessarily mean that more adult women have asthma.[176]

[edit] History
This section requires expansion.

Asthma was first recognized and named by Hippocrates circa 450 BC. During the 1930s50s, asthma was considered as being one of the 'holy seven' psychosomatic illnesses. Its aetiology was considered to be psychological, with treatment often based on psychoanalysis and other 'talking cures'.[177] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, so they considered that the treatment of depression was especially important for individuals with asthma.[177] among the first papers in modern medicine, is one that was published in 1873 and this paper tried to explain the pathophysiology of the disease.[178] And one of the first papers discussing treatment of asthma was released in 1872, the author concluded in his paper that asthma can be cured by rubbing the chest with chloroform liniment.[179] Among the first times researchers referred to medical treatment was in 1880, when Dr. J. B. Berkart used IV therapy to administer doses of a drug called pilocarpin.[180][181] In 1886, F.H. Bosworth FH suspected a connection between asthma and hay fever.[182] Epinephrine was first referred to in the treatment of asthma in 1905,[183] and for acute asthma in 1910.[184]

Drowning Drowning
From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Drowning (disambiguation) and Drown (disambiguation).

Drowning / Near Drowning

Classification and external resources

Vasily Perov: The drowned, 1867

ICD-10

T75.1

ICD-9

994.1

DiseasesDB

3957

MedlinePlus

000046

eMedicine

emerg/744

MeSH

C23.550.260.393

Drowning is death from asphyxia due to suffocation caused by water entering the lungs and preventing the absorption of oxygen leading to cerebral hypoxia.[1] Near drowning is the survival of a drowning event involving unconsciousness or water inhalation and can lead to serious secondary complications, including death, after the event.[1][2] According to the World Health Organization, drowning is the 3rd leading cause of unintentional injury death worldwide, accounting for 7% of all injury related deaths (est. 388,000 deaths by drowning in 2004, excluding those due to natural disasters), with 96% of these deaths occurring in low- and middle-income countries.[3] In many countries, drowning is one of the leading causes of death for children under 12 years old. For example, in the United States, it is the second leading cause of death (after motor vehicle crashes) in children 12 and younger.[4] The rate of drowning in populations around the world varies widely according to their access to water, the climate and the national swimming culture. Drowning itself is quick and silent, although it may be preceded by distress which is more visible.[5] A person drowning is unable to shout or call for help, or seek attention, as they cannot obtain enough air. The instinctive drowning response is the final set of autonomic reactions in

the 20 60 seconds before sinking underwater, and to the untrained eye can look similar to calm safe behavior.[5][6] Lifeguards and other persons trained in rescue learn to recognize drowning people by watching for these instinctive movements.[5] Drowning occurs more frequently in males and the young.[4] Surveys indicate that 10% of children under 5 have experienced a situation with a high risk of drowning.

Contents
[hide]

1 Classification 2 Behavior, signs and symptoms 3 Cause 4 Pathophysiology o 4.1 Clinical background o 4.2 Overview o 4.3 Body's reaction to submersion o 4.4 Oxygen deprivation o 4.5 Water inhalation 5 Management o 5.1 Surveillance 6 Epidemiology 7 Society and culture 8 References 9 External links

[edit] Classification
Experts differentiate between distress and drowning. They also divide drowning into passive and secondary:

Distress - these are people in trouble and distress, but who still have the ability to keep afloat, signal for help and take actions. Drowning - these are people suffocating and in imminent danger of death within seconds, and fall into two categories:

Passive drowning - people who suddenly sink or have sunk due to a change in their circumstances. Examples include people who drown in an accident, or due to sudden loss of consciousness or sudden medical condition.

Active drowning - people such as non-swimmers and the exhausted or hypothermic at the surface, who are unable to hold their mouth above water and are suffocating due to lack of air. Instinctively, people in such cases perform well known behaviors

in the last 20 - 60 seconds before being submerged, representing the body's last efforts to obtain air. Notably such people are unable to call for help, talk, reach for rescue equipment, or alert swimmers even feet away, and they may drown quickly and silently close to other swimmers or safety.

[edit] Behavior, signs and symptoms

Main article: Instinctive drowning response

Drowning is most often quick and unspectacular. Its media depictions as a loud, violent struggle have much more in common with distressed non-swimmers, who may well drown but have not yet begun. In particular, an asphyxiating person is seldom able to call for help.[7] The instinctive drowning response covers many signs or behaviors associated with drowning or near-drowning:

Head low in the water, mouth at water level Head tilted back with mouth open Eyes glassy and empty, unable to focus Eyes open, with fear evident on the face Hyperventilating or gasping Trying to swim in a particular direction but not making headway Trying to roll over on the back to float Uncontrollable movement of arms and legs, rarely out of the water.

Pia notes that drowning begins at the point a person is unable to keep their mouth above water; inhalation of water takes place at a later stage.[8] Most victims demonstrating the instinctive drowning response do not show prior evidence of distress.[8]

[edit] Cause

Children have drowned in buckets and toilets.

Most drownings occur when the victim is in water (90% in freshwater (rivers, lakes and pools), 10% in seawater). Drownings in other fluids are rare, and are often related to industrial accidents.[citation needed] People have drowned in as little as 30 mm of water lying face down, in one case in a wheel rut.[citation needed] Children have drowned in baths, buckets and toilets; inebriates or those under the influence of drugs have died in puddles. Drowning can take place in other circumstances than those in popular awareness, for instance:

Deep water blackout - caused by latent hypoxia upon ascent from depth, where the partial pressure of oxygen in the lungs under pressure at the bottom of a deep free-dive is adequate to support consciousness but drops below the blackout threshold as the water pressure decreases on the ascent. It usually strikes upon arriving near the surface as the pressure approaches normal atmospheric pressure. Shallow water blackout - caused by hyperventilation prior to swimming or diving. The primary urge to breathe (more precisely: to exhale) is triggered by rising carbon dioxide (CO2) levels in the bloodstream.[9] The body detects CO2 levels very accurately and relies on this to control breathing.[9] Hyperventilation artificially depletes this, but leaves the diver susceptible to sudden loss of consciousness without warning from hypoxia. There is no bodily sensation that warns a diver of an impending blackout, and victims (often capable swimmers swimming under the surface in shallow water) become unconscious and drown quietly without alerting anyone to the fact that there is a problem; they are typically found on the bottom.

Secondary drowning - Inhaled fluid can act as an irritant inside the lungs. Physiological responses to even small quantities include the extrusion of liquid into the lungs (pulmonary edema) over the following hours, but this reduces the ability to exchange air and can lead to a person "drowning in their own body fluid". Certain poisonous vapors or gases (as for example in chemical warfare), or vomit can have a similar effect. The reaction can take place up to 72 hours after a near drowning incident, and may lead to a serious condition or death.

[edit] Pathophysiology
[edit] Clinical background

A continued lack of oxygen in the brain, known as hypoxia, will quickly render a victim unconscious usually around a blood partial pressure of oxygen of 25-30 mmHg. An unconscious victim rescued with an airway still sealed from Laryngospasm (involuntary sealing of the throat) stands a good chance of a full recovery. Artificial respiration is also much more effective without water in the lungs. At this point the victim stands a good chance of recovery if attended to within minutes.

[edit] Overview This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (March 2011) This section's factual accuracy may be compromised due to out-of-date information. Please help improve the article by updating it. There may be additional information on the talk page. (January 2011)

A continued lack of oxygen in the brain, hypoxia, will quickly render a victim unconscious usually around a blood partial pressure of oxygen of 25-30mmHg. An unconscious victim rescued with an airway still sealed from laryngospasm stands a good chance of a full recovery. Artificial respiration is also much more effective without water in the lungs. At this point the victim stands a good chance of recovery if attended to within minutes. Latent hypoxia is a special condition leading to unconsciousness where the partial pressure of oxygen in the lungs under pressure at the bottom of a deep free-dive is adequate to support consciousness but drops below the blackout threshold as the water pressure decreases on the ascent, usually close to the surface as the pressure approaches normal atmospheric pressure. A blackout on ascent like this is called a deep water blackout. The brain cannot survive long without oxygen and the continued lack of oxygen in the blood combined with the cardiac arrest will lead to the deterioration of brain cells causing first brain damage and eventually brain death from which recovery is generally considered impossible. A lack of oxygen or chemical changes in the lungs may cause the heart to stop beating; this cardiac arrest stops the flow of blood and thus stops the transport of oxygen to the brain. Cardiac arrest used to be the traditional point of death but at this point there is still a chance of recovery. The brain will die after approximately six minutes without oxygen but special conditions may prolong this (see 'cold water drowning' below). As well as the direct effect of oxygen deprivation, there are also dangerous effects on blood chemistry if water is taken into the lungs. The mechanism for this is different for fresh and seawater.

Freshwater taken into the lungs will be pulled into the pulmonary circulation by osmosis. The dilution of blood leads to hemolysis (bursting of red blood cells). The resulting elevation of plasma K+ (potassium) level and depression of Na+ (sodium) level alter the electrical activity of the heart often causing ventricular fibrillation. In animal experiments this effect was shown to be capable of causing cardiac arrest in 2 to 3 minutes. Acute renal failure can also result from hemoglobin from the burst blood cells accumulating in the kidneys, and cardiac arrest can also result if cold freshwater taken into the bloodstream sufficiently cools the heart.

Sea water is hypertonic to blood (more salty). It poses the opposite danger. Osmosis will instead pull water from the bloodstream into the lungs, thickening the blood. In animal experiments the thicker blood requires more work from the heart leading to cardiac arrest in 8 to 10 minutes.

Autopsies on human drowning victims show no indications of these effects and there appears to be little difference between drownings in salt water and fresh water. After death, rigor mortis will set in and remains for about two days, depending on many factors including water temperature.
[edit] Body's reaction to submersion

Submerging the face in water colder than about 21 C (70 F) triggers the mammalian diving reflex, found in mammals, and especially in marine mammals such as whales and seals. This reflex protects the body by putting it into energy saving mode to maximize the time it can stay under water. The strength of this reflex is greater in colder water and has three principal effects:

Bradycardia, a slowing of the heart rate by up to 50% in humans. Peripheral vasoconstriction, the restriction of the blood flow to the extremities to increase the blood and oxygen supply to the vital organs, especially the brain. Blood Shift, the shifting of blood to the thoracic cavity, the region of the chest between the diaphragm and the neck, to avoid the collapse of the lungs under higher pressure during deeper dives.

The reflex action is automatic and allows both a conscious and an unconscious person to survive longer without oxygen under water than in a comparable situation on dry land. The exact mechanism for this effect has been debated and may be a result of brain cooling similar to the protective effects seen in patients treated with deep hypothermia.[10][11]
[edit] Oxygen deprivation

A conscious victim will hold his or her breath (see Apnea) and will try to access air, often resulting in panic, including rapid body movement. This uses up more oxygen in the blood stream and reduces the time to unconsciousness. The victim can voluntarily hold his or her breath for some time, but the breathing reflex will increase until the victim will try to breathe, even when submerged. The breathing reflex in the human body is weakly related to the amount of oxygen in the blood but strongly related to the amount of carbon dioxide (see Hypercapnia). During apnea, the oxygen in the body is used by the cells, and excreted as carbon dioxide. Thus, the level of oxygen in the blood decreases, and the level of carbon dioxide increases. Increasing carbon dioxide levels lead to a stronger and stronger breathing reflex, up to the breath-hold breakpoint, at which the victim can no longer voluntarily hold his or her breath. This typically occurs at an arterial partial pressure

of carbon dioxide of 55 mm Hg, but may differ significantly from individual to individual and can be increased through training. The breath-hold break point can be suppressed or delayed either intentionally or unintentionally. Hyperventilation before any dive, deep or shallow, flushes out carbon dioxide in the blood resulting in a dive commencing with an abnormally low carbon dioxide level; a potentially dangerous condition known as hypocapnia. The level of carbon dioxide in the blood after hyperventilation may then be insufficient to trigger the breathing reflex later in the dive and a blackout may occur without warning and before the diver feels any urgent need to breathe. This can occur at any depth and is common in distance breath-hold divers in swimming pools. Hyperventilation is often used by both deep and distance free-divers to flush out carbon dioxide from the lungs to suppress the breathing reflex for longer. It is important not to mistake this for an attempt to increase the body's oxygen store. The body at rest is fully oxygenated by normal breathing and cannot take on any more. Breath holding in water should always be supervised by a second person, as by hyperventilating, one increases the risk of shallow water blackout because insufficient carbon dioxide levels in the blood fail to trigger the breathing reflex.
[edit] Water inhalation

If water enters the airways of a conscious victim, the victim will try to cough up the water or swallow it, thus inhaling more water involuntarily. Upon water entering the airways, both conscious and unconscious victims experience laryngospasm, that is the larynx or the vocal cords in the throat constrict and seal the air tube. This prevents water from entering the lungs. Because of this laryngospasm, water enters the stomach in the initial phase of drowning and very little water enters the lungs. Unfortunately, this can interfere with air entering the lungs, too. In most victims, the laryngospasm relaxes some time after unconsciousness and water can enter the lungs causing a "wet drowning". However, about 10-15% of victims maintain this seal until cardiac arrest. This is called "dry drowning", as no water enters the lungs. In forensic pathology, water in the lungs indicates that the victim was still alive at the point of submersion. Absence of water in the lungs may be either a dry drowning or indicates a death before submersion.

[edit] Management
Rescue involves bringing the persons mouth and nose above the water surface. A drowning person may cling to the rescuer and try to pull himself out of the water, submerging the rescuer in the process. Thus it is advised that the rescuer approach with a buoyant object, or from behind, twisting the person's arm on the back to restrict movement. If the rescuer does get pushed under water, they should dive downwards to escape the person. After a successful approach, negatively buoyant objects such as a weight belt are removed. The priority is then to transport the person to the water's edge in

preparation for removal from the water. The person is turned on their back with a secure grip used to tow from behind. If the person is cooperative they may be towed in a similar fashion held at the armpits. If the person is unconscious they may be pulled in a similar fashion held at the chin and cheeks, ensuring that the mouth and nose are well above the water. Special care has to be taken for people with suspected spinal injuries, and a back board (spinal board) may be needed for the rescue. In water, CPR is ineffective, and the goal should be to bring the person to a stable ground quickly and then to start CPR. Once on ground chest compressions are performed if the patient is pulseless, and if they are not breathing rescue breaths.[12] 100% oxygen is neither recommended nor discouraged.[13] Treatment for hypothermia may also be necessary. The Heimlich maneuver is not recommended;[14] the technique may have relevance in situations where airways are obstructed by solids but not fluids. Performing the manoeuver on drowning people not only delays ventilation but may induce vomiting, which if aspirated will place the patient in a far worse situation. Moreover, the use of the Heimlich manoeuver in any choking situation involving solids or fluids has become controversial and is generally no longer taught. For more information on this debate refer to the article Henry Heimlich. Because of the mammalian diving reflex (see above), person submerged in cold water and apparently drowned may revive after a relatively long period. Rescuers retrieving an apparently dead person from water significantly below body temperature should not consider the rescued person dead until he or she is warm and dead.
[edit] Surveillance

Many pools and designated bathing areas either have lifeguards, a pool safety camera system for local or remote monitoring, or computer aided drowning detection. However, bystanders play an important role in drowning detection and either intervention or the notification of authorities by phone or alarm.

[edit] Epidemiology

Disability-adjusted life year for drowning per 100,000 inhabitants in 2004.[15]

no data < 100 100-150 150-200 200-250 250-300 300-350 350-400 400-450 450-500 500-600 600-700 > 700

In the United States in 2006, 1100 people under 20 years of age died from drowning.[16] Typically the United Kingdom suffers 450 drownings per annum or 1 per 150,000 of population whereas the United States suffers 6,500 drownings or around 1 per 50,000 of population. In Asia, according to a study by The Alliance for Safe Children, suffocation and drowning were the most easily preventable causes of death for children under five years of age;[17][18] a 2008 report by the organization found that in Bangladesh, for instance, 46 children drown each day.[19] People who drown are more likely to be male, young or adolescent.[4] Surveys indicate that 10% of children under 5 have experienced a situation with a high risk of drowning. About 175,000 children die through drowning every year.[20] The causes of drowning cases in the US from 1999 to 2006 are as follows[21]: 31.0% Drowning and submersion while in natural water 27.9% Unspecified drowning and submersion 14.5% Drowning and submersion while in swimming pool 9.4% Drowning and submersion while in bathtub 7.2% Drowning and submersion following fall into natural water 6.3% Other specified drowning and submersion 2.9% Drowning and submersion following fall into swimming pool 0.9% Drowning and submersion following fall into bathtub

[edit] Society and culture

In Europe, drowning was used as capital punishment. In fact, during the Middle Ages, a sentence of death was read using the words "cum fossa et furca," or "with drowning-pit and gallows." Furthermore, drowning was used as a way to determine if a woman was a witch. The idea was that witches would float and innocent women would drown. For more details, see trial by drowning. It is understood that drowning was used as the least brutal form of execution, and was therefore reserved primarily for women, although favoured men were executed in this way as well. Drowning survived as a method of execution in Europe until the 17th and 18th centuries. England had abolished the practice by 1623, Scotland by 1685, Switzerland in 1652, Austria in 1776, Iceland in 1777, and Russia by the beginning of the 1800s. France revived the practice during the French Revolution (17891799) and was carried out by Jean-Baptiste Carrier at Nantes.[22]

Choking Choking
From Wikipedia, the free encyclopedia Jump to: navigation, search "Chocking" redirects here. For the mechanical tool, see Wheel chock. For the act of compressing someone's neck, see Strangling. For other uses, see Choke.

Choking
Classification and external resources

ICD-10

F41.0, R06.8, T17, W78-W80

ICD-9

784.9, 933.1

MeSH

D000402

Choking is the mechanical obstruction of the flow of air from the environment into the lungs. Choking prevents breathing, and can be partial or complete, with partial choking allowing some,

although inadequate, flow of air into the lungs. Prolonged or complete choking results in asphyxia which leads to anoxia and is potentially fatal. Oxygen stored in the blood and lungs keep the victim alive for several minutes after breathing is stopped completely.[1] Choking can be caused by:

Physical obstruction of the airway by a foreign body. Respiratory diseases that involve obstruction of the airway. Compression of the laryngopharynx, larynx or vertebrate trachea in strangulation.

Contents
[hide]

1 Foreign objects 2 Symptoms and clinical signs 3 Treatment o 3.1 Encouraging the victim to cough o 3.2 Back slaps o 3.3 Abdominal thrusts 3.3.1 Self treatment with abdominal thrusts o 3.4 Modified chest thrusts o 3.5 Finger sweeping o 3.6 Direct vision removal 4 CPR 5 Notable victims 6 Other uses of abdominal thrusts 7 References 8 External links

[edit] Foreign objects

The type of choking most commonly recognized as such by the public is the lodging of foreign objects (also known as foreign bodies, but consisting of any object which comes from outside the body itself, including food, toys or household objects) in the airway.[2] This type of choking is often suffered by small children, who are unable to appreciate the hazard inherent in putting small objects in their mouth.[3] In adults, it mostly occurs whilst the patient is eating. In one study, peanuts were the most common obstruction.[4]

[edit] Symptoms and clinical signs

The person cannot speak or cry out, or has great difficulty and limited ability to do so. Breathing, if possible, is labored, producing gasping or wheezing.

The person has a violent and largely involuntary cough, gurgle, or vomiting noise, though more serious choking victims will have a limited (if any) ability to produce these symptoms since they require at least some air movement. The person desperately clutches his or her throat or mouth, or attempts to induce vomiting by putting their fingers down their throat. If breathing is not restored, the person's face turns blue (cyanosis) from lack of oxygen. The person does any or all of the above, and if breathing is not restored, then becomes unconscious.

[edit] Treatment
Choking can be treated with a number of different procedures, with both basic techniques available for first aiders and more advanced techniques available for health professionals. Many members of the public associate abdominal thrusts, also known as the Heimlich Maneuver with the correct procedure for choking, which is partly due to the widespread use of this technique in movies, which in turn was based on the widespread adoption of this technique in the United States at the time. Most modern protocols, including those of the American Heart Association and the American Red Cross, who changed policy in 2006[5] from recommending only abdominal thrusts) involve several stages, designed to apply increasingly more pressure. The key stages in most modern protocols include:
[edit] Encouraging the victim to cough

This stage was introduced in many protocols as it was found that many people were too quick to undertake potentially dangerous interventions, such as abdominal thrusts, for items which could have been dislodged without intervention. Also, if the choking is caused by an irritating substance rather than an obstructing one, and if conscious, the patient should be allowed to drink water on their own to try to clear the throat. Since the airway is already closed, there is very little danger of water entering the lungs. Coughing is normal after most of the irritant has cleared, and at this point the patient will probably refuse any additional water for a short time.
[edit] Back slaps

The majority of protocols now advocate the use of hard blows with the heel of the hand on the upper back of the victim. The number to be used varies by training organization, but is usually between five and twenty. The back slap is designed to use percussion to create pressure behind the blockage, assisting the patient in dislodging the article. In some cases the physical vibration of the action may also be enough to cause movement of the article sufficient to allow clearance of the airway.

Almost all protocols give back slaps as a technique to be used before to the consideration of potentially damaging interventions such as abdominal thrusts,[6][7] but Henry Heimlich, noted for promulgating abdominal thrusts, wrote in a letter to the New York Times that back slaps were proven to cause death by lodging foreign objects in to the windpipe.[8] The findings of a 1982 Yale study by Day, DuBois, and Crelin that "persuaded the American Heart Association to stop recommending back blows for dealing with choking...was partially funded by Heimlich's own foundation."[9] According to Roger White MD of the Mayo Clinic and American Heart Association (AHA), "There was never any science here. Heimlich overpowered science all along the way with his slick tactics and intimidation, and everyone, including us at the AHA, caved in."[10]
[edit] Abdominal thrusts

A demonstration of abdominal thrusts

Abdominal thrusts, also known by the proprietary name the Heimlich Maneuver (after Henry Heimlich, who first described the procedure in a June 1974 informal article entitled "Pop Goes the Cafe Coronary", published in the journal Emergency Medicine). Edward A. Patrick, MD, PhD, an associate of Heimlich, has claimed to be the uncredited co-developer of the procedure.[11] Heimlich has objected to the name "abdominal thrusts" on the grounds that the vagueness of the term "abdomen" could cause the rescuer to exert force at the wrong site.[12]

Performing abdominal thrusts involves a rescuer standing behind a patient and using their hands to exert pressure on the bottom of the diaphragm. This compresses the lungs and exerts pressure on any object lodged in the trachea, hopefully expelling it. This amounts to an artificial cough. Due to the forceful nature of the procedure, even when done correctly it can injure the person on whom it is performed. Bruising to the abdomen is highly likely and more serious injuries can occur, including fracture of the xiphoid process or ribs.[13] In some areas, such as Australia, authorities believe that there is not enough scientific evidence to support the use of Abdominal thrusts and their use is not recommended in first aid.[14] [edit] Self treatment with abdominal thrusts A person may also perform abdominal thrusts on themselves by using a fixed object such as a railing or the back of a chair to apply pressure where a rescuer's hands would normally do so. As with other forms of the procedure, it is possible that internal injuries may result.
[edit] Modified chest thrusts

A modified version of the technique is sometimes taught for use with pregnant and/or obese patients. The rescuer places their hand in the center of the chest to compress, rather than in the abdomen.
[edit] Finger sweeping

The American Medical Association advocates sweeping the fingers across the back of the throat to attempt to dislodge airway obstructions, once the choking victim becomes unconscious.[15] Some protocols advocate the use of the rescuer's finger to 'sweep' foreign objects away once they have reached the mouth.[citation needed] However, many modern protocols recommend against the use of the finger sweep as if the patient is conscious, they will be able to remove the foreign object themselves, or if they are unconscious, the rescuer should simply place them in the recovery position (where the object should fall out due to gravity). There is also a risk of causing further damage (for instance inducing vomiting) by using a finger sweep technique.
[edit] Direct vision removal

The advanced medical procedure to remove such objects is inspection of the airway with a laryngoscope or bronchoscope, and removal of the object under direct vision, followed by CPR if the patient does not start breathing on their own. Severe cases where there is an inability to remove the object may require cricothyrotomy.

[edit] CPR
In most protocols, once the patient has become unconscious, the emphasis switches to performing CPR, involving both chest compressions and artificial respiration. These actions are

often enough to dislodge the item sufficiently for air to pass it, allowing gaseous exchange in the lungs.

[edit] Notable victims

United States President George W. Bush survived choking on a pretzel on January 13, 2002, receiving major media coverage.[16] Jimmie Foxx, a famous Major League Baseball player, died by choking on a bone.[17] Tennessee Williams, the playwright, died after choking on a bottle cap.[18] An urban legend states that obese singer Mama Cass choked to death on a ham sandwich. This was borne out of a quickly discarded speculation by the coroner, who noted a partly eaten ham sandwich and figured she may have choked to death. In fact, she died of a heart condition, often wrongly referred to in the media as heart failure.[19] The Queen Mother was admitted to a UK Hospital for an operation in May 1993 after choking on a fish bone.[20]

[edit] Other uses of abdominal thrusts

Dr. Heimlich also advocates the use of the technique as a treatment for drowning[21] and asthma[22] attacks, but Heimlich's promotion to use the maneuver to treat these conditions resulted in marginal acceptance. Criticism of these uses has been the subject of numerous print and television reports which resulted from an internet and media campaign by his son, Peter M. Heimlich, who alleges that in August 1974 his father published the first of a series of fraudulent case reports in order to promote the use of abdominal thrusts for near-drowning rescue.[23]

Dyspnea Dyspnea
From Wikipedia, the free encyclopedia Jump to: navigation, search

Dyspnea
ICD-10 R06.0

ICD-9

786.09

DiseasesDB

15892

MedlinePlus

003075

MeSH

D004417

Dyspnea ( /dspni/ disp-NEE-; also dyspnoea; Latin: dyspnoea; Greek: , dspnoia), shortness of breath (SOB), or air hunger,[1] is the subjective symptom of breathlessness.[2][3] It is a normal symptom of heavy exertion but becomes pathological if it occurs in unexpected situations.[2] In 85% of cases it is due to either asthma, pneumonia, cardiac ischemia, interstitial lung disease, congestive heart failure, chronic obstructive pulmonary disease, or psychogenic causes.[4] Treatment typically depends on the underlying cause.[5]

Contents
[hide]

1 Definition 2 Differential diagnosis o 2.1 Acute coronary syndrome o 2.2 Congestive heart failure o 2.3 Chronic obstructive pulmonary disease o 2.4 Asthma o 2.5 Pneumothorax o 2.6 Pneumonia o 2.7 Pulmonary embolism o 2.8 Pulmonary hypertension o 2.9 Other 3 Pathophysiology 4 Evaluation o 4.1 Blood tests o 4.2 Imaging 5 Treatment 6 Physiotherapy o 6.1 Palliative 7 Epidemiology 8 Etymology 9 See also 10 References 11 External links

[edit] Definition
Dyspnea does not have a well-defined or universally accepted definition.[4] It is defined by the American Thoracic Society as the "subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses."[6] Other definitions of dyspnea include "difficulty in breathing",[7] "disordered or inadequate breathing",[8] "uncomfortable awareness of breathing",[3] or simple "breathlessness".[2] Acute breathlessness is defined as severe shortness of breath that develops over minutes to hours.[5] Chronic breathlessness on the other hand comes on over weeks or months.[9] Dyspnea is distinct from labored breathing, which is rather a common physical presentation of respiratory distress.

[edit] Differential diagnosis

Main article: Differential diagnosis of dyspnea

While shortness of breath is generally caused by disorders of the cardiac or respiratory system other system such as neurological,[10] musculoskeletal, endocrine, hematologic, and psychiatric may be the cause.[4] DiagnosisPro, an online medical expert system, listed 497 distinct causes in October 2010.[11] The most common cardiovascular causes are acute myocardial infarction and congestive heart failure while common pulmonary causes include chronic obstructive pulmonary disease, asthma, pneumothorax, and pneumonia.[2] On a pathophysiological basis the causes can be divided into: (1) an increased awareness of normal breathing such as during an anxiety attack, (2) an increase in the work of breathing and (3) an abnormality in the ventilatory system.[10]
[edit] Acute coronary syndrome

Acute coronary syndrome frequently presents with retrosternal chest discomfort and difficulty catching the breath.[2] It however may atypically present with shortness of breath alone.[12] Risk factors include old age, smoking, hypertension, hyperlipidemia, and diabetes.[12] An electrocardiogram and cardiac enzymes are important both for diagnosis and directing treatment.[12] Treatment involves measures to decrease the oxygen requirement of the heart and efforts to increase blood flow.[2]
[edit] Congestive heart failure

Congestive heart failure frequently presents with SOB with exertion, orthopnea, and paroxysmal nocturnal dyspnea.[2] It affects between 1-2% of the general United States population and occurs in 10% of those over 65 years old.[2][12] Risk factors for acute decompensation include high dietary salt intake, medication noncompliance, cardiac ischemia, dysrhythmias, renal failure, pulmonary emboli, hypertension, and infections.[12] Treatment efforts are directed towards decreasing lung congestion.[2]

[edit] Chronic obstructive pulmonary disease

People with chronic obstructive pulmonary disease (COPD), most commonly emphysema or chronic bronchitis, frequently have chronic shortness of breath and a chronic productive cough.[2] An acute exacerbation presents with increased shortness of breath and sputum production.[2] COPD is a risk factor for pneumothorax; thus this condition should be ruled out.[2] In an acute exacerbation treatment is with a combination of anticholinergics, beta2-adrenoceptor agonists, steroids and possibly positive pressure ventilation.[2]
[edit] Asthma

Asthma is the most common reason for presenting to the emergency with shortness of breath.[2] It is the most common lung disease in both developing and developed countries affecting about 5% of the population.[2] Other symptoms include wheezing, tightness in the chest, and a non productive cough.[2] Inhaled beta2-adrenergic agonist (salbutamol) are first line therapy and usually lead to prompt improvement.[2]
[edit] Pneumothorax

Pneumothorax presents typically with pleuritic chest pain of acute onset and shortness of breath not improved with oxygen.[2] Physical findings may include absent breath sounds on one side of the chest, jugular venous distension, and tracheal deviation.[2]
[edit] Pneumonia

The symptoms of pneumonia are fever, productive cough, shortness of breath, and pleuritic chest pain.[2] Inspiratory crackles may be heard on exam.[2] A chest x-ray can be useful to differential pneumonia from congestive heart failure.[2] As the cause is usually a bacterial infections antibiotics are typically used for treatment.[2]
[edit] Pulmonary embolism

Pulmonary embolism classically presents with an acute onset of shortness of breath.[2] Other presenting symptoms include pleuritic chest pain, cough, hemoptysis, and fever.[2] Risk factors include deep vein thrombosis, recent surgery, cancer, and previous thromboembolism.[2] It must always be considered in those with acute onset of shortness of breath due to its high risk of mortality.[2] Diagnosis however may be difficult.[2] Treatment is typically with anticoagulants.[2]
[edit] Pulmonary hypertension

Pulmonary hypertension is high blood pressure in the arteries of the lungs that can lead to heart failure. PH may be associated with shortness of breath, dizziness and fatigue, and the severity of symptoms usually correlates with the progression of the disease. Diagnosis of PH is often delayed as it is relatively rare and the symptoms are atypical. PH affects people of all ages, races and ethnic backgrounds. Although anyone can get PH, there are risk factors that make some people more susceptible. There are a number of different tests used to diagnose PH. The

definitive test is right hear catheterization. While there is currently no cure for PH, different treatment options are available to help manage the disease and prolong life.
[edit] Other

Other important or common causes of shortness of breath include cardiac tamponade, anemia, anaphylaxis, interstitial lung disease and panic attacks.[4][5][13] Cardiac tamponade presents with dyspnea, tachycardia, elevated jugular venous pressure, and pulsus paradoxus.[13] The gold standard for diagnosis is ultrasound.[13] Anemia, that develops gradually, usually presents with exertional dyspnea, fatigue, weakness, and tachycardia.[13] It may lead to heart failure.[13] Anaphylaxis typically begins over a few minutes in a person with a previous history of the same.[5] Other symptoms include urticaria, throat swelling, and gastrointestinal upset.[5] The primary treatment is epinephrine.[5] Interstitial lung disease presents with gradual onset of shortness of breath typically with a history of a predisposing environmental exposure.[4] Shortness of breath is often the only symptom in those with tachydysrhythmias.[12] Panic attacks typically present with hyperventilation, sweating, and numbness.[5] They are however a diagnosis of exclusion.[4] Around 2/3 of women experience shortness of breath as a part of a normal pregnancy.[8] Neurological conditions such as spinal cord injury, phrenic nerve injuries, GuillainBarre syndrome, amyotrophic lateral sclerosis, multiple sclerosis and muscular dystrophy can all cause an individual to experience shortness of breath.[10]

[edit] Pathophysiology
A number of different physiological pathway may lead to shortness of breath including via chemoreceptors, mechanoreceptors, and lung receptors.[12] It is currently thought that there are three main components that contribute to dyspnea: afferent signals, efferent signals, and central information processing. It is believed that the central processing in the brain compares the afferent and efferent signals, and that a "mismatch" results in the sensation of dyspnea. In other words, dyspnea may result when the need for ventilation (afferent signaling) is not being met by the physical breathing that is occurring (efferent signaling).[14] Afferent signals are sensory neuronal signals that ascend to the brain. Afferent neurons significant in dyspnea arise from a large number of sources including the carotid bodies, medulla, lungs, and chest wall. Chemoreceptors in the carotid bodies and medulla supply information regarding the blood gas levels of O2, CO2 and H+. In the lungs, juxtacapillary (J) receptors are sensitive to pulmonary interstitial edema, while stretch receptors signal bronchoconstriction. Muscle spindles in the chest wall signal the stretch and tension of the respiratory muscles. Thus, poor ventilation leading to hypercapnia, left heart failure leading to interstitial edema (impairing gas exchange), asthma causing bronchoconstriction (limiting airflow) and muscle fatigue leading to ineffective respiratory muscle action could all contribute to a feeling of dyspnea.[14] Efferent signals are the motor neuronal signals descending to the respiratory muscles. The most important respiratory muscle is the diaphragm. Other respiratory muscles include the external and internal intercostal muscles, the abdominal muscles and the accessory breathing muscles.

As the brain receives its plentiful supply of afferent information relating to ventilation, it is able to compare it to the current level of respiration as determined by the efferent signals. If the level of respiration is inappropriate for the body's status then dyspnea might occur. It is worth noting that there is a psychological component of dyspnea as well, as some people may become aware of their breathing in such circumstances but not experience the distress typical of dyspnea.[14]

[edit] Evaluation
mMRC Breathlessness Scale Grade 0 1 2 3 4 Degree of dyspnea no dyspnea except with strenuous exercise dyspnea when walking up an incline or hurrying on the level walks slower than most on the level, or stops after 15 minutes of walking on the level stops after a few minutes of walking on the level with minimal activity such as getting dressed, too dyspneic to leave the house

The initial approach to evaluation begins by assessment of the airway, breathing, and circulation followed by a medical history and physical examination.[2] Signs that represent significant severity include hypotension, hypoxemia, tracheal deviation, altered mental status, unstable dysrhythmia, stridor, intercostal indrawing, cyanosis, and absent breath sounds.[4] A number of scales may be used to quantify the degree of shortness of breath.[15] It may be subjectively rated on a scale from 1 to 10 with descriptors associated with the number (The Modified Borg Scale).[15] Alternatively a scale such as the MRC Breathlessness Scale might be used - it suggests five different grades of dyspnea based on the circumstances in which it arises.[16]
[edit] Blood tests

A number of labs maybe helpful in determining the cause of shortness of breath. D-dimer while useful to rule out a pulmonary embolism in those who are at low risk is not of much value if it is positive as it may be positive in a number of conditions that lead to shortness of breath.[12] A low level of brain natriuretic peptide is useful in ruling out congestive heart failure however a high level while supportive of the diagnosis could also be due to advanced age, renal failure, acute coronary syndrome, or a large pulmonary embolism.[12]

[edit] Imaging

A chest x-ray is useful to confirm or rule out a pneumothorax, pulmonary edema, or pneumonia.[12] Spiral computed tomography with intravenousradiocontrast is the imaging study of choice to evaluate for pulmonary embolism.[12]

[edit] Treatment
In those who are not palliative the primary treatment of shortness of breath is directed at its underlying cause.[5] Extra oxygen is effective in those with hypoxia however has no effect in those with normal blood oxygen saturations even in those with who are palliative.[3][17]

[edit] Physiotherapy
Individuals can benefit from a variety of physical therapy interventions.[18] Persons with neurological/neuromuscular abnormalities may have breathing difficulties due to weak or paralyzed intercostal, abdominal and/or other muscles needed for ventilation.[19] Some physical therapy interventions for this population include active assisted cough techniques,[20] volume augmentation such as breath stacking,[21] education about body position and ventilation patterns[22] and movement strategies to facilitate breathing.[21]
[edit] Palliative

Along with the measure above, systemic immediate release opioids are beneficial in reducing the symptom of shortness of breath due to both cancer and non cancer causes.[3][23] There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitivebehavioral therapy.[24]

[edit] Epidemiology
Shortness of breath is the primary reason 3.5% of people present to the emergency department in the United States. Of these approximately 51% are admitted to hospital and 13% are dead within a year.[25] Some studies have suggested that up to 27% of people suffer from dyspnea,[26] while in dying patients 75% will experience it.[14] Acute shortness of breath is the most common reason people who are palliative visit an emergency department.[3]

Anaphylaxis Anaphylaxis
From Wikipedia, the free encyclopedia Jump to: navigation, search

Anaphylaxis
Classification and external resources

A rash on the back of a person with anaphylaxis.

ICD-10

T78.2

DiseasesDB

29153

eMedicine

med/128

MeSH

D000707

Anaphylaxis is defined as "a serious allergic reaction that is rapid in onset and may cause death".[1] It can result in a number of symptoms including throat swelling, an itchy rash, and low blood pressure. On a pathophysiologic level it is an acute multi-system type I hypersensitivity reaction. The term comes from the Greek words ana, against, and phylaxis, protection.[2] Due in part to the variety of definitions, between 1% and 15% of the population of the United States can be considered "at risk" for having an anaphylactic reaction if they are exposed to one or more allergens. Of those people who actually experience anaphylaxis, up to 1% may die as a result.[3] Anaphylaxis results in approximately 1,500 deaths per year in the United States.[4][5] In the United Kingdom, mortality rates for anaphylaxis have been reported as up to 0.05 per 100,000 population, or around 10-20 a year.[6] Anaphylactic reactions requiring hospital treatment appear to be increasing, with authorities in the UK reporting a threefold increase between 1994 and 2004.[7]

Based on the pathophysiology, anaphylaxis can be divided into "true anaphylaxis" and "pseudoanaphylaxis" or "anaphylactoid reaction." The symptoms, treatment, and risk of death are the same; however, "true" anaphylaxis is caused by degranulation of mast cells or basophils mediated by immunoglobulin E (IgE), and pseudo-anaphylaxis occurs without IgE mediation.[8]

Contents
[hide]

1 Signs and symptoms 2 Causes o 2.1 Food o 2.2 Medication o 2.3 Venom o 2.4 Risk factors 3 Pathophysiology 4 Diagnosis o 4.1 Classification o 4.2 Differential diagnosis 5 Prevention 6 Management o 6.1 Epinephrine o 6.2 Adjuncts o 6.3 Preparedness o 6.4 Prognosis 7 Epidemiology 8 References 9 External links

[edit] Signs and symptoms

Anaphylaxis can present with many different symptoms due to the systemic effects of histamine release.[9] These usually develop over minutes to hours.[10] The most common areas affected include: skin (80% to 90%), respiratory (70%), gastrointestinal (30% to 45%), heart and vasculature (10% to 45%), and central nervous system (10% to 15%)[10] with usual two or more being involved.[11] Skin involvement may include generalized hives, itchiness, flushing, and swelling of the lips, tongue, or throat.[12] Respiratory symptoms may include shortness of breath, wheezes or stridor, and low oxygen.[12] Gastrointestinal symptoms may include crampy abdominal pain, diarrhea, and vomiting.[12] Due to the presence of histamine-releasing cells in the heart, coronary artery spasm may occur with subsequent myocardial infarction or dysrhythmia even in the absence of epinephrine use.[10][11] A drop in blood pressure may result in a feeling of lightheadedness or loss

of consciousness. There may be a loss of bladder control[12] a feeling of anxiety or of "impending doom".[11]

[edit] Causes
Anaphylaxis can occur in response to any allergen. Common triggers include insect bites or stings, foods, medication, and latex rubber.[13] Foods are the most common trigger in children and young adults while medications and insect bites and stings are more common in older adults.[11] Physical factors such as exercise or temperature may also act as trigger.[11]
[edit] Food

Many foods can trigger anaphylaxis. The most common are peanuts, wheat, tree nuts, shellfish, fish, milk, and eggs in Western cultures.[10][11] In the Middle East sesame is common and rice and chickpeas occur more frequently in Asia.[11] Severe cases are usually the result of ingesting the allergen.
[edit] Medication

Any medication may potentially trigger anaphylaxis. The most common to do so include antibiotics (-lactam antibiotics in particular), aspirin, ibuprofen, and other analgesics.[10] Chemotherapy agents and herbal preparations have also been implicated.[11] Some medications (polymyxin, morphine, x-ray contrast among others) may cause an anaphylactoid reaction (anaphylactic-like reaction) on the first exposure.[14] This is usually due to a toxic reaction, rather than the immune system mechanism that occurs with "true" anaphylaxis. The symptoms, risk for complications without treatment, and treatment are the same, however, for both types of reactions. Some vaccinations are also known to cause anaphylactoid reactions.[15]
[edit] Venom

Venom from stinging or biting insects such as Hymenoptera (bees and wasps) or Hemiptera (kissing bugs) may induce anaphylaxis in susceptible people.[10]
[edit] Risk factors

People with atopic diseases such as asthma are at high risk of anaphylaxis. As are those with mastocytosis.[11]

[edit] Pathophysiology
Anaphylaxis is a severe, whole-body allergic reaction. After an initial exposure "sensitizing dose" to a substance like bee sting toxin, the person's immune system becomes sensitized to that

allergen. On a subsequent exposure "shocking dose", an allergic reaction occurs. This reaction is sudden, severe, and involves the whole body. Classified as a type I hypersensitivity, anaphylaxis is triggered when an antigen binds to IgE antibodies on mast cells based in connective tissue throughout the body, which leads to degranulation of the mast cells (the release of inflammatory mediators).[16] These immune mediators cause many symptoms, including common symptoms of allergic reactions, such as itching, hives, and swelling. Anaphylactic shock is an allergic reaction to an antigen that causes circulatory collapse and suffocation due to bronchial and tracheal swelling. Different classes of antibodies are produced by B cells to bind and destroy substances that the immune system has identified as potentially dangerous pathogens. Each B cell produces thousands of identical antibodies that can attack a single, small part of a pathogen. In susceptible individuals, antibodies may be produced against innocuous antigens or allergens, such as components of common foods or plants. One class, the IgE antibodies, can trigger anaphylaxis. Production of IgE antibodies may persist for months, even in the complete absence of the allergen. These IgE antibodies associate with a receptor on the surface of mast cells. If the antibody binds to its specific antigen, then the antibody triggers degranulation of the mast cell. Mast cells become the major effector cells for immediate hypersensitivity and chronic allergic reactions.[17] Mast cells are large cells found in particularly high concentrations in vascularized connective tissues just beneath epithelial surfaces, including the submucosal tissues of the gastrointestinal and respiratory tracts, and the dermis that lies just below the surface of the skin.[16] They contain large granules that store a variety of mediator molecules including the vasoactive amine histamine. Histamine causes dilation of local blood vessels and smooth-muscle contraction. Other molecules in the mast cell granules include lipid inflammatory mediators such as prostaglandin D2 and leukotriene C4 as well as tumor necrosis factor- (TNF-), a cytokine.[16] The importance of TNF- is most noted in the activation of the endothelium. TNF-, the prototype of the TNF family cytokines, can induce endothelial cells to present E-selectin and ICAM-1, both of which are cell adhesion molecules (CAM) that mediate the roll and stick mechanism of leukocyte extravasation, termed diapedesis. While this process is essential for the recruitment of leukocytes to a localized area during an inflammatory response, it can be catastrophic in cases of systemic infection. Point in case, the presence of said infection in the bloodstream, or sepsis, is accompanied by the release of TNF- by macrophages in liver, spleen, and other systemic sites. The systemic release of TNF- causes vasodilatation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually to shock.[16] TNF-, along with the other aforementioned mast cell granule contents become exocytosed upon activation of the mast cell. Activation is achieved only when IgE, bound to the high-affinity Fc receptors (FcR1), are cross-linked by multivalent antigen. The FcR1 is a tetrameric receptor composed of a single chain, responsible for binding the IgE, associated with a single chain and a disulfide linked homodimer of chains that initiate the cell signal pathway.[18] Once the FcR1 are aggregated by the cross-linking process, the immunoreceptor tryrosine-based

activation motifs (ITAMs) in both the and chains are phosphorylated by LYN, a protein tryrosine kinase (PTK) belonging to the Src family. The ITAM domain is simply conserved sequence motif generally composed of two YXXL/I sequences separated by about six to nine amino acids, where Y is tyrosine, L is leucine, I isoleucine, and X any amino acid.[16] Their phosphorylation in the and chains provide high-affinity docking sites for the SH2 domains of additional LYN and the SYK (spleen tyrosine kinase), respectively.[19] These SH2 domains (Src homology 2 domian) are found in a numerous cell-signaling proteins and bind to phosphotyrosine through a very specific sequence.[16] As the signal continues to propagate through the pathway, the membrane-bound molecule, named linker for activation of T cells (LAT), is phosphoyraleted by the LYN and SYK and acts as a scaffold protein, organizing other molecules that complete the degranulation of mast cells, as well as promote further cytokine production.[20] The most notable of these LAT affected molecules is Phospholipase C (PLC). As in many cell signaling pathways PLC hydrolyzes the phosphodiester bond in phosphoatidylinositol-4,5-bisphosphate [PI(4,5)P2] to yield diacylglycerol (DAG) and inositol-1,4,5-triphosphate (IP3). A well-characterized second messenger, IP3, signals the release of calcium from the endoplasmic reticulum. The influx of cytosolic Ca2+ and phosphoatidylserine further active Phosphokinase C (PKC) bound to DAG. Together, it is the cytosolic Ca2+ and PKC signal the degranulation of the mast cell.4 Although less well-mapped, similarly prevailing cell signaling molecules, such as Ras, a monomeric G protein, SOS (son of sevenless homologue) and MAPK (mitogen-activated protein kinase) lead to the upregulation of cytokines and the previously mentioned eicosanoids, prostaglandin D2, and leukotriene C4.[19] While this cell single pathway is sufficient to induce degranulation, it is not the only effective mechanism. Studies with LYK-deficient mice have shown that degranulation is still inducible.[20] Consequently, several alternative pathways leading to mast cell degranulation have been mapped. The first of which, dubbed the complementary pathway, determined that the crosstalk between LYK and another Src family PTK, called FYN, is an essential interaction to degranulation, along with the preferential activity of Phosphoatidylinositol 3-kinase (PI-3K) over PLC. Studies have also elucidated subsequent pathways that utilize the integration of G-proteincoupled receptors to mediate the degranulation and cytokine production mechanism of activated mast cells.[19] IgE binding to FcR1 in the absence of a specific antigen still induces the up-regulation of FcR1 surface expression in mast cells through autocrine signaling of cytokines.[21] However, not all IgE are equally capable of inducing such as secretion. Therefore, researchers have divided all invariant IgEs into two major categories: highly cytokinergic(HC), where the production and secretion of various cytokines and other activation events including degranulation is inducible, and poorly cytokinergic (PC) in which no autocrine signaling is observed. The former, HC IgE, brings forward a reaction in which cytokines are exocytosed and act as autocrine and paracrine signaling molecules. As such, mast cells with bound HC IgE attract other mast cells even in the absence of antigen crosslinking.[18] While the exact structural features that account for the function differences between HC and PC IgE has yet to be determined, their effects are thought to be the result of intracellular cell signaling.[21] IgE binding to FcR1 leads to a greater stability of the mast cell and increased production of surface receptors. The newly expressed FcR1 then

aggregate on the surface, independent of antigen binding. The cell signaling pathway then initiates and appears to involve components used in the alternative mechanisms. Mast cell migration is dependent on soluble factors such as adenosine, leukotriene B4, and other chemokines, whose secretion is dependent upon the activity of LYN and SYK. The degranulation of mast cells in the absence of antigen can then be initiated by G-protein-coupled receptors (GPCR) stimulated by soluble factors agonists and completed by downstream activity of PI3K.[18]

[edit] Diagnosis
Anaphylaxis is diagnosed based on clinical criteria.[11] When any one of the following three is true there is a high likelihood of anaphylaxis:[11]
1. Symptom onset within minutes to several hours with involvement of the skin or mucosal tissue plus either respiratory difficulty or a low blood pressure. 2. Any two or more of the following symptoms within minutes to several hours of allergen exposure: a. involvement of the skin or mucosa b. respiratory difficulties c. low blood pressure d. gastrointestinal symptoms 3. Low blood pressure within minutes to several hours after exposure to known allergen

During an attack blood tests for tryptase or histamine (released from mast cells) might be useful in diagnosing anaphylaxis due to insect stings or medications but are of limited utility if the cause is food or the person has a normal blood pressure.[11] Allergy testing may help in determining what triggered the anaphylaxis. In this setting, skin allergy testing (with or without patch testing) or RAST blood tests can sometimes identify the cause.
[edit] Classification

Biphasic anaphylaxis is the recurrence of symptoms within 1-72 hours with no further exposure to the allergen.[11] It occurs in between 120% of cases depending on the study examined.[22] It is managed in the same manner as anaphylaxis.[10] Anaphylactic shock is anaphylaxis associated with systemic vasodilation that results in low blood pressure. It is also associated with severe bronchoconstriction to the point where the individual is unable to breathe. Pseudoanaphylaxis has a similar presentation and treatment to that of anaphylaxis, however, it does not involve an allergic reaction but is due to direct mast cell degranulation.[23] This can result from morphine, radiocontrast, aspirin and muscle relaxants.[24] Active anaphylaxis is what is naturally observed. Two weeks or so after an animal, including humans, is exposed to certain allergens, active anaphylaxis (which is simply called "anaphylaxis") would be elicited upon exposure to the same allergens.

Passive anaphylaxis is induced in native animals that receive transfer of the serum experimentally from sensitized animals with certain allergens. Passive anaphylaxis would be provoked in the recipient animals after exposure to the same allergens.[25]

[edit] Differential diagnosis

It can sometimes be difficult to distinguish anaphylaxis from asthma, syncopy, and panic attacks.[11] Asthma however typically does not have itching or gastrointestinal symptoms, syncope presents with pallor rather than a rash, and panic attacks while it may have flushing does not have hives.[11]

[edit] Prevention
Avoidance of the trigger of anaphylaxis is recommended. In cases where this may not be possible or exposure is important, desensitization may be an option. Immunotherapy with Hymenoptera venoms is effective at desensitizing 80-90% of adults and 98% of children against allergies to bees, wasps, hornets, yellowjackets, and fire ants. Oral immunotherapy may be effective at desensitizing some people to certain food including mild, eggs, nuts and peanuts however adverse effects are common. Desensitization is also possible for many medications however it is advised that most people simply avoid the agent in question. In those who react to latex it may be important to avoid cross reactive foods such as avocados, bananas, and potatoes among others.[11]

[edit] Management
Anaphylaxis is a medical emergency that may require resuscitation measures such as airway management, supplemental oxygen, large volumes of intravenous fluids, and close monitoring.[10] Administration of epinephrine is the treatment of choice with antihistamines and steroids often used as adjuncts.[11] A period of in hospital observation for between 6 and 24 hours is recommended for people once they have returned to normal due to concerns of biphasic anaphylaxis.[22][26]
[edit] Epinephrine

Epinephrine (adrenaline) is the primary treatment for anaphylaxis with no absolute contraindication to its use.[10] It is recommended that it be given intramuscularly into the mid anterolaterial thigh as soon as the diagnosis is suspected.[11] The recommended dose is 0.5 mg / 500 g or 0.5 mL in adults and 0.01 mg/kg in children to a maximum of 0.3 mg of 1 in 1000 solution.[11] The dose may be repeated if there is insufficient response every 5 to 15-minute.[11] More than two doses is rarely required.[11] Minor adverse effects from epinephrine include tremors, anxiety, headaches, and palpitations.[11] If necessary, it can also be given intravenously using a dilute 1 in 10,000 epinephrine solution. Epinephrine autoinjector used for self-administration contain a dose of 300 g (0.3 mL) 1 in 1000 solution.

[edit] Adjuncts

Antihistamines, while commonly used and assumed effective based on theoretical reasoning, are poorly supported by evidence. A 2007 Cochrane review did not find any good-quality studies upon which to base recommendations.[27] Corticosteroids are unlikely to make a difference in the current episode of anaphylaxis, but may be used in the hope of decreasing the risk of biphasic anaphylaxis. How effective they are at achieving this, however, is uncertain.[22]
[edit] Preparedness

People prone to anaphylaxis are advised to have an "allergy action plan", and parents are advised to inform schools, etc. of their children's allergies and what to do in case of an anaphylactic emergency.[28] The action plan usually includes use of epinephrine auto-injectors, the recommendation to wear a medical alert bracelet, and counseling on avoidance of triggers.[29] Immunotherapy is available for certain triggers to prevent future episodes of anaphylaxis. A multiyear course of subcutaneous desensitization has been found effective against stinging insects, while oral desensitization is effective for many foods.[10]
[edit] Prognosis

There have been cases of death occurring with minutes.[11]

[edit] Epidemiology
Lifetime prevalence of anaphylaxis is estimated at between 0.05-2% globally with rates appearing to be increasing.[11] The rate in the 1980s was 21 per 100,000 per year, while in the 1990s it had increased to 50 per 100,000 per year.[10] The risk is greatest in young people and females. The trigger in the young is usually food related while in adults, medications and insect venoms are more common causes.[10] Due in part to the variety of definitions, between 1% and 15% of the population of the United States can be considered "at risk" for having an anaphylactic reaction if they are exposed to one or more allergens, especially penicillin and insect stings. Most of these people successfully avoid their allergens and will never experience anaphylaxis. Of those people who actually experience anaphylaxis, up to 1% may die as a result.[3] Anaphylaxis results in approximately 1,500 deaths per year in the U.S.[4] (one out of every 1,600 of the 2.4 million deaths from all causes each year in the U.S.;[5]). The most common presentation includes sudden cardiovascular collapse (88% of reported cases of severe anaphylaxis). In England, mortality rates for anaphylaxis have been reported as up to 0.05 per 100,000 population, or around 10-20 a year.[6] Anaphylactic reactions requiring hospital treatment appear to be increasing, with authorities in England reporting a threefold increase between 1994 and 2004.[7]

Pneumonia Pneumonia
From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Pneumonia (disambiguation).

Pneumonia
Classification and external resources

A chest X-ray showing a very prominent wedge-shaped bacterial pneumonia in the right lung.

ICD-10

J12., J13., J14., J15., J16., J17., J18., P23.

ICD-9

480-486, 770.0

DiseasesDB

10166

MedlinePlus

000145

eMedicine

topic list

MeSH

D011014

Pneumonia is an inflammatory condition of the lungespecially affecting the microscopic air sacs (alveoli)associated with fever, chest symptoms, and a lack of air space (consolidation) on a chest X-ray.[1][2] Pneumonia is typically caused by an infection but there are a number of other causes.[1] Infectious agents include: bacteria, viruses, fungi, and parasites.[3] Typical symptoms include cough, chest pain, fever, and difficulty breathing.[4] Diagnostic tools include x-rays and examination of the sputum. Vaccines to prevent certain types of pneumonia are available. Treatment depends on the underlying cause with presumed bacterial pneumonia being treated with antibiotics. Although pneumonia was regarded by William Osler in the 19th century as "the captain of the men of death", the advent of antibiotic therapy and vaccines in the 20th century have seen radical improvements in survival outcomes. Nevertheless, in the third world, and among the very old, the very young and the chronically ill, pneumonia remains a leading cause of death.[5]

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Cause o 3.1 Bacteria o 3.2 Viruses o 3.3 Fungi o 3.4 Parasites o 3.5 Idiopathic 4 Pathophysiology o 4.1 Viral o 4.2 Bacterial 5 Diagnosis o 5.1 Imaging o 5.2 Microbiology o 5.3 Differential diagnosis 6 Prevention o 6.1 Vaccination o 6.2 Environmental o 6.3 Other 7 Management o 7.1 Bacterial o 7.2 Viral o 7.3 Aspiration 8 Prognosis o 8.1 Clinical prediction rules o 8.2 Pleural effusion, empyema, and abscess o 8.3 Respiratory and circulatory failure

9 Epidemiology o 9.1 Children 10 History 11 Society and culture 12 References

Classification
Main article: Classification of pneumonia

Pneumonitis refers to lung inflammation; pneumonia refers to pneumonitis, usually due to infection but sometimes non infectious, that has the additional feature of pulmonary consolidation.[6] Pneumonia can be classified in several ways. It is most commonly classified by where or how it was acquired (community-acquired, aspiration, healthcare-associated, hospitalacquired, and ventilator-associated pneumonia),[7] but may also be classified by the area of lung affected (lobar pneumonia, bronchial pneumonia and acute interstitial pneumonia),[7] or by the causative organism.[8] Pneumonia in children may additionally be classified based on signs and symptoms as non-severe, severe, or very severe.[9]

Signs and symptoms

Main symptoms of infectious pneumonia

People with infectious pneumonia often have a productive cough, fever accompanied by shaking chills, shortness of breath, sharp or stabbing chest pain during deep breaths, confusion, and an increased respiratory rate.[10] In the elderly, confusion may be the most prominent symptom.[10] The typical symptoms in children under five are fever, cough, and fast or difficult breathing.[11] Fever, however, is not very specific, as it occurs in many other common illnesses, and may be absent in those with severe disease or malnutrition. Additionally, a cough is frequently absent in

children less than 2 months old.[11] More severe symptoms may include: central cyanosis, decreased thirst, convulsions, persistent vomiting, or a decreased level of consciousness.[11]
Symptoms frequency in pneumonia[12]

Some causes of pneumonia are associated with classic, but non-specific, clinical characteristics. Pneumonia caused by Symptom Legionella may occur with abdominal pain, diarrhea, or confusion,[13] while pneumonia caused by Streptococcus Cough pneumoniae is associated with rusty colored sputum,[14] and pneumonia caused by Klebsiella may have bloody sputum Fatigue often described as "currant jelly".[12]
Fever

Frequency 7991% 90% 7175%

Physical examination may sometimes reveal low blood pressure, a high heart rate, or a low oxygen saturation. Shortness of breath 6775% Examination of the chest may be normal, but may show decreased chest expansion on the affected side. Harsh Sputum 6065% breath sounds from the larger airways that are transmitted through the inflamed lung are termed bronchial breathing, Chest pain 3949% and are heard on auscultation with a stethoscope. Rales (or crackles) may be heard over the affected area during inspiration. Percussion may be dulled over the affected lung, and increased, rather than decreased, vocal resonance distinguishes pneumonia from a pleural effusion.[10] Struggling to breathe, confusion, and blue-tinged skin are signs of a medical emergency.

Cause
Pneumonia is primarily due to infections, with less common causes including irritants and the unknown. Although more than one hundred strains of micro organisms can cause pneumonia, only a few are responsible for most cases. The most common types of infectious are viruses and bacteria with it being less commonly due to fungi or parasites. Mixed infections with both viruses and bacterial may occur in up to 45% of infections in children and 15% of infections in adults.[15] A causative agent is not isolated in approximately half of cases despite careful testing.[16] The term pneumonia is sometimes more broadly applied to inflammation of the lung (for example caused by autoimmune disease, chemical burns or drug reactions), however this is more accurately referred to as pneumonitis.[17][18]
Bacteria Main article: Bacterial pneumonia

The bacterium Streptococcus pneumoniae, a common cause of pneumonia, imaged by an electron microscope

Bacteria are the most common cause of community acquired pneumonia, with Streptococcus pneumoniae isolated in nearly 50% of cases.[19][7] Other commonly isolated bacteria include: Haemophilus influenzae in 20%, Chlamydophila pneumoniae in 13%, Mycoplasma pneumoniae in 3%,[7], Staphylococcus aureus, Moraxella catarrhalis, Legionella pneumophila and gramnegative bacilli.[16] Risk factors for infection depend on the organism involved.[16] Alcoholism is associated with Streptococcus pneumoniae, anaerobic organisms, and Mycobacterium tuberculosis, smoking is associated with Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Legionella pneumophila, exposure to bird with Chlamydia psittaci, farm animals with Coxiella burnetti, aspiration of stomach contents with anaerobes, and cystic fibrosis with Pseudomonas aeruginosa and Staphylococcus aureus.[16] Streptococcus pneumoniae is more common in the winter.[16]
Viruses Main article: Viral pneumonia

In adults viruses account for approximately a third of pneumonia cases.[15] Commonly implicated agents include: rhinoviruses,[15]coronaviruses,[15] influenza virus,[20] respiratory syncytial virus (RSV),[20] adenovirus,[20] and parainfluenza.[20] Herpes simplex virus is a rare cause of pneumonia, except in newborns. People with weakened immune systems are at increased risk of pneumonia caused by cytomegalovirus (CMV).
Fungi Main article: Fungal pneumonia

Fungal pneumonia is uncommon,[16] but it may occur in individuals with weakened immune systems due to AIDS, immunosuppressive drugs, or other medical problems. The pathophysiology of pneumonia caused by fungi is similar to that of bacterial pneumonia. Fungal pneumonia is most often caused by Histoplasma capsulatum, blastomyces, Cryptococcus neoformans, Pneumocystis jiroveci, and Coccidioides immitis. Histoplasmosis is most common

in the Mississippi River basin, and coccidioidomycosis is most common in the southwestern United States.[16]
Parasites Main article: Parasitic pneumonia

A variety of parasites can affect the lungs. These parasites typically enter the body through the skin or the mouth. Once inside the body, they travel to the lungs, usually through the blood. In parasitic pneumonia, as with other kinds of pneumonia, a combination of cellular destruction and immune response causes disruption of oxygen transportation. One type of white blood cell, the eosinophil, responds vigorously to parasite infection. Eosinophils in the lungs can lead to eosinophilic pneumonia, thus complicating the underlying parasitic pneumonia. The most common parasites causing pneumonia are Toxoplasma gondii, Strongyloides stercoralis, and Ascariasis.
Idiopathic Main article: Idiopathic interstitial pneumonia

Idiopathic interstitial pneumonia or noninfectious pneumonia[21] are a class of diffuse lung diseases. They include: diffuse alveolar damage, organizing pneumonia, nonspecific interstitial pneumonia, lymphocytic interstitial pneumonia, desquamative interstitial pneumonia, respiratory bronchiolitis interstitial lung disease, and usual interstitial pneumonia.[22]

Pathophysiology

Pneumonia fills the lung's alveoli with fluid, hindering oxygenation. The alveolus on the left is normal, while on the right it is full of fluid from pneumonia.

Pneumonia frequently starts as a upper respiratory tract infection that moves into the lower respiratory tract.[23]
Viral

Viruses invade cells in order to reproduce. Typically, a virus reaches the lungs when airborne droplets are inhaled through the mouth or nose. Once in the lungs, the virus invades the cells lining the airways and alveoli. This invasion often leads to cell death, either from damage to the cell by the virus, or from a protective process called apoptosis in which the infected cell destroys itself before it can be used as a conduit for virus reproduction. When the immune system responds to the viral infection, even more lung damage occurs. White blood cells, mainly lymphocytes, activate certain chemical cytokines which allow fluid to leak into the alveoli. This combination of cell destruction and fluid-filled alveoli interrupts the normal transportation of oxygen into the bloodstream. As well as damaging the lungs, many viruses affect other organs and thus disrupt many body functions. Viruses can also make the body more susceptible to other bacterial infections; in this way bacterial pneumonia can arrise as a co-morbid condition.[20]
Bacterial

Bacteria typically enter the lung when airborne droplets are inhaled, but can also reach the lung through the bloodstream when there is an infection in another part of the body. Many bacteria live in parts of the upper respiratory tract, such as the nose, mouth and sinuses, and can easily be inhaled into the alveoli. Once inside, bacteria may invade the spaces between cells and between alveoli through connecting pores. This invasion triggers the immune system to send neutrophils, a type of defensive white blood cell, to the lungs. The neutrophils engulf and kill the offending organisms, and also release cytokines, causing a general activation of the immune system. This leads to the fever, chills, and fatigue common in bacterial and fungal pneumonia. The neutrophils, bacteria, and fluid from surrounding blood vessels fill the alveoli and interrupt normal oxygen transportation.

Diagnosis
Crackles

Crackles heard in the lungs of a person with pneumonia using a stethoscope.

Problems listening to this file? See media help.

Pneumonia is typically diagnosed based on a combination of physical signs and a chest X-ray.[24] Confirming the underlying cause can be difficult, however, with no definitive test able to distinguish between bacterial and not-bacterial origin.[15][24] The World Health Organization has defined pneumonia in children clinically based on a either a cough or difficulty breathing and a rapid respiratory rate, chest indrawing, or a decreased level of consciousness.[25] A rapid respiratory rate is defined as greater than 60 breaths per minute in children under 2 months old, 50 breaths per minute in children two months to one year old, or greater than 40 breaths per minute in children one to five years old.[25] In children, an increased respiratory rate and lower chest indrawing are more sensitive than hearing chest crackles with a stethoscope.[11] In adults investigations are generally not needed in mild cases[26] as if all vital signs and auscultation are normal the risk of pneumonia is very low.[27]In those requiring admission to a hospital, pulse oximetry, chest radiography, and blood tests including a complete blood count, serum electrolytes, C-reactive protein, and possibly liver function tests are recommended.[26] The diagnosis of influenza-like illness can be made based on presenting signs and symptoms however verification of an influenza infection requires testing.[28] Thus treatment is frequently based on the presence of influenza in the community or a rapid influenza test.[28]
Imaging

CT of the chest demonstrating right sided pneumonia (left side of the image).

A chest radiograph is frequently used in diagnosis.[11] In people with mild disease imaging is only needed in those with potential complications, those who have not improved with treatment, or those in which the cause in uncertain.[11][26] If a person is sufficiently sick to require hospitalization, a chest radiograph is recommended.[26] Findings do not always correlate with severity of disease and do not reliably distinguish between bacterial versus viral infection.[11] X-ray signs of bacterial community acquired pneumonia classically show lung consolidation of one lung segmental lobe.[7] However, radiographic findings may be variable, especially in other types of pneumonia.[7] Aspiration pneumonia may present with bilateral opacities primarily in the bases of the lungs and on the right side.[7] Radiographs of viral pneumonia cases may appear normal, hyper-inflated, have bilateral patchy areas, or present similar to bacterial pneumonia with lobar consolidation.[7] A CT scan can give additional information in indeterminate cases.[7]

Microbiology

For people managed in the community figuring out the causative agent is not cost effective, and typically does not alter management.[11] For those who do not respond to treatment, sputum culture should be considered, and culture for Mycobacterium tuberculosis should be carried out in those with a chronic productive cough.[26] Testing for other specific organisms may be recommended during outbreaks, for public health reasons.[26] In those who are hospitalized for severe disease both sputum and blood cultures are recommended.[26] Viral infections can be confirmed via detection of either the virus or its antigens with culture or polymerase chain reaction (PCR) among other techniques.[15] With routine microbiological testing a causative agent is determined in only 15% of cases.[10]
Differential diagnosis

Several diseases can present similar to pneumonia, including: chronic obstructive pulmonary disease (COPD), asthma, pulmonary edema, bronchiectasis, lung cancer and pulmonary emboli.[10] Unlike pneumonia, asthma and COPD typically present with wheezing, pulmonary edema presents with an abnormal electrocardiogram, cancer and bronchiectasis present with a cough of longer duration, and pulmonary emboli presents with acute onset sharp chest pain and shortness of breath.[10]

Prevention
Prevention includes vaccination, environmental measures, and appropriately treating other diseases.[11]
Vaccination

Vaccination is effective for preventing certain bacterial and viral pneumonias in both children and adults. Influenza vaccines are modestly effective against influenza A and B.[15][29] The Center for Disease Control and Prevention (CDC) recommends that everyone 6 months and older get yearly vaccination.[30] When an influenza outbreak is occurring, medications such as amantadine, rimantadine, zanamivir, and oseltamivir can help prevent influenza.[31][32] Vaccinations against Haemophilus influenzae and Streptococcus pneumoniae have good evidence to support their use.[23] Vaccinating children against Streptococcus pneumoniae has also led to a decreased incidence of these infections in adults, because many adults acquire infections from children. A vaccine against Streptococcus pneumoniae is also available for adults, and has been found to decrease the risk of invasive pneumococcal disease.[33]
Environmental

Reducing indoor air pollution is recommended[11] as is smoking cessation.[26]

Other

Appropriately treating underlying illnesses (such as AIDS) can decrease a person's risk of pneumonia. There are several ways to prevent pneumonia in newborn infants. Testing pregnant women for Group B Streptococcus and Chlamydia trachomatis, and giving antibiotic treatment, if needed, reduces pneumonia in infants. Suctioning the mouth and throat of infants with meconium-stained amniotic fluid decreases the rate of aspiration pneumonia.

Management
Typically, oral antibiotics, rest, simple analgesics, and fluids CURB-65 are sufficient for complete resolution.[26] However, those with other medical conditions, the elderly, or those with Symptom Points significant trouble breathing may require more advanced care. If the symptoms worsen, the pneumonia does not Confusion 1 improve with home treatment, or complications occur, hospitalization may be required.[26] Worldwide, Urea>7mmol/l 1 approximately 713% of cases in children result in hospitalization[11] while in the developed world between 22 Respiratory rate>30 1 42% of adults with community acquired pneumonia are admitted.[26] The CURB-65 score is useful for determining SBP<90mmHg, DBP<60mmHg 1 the need for admission in adults.[26] If the score is 0 or 1 people can typically be managed at home, if it is 2 a short Age>=65 1 hospital stay or close follow up is needed, if it is 35 hospitalization is recommended.[26] In children those with respiratory distress or oxygen saturation's of less than 90% should be hospitalized.[34] The utility of chest physiotherapy in pneumonia has not yet been determined.[35] Over the counter cough medicine has not been found to be effective.[36]
Bacterial

Antibiotics improve outcomes in those with bacterial pneumonia.[37] Initially antibiotic choice depends on the characteristics of the person affected, such as age, underlying health, and the location the infection was acquired. In the UK empiric treatment with amoxicillin is recommended first line for community-acquired pneumonia with doxycycline or clarithromycin as alternatives.[26] In North America, where the "atypical" forms of community-acquired pneumonia are more common, macrolides (such as azithromycin), and doxycycline have displaced amoxicillin as first-line outpatient treatment in adults.[19][38] In children with mild or moderate symptoms amoxicillin is still the first line.[34] The use of fluoroquinolones in uncomplicated cases is discouraged due to concerns of side effects and resistance.[19] The duration of treatment has traditionally been seven to ten days, but there is increasing evidence that short courses (three to five days) are similarly effective.[39] Antibiotics recommended for hospital-acquired pneumonia include third- and fourth-generation cephalosporins, carbapenems,

fluoroquinolones, aminoglycosides, and vancomycin.[40] These antibiotics are often given intravenously, and may be used in combination.
Viral

Neuraminidase inhibitors may be used to treat viral pneumonia caused by influenza viruses (influenza A and influenza B).[15] No specific antiviral medications are recommended for other types of community acquired viral pneumonias including SARS coronavirus, adenovirus, hantavirus, and parainfluenza virus.[15] Influenza A may be treated with rimantadine or amantadine, while influenza A or B may be treated with oseltamivir, zanamivir or peramivir.[15] These are of most benefit if they are started within 48 hours of the onset of symptoms.[15] Many strains of H5N1 influenza A, also known as avian influenza or "bird flu," have shown resistance to rimantadine and amantadine.[15] The use of antibiotics in viral pneumonia is recommended by some experts as it is impossible to rule out a complicating bacterial infection.[15] The British Thoracic Society recommends that antibiotics be withheld in those with mild disease.[15] The use of corticosteroids is controversial.[15]
Aspiration

Aspiration pneumonitis is generally treated conservatively with antibiotics only indicated for aspiration pneumonia.[41] The choice of antibiotic will depend on several factors, including the suspected causative organism and whether pneumonia was acquired in the community or developed in a hospital setting. Common options include clindamycin, a combination of a betalactam antibiotic and metronidazole, or an aminoglycoside.[42] Corticosteroids are commonly used in aspiration pneumonia, but there is no evidence to support their effectiveness.[42]

Prognosis
With treatment, most types of bacterial pneumonia can be cleared within two to four weeks[43] and mortality is very low.[15] Viral pneumonia may last longer, and mycoplasmal pneumonia may take four to six weeks to resolve completely.[43] The eventual outcome of an episode of pneumonia depends on how ill the person is when he or she was first diagnosed.[43] Before the advent of antibiotics mortality was typically 30% for hospitalized patients.[16] In the United States, about 5% of those diagnosed with pneumococcal pneumonia will die. In cases where the pneumonia progresses to blood infection, just over 20% will die.[44] The death rate (or mortality) also depends on the underlying cause of the pneumonia. Pneumonia caused by Mycoplasma, for instance, is associated with lower mortality. However, about half of the people who develop methicillin-resistant Staphylococcus aureus (MRSA) pneumonia while on a ventilator will die.[45] In regions of the world without advanced health care systems, pneumonia is even more deadly. Limited access to clinics and hospitals, limited access to x-rays, limited antibiotic choices, and inability to diagnose and treat underlying conditions inevitably lead to higher rates of death from pneumonia. For these reasons, the majority of deaths in children under five due to pneumococcal disease occur in developing countries.[46]

Adenovirus can cause severe necrotizing pneumonia in which all or part of a lung has increased translucency radiographically, which is called Swyer-James Syndrome.[47] Severe adenovirus pneumonia also may result in bronchiolitis obliterans, a subacute inflammatory process in which the small airways are replaced by scar tissue, resulting in a reduction in lung volume and lung compliance.[47] Sometimes pneumonia can lead to additional complications. Complications are more frequently associated with bacterial pneumonia than with viral pneumonia. The most important complications include respiratory and circulatory failure and pleural effusions, empyema or abscesses.
Clinical prediction rules

Clinical prediction rules have been developed to more objectively prognosticate outcomes in pneumonia. Although these rules are often used in deciding whether or not to hospitalize the person, they were derived simply to inform on prognosis; neither index was designed or tested as guide to determine whether the person would benefit by hospital admission.

Pneumonia severity index (or PORT Score)[48] online calculator CURB-65 score, which takes into account the severity of symptoms, any underlying diseases, and age[49] online calculator

Pleural effusion, empyema, and abscess

A pleural effusion as seen on chest x-ray. The A arrow indicates fluid layering in the right chest. The B arrow indicates the width of the right lung. The volume of the lung is reduced because of the collection of fluid around the lung.

In pneumonia, a collection of fluid (pleural effusion) often forms in the space that surrounds the lung (the pleural cavity). Occasionally, microorganisms will infect this fluid, causing what is called an empyema. To distinguish an empyema from the more common simple parapneumonic effusion, the fluid is collected with a needle (thoracentesis), and examined. If this shows evidence of empyema, complete drainage of the fluid may be necessary, often requiring a chest tube. In severe cases of empyema, surgery may be needed. If the infected fluid is not drained, the infection may persist, because antibiotics do not penetrate well into the pleural cavity. If the fluid is sterile, it need only be drained if it is causing symptoms or remains unresolved.

Rarely, bacteria in the lung will form a pocket of infected fluid called a lung abscess. Lung abscesses can usually be seen with a chest x-ray or chest CT scan. Abscesses typically occur in aspiration pneumonia, and often contain several types of bacteria. Antibiotics are usually adequate to treat a lung abscess, but sometimes the abscess must be drained by a surgeon or radiologist.
Respiratory and circulatory failure

Because pneumonia affects the lungs, people with pneumonia often have difficulty breathing, sometimes to the point where mechanical assistance is required. Non-invasive breathing assistance may be helpful, such as with a bi-level positive airway pressure machine. In other cases, placement of an endotracheal tube (breathing tube) may be necessary, and a ventilator may be used to help the person breathe. Pneumonia can also cause respiratory failure by triggering acute respiratory distress syndrome (ARDS), which results from a combination of infection and inflammatory response. The lungs quickly fill with fluid and become very stiff. This stiffness, combined with severe difficulties extracting oxygen due to the alveolar fluid, creates a need for mechanical ventilation. Sepsis and septic shock are potential complications of pneumonia. Sepsis occurs when microorganisms enter the bloodstream and the immune system responds by secreting cytokines. Sepsis most often occurs with bacterial pneumonia; Streptococcus pneumoniae is the most common cause. Individuals with sepsis or septic shock need hospitalization in an intensive care unit. They often require intravenous fluids and medications to help keep their blood pressure up. Sepsis can cause liver, kidney, and heart damage, among other problems, and it is often fatal.

Epidemiology
Main article: Epidemiology of pneumonia

Age-standardized death from lower respiratory tract infections per 100,000 inhabitants in 2004.[50] no data <100 100-700 3500-4200 4200-4900 4900-5600

700-1400 1400-2100 2100-2800 2800-3500

5600-6300 6300-7000 >7000

Pneumonia is a common illness affecting approximately 450 million people a year and occurring in all parts of the world.[15] It is a major cause of death among all age groups resulting in 4 million deaths (7% of the world's yearly total).[37][15] Rates are greatest in children less than five, and adults older than 75 years of age.[15] It occurs about five times more frequently in the developing world versus the developed world.[15] Viral pneumonia accounts for about 200 million cases.[15]
Children

In 2008 pneumonia occurred in approximately 156 million children (151 million in the developing world and 5 million in the developed world).[15] It resulted in 1.6 million deaths, or 2834% of all deaths in those under five years of age, of which 95% occurred in the developing world.[15][11] Countries with the greatest burden of disease include: India (43 million), China (21 million) and Pakistan (10 million).[51] It is the leading cause of death among children in low income countries.[37][15] Many of these deaths occur in the newborn period. The World Health Organization estimates that one in three newborn infant deaths are due to pneumonia.[52] Approximately half of these deaths are theoretically preventable, as they are caused by the bacteria for which an effective vaccine is available.[53]

History

WPA poster, 1936/1937

Pneumonia has been a common disease throughout human history.[54] The symptoms were described by Hippocrates (c. 460 BC 370 BC):[54] "Peripneumonia, and pleuritic affections, are to be thus observed: If the fever be acute, and if there be pains on either side, or in both, and if expiration be if cough be present, and the sputa expectorated be of a blond or livid color, or likewise thin, frothy, and florid, or having any other character different from the common... When pneumonia is at its height, the case is beyond remedy if he is not purged, and it is bad if he has dyspnoea, and urine that is thin and acrid, and if sweats come out about the neck and head, for such sweats are bad, as proceeding from the suffocation, rales, and the violence of the disease which is obtaining the upper hand."[55] However, Hippocrates referred to pneumonia as a disease "named by the ancients." He also reported the results of surgical drainage of empyemas. Maimonides (11351204 AD) observed "The basic symptoms which occur in pneumonia and which are never lacking are as follows: acute fever, sticking [pleuritic] pain in the side, short rapid breaths, serrated pulse and cough."[56] This clinical description is quite similar to those found in modern textbooks, and it reflected the extent of medical knowledge through the Middle Ages into the 19th century. Bacteria were first seen in the airways of individuals who died from pneumonia by Edwin Klebs in 1875.[57] Initial work identifying the two common bacterial causes Streptococcus pneumoniae and Klebsiella pneumoniae was performed by Carl Friedlnder[58] and Albert Frnkel[59] in 1882 and 1884, respectively. Friedlnder's initial work introduced the Gram stain, a fundamental laboratory test still used today to identify and categorize bacteria. Christian Gram's paper describing the procedure in 1884 helped differentiate the two different bacteria, and showed that pneumonia could be caused by more than one microorganism.[60]

Sir William Osler, known as "the father of modern medicine," appreciated the death and disability cause by pneumonia, describing it as the "captain of the men of death" in 1918, as it had overtaken tuberculosis as one of the leading causes of death in this time. This phrase was originally coined by John Bunyan in reference to "consumption" (tuberculosis).[61][62] Osler also described pneumonia as "the old man's friend" as death was often quick and painless when there was many slower more painful ways to die.[16] Several developments in the 1900s improved the outcome for those with pneumonia. With the advent of penicillin and other antibiotics, modern surgical techniques, and intensive care in the twentieth century, mortality from pneumonia, which had approached 30%, dropped precipitously in the developed world. Vaccination of infants against Haemophilus influenzae type B began in 1988 and led to a dramatic decline in cases shortly thereafter.[63] Vaccination against Streptococcus pneumoniae in adults began in 1977, and in children in 2000, resulting in a similar decline.[64]

Society and culture

See also: List of pneumonia victims

Because of the combination of a very high burden of disease in developing countries and a relatively low awareness of the disease in industrialized countries, the global health community has declared November 12 to be World Pneumonia Day, a day for concerned citizens and policy makers to take action against the disease.[65]

Severe acute respiratory syndrome Severe acute respiratory syndrome

From Wikipedia, the free encyclopedia Jump to: navigation, search "SARS" redirects here. For other uses, see SARS (disambiguation). Further information: Progress of the SARS outbreak

Severe Acute Respiratory Syndrome

Classification and external resources

SARS coronavirus (SARS-CoV) is causative of the syndrome.

ICD-10

U04.

ICD-9

079.82

DiseasesDB

32835

eMedicine

med/3662

MeSH

D045169

Severe acute respiratory syndrome (SARS, /srz/ SARZ) is a respiratory disease in humans which is caused by the SARS coronavirus (SARS-CoV).[1] Between November 2002 and July 2003 an outbreak of SARS in Hong Kong nearly became a pandemic, with 8,422 cases and 916 deaths worldwide [2] (10.9% fatality) according to the WHO.[3] Within weeks SARS spread from Hong Kong to infect individuals in 37 countries in early 2003.[4] As of today, the spread of SARS has been fully contained, with the last infected human case seen in June 2003 (disregarding a laboratory induced infection case in 2004). However, SARS is not claimed to have been eradicated (unlike smallpox), as it may still be present in its natural host reservoirs (animal populations) and may potentially return into the human population in the future. Mortality is less than 1% for people aged 24 or younger, 6% for those 25 to 44, 15% for those 45 to 64, and more than 50% for those over 65.[5] For comparison, the fatality rate for influenza is usually around 0.6% (primarily among the elderly) but can rise as high as 33% in severe epidemics of new strains.

Contents

[hide]

1 Signs and symptoms 2 Cause o 2.1 Viral replication 3 Diagnosis 4 Prevention 5 Treatment 6 Prognosis 7 Epidemiology 8 History o 8.1 Outbreak in south China o 8.2 Spread to other countries and regions 9 Culture o 9.1 China o 9.2 Hong Kong o 9.3 Taiwan o 9.4 Businesses o 9.5 Canada o 9.6 United States 10 Research o 10.1 Antiviral research o 10.2 Vaccine development 11 See also 12 Notes 13 Further reading 14 External links

[edit] Signs and symptoms

Initial symptoms are flu-like and may include: fever, myalgia, lethargy, gastrointestinal symptoms, cough, sore throat and other non-specific symptoms. The only symptom that is common to all patients appears to be a fever above 38 C (100.4 F). Shortness of breath may occur later.

[edit] Cause
The following text needs to be harmonized with text in SARS coronavirus. Main article: SARS coronavirus

Coronaviruses are positive-strand, enveloped RNA viruses that are important pathogens of mammals and birds. This group of viruses cause enteric or respiratory tract infections in a variety of animals including humans, livestock and pets.[1] Initial electron microscopic examination in Hong Kong and Germany found viral particles with structures suggesting paramyxovirus in respiratory secretions of SARS patients. Subsequently, in Canada, electron microscopic examination found viral particles with structures suggestive of metapneumovirus (a subtype of paramyxovirus) in respiratory secretions. Chinese researchers also reported that a Chlamydophila-like disease may be behind SARS. The Pasteur Institute in Paris identified coronavirus in samples taken from six patients, so did the laboratory of Malik Peiris at the University of Hong Kong, which in fact was the first to announce (on 21 March 2003) the discovery of a new coronavirus as the possible cause of SARS after successfully cultivating it from tissue samples and was also amongst the first to develop a test for the presence of the virus. The CDC noted viral particles in affected tissue (finding a virus in tissue rather than secretions suggests that it is actually pathogenic rather than an incidental finding). Upon electron microscopy, these tissue viral inclusions resembled coronaviruses, and comparison of viral genetic material obtained by PCR with existing genetic libraries suggested that the virus was a previously unrecognized coronavirus. Sequencing of the virus genome which computers at the British Columbia Cancer Agency in Vancouver completed at 4 a.m. Saturday, 12 April 2003 was the first step toward developing a diagnostic test for the virus, and possibly a vaccine.[6] A test was developed for antibodies to the virus, and it was found that patients did indeed develop such antibodies over the course of the disease, which is highly suggestive of a causative role. On 16 April 2003, the WHO issued a press release stating that a coronavirus identified by a number of laboratories was the official cause of SARS.[7] Scientists at Erasmus University in Rotterdam, the Netherlands demonstrated that the SARS coronavirus fulfilled Koch's postulates thereby confirming it as the causative agent. In the experiments, macaques infected with the virus developed the same symptoms as human SARS victims.[8] An article published in The Lancet identifies a coronavirus as the probable causative agent. In late May 2003, studies from samples of wild animals sold as food in the local market in Guangdong, China found that the SARS coronavirus could be isolated from palm civets (Paguma sp.), but the animals did not always show clinical signs. The preliminary conclusion was that the SARS virus crossed the xenographic barrier from palm civet to humans, and more than 10,000 masked palm civets were destroyed in Guangdong Province. Virus was also later found in raccoon dogs (Nyctereuteus sp.), ferret badgers (Melogale spp.) and domestic cats. In 2005, two studies identified a number of SARS-like coronaviruses in Chinese bats.[9][10] Phylogenetic analysis of these viruses indicated a high probability that SARS coronavirus originated in bats and spread to humans either directly, or through animals held in Chinese markets. The bats did not show any visible signs of disease, but are the likely natural reservoirs of SARS-like coronaviruses. In late 2006, scientists from the Chinese Centre for Disease Control and Prevention of Hong Kong University and the Guangzhou Centre for Disease Control and Prevention established a genetic link between the SARS coronavirus appearing in civet cats and humans, bearing out claims that the disease had jumped across species.[11]

[edit] Viral replication

Coronavirus (CoV) genome replication takes place in the cytoplasm in a membrane-protected microenvironment and starts with the translation of the genome to produce the viral replicase. CoV transcription involves a discontinuous RNA synthesis (template switch) during the extension of a negative copy of the subgenomic mRNAs. The requirement for base pairing during transcription has been formally demonstrated in arteriviruses and CoVs. The CoV N protein is required for coronavirus RNA synthesis and has RNA chaperon activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. CoVs initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after CoV infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation and immune and stress responses. The balance between genes up- and down-regulated could explain the pathogenesis caused by these viruses. Coronavirus expression systems based on single genome constructed by targeted recombination, or by using infectious cDNAs, have been developed. The possibility of expressing different genes under the control of transcription regulating sequences (TRSs) with programmable strength and engineering tissue and species tropism indicates that CoV vectors are flexible. CoV based vectors have emerged with high potential vaccine development and possibly for gene therapy.[12]

[edit] Diagnosis

A chest x-ray showing increased opacity in both lungs, indicative of pneumonia, in a patient with SARS.

SARS may be suspected in a patient who has:

1. Any of the symptoms, including a fever of 38 C (100.4 F) or higher, and 2. Either a history of: 1. Contact (sexual or casual, including tattooes) with someone with a diagnosis of SARS within the last 10 days OR

2. Travel to any of the regions identified by the WHO as areas with recent local transmission of SARS (affected regions as of 10 May 2003[13] were parts of China, Hong Kong, Singapore and the province of Ontario, Canada).

A probable case of SARS has the above findings plus positive chest X-ray findings of atypical pneumonia or respiratory distress syndrome. With the advent of diagnostic tests for the coronavirus probably responsible for SARS, the WHO has added the category of "laboratory confirmed SARS" for patients who would otherwise fit the above "probable" category who do not (yet) have the chest x-ray changes but do have positive laboratory diagnosis of SARS based on one of the approved tests (ELISA, immunofluorescence or PCR). The chest X-ray (CXR) appearance of SARS is variable. There is no pathognomonic appearance of SARS but is commonly felt to be abnormal with patchy infiltrates in any part of the lungs. The initial CXR may be clear. White blood cell and platelet counts are often low. Early reports indicated a tendency to relative neutrophilia and a relative lymphopenia relative because the total number of white blood cells tends to be low. Other laboratory tests suggest raised lactate dehydrogenase and slightly raised creatine kinase and C-Reactive protein levels. With the identification and sequencing of the RNA of the coronavirus responsible for SARS on 12 April 2003, several diagnostic test kits have been produced and are now being tested for their suitability for use. Three possible diagnostic tests have emerged, each with drawbacks. The first, an ELISA (enzyme-linked immunosorbent assay) test detects antibodies to SARS reliably but only 21 days after the onset of symptoms. The second, an immunofluorescence assay, can detect antibodies 10 days after the onset of the disease but is a labour and time intensive test, requiring an immunofluorescence microscope and an experienced operator. The last test is a polymerase chain reaction (PCR) test that can detect genetic material of the SARS virus in specimens ranging from blood, sputum, tissue samples and stools. The PCR tests so far have proven to be very specific but not very sensitive. This means that while a positive PCR test result is strongly indicative that the patient is infected with SARS, a negative test result does not mean that the patient does not have SARS. The WHO has issued guidelines for using these diagnostic tests.[13] There is currently no rapid screening test for SARS and research is ongoing.

[edit] Prevention
The WHO set up a network for doctors and researchers dealing with SARS, consisting of a secure web site to study chest x-rays and a teleconference.

A SARS-treating hospital in Taiwan.

Attempts were made to control further SARS infection through the use of quarantine. Over 1200 were under quarantine in Hong Kong, while in Singapore and Taiwan, 977 and 1147 were quarantined respectively. Canada also put thousands of people under quarantine.[14] In Singapore, schools were closed for 10 days and in Hong Kong they were closed until 21 April to contain the spread of SARS.[15] On 27 March 2003, the WHO recommended the screening of airline passengers for the symptoms of SARS.[16] In Singapore, a single hospital, Tan Tock Seng Hospital, was designated as the sole treatment and isolation centre for all confirmed and probable cases of the disease on 22 March. Subsequently, all hospitals implemented measures whereby all staff members were required to submit to temperature checks twice a day, visitorship was restricted only to pediatric, obstetric and selected other patients, and even then, only one person was allowed to visit at a time. To overcome this inconvenience, videoconferencing was utilised. A dedicated phoneline was designated to report SARS cases, whereupon a private ambulance service was dispatched to transport them to Tan Tock Seng Hospital. On 24 March, Singapore's Ministry of Health invoked the Infectious Diseases Act, allowing for a 10-day mandatory home quarantine to be imposed on all who may have come in contact with SARS patients. SARS patients who have been discharged from hospitals were under 21 days of home quarantine, with telephone surveillance requiring them to answer the phone when randomly called up. Discharged probable SARS patients and some recovered cases of suspected SARS patients are similarly required to be home quarantined for 14 days. Security officers from CISCO, a Singaporean auxiliary police force, were utilised to serve quarantine orders to their homes, and installed an electronic picture (ePIC) camera outside the doors of each contact. Sparked in particular by the news surrounding an elderly man who disregarded the quarantine order, flashing it to the public as he strolled to eating outlets and causing a minor exodus of patrons which persisted until the fears over the disease abated, the Singapore government called for an urgent meeting in Parliament on 24 April to amend the Infectious Disease Act and include penalties for violations, revealing at least 11 other violators of quarantine orders. These amendments included:

the requirement of suspected persons of infectious diseases to be brought to designated treatment centres, and their prohibition from going to public places;

the designation of contaminated areas and the restriction of access to them, and the destruction of suspected sources of infection; the introduction of the power to tag offenders who break home quarantine (persons who failed to be contacted three times by phone consecutively) with electronic wrist tags, and the imposition of fines without court trial; the ability to charge repeated offenders in court which may lead to imprisonment; and the prosecution of anyone caught lying to health officials about their travel to SARS-affected areas or contacts with SARS patients.

Thermal imaging at Taoyuan Airport's International checkpoint.

On 23 April the WHO advised against all but essential travel to Toronto, noting that a small number of persons from Toronto appear to have "exported" SARS to other parts of the world. Toronto public health officials noted that only one of the supposedly exported cases had been diagnosed as SARS and that new SARS cases in Toronto were originating only in hospitals. Nevertheless, the WHO advisory was immediately followed by similar advisories by several governments to their citizens. On 29 April WHO announced that the advisory would be withdrawn on 30 April. Toronto tourism suffered as a result of the WHO advisory, prompting The Rolling Stones and others to organize the massive Molson Canadian Rocks for Toronto concert, commonly known as SARSstock, to revitalize the city's tourism trade. Also on 23 April, Singapore instituted thermal imaging scans to screen all passengers departing Singapore from Singapore Changi Airport. It also stepped up screening of travelers at its Woodlands and Tuas checkpoints with Malaysia. Singapore had previously implemented this screening method for incoming passengers from other SARS affected areas but was to include all travelers into and out of Singapore by mid- to late May. In addition, students and teachers in Singapore were issued with free personal oral digital thermometers. Students took their temperatures daily, usually two or three times a day, but the temperature-taking exercises were suspended with the waning of the outbreak. Taiwan Taoyuan International Airport also added SARS checkpoints with an infrared screening system similar to Singapore's Changi Airport.

[edit] Treatment

Antibiotics are ineffective as SARS is a viral disease. Treatment of SARS so far has been largely supportive with antipyretics, supplemental oxygen and ventilatory support as needed. Suspected cases of SARS must be isolated, preferably in negative pressure rooms, with complete barrier nursing precautions taken for any necessary contact with these patients. There was initially anecdotal support for steroids and the antiviral drug ribavirin, but no published evidence has supported this therapy. Researchers are currently testing all known antiviral treatments for other diseases including AIDS, hepatitis, influenza and others on the SARS-causing coronavirus. There is some evidence that some of the more serious damage in SARS is due to the body's own immune system overreacting to the virus - a cytokine storm. Research is continuing in this area. In December 2004 it was reported that Chinese researchers had produced a SARS vaccine, it has been tested on a group of 36 volunteers, 24 of whom developed antibodies against the virus.[17] A 2006 systematic review of all the studies done on the 2003 SARS epidemic found no evidence that antivirals, steroids or other therapies helped patients. A few suggested they caused harm.[18] The clinical treatment of SARS has been relatively ineffective with most high risk patients requiring artificial ventilation. Currently, corticosteroids and Ribavirin are the most common drugs used for treatment of SARS (Wu et al., 2004). In vitro studies of Ribavirin have yielded little results at clinical, nontoxic concentrations. Better combinations of drugs that have yielded a more positive clinical outcome (when administered early) have included the use of Kaletra, Ribavirin and corticosteroids. The administration of corticosteroids, marketed as Prednisone, during viral infections has been controversial. Lymphopenia can also be a side effect of corticosteroids even further decreasing the immune response and allowing a spike in the viral load; yet physicians must balance the need for the anti-inflammatory treatment of corticosteroids (Murphy 2008). Clinicians have also noticed positive results during the use of human interferon and Glycyrrhizin. No compounds have yielded inhibitory results of any significance. The HIV protease inhibitors Ritonavir and Saquinavir did not show any inhibitory effect at nontoxic levels. Iminocyclitol 7 has been found to have an inhibitory effect on SARS-CoV in that it disrupts the envelope glycoprotein processing. Iminocyclitol 7 specifically inhibits the production of human fucosidase and in vitro trials yielded promising results in the treatment of SARS, yet one problem exists. A deficiency of fucosidase can lead to a condition known as fucosidosis in which there is a decrease in neurological function.

[edit] Prognosis
Several consequent reports from China on some recovered SARS patients show that severe longtime sequelae exist. The most typical diseases include, among other things, pulmonary fibrosis, osteoporosis, and femoral necrosis, which have led to the complete loss of working ability or even self-care ability of these cases. And as a result some of the post-SARS patients suffer from major depressive disorder.[19]

[edit] Epidemiology
SARS is still considered a relatively rare disease with 8,273 cases as of 2003.[20]

[edit] History
Probable cases of SARS by country, 1 November 2002 31 July 2003. SARS cases Country or dead Fatality Cases Deaths due to (%) Region other causes China * Hong Kong * Canada Taiwan Singapore Vietnam United States Philippines Mongolia Macau * Kuwait Ireland 5328 1755 251 346** 238 63 27 14 9 1 1 1 349 299 44 37 33 5 0 2 0 0 0 0 19 5 0 36 0 0 0 0 0 0 0 0 6.6 17 18 11 14 8 0 14 0 0 0 0

Romania Russian Federation Spain Switzerland South Korea

1 1 1 1 1

0 0 0 0 0 775

0 0 0 0 0 60

0 0 0 0 0 9.6

Total 8273

(*) Figures for the People's Republic of China exclude the Special Administrative Regions (Macau SAR, Hong Kong SAR) which are reported separately by the WHO. (**) Since 11 July 2003, 325 Taiwanese cases have been 'discarded'. Laboratory information was insufficient or incomplete for 135 discarded cases; 101 of these patients died.

Source:WHO.[13] [edit] Outbreak in south China Main article: Progress of the SARS outbreak

The epidemic of SARS appears to have started in Guangdong Province, China in November 2002. The first case of SARS was reportedly originated in Shunde, Foshan, Guangdong in Nov 2002, and the patient, a farmer, was treated in the First People's Hospital of Foshan (Mckay Dennis). The patient died soon after, and no definite diagnosis was made on his cause of death. Despite taking some action to control it, Chinese government officials did not inform the World Health Organization of the outbreak until February 2003. This lack of openness caused delays in efforts to control the epidemic, resulting in criticism of the Peoples Republic of China from the international community. China has since officially apologized for early slowness in dealing with the SARS epidemic.[21] The first clue of the outbreak appears to be 27 November 2002 when Canada's Global Public Health Intelligence Network (GPHIN), an electronic warning system which is part of the World Health Organization's (WHO) Global Outbreak and Alert Response Network (GOARN), picked up reports of a "flu outbreak" in China through Internet media monitoring and analysis and sent them to the WHO. Importantly, while GPHIN's capability had recently been upgraded to enable

Arabic, Chinese, English, French, Russian and Spanish translation, the system was limited to English or French in presenting this information. Thus, while the first reports of an unusual outbreak were in Chinese, an English report was not generated until 21 January 2003.[22][22][23] Subsequently, the WHO requested information from Chinese authorities on 5 and 11 December. Despite the successes of the network in previous outbreak of diseases, it was proven rather defective after receiving intelligence on the media reports from China several months after the outbreak of SARS. Along with the second alert, WHO released the name, definition, as well as an activation of a coordinated global outbreak response network that brought sensitive attention and containment procedures (Dr. Heymann, 2003). However, by then although the new definitions do give nations a guideline to contain SARS, over five hundred deaths and an additional two thousand cases had already occurred worldwide.[23] In early April, there appeared to be a change in official policy when SARS began to receive a much greater prominence in the official media. Some have directly attributed this to the death of American James Earl Salisbury.[24] However, it was also in early April that accusations emerged regarding the undercounting of cases in Beijing military hospitals. After intense pressure, Chinese officials allowed international officials to investigate the situation there. This revealed problems plaguing the aging mainland Chinese healthcare system, including increasing decentralization, red tape, and inadequate communication.
[edit] Spread to other countries and regions

The epidemic reached the public spotlight in February 2003, when an American businessman traveling from China became afflicted with pneumonia-like symptoms while on a flight to Singapore. The plane stopped at Hanoi, Vietnam, where the victim died in The French Hospital of Hanoi. Several of the medical staff who treated him soon developed the same disease despite basic hospital procedures. Italian doctor Carlo Urbani identified the threat and communicated it to WHO and the Vietnamese government; he later succumbed to the disease. The severity of the symptoms and the infection of hospital staff alarmed global health authorities fearful of another emergent pneumonia epidemic. On 12 March 2003, the WHO issued a global alert, followed by a health alert by the United States Centers for Disease Control and Prevention (CDC). Local transmission of SARS took place in Toronto, Ottawa, San Francisco, Ulan Bator, Manila, Singapore, Taiwan, Hanoi and Hong Kong whereas within mainland China it spread to Guangdong, Jilin, Hebei, Hubei, Shaanxi, Jiangsu, Shanxi, Tianjin and Inner Mongolia. In Hong Kong the first cohort of affected people were discharged from the hospital on 29 March 2003. The disease spread in Hong Kong from a mainland doctor who arrived in February and stayed at the 9th floor of the Metropole Hotel in Kowloon Peninsula, infecting 16 of the hotel visitors. Those visitors traveled to Canada, Singapore, Taiwan and Vietnam, spreading SARS to those locations.[25] Another, larger, cluster of cases in Hong Kong centred on the Amoy Gardens housing estate. Its spread is suspected to have been facilitated by defects in the sewage system of the estate. Concerned citizens in Hong Kong worried that information was not reaching people quickly enough and created a website called sosick.org, eventually forced the Hong Kong government to provide information related to SARS in a timely manner.

[edit] Culture

[edit] China

The usually jam-packed Beijing Subway, as seen during the SARS outbreak. During the epidemic many chose not to take public transport. (11 May 2003)

The 2003 FIFA Women's World Cup, originally scheduled for China, was moved to the United States. China was allowed to keep its automatic qualification, and was awarded the 2007 Women's World Cup as compensation. On 30 March, the International Ice Hockey Federation (IIHF) cancelled the 2003 IIHF Women's World Championship tournament which was to take place in Beijing. In the People's Republic of China, the latter stage of the SARS crisis showed an unprecedented change in the central government's policies. In the past, rarely had officials stepped down purely because of administrative mistakes, but the case was different with SARS, when these mistakes caused international scrutiny. This change in policy has been largely credited to President Hu Jintao and Premier Wen Jiabao. At the heart of the crisis, Hu made a high-profile trip to Guangdong and Wen ate lunch with students at Peking University.
[edit] Hong Kong

Some members of Hong Kong Legislative Council recommended editing the budget for increased spending on medical services. Hong Kong merchants withdrew from an international jewelry and timepiece exhibition at Zrich. Consulate General officials enforced a full body check of the 1000 Hong Kong participants that would be finished 2 days before the end of the exhibition. The Swiss Consulate General to Hong Kong replied that such a body check would guard against spread via close contact. A merchant union leader alleged probable racial discrimination towards Chinese merchants, as the exhibition committee allowed the merchants to participate in the exhibition but not to promote their own goods. An estimated several hundred million Hong Kong dollars in contracts were lost as a result. However, exhibitors from Hong Kong were not barred from selling their products in their hotel rooms. Hong Kong was somehow hit hard. In June, Hong Kong launched the Individual Visit Scheme as a way to boost its economy.

[edit] Taiwan

SARS checkpoint at Taiwan Taoyuan International Airport's International Arrivals in Terminal 1.

Both China and Taiwan were dealing with SARS epidemics at the same time, and the cross-strait politics inevitably complicated the way the disease was handled. Since the People's Republic of China insisted on representing the 23 million Taiwanese people in the WHO by itself and forbid the ROC government's participation, Taiwan, which was one of the most endemic areas in the world, did not receive direct advice from WHO. Even though the ROC government actively reported the situation to WHO, the authority received SARS information only through the WHO website. The ROC claimed that the lack of direct communication with the WHO precluded proper handling of the disease and caused unnecessary deaths on the island. On the other hand, the PRC claimed that video conferences held between her experts and Taiwanese experts already facilitated information distribution and improved the way SARS was being treated in Taiwan. The ROC further advocated its own seats in WHO and used the case of SARS to illustrate the importance of having Taiwan included in the global health monitoring system. However, the PRC saw this as a politically motivated move towards Taiwanese independence. During the WHO general assembly, the People's Republic of China fiercely snubbed the proposal for Taiwan's participation. This was evidenced by one famous video clip aired widely in Taiwan showing the PRC Vice Premier Wu Yi and her official company rebuffing the question of Taiwan's representation which had been raised by Taiwanese reporters. Under pressure from the PRC, Taiwan was excluded from several major SARS conferences held by WHO. WHO eventually sent its experts to Taiwan to conduct inspections at the end of the SARS endemic.
[edit] Businesses

Severe customer drop of Chinese cuisine restaurants in Guangdong, China, Hong Kong and Chinatowns in North America, 90% decrease in some cases. Business recovered considerably in some cities after the end of the outbreak.[citation needed]

[edit] Canada

Most conferences and conventions scheduled for Toronto were cancelled, and the production of at least one movie was moved out of the city. On 22 April, the CBC reported that the hotel occupancy rate in Toronto was only half the normal rate, and that tour operators were reporting large declines in business. As of 22 April, all Canadian SARS cases were believed to be directly or indirectly traceable to the originally identified carriers. SARS was not loose in the community at large in Canada, although a few infected persons had broken quarantine and moved among the general population. No new cases had originated outside hospitals for 20 days.[citation needed] Nonetheless, on 23 April the WHO extended its travel advice urging postponement of nonessential travel to include Toronto. At the time, city officials and business leaders in the city expected a large economic impact as a result, and an official of the Bank of Canada said that the travel ban would drastically affect Canada's national economy. On 29 April, WHO announced that its advisory against unnecessary travel to Toronto would be withdrawn on 30 April.[citation
needed]

The U.S. Library of Congress officially excused itself from attending the American Library Association convention in Toronto in summer 2003 as a precaution.[citation needed] On July 30, 2003, the Molson Canadian Rocks for Toronto concert featuring AC/DC and the Rolling Stones was held to help revive the local economy and recoup tourist losses resulting from the SARS outbreak. With an estimated attendance of about 450,000 and also referred to as "SARSStock" (harking of the 1969 Woodstock concerts), it would turn out to be the largest ticketed event ever in Canada and one of the largest in North America. In 2005 and 2006, The Rumoli Brothers[26] (a comedy duo based in Toronto) put on SARSical, a musical that explored the lighter side of the epidemic and poked fun at the media's overreaction to the 44 deaths that occurred in Toronto.[27]
[edit] United States

SARS illustrated that responses to a deadly epidemic can occur far beyond the region experiencing actual infections, particularly in the age of the Internet. In the United States, which suffered no SARS-related deaths, there were 8 people with laboratory-confirmed cases of SARS infection, all of whom contracted the virus abroad.[28] However, mainstream media reports fixated on the possibility of a domestic epidemic, and often used metaphors that described SARS as the product of Chinese "culture".[29] The ubiquitous media image of Asians in facemasks and emails circulating rumors of domestic infections in Chinatowns across the country helped to establish the association between Asian peoples and SARS infection.[citation needed] The first SARS case in the US was in Bergen County, New Jersey at Holy Name Hospital in Teaneck. Dr. Thomas Birch, the head of Infectious Diseases at Holy Name, was the first doctor to treat SARS in the United States.[30][31]

A national survey conducted by the Harvard School of Public Health revealed that by mid-April, 93% of Americans had heard of SARS. Further, the survey showed that fourteen percent of Americans nationally avoided Asian businesses.[32] While the latter is not an overwhelming statistic, many Asian communities began reporting losses in business and tourism, indicating that a larger percentage of people in areas near Asian communities might have avoided Asian businesses.[citation needed] New York Citys Chinatown was particularly affected, as rumors of local infections circulated fear around the community and many Asian Americans felt stigmatized in the general public. Even without a local epidemic, SARS caused economic damage to Chinatowns economy that was already struggling from the nearby terrorist attacks of 9/11. Tourism plummeted as the public avoided what they perceived as an infected space and people. Restaurants in particular suffered losses after one particular rumor reported that a local restaurant owner had spread SARS to his employees before dying. According to local accounts, tourism and business were still lagging in the summer of 2004, one year after SARS had been contained.[29] Even without a single infection, Chinatown was quickly identified as a site of contagion and risk.[citation needed] Chinatown community members responded by organizing demonstrations to refute rumors of local infections. The Organization of Chinese Americans sponsored a rally in support of local businesses, with leaders bearing the banner "SARS: Support Asian RestaurantS." Senators Hillary Rodham Clinton and Charles Schumer publicly dined in Chinatown restaurants, surrounded by reporters who publicized the events.[citation needed] However, Chinatown community members did not universally dismiss the dominant discourses of risk and responsibility that blamed SARS on Chinese "culture". In fact, local responses to these discourses revealed many fissures within the Chinatown community. Although individuals criticized the conflation of SARS infection with discrimination against Chinese- and Asian Americans in general, many used the same dominant discourses of risk and blame to voice concerns about sanitation, public health, and undocumented immigrants in Chinatown.[29]

[edit] Research
[edit] Antiviral research

Before the emergence of SARS-CoV, no efforts were put into the search for Antiviral drugs against coronaviruses. The rapid transmission and high mortality rate made SARS a global threat for which no efficacious therapy was available and empirical strategies had to be used to treat the patients. New insights into the field of the SARS-CoV genome structure and pathogenesis revealed novel potential anti-coronavirus targets. Several proteins encoded by the SARS-CoV could be considered as targets for therapeutic intervention: the spike protein, the main protease, the NTPase/helicase, the RNA dependent RNA polymerase and different other viral proteinmediated processes. Potential anti-SARS-CoV drugs are currently being developed in vivo. The development of effective drugs against SARS-CoV may also provide new strategies for the prevention or treatment of other coronavirus diseases in animals or humans.[1]

[edit] Vaccine development

The emergence and identification of several common and rare human coronaviruses that cause severe lower respiratory tract infection argues for the judicious development of robust coronavirus vaccines and vector platforms. Currently, limited information is available on the correlates of protection against SARS-CoV and other severe lower respiratory tract human coronavirus infections, a clear priority for future research. Dr. Zobel de Ayala along with other medical researchers from Harvard University of Medicine gathered together in a 7-day all laboratory research, the research was rather successful. Passive immunization has been successful in establishing protection from SARS-CoV suggesting an important role for neutralizing antibodies. One important property of future vaccine candidates is the ability to confer protection against multiple variant strains of SARS-CoV, especially in senescent populations that are most at risk for severe disease. Many vaccine candidates are capable of inducing humoral and cellular responses. The development of infectious clones for coronaviruses has facilitated the identification of attenuating mutations, deletions and recombinations which could ultimately result in live attenuated vaccine candidates. Stable vaccine platforms should be developed that allow for rapid intervention strategies against any future emergence coronaviruses. Vaccine correlates that enhance disease after challenge should be thoroughly investigated and mechanisms devised to circumvent vaccine-associated complications.[1]

Aspiration (medicine) - Pulmonary edema

Death Death
From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Death (disambiguation) and Dead (disambiguation). "Dying" redirects here. For the process of coloring, see Dyeing. For other uses, see Near-death (disambiguation).

The human skull, widely considered a symbol of death

Death is the permanent termination of the biological functions that sustain a living organism. Phenomena which commonly bring about death include old age, predation, malnutrition, disease, and accidents or trauma resulting in terminal injury. The nature of death has been for millennia a central concern of the world's religious traditions and of philosophical enquiry, and belief in some kind of afterlife or rebirth has been a central aspect of religious faith.

Contents
[hide]

1 Etymology 2 Senescence 3 Symptoms of death 4 Diagnosis o 4.1 Problems of definition o 4.2 Legal o 4.3 Misdiagnosed 5 Causes

o 5.1 Autopsy 6 Life extension 7 Location 8 Society and culture 9 In biology o 9.1 Natural selection o 9.2 Extinction o 9.3 Evolution of aging 10 See also 11 References 12 Further reading 13 External links

[edit] Etymology
The word death comes from Old English dea, which in turn comes from Proto-Germanic *dauaz (reconstructed by etymological analysis). This comes from the Proto-Indo-European stem *dheu- meaning the 'Process, act, condition of dying'.

[edit] Senescence
Almost all animals who survive external hazards to their biological functioning eventually die from senescence. The only known exception is the jellyfish Turritopsis nutricula, thought to be, in effect, immortal.[1] Causes of death in humans as a result of intentional activity include suicide and homicide. From all causes, roughly 150,000 people die around the world each day.[2] Physiological death is now seen as a process, more than an event: conditions once considered indicative of death are now reversible.[3] Where in the process a dividing line is drawn between life and death depends on factors beyond the presence or absence of vital signs. In general, clinical death is neither necessary nor sufficient for a determination of legal death. A patient with working heart and lungs determined to be brain dead can be pronounced legally dead without clinical death occurring. Precise medical definition of death, in other words, becomes more problematic, paradoxically, as scientific knowledge and medicine advance.[4]

[edit] Symptoms of death

Signs of death or strong indications that an animal is no longer alive are:

Cessation of breathing Cardiac arrest (No pulse) Pallor mortis, paleness which happens in the 15120 minutes after death Livor mortis, a settling of the blood in the lower (dependent) portion of the body Algor mortis, the reduction in body temperature following death. This is generally a steady decline until matching ambient temperature

Rigor mortis, the limbs of the corpse become stiff (Latin rigor) and difficult to move or manipulate Decomposition, the reduction into simpler forms of matter, accompanied by a strong, unpleasant odor.

[edit] Diagnosis
[edit] Problems of definition

A flower, a skull and an hourglass stand in for Life, Death and Time in this 17th-century painting by Philippe de Champaigne

The concept of death is a key to human understanding of the phenomenon.[5] There are many scientific approaches to the concept. For example, brain death, as practiced in medical science, defines death as a point in time at which brain activity ceases.[6][7][8][9] One of the challenges in defining death is in distinguishing it from life. As a point in time, death would seem to refer to the moment at which life ends. However, determining when death has occurred requires drawing precise conceptual boundaries between life and death. This is problematic because there is little consensus over how to define life. It is possible to define life in terms of consciousness. When consciousness ceases, a living organism can be said to have died. One of the notable flaws in this approach, however, is that there are many organisms which are alive but probably not conscious (for example, single-celled organisms). Another problem with this approach is in defining consciousness, which has many different definitions given by modern scientists, psychologists and philosophers. This general problem of defining death applies to the particular challenge of defining death in the context of medicine. Other definitions for death focus on the character of cessation of something.[10] In this context "death" describes merely the state where something has ceased, for example, life. Thus, the definition of "life" simultaneously defines death. Historically, attempts to define the exact moment of a human's death have been problematic. Death was once defined as the cessation of heartbeat (cardiac arrest) and of breathing, but the development of CPR and prompt defibrillation have rendered that definition inadequate because breathing and heartbeat can sometimes be restarted. Events which were causally linked to death in the past no longer kill in all circumstances; without a functioning heart or lungs, life can

sometimes be sustained with a combination of life support devices, organ transplants and artificial pacemakers. Today, where a definition of the moment of death is required, doctors and coroners usually turn to "brain death" or "biological death" to define a person as being clinically dead; people are considered dead when the electrical activity in their brain ceases. It is presumed that an end of electrical activity indicates the end of consciousness. However, suspension of consciousness must be permanent, and not transient, as occurs during certain sleep stages, and especially a coma. In the case of sleep, EEGs can easily tell the difference. However, the category of "brain death" is seen by some scholars to be problematic. For instance, Dr. Franklin Miller, senior faculty member at the Department of Bioethics, National Institutes of Health, notes: "By the late 1990s, however, the equation of brain death with death of the human being was increasingly challenged by scholars, based on evidence regarding the array of biological functioning displayed by patients correctly diagnosed as having this condition who were maintained on mechanical ventilation for substantial periods of time. These patients maintained the ability to sustain circulation and respiration, control temperature, excrete wastes, heal wounds, fight infections and, most dramatically, to gestate fetuses (in the case of pregnant "brain-dead" women)."[11] Those people maintaining that only the neo-cortex of the brain is necessary for consciousness sometimes argue that only electrical activity should be considered when defining death. Eventually it is possible that the criterion for death will be the permanent and irreversible loss of cognitive function, as evidenced by the death of the cerebral cortex. All hope of recovering human thought and personality is then gone given current and foreseeable medical technology. However, at present, in most places the more conservative definition of death irreversible cessation of electrical activity in the whole brain, as opposed to just in the neo-cortex has been adopted (for example the Uniform Determination Of Death Act in the United States). In 2005, the Terri Schiavo case brought the question of brain death and artificial sustenance to the front of American politics. Even by whole-brain criteria, the determination of brain death can be complicated. EEGs can detect spurious electrical impulses, while certain drugs, hypoglycemia, hypoxia, or hypothermia can suppress or even stop brain activity on a temporary basis. Because of this, hospitals have protocols for determining brain death involving EEGs at widely separated intervals under defined conditions. In certain cultures, death is more of a process than a single event. It implies a slow shift from one spiritual state to another[12].
[edit] Legal See also: Legal death

A dead Confederate soldier sprawled out in Petersburg, Virginia, 1865, during the American Civil War

In the United States, a person is dead by law if a Statement of Death or Death certificate is approved by a licensed medical practitioner. Various legal consequences follow death, including the removal from the person of what in legal terminology is called personhood. The possession of brain activities, or capability to resume brain activity, is a necessary condition to legal personhood in the United States. "It appears that once brain death has been determined ... no criminal or civil liability will result from disconnecting the life-support devices." (Dority v. Superior Court of San Bernardino County, 193 Cal.Rptr. 288, 291 (1983))
[edit] Misdiagnosed See also: Premature burial

There are many anecdotal references to people being declared dead by physicians and then "coming back to life", sometimes days later in their own coffin, or when embalming procedures are about to begin. From the mid-18th century onwards, there was an upsurge in the public's fear of being mistakenly buried alive,[13] and much debate about the uncertainty of the signs of death. Various suggestions were made to test for signs of life before burial, ranging from pouring vinegar and pepper into the corpse's mouth to applying red hot pokers to the feet or into the rectum.[14] Writing in 1895, the physician J.C. Ouseley claimed that as many as 2,700 people were buried prematurely each year in England and Wales, although others estimated the figure to be closer to 800.[15] In cases of electric shock, cardiopulmonary resuscitation (CPR) for an hour or longer can allow stunned nerves to recover, allowing an apparently dead person to survive. People found unconscious under icy water may survive if their faces are kept continuously cold until they arrive at an emergency room.[16] This "diving response", in which metabolic activity and oxygen requirements are minimal, is something humans share with cetaceans called the mammalian diving reflex.[16] As medical technologies advance, ideas about when death occurs may have to be re-evaluated in light of the ability to restore a person to vitality after longer periods of apparent death (as happened when CPR and defibrillation showed that cessation of heartbeat is inadequate as a decisive indicator of death). The lack of electrical brain activity may not be enough to consider

someone scientifically dead. Therefore, the concept of information theoretical death has been suggested as a better means of defining when true death occurs, though the concept has few practical applications outside of the field of cryonics. There have been some scientific attempts to bring dead organisms back to life, but with limited success.[17] In science fiction scenarios where such technology is readily available, real death is distinguished from reversible death.

[edit] Causes
See also: List of causes of death by rate and List of preventable causes of death

The leading cause of death in developing countries is infectious disease. The leading causes of death in developed countries are atherosclerosis (heart disease and stroke), cancer, and other diseases related to obesity and aging. These conditions cause loss of homeostasis, leading to cardiac arrest, causing loss of oxygen and nutrient supply, causing irreversible deterioration of the brain and other tissues. Of the roughly 150,000 people who die each day across the globe, about two thirds die of age-related causes.[2] In industrialized nations, the proportion is much higher, reaching 90%.[2] With improved medical capability, dying has become a condition to be managed. Home deaths, once commonplace, are now rare in the developed world.

The body of Pope John Paul II lying in state in St. Peter's Basilica, 2005

In developing nations, inferior sanitary conditions and lack of access to modern medical technology makes death from infectious diseases more common than in developed countries. One such disease is tuberculosis, a bacterial disease which killed 1.7 million people in 2004.[18] Malaria causes about 400900 million cases of fever and 13 million deaths annually.[19] AIDS death toll in Africa may reach 90100 million by 2025.[20][21] According to Jean Ziegler, who was the United Nations Special reporter on the Right to Food from 2000 to March 2008; mortality due to malnutrition accounted for 58% of the total mortality rate in 2006. Ziegler says worldwide approximately 62 million people died from all causes and of those deaths more than 36 million died of hunger or diseases due to deficiencies in micronutrients.[22]

Tobacco smoking killed 100 million people worldwide in the 20th century and could kill 1 billion people around the world in the 21st century, a WHO Report warned.[23][24] Many leading developed world causes of death can be postponed by diet and physical activity, but the accelerating incidence of disease with age still imposes limits on human longevity. The evolutionary cause of aging is, at best, only just beginning to be understood. It has been suggested that direct intervention in the aging process may now be the most effective intervention against major causes of death.[25]
[edit] Autopsy

An autopsy, also known as a postmortem examination or an obduction, is a medical procedure that consists of a thorough examination of a human corpse to determine the cause and manner of a person's death and to evaluate any disease or injury that may be present. It is usually performed by a specialized medical doctor called a pathologist.

Rembrandt turns an autopsy into a masterpiece: The Anatomy Lesson of Dr. Nicolaes Tulp

Autopsies are either performed for legal or medical purposes. A forensic autopsy is carried out when the cause of death may be a criminal matter, while a clinical or academic autopsy is performed to find the medical cause of death and is used in cases of unknown or uncertain death, or for research purposes. Autopsies can be further classified into cases where external examination suffices, and those where the body is dissected and an internal examination is conducted. Permission from next of kin may be required for internal autopsy in some cases. Once an internal autopsy is complete the body is generally reconstituted by sewing it back together. Autopsy is important in a medical environment and may shed light on mistakes and help improve practices. A "necropsy" is an older term for a postmortem examination, unregulated, and not always a medical procedure. In modern times the term is more often used in the postmortem examination of the corpses of animals.

[edit] Life extension

Main article: Life extension

Life extension refers to an increase in maximum or average lifespan, especially in humans, by slowing down or reversing the processes of aging. Average lifespan is determined by vulnerability to accidents and age or lifestyle-related afflictions such as cancer, or cardiovascular disease. Extension of average lifespan can be achieved by good diet, exercise and avoidance of hazards such as smoking. Maximum lifespan is determined by the rate of aging for a species inherent in its genes. Currently, the only widely recognized method of extending maximum lifespan is calorie restriction. Theoretically, extension of maximum lifespan can be achieved by reducing the rate of aging damage, by periodic replacement of damaged tissues, or by molecular repair or rejuvenation of deteriorated cells and tissues. Researchers of life extension are a subclass of biogerontologists known as "biomedical gerontologists". They try to understand the nature of aging and they develop treatments to reverse aging processes or to at least slow them down, for the improvement of health and the maintenance of youthful vigor at every stage of life. Those who take advantage of life extension findings and seek to apply them upon themselves are called "life extensionists" or "longevists". The primary life extension strategy currently is to apply available anti-aging methods in the hope of living long enough to benefit from a complete cure to aging once it is developed, which given the rapidly advancing state of biogenetic and general medical technology, could conceivably occur within the lifetimes of people living today.

[edit] Location
Before about 1930, most people died in their own homes, surrounded by family, and comforted by clergy, neighbors, and doctors making house calls.[26] By the mid-20th century, half of all Americans died in a hospital.[27] By the start of the 21st century, only about 20 to 25% of people in developed countries died in the community.[27][28][29] The shift away from dying at home, towards dying in a professionalized medical environment, has been termed the "Invisible Death".[27]

[edit] Society and culture

Main article: Death and culture

The regent duke Charles (later king Charles IX of Sweden) insulting the corpse of Klaus Fleming. Albert Edelfelt, 1878.

Dead bodies can be mummified either naturally, as this one from Guanajuato, or by intention, as those in ancient Egypt.

Death is the center of many traditions and organizations; customs relating to death are a feature of every culture around the world. Much of this revolves around the care of the dead, as well as the afterlife and the disposal of bodies upon the onset of death. The disposal of human corpses does, in general, begin with the last offices before significant time has passed, and ritualistic ceremonies often occur, most commonly interment or cremation. This is not a unified practice, however, as in Tibet for instance the body is given a sky burial and left on a mountain top. Proper preparation for death and techniques and ceremonies for producing the ability to transfer one's spiritual attainments into another body (reincarnation) are subjects of detailed study in Tibet.[30] Mummification or embalming is also prevalent in some cultures, to retard the rate of decay. Legal aspects of death are also part of many cultures, particularly the settlement of the deceased estate and the issues of inheritance and in some countries, inheritance taxation.

Gravestones in Kyoto, Japan

Capital punishment is also a culturally divisive aspect of death. In most jurisdictions where capital punishment is carried out today, the death penalty is reserved for premeditated murder, espionage, treason, or as part of military justice. In some countries, sexual crimes, such as adultery and sodomy, carry the death penalty, as do religious crimes such as apostasy, the formal renunciation of one's religion. In many retentionist countries, drug trafficking is also a capital offense. In China human trafficking and serious cases of corruption are also punished by the death penalty. In militaries around the world courts-martial have imposed death sentences for offenses such as cowardice, desertion, insubordination, and mutiny.[31] Death in warfare and in suicide attack also have cultural links, and the ideas of dulce et decorum est pro patria mori, mutiny punishable by death, grieving relatives of dead soldiers and death notification are embedded in many cultures. Recently in the western world, with the supposed increase in terrorism following the September 11 attacks, but also further back in time with suicide bombings, kamikaze missions in World War II and suicide missions in a host of other conflicts in history, death for a cause by way of suicide attack, and martyrdom have had significant cultural impacts. Suicide in general, and particularly euthanasia, are also points of cultural debate. Both acts are understood very differently in different cultures. In Japan, for example, ending a life with honor by seppuku was considered a desirable death, whereas according to traditional Christian and Islamic cultures, suicide is viewed as a sin. Death is personified in many cultures, with such symbolic representations as the Grim Reaper, Azrael and Father Time.

[edit] In biology
After death the remains of an organism become part of the biogeochemical cycle. Animals may be consumed by a predator or a scavenger. Organic material may then be further decomposed by detritivores, organisms which recycle detritus, returning it to the environment for reuse in the food chain. Examples of detritivores include earthworms, woodlice and dung beetles. Microorganisms also play a vital role, raising the temperature of the decomposing matter as they break it down into yet simpler molecules. Not all materials need to be decomposed fully, however. Coal, a fossil fuel formed over vast tracts of time in swamp ecosystems, is one example.
[edit] Natural selection Main articles: competition (biology), natural selection, and extinction

Contemporary evolutionary theory sees death as an important part of the process of natural selection. It is considered that organisms less adapted to their environment are more likely to die having produced fewer offspring, thereby reducing their contribution to the gene pool. Their genes are thus eventually bred out of a population, leading at worst to extinction and, more positively, making the process possible, referred to as speciation. Frequency of reproduction plays an equally important role in determining species survival: an organism that dies young but

leaves numerous offspring displays, according to Darwinian criteria, much greater fitness than a long-lived organism leaving only one.
[edit] Extinction Main article: Extinction

A dodo, the bird that became a byword in English for species extinction[32]

Extinction is the cessation of existence of a species or group of taxa, reducing biodiversity. The moment of extinction is generally considered to be the death of the last individual of that species (although the capacity to breed and recover may have been lost before this point). Because a species' potential range may be very large, determining this moment is difficult, and is usually done retrospectively. This difficulty leads to phenomena such as Lazarus taxa, where a species presumed extinct abruptly "reappears" (typically in the fossil record) after a period of apparent absence. New species arise through the process of speciation, an aspect of evolution. New varieties of organisms arise and thrive when they are able to find and exploit an ecological niche and species become extinct when they are no longer able to survive in changing conditions or against superior competition.
[edit] Evolution of aging Main article: Evolution of ageing

Inquiry into the evolution of aging aims to explain why so many living things and the vast majority of animals weaken and die with age (a notable exception being hydra, which may be biologically immortal). The evolutionary origin of senescence remains one of the fundamental puzzles of biology. Gerontology specializes in the science of human aging processes.

By intensive care and emergency medicine

CPR Cardiopulmonary resuscitation

From Wikipedia, the free encyclopedia Jump to: navigation, search "CPR" redirects here. For other uses, see CPR (disambiguation).

Cardiopulmonary resuscitation
Intervention

CPR being performed on a mannequin

ICD-9:

99.60

MeSH

D016887

OPS-301 code:

8-771

Cardiopulmonary resuscitation (CPR) is an emergency procedure which is performed in an effort to manually preserve intact brain function until further measures are taken to restore spontaneous blood circulation and breathing in a person in cardiac arrest. It is indicated in those who are unresponsive with no breathing or abnormal breathing, for example agonal respirations. It may be performed both in and outside of a hospital. CPR involves chest compressions at least 5 cm deep and at a rate of at least 100 per minute in an effort to create artificial circulation by manually pumping blood through the heart. In addition, the rescuer may provide breaths by either exhaling into the subject's mouth or utilizing a device that pushes air into the subject's lungs. This process of externally providing ventilation is termed artificial respiration. Current recommendations place emphasis on high-quality chest

compressions over artificial respiration; a simplified CPR method involving chest compressions only is recommended for untrained rescuers. CPR alone is unlikely to restart the heart; its main purpose is to restore partial flow of oxygenated blood to the brain and heart. The objective is to delay tissue death and to extend the brief window of opportunity for a successful resuscitation without permanent brain damage. Administration of an electric shock to the subject's heart, termed defibrillation, is usually needed in order to restore a viable or "perfusing" heart rhythm. Defibrillation is only effective for certain heart rhythms, namely ventricular fibrillation or pulseless ventricular tachycardia, rather than asystole or pulseless electrical activity. CPR may succeed in inducing a heart rhythm which may be shockable. CPR is generally continued until the subject regains return of spontaneous circulation (ROSC) or is declared dead.

Contents
[hide]

1 Medical uses 2 Methods o 2.1 Standard o 2.2 Compression only o 2.3 In pregnancy o 2.4 Other 3 Effectiveness 4 Pathophysiology 5 Adjunct devices o 5.1 Timing devices o 5.2 Manual assist devices o 5.3 Automatic devices 6 Prevalence o 6.1 Chance of receiving CPR o 6.2 Chance of receiving CPR in time 7 Society and culture o 7.1 Portrayed effectiveness o 7.2 Stage CPR o 7.3 Self-CPR hoax o 7.4 CPR learned from movies and television o 7.5 Hands-Only CPR portrayed as more palatable version 8 History 9 In other animals 10 References 11 External links

[edit] Medical uses

CPR is indicated for any person who is unresponsive with no breathing, or who is only breathing in occasional agonal gasps, as it is most likely that they are in cardiac arrest.[1]:S643 If a person still has a pulse, but is not breathing (respiratory arrest), artificial respirations may be more appropriate, but due to the difficulty people have in accurately assessing the presence or absence of a pulse, CPR guidelines recommend that lay persons should not be instructed to check the pulse, while giving health care professionals the option to check a pulse.[2] In those with cardiac arrest due to trauma CPR is considered futile but still recommended.[3]

[edit] Methods

CPR training: CPR is being administered while a second rescuer prepares for defibrillation.

In 2010, the American Heart Association and International Liaison Committee on Resuscitation updated their CPR guidelines.[1]:S640[4] The importance of high quality CPR (sufficient rate and depth without excessively ventilating) was emphasized.[1]:S640 The order of interventions was changed for all age groups except newborns from airway, breathing, chest compressions (ABC) to chest compressions, airway, breathing (CAB).[1]:S642 An exception to this recommendation is for those who are believed to be in a respiratory arrest (drowning, etc.).[1]:S642
[edit] Standard

A universal compression to ventilation ratio of 30:2 is recommended for adult and in children and infant if only a single rescuer is present.[5]:8 If at least 2 rescuers are present a ratio of 15:2 is preferred in children and infants.[5]:8 In newborns a rate of 3:1 is recommended unless a cardiac cause is known in which case a 15:2 ratio is reasonable.[1]:S647 If an advanced airway such as an endotracheal tube or laryngeal mask airway is in place delivery of respirations should occur without pauses in compressions at a rate of 8-10 per minute.[6] The recommended order of interventions is chest compressions, airway, breathing or CAB in most situations.[1]:S642 With a compression rate of at least 100 per minute in all groups.[5]:8 Recommended compression depth in adults and children is about 5 cm (2 inches) and in infants it is 4 cm (1.5 inches.[5]:8 As of 2010 the Resuscitation Council (UK) still recommends ABC for children.[7] As it can be difficult to determine the presence or absence of a pulse the pulse check has been removed for lay providers and should not be performed for more than 10 seconds by health care providers.[5]:8 In adults rescuers should use two hands for the chest compressions, while in children they should use one, and with infants two fingers (index and middle fingers).[8]

[edit] Compression only

Compression only (hands-only or cardiocerebral resuscitation) CPR is a technique that involves chest compressions without artificial respiration.[1]:S643 It is recommended as the method of choice for the untrained rescuer or those who are not proficient as it is easier to perform and instructions are easier to give over the phone.[1]:S643[5]:8[9] In adults with out-of-hospital cardiac arrest, compression-only CPR by the lay public has a higher success rate than standard CPR.[9] The exceptions are cases of drownings, drug overdose, and arrest in children. Children who receive compression only CPR have the same outcomes as those who received no CPR.[1]:S646 The method of delivering chest compressions remains the same, as does the rate (at least 100 per minute). It is hoped that the use of compression only delivery will increase the chances of the lay public delivering CPR.[10] As per the American Heart Association, the beat of the Bee Gees' song Stayin' Alive provides an ideal amount of beats-per-minute to use for hands-only CPR.[11] For those with non cardiac arrest and people less than 20 years of age standard CPR is superior to compression only CPR.[12][13]
[edit] In pregnancy

During pregnancy when a woman is lying on her back the uterus may compress the inferior vena cava and thus decrease venous return.[3] It is recommended for this reason that the uterus be pushed to the persons left and if this is not effective either roll the person 30s or consider emergency cesarean section.[3]
[edit] Other

Interposed abdominal compressions may be beneficial in the in hospital environment.[14] There is however no evidence of benefit pre hospital or in children.[14] Internal cardiac massage is manual squeezing of the heart carried out through a surgical incision into the chest cavity. This may be carried out if the chest is already open for cardiac surgery.

[edit] Effectiveness
Type of Arrest Witnessed In-Hospital Cardiac Arrest Unwitnessed In-Hospital Cardiac Arrest Bystander Cardiocerebral Resuscitation ROSC Survival Source 48% 21% 40% 22% 1% 6% 4% 2%
[15]

[15]

[16]

Bystander Cardiopulmonary Resuscitation 40% No Bystander CPR (Ambulance CPR) 15%

[16]

[16]

Defibrillation within 35 minutes

74%

30%

[17][18]

Used alone, CPR will result in few complete recoveries, and those who do survive often develop serious complications. Estimates vary, but many organizations stress that CPR does not "bring anyone back," it simply preserves the body for defibrillation and advanced life support.[17] However, in the case of "non-shockable" rhythms such as Pulseless Electrical Activity (PEA), defibrillation is not indicated, and the importance of CPR rises. On average, only 510% of people who receive CPR survive.[19] The purpose of CPR is not to "start" the heart, but rather to circulate oxygenated blood, and keep the brain alive until advanced care (especially defibrillation) can be initiated. As many of these patients may have a pulse that is impalpable by the layperson rescuer, the current consensus is to perform CPR on a patient who is not breathing. Studies have shown the importance of immediate CPR followed by defibrillation within 35 minutes of sudden VF cardiac arrest improve survival. In cities such as Seattle where CPR training is widespread and defibrillation by EMS personnel follows quickly, the survival rate is about 30 percent. In cities such as New York, without those advantages, the survival rate is only 12 percent.[18] In most cases, there is a higher proportion of patients who achieve a Return of Spontaneous Circulation (ROSC), where their heart starts to beat on its own again, than ultimately survive to be discharged from hospital (see table below). This is due to medical staff either being ultimately unable to address the cause of the arrhythmia or cardiac arrest, or in some instances due to other co-morbidities, due to the patient being gravely ill in more than one way. Compression-only CPR is less effective in children than in adults, as cardiac arrest in children is more likely to have a non-cardiac cause. In a 2010 prospective study of cardiac arrest in children (age 117), for arrests with a non-cardiac cause provision by bystanders of conventional CPR with rescue breathing yielded a favorable neurological outcome at one month more often that did compression-only CPR (OR 5.54; 95% confidence interval 2.5216.99). For arrests with a cardiac cause in this cohort, there was no difference between the two techniques (OR 1.20; 95% confidence interval 0.552.66).[20] This is consistent with American Heart Association guidelines for parents.[21]

[edit] Pathophysiology
CPR is used on people in cardiac arrest in order to oxygenate the blood and maintain a cardiac output to keep vital organs alive. Blood circulation and oxygenation are required to transport oxygen to the tissues. The brain may sustain damage after blood flow has been stopped for about four minutes and irreversible damage after about seven minutes.[22][23][24][25][26] Typically if blood flow ceases for one to two hours, the cells of the body die. Because of that CPR is generally only effective if performed within seven minutes of the stoppage of blood flow.[27] The heart also rapidly loses the ability to maintain a normal rhythm. Low body temperatures as sometimes seen in near-drownings prolong the time the brain survives. Following cardiac arrest, effective CPR enables enough oxygen to reach the brain to delay brain death, and allows the heart to remain responsive to defibrillation attempts.

[edit] Adjunct devices

While several adjunctive devices are available none other than defibrillation as of 2010 have consistently been found to be better than standard CPR for out of hospital cardiac arrest.[1]:S644 These devices can be split in to three broad groups - timing devices, those that assist the rescuer to achieve the correct technique, especially depth and speed of compressions, and those which take over the process completely.
[edit] Timing devices

They can feature a metronome (an item carried by many ambulance crews) in order to assist the rescuer in getting the correct rate. Some units can also give timing reminders for performing compressions, breathing and changing operators.[28]
[edit] Manual assist devices

Mechanical devices have not been found to have greater benefit than harm and thus are not currently recommended for widespread use.[29] Audible and visual prompting may improve the quality of CPR and prevent the decrease of compression rate and depth that naturally occurs with fatigue,[30][31][32][33][34][35] and to address this potential improvement, a number of devices have been developed to help improve CPR technique. These items can be devices to placed on top of the chest, with the rescuers hands going over the device, and a display or audio feedback giving information on depth, force or rate,[36] or in a wearable format such as a glove.[37] Several published evaluations show that these devices can improve the performance of chest compressions.[38][39] As well as use during actual CPR on a cardiac arrest victim, which relies on the rescuer carrying the device with them, these devices can also be used as part of training programs to improve basic skills in performing correct chest compressions.[40]
[edit] Automatic devices

There are also some automated devices available which take over the chest compressions for the rescuer. These have several advantages: they allow rescuers to focus on performing other interventions; they do not fatigue and begin to perform less effective compressions, as humans do; and they are able to perform effective compressions in limited-space environments such as air ambulances, where manual compressions are difficult. These devices use either pneumatic (high-pressure gas) or electrical power sources to drive a compressing pad on to the chest of the patient. One such device, known as the LUCAS, was developed at the University Hospital of Lund, is powered by the compressed oxygen supplies already standard in ambulances and hospitals, and has undergone numerous clinical trials, showing a marked improvement in coronary perfusion pressure[41] and return of spontaneous circulation.[42]

Another system called the AutoPulse is electrically powered and uses a large band around the patients chest which contracts in rhythm in order to deliver chest compressions. This is also backed by clinical studies showing increased successful return of spontaneous circulation.[43][44]

[edit] Prevalence
[edit] Chance of receiving CPR

Various studies suggest that in out-of-home cardiac arrest, bystanders, lay persons or family members attempt CPR in between 14%[45] and 45%[46] of the time, with a median of 32%. This indicates that around a third of out-of-home arrests have a CPR attempt made on them. However, the effectiveness of this CPR is variable, and the studies suggest only around half of bystander CPR is performed correctly.[47][48] There is a clear correlation between age and the chance of CPR being commenced, with younger people being far more likely to have CPR attempted on them prior to the arrival of emergency medical services.[45][49] It was also found that CPR was more commonly given by a bystander in public than when an arrest occurred in the patient's home, although health care professionals are responsible for more than half of out-of-hospital resuscitation attempts.[46] This is supported by further research, which suggests that people with no connection to the victim are more likely to perform CPR than a member of their family.[50] This is likely because of the shock experienced by finding a family member in need of CPR; it is easier to remain calm - and think clearly - when the person in need of CPR is a complete stranger, as in this case one will not be as frightened. There is also a correlation between the cause of arrest and the likelihood of bystander CPR being initiated. Lay persons are most likely to give CPR to younger cardiac arrest victims in a public place when it has a medical cause; victims in arrest from trauma, exsanguination or intoxication are less likely to receive CPR.[50] Finally, it has been claimed that there is a higher chance of CPR being performed if the bystander is told to only perform the chest compression element of the resuscitation.[10]
[edit] Chance of receiving CPR in time

CPR is only likely to be effective if commenced within 6 minutes after the blood flow stops,[51] because permanent brain cell damage occurs when fresh blood infuses the cells after that time, since the cells of the brain become dormant in as little as 46 minutes in an oxygen deprived environment and the cells are unable to survive the reintroduction of oxygen in a traditional resuscitation. Research using cardioplegic blood infusion resulted in a 79.4% survival rate with cardiac arrest intervals of 7243 minutes, traditional methods achieve a 15% survival rate in this scenario, by comparison. New research is currently needed to determine what role CPR, electroshock, and new advanced gradual resuscitation techniques will have with this new knowledge[52] A notable exception is cardiac arrest occurring in conjunction with exposure to very cold temperatures. Hypothermia seems to protect by slowing down metabolic and physiologic processes, greatly decreasing the tissues' need for oxygen.[53] There are cases where

CPR, defibrillation, and advanced warming techniques have revived victims after substantial periods of hypothermia.[54]

[edit] Society and culture

[edit] Portrayed effectiveness

CPR is often severely misrepresented in movies and television as being highly effective in resuscitating a person who is not breathing and has no circulation. A 1996 study published in the New England Journal of Medicine showed that CPR success rates in television shows was 75% for immediate circulation, and 67% survival to discharge.[55][56] This gives members of the public an unrealistic expectation of a successful outcome.[55] When educated on the actual survival rates, the proportion of patients over 60 years of age desiring CPR should they suffer a cardiac arrest drops from 41% to 22%.[57]
[edit] Stage CPR

Chest compressions are capable of causing significant local blunt trauma, including bruising or fracture of the sternum or ribs.[58] Performing CPR on a healthy person may or may not disrupt normal heart rhythm, but regardless the technique should not be performed on a healthy person because of the risk of trauma. The portrayal of CPR technique on television and film often is purposely incorrect. Actors simulating the performance of CPR may bend their elbows while appearing to compress, to prevent force from reaching the chest of the actor portraying the victim. Other techniques, such as substituting a mannequin torso for the "victim" in some shots, may also be used to avoid harming actors.
[edit] Self-CPR hoax

A form of "self-CPR" termed "Cough CPR" was the subject of a hoax chain e-mail entitled "How to Survive a Heart Attack When Alone" which wrongly cited "ViaHealth Rochester General Hospital" as the source of the technique. Rochester General Hospital has denied any connection with the technique.[59][60] Cough CPR cannot be used outside the hospital because the first symptom of cardiac arrest is unconsciousness[61] in which case coughing is impossible, although myocardial infarction (heart attack) may occur to give rise to the cardiac arrest, so a patient may not be immediately unconscious. Further, the vast majority of people suffering chest pain from a heart attack will not be in cardiac arrest and CPR is not needed. In these cases attempting cough CPR will increase the workload on the heart and may be harmful. When coughing is used on trained and monitored patients in hospitals, it has only been shown to be effective for 90 seconds.[62] The American Heart Association (AHA) and other resuscitation bodies[62] do not endorse "Cough CPR", which it terms a misnomer as it is not a form of resuscitation. The AHA does recognize a limited legitimate use of the coughing technique: "This coughing technique to

maintain blood flow during brief arrhythmias has been useful in the hospital, particularly during cardiac catheterization. In such cases the patients ECG is monitored continuously, and a physician is present."[63]
[edit] CPR learned from movies and television

In at least one case, it has been claimed that CPR allegedly learned from a movie was used to save a person's life. In April 2011, it was claimed that nine-year-old Tristin Saghin saved his sister's life by administering CPR on her after she fell into a swimming pool, using only the knowledge of CPR that he had gleaned from a motion picture, Black Hawk Down.[64]
[edit] Hands-Only CPR portrayed as more palatable version

Less than 1/3 of those people who experience a cardiac arrest at home, work or in a public location have CPR performed on them. Most bystanders are worried that they might do something wrong.[65] On October 28, 2009 The American Heart Association and the Ad Council launched a Hands Only CPR PSA and website as a means to address this issue.[66] In July 2011, new content was added to the website including a digital app that helps a user learn how to perform Hands-Only CPR.[67]

[edit] History
Main article: History of CPR

Sign showing old Silvester and Holger-Nielsen methods of resuscitation

In the 19th century, Doctor H. R. Silvester described a method (The Silvester Method) of artificial respiration in which the patient is laid on their back, and their arms are raised above their head to aid inhalation and then pressed against their chest to aid exhalation.[68] The

procedure is repeated sixteen times per minute. This type of artificial respiration is occasionally seen in films made in the early part of the 20th century. A second technique, called the Holger Neilson technique, described in the first edition of the Boy Scout Handbook in the United States in 1911, described a form of artificial respiration where the person was laid on their front, with their head to the side, resting on the palms of both hands. Upward pressure applied at the patients elbows raised the upper body while pressure on their back forced air into the lungs, essentially the Silvester Method with the patient flipped over. This form is seen well into the 1950s (it is used in an episode of Lassie during the Jeff Miller era), and was often used, sometimes for comedic effect, in theatrical cartoons of the time (see Tom and Jerry's "The Cat and the Mermouse"). This method would continue to be shown, for historical purposes, side-by-side with modern CPR in the Boy Scout Handbook until its ninth edition in 1979. The technique was later banned from first-aid manuals in the U.K. However, it was not until the middle of the 20th century that the wider medical community started to recognize and promote artificial respiration combined with chest compressions as a key part of resuscitation following cardiac arrest. The combination was first seen in a 1962 training video called "The Pulse of Life" created by James Jude, Guy Knickerbocker and Peter Safar. Jude and Knickerbocker, along with William Kouwenhoven and Joseph S. Redding had recently discovered the method of external chest compressions, whereas Safar had worked with Redding and James Elam to prove the effectiveness of artificial respiration. It was at Johns Hopkins University where the technique of CPR was originally developed. The first effort at testing the technique was performed on a dog by Redding, Safar and JW Perason. Soon afterward, the technique was used to save the life of a child.[69] Their combined findings were presented at annual Maryland Medical Society meeting on September 16, 1960 in Ocean City, and gained rapid and widespread acceptance over the following decade, helped by the video and speaking tour they undertook. Peter Safar wrote the book ABC of resuscitation in 1957. In the U.S., it was first promoted as a technique for the public to learn in the 1970s.[70] Artificial respiration was combined with chest compressions based on the assumption that active ventilation is necessary to keep circulating blood oxygenated, and the combination was accepted without comparing its effectiveness with chest compressions alone. However, research over the past decade has shown that assumption to be in error, resulting in the AHA's acknowledgment of the effectiveness of chest compressions alone (see Cardiocerebral resuscitation in this article).[71]

[edit] In other animals

It is feasible to perform CPR on animals, including cats and dogs. The principles and practices are virtually identical to CPR for humans. One difference is that resuscitation is usually done through the animal's nose, not the mouth. One is cautioned to only perform CPR on unconscious animals to avoid the risk of being bitten and that animals, depending on species, have a lower bone density than humans, causing bones to become weakened after CPR is performed.[72]

Mechanical ventilation

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Mechanical ventilation
From Wikipedia, the free encyclopedia Jump to: navigation, search In architecture and climate control, mechanical or forced ventilation is the use of powered equipment, e.g. fans and blowers, to move air see ventilation (architecture).

Mechanical ventilation
Intervention

Nasotracheal intubation

ICD-9:

93.90 96.7

MeSH

D012121

OPS-301 code:

8-71

In medicine, mechanical ventilation is a method to mechanically assist or replace spontaneous breathing. This may involve a machine called a ventilator or the breathing may be assisted by a physician or other suitable person compressing a bag or set of bellows. Traditionally divided into negativepressure ventilation, where air is essentially sucked into the lungs, or positive pressure ventilation, where air (or another gas mix) is pushed into the trachea. It can be used as a short term measure, for example during an operation or critical illness (often in the setting of an intensive care unit). It may be used at home or in a nursing or rehabilitation institution if patients have chronic illnesses that require long-term ventilatory assistance. Owing to the anatomy of the human pharynx, larynx, and esophagus and the circumstances for which ventilation is required then additional measures are often required to "secure" the airway during positive pressure ventilation to allow unimpeded passage of air into the trachea and avoid air passing into the esophagus and stomach. Commonly this is by insertion of a tube into the trachea which provides a clear route for the air. This can be either an endotracheal tube, inserted through the natural openings of mouth or nose or a tracheostomy inserted through an artificial opening in the neck. In other circumstances simple airway maneuvres, an oropharyngeal airway or laryngeal mask airway may be employed. If the patient is able to protect their own airway such as in non-invasive ventilation or negative-pressure ventilation then no airway adjunct may be needed. Mechanical ventilation is often a life-saving intervention, but carries many potential complications including pneumothorax, airway injury, alveolar damage, and ventilatorassociated pneumonia.[citation needed]. In many healthcare systems prolonged ventilation as part of intensive care is a limited resource (in that there are only so many patients that can receive care at any given moment). It is used to support a single failing organ system (the lungs) and cannot reverse any underlying disease process (such as terminal cancer). For this reason there can be (occasionally difficult) decisions to be made about whether it is suitable to commence someone on mechanical ventilation. Equally many ethical issues surround the decision to discontinue mechanical ventilation.

Contents
[hide]

1 History o 1.1 Negative pressure machines o 1.2 Positive pressure machines 2 Indications for use 3 Associated risk 4 Types of ventilators o 4.1 Mechanical ventilators 5 Ventilation process in conventional mechanical ventilation o 5.1 Breath termination o 5.2 Breath initiation 6 Modes of mechanical ventilation o 6.1 Volume controlled continuous mandatory ventilation o 6.2 Volume controlled intermittent mandatory ventilation o 6.3 Pressure controlled continuous mandatory ventilation o 6.4 Pressure controlled intermittent mandatory ventilation o 6.5 High frequency ventilation o 6.6 Continuous spontaneous ventilation 6.6.1 Pressure Support Ventilation 6.6.2 Continuous positive airway pressure 7 Choosing amongst ventilator modes 8 Initial ventilator settings o 8.1 Tidal volume, rate, and pressures o 8.2 Sighs o 8.3 Initial FiO2 o 8.4 Positive end-expiratory pressure o 8.5 Positioning o 8.6 Sedation and paralysis o 8.7 Prophylaxis 9 Modification of settings o 9.1 When to withdraw mechanical ventilation 10 Respiratory monitoring 11 Connection to ventilators 12 Terminology 13 References 14 External links

[edit] History
The Roman physician Galen may have been the first to describe mechanical ventilation: "If you take a dead animal and blow air through its larynx [through a reed], you will fill its bronchi and watch its lungs attain the greatest distention."[1] Vesalius too describes ventilation by inserting a

reed or cane into the trachea of animals.[2] In 1908 George Poe demonstrated his mechanical respirator by asphyxiating dogs and seemingly bringing them back to life.[3]
[edit] Negative pressure machines

An Iron Lung Main article: Iron Lung

The iron lung, also known as the Drinker and Shaw tank, was developed in 1929 and was one of the first negative-pressure machines used for long-term ventilation. It was refined and used in the 20th century largely as a result of the polio epidemic that struck the world in the 1940s. The machine is effectively a large elongated tank, which encases the patient up to the neck. The neck is sealed with a rubber gasket so that the patient's face (and airway) are exposed to the room air. While the exchange of oxygen and carbon dioxide between the bloodstream and the pulmonary airspace works by diffusion and requires no external work, air must be moved into and out of the lungs to make it available to the gas exchange process. In spontaneous breathing, a negative pressure is created in the pleural cavity by the muscles of respiration, and the resulting gradient between the atmospheric pressure and the pressure inside the thorax generates a flow of air. In the iron lung by means of a pump, the air is withdrawn mechanically to produce a vacuum inside the tank, thus creating negative pressure. This negative pressure leads to expansion of the chest, which causes a decrease in intrapulmonary pressure, and increases flow of ambient air into the lungs. As the vacuum is released, the pressure inside the tank equalizes to that of the ambient pressure, and the elastic coil of the chest and lungs leads to passive exhalation. However, when the vacuum is created, the abdomen also expands along with the lung, cutting off venous flow back to the heart, leading to pooling of venous blood in the lower extremities. There are large portholes for nurse or home assistant access. The patients can talk and eat normally, and can see the world through a well-placed series of mirrors. Some could remain in these iron lungs for years at a time quite successfully. Today, negative pressure mechanical ventilators are still in use, notably with the polio wing hospitals in England such as St Thomas' Hospital in London and the John Radcliffe in Oxford. The prominent device used is a smaller device known as the cuirass. The cuirass is a shell-like unit, creating negative pressure only to the chest using a combination of a fitting shell and a soft

bladder. Its main use is in patients with neuromuscular disorders who have some residual muscular function. However, it was prone to falling off and caused severe chafing and skin damage and was not used as a long term device. In recent years this device has re-surfaced as a modern polycarbonate shell with multiple seals and a high pressure oscillation pump in order to carry out biphasic cuirass ventilation.
[edit] Positive pressure machines

Neonatal mechanical ventilator

The design of the modern positive-pressure ventilators were mainly based on technical developments by the military during World War II to supply oxygen to fighter pilots in high altitude. Such ventilators replaced the iron lungs as safe endotracheal tubes with high volume/low pressure cuffs were developed. The popularity of positive-pressure ventilators rose during the polio epidemic in the 1950s in Scandinavia and the United States and was the beginning of modern ventilation therapy. Positive pressure through manual supply of 50% oxygen through a tracheostomy tube led to a reduced mortality rate among patients with polio and respiratory paralysis. However, because of the sheer amount of man-power required for such manual intervention, mechanical positive-pressure ventilators became increasingly popular. Positive-pressure ventilators work by increasing the patient's airway pressure through an endotracheal or tracheostomy tube. The positive pressure allows air to flow into the airway until the ventilator breath is terminated. Subsequently, the airway pressure drops to zero, and the elastic recoil of the chest wall and lungs push the tidal volume -- the breathout through passive exhalation.

[edit] Indications for use

Mechanical ventilation is indicated when the patient's spontaneous ventilation is inadequate to maintain life. It is also indicated as prophylaxis for imminent collapse of other physiologic functions, or ineffective gas exchange in the lungs. Because mechanical ventilation only serves

to provide assistance for breathing and does not cure a disease, the patient's underlying condition should be correctable and should resolve over time. In addition, other factors must be taken into consideration because mechanical ventilation is not without its complications (see below) Common medical indications for use include:

Acute lung injury (including ARDS, trauma) Apnea with respiratory arrest, including cases from intoxication Chronic obstructive pulmonary disease (COPD) Acute respiratory acidosis with partial pressure of carbon dioxide (pCO2) > 50 mmHg and pH < 7.25, which may be due to paralysis of the diaphragm due to Guillain-Barr syndrome, Myasthenia Gravis, spinal cord injury, or the effect of anaesthetic and muscle relaxant drugs Increased work of breathing as evidenced by significant tachypnea, retractions, and other physical signs of respiratory distress Hypoxemia with arterial partial pressure of oxygen (PaO2) < 55 mm Hg with supplemental fraction of inspired oxygen (FiO2) = 1.0 Hypotension including sepsis, shock, congestive heart failure Neurological diseases such as Muscular Dystrophy and Amyotrophic Lateral Sclerosis

[edit] Associated risk

Barotrauma Pulmonary barotrauma is a well-known complication of positive pressure mechanical ventilation[4]. This includes pneumothorax, subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum[4]. Ventilator-associated lung injury Ventilator-associated lung injury (VALI) refers to acute lung injury that occurs during mechanical ventilation. It is clinically indistinguishable from acute lung injury or acute respiratory distress syndrome (ALI/ARDS)[5]. Diaphragm Controlled mechanical ventilation may lead to a rapid type of disuse atrophy involving the diaphragmatic muscle fibers, which can develop within the first day of mechanical ventilation[6]. This cause of atrophy in the diaphragm is also a cause of atrophy in all respiratory related muscles during controlled mechanical ventilation[7]. Motility of mucocilia in the airways Positive pressure ventilation appears to impair mucociliary motility in the airways. Bronchial mucus transport was frequently impaired and associated with retention of secretions and pneumonia[8].

[edit] Types of ventilators

SMART BAG MO Bag-Valve-Mask Resuscitator

Ventilators come in many different styles and method of giving a breath to sustain life. Hand controlled Manual ventilators such as Bag valve masks and anesthesia bags require the user to hold the ventilator to the face or to an artificial airway and maintain breaths with their hands.
[edit] Mechanical ventilators

Mechanical ventilators typically require power by a battery or a wall outlet (DC or AC) though some ventilators work on a pneumatic system not requiring power. Transport ventilators These ventilators are small, more rugged, and can be powered pneumatically or via AC or DC power sources. Intensive-care ventilators These ventilators are larger and usually run on AC power (though virtually all contain a battery to facilitate intra-facility transport and as a back-up in the event of a power failure). This style of ventilator often provides greater control of a wide variety of ventilation parameters (such as inspiratory rise time). Many ICU ventilators also incorporate graphics to provide visual feedback of each breath. Neonatal ventilators Designed with the preterm neonate in mind, these are a specialized subset of ICU ventilators which are designed to deliver the smaller, more precise volumes and pressures required to ventilate these patients. Positive airway pressure ventilators (PAP) These ventilators are specifically designed for non-invasive ventilation. this includes ventilators for use at home for treatment of chronic conditions such as sleep apnea or COPD.

[edit] Ventilation process in conventional mechanical ventilation

The three traditional categories of ventilators are listed below. As microprocessor technology is incorporated into ventilator design, the distinction among these types has become less clear as

ventilators may use combinations of all of these modes as well as flow-sensing, which controls the ventilator breath based on the flow-rate of gas versus a specific volume, pressure, or time.
[edit] Breath termination

Modes of ventilation are classified by the means that they determine the inspired breath is complete. This is sensed by either pressure or volume.

Volume ventilation - A predetermined tidal volume (Vt) is set for the patient and is delivered with each inspiration. The amount of pressure necessary to deliver this volume will fluctuate from breath to breath based on the resistance and compliance of the patient and ventilator circuit. If the tidal volume is set at 500ml, the ventilator will continue to inspire gas until it reaches its goal. Upon completion of the inspired volume, the ventilator will open a valve allowing the patient to passively exhale. Pressure ventilation - A predetermined peak inspiratory pressure (PIP) is determined based on the patient's condition and pathophysiology. The ventilator will flow gas into the patient until this set pressure is reached. Upon reaching the preset PIP, the ventilator allows for passive exhalation. Caution and close observation must be given in this mode due to potential for either hypoventilation or hyperventilation because the tidal volume is variable.

Several manufactures have incorporated features from both of theses modes in an attempt to accommodate patients needs. These modes are flow-variable, volume-targeted, pressure-regulated, time-limited modes (for example, pressure regulated volume control - PRVC). This means that instead of providing an exact tidal volume each breath, a target volume is set and the ventilator will vary the inspiratory flow at each breath to achieve the target volume at the lowest possible peak pressure. The inspiratory time (Ti) limits the length of the inspiratory cycle and therefore the I:E ratio. Pressure regulated modes such as PRVC, Auto-flow (Draeger)or Average Volume Assured Pressure Support (AVAPS) from Philips can most easily be thought of as turning a volume mode into a pressure mode with the added benefit of maintaining more control over tidal volume than with strictly pressure-control.
[edit] Breath initiation

The other method of classifying mechanical ventilation is based on how to determine when to start giving a breath. Similar to the termination classification noted above, microprocessor control has resulted in a myriad of hybrid modes that combine features of the traditional classifications. Note that most of the timing initiation classifications below can be combined with any of the termination classifications listed above.

[edit] Modes of mechanical ventilation

Main article: Modes of mechanical ventilation

Mechanical ventilation utilizes several separate systems for ventilation referred to as the "mode". Modes come in many different delivery concepts but all modes generally fall into one of the few main flagship categories such as volume controlled continuous mandatory ventilation, volume controlled intermittent mandatory ventilation, pressure controlled continuous mandatory ventilation, pressure controlled intermittent mandatory ventilation, continuous spontaneous ventilation and the high frequency ventilation systems.
[edit] Volume controlled continuous mandatory ventilation

Controlled mechanical ventilation (CMV) In this mode the ventilator provides a mechanical breath on a preset timing. Patient respiratory efforts are ignored. This is generally uncomfortable for children and adults who are conscious and is usually only used in an unconscious patient. It may also be used in infants who often quickly adapt their breathing pattern to the ventilator timing. Since CMV is no longer contained in its original form the term volume controlled continuous mandatory ventilation has consumed it into its definition and overall has combined any CMV mode for mechanical ventilation into the more accepted term in nomenclature for mechanical ventilation. Volume controlled continuous mandatory ventilation In this mode the ventilator provides a mechanical breath with either a pre-set tidal volume or peak pressure every time the patient initiates a breath. Traditional assist-control used only a pre-set tidal volumewhen a preset peak pressure is used this is also sometimes termed intermittent positive pressure ventilation (IPPV). However, the initiation timing is the sameboth provide a ventilator breath with every patient effort. In most ventilators a back-up minimum breath rate can be set in the event that the patient becomes apnoeic. Although a maximum rate is not usually set, an alarm can be set if the ventilator cycles too frequently. This can alert that the patient is tachypneic or that the ventilator may be auto-cycling (a problem that results when the ventilator interprets fluctuations in the circuit due to the last breath termination as a new breath initiation attempt).
[edit] Volume controlled intermittent mandatory ventilation

Volume controlled intermittent mandatory ventilation (VC-IMV). Formerly known as synchronized intermittent mandatory ventilation (SIMV). In this mode the ventilator provides a pre-set mechanical breath (volume limited) every specified number of seconds (determined by dividing the respiratory rate into 60 seconds - thus a respiratory rate of 12 results in a 5 second cycle time). Within that cycle time the ventilator waits for the patient to initiate a breath using either a pressure or flow sensor. When the ventilator senses the first patient breathing attempt within the cycle, it delivers the preset ventilator breath. If the patient fails to initiate a breath, the ventilator delivers a mechanical breath at the end of the breath cycle. Additional spontaneous breaths after the first one within the breath cycle do not trigger another SIMV breath. However, SIMV may be combined with pressure support (see below). SIMV is frequently employed as a method of decreasing ventilatory support (weaning) by turning down the rate, which requires the patient to take additional breaths beyond the SIMV triggered breath.

[edit] Pressure controlled continuous mandatory ventilation

Pressure controlled continuous mandatory ventilation (PC-CMV) mechanical ventilation with preset inspiratory pressure (PIP) and inspiratory time (Ti). Every breath is machine initiated and mandatory.
[edit] Pressure controlled intermittent mandatory ventilation

Pressure controlled intermittent mandatory ventilation (formerly known as SIMV) In this mode the ventilator provides a pre-set pressure limited mechanical breath every specified number of seconds SIMV is frequently employed as a method of decreasing ventilatory support (weaning) by turning down the rate, which requires the patient to take additional breaths beyond the SIMV triggered breath. PC-IMV is fundamentally the same as VC-IMV with an emphasis on pressure support and control instead of volume. An example of PC-IMV is in the mode pressure regulated volume control.
[edit] High frequency ventilation

High frequency ventilation refers to ventilation that occurs at rates significantly above that found in natural breathing. High frequency ventilation is further defined as any ventilation with a respiratory rate (Vf) greater than 150 respirations per minute. Within the category of highfrequency ventilation, the two principal types are high-frequency ventilation (passive) (ie. highfrequency jet ventilation) and high-frequency ventilation (active) (ie. high-frequency oscillatory ventilation).
[edit] Continuous spontaneous ventilation

[edit] Pressure Support Ventilation Pressure support ventilation (PSV). When a patient attempts to breathe spontaneously through an endotracheal tube, the narrowed diameter of the airway results in higher resistance to airflow, and thus a higher work of breathing. PSV was developed as a method to decrease the work of breathing in-between ventilator mandated breaths by providing an elevated pressure triggered by spontaneous breathing that "supports" ventilation during inspiration. Thus, for example, SIMV might be combined with PSV so that additional breaths beyond the SIMV programmed breaths are supported. However, while the SIMV mandated breaths have a preset volume or peak pressure, the PSV breaths are designed to cut short when the inspiratory flow reaches a percentage of the peak inspiratory flow (e.g. 10-25%). New generation of ventilators provides user-adjustable inspiration cycling off threshold, and some even are equipped with automatic inspiration cycling off threshold function. This helps the patient ventilator synchrony.[9] The peak pressure set for the PSV breaths is usually a lower pressure than that set for the full ventilator mandated breath. PSV can be also be used as an independent mode. [edit] Continuous positive airway pressure

Continuous positive airway pressure (CPAP). A continuous level of elevated pressure is provided through the patient circuit to maintain adequate oxygenation, decrease the work of breathing, and decrease the work of the heart (such as in left-sided heart failure CHF). Note that no cycling of ventilator pressures occurs and the patient must initiate all breaths. In addition, no additional pressure above the CPAP pressure is provided during those breaths. CPAP may be used invasively through an endotracheal tube or tracheostomy or non-invasively with a face mask or nasal prongs.

[edit] Choosing amongst ventilator modes

Assist-control mode minimizes patient effort by providing full mechanical support with every breath. This is often the initial mode chosen for adults because it provides the greatest degree of support. In patients with less severe respiratory failure, other modes such as SIMV may be appropriate. Assist-control mode should not be used in those patients with a potential for respiratory alkalosis, in which the patient has an increased respiratory drive. Such hyperventilation and hypocapnia (decreased systemic carbon dioxide due to hyperventilation) usually occurs in patients with end-stage liver disease, hyperventilatory sepsis, and head trauma. Respiratory alkalosis will be evident from the initial arterial blood gas obtained, and the mode of ventilation can then be changed if so desired. Positive End Expiratory Pressure may or may not be employed to prevent atelectasis in adult patients. It is almost always used for pediatric and neonatal patients due to their increased tendency for atelectasis. High frequency oscillation is used most frequently in neonates, but is also used as an always alternative mode in adults with severe ARDS. Pressure regulated volume control is another option.

[edit] Initial ventilator settings

The following are general guidelines that may need to be modified for the individual patient. As a general rule, whenever possible, spontaneous breathing must be maintained or supported, to avoid muscular atrophy of the diaphragm (Ventilator Induced Dysfunction of Diaphragm, VIDD) . To limit VALI and VILI, protective ventilation pattern should be applied to the patient. If this results in severe hypercapnia, exceeding accepted levels for permissive hypercapnia (pH below 7.2), measures for extracorporeal CO2 removal (iLA Membranventilator, Novalung) should be installed at an early stage of mechanical ventilation, to terminate cascades of inflammatory response from the lung tissue, resulting in multiorgan failure respective.
[edit] Tidal volume, rate, and pressures

For adult patients and older children

tidal volume(Vt) is calculated in milliliters per kilogram. Traditionally 10 ml/kg was used but has been shown to cause barotrauma, or injury to the lung by overextension, so 6 to 8 ml/kg IBW (ideal body weight) is now common practice in ICU. Hence a patient weighing 70 kg would get a Vt of 420560 ml. In adults a rate of 12 breaths per minute is generally used. o with acute respiratory distress syndrome (ARDS) most commonly, a tidal volume of 68 ml/kg is used with a rate of 1012 per minute. This reduced tidal volume allows for minimal volutrauma but may result in an elevated pCO2 (due to the relative decreased oxygen delivered) but this elevation does not need to be corrected (termed permissive hypercapnia) For infants and younger children o without existing lung diseasea tidal volume of 48 ml/kg to be delivered at a rate of 3035 breaths per minute o with ARDSdecrease tidal volume and increase respiratory rate sufficient to maintain pCO2 between 45 and 55[vague]. Allowing higher pCO2 (sometimes called permissive hypercapnia) may help prevent ventilator induced lung injury

As the amount of tidal volume increases, the pressure required to administer that volume is increased. This pressure is known as the peak airway pressure. If the peak airway pressure is persistently above 45 cmH2O (4.4 kPa) for adults, the risk of barotrauma is increased (see below) and efforts should be made to try to reduce the peak airway pressure (such as acceptable alarm limits). In infants and children it is unclear what level of peak pressure may cause damage. In general, keeping peak pressures below 30 cmH2O (2.9 kPa) is desirable. Monitoring for barotrauma can also involve measuring the plateau pressure, which is the pressure after the delivery of the tidal volume but before the patient is allowed to exhale. Normal breathing pattern involves inspiration, then expiration. The ventilator is programmed so that after delivery of the tidal volume (inspiration), the patient is not allowed to exhale for a half a second. Therefore, pressure must be maintained in order to prevent exhalation, and this pressure is the plateau pressure. Barotrauma is minimized when the plateau pressure is maintained < 3035 cmH2O.
[edit] Sighs

An adult patient breathing spontaneously will usually sigh about 68 times per hour to prevent microatelectasis, and this has led some to propose that ventilators should deliver 12 times the amount of the preset tidal volume 68 times per hour to account for the sighs. However, such high quantity of volume delivery requires very high peak pressure that predisposes to barotrauma. Currently, accounting for sighs is not recommended if the patient is receiving 10-12 mL/kg or is on PEEP. If the tidal volume used is lower, the sigh adjustment can be used, as long as the peak and plateau pressures are acceptable. Sighs are not generally used with ventilation of infants and young children.
[edit] Initial FiO2

Because the mechanical ventilator is responsible for assisting in a patient's breathing, it must then also be able to deliver an adequate amount of oxygen in each breath. The FiO2 stands for fraction of inspired oxygen, which means the percent of oxygen in each breath that is inspired.

(Note that normal room air has ~21% oxygen content or an FiO2 of 0.21). In adult patients who can tolerate higher levels of oxygen for a period of time, the initial FiO2 may be set at 100% until arterial blood gases can document adequate oxygenation. An FiO2 of 100% for an extended period of time can cause atelectasis, but it can protect against hypoxemia from unexpected intubation problems. For infants, and especially in premature infants, avoiding high levels of FiO2 (>60%) is very important to avoid lung injury and apnea of prematurity. Fraction of inspired oxygen should always be titrated to meet the patients needs and to avoid unnecessary lung injury.
[edit] Positive end-expiratory pressure Main article: Positive end-expiratory pressure

PEEP is an adjuvant to the mode of ventilation used to help maintain functional residual capacity (FRC). At the end of expiration, the PEEP exerts pressure to oppose passive emptying of the lung and to keep the airway pressure above the atmospheric pressure. The presence of PEEP opens up collapsed or unstable alveoli and increases the FRC and surface area for gas exchange, thus reducing the size of the shunt. For example, if a large shunt is found to exist based on the estimation from 100% FiO2 (see above), then PEEP can be considered and the FiO2 can be lowered (< 60%) in order to maintain an adequate PaO2, thus reducing the risk of oxygen toxicity. In addition to treating a shunt, PEEP may also be useful to decrease the work of breathing. In pulmonary physiology, compliance is a measure of the "stiffness" of the lung and chest wall. The mathematical formula for compliance (C) equals change in volume divided by change in pressure. The higher the compliance, the more easily the lungs will inflate in response to positive pressure. An underinflated lung will have low compliance and PEEP will improve this initially by increasing the FRC, since the partially inflated lung takes less energy to inflate further. Excessive PEEP can however produce overinflation, which will again decrease compliance. Therefore it is important to maintain an adequate, but not excessive FRC. Indications. PEEP can cause significant haemodynamic consequences through decreasing venous return to the right heart and decreasing right ventricular function. As such, it should be judiciously used and is indicated for adults in two circumstances.

If a PaO2 of 60 mmHg cannot be achieved with a FiO2 of 60% If the initial shunt estimation is greater than 25%

If used, PEEP is usually set with the minimal positive pressure to maintain an adequate PaO2 with a safe FiO2. As PEEP increases intrathoracic pressure, there can be a resulting decrease in venous return and decrease in cardiac output. A PEEP of less than 10 cmH2O (1 kPa) is usually safe in adults if intravascular volume depletion is absent. Lower levels are used for pediatric patients. Older literature recommended routine placement of a Swan-Ganz catheter if the amount of PEEP used is greater than 10 cmH2 for hemodynamic monitoring. More recent literature has failed to find outcome benefits with routine PA catheterisation when compared to simple central venous pressure monitoring.[10] If cardiac output measurement is required, minimally invasive techniques, such as oesophageal doppler monitoring or arterial waveform contour monitoring

may be sufficient alternatives.[11][12]. When withdrawing, it is decreased through 12 cmH2O decrements while monitoring haemoglobin-oxygen saturations. Any unacceptable haemoglobinoxygen saturation should prompt reinstitution of the last PEEP level that maintained good saturation.
[edit] Positioning

Prone (face down) positioning has been used in patients with ARDS and severe hypoxemia. It improves FRC, drainage of secretions, and ventilation-perfusion matching (efficiency of gas exchange). It may improve oxygenation in > 50% of patients, but no survival benefit has been documented.
[edit] Sedation and paralysis

Most intubated patients receive intravenous sedation through a continuous infusion or scheduled dosing to help with anxiety or psychological stress. Sedation also helps the patient tolerate the constant irritation of the endotracheal tube in their mouth, pharynx and trachea. Without some form of sedation and analgesia, it is common for patients to "fight" the ventilator. This fighting increases work of breathing and may cause further lung injury. Daily interruption of sedation is commonly helpful to the patient for reorientation and appropriate weaning. These interruptions are frequently described as "sedation vacations" and have been shown to reduce the time patients stay on mechanical ventilation.[13] It is not uncommon for patients on a mechanical ventilator to be given a muscle relaxant or paralytic to aid in ventilation. These "neuromuscular blockades" prevent skeletal muscle from contracting and thereby stop all patient movement including respiratory efforts. These types of pharmaceutical agents must always be given in conjunction with sedation as the effects of the paralytics is not only uncomfortable but would cause significant psychological stress and anxiety.
[edit] Prophylaxis

To protect against ventilator-associated pneumonia, patients' beds are often elevated to about 30. Deep vein thrombosis prophylaxis with heparin or sequential compression device is important in older children and adults. A histamine receptor (H2) blocker or proton-pump inhibitor may be used to prevent gastrointestinal bleeding, which has been associated with mechanical ventilation

[edit] Modification of settings

In adults when 100% FiO2 is used initially, it is easy to calculate the next FiO2 to be used and easy to estimate the shunt fraction. The estimated shunt fraction refers to the amount of oxygen not being absorbed into the circulation. In normal physiology, gas exchange (oxygen/carbon dioxide) occurs at the level of the alveoli in the lungs. The existence of a shunt refers to any process that hinders this gas exchange, leading to wasted oxygen inspired and the flow of un-

oxygenated blood back to the left heart (which ultimately supplies the rest of the body with unoxygenated blood). When using 100% FiO2, the degree of shunting is estimated by subtracting the measured PaO2 (from an arterial blood gas) from 700 mmHg. For each difference of 100 mmHg, the shunt is 5%. A shunt of more than 25% should prompt a search for the cause of this hypoxemia, such as mainstem intubation or pneumothorax, and should be treated accordingly. If such complications are not present, other causes must be sought after, and PEEP should be used to treat this intrapulmonary shunt. Other such causes of a shunt include:

Alveolar collapse from major atelectasis Alveolar collection of material other than gas, such as pus from pneumonia, water and protein from acute respiratory distress syndrome, water from congestive heart failure, or blood from haemorrhage

[edit] When to withdraw mechanical ventilation

Withdrawal from mechanical ventilationalso known as weaningshould not be delayed unnecessarily, nor should it be done prematurely. Patients should have their ventilation considered for withdrawal if they are able to support their own ventilation and oxygenation, and this should be assessed continuously. There are several objective parameters to look for when considering withdrawal, but there is no specific criteria that generalizes to all patients. Trials of spontaneous breathing have been shown to accurately predict the success of spontaneous breathing. (Yang K, Tobin MJ. A prospective study of indexes predicting the outcome of weaning from mechanical ventilation. N Engl J Med 1991;324:14451450).

[edit] Respiratory monitoring

Respiratory mechanics monitor

One of the main reasons why a patient is admitted to an ICU is for delivery of mechanical ventilation. Monitoring a patient in mechanical ventilation has many clinical applications: Enhance understanding of pathophysiology, aid with diagnosis, guide patient management, avoid complications and assessment of trends[14].

Most of modern ventilators have basic monitoring tools. There are also monitors that work independently of the ventilator, which allow to measure patients after the ventilator has been removed, such as a T tube test.

[edit] Connection to ventilators

There are various procedures and mechanical devices that provide protection against airway collapse, air leakage, and aspiration:

Face mask - In resuscitation and for minor procedures under anaesthesia, a face mask is often sufficient to achieve a seal against air leakage. Airway patency of the unconscious patient is maintained either by manipulation of the jaw or by the use of nasopharyngeal or oropharyngeal airway. These are designed to provide a passage of air to the pharynx through the nose or mouth, respectively. Poorly fitted masks often cause nasal bridge ulcers, a problem for some patients. Face masks are also used for non-invasive ventilation in conscious patients. A full face mask does not, however, provide protection against aspiration. Laryngeal mask airway - The laryngeal mask airway (LMA) causes less pain and coughing than a tracheal tube. However, unlike tracheal tubes it does not seal against aspiration, making careful individualised evaluation and patient selection mandatory. Tracheal intubation is often performed for mechanical ventilation of hours to weeks duration. A tube is inserted through the nose (nasotracheal intubation) or mouth (orotracheal intubation) and advanced into the trachea. In most cases tubes with inflatable cuffs are used for protection against leakage and aspiration. Intubation with a cuffed tube is thought to provide the best protection against aspiration. Tracheal tubes inevitably cause pain and coughing. Therefore, unless a patient is unconscious or anaesthetized for other reasons, sedative drugs are usually given to provide tolerance of the tube. Other disadvantages of tracheal intubation include damage to the mucosal lining of the nasopharynx or oropharynx and subglottic stenosis. Esophageal obturator airway - sometimes used by emergency medical technicians and basic EMS providers not trained to intubate. It is a tube which is inserted into the esophagus, past the epiglottis. Once it is inserted, a bladder at the tip of the airway is inflated, to block ("obturate") the esophagus, and oxygen is delivered through a series of holes in the side of the tube which is then forced into the lungs. Cricothyrotomy - Patients who require emergency airway management, in whom tracheal intubation has been unsuccessful, may require an airway inserted through a surgical opening in the cricothyroid membrane. This is similar to a tracheostomy but a cricothyrotomy is reserved for emergency access.[1] Tracheostomy - When patients require mechanical ventilation for several weeks, a tracheostomy may provide the most suitable access to the trachea. A tracheostomy is a surgically created passage into the trachea. Tracheostomy tubes are well tolerated and often do not necessitate any use of sedative drugs. Tracheostomy tubes may be inserted early during treatment in patients with preexisting severe respiratory disease, or in any patient who is expected to be difficult to wean from mechanical ventilation, i.e., patients who have little muscular reserve. Mouthpiece - Less common interface, does not provide protection against aspiration. There are lipseal mouthpieces with flanges to help hold them in place if patient is unable.

Intubation Intubation
From Wikipedia, the free encyclopedia

Jump to: navigation, search

Intubation
Intervention

ICD-9-CM

96.0

MeSH

D007440

Intubation, sometimes entubation,[1] is the insertion of a tube into an external or internal orifice of the body for the purpose of adding or removing fluids or air. It is sometimes considered synonymous with tracheal intubation, but it can also involve the gastrointestinal tract, as with balloon tamponade with a Sengstaken-Blakemore tube. Intubation into the trachea may be performed through the mouth (orotracheal intubation) or through the nose (nasotracheal intubation). Successful intubation depends on three requirements:

correct patient positioning; depression of pharyngeal reflex; immobilization of the patient.

The highest priority in an emergency is to enable a patient to breathe by securing their airway (passage from the nose and mouth into the lungs). Endotracheal intubation is one of various ways to secure the airway. A Cochrane review, examines whether emergency endotracheal intubation, as opposed to other airway management techniques, improves the outcome and no difference was found between endotracheal intubation and other airway securing strategies for reducing deaths after acute illness or injury.[2]

Negative pressure ventilator

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(Redirected from Iron lung)

Jump to: navigation, search This article is about the medical device. For the band, see Iron Lung (band). This article's lead section may not adequately summarize its contents. Please consider expanding the lead to provide an accessible overview of the article's key points. (August 2011)

Negative pressure ventilator

Intervention

An Emerson iron lung. The patient lies within the chamber, which when sealed provides an effectively oscillating atmospheric pressure. This particular machine was donated to the Centers for Disease Control and Prevention Museum by the family of poliomyelitis patient Barton Hebert of Covington, Louisiana, who had used the device from the late 1950s until his death in 2003.

ICD-9-CM

93.99

MeSH

D015919

A negative pressure ventilator (often referred to colloquially as an iron lung) is a form of medical ventilator that enables a person to breathe when normal muscle control has been lost or the work of breathing exceeds the person's ability.

Contents
[hide]

1 Method and use 2 Invention and early use 3 Modern usage 4 See also 5 References 6 Further reading 7 External links

[edit] Method and use

Humans, like most other animals, breathe by negative pressure breathing:[1] the rib cage expands and the diaphragm pulls down, expanding the chest cavity. This causes the pressure in the chest cavity to decrease, and the lungs expand to fill the space. This, in turn, causes the pressure of the air inside the lungs to fill (it becomes negative, relative to the atmosphere), and air flows into the lungs from the atmosphere: inhalation. When the chest cavity is contracted, the reverse happens and the person exhales. If a person loses part or all of the ability to control the muscles involved, breathing becomes difficult or impossible.

Iron lung ward filled with polio patients, Rancho Los Amigos Hospital, California (1953) The person using the iron lung is placed into the central chamber, a cylindrical steel drum. A door allowing the head and neck to remain free is then closed, forming a sealed, air-tight compartment enclosing the rest of the person's body. Pumps that control airflow periodically decrease and increase the air pressure within the chamber, and particularly, on the chest. When the pressure is below that within the lungs, the lungs expand and atmospheric pressure pushes air from outside the chamber in via the person's nose and airways to keep the lungs filled; when the pressure goes above that within the lungs, the reverse occurs, and air is expelled. In this manner, the iron lung mimics the physiological action of breathing: by periodically altering intrathoracic pressure, it causes air to flow in and out of the lungs. The iron lung is a form of non-invasive therapy.

[edit] Invention and early use

Staff in a Rhode Island hospital are examining a patient in an iron lung tank respirator during the 1960 polio epidemic. The iron lung encased the thoracic cavity in an air-tight chamber. The chamber was used to create a negative pressure around the thoracic cavity, thereby causing air to enter the lungs to equalize intrapulmonary pressure. The first negative pressure ventilator was described by Scottish physician John Dalziel in 1832. Successful use of similar devices was described a few years later. The first of these devices to be widely used however was developed by Drinker and Shaw in 1928.[2] The iron lung, often referred to in the early days as the "Drinker respirator", was invented by Phillip Drinker (1894 1972) and Louis Agassiz Shaw Junior, professors of industrial hygiene at the Harvard School of Public Health.[3][4][5][6] The machine was powered by an electric motor with air pumps from two vacuum cleaners. The air pumps changed the pressure inside a rectangular, airtight metal box, pulling air in and out of the lungs.[7] The first clinical use of the Drinker respirator on a human was on October 12, 1928 at the Children's Hospital in Boston.[4][8] The subject was an eight-year-old girl who was nearly dead as a result of respiratory failure due to poliomyelitis (often called polio or infantile paralysis).[6] Her dramatic recovery, within less than a minute of being placed in the chamber, helped popularize the new device.[5] Boston manufacturer Warren E. Collins began production of the iron lung that year.[9][10] Although it was initially developed for the treatment of victims of coal gas poisoning, it was most famously used in the mid-20th century for the treatment of respiratory failure caused by poliomyelitis.[3] In 1931, John Haven Emerson (February 5, 1906 February 4, 1997) introduced an improved and less expensive iron lung.[11][12] The Emerson iron lung had a bed that could slide in and out of the cylinder as needed, and the tank had portal windows which allowed attendants to reach in and adjust limbs, sheets, or hot packs.[7] Drinker and Harvard University sued Emerson, claiming he had infringed on patent rights. Emerson defended himself by making the case that such lifesaving devices should be freely available to all.[7] Emerson also demonstrated that every aspect of Drinker's patents had been patented by others at earlier times. Emerson won the case, and Drinker's patents were declared invalid.

[edit] Modern usage

Rows of irons lungs filled hospital wards at the height of the polio outbreaks of the 1940s and 1950s. Polio vaccination programs have virtually eradicated new cases of poliomyelitis in the United States. Because of this, and also the development of modern ventilators and widespread use of tracheal intubation and tracheotomy, the iron lung has virtually disappeared from modern medicine. For example, in 1959, there were 1,200 people using tank respirators in the United States, but by 2004 there were only 39.[7] Positive pressure ventilation systems are now more common than negative pressure systems. Positive pressure ventilators work by blowing air into the patient's lungs via intubation through the airway; they were used for the first time in Blegdams Hospital, Copenhagen, Denmark during a polio outbreak in 1952.[13][14] It proved a success and soon superseded the iron lung throughout Europe. The iron lung now has a marginal place in modern respiratory therapy. Most patients with paralysis of the breathing muscles use modern mechanical ventilators that push air into the airway with positive pressure. These are generally efficacious and have the advantage of not restricting patients' movements or caregivers' ability to examine the patients as significantly as an iron lung does. However, negative pressure ventilation is a truer approximation of normal physiological breathing and results in more normal distribution of air in the lungs. It may also be preferable in certain rare conditions, such as Ondine's curse, in which failure of the medullary respiratory centers at the base of the brain result in patients having no autonomic control of breathing. At least one reported polio patient, Dianne Odell, had a spinal deformity that caused the use of mechanical ventilators to be contraindicated.[15] There are patients who today still use the older machines, often in their homes, despite the occasional difficulty of finding the various replacement parts. Joan Headley of Post-Polio Health International stated to CNN that there are approximately 30 patients in the USA still using an iron lung.[16] That figure may be inaccurately low; Houston alone had 19 iron lung patients living at home in 2008.[17] Martha Mason of Lattimore, North Carolina died on May 4, 2009, after spending 60 of her 72 years in an iron lung.[18] On the 30th of October 2009, June Middleton of Melbourne, Australia, who had been entered in the Guinness Book of Records as the person who spent the longest time in an iron lung, died aged 83, having spent more than 60 years in her iron lung.[19] Biphasic Cuirass Ventilation is a modern development of the iron lung, consisting of a wearable rigid upper-body shell (a cuirass) which functions as a negative pressure ventilator.

Iron lung

Intensive care medicine Intensive-care medicine

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(Redirected from Intensive care medicine) Jump to: navigation, search "Intensive Care" redirects here. For the album by pop singer Robbie Williams, see Intensive Care (album). "CICU" redirects here. For the radio station, see CICU-FM. "High dependency unit" redirects here. For the New Zealand psychedelic rock band, see High Dependency Unit (band). This article includes a list of references, but its sources remain unclear because it has insufficient inline citations. Please help to improve this article by introducing more precise citations. (July 2009)

Mechanical ventilation may be required if a patient's unassisted breathing is insufficient to oxygenate the blood.

Intensive-care medicine or critical-care medicine is a branch of medicine concerned with the diagnosis and management of life threatening conditions requiring sophisticated organ support and invasive monitoring.

Contents
[hide]

1 Overview 2 Organ systems 3 Equipment and systems 4 Medical specialties

5 History o 5.1 Florence Nightingale era o 5.2 Dandy era o 5.3 Ibsen era o 5.4 Safar era 6 See also 7 Notes 8 References 9 External links

[edit] Overview
Patients requiring intensive care may require support for hemodynamic instability (hypertension/hypotension), airway or respiratory compromise (such as ventilator support), acute renal failure, potentially lethal cardiac arrhythmias, or the cumulative effects of multiple organ failure, more commonly referred to now as multiple organ dysfunction syndrome. They may also be admitted for intensive/invasive monitoring, such as the crucial hours after major surgery when deemed too unstable to transfer to a less intensively monitored unit. Intensive care is usually only offered to those whose condition is potentially reversible and who have a good chance of surviving with intensive care support. Since the critically ill are so close to dying, the outcome of this intervention is difficult to predict.[citation needed] A prime requisite for admission to an Intensive Care Unit is that the underlying condition can be overcome. Medical studies suggest a relation between intensive care unit (ICU) volume and quality of care for mechanically ventilated patients.[1] After adjustment for severity of illness, demographic variables, and characteristics of the ICUs (including staffing by intensivists), higher ICU volume was significantly associated with lower ICU and hospital mortality rates. For example, adjusted ICU mortality (for a patient at average predicted risk for ICU death) was 21.2% in hospitals with 87 to 150 mechanically ventilated patients annually, and 14.5% in hospitals with 401 to 617 mechanically ventilated patients annually. Hospitals with intermediate numbers of patients had outcomes between these extremes. In general, it is the most expensive, technologically advanced and resource-intensive area of medical care. In the United States, estimates of the 2000 expenditure for critical care medicine ranged from US$1555 billion, accounting for about 0.5% of GDP and about 13% of national health care expenditure (Halpern, 2004).

[edit] Organ systems

Intensive care usually takes a system by system approach to treatment, rather than the SOAP (subjective, objective, analysis, plan) approach of high dependency care. The nine key systems (see below) are each considered on an observation-intervention-impression basis to produce a

daily plan. As well as the key systems, intensive-care treatment raises other issues including psychological health, pressure points, mobilisation and physiotherapy, and secondary infections. The nine key IC systems are (alphabetically): cardiovascular system, central nervous system, endocrine system, gastro-intestinal tract (and nutritional condition), hematology, microbiology (including sepsis status), peripheries (and skin), renal (and metabolic), respiratory system. The provision of intensive care is, in general, administered in a specialized unit of a hospital called the intensive-care unit (ICU) or critical-care unit (CCU). Many hospitals also have designated intensive-care areas for certain specialities of medicine, such as the coronary intensive-care unit (CCU or sometimes CICU, depending on hospital) for heart disease, medical intensive-care unit (MICU), surgical intensive-care unit (SICU), pediatric intensive-care unit (PICU), neuroscience critical-care unit (NCCU), overnight intensive-recovery (OIR), shock/trauma intensive-care unit (STICU), neonatal intensive-care unit (NICU), and other units as dictated by the needs and available resources of each hospital. The naming is not rigidly standardized. For a time in the early 1960s, it was not clear that specialized intensive care units were needed, so intensive-care resources (see below) were brought to the room of the patient that needed the additional monitoring, care, and resources. It became rapidly evident, however, that a fixed location where intensive-care resources and personnel were available provided better care than ad hoc provision of intensive care services spread throughout a hospital.

[edit] Equipment and systems

An endotracheal tube

Common equipment in an intensive-care unit (ICU) includes mechanical ventilation to assist breathing through an endotracheal tube or a tracheotomy; hemofiltration equipment for acute renal failure; monitoring equipment; intravenous lines for drug infusions fluids or total parenteral nutrition, nasogastric tubes, suction pumps, drains and catheters; and a wide array of drugs including inotropes, sedatives, broad spectrum antibiotics and analgesics.

[edit] Medical specialties

Critical-care medicine is a relatively new but increasingly important medical specialty. Physicians with training in critical-care medicine are referred to as intensivists.[2] The specialty requires additional fellowship training for physicians having completed their primary residency training in internal medicine, anesthesiology, or surgery. Board certification in critical care medicine is available through all three specialty boards. Respiratory Therapists though already specialists in cardiopulmonary critical care have additional credentialing in Adult Critical Care (ACCS) and Neonatal and Pediatric (NPS) specialties. Nurse intensivists receive their training after basic education through ASTNA. Paramedics are certified to levels of CCEMTP or FP-C. Intensivists-physicians with a primary training in internal medicine sometimes pursue combined fellowship training in another subspecialty such as pulmonary medicine, cardiology, infectious disease, or nephrology. The Society of Critical Care Medicine is a well-established multiprofessional society for practitioners working in the ICU, including intensivists. Most medical research has demonstrated that ICU care provided by intensivists produces better outcomes and more cost-effective care.[3] This has led the Leapfrog Group to make a primary recommendation that all ICU patients be managed or co-managed by a dedicated intensivist who is exclusively responsible for patients in one ICU. However, there is a critical shortage of intensivists in the United States, and most hospitals lack this critical physician team member. Patient management in intensive-care differs significantly between countries. In Australia, where Intensive Care Medicine is a well-established speciality, ICUs are described as 'closed'. In a closed unit the intensive-care specialist takes on the senior role where the patient's primary doctor now acts as a consultant. The advantage of this system is a more coordinated management of the patient based on a team who work exclusively in ICU. Other countries have open Intensive Care Units, where the primary doctor chooses to admit and, in general, makes the management decisions. There is increasingly strong evidence that 'closed' Intensive-Care Units staffed by Intensivists provide better outcomes for patients.[4][5]

[edit] History
[edit] Florence Nightingale era

Florence Nightingale

The ICU's roots can be traced back to the Monitoring Unit of critical patients through nurse Florence Nightingale. The Crimean War began in 1853 when Britain, France, and Turkey declared war on Russia. Because of the lack of critical care and the high rate of infection, there was a high mortality rate of hospitalised soldiers, reaching as high as 40% of the deaths recorded during the war. Nightingale and 38 other volunteers had to leave for the Fields of Scurati, and took their "critical care protocol" with them. Upon arriving, and practicing, the mortality rate fell to 2%. Nightingale contracted typhoid, and returned in 1856 from the war. A school of nursing dedicated to her was formed in 1859 in England. The school was recognised for its professional value and technical calibre, receiving prizes throughout the British government. The school of nursing was established in Saint Thomas Hospital, as a one-year course, and was given to doctors. It used theoretical and practical lessons, as opposed to purely academic lessons. Nightingale's work, and the school, paved the way for intensive care medicine.
[edit] Dandy era

Walter Edward Dandy was born in Sedalia, Missouri. He received his BA in 1907 through the University of Missouri and his M.D. in 1910 through the Johns Hopkins University School of Medicine. Dandy worked one year with Dr. Harvey Cushing in the Hunterian Laboratory of Johns Hopkins before entering its boarding school and residence in the Johns Hopkins Hospital. He worked in the Johns Hopkins College in 1914 and remained there until his death in 1946. One of the most important contributions he made for neurosurgery was the air method in ventriculography, in which the cerebrospinal fluid is substituted with air to help an image form on an X-Ray of the ventricular space in the brain. This technique was extremely successful for identifying brain injuries. Dr. Dandy was also a pioneer in the advances in operations for illnesses of the brain affecting the glossopharyngeal as well as Mnire's syndrome, and he published studies that show that high activity can cause sciatic pain. Dandy created the first ICU in the world, 03 beds in Boston in 1926.
[edit] Ibsen era

Bjrn Aage Ibsen (19152007) graduated in 1940 from medical school at the University of Copenhagen and trained in anesthesiology from 1949 to 1950 at the Massachusetts General Hospital, Boston. He became involved in the 1952 poliomyelitis outbreak in Denmark[6], where 2722 patients developed the illness in a 6 month period, with 316 suffering respiratory or airway paralysis. Treatment had involved the use of the few negative pressure respirators available, but these devices, while helpful, were limited and did not protect against aspiration of secretions. Ibsen changed management directly, instituting protracted positive pressure ventilation by means of intubation into the trachea, and enlisting 200 medical students to manually pump oxygen and air into the patients lungs[7]. At this time Carl-Gunnar Engstrm had developed one of the first positive pressure volume controlled ventilators, which eventually replaced the medical students. In this fashion, mortality declined from 90% to around 25%. Patients were managed in 3 special 35 bed areas, which aided charting and other management. In 1953, Ibsen set up what became

the world's first Medical/Surgical ICU in a converted student nurse classroom in Kommunehospitalet (The Municipal Hospital) in Copenhagen[8], and provided one of the first accounts of the management of tetanus with muscle relaxants and controlled ventilation. In 1954 Ibsen was elected Head of the Department of Anaesthesiology at that institution. He jointly authored the first known account of ICU management principles in Nordisk Medicin, September 18, 1958: Arbejdet p en Ansthesiologisk Observationsafdeling (The Work in an Anaesthesiologic Observation Unit) with Tone Dahl Kvittingen from Norway. He died in 2007.
[edit] Safar era

Peter Safar, the first Intensivist doctor in the USA,[citation needed] was born in Austria as the son of two doctors. He first migrated to the United States in 1949. Safar first got certification as an anesthesiologist, and, in the 1950s, he started and praised the "Urgency & Emergency" room setup (now known as an ICU)[citation needed]. It was at this time the ABC (Airway, Breathing, and Circulation) protocols were formed, and artificial ventilation as well as cardiopulmonary resuscitation became popular.[citation needed] These experiments counted on volunteers of its team, and used only minimal sedation. It was through these experiments that the techniques for maintaining life in the critical patient were established.[citation needed] The first surgical ICU was established in Baltimore, and, in 1962, in the University of Pittsburgh, the first Critical Care Residency was established in the United States. It was around this time that the induction of hypothermia in critical patients was also tested.[citation needed] In 1970, the Society of Critical Care Medicine was formed.[9]

Liquid breathing Liquid breathing

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This article may be too technical for most readers to understand. Please help improve this article to make it understandable to non-experts, without removing the technical details. The talk page may contain suggestions. (August 2009)

Liquid breathing

Intervention

MeSH

D021061

This article needs attention from an expert on the subject. See the talk page for details. WikiProject SCUBA may be able to help recruit an expert. (March 2010)

Liquid breathing is a form of respiration in which a normally air-breathing organism breathes an oxygen-rich liquid (such as a perfluorocarbon), rather than breathing air.

Computer models of three perfluorochemical molecules used for biomedical applications and for liquid ventilation studies: a) FC-75, b) perflubron, and c) perfluorodecalin.

Perfluorochemical (perfluorocarbon) molecules have very different structures that impart different physical properties such as respiratory gas solubility, density, viscosity, vapor pressure, and lipid solubility.[1] Thus, it is critical to select the appropriate PFC for a specific biomedical

application, such as liquid ventilation, drug delivery, blood substitutes, etc. The physical properties of PFC liquids vary substantially; however, the one common property is their high solubility for respiratory gases. In fact, these liquids carry more oxygen and carbon dioxide than blood.[2] In theory, liquid breathing could assist in the treatment of patients with severe pulmonary or cardiac trauma, especially in pediatric cases. Liquid breathing has also been proposed for use in deep diving[3][4] and space travel.[5] Despite some recent advances in liquid ventilation, a standard mode of application has not been established yet. Liquid breathing is sometimes called "fluid breathing", but this can be misleading, as normal atmospheric air is also a fluid.
Physicochemical properties (37C at 1 atm) of 18 perfluorochemical liquids used for biomedical applications. This table characterizes the most significant physical properties related to systemic physiology and their range of properties. gas solubility Oxygen Carbon dioxide vapor pressure density viscosity 33-66 mL / 100 mL PFC 140-166 mL / 100 mL PFC 0.2-400 torr 1.58-2.0 g/mL 0.8-8.0 cS

Contents
[hide]

1 Approaches o 1.1 Total liquid ventilation o 1.2 Partial liquid ventilation o 1.3 PFC vapor o 1.4 Aerosol-PFC 2 Proposed uses o 2.1 Diving o 2.2 Medical treatment o 2.3 Space travel 3 Examples in fiction 4 See also 5 References

6 External links

[edit] Approaches
Because liquid breathing is still a highly experimental technique, there are several proposed approaches.
[edit] Total liquid ventilation

Although total liquid ventilation (TLV) with completely liquid-filled lungs can be beneficial,[6] the complex liquid-filled tube system required is a disadvantage compared to gas ventilation - the system must incorporate a membrane oxygenator, heater, and pumps to deliver to, and remove from the lungs tidal volume aliquots of conditioned perfluorocarbon (PFC). One research group led by Thomas H. Shaffer has maintained that with the use of microprocessors and new technology, it is possible to maintain better control of respiratory variables such as liquid functional residual capacity and tidal volume during TLV, than with gas ventilation.[1][7][8][9] Consequently, the total liquid ventilation necessitates a dedicated liquid ventilator similar to a medical ventilator except that it uses a breatheable liquid. Many prototypes are used for animal experimentations, but experts recommend continued development of a liquid ventilator toward clinical applications.[10]
[edit] Partial liquid ventilation

In contrast, partial liquid ventilation (PLV) is a technique in which a PFC is instilled into the lung to a volume approximating functional residual capacity (approximately 40% of Total Lung Capacity (TLC)). Conventional mechanical ventilation delivers tidal volume breaths on top of it. This mode of liquid ventilation currently seems technologically more feasible than total liquid ventilation, because PLV could utilise technology currently in place in many neonatal intensivecare units (NICU) worldwide. The influence of PLV on oxygenation, carbon dioxide removal and lung mechanics has been investigated in several animal studies using different models of lung injury[11] Clinical applications of PLV have been reported in patients with acute respiratory distress syndrome (ARDS), meconium aspiration syndrome, congenital diaphragmatic hernia and respiratory distress syndrome (RDS) of neonates. In order to correctly and effectively conduct PLV, it is essential to
1. properly dose a patient to a specific lung volume (10-15 ml/kg) to recruit alveolar volume and 2. redose the lung with PFC liquid (1-2 ml/kg/hr) to oppose PFC evaporation from the lung.

If PFC liquid is not maintained in the lung, PLV can not effectively protect the lung from biophysical forces associated with the gas ventilator. New application modes for PFC have been developed.[12]

[edit] PFC vapor

Vaporization of perfluorohexane with two anesthetic vaporizers calibrated for perfluorohexane has been shown to improve gas exchange in oleic acid-induced lung injury in sheep.[13] Predominantly PFCs with high vapor pressure are suitable for vaporization
[edit] Aerosol-PFC

With aerosolized perfluorooctane, significant improvement of oxygenation and pulmonary mechanics was shown in adult sheep with oleic acid-induced lung injury. In surfactant-depleted piglets, persistent improvement of gas exchange and lung mechanics was demonstrated with Aerosol-PFC.[14] The aerosol device is of decisive importance for the efficacy of PFC aerosolization, as aerosolization of PF5080 (a less purified FC77) has been shown to be ineffective using a different aerosol device in surfactant-depleted rabbits. Partial liquid ventilation and Aerosol-PFC reduced pulmonary inflammatory response.[15]

[edit] Proposed uses

[edit] Diving

Gas pressure increases with depth, rising 1 bar every 10 meters to over 1,000 bar at the bottom of the Mariana Trench. Diving becomes more dangerous as depth increases, and deep diving presents many hazards. All surface-breathing animals are subject to decompression sickness, including aquatic mammals[16] and free-diving humans (see taravana). Breathing at depth can cause nitrogen narcosis and oxygen toxicity. Ascending after breathing at depth can cause air embolisms, burst lung, and collapsed lung. Special breathing gas mixes such as trimix or heliox ameliorate the risk of decompression illness but do not eliminate it. Heliox further eliminates the risk of nitrogen narcosis but introduces the risk of helium tremors below 500 feet (152 meters). Atmospheric diving suits maintain body and breathing pressure at 1 bar, eliminating most of the hazards of descending, ascending, and breathing at depth. However, the rigid suits are bulky, clumsy, and very expensive. Liquid breathing offers a third option,[3][17] promising the mobility available with flexible dive suits and the reduced risks of rigid suits. With liquid in the lungs, the pressure within the diver's lungs could accommodate changes in the pressure of the surrounding water without the huge gas partial pressure exposures required when the lungs are filled with gas. Liquid breathing would not result in the saturation of body tissues with high pressure nitrogen or helium that occurs with the use of non-liquids, thus would reduce or remove the need for slow decompression. A significant problem, however, arises from the high viscosity of the liquid and the corresponding reduction in its ability to remove CO2.[3][18] All uses of liquid breathing for diving must involve total liquid ventilation (see above). Total liquid ventilation, however, has difficulty moving enough liquid to carry away CO2, because no matter how great the total pressure is, the

amount of partial CO2 gas pressure available to dissolve CO2 into the breathing liquid can never be much more than the pressure at which CO2 exists in the blood (about 40 mm of mercury (Torr)).[18] At these pressures, most fluorocarbon liquids require about 70 mL/kg minute-ventilation volumes of liquid (about 5 L/min for a 70 kg adult) to remove enough CO2 for normal resting metabolism.[19] This is a great deal of fluid to move, particularly as liquids are generally more viscous than gases, (for example water is about 850 times the viscosity of air[20]). Any increase in the diver's metabolic activity also increases CO2 production and the breathing rate, which is already at the limits of realistic flow rates in liquid breathing.[3][21][22] It seems unlikely that a person would move 10 liters/min of fluorocarbon liquid without assistance from a mechanical ventilator, so "free breathing" may be unlikely.
[edit] Medical treatment

Computer-generated model of perflubron and gentamicin molecules in liquid suspension for pulmonary administration

The most promising area for the use of liquid ventilation is in the field of pediatric medicine.[23][24][25] The first medical use of liquid breathing was treatment of premature babies[26][27][28][29] and adults with acute respiratory distress syndrome (ARDS) in the 1990s. Liquid breathing was used in clinical trials after the development by Alliance Pharmaceuticals of the fluorochemical perfluorooctyl bromide, or perflubron for short. Current methods of positivepressure ventilation can contribute to the development of lung disease in pre-term neonates, leading to diseases such as bronchopulmonary dysplasia. Liquid ventilation removes many of the high pressure gradients responsible for this damage. Furthermore, perfluorocarbons have been demonstrated to reduce lung inflammation,[30][31][32] improve ventilation-perfusion mismatch and to provide a novel route for the pulmonary administration of drugs.[33][34][35] In order to explore drug delivery techniques that would be useful for both partial and total liquid ventilation, more recent studies have focused on PFC drug delivery using a nanocrystal suspension. The first image is a computer model of a PFC liquid (perflubron) combined with gentamicin molecules.

The second image shows experimental results comparing both plasma and tissue levels of gentamicin after an intratracheal (IT) and intravenous (IV) dose of 5 mg/kg in a newborn lamb during gas ventilation. Note that the plasma levels of the IV dose greatly exceed the levels of the IT dose over the 4 hour study period; whereas, the lung tissue levels of gentamicin when delivered by an intratracheal (IT) suspension, uniformly exceed the intravenous (IV) delivery approach after 4 hours. Thus, the IT approach allows more effective delivery of the drug to the target organ while maintaining a safer level systemically. Both images represent the in-vivo time course over 4 hours. Numerous studies have now demonstrated the effectiveness of PFC liquids as a delivery vehicle to the lungs.[36][37][38][39][40][41][42][43][44][45]

Comparison of IT and IV administration of gentamicin.

Clinical trials with premature infants, children and adults were conducted. Since the safety of the procedure and the effectiveness were apparent from an early stage, the US Food and Drug Administration (FDA) gave the product "fast track" status (meaning an accelerated review of the product, designed to get it to the public as quickly as is safely possible) due to its life-saving potential. Clinical trials showed that using perflubron with ordinary ventilators improved outcomes as much as using high frequency oscillating ventilation (HFOV). But because perflubron was not better than HFOV, the FDA did not approve perflubron, and Alliance is no longer pursuing the partial liquid ventilation application. Whether perflubron would improve outcomes when used with HFOV remains an open question. In 1996 Mike Darwin and Dr. Steven B. Harris proposed using cold liquid ventilation with perfluorocarbon to quickly lower the body temperature of victims of cardiac arrest and other brain trauma to allow the brain to better recover.[46] The technology came to be called gas/liquid ventilation (GLV), and was shown able to achieve a cooling rate of 0.5 C per minute in large animals.[47] It has not yet been tried in humans. Most recently, hypothermic brain protection has been associated with rapid brain cooling. In this regard, a new therapeutic approach is the use of intranasal perfluorochemical spray for preferential brain cooling.[48] The nasopharyngeal (NP) approach is unique for brain cooling due to anatomic proximity to the cerebral circulation and arteries. Based on preclinical studies in adult sheep, it was shown that independent of region, brain cooling was faster during NPperfluorochemical versus conventional whole body cooling with cooling blankets. To date, there have been four human studies including a completed randomized intra-arrest study (200

patients).[49][50] Results clearly demonstrated that prehospital intra-arrest transnasal cooling is safe, feasible and is associated with an improvement in cooling time.
[edit] Space travel

Liquid immersion provides a way to reduce the physical stress of G forces. Forces applied to fluids are distributed as omnidirectional pressures. Because liquids cannot be practically compressed, they do not change density under high acceleration such as performed in aerial maneuvers or space travel. A person immersed in liquid of the same density as tissue has acceleration forces distributed around the body, rather than applied at a single point such as a seat or harness straps. This principle is used in a new type of G-suit called the Libelle G-suit, which allows aircraft pilots to remain conscious and functioning at more than 10 G acceleration by surrounding them with water in a rigid suit. Acceleration protection by liquid immersion is limited by the differential density of body tissues and immersion fluid, limiting the utility of this method to about 15 to 20 G.[51] Extending acceleration protection beyond 20 G requires filling the lungs with fluid of density similar to water. An astronaut totally immersed in liquid, with liquid inside all body cavities, will feel little effect from extreme G forces because the forces on a liquid are distributed equally, and in all directions simultaneously. However effects will be felt because of density differences between different body tissues, so an upper acceleration limit still exists. Liquid breathing for acceleration protection may never be practical because of the difficulty of finding a suitable breathing medium of similar density to water that is compatible with lung tissue. Perfluorocarbon fluids are twice as dense as water, hence unsuitable for this application.[2] On the other hand, although perfluorochemicals are denser than water, lung tissue floats within the PFC filled lungs, and if the lungs are not over-filled, there is no compromise in pulmonary or systemic blood flow.[52] Therefore, if the astronaut is immersed in liquid and their lungs are filled with liquid PFC, they should not experience adverse effects, in spite of the almost twofold density difference. Based on interviews with adult patients that experienced partial liquid ventilation, when they became conscious they were unaware that 20-30 ml/kg of PFC was in their lungs during recovery.

[edit] Examples in fiction

Joe Haldeman's 1975 Novel The Forever War describes liquid immersion and breathing in great detail as a key technology to allow space travel and combat with acceleretion up to 25 G. In The Lost Symbol by Dan Brown, Robert Langdon (the protagonist) is completely submerged in breathable liquid mixed with hallucination agents and sedatives as a torture technique by Mal'akh (the antagonist). He goes through a near death experience when he inhales the liquid and blacks out, losing control over his body, but is soon revived. The James Cameron film The Abyss features a character using liquid breathing to dive thousands of feet without compressing. The Abyss also features a scene with a rat submerged in and breathing fluorocarbon liquid, filmed in real life.[53]

In the anime Neon Genesis Evangelion, the cockpits of the titular Mecha are filled with a fictional oxygenated liquid called LCL which helps to dampen impacts on the pilot in battle and helps him to better psychically-synchronize with his biomechanical vehicle. The aliens in the Gerry Anderson UFO series use liquid-breathing spacesuits. Hal Clement's 1973 novel Ocean on Top portrays a small underwater civilization living in a 'bubble' of oxygenated fluid denser than seawater. In an episode of the Adult Swim cartoon series Metalocalypse, the other members of the band submerge guitarist Toki in a "liquid oxygen isolation chamber" while recording an album in the Mariana Trench. In an episode of the SyFy Channel show Eureka, Sheriff Jack Carter is submerged in a tank of "oxygen rich plasma" to be cured of the effects of a scientific accident. In the movies Mission to Mars and Event Horizon, a character is depicted as being immersed in apparent breathable fluid before a high-acceleration launch. In season 1, episode 13 of Seven Days chrononaut Frank Parker is seen breathing a hyperoxygenated perfluorocarbon liquid that is pumped through a sealed full body suit that he is wearing. This suit and liquid combination allow him to board a Russian submarine through open ocean at a depth of almost 1000 feet. Upon boarding the submarine he removes his helmet, expels the liquid from his lungs and is able to breathe air again. Ben Bova's novel Jupiter features a craft in which the crew are suspended in a breathable liquid that allows them to survive in the high pressure environment of Jupiter's atmosphere. In the book Mechanicum from the Horus Heresy series of novels in the Warhammer 40,000 setting, physically crippled Titan pilots are encased in nutrient fluid tanks to allow them to continue operating beyond the limits normally imposed by the body. In the classic PC Turn-Based Strategy game X-COM: Terror from the Deep, "Aquanauts" fighting deep ocean conditions breathe a dense oxygen-carrying fluid. In the Star Trek: The Next Generation novel "The Children of Hamlin" the crew of the Enterprise-D encounter an alien race whose ships contain a breathable liquid environment.

ECMO Extracorporeal membrane oxygenation

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Extracorporeal membrane oxygenation

Intervention

ICD-9-CM

39.65

In intensive care medicine, extracorporeal membrane oxygenation (ECMO) is an extracorporeal technique of providing both cardiac and respiratory support oxygen to patients whose heart and lungs are so severely diseased or damaged that they can no longer serve their function. Initial cannulation of a patient receiving ECMO is performed by a surgeon and maintenance of the patient is the responsibility of the ECMO Specialist and gives 24/7 monitoring care during the duration of the ECMO treatment.

Contents
[hide]

1 Uses 2 Procedure 3 Types 4 Duration 5 Complications 6 References 7 External links 8 See also

[edit] Uses
[citation needed]

One of the new uses is in adults and children with the H1N1 flu.[1] It is also used with children who have respiratory syncytial virus infections.[2] ECMO treatment provides oxygenation until their lung function has sufficiently recovered to maintain appropriate O2 saturation. It is often a last resort. It is around 75% effective in saving the newborn's life.[3] Newborns cannot be placed on ECMO if they are under 4.5 pounds (2 kg), because they have extremely small vessels for cannulation, thus hindering adequate flow because of limitations from cannula size and subsequent higher resistance to blood flow (compare with vascular resistance).[4] Therefore, the device cannot be used for most premature newborns. Newborn infants are occasionally placed on ECMO due to the lack of a fully functioning respiratory system or other birth defect, but the survival rates drops to roughly 33%.[citation needed]

ECMO has proven to be useful in treating some severe trauma/polytrauma patients.[5] ECMO use on cadavers can increase the viability rate of transplanted organs.[6]

[edit] Procedure

ECMO schema An ECMO machine is similar to a heart-lung machine. To initiate ECMO, cannulae are placed in large blood vessels to provide access to the patient's blood. Anticoagulant drugs, usually heparin, are given to prevent blood clotting. The ECMO machine continuously pumps blood from the patient through a membrane oxygenator that imitates the gas exchange process of the lungs, i.e. it removes carbon dioxide and adds oxygen. Oxygenated blood is then returned to the patient. Management of the ECMO circuit is done by a team of ECMO specialists that includes intensive care unit (ICU) physicians, physician assistants, perfusionists, Registered Nurses, respiratory therapists, and Medical Laboratory Technologists that have received training in this specialty.

ECMO in H1N1 patient

[edit] Types
There are several forms of ECMO, the two most common of which are veno-arterial (VA) and veno-venous (VV). In both modalities, blood drained from the venous system is oxygenated outside of the body. In VA ECMO, this blood is returned to the arterial system and in VV ECMO the blood is returned to the venous system. In VV ECMO, no cardiac support is provided.

[edit] Duration
VV ECMO can provide sufficient oxygenation for several weeks, allowing diseased lungs to heal while the potential additional injury of aggressive mechanical ventilation is avoided. It may therefore be life-saving for some patients. However, due to the high technical demands, cost, and

risk of complications, such as bleeding under anticoagulant medication, ECMO is usually only considered as a last resort. The time limit for a newborn on ECMO is usually around 21 days. The record for the longest survivor on ECMO occurred on January 30, 2008, when a patient at NTU hospital, Taiwan survived a drowning accident after 117 days of ECMO application.[7]

[edit] Complications
A common consequence in ECMO-treated adults is neurological injury, which may include subarachnoid hemorrhage, ischemic watershed infarctions, hypoxic-ischemic encephalopathy, unexplained coma, and brain death [8] Fatal sepsis may occur when the large catheters inserted in the neck provide fertile field for infection.[9][citation needed] Additional risks include bleeding. In adults, ECMO survival rates are around 60%. ECMO has yet to have proven survival benefit in adults with acute respiratory distress syndrome (ARDS). In VA ECMO, patients whose cardiac function does not recover sufficiently to be weaned from ECMO may be bridged to a ventricular assist device (VAD) or transplant. In infants aged less than 34 weeks of gestation several physiologic systems are not welldeveloped, specially the cerebral vasculature and germinal matrix, resulting in high sensitivity to slight changes in pH, PaO2, and intracranial pressure.[4] Preterm infants are at unacceptably high risk for intraventricular hemorrhage (IVH) if administered ECMO at a gestational age less than 32 weeks.[10] Also later, given the risk of IVH, it has become standard practice to ultrasound the brain prior to administering ECMO.[4]

Oxygen toxicity Oxygen toxicity

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Oxygen toxicity
Classification and external resources

In 194243 the UK Government carried out extensive testing for oxygen toxicity in divers. The chamber is pressurised with air to 3.7 bar. The subject in the centre is breathing 100% oxygen from a mask.[1]

ICD-10

T59.8

ICD-9

987.8

MeSH

D018496

Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen (O2) at elevated partial pressures. It is also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning. Historically, the central nervous system condition was called the Paul Bert effect, and the pulmonary condition the Lorrain Smith effect, after the researchers who pioneered its discovery and description in the late 19th century. Severe cases can result in cell damage and death, with effects most often seen in the central nervous system, lungs and eyes. Oxygen toxicity is a concern for scuba divers, those on high concentrations of supplemental oxygen (particularly premature babies), and those undergoing hyperbaric oxygen therapy. The result of breathing elevated concentrations of oxygen is hyperoxia, an excess of oxygen in body tissues. The body is affected in different ways depending on the type of exposure. Central nervous system toxicity is caused by short exposure to high concentrations of oxygen at greater than atmospheric pressure. Pulmonary and ocular toxicity result from longer exposure to elevated oxygen levels at normal pressure. Symptoms may include disorientation, breathing problems, and vision changes such as myopia. Prolonged or very high oxygen concentrations can cause oxidative damage to cell membranes, the collapse of the alveoli in the lungs, retinal detachment, and seizures. Oxygen toxicity is managed by reducing the exposure to elevated

oxygen levels. Studies show that, in the long term, a robust recovery from most types of oxygen toxicity is possible. Protocols for avoidance of hyperoxia exist in fields where oxygen is breathed at higher-thannormal partial pressures, including underwater diving using compressed breathing gases, hyperbaric medicine, neonatal care and human spaceflight. These protocols have resulted in the increasing rarity of seizures due to oxygen toxicity, with pulmonary and ocular damage being mainly confined to the problems of managing premature infants. In recent years, oxygen has become available for recreational use in oxygen bars. The US Food and Drug Administration has warned those suffering from problems such as heart or lung disease not to use oxygen bars. Scuba divers use breathing gases containing up to 100% oxygen, and should have specific training in using such gases.

Contents
[hide]

1 Classification 2 Signs and symptoms o 2.1 Central nervous system o 2.2 Pulmonary o 2.3 Ocular 3 Causes o 3.1 Central nervous system toxicity o 3.2 Pulmonary toxicity o 3.3 Ocular toxicity 4 Mechanism 5 Diagnosis 6 Prevention o 6.1 Underwater o 6.2 Hyperbaric setting o 6.3 Normobaric setting o 6.4 Hypobaric setting 7 Management 8 Prognosis 9 Epidemiology 10 History 11 Society and culture 12 See also 13 References 14 Sources 15 Further reading 16 External links

[edit] Classification

The effects of oxygen toxicity may be classified by the organs affected, producing three principal forms:[2][3][4]

Central nervous system, characterised by convulsions followed by unconsciousness, occurring under hyperbaric conditions; Pulmonary (lungs), characterised by difficulty in breathing and pain within the chest, occurring when breathing elevated pressures of oxygen for extended periods; Ocular (retinopathic conditions), characterised by alterations to the eyes, occurring when breathing elevated pressures of oxygen for extended periods.

Central nervous system oxygen toxicity can cause seizures, brief periods of rigidity followed by convulsions and unconsciousness, and is of concern to divers who encounter greater than atmospheric pressures. Pulmonary oxygen toxicity results in damage to the lungs, causing pain and difficulty in breathing. Oxidative damage to the eye may lead to myopia or partial detachment of the retina. Pulmonary and ocular damage are most likely to occur when supplemental oxygen is administered as part of a treatment, particularly to newborn infants, but are also a concern during hyperbaric oxygen therapy. Oxidative damage may occur in any cell in the body but the effects on the three most susceptible organs will be the primary concern. It may also be implicated in red blood cell destruction (haemolysis),[5][6] damage to liver (hepatic),[7] heart (myocardial),[8] endocrine glands (adrenal, gonads, and thyroid),[9][10][11] or kidneys (renal),[12] and general damage to cells.[2][13] In unusual circumstances, effects on other tissues may be observed: it is suspected that during spaceflight, high oxygen concentrations may contribute to bone damage.[14] Hyperoxia can also indirectly cause carbon dioxide narcosis in patients with lung ailments such as chronic obstructive pulmonary disease or with central respiratory depression.[14] Oxygen toxicity is not associated with hyperventilation, because breathing air at atmospheric pressure always has a

partial pressure of oxygen (ppO2) of 0.21 bar (21 kPa) and the lower limit for toxicity is more than 0.3 bar (30 kPa).[15]

Oxygen Poisoning at 90 ft (27 m) in the Dry in 36 Subjects in Order of Performance K W Donald[1] Exposure Num. of (mins.) Subjects 96 6069 5055 3135 2130 1620 1115 610 1 3 4 4 6 8 4 6 Symptoms Prolonged dazzle; severe spasmodic vomiting Severe lip-twitching; Euphoria; Nausea and vertigo; arm twitch Severe lip-twitching; Dazzle; Blubbering of lips; fell asleep; Dazed Nausea, vertigo, lip-twitching; Convulsed Convulsed; Drowsiness; Severe lip-twitching; epigastric aura; twitch L arm; amnesia Convulsed; Vertigo and severe lip twitching; epigastric aura; spasmodic respiration; Inspiratory predominance; lip-twitching and syncope; Nausea and confusion Dazed and lip-twitching; paraesthesiae; vertigo; "Diaphragmatic spasm"; Severe nausea

[edit] Signs and symptoms

[edit] Central nervous system

Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), irritability (personality changes, anxiety, confusion, etc.), and dizziness. This may be followed by a tonicclonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic). The seizure ends with a period of unconsciousness (the postictal state).[16][17] The onset of seizure depends upon the partial pressure of oxygen (ppO2) in the breathing gas and exposure duration. However, exposure time before onset is unpredictable, as tests have shown a wide variation, both amongst individuals, and in the same individual from day to day.[16][18][19] In addition, many external factors, such as underwater immersion, exposure to cold, and exercise will decrease the time to onset of central nervous system symptoms.[1] Decrease of tolerance is closely linked to retention of carbon dioxide.[20][21][22] Other factors, such

as darkness and caffeine, increase tolerance in test animals, but these effects have not been proven in humans.[23][24]
[edit] Pulmonary

Pulmonary toxicity symptoms result from an inflammation that starts in the airways leading to the lungs and then spreads into the lungs (tracheobronchial tree). The symptoms appear in the upper chest region (substernal and carinal regions).[25][26][27] This begins as a mild tickle on inhalation and progresses to frequent coughing.[25] If breathing elevated partial pressures of oxygen is not discontinued, patients experience a mild burning on inhalation along with uncontrollable coughing and occasional shortness of breath (dyspnoea).[25] Physical findings related to pulmonary toxicity have included bubbling sounds heard through a stethoscope (bubbling rales), fever, and increased blood flow to the lining of the nose (hyperaemia of the nasal mucosa).[27] The radiological finding from the lungs shows inflammation and swelling (pulmonary oedema).[25][26] Pulmonary function measurements are reduced, as noted by a reduction in the amount of air that the lungs can hold (vital capacity) and changes in expiratory function and lung elasticity.[27][28] Tests in animals have indicated a variation in tolerance similar to that found in central nervous system toxicity, as well as significant variations between species. When the exposure to oxygen above 0.5 bar (50 kPa) is intermittent, it permits the lungs to recover and delays the onset of toxicity.[29]
[edit] Ocular

In premature babies, signs of damage to the eye (retinopathy of prematurity, or ROP) are observed via an ophthalmoscope as a demarcation between the vascularised and nonvascularised regions of an infant's retina. The degree of this demarcation is used to designate four stages: (I) the demarcation is a line; (II) the demarcation becomes a ridge; (III) growth of new blood vessels occurs around the ridge; (IV) the retina begins to detach from the inner wall of the eye (choroid).[30]

[edit] Causes
Oxygen toxicity is caused by exposure to oxygen at partial pressures greater than those to which the body is normally exposed. This occurs in three principal settings: underwater diving, hyperbaric oxygen therapy and the provision of supplemental oxygen, particularly to premature infants. In each case, the risk factors are markedly different.
[edit] Central nervous system toxicity See also: Technical diving

Exposures, from minutes to a few hours, to partial pressures of oxygen above 1.6 bars (160 kPa)about eight times the atmospheric concentrationare usually associated with central nervous system oxygen toxicity and are most likely to occur among patients undergoing hyperbaric oxygen therapy and divers. Since atmospheric pressure is about 1 bar (100 kPa), central nervous system toxicity can only occur under hyperbaric conditions, where ambient pressure is above normal.[31][32] Divers breathing air at depths greater than 60 m (200 ft) face an

increasing risk of an oxygen toxicity "hit" (seizure). Divers breathing a gas mixture enriched with oxygen, such as nitrox, can similarly suffer a seizure at shallower depths, should they descend below the maximum depth allowed for the mixture.[33]
[edit] Pulmonary toxicity

The lungs, as well as the remainder of the respiratory tract, are exposed to the highest concentration of oxygen in the human body and are therefore the first organs to show toxicity. Pulmonary toxicity occurs with exposure to concentrations of oxygen greater than 0.5 bar (50 kPa), corresponding to an oxygen fraction of 50% at normal atmospheric pressure. Signs of pulmonary toxicity begins with evidence of tracheobronchitis, or inflammation of the upper airways, after an asymptomatic period between 4 and 22 hours at greater than 95% oxygen,[34] with some studies suggesting symptoms usually begin after approximately 14 hours at this level of oxygen.[35] At partial pressures of oxygen of 2 to 3 bar (200 to 300 kPa)100% oxygen at 2 to 3 times atmospheric pressurethese symptoms may begin as early as 3 hours after exposure to oxygen.[34] Experiments on rats show pulmonary manifestations of oxygen toxicity are not the same for normobaric conditions as they are for hyperbaric conditions.[36] Evidence of decline in lung function as measured by pulmonary function testing can occur as quickly as 24 hours of continuous exposure to 100% oxygen,[35] with evidence of diffuse alveolar damage and the onset of acute respiratory distress syndrome usually occurring after 48 hours on 100% oxygen.[34] Breathing 100% oxygen also eventually leads to collapse of the alveoli (atelectasis), whileat the same partial pressure of oxygenthe presence of significant partial pressures of inert gases, typically nitrogen, will prevent this effect.[37] Preterm newborns are known to be at higher risk for bronchopulmonary dysplasia with extended exposure to high concentrations of oxygen.[38] Other groups at higher risk for oxygen toxicity are patients on mechanical ventilation with exposure to levels of oxygen greater than 50%, and patients exposed to chemicals that increase risk for oxygen toxicity such the chemotherapeutic agent bleomycin.[35] Therefore, current guidelines for patients on mechanical ventilation in intensive care suggests keeping oxygen concentration less than 60%.[34] Likewise, divers who undergo treatment of decompression sickness are at increased risk of oxygen toxicity as treatment entails exposure to long periods of oxygen breathing under hyperbaric conditions, in addition to any oxygen exposure during the dive.[31]
[edit] Ocular toxicity See also: Retinopathy of prematurity

Prolonged exposure to high inspired fractions of oxygen causes damage to the retina.[39][40][41] Damage to the developing eye of infants exposed to high oxygen fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions.[42][43] Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants.[42][44] In preterm infants, the retina is often not fully vascularised. Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of

these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of retinopathy of prematurity, and may raise the risk of hypoxia-related systemic complications.[42] Hyperoxic myopia has occurred in closed circuit oxygen rebreather divers with prolonged exposures.[43][45][46] It also occurs frequently in those undergoing repeated hyperbaric oxygen therapy.[40][47] This is due to an increase in the refractive power of the lens, since axial length and keratometry readings do not reveal a corneal or length basis for a myopic shift.[47][48] It is usually reversible with time.[40][47]

[edit] Mechanism
Main articles: Reactive oxygen species and Oxidative stress

The lipid peroxidation mechanism shows a single radical initiating a chain reaction which converts unsaturated lipids to lipid peroxides,

The biochemical basis for the toxicity of oxygen is the partial reduction of oxygen by one or two electrons to form reactive oxygen species,[49] which are natural by-products of the normal metabolism of oxygen and have important roles in cell signalling.[50] One species produced by the body, the superoxide anion (O2),[51] is possibly involved in iron acquisition.[52] Higher than normal concentrations of oxygen lead to increased levels of reactive oxygen species.[53] Oxygen is necessary for cell metabolism, and the blood supplies it to all parts of the body. When oxygen is breathed at high partial pressures, a hyperoxic condition will rapidly spread, with the most vascularised tissues being most vulnerable. During times of environmental stress, levels of reactive oxygen species can increase dramatically, which can damage cell structures and produce oxidative stress.[19][54]

While all the reaction mechanisms of these species within the body are not yet fully understood,[55] one of the most reactive products of oxidative stress is the hydroxyl radical (OH), which can initiate a damaging chain reaction of lipid peroxidation in the unsaturated lipids within cell membranes.[56] High concentrations of oxygen also increase the formation of other free radicals, such as nitric oxide, peroxynitrite, and trioxidane, which harm DNA and other biomolecules.[19][57] Although the body has many antioxidant systems such as glutathione that guard against oxidative stress, these systems are eventually overwhelmed at very high concentrations of free oxygen, and the rate of cell damage exceeds the capacity of the systems that prevent or repair it.[58][59][60] Cell damage and cell death then result.[61]

[edit] Diagnosis
Diagnosis of central nervous system oxygen toxicity in divers prior to seizure is difficult as the symptoms of visual disturbance, ear problems, dizziness, confusion and nausea can be due to many factors common to the underwater environment such as narcosis, congestion and coldness. However, these symptoms may be helpful in diagnosing the first stages of oxygen toxicity in patients undergoing hyperbaric oxygen therapy. In either case, unless there is a prior history of epilepsy or tests indicate hypoglycaemia, a seizure occurring in the setting of breathing oxygen at partial pressures greater than 1.4 bar (140 kPa) suggests a diagnosis of oxygen toxicity.[62] Diagnosis of bronchopulmonary dysplasia in new-born infants with breathing difficulties is difficult in the first few weeks. However, if the infant's breathing does not improve during this time, blood tests and x-rays may be used to confirm bronchopulmonary dysplasia. In addition, an echocardiogram can help to eliminate other possible causes such as congenital heart defects or pulmonary arterial hypertension.[63] The diagnosis of retinopathy of prematurity in infants is typically suggested by the clinical setting. Prematurity, low birth weight and a history of oxygen exposure are the principal indicators, while no hereditary factors have been shown to yield a pattern.[64]

[edit] Prevention

The label on the diving cylinder shows that it contains oxygen-rich gas (36%) and is boldly marked with a maximum operating depth of 28 metres.

The prevention of oxygen toxicity depends entirely on the setting. Both underwater and in space, proper precautions can eliminate the most pernicious effects. Premature infants commonly require supplemental oxygen to treat complications of preterm birth. In this case prevention of bronchopulmonary dysplasia and retinopathy of prematurity must be carried out without compromising a supply of oxygen adequate to preserve the infant's life.
[edit] Underwater See also: Maximum operating depth

A seizure caused by oxygen toxicity to the central nervous system is a deadly but avoidable event while diving.[33] The diver may experience no warning symptoms.[17] The effects are sudden convulsions and unconsciousness, during which victims can lose their regulator and drown.[65] One of the advantages of a full-face diving mask is prevention of regulator loss in the event of a seizure. As there is an increased risk of central nervous system oxygen toxicity on deep dives, long dives and dives where oxygen-rich breathing gases are used, divers are taught to calculate a maximum operating depth for oxygen-rich breathing gases, and cylinders containing such mixtures must be clearly marked with that depth.[22][66] In some diver training courses for these types of diving, divers are taught to plan and monitor what is called the oxygen clock of their dives.[66] This is a notional alarm clock, which ticks more quickly at increased ppO2 and is set to activate at the maximum single exposure limit recommended in the National Oceanic and Atmospheric Administration Diving Manual.[22][66] For the following partial pressures of oxygen the limit is: 45 minutes at 1.6 bar (160 kPa), 120 minutes at 1.5 bar (150 kPa), 150 minutes at 1.4 bar (140 kPa), 180 minutes at 1.3 bar (130 kPa) and 210 minutes at 1.2 bar (120 kPa), but is impossible to predict with any reliability whether or when toxicity symptoms will occur.[67][68] Many nitrox-capable dive computers calculate an

oxygen loading and can track it across multiple dives. The aim is to avoid activating the alarm by reducing the ppO2 of the breathing gas or the length of time breathing gas of higher ppO2. As the ppO2 depends on the fraction of oxygen in the breathing gas and the depth of the dive, the diver obtains more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas, or by shortening the duration of exposure to oxygen-rich gases.[69][70] Diving below 60 m (200 ft) on air would expose a diver to increasing danger of oxygen toxicity as the partial pressure of oxygen exceeds 1.4 bar (140 kPa), so a gas mixture must be used which contains less than 21% oxygen (a hypoxic mixture). Increasing the proportion of nitrogen is not viable, since it would produce a strongly narcotic mixture. However, helium is not narcotic, and a usable mixture may be blended either by completely replacing nitrogen with helium (the resulting mix is called heliox), or by replacing part of the nitrogen with helium, producing a trimix.[71] Pulmonary oxygen toxicity is an entirely avoidable event while diving. The limited duration and naturally intermittent nature of most diving makes this a relatively rare (and even then, reversible) complication for divers.[15] Guidelines have been established that allow divers to calculate when they are at risk of pulmonary toxicity.[72][73][74]
[edit] Hyperbaric setting

The presence of a fever or a history of seizure is a relative contraindication to hyperbaric oxygen treatment.[75] The schedules used for treatment of decompression illness allow for periods of breathing air rather than 100% oxygen (oxygen breaks) to reduce the chance of seizure or lung damage. The U.S. Navy uses treatment tables based on periods alternating between 100% oxygen and air. For example, U.S.N. table 6 requires 75 minutes (three periods of 20 minutes oxygen/5 minutes air) at an ambient pressure of 2.8 standard atmospheres (280 kPa), equivalent to a depth of 18 metres (60 ft). This is followed by a slow reduction in pressure to 1.9 atm (190 kPa) over 30 minutes on oxygen. The patient then remains at that pressure for a further 150 minutes, consisting of two periods of 15 minutes air/60 minutes oxygen, before the pressure is reduced to atmospheric over 30 minutes on oxygen.[76] Vitamin E and selenium were proposed and later rejected as a potential method of protection against pulmonary oxygen toxicity.[77][78][79] There is however some experimental evidence in rats that vitamin E and selenium aid in preventing in vivo lipid peroxidation and free radical damage, and therefore prevent retinal changes following repetitive hyperbaric oxygen exposures.[80]
[edit] Normobaric setting

Bronchopulmonary dysplasia is reversible in the early stages by use of break periods on lower pressures of oxygen, but it may eventually result in irreversible lung injury if allowed to progress to severe damage. One or two days of exposure without oxygen breaks are needed to cause such damage.[14]

Retinopathy of prematurity is largely preventable by screening. Current guidelines require that all babies of less than 32 weeks gestational age or having a birth weight less than 1.5 kg (3.3 lb) should be screened for retinopathy of prematurity at least every two weeks.[81] The National Cooperative Study in 1954 showed a causal link between supplemental oxygen and retinopathy of prematurity, but subsequent curtailment of supplemental oxygen caused an increase in infant mortality. To balance the risks of hypoxia and retinopathy of prematurity, modern protocols now require monitoring of blood oxygen levels in premature infants receiving oxygen.[82]
[edit] Hypobaric setting

In low-pressure environments oxygen toxicity may be avoided since the toxicity is caused by high partial pressure of oxygen, not merely by high oxygen fraction. This is illustrated by modern pure oxygen use in spacesuits, which must operate at low pressure (also historically, very high percentage oxygen and lower than normal atmospheric pressure was used in early spacecraft, for example, the Gemini and Apollo spacecraft).[83] In such applications as extravehicular activity, high-fraction oxygen is non-toxic, even at breathing mixture fractions approaching 100%, because the oxygen partial pressure is not allowed to chronically exceed 0.3 bar (4.4 psi).[83]

[edit] Management

The retina (red) is detached at the top of the eye.

The silicone band (scleral buckle, blue) is placed around the eye. This brings the wall of the eye into contact with the detached retina, allowing the retina to re-attach.

During hyperbaric oxygen therapy, the patient will usually breathe 100% oxygen from a mask, while inside a hyperbaric chamber pressurised with air to about 2.8 bar (280 kPa). Seizures during the therapy are managed by removing the mask from the patient, thereby dropping the partial pressure of oxygen inspired below 0.6 bar (60 kPa).[17] A seizure underwater requires that the diver is brought to the surface as soon as practicable. Although for many years the recommendation has been not to raise the diver during the seizure itself, owing to the danger of arterial gas embolism,[84] there is no evidence of expiratory obstruction during seizure and benefit may be gained by raising the diver during the seizure's clonic phase.[85] Rescuers need to ensure that their own safety is not compromised during the convulsive phase. They then ensure that the victim's air supply is established and maintained, and carry out a controlled buoyant lift. Lifting an unconscious body is taught by most diver training agencies. Upon reaching the surface, emergency services are always contacted as there is a possibility of further complications requiring medical attention.[86] The U.S. Navy has procedures for completing the decompression stops where a recompression chamber is not immediately available.[87] The occurrence of symptoms of bronchopulmonary dysplasia or acute respiratory distress syndrome is treated by lowering the fraction of oxygen administered, along with a reduction in the periods of exposure and an increase in the break periods where normal air is supplied. Where supplemental oxygen is required for treatment of another disease (particularly in infants), a ventilator may be needed to ensure that the lung tissue remains inflated. Reductions in pressure and exposure will be made progressively and medications such as bronchodilators and pulmonary surfactants may be used.[88] Retinopathy of prematurity may regress spontaneously, but should the disease progress beyond a threshold (defined as five contiguous or eight cumulative hours of stage 3 retinopathy of prematurity), both cryosurgery and laser surgery have been shown to reduce the risk of blindness as an outcome. Where the disease has progressed further, techniques such as scleral buckling and vitrectomy surgery may assist in re-attaching the retina.[89]

[edit] Prognosis
Although the convulsions caused by central nervous system oxygen toxicity may lead to incidental injury to the victim, it remained uncertain for many years whether damage to the nervous system following the seizure could occur and several studies searched for evidence of such damage. An overview of these studies by Bitterman in 2004 concluded that following removal of breathing gas containing high fractions of oxygen, no long-term neurological damage from the seizure remains.[19][90]

The majority of infants who have survived following an incidence of bronchopulmonary dysplasia will eventually recover near-normal lung function, since lungs continue to grow during the first 57 years and the damage caused by bronchopulmonary dysplasia is to some extent reversible (even in adults). However, they are likely be more susceptible to respiratory infections for the rest of their lives and the severity of later infections is often greater than that in their peers.[91][92] Retinopathy of prematurity (ROP) in infants frequently regresses without intervention and eyesight may be normal in later years. Where the disease has progressed to the stages requiring surgery, the outcomes are generally good for the treatment of stage 3 ROP, but are much worse for the later stages. Although surgery is usually successful in restoring the anatomy of the eye, damage to the nervous system by the progression of the disease leads to comparatively poorer results in restoring vision. The presence of other complicating diseases also reduces the likelihood of a favourable outcome.[93]

[edit] Epidemiology

Retinopathy of prematurity (ROP) is more common in middle income countries where neonatal intensive care services are increasing; but greater awareness of the problem, leading to preventive measures, has not yet occurred.[94]

The incidence of central nervous system toxicity among divers has decreased since the Second World War, as protocols have developed to limit exposure and partial pressure of oxygen inspired. In 1947, Donald recommended limiting the depth allowed for breathing pure oxygen to 7.6 m (25 ft), or a ppO2 of 1.8 bar (180 kPa).[95] This limit has been reduced, until today a limit

of 1.4 bar (140 kPa) during a recreational dive and 1.6 bar (160 kPa) during shallow decompression stops is accepted. Oxygen toxicity has now become a rare occurrence other than when caused by equipment malfunction and human error. Historically, the U.S. Navy has refined its Navy Diving Manual Tables to reduce oxygen toxicity incidents. Between 1995 and 1999, reports showed 405 surface-supported dives using the heliumoxygen tables; of these, oxygen toxicity symptoms were observed on 6 dives (1.5%). As a result, the U.S. Navy in 2000 modified the schedules and conducted field tests of 150 dives, none of which produced symptoms of oxygen toxicity. Revised tables were published in 2001.[96] The variability in tolerance and other variable factors such as workload have resulted in the U.S. Navy abandoning screening for oxygen tolerance. Of the 6,250 oxygen-tolerance tests performed between 1976 and 1997, only 6 episodes of oxygen toxicity were observed (0.1%).[97][98] Central nervous system oxygen toxicity among patients undergoing hyperbaric oxygen therapy is rare, and is influenced by a number of a factors: individual sensitivity and treatment protocol; and probably therapy indication and equipment used. A study by Welslau in 1996 reported 16 incidents out of a population of 107,264 patients (0.015%), while Hampson and Atik in 2003 found a rate of 0.03%.[99][100] Yildiz, Ay and Qyrdedi, in a summary of 36,500 patient treatments between 1996 and 2003, reported only 3 oxygen toxicity incidents, giving a rate of 0.008%.[99] A later review of over 80,000 patient treatments revealed an even lower rate: 0.0024%. The reduction in incidence may be partly due to use of a mask (rather than a hood) to deliver oxygen.[101] Bronchopulmonary dysplasia is among the most common complications of prematurely born infants and its incidence has grown as the survival of extremely premature infants has increased. Nevertheless, the severity has decreased as better management of supplemental oxygen has resulted in the disease now being related mainly to factors other than hyperoxia.[38] In 1997 a summary of studies of neonatal intensive care units in industrialised countries showed that up to 60% of low birth weight babies developed retinopathy of prematurity, which rose to 72% in extremely low birth weight babies, defined as less than 1 kg (2.2 lb) at birth. However, severe outcomes are much less frequent: for very low birth weight babiesthose less than 1.5 kg (3.3 lb) at birththe incidence of blindness was found to be no more than 8%.[94]

[edit] History

Paul Bert, a French physiologist, first described oxygen toxicity in 1878.

Central nervous system toxicity was first described by Paul Bert in 1878.[102][103] He showed that oxygen was toxic to insects, arachnids, myriapods, molluscs, earthworms, fungi, germinating seeds, birds, and other animals. Central nervous system toxicity may be referred to as the "Paul Bert effect".[14] Pulmonary oxygen toxicity was first described by J. Lorrain Smith in 1899 when he noted central nervous system toxicity and discovered in experiments in mice and birds that 0.43 bar (43 kPa) had no effect but 0.75 bar (75 kPa) of oxygen was a pulmonary irritant.[29] Pulmonary toxicity may be referred to as the "Lorrain Smith effect".[14] The first recorded human exposure was undertaken in 1910 by Bornstein when two men breathed oxygen at 2.8 bar (280 kPa) for 30 minutes while he went on to 48 minutes with no symptoms. In 1912, Bornstein developed cramps in his hands and legs while breathing oxygen at 2.8 bar (280 kPa) for 51 minutes.[3] Smith then went on to show that intermittent exposure to a breathing gas with less oxygen permitted the lungs to recover and delayed the onset of pulmonary toxicity.[29] Albert R. Behnke et al. in 1935 were the first to observe visual field contraction (tunnel vision) on dives between 1.0 bar (100 kPa) and 4.1 bar (410 kPa).[104][105] During World War II, Donald and Yarbrough et al. performed over 2,000 experiments on oxygen toxicity to support the initial use of closed circuit oxygen rebreathers.[39][106] Naval divers in the early years of oxygen rebreather diving developed a mythology about a monster called "Oxygen Pete", who lurked in the bottom of the Admiralty Experimental Diving Unit "wet pot" (a water-filled hyperbaric chamber) to catch unwary divers. They called having an oxygen toxicity attack "getting a Pete".[107][108] In the decade following World War II, Lambertsen et al. made further discoveries on the effects of breathing oxygen under pressure as well as methods of prevention.[109][110] Their work on intermittent exposures for extension of oxygen tolerance and on a model for prediction of pulmonary oxygen toxicity based on pulmonary function are key documents in the development of standard operating procedures when breathing elevated pressures of oxygen.[15] Lambertsen's

work showing the effect of carbon dioxide in decreasing time to onset of central nervous system symptoms has influenced work from current exposure guidelines to future breathing apparatus design.[21][22][111] Retinopathy of prematurity was not observed prior to World War II, but with the availability of supplemental oxygen in the decade following, it rapidly became one of the principal causes of infant blindness in developed countries. By 1960 the use of oxygen had become identified as a risk factor and its administration restricted. The resulting fall in retinopathy of prematurity was accompanied by a rise in infant mortality and hypoxia-related complications. Since then, more sophisticated monitoring and diagnosis have established protocols for oxygen use which aim to balance between hypoxic conditions and problems of retinopathy of prematurity.[94] Bronchopulmonary dysplasia was first described by Northway in 1967, who outlined the conditions that would lead to the diagnosis.[112] This was later expanded by Bancalari and in 1988 by Shennan, who suggested the need for supplemental oxygen at 36 weeks could predict long-term outcomes.[113] Nevertheless, Palta et al. in 1998 concluded that radiographic evidence was the most accurate predictor of long-term effects.[114] Bitterman et al. in 1986 and 1995 showed that darkness and caffeine would delay the onset of changes to brain electrical activity in rats.[23][24] In the years since, research on central nervous system toxicity has centred on methods of prevention and safe extension of tolerance.[115] Sensitivity to central nervous system oxygen toxicity has been shown to be affected by factors such as circadian rhythm, drugs, age, and gender.[116][117][118][119] In 1988, Hamilton et al. wrote procedures for the National Oceanic and Atmospheric Administration to establish oxygen exposure limits for habitat operations.[72][73][74] Even today, models for the prediction of pulmonary oxygen toxicity do not explain all the results of exposure to high partial pressures of oxygen.[120]

[edit] Society and culture

See also: Nitrox and Oxygen bar

Recreational scuba divers commonly breathe nitrox containing up to 40% oxygen, while technical divers use pure oxygen or nitrox containing up to 80% oxygen. Divers who breathe oxygen fractions greater than in air (21%) need to be trained in the dangers of oxygen toxicity and how to prevent them.[66] In order to buy nitrox, a diver has to show evidence of such qualification.[121] Since the late 1990s the recreational use of oxygen has been promoted by oxygen bars, where customers breathe oxygen through a nasal cannula. Claims have been made that this reduces stress, increases energy, and lessens the effects of hangovers and headaches, despite the lack of any scientific evidence to support them.[122] There are also devices on sale that offer "oxygen massage" and "oxygen detoxification" with claims of removing body toxins and reducing body fat.[123] The American Lung Association has stated "there is no evidence that oxygen at the low flow levels used in bars can be dangerous to a normal person's health", but the U.S. Center for

Drug Evaluation and Research cautions that people with heart or lung disease need their supplementary oxygen carefully regulated and should not use oxygen bars.[122] Victorian society had a fascination for the rapidly expanding field of science. In "Dr. Ox's Experiment", a short story written by Jules Verne in 1872, the eponymous doctor uses electrolysis of water to separate oxygen and hydrogen. He then pumps the pure oxygen throughout the town of Quiquendone, causing the normally tranquil inhabitants and their animals to become aggressive and plants to grow rapidly. An explosion of the hydrogen and oxygen in Dr Ox's factory brings his experiment to an end. Verne summarised his story by explaining that the effects of oxygen described in the tale were his own invention.[124] There is also a brief episode of oxygen intoxication in his "From the Earth to the Moon".[125]

Medical ventilator Medical ventilator

From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Modes of mechanical ventilation. For other uses, see ventilation (physiology).

The Bird VIP Infant ventilator

A medical ventilator can be defined as any machine designed to mechanically move breatheable air into and out of the lungs, to provide the mechanism of breathing for a patient who is physically unable to breathe, or breathing insufficiently.

While modern ventilators are generally thought of as computerized machines, patients can be ventilated indefinitely with a bag valve mask, a simple hand-operated machine. After Hurricane Katrina, dedicated staff "bagged" patients in New Orleans hospitals for days with simple bag valve masks. Ventilators are chiefly used in intensive care medicine, home care, and emergency medicine (as standalone units) and in anesthesia (as a component of an anesthesia machine).

Contents
[hide]

1 Function o 1.1 Life-critical system 2 Ventilation o 2.1 Biphasic Cuirass Ventilation 3 See also 4 References 5 External links

[edit] Function
In its simplest form, a modern positive pressure ventilator consists of a compressible air reservoir or turbine, air and oxygen supplies, a set of valves and tubes, and a disposable or reusable "patient circuit". The air reservoir is pneumatically compressed several times a minute to deliver room-air, or in most cases, an air/oxygen mixture to the patient. If a turbine is used, the turbine pushes air through the ventilator, with a flow valve adjusting pressure to meet patient-specific parameters. When overpressure is released, the patient will exhale passively due to the lungs' elasticity, the exhaled air being released usually through a one-way valve within the patient circuit called the patient manifold. The oxygen content of the inspired gas can be set from 21 percent (ambient air) to 100 percent (pure oxygen). Pressure and flow characteristics can be set mechanically or electronically. Ventilators may also be equipped with monitoring and alarm systems for patient-related parameters (e.g. pressure, volume, and flow) and ventilator function (e.g. air leakage, power failure, mechanical failure), backup batteries, oxygen tanks, and remote control. The pneumatic system is nowadays often replaced by a computer-controlled turbopump. Modern ventilators are electronically controlled by a small embedded system to allow exact adaptation of pressure and flow characteristics to an individual patient's needs. Fine-tuned ventilator settings also serve to make ventilation more tolerable and comfortable for the patient. In Germany, Canada, and the United States, respiratory therapists are responsible for tuning these settings while biomedical technologists are responsible for the maintenance.

The patient circuit usually consists of a set of three durable, yet lightweight plastic tubes, separated by function (e.g. inhaled air, patient pressure, exhaled air). Determined by the type of ventilation needed, the patient-end of the circuit may be either noninvasive or invasive. Noninvasive methods, which are adequate for patients who require a ventilator only while sleeping and resting, mainly employ a nasal mask. Invasive methods require intubation, which for long-term ventilator dependence will normally be a tracheotomy cannula, as this is much more comfortable and practical for long-term care than is larynx or nasal intubation.
[edit] Life-critical system

Because the failure of a mechanical ventilation system may result in death, it is classed as a lifecritical system, and precautions must be taken to ensure that mechanical ventilation systems are highly reliable. This includes their power-supply provision. Mechanical ventilators are therefore carefully designed so that no single point of failure can endanger the patient. They usually have manual backup mechanisms to enable hand-driven respiration in the absence of power. Some systems are also equipped with compressed-gas tanks and backup batteries to provide ventilation in case of power failure or defective gas supplies, and methods to operate or call for help if their mechanisms or software fail.]]

[edit] Ventilation
The early history of mechanical ventilation begins with various versions of what was eventually called the iron lung, a form of noninvasive negative pressure ventilator widely used during the polio epidemics of the 20th century after the introduction of the "Drinker respirator" in 1928, and the subsequent improvements introduced by John Haven Emerson in 1931.[1] Other forms of noninvasive ventilators, also used widely for polio patients, include Biphasic Cuirass Ventilation, the rocking bed, and rather primitive positive pressure machines.[1] In 1949, John Haven Emerson developed a mechanical assister for anesthesia with the cooperation of the anesthesia department at Harvard University. Mechanical ventilators began to be used increasingly in anesthesia and intensive care during the 1950s. Their development was stimulated both by the need to treat polio patients and the increasing use of muscle relaxants during anesthesia. Relaxant drugs paralyze the patient and improve operating conditions for the surgeon, but also paralyze the respiratory muscles

In the United Kingdom, the East Radcliffe and Beaver models were early examples, the later using an automotive wiper motor to drive the bellows used to inflate the lungs.[2] Electric motors were, however, a problem in the operating theatres of that time, as their use caused an explosion hazard in the presence of flammable anesthetics such as ether and cyclopropane. In 1952, Roger Manley of the Westminster Hospital, London, developed a ventilator which was entirely gas driven, and became the most popular model used in Europe. It was an elegant design, and became a great favourite with European anesthetists for four decades, prior to the introduction of models controlled by electronics. It was independent of electrical power, and caused no

explosion hazard. The original Mark I unit was developed to become the Manley Mark II in collaboration with the Blease company, who manufactured many thousands of these units. Its principle of operation was very simple, an incoming gas flow was used to lift a weighted bellows unit, which fell intermittently under gravity, forcing breathing gases into the patient's lungs. The inflation pressure could be varied by sliding the movable weight on top of the bellows. The volume of gas delivered was adjustable using a curved slider, which restricted bellows excursion. Residual pressure after the completion of expiration was also configurable, using a small weighted arm visible to the lower right of the front panel. This was a robust unit and its availability encouraged the introduction of positive pressure ventilation techniques into mainstream European anesthetic practice. The 1955 release of Forrest Bird's "Bird Universal Medical Respirator" in the United States, changed the way mechanical ventilation was performed with the small green box becoming a familiar piece of medical equipment.[3] The unit was sold as the Bird Mark 7 Respirator and informally called the "Bird". It was a pneumatic device and therefore required no electrical power source to operate. Intensive care environments around the world revolutionalized in 1971 by the introduction of the first SERVO 900 ventilator (Elema-Schnander). It was a small, silent and effective electronic ventilator, with the famous SERVO feedback system controlling what had been set and regulating delivery. For the first time, the machine could deliver the set volume in volume control ventilation. Ventilators used under increased pressure (hyperbaric) require special precautions and few ventilators can operate under these conditions.[4] In 1979, Sechrist Industries introduced their Model 500A ventilator which was specifically designed for use with hyperbaric chambers.[5] In 1991 the SERVO 300 ventilator series was introduced. The platform of the SERVO 300 series enabled treatment of all patient categories, from adult to neonate, with one single ventilator. The SERVO 300 series provided a completely new and unique gas delivery system, with rapid flowtriggering response. A modular concept, meaning that the hospital has one ventilator model throughout the ICU department instead of a fleet with different models and brands for the different user needs, was introduced with SERVO-i in 2001. With this modular concept the ICU departments could choose the modes and options, software and hardware needed for a particular patient category.
[edit] Biphasic Cuirass Ventilation

Biphasic Cuirass Ventilation (BCV) is a method of ventilation which requires the patient to wear an upper body shell or cuirass, so named after the body armor worn by medieval soldiers. The ventilation is biphasic because the cuirass is attached to a pump which actively controls both the inspiratory and expiratory phases of the respiratory cycle. This method has also been described as 'Negative Pressure Ventilation' (NPV), 'External Chest Wall Oscillation' (ECWO), 'External Chest Wall Compression' (ECWC) and 'External High Frequency Oscillation' (EHFO). BCV may be considered a refinement of the iron lung ventilator. Biphasic Cuirass Ventilation

was developed by the late Dr Zamir Hayek, a pioneer in the field of assisted ventilation. Some of Dr Hayek's previous inventions include the Hayek Oscillator, an early form of the technology.

Paramedic Paramedic
From Wikipedia, the free encyclopedia Jump to: navigation, search This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed.
(May 2011)

Paramedics of the Australian Capital Territory Ambulance Service during a training regime

A paramedic is a healthcare professional that works in emergency medical situations. Paramedics provide advanced levels of care for medical emergencies and trauma.[1] The majority of paramedics are based in the field in ambulances, emergency response vehicles, or in specialist mobile units such as cycle response. Paramedics provide out-of-hospital treatment and some diagnostic services[2][3], although some may undertake hospital-based roles, such as in the treatment of minor injuries.

Contents
[hide]

1 History of paramedics o 1.1 Early history o 1.2 Early ambulance services o 1.3 Pre-hospital emergency care

1.4 Public notability 1.5 Evolution and growth 1.5.1 Canada 1.5.2 United Kingdom o 1.6 Current practice 2 Structure of employment 3 Paramedic skills o 3.1 Common skills o 3.2 Medications administered o 3.3 Skills by certification level 4 Medicolegal authority 5 In entertainment 6 See also 7 References 8 External links

o o

[edit] History of paramedics

See also: History of the ambulance [edit] Early history

Throughout the evolution of paramedic care, there has been an ongoing association with military conflict. One of the first indications of a formal process for managing injured people dates from the Imperial Legions of Rome, where aging Centurions, no longer able to fight, were given the task of organizing the removal of the wounded from the battlefield and providing some form of care. Such individuals, although not physicians, were probably among the world's earliest surgeons by default, being required to suture wounds and complete amputations. A similar situation existed in the Crusades, with the Knights Hospitallers of the Order of St. John of Jerusalem filling a similar function; this organisation continued, and evolved into what is now known throughout the Commonwealth of Nations as the St. John Ambulance.
[edit] Early ambulance services

While civilian communities had organized ways to deal with the care and transportation of the sick and dying as far back as the bubonic plague in London between 1598 and 1665, such arrangements were typically temporary. In time, however, these arrangements began to formalize and become permanent. During the American Civil War, Jonathan Letterman devised a system of mobile field hospitals employing the first uses of the principles of triage. After returning home, some veterans began to attempt to apply what had they had seen on the battlefield to their own communities, and commenced the creation of volunteer life-saving squads and ambulance corps.

German Red Cross paramedics training in 1931

These early developments in formalised ambulance services were decided at local levels, and this led to services being provided by diverse operators such as the local hospital, police, fire brigade, or even funeral directors who often possessed the only local transport allowing a passenger to lie down. In most cases these ambulances were operated by drivers and attendants with little or no medical training, and it was some time before formal training began to appear in some units. An early example was the members of the Toronto Police Ambulance Service receiving a mandatory five days of training from St. John as early as 1889.[4] Prior to World War I motorized ambulances started to be developed, but once they proved their effectiveness on the battlefield during the war the concept spread rapidly to civilian systems. In terms of advanced skills, once again the military led the way. During World War II and the Korean War battlefield medics administered painkilling narcotics by injection in emergency situations, and pharmacists' mates on warships were permitted to do even more without the guidance of a physician. The Korean War also marked the first widespread use of helicopters to evacuate the wounded from forward positions to medical units, leading to the rise of the term "medivac". These innovations would not find their way into the civilian sphere for nearly twenty more years.
[edit] Pre-hospital emergency care

By the early 1960s experiments in improving care had begun in some civilian centres. One early experiment involved the provision of pre-hospital cardiac care by physicians in Belfast, Northern Ireland, in 1966.[5] This was repeated in Toronto, Canada in 1968 using a single ambulance called Cardiac One, which was staffed by a regular ambulance crew, along with a hospital intern to perform the advanced procedures. While both of these experiments had certain levels of success, the technology had not yet reached a sufficiently advanced level to be fully effective; for example, the Toronto portable defibrillator and heart monitor was powered by lead-acid car batteries, and weighed around 45 kilograms (99 lb).

Paramedics caring for a collapsed woman in New York

In 1966 a report called Accidental Death and Disability: The Neglected Disease of Modern Societycommonly known as The White Paperwas published in the United States. This paper presented data showing that soldiers who were seriously wounded on the battlefields during the Vietnam War had a better survival rate than individuals who were seriously injured in motor vehicle accidents on California's freeways.[6] Key factors allowing the victim to survive the journey to definitive care such as a hospital were stated to be comprehensive trauma care, rapid transport to designated trauma facilities, and the presence of medical corpsman who were trained to perform certain critical advanced medical procedures such as fluid replacement and airway management. As a result of the The White Paper the Federal government moved to develop minimum standards for ambulance attendant training, ambulance equipment and vehicle design. These new standards were incorporated into Federal Highway Safety legislation and the state were advised to either adopt these standards into state laws or risk a reduction in Federal highway safety fundings. The "White Paper" also prompted the inception of of a number of emergency medical service (EMS)pilot units across the US including paramedic programs. The success of these units led to a rapid transition to make them fully operational, with the first paramedic program being in Miami, Florida. New York City's Saint Vincent's Hospital developed America's first Mobile Coronary Care Unit (MCCU) under the medical direction of William Grace, MD and was based on Dr. Frank Pantridge's Belfast, Northern Ireland MCCU project. In 1967 Eugene Nagle, MD and Jim Hirschmann, MD helped pioneer America's first EKG telemetry transmission to a hospital and then in 1968, a functional paramedic program in conjunction with the City of Miami Fire Department. In 1969. the City of Columbus Fire Services joined together with the Ohio State University Medical Center and developed the "HEARTMOBILE" paramedic program under the medical direction of James Warren, MD and Richard Lewis, MD. In 1969. the Haywood County (NC) Volunteer Rescue Squad developed a paramedic program under the medical direction of Ralph Fleicher, MD. In 1969, the initial Los Angeles paramedic training program was instituted in conjunction with Harbor General Hospital under the medical direction of Michael Criley, MD and James Lewis, MD. In 1969, the Seattle "Medic 1" paramedic program was developed in conjunction with the Harborview Medical Center under the medical direction of Leonard, Cobb. The Marietta (GA) initial paramedic project was instituted in the Fall of 1970 in conjunction

with Kennestone Hospital and Metro Ambulance Service, Inc. under the medical direction of Luther Fortson, MD. The Los Angeles county and city established paramedic programs following the passage of The Wedworth-Townsend Act in 1970. This was followed by other cities and states passing their own paramedic bills, leading to the formation of services across the US. Many other countries also followed suit, with paramedic units quickly being formed around the world.

In the military, however, the required telemetry and miniaturization technologies were more advanced, particularly due to initiatives such as the space program, but it would take several more years before these technologies drifted through to civilian applications. In North America, physicians were judged to be too expensive to be used in the pre-hospital setting, although such initiatives were implemented, and sometimes still operate, in European countries and Latin America.

[edit] Public notability

While doing background research at Los Angeles' UCLA Harbor Medical Center for a proposed new show about doctors, television producer Robert A. Cinader, working for Jack Webb, happened to encounter "firemen who spoke like doctors and worked with them".[citation needed] This concept developed into the television series Emergency!, which ran from 1972 to 1979, portraying the exploits of this new profession called paramedics. The show gained popularity with emergency services personnel, the medical community, and the general public. When the show first aired in 1972, there were just six paramedic units operating in three pilot programs in the whole of the US, and the term paramedic was essentially unknown. By the time the program ended in 1979, there were paramedics operating in all fifty states. The show's technical advisor, James O. Page, was a pioneer of paramedicine and responsible for the UCLA paramedic program; he would go on to help establish paramedic programs throughout the US, and was the founding publisher of the Journal of Emergency Medical Services (JEMS). The JEMS magazine creation resulted from Page's previous purchase of the "PARAMEDICS International" magazine.
[edit] Evolution and growth

Throughout the 1970s and 80s, the paramedic field continued to evolve, with a shift in emphasis from patient transport to treatment both on scene and en-route to hospitals. This led to some services changing their descriptions from "ambulance services" to "emergency medical services".

Bicycle paramedics in Los Angeles indicate the changing nature of the job

The training, knowledge-base, and skill sets of both paramedics and emergency medical technicians (EMTs) were typically determined by local medical directors, what it was felt the community needed, and what was affordable. There were also large differences between localities in the amount and type of training required, and how it would be provided. This ranged from in-service training in local systems, through community colleges, and up to university level education. This emphasis on increasing qualifications has followed the progression of other health professions such as nursing, which also progressed from on the job training to university level qualifications. The variations in educational approaches and standards required for paramedics has led to large differences in the required qualifications between locationsboth within individual countries and from country to country. This has led to many countries passing laws to protect the title of "paramedic" (or its local equivalent) from use by anyone except those qualified and experienced to a defined standard. This usually means that paramedics must be registered with the appropriate body in their country, for example all paramedics in the United Kingdom must by registered with the Health Professions Council in order to call themselves a paramedic. In the United States, a similar system is operated by the National Registry of Emergency Medical Technicians (NREMT), although this is only accepted by forty of the fifty states. As paramedicine has evolved a great deal of both the curriculum and skill set has existed in a state of flux. Requirements often originated and evolved at the local level, and were based upon the preferences of physician advisers and medical directors. Recommended treatments would change regularly, often changing more like a fashion than a scientific discipline. Associated technologies also rapidly evolved and changed, with medical equipment manufacturers having to adapt equipment that worked adequately the hospital environment to be able to cope with the less controlled pre-hospital environment. Physicians began to take more interest in paramedics from a research perspective as well. By about 1990, the fluctuating trends began to diminish, being replaced by outcomes-based research. This research then drove further evolution of the practice of both paramedics and the

emergency physicians who oversaw their work, with changes to procedures and protocols occurring only after significant research demonstrated their need and effectiveness. Such changes affected everything from simple procedures, such as CPR, to changes in drug protocols. As the profession grew, some paramedics went on to become not just research participants, but researchers in their own right, with their own projects and journal publications. Changes in procedures also included the manner in which the work of paramedics was overseen and managed. In the early days medical control and oversight was direct and immediate, with paramedics calling into a local hospital and receiving orders for every individual procedure or drug. While this still occurs in some jurisdictions, it has become increasingly rare, with physicians building an increasing confidence and trust in the work of paramedics. Day-to-day operations largely moved from direct and immediate medical control to pre-written protocols or standing orders, with the paramedic typically seeking advice after the options in the standing orders had been exhausted. [edit] Canada

First responders from St. John Ambulance and local fire departments assist paramedics during an exercise in Canada

While the evolution of paramedicine described above is focussed largely on the US, many other countries followed a similar pattern, although often with significant variations. Canada, for example, attempted a pilot paramedic training program at Queen's University, Kingston, Ontario, in 1972. The program, which intended to upgrade the then mandatory 160 hours of training for ambulance attendants, was found to be too costly and premature. The program was abandoned after two years, and it was more than a decade before the legislative authority for its graduates to practice was put into place. An alternative program which provided 1,400 hours of training at the community college level prior to commencing employment was then tried, and made mandatory in 1977, with formal certification examinations being introduced in 1978. Similar programs occurred at roughly the same time in Alberta and British Columbia, with other Canadian provinces gradually following, but with their own education and certification requirements. Advanced Care Paramedics were not introduced until 1984, when Toronto trained its first group internally, before the process spread across the country. By 2010 the Ontario system involved a two year community college based program, including both hospital and field clinical components, prior to designation as a Primary Care Paramedic, although it is starting to head

towards a university degree-based program. Some services, such as Toronto EMS, continue to train advnaced care paramedics internally. [edit] United Kingdom In the United Kingdom, ambulances became largely municipal services shortly after the end of World War II. Training was frequently conducted internally, although national levels of coordination led to more standardization of staff training. As of 2010 public ambulance services were operated by regional entities, most often trusts, under the authority of the National Health Service, with significant standardization of training and skills. The UK model utilizes two levels of ambulance staff, internally trained Ambulance Technicians, which are similar to EMTs in the US, and paramedics with advanced life support skills. Initially paramedics were mainly trained internally, with experienced ambulance technicians often progressing to the role of paramedic. Increasingly, however, university qualifications are being expected for paramedics, with the entry level being an Honours Bachelor of Science degree in Pre-Hospital or Paramedic Care. Some British paramedics have gone on to become Paramedic Practitioners, a role that practices independently in the pre-hospital environment in a capacity similar to that of a nurse practitioner, but with more of an acute care orientation.
[edit] Current practice

Paramedicine continues to grow and evolve into a formal profession in its own right, complete with its own standards and body of knowledge, and in many locations paramedics have formed their own professional bodies. The early technicians with limited training, performing a small and specific set of procedures, has become a profession requiring a university qualification in countries such as Australia, South Africa, and the UK, and increasingly so in the US and Canada. In some locations paramedics are evolving into a second tier medical practitioner and being granted the legal status of self-regulated health professionals. This requires them to meet set standards of education and proficiency, deals with complaints regarding individual practitioners, and will usually involve government regulation.

[edit] Structure of employment

See also: Paramedics by country

Firefighter paramedics assist a simulated burn victim during a US Navy mass casualty drill

Paramedics are employed by a variety of different organizations, and the services provided by paramedics may occur under differing organizational structures, depending on the part of the world. A new and evolving role for paramedics involves the expansion of their practice into the provision of relatively basic primary health care and assessment services. Some paramedics have begun to specialize their practice, frequently in association with the environment in which they will work. Some early examples of this involved aviation medicine

and the use of helicopters, and the transfer of critical care patients between facilities. While some jurisdictions still use physicians, nurses, and technicians for transporting patients, increasingly this role falls to specialized senior and experienced paramedics. Other areas of specialization include such roles as tactical paramedics working in police units, marine paramedics, hazardous materials (Hazmat) teams, Heavy Urban Search and Rescue, and paramedics on offshore oil platforms, oil and mineral exploration teams, and in the military. The majority of paramedics are employed by the municipal emergency medical service for their area, although this employer could be itself be working under a number of models, including a specific autonomous public ambulance service, a fire department, a hospital based service or a private company working under contract. There are also legions of paramedics who volunteer for backcountry rescue teams, small town rescue squads, and the like. The provision of municipal ambulance services, and paramedics, can vary by area, even within the same country or state. For instance, in Canada, the province of British Columbia operates a province-wide service (the British Columbia Ambulance Service) whereas in Ontario, the service is provided by each municipality, either as a disctinct service, linked to the fire brigade, or contracted out to a third party.

[edit] Paramedic skills

[edit] Common skills

While there are varying degrees of training and expectations around the world, a general set of skills shared by essentially all paramedics and EMTs includes:

Spinal injury management, including immobilization and safe transport Fracture management, including assessment, splinting, and use of traction splints where appropriate Obstetrics, including assessment, assisting with uncomplicated childbirth, and recognition of and procedures for obstetrical emergencies such as breech presentation, cord presentation, and placental abruption Management of burns, including classification, estimate of surface area, recognition of more serious burns, and treatment Triage of patients in a mass casualty incident Assessment and evaluation of general incident scene safety Effective verbal and written reporting skills (charting) Routine medical equipment maintenance procedures Routine radio operating procedures Emergency vehicle operation

[edit] Medications administered

Paramedics in most jurisdictions administer a variety of emergency medications. The specific medications they are permitted to administer vary widely, based on local standards of care and legal restrictions, and physician or medical director preferences. For an accurate description of

permitted drugs or procedures in a given location, it is necessary to contact that jurisdiction directly. A representative list of medications may commonly include:

A paramedic preparing an intravenous infusion for a patient

Analgesic medications such as aspirin, ketorolac, paracetamol and Tylenol used to relieve pain or decrease nausea and vomiting Narcotics like morphine, pethidine, fentanyl, and dilaudid, used to treat severe pain, such as with burns and fractures Adenosine, calcium channel blockers Diltiazem and Verapamil used to slow down excessively high heart rates Parasympatholytic drug such as Atropine, used to speed up slow bradycardia heart rates Sympathomimetics such as dopamine, dobutamine used for severe hypotension (low blood pressure) and cardiogenic shock D50W (a solution of 50% dextrose in water), used to treat hypoglycemia (low blood sugar) Sedatives like midazolam, lorazepam, and etomidate, used to reduce the irritability or agitation of patients Paralytics such as succinylcholine, rocuronium, and vecuronium, used when an emergency procedure such as rapid sequence induction (RSI) is required Antipsychotics like haloperidol or ziprasidone, used to sedate combative patients Respiratory medications such as salbutamol, Ipratropium bromide and methylprednisolone, used to treat conditions such as asthma and acute bronchitis Cardiac medications such as nitroglycerin, aspirin, and morphine, fentanyl used to treat cardiac ailments such as angina and heart attacks Antiarrhythmics such as amiodarone, lidocaine and magnesium sulfate used to treat cardiac arrhythmias such as ventricular tachycardia and ventricular fibrillation Ondansetron used for nausea and vomiting Naloxone used to treat opioid drug overdose

[edit] Skills by certification level

As described above, many jurisdictions have different levels of paramedic training, leading to variations in what procedures different paramedics may perform depending upon their qualifications. Three common general divisions of paramedic training are the basic technician, general paramedic or advanced technician, and advanced paramedic. Common skills that these

three certification levels may practice are summarized in the table below. The skills for the higher levels automatically also assume those listed for lower levels.
Treatment issue Common technician skills Paramedic/advanced technician skills Tracheal intubation, and sometimes nasopharyngeal intubation, advanced airway management, ETT, LMA, and combitube, deep suctioning, use of Magill forceps Pulse oximetry, active oxygen administration by endotracheal tube or other device using BVM, side stream, or inline end tidal carbon dioxide, capnography Advanced paramedic skills Rapid sequence induction, surgical airway procedures including needle cricothyrotomy and surgical cricothyrotomy

Airway Assessment, manual management repositioning, oropharyngeal and nasopharyngeal airway adjuncts, manual removal of obstructions, suctioning

Breathing

Assessment (rate, effort, symmetry, skin color), obstructed airway maneuver, passive oxygen administration by nasal canula, rebreathing and nonrebreathing mask, active oxygen administration by bag valve mask (BVM) Assessment of pulse (rate, rhythm, volume), blood pressure, skin color, and capillary refill, patient positioning to enhance circulation, recognition and control of hemorrhage of all types using direct and indirect pressure, tourniquets, and obtaining intravenous access

Use of mechanical transport ventilators, active oxygen administration by surgical airway, decompression of chest cavity using needle or valve device (needle thoracotomy)

Circulation

Ability to interpret assessment findings in terms of levels of perfusion, intravenous fluid replacement, use of vasoconstriction drugs

Intravenous plasma volume expanders, blood transfusion, intraosseous (IO) cannulation (placement of needle into marrow space of a large bone), central venous access (using central venous catheter by way of external jugular or subclavian)

Cardiac arrest Cardiopulmonary resuscitation, airway management, manual ventilation with BVM, automatic external defibrillator

Dynamic resuscitation including intubation, drug administration (includes antiarrhythmics), ECG interpretation (may be limited to three-lead), semiautomatic and/or manual

Expanded drug therapy options, ECG interpretation (twelve-lead), manual defibrillator, synchronized mechanical or chemical cardioversion, external pacing of the heart

defibrillator, cardioversion, and external cardiac pacing Cardiac Monitoring Cardiac monitoring and interpretation of ECGs Twelve-lead ECG monitoring Eighteen-lead ECG monitoring and and interpretation interpretation Intramuscular, endotracheal tube, rectal subcutaneous, intravenous tube, infusion pump injection (bolus), intravenous drip, transdermal and intraosseous Considerable expansion of permitted drugs, but still typically limited to about twenty, including analgesics (may include narcotics), antiarrhythmics, major cardiac resuscitation drugs, bronchodilators, vasoconstrictors, sedatives Significantly expanded drug list (up to sixty); in some jurisdictions advanced levels of paramedics are permitted to administer any drug, as long as they are familiar with it, and may have limited authority to prescribe

Drug Oral, nebulized, and administration intramuscular injection

Drug types permitted

Low-risk and immediate requirements, e.g., aspirin and nitroglycerin (chest pain), oral glucose and glucagon (diabetes), epinephrine (allergic reaction), salbutamol (asthma), sometimes naloxone (narcotic overdose)

Patient assessment

Basic physical assessment, More detailed physical vital signs, history of general assessment and history, auscultation, interpretation and current condition of assessment findings, ECG interpretation, glucometry, capnography, pulse oximetry

Interpretation of lab results, interpretation of chest xrays, interpretation of cranial CT scan, limited diagnosis (e.g. rule out fracture using Ottawa ankle rules), ultrasonography[7] Wound cleansing, wound closure with butterfly stitches, suturing

Wound Assessment, control of management bleeding, application of pressure dressings and other types of dressings

[edit] Medicolegal authority

The medicolegal framework for paramedics is highly dependant on the overall structure of emergency medical services in the territory where they are working.

Paramedics load an injured woman into a helicopter ambulance after a head-on collision in Canada

In places where paramedics are recognized health care professionals registered with an appropriate body, they can conduct all procedures authorised for their profession, including the administration of prescription medication, and are personally answerable to a regulator. For example, in the United Kingdom, the Health Professions Council regulates paramedics and can censure or strike a paramedic from the register. In some cases paramedics may gain further qualifications to extend their status to that of a paramedic practitioner, which provides the right to prescribe, rather than just administer, medication. In other places paramedics operate as a direct extension of a physician medical director, and practice as an extension of the medical director's license to practice medicine. The authority to practice in this semi-autonomous manner is granted in the form of standing order protocols (offline medical control), and, in some cases, direct physician consultation via phone or radio (online medical control). Under this paradigm, paramedics effectively assume the role of out-ofhospital field agents to regional emergency physicians, with independent clinical decisionmaking authority that is typically enjoyed only by expert clinicians within the hospital setting. In some locations paramedics are only permitted to practice many advanced skills while assisting a physician who is physically present, except for with immediately life-threatening emergencies.

[edit] In entertainment

Emergency! was a popular 1970s television series which centered on the work of paramedics in the Los Angeles County Fire Department, and the staff at the fictional Rampart Emergency Hospital. Emergency! has been widely credited with inspiring many municipalities in the United States to develop their own paramedic programs, and acted as an inspiration for many individuals to enter the fields of emergency medicine.[citation needed] The show rated well for its entire production run (197279), as well as in syndicated reruns, and inspired a related cartoon series. Mother, Jugs & Speed is a 1976 comedy film, starring Bill Cosby, Raquel Welch, and Harvey Keitel. The film depicts a private ambulance company struggling to survive in Los Angeles, and gives an indication of the state of the ambulance industry just prior to its increased professionalism. Trauma Center is a 1983 American television medical drama focussing on the McKee Hospital Trauma Center, and two paramedics who had to rescue or save injured people before delivering them to the trauma center.

Casualty is a long-running British BBC television series (1986present), depicting the fictional Holby City Hospital's Accident and Emergency Department, and the related paramedics. Casualty has inspired the spin-off series, Holby City, and a number of made-for-television films. Paramedics is a 1988 American comedy film focussing on a group of paramedics in a US city. Paramedic: On the Front Lines of Medicine, is a 1988 autobiographical account of a paramedic's first year on the job by Peter Canning. A sequel, Rescue 471: A Paramedic's Stories was released in 2000. Bringing Out the Dead is a 1999 American drama film, directed by Martin Scorsese and starring Nicolas Cage, showing forty-eight hours in the life of a burnt-out paramedic in New York's Hell's Kitchen. The film is based on the novel of the same name by Joe Connelly, a former New York City paramedic. Paramedics is an American reality television show that originally screened from 1999 to 2001, and now runs intermittently on the Discovery Health Channel. The show features the life and work of emergency medical squads in major urban centers in the United States. Third Watch (19992005) is an American television drama, parts of which focussed on the firefighters and paramedics of the New York City Fire Department. Into the Breach: A Year of Life and Death with EMS is a 2002 book written by J. A. Karam, focussing on real-life stories of paramedics, emergency medical technicians, and heavy-rescue specialists fighting to control trauma and medical emergencies. Saved is a 2006 medical television drama centered on a fictional paramedic, his partner, and their chaotic lives on and off the job. Black Flies is a 2008 American novel written by Shannon Burke, based on his experiences working as a paramedic in Harlem, New York. Trauma is a 200910 American television drama series focussing on a group of San Francisco Fire Department paramedics working in conjunction with the fictional trauma center of San Francisco City Hospital.

Denise Sherwood, from "Army Wives" was a paramedic, having been a nurse beforehand and a 911 dispatcher later on.

Life support Life support

From Wikipedia, the free encyclopedia

Jump to: navigation, search This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (April 2008) For other uses of "life support", see Life support (disambiguation) Life support, in medicine is a broad term that applies to any therapy used to sustain a patient's life while they are critically ill or injured. There are many therapies and techniques that may be used by clinicians to achieve the goal of sustaining life. Some examples include:

Feeding tubes Inotropes

Total parenteral nutrition Mechanical ventilation Heart/Lung bypass Urinary catheterization Dialysis Cardiopulmonary resuscitation Defibrillation Artificial pacemaker

These techniques are applied most commonly in the Emergency Department, Intensive Care Unit and, Operating Rooms. As various life support technologies have improved and evolved they are used increasingly outside of the hospital environment. For example a patient who requires a ventilator for survival are commonly discharged home with these devices. Another example includes the now ubiquitous presence of Automated external defibrillator in public venues which allow lay people to deliver life support in a prehospital environment. The ultimate goals of life support depend on the specific patient situation. Typically life support is used to sustain life while the underlying injury or illness is being treated or evaluated for prognosis. Life support techniques may also be used indefinitely if the underlying medical condition cannot be corrected but a reasonable quality of life can still be expected.

General anaesthesia General anaesthesia

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Jump to: navigation, search

General anaesthesia
Intervention

MeSH

D000768

General anaesthesia (or general anesthesia) is a state of unconsciousness and loss of protective reflexes resulting from the administration of one or more general anaesthetic agents. A variety of medications may be administered, with the overall aim of ensuring hypnosis, amnesia, analgesia, relaxation of skeletal muscles, and loss of control of reflexes of the autonomic nervous system. The optimal combination of these agents for any given patient and procedure is typically selected by an anaesthesiologist or another provider such as an anaesthesiologist assistant or nurse anaesthetist, in consultation with the patient and the medical or dental practitioner performing the operative procedure.

Contents
[hide]

1 History 2 Purpose 3 Biochemical mechanism of action 4 Preanaesthetic evaluation 5 Premedication 6 Stages of anaesthesia 7 Induction o 7.1 Physiologic monitoring o 7.2 Airway management o 7.3 Neuromuscular blockade 8 Maintenance 9 Emergence 10 Postoperative care 11 Perioperative mortality 12 See also 13 References 14 External links

[edit] History
Main article: History of general anesthesia Further information: History of tracheal intubation

[edit] Purpose
General anaesthesia has many purposes including: 1. 2. 3. 4. 5. Analgesia loss of response to pain, Amnesia loss of memory, Immobility loss of motor reflexes, Hypnosis loss of consciousness, Skeletal muscle relaxation.

[edit] Biochemical mechanism of action

The biochemical mechanism of action of general anaesthetics is not yet well understood. To induce unconsciousness, anaesthetics affect the GABA and NMDA systems. For example, halothane is a GABA agonist,[1] and ketamine is an NMDA receptor antagonist.[2]

[edit] Preanaesthetic evaluation

Prior to planned operation or procedure, the anaesthetist reviews the medical record and/or interviews the patient to determine the best combination of drugs and dosages and the degree to which monitoring will be required to ensure a safe and effective procedure. Key factors of this evaluation are the patient's age, body mass index, medical and surgical history, current medications, and fasting time. Thorough and accurate answering of the questions is important so that the anaesthetist can select the proper anaesthetic drugs and procedures. For example, a patient who consumes significant quantities of alcohol or illicit drugs could be undermedicated if s/he fails to disclose this fact. This in turn could then lead to anaesthesia awareness or dangerously high blood pressure.[citation needed] Commonly used medications (e.g., sildenafil) can interact with anaesthesia drugs; failure to disclose such usage can also increase the risk to the patient.[citation needed] There are some situations (where patients are on a certain medication and must undergo a given procedure) in which local anaesthesia or regional anaesthesia can be given, but instead general anaesthesia is chosen, though this is not extremely common due to the fact that general anaesthesia is by nature more dangerous and the agents used react with many more medications. An important aspect of the preanaesthetic evaluation is that of the patient's airway, involving inspection of the mouth opening and visualisation of the soft tissues of the pharynx. The condition of teeth and location of dental crowns and caps are checked, neck flexibility and head extension observed. If a tracheal tube is indicated and airway management is deemed difficult, then alternative methods of tracheal intubation, such as fibreoptic intubation, may be required as part of the anaesthetic management.

[edit] Premedication
Anaesthesiologists may prescribe or administer a premedication prior to administration of a general anaesthetic. Anaesthetic premedication consists of a drug or combination of drugs that serve to complement or otherwise improve the quality of the anaesthetic. One example of this is the preoperative administration of clonidine, an alpha-2 adrenergic agonist. Clonidine premedication reduces the need for anaesthetic induction agents[citation needed], as well as the need for volatile anaesthetic agents during maintenance of general anaesthesia,[citation needed] and the need for postoperative analgesics.[citation needed] Clonidine premedication also reduces postoperative shivering[citation needed], postoperative nausea and vomiting and emergence delirium.[citation needed] In children, clonidine premedication is at least as effective as benzodiazepines, in addition to having a more favourable side effect profile.[citation needed] It also reduces the incidence of post-operative delirium associated with sevoflurane anaesthesia.[citation needed] As a result clonidine has become a popular agent for anaesthetic premedication.[3][4] Drawbacks of oral clonidine include the fact that it can take up to 45 minutes to take full effect,[5] hypotension and bradycardia.[citation needed] Midazolam, a benzodiazepine characterized by a rapid onset and short duration relative to other benzodiazepines, is effective in reducing preoperative anxiety, including separation anxiety

associated with separation of children from their parents and induction of anaesthesia.[6] Dexmedetomidine and certain atypical antipsychotic agents are other drugs that are used in particular in very uncooperative children.[7] Melatonin has been found to be effective as an anaesthetic premedication in both adults and children due to its hypnotic, anxiolytic, sedative, antinociceptive, and anticonvulsant properties. Unlike midazolam, melatonin does not impair psychomotor skills or adversely affect the quality of recovery. Recovery is more rapid after melatonin premedication than with midazolam, and there is also a reduced incidence of post-operative agitation and delirium.[8] Melatonin premedication also reduces the required induction dose of propofol and thiopental.[8] Another example of anaesthetic premedication is the preoperative administration of beta adrenergic antagonists to reduce the incidence of postoperative hypertension, cardiac dysrhythmia or myocardial infarction.[citation needed] One may choose to administer an antiemetic agent such as droperidol or dexamethasone to reduce the incidence of postoperative nausea and vomiting,[citation needed] or subcutaneous heparin or enoxaparin to reduce the incidence of deep vein thrombosis.[citation needed] Other commonly used premedication agents include opioids such as fentanyl or sufentanil, gastrokinetic agents such as metoclopramide, and histamine antagonists such as famotidine. Non-pharmacologic preanaesthetic interventions include playing relaxing music, massage, and reducing ambient light and noise levels in order to maintain the sleep-wake cycle.[9] These techniques are particularly useful for paediatric and mentally retarded patients. Other options for children who refuse or cannot tolerate pharmacologic premedication include interventions by clowns and child life specialists. Minimizing sensory stimulation or distraction by video games may also help to reduce anxiety prior to or during induction of general anaesthesia.[10]

[edit] Stages of anaesthesia

The four stages of anaesthesia were described in 1937.[11] Despite newer anaesthetic agents and delivery techniques, which have led to more rapid onset and recovery from anaesthesia, with greater safety margins, the principles remain. Stage 1 Stage 1 anaesthesia, also known as the "induction", is the period between the initial administration of the induction agents and loss of consciousness. During this stage, the patient progresses from analgesia without amnesia to analgesia with amnesia. Patients can carry on a conversation at this time. Stage 2 Stage 2 anaesthesia, also known as the "excitement stage", is the period following loss of consciousness and marked by excited and delirious activity. During this stage, respirations and heart rate may become irregular. In addition, there may be uncontrolled movements, vomiting, breath holding, and pupillary dilation. Since the combination of spastic movements, vomiting, and irregular respirations may lead to airway compromise, rapidly acting drugs are used to minimize time in this stage and reach stage 3 as fast as possible.

Stage 3 Stage 3, "surgical anaesthesia". During this stage, the skeletal muscles relax, and the patient's breathing becomes regular. Eye movements slow, then stop, and surgery can begin. It has been divided into 4 planes: 1. 2. 3. 4. eyes initially rolling, then becoming fixed loss of corneal and laryngeal reflexes pupils dilate and loss of light reflex intercostal paralysis, shallow abdominal respiration, dilated pupils

Stage 4 Stage 4 anaesthesia, also known as "overdose", is the stage where too much medication has been given relative to the amount of surgical stimulation and the patient has severe brain stem or medullary depression. This results in a cessation of respiration and potential cardiovascular collapse. This stage is lethal without cardiovascular and respiratory support.

[edit] Induction
Induction of general anaesthesia is usually conducted in a medical facility, most commonly in an operating room. However, general anaesthesia may also be conducted in many other locations, such as an endoscopy suite, radiology or cardiology department, emergency department, ambulance, or at the site of a disaster where extrication of the patient may be impossible or impractical. Anaesthetic agents may be administered by various routes, including inhalation, injection (intravenous, intramuscular or subcutaneous), oral, and rectal. After administration by one or more of these routes, the agents gain access to the blood. Once in the circulatory system, they are transported to their biochemical sites of action in the central and autonomic nervous systems, where they exert their pharmacologic effects. Most general anaesthetics today are induced either with a needle, by intravenous injection, or by breathing a volatile anaesthetic through an anaesthetic circuit (inhalational induction). Onset of anaesthesia is faster with intravenous injection than with inhalation, taking about 1020 seconds to induce total unconsciousness.[citation needed] This has the advantage of avoiding the excitatory phase of anaesthesia (see above), and thus reduces complications related to induction of anaesthesia.[citation needed] Commonly used intravenous induction agents include propofol, sodium thiopental, etomidate, and ketamine. An inhalational induction may be chosen by the anaesthesiologist where intravenous access is difficult to obtain, where difficulty maintaining the airway is anticipated, or due to patient preference (e.g., children). Sevoflurane is currently the most commonly used agent for inhalational induction, because it is less irritating to the tracheobronchial tree than other volatile anaesthetic agents.[citation
needed]

[edit] Physiologic monitoring

Monitoring involves the use of several technologies to allow for a controlled induction of, maintenance of and emergence from general anaesthesia. 1. Continuous Electrocardiography (ECG): The placement of electrodes that monitor heart rate and rhythm. This may also help the anaesthetist to identify early signs of heart ischaemia. 2. Continuous pulse oximetry (SpO2): The placement of this device (usually on one of the fingers) allows for early detection of a fall in a patient's haemoglobin saturation with oxygen (hypoxaemia). 3. Blood Pressure Monitoring (NIBP or IBP): There are two methods of measuring the patient's blood pressure. The first, and most common, is called non-invasive blood pressure (NIBP) monitoring. This involves placing a blood pressure cuff around the patient's arm, forearm or leg. A blood pressure machine takes blood pressure readings at regular, preset intervals throughout the surgery. The second method is called invasive blood pressure (IBP) monitoring. This method is reserved for patients with significant heart or lung disease, the critically ill, major surgery such as cardiac or transplant surgery, or when large blood losses are expected. The invasive blood pressure monitoring technique involves placing a special type of plastic cannula in the patient's artery - usually at the wrist or in the groin. 4. Agent concentration measurement - Common anaesthetic machines have monitors to measure the per cent of inhalational anaesthetic agent used (e.g. sevoflurane, isoflurane, desflurane, halothane etc.). The monitors also usually measure nitrous oxide and oxygen percentages and could give a MAC level. 5. Low oxygen alarm - Almost all circuits have a backup alarm in case the oxygen delivery to the patient becomes compromised. This warns if the fraction of inspired oxygen drops lower than minimum alarm setting and allows the anaesthetist to take immediate remedial action. 6. Circuit disconnect alarm or low pressure alarm indicates failure of circuit to achieve a given pressure during mechanical ventilation. 7. Carbon dioxide measurement (capnography)- measures the amount of carbon dioxide expired by the patient's lungs in per cent or mmHg, mmHg is usually used to allow the anaesthesia provider to see more subtle changes in CO2. It allows the anaesthetist to assess the adequacy of ventilation 8. Temperature measurement to discern hypothermia or fever, and to aid early detection of malignant hyperthermia. 9. EEG or other system to verify depth of anaesthesia may also be used. This reduces the likelihood that a patient will be mentally awake, although unable to move because of the paralytic agents. It also reduces the likelihood of a patient receiving significantly more amnesic drugs than actually necessary to do the job.

[edit] Airway management

With the loss of consciousness caused by general anaesthesia, there is loss of protective airway reflexes (such as coughing), loss of airway patency and sometimes loss of a regular breathing pattern due to the effect of anaesthetics, opioids, or muscle relaxants. To maintain an open airway and regulate breathing within acceptable parameters, some form of "breathing tube" is inserted in the airway after the patient is unconscious. To enable mechanical ventilation, an endotracheal tube is often used (intubation), although there are alternative devices such as face masks or laryngeal mask airways.

[edit] Neuromuscular blockade

"Paralysis" or temporary muscle relaxation with a neuromuscular blocker is an integral part of modern anaesthesia. The first drug used for this purpose was curare, introduced in the 1940s, which has now been superseded by drugs with fewer side effects and generally shorter duration of action. Muscle relaxation allows surgery within major body cavities, e.g. abdomen and thorax without the need for very deep anaesthesia, and is also used to facilitate endotracheal intubation. Acetylcholine, the natural neurotransmitter substance at the neuromuscular junction, causes muscles to contract when it is released from nerve endings. Muscle relaxants work by preventing acetylcholine from attaching to its receptor. Paralysis of the muscles of respiration, i.e. the diaphragm and intercostal muscles of the chest requires that some form of artificial respiration be implemented. As the muscles of the larynx are also paralysed, the airway usually needs to be protected by means of an endotracheal tube. Monitoring of paralysis is most easily provided by means of a peripheral nerve stimulator. This device intermittently sends short electrical pulses through the skin over a peripheral nerve while the contraction of a muscle supplied by that nerve is observed. The effects of muscle relaxants are commonly reversed at the termination of surgery by anticholinesterase drugs. Examples of skeletal muscle relaxants in use today are pancuronium, rocuronium, vecuronium, atracurium, mivacurium, and succinylcholine.

[edit] Maintenance
This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (September 2010) The duration of action of intravenous induction agents is in general 5 to 10 minutes, after which time spontaneous recovery of consciousness will occur. In order to prolong anaesthesia for the required duration (usually the duration of surgery), anaesthesia must be maintained. Usually this is achieved by allowing the patient to breathe a carefully controlled mixture of oxygen, nitrous oxide, and

a volatile anaesthetic agent or by having a carefully controlled infusion of medication, usually propofol, through an intravenous catheter. The inhalation agents are transferred to the patient's brain via the lungs and the bloodstream, and the patient remains unconscious. Inhaled agents are frequently supplemented by intravenous anaesthetics, such as opioids (usually fentanyl or a fentanyl derivative) and sedative-hypnotics (usually propofol or midazolam), though, for a propofol-based anaesthetic, supplementation by inhalation agents is not required. At the end of surgery, the volatile or intravenous anaesthetic is discontinued. Recovery of consciousness occurs when the concentration of anaesthetic in the brain drops below a certain level (usually within 1 to 30 minutes, depending upon the duration of surgery). In the 1990s, a novel method of maintaining anaesthesia was developed in Glasgow, UK. Called TCI (target controlled infusion), this involves using a computer-controlled syringe driver (pump) to infuse propofol throughout the duration of surgery, removing the need for a volatile anaesthetic, and allowing pharmacologic principles to more precisely guide the amount of infusion of the drug. Purported advantages include faster recovery from anaesthesia, reduced incidence of post-operative nausea and vomiting, and absence of a trigger for malignant hyperthermia. At present, TCI is not permitted in the United States.[citation needed] Other medications will occasionally be given to anaesthetized patients to treat side-effects or prevent complications. These medications include antihypertensives to treat high blood pressure, drugs like ephedrine and phenylephrine to treat low blood pressure, drugs like salbutamol to treat asthma or laryngospasm/bronchospasm, and drugs like epinephrine or diphenhydramine to treat allergic reactions. Sometimes glucocorticoids or antibiotics are given to prevent inflammation and infection, respectively.

[edit] Emergence
Emergence is the process of return to baseline physiologic function of all organ systems after the cessation of administration of general anaesthetic agent(s). This stage of general anaesthesia may be accompanied by certain unusual but temporary neurologic phenomena, such as delirium (acute mental confusion), aphasia (impaired production or comprehension of speech), or focal impairment in sensory or motor function. Shivering is also fairly common and can be clinically significant since it results in an increase in oxygen consumption, carbon dioxide production, cardiac output, heart rate, and systemic blood pressure. The proposed mechanism is based on the observation that the spinal cord recovers at a faster rate than the brain. This results in uninhibited spinal reflexes manifested as clonic activity (shivering). This theory is supported by the fact that doxapram, a CNS stimulant, is somewhat effective in abolishing postoperative shivering.[12] Cardiovascular events such as increased or decreased blood pressure, rapid heart rate or other cardiac dysrhythmias are also common during emergence from general anaesthesia, as are respiratory symptoms such as dyspnoea.

[edit] Postoperative care

This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (September 2010) The anaesthesia should conclude with a pain-free awakening and a management plan for postoperative pain relief. This may be in the form of regional analgesia, oral, transdermal, or parenteral medication. Minor surgical procedures are amenable to oral pain relief medications such as paracetamol and NSAIDs such as ibuprofen. Moderate levels of pain require the addition of mild opiates such as tramadol. Major surgical procedures may require a combination of modalities to confer adequate pain relief. Parenteral methods include patient-controlled analgesia (PCA) involving a strong opiate such as morphine, fentanyl, or oxycodone. Here, to activate a syringe device, the patient presses a button and receives a preset dose or "bolus" of the drug (e.g., one milligram of morphine). The PCA device then "locks out" for a preset period, e.g. 5 minutes, to allow the drug to take effect. If the patient becomes too sleepy or sedated, he or she make no more morphine requests. This confers a fail-safe aspect that is lacking in continuous-opiate infusion techniques. Shivering is a frequent occurrence in the post-operative period. Apart from causing discomfort and exacerbating postoperative pain, shivering has been shown to increase oxygen consumption, catecholamine release, cardiac output, heart rate, blood pressure, and intra-ocular pressure. There is a number of techniques used to reduce this occurrence, such as increasing the ambient temperature in theatre, using conventional or forced warm air blankets, and using warmed intravenous fluids.[13] In many cases, opioids used in general anaesthesia can cause post-operative ileus even in non-abdominal surgery. Administration of a -opioid antagonist such as alvimopan immediately after recovery can help reduce the severity and duration of ileus.[14]

[edit] Perioperative mortality

Main article: Perioperative mortality Most perioperative mortality is attributable to complications from the operation (such as haemorrhage, sepsis, and failure of vital organs. This also may include memory loss or slowing down of the thought processes) or pre-existing medical conditions.[citation needed] Most current estimates of perioperative mortality range from 1 death in 53 anaesthetics to 1 in 5,417 anaesthetics.[15][16] However, a 1997 Canadian retrospective review of 2,830,000 oral surgical procedures in Ontario between 19731995 reported only four deaths in cases in which either an oral and maxillofacial surgeon or a dentist with specialized training in anaesthesia administered the general anaesthetic or deep sedation. The authors calculated an

overall mortality rate of 1.4 per 1,000,000.[17] The largest and most recent study of postoperative mortality was published in 2010. In this review of 3.7 million elective open surgical procedures performed on inpatients at 102 hospitals in the Netherlands during 19912005, postoperative mortality from all causes was observed in 67,879 patients, for an overall rate of 1.85%.[18] The wide disparity between the results of these studies may be the result of differences in operational definitions and reporting sources.[15] Mortality directly related to anaesthetic management is significantly less common, and may include such causes as pulmonary aspiration of gastric contents,[19] asphyxiation[20] and anaphylaxis.[21] These in turn may result from malfunction of anaesthesia-related equipment or more commonly, human error. A 1978 study found that 82% of preventable anaesthesia mishaps were the result of human error.[22] In a 1954 review of 599,548 surgical procedures at 10 hospitals in the United States between 19481952, 384 deaths were attributed to anaesthesia, for an overall mortality rate of 0.064%.[23] In 1984, after a television programme highlighting anaesthesia mishaps aired in the United States, American anaesthesiologist Ellison C. Pierce appointed a committee called the Anesthesia Patient Safety and Risk Management Committee of the American Society of Anesthesiologists.[24] This committee was tasked with determining and reducing the causes of peri-anaesthetic morbidity and mortality.[24] An outgrowth of this committee, the Anesthesia Patient Safety Foundation was created in 1985 as an independent, nonprofit corporation with the vision that "that no patient shall be harmed by anesthesia".[25] As with perioperative mortality rates in general, the current mortality attributable to the management of general anaesthesia is controversial.[26] The incidence of perioperative mortality that is directly attributable to anaesthesia ranges from 1 in 6,795 to 1 in 200,200 anaesthetics.[15

Laryngoscope Laryngoscopy
From Wikipedia, the free encyclopedia (Redirected from Laryngoscope) Jump to: navigation, search

Laryngoscopy
Intervention

View of the glottis as seen during laryngoscopy

ICD-9-CM

31.42

MeSH

D007828

OPS-301 code:

1-610

Laryngoscopy (larynx + scopy) is a medical procedure that is used to obtain a view of the vocal folds and the glottis. Laryngoscopy may be performed to facilitate tracheal intubation during general anesthesia or cardiopulmonary resuscitation or for procedures on the larynx or other parts of the upper tracheobronchial tree. Direct laryngoscopy is carried out (usually) with the patient lying on his or her back; the laryngoscope is inserted into the mouth on the right side and flipped to the left to trap and move the tongue out of the line of sight, and, depending on the type of blade used, inserted either anterior or posterior to the epiglottis and then lifted with an upwards and forward motion ("away from you and towards the roof "). This move makes a view of the glottis possible. There are at least ten different types of laryngoscope used for this procedure, each of which has a specialized use for the otolaryngologist. This procedure is most often employed in direct diagnostic laryngoscopy with biopsy. It is extremely uncomfortable and is not typically performed on conscious patients, or on patients with an intact gag reflex. Another type of procedure performed by many ENT specialists in clinics is referred to as indirect laryngoscopy. It utilizes a straight rod-mounted mirror (laryngeal mirror; vide Instruments used in otolaryngology) that is inserted into the throat and used to look at the laryngeal inlet.

Contents
[hide]

1 History

2 Applications 3 Conventional laryngoscope o 3.1 Laryngoscope blades 4 Fiberoptic laryngoscopes 5 Video laryngoscope o 5.1 Glidescope o 5.2 Other video laryngoscopes 6 Other noninvasive intubation devices 7 References 8 External links

[edit] History
See also: Tracheal intubation

The laryngoscopy. From Garca, 1884

Eugne Bouchut

Some historians (for example, Morell Mackenzie) credit Benjamin Guy Babington (17941866), who called his device the "glottiscope", with the invention of the laryngoscope.[1] Philipp von

Bozzini (17731809)[2][3] and Garignard de la Tour were other early physicians to use mouth mirrors to inspect the oropharynx and hypopharynx.[4] In 1854, a Spanish vocal pedagogist named Manuel Garca (18051906) became the first man to view the functioning glottis and larynx in a living human. Garca developed a tool that used two mirrors for which the Sun served as an external light source.[5][6] Using this device, he was able to observe the function of his own glottic apparatus and the uppermost portion of his trachea. He presented his findings at the Royal Society of London in 1855.[7] All previous observations of the glottis and larynx had been performed under indirect vision (using mirrors) until 23 April 1895, when Alfred Kirstein (18631922) of Germany first described direct visualization of the vocal cords. Kirstein performed the first direct laryngoscopy in Berlin, using an esophagoscope he had modified for this purpose; he called this device an autoscope.[8] It is believed that the death in 1888 of Emperor Frederick III[9] motivated Kirstein to develop the autoscope.[10] In 1913, Chevalier Jackson was the first to report a high rate of success for the use of direct laryngoscopy as a means to intubate the trachea.[11] Jackson introduced a new laryngoscope blade that had a light source at the distal tip, rather than the proximal light source used by Kirstein.[12] This new blade incorporated a component that the operator could slide out to allow room for passage of an endotracheal tube or bronchoscope.[13] That same year, Henry H. Janeway (18731921) published results he had achieved using another new laryngoscope he had recently developed.[14] An American anesthesiologist practicing at Bellevue Hospital in New York City, Janeway believed that direct intratracheal insufflation of volatile anesthetics would provide improved conditions for surgery of the nose, mouth and throat. With this in mind, he developed a laryngoscope designed for the sole purpose of tracheal intubation. Similar to Jackson's device, Janeway's instrument incorporated a distal light source. Unique however was the inclusion of batteries within the handle, a central notch in the blade for maintaining the tracheal tube in the midline of the oropharynx during intubation, and a slight curve to the distal tip of the blade to help guide the tube through the glottis. The success of this design led to its subsequent use in other types of surgery. Janeway was thus instrumental in popularizing the widespread use of direct laryngoscopy and tracheal intubation in the practice of anesthesiology.[10]

[edit] Applications

Helps in intubation during the administration of general anaesthesia or for mechanical ventilation. Detects causes of voice problems, such as breathing voice, hoarse voice, weak voice, or no voice. Detects causes of throat and ear pain. Evaluates difficulty in swallowing : a persistent sensation of lump in the throat, or mucous with blood. Detects strictures or injury to the throat, or obstructive masses in the airway.

[edit] Conventional laryngoscope

Laryngoscope handles with an assortment of Miller blades (large adult, small adult, pediatric, infant, and neonate)

Laryngoscope handle with an assortment of Macintosh blades (large adult, small adult, pediatric, infant, and neonate)

The vast majority of tracheal intubations involve the use of a viewing instrument of one type or another. Since its introduction by Kirstein in 1895,[8] the conventional laryngoscope has been the most popular device used for this purpose. Today, the conventional laryngoscope consists of a handle containing batteries with a light source, and a set of interchangeable blades.

[edit] Laryngoscope blades

Early laryngoscopes used a straight "Magill Blade", and this design is still the standard pattern veterinary laryngoscopes are based upon; however the blade is difficult to control in adult humans and can cause pressure on the vagus nerve, which can cause unexpected cardiac arrhythmias to spontaneously occur in adults. Two basic styles of laryngoscope blade are currently commercially available: the curved blade and the straight blade. The Macintosh blade is the most widely used of the curved laryngoscope blades,[15] while the Miller blade[16] is the most popular style of straight blade.[17] Both Miller and Macintosh laryngoscope blades are available in sizes 0 (neonatal) through 4 (large adult). There are many other styles of curved and straight blades (e.g., Phillips, Robertshaw, Sykes, Wisconsin, Wis-Hipple, etc.) with accessories such as mirrors for enlarging the field of view and even ports for the administration of oxygen. These specialty blades are primarily designed for use by anesthetists, most commonly in the operating room.[18] The Macintosh blade is positioned in the vallecula, anterior to the epiglottis, lifting it out of the visual pathway, while the Miller blade is positioned posterior to the epiglottis, trapping it while exposing the glottis and vocal folds. Incorrect usage can cause trauma to the front incisors; the correct technique is to displace the chin upwards and forward at the same time, not to use the blade as a lever with the teeth serving as the fulcrum. The Miller, Wisconsin, Wis-Hipple, and Robertshaw blades are commonly used for infants. It is easier to visualize the glottis using these blades than the Macintosh blade in infants, due to the larger size of the epiglottis relative to that of the glottis.
Blade Named for Year introduced 1963 Comments straight, no flange straight straight 1999 1943 1921 1941 curved reduced flange at heel curved straight straight

Cranwall[citation needed] George D. Cranton and Barry L. Wall Jackson Janeway Chevalier Jackson Henry H. Janeway

Reduced Flange (RF George D. Cranton Mac)[citation needed] Macintosh[19] Magill[20] Miller Robert Reynolds Macintosh Ivan Magill Robert A. Miller

Blade Parrott Phillips Robertshaw Siker Soper Wis-Hipple Wisconsin R.I. Soper C.M. Parrott

Named for

Year introduced 1951 1973 curved

Comments

straight straight

1956 1947

curved, with integrated mirror straight straight straight

[edit] Fiberoptic laryngoscopes

Besides the conventional laryngoscopes, many other devices have been developed as alternatives to direct laryngoscopy. These include a number of indirect fiberoptic viewing laryngoscopes such as the flexible fiberoptic bronchoscope. The flexible fiberoptic bronchoscope or rhinoscope can be used for office-based diagnostics or for tracheal intubation. The patient can remain conscious during the procedure, so that the vocal folds can be observed during phonation. Surgical instruments passed through the scope can be used for performing procedures such as biopsies of suspicious masses. These instruments have become indispensable within the otolaryngology, pulmonology and anesthesia communities. Other available fiberoptic devices include the Bullard scope,[21] UpsherScope,[22][23] and the WuScope.[24] These devices are widely employed for tracheal intubation, especially in the setting of the difficult intubation (see below).

[edit] Video laryngoscope

Glidescope video laryngoscope, showing 60-degree angulated blade. The CMOS active pixel sensor (CMOS APS) video camera and light source are located at the point of angulation of the blade. An anesthesia machine is visible on the high resolution LCD monitor.

The conventional direct laryngoscope uses a line of sight provided by a rigid viewing instrument with a light on the blade or intra-oral portion which requires a direct view of the target larynx; this view is clearly seen in 80-90% of attempts. The frequent failure of direct laryngoscopy to provide an adequate view for tracheal intubation led to the development of alternative devices such as the lighted stylet, and a number of indirect fiberoptic viewing laryngoscopes, such as the fiberscope, Bullard scope, Upsher scope, and the WuScope. Though these devices can be effective alternatives to direct laryngoscopy, they each have certain limitations, and none of them is effective under all circumstances. One important limitation commonly associated with these devices is fogging of the lens.[25] In an attempt to address some of these limitations, Dr. Jon Berall, a New York City internist and emergency medicine physician, designed the camera screen straight video laryngoscope in 1998. The Digital Revolution has brought new technology to the practice of tracheal intubation. Several manufacturers have developed video laryngoscopes which employ digital technology such as the CMOS active pixel sensor (CMOS APS) to generate a view of the glottis so that the trachea may be intubated. The Glidescope video laryngoscope is one example of such a device. Other examples include the McGrath laryngoscope, Daiken Medical Coopdech C-scope vlp-100, the Storz C-Mac, Pentax AWS, and the Berci DCI laryngoscopes.

[edit] Glidescope

Anesthesiologist using Glidescope video laryngoscope to intubate the trachea of a morbidly obese patient with challenging airway anatomy

In 2001, the Glidescope (designed by vascular and general surgeon John Allen Pacey) became the first commercially available video laryngoscope. It incorporates a high resolution digital camera, connected by a video cable to a high resolution LCD monitor. It can be used for tracheal intubation to provide controlled mechanical ventilation, as well as for removal of foreign bodies from the airway. The Glidescope owes its superior results to a combination of five key factors:
1. The steep 60-degree angulation of its blade improves the view of the glottis by reducing the requirement for anterior displacement of the tongue. 2. The CMOS APS digital camera is located at the point of angulation of the blade (rather than at the tip). This placement allows the operator to more effectively view the field in front of the camera. 3. The video camera is recessed for protection from blood and secretions which might otherwise obstruct the view. 4. The video camera has a relatively wide viewing angle of 50 degrees. 5. The heated lens innovation helps to prevent fogging of the lens, which might otherwise obscure the view.

Tracheal intubation with the GlideScope can be facilitated by the use of the Verathon Stylet, a rigid stylet that is curved to follow the 60 angulation of the blade.[26] To achieve a 99% successful rate of intubation with the GlideScope requires the operator to acquire a new skill set with this stylet. In a 2003 study, the authors noted that the GlideScope provided adequate vision of the glottis (Cormack and Lehane grade I-II) [27][28] even when the oral, pharyngeal and laryngeal axes could not be optimally aligned due to the presence of a cervical collar. Despite this significant limitation, the average time to intubate the trachea with the GlideScope was only 38 seconds.[26] In 2005, the first major clinical study comparing the Glidescope to the conventional laryngoscope was published. In 133 patients in whom both Glidescope and conventional laryngoscopy were performed, excellent or good laryngeal exposure was obtained in 124/133 (93%) of Glidescope laryngoscopy patients, compared with only 98/133 (74%) of patients in

whom conventional laryngoscopy was used. Intubation was successful in 128/133 (96%) of Glidescope laryngoscopy patients.[29] These early results suggest that this device may be a useful alternative in the management of difficult tracheal intubation. The Verathon design team later produced the Ranger Video Laryngoscope for a United States Air Force requirement that is now rolling forward into EMS and military use. The Cobalt series of Glidescopes then introduced a single use variant that encompasses weights from 1000 grams to morbid obesity and is successful in many airway syndromes as well. The Glidescope Ranger is a variant designed for use in pre-hospital airway management including air, land, and sea applications. This device weighs 1.5 pounds, and is waterproof as well as airworthy to 20,000 feet altitude. The Glidescope Cobalt is a variant that has a reusable video camera with lightemitting core which has a disposable or single use external shell for prevention of cross infection. In August 2009, the team at Verathon collaborated with Professor John Sakles from the University of Arizona Emergency Department in achieving the world's first tracheal intubation conducted with the assistance of telemedicine technology. During this demonstration, Dr. Sakles and the University of Arizona Telemedicine service guided physicians in a rural hospital as they performed a tracheal intubation using the Glidescope.
[edit] Other video laryngoscopes

Several types of video laryngoscopes are also currently available, such as the Glidescope,[26][29] McGrath laryngoscope,[30] Daiken Medical Coopdech C-scope VLP-100,[31] the Storz C-Mac,[32] Pentax AWS,[33][34][35][36] Video Macintosh Intubating Laryngoscope System (VMS),[37] the Berci DCI,[38] and the Copilot VL.[39] These laryngoscopes employ a variety of features such as a monitor on the handle and or channels to assist in guiding the endotracheal tube into the trachea. The superior performance of video laryngoscopes in airway management where cervical spine injury is possible has raised the question of whether these scopes should supersede direct laryngoscopy in routine airway management.[26]

[edit] Other noninvasive intubation devices

Other "noninvasive" devices which can be employed to assist in tracheal intubation are the laryngeal mask airway[40][41][42][43][44][45][46] (used as a conduit for endotracheal tube placement), the lighted stylet,[47][48] and the AirTraq.[49] Due to the widespread availability of such devices, the technique of blind digital intubation[50] of the trachea is rarely practiced today, though it may still be useful in emergency situations under austere conditions such as natural or man-made disasters.[51]

By other medical topics

Respiratory therapy Respiratory therapy

From Wikipedia, the free encyclopedia Jump to: navigation, search

Respiratory Therapist

A symbol of Respiratory Therapy

Occupation

Names

Respiratory Therapist, Cardiopulmonary Therapist

Activity sectors

Medicine, Allied Health

Description

Education required

Associate of Science, Bachelors Degree, Masters Degree

Respiratory therapy is a healthcare profession in which specialists work with patients suffering from either acute or chronic respiratory problems. These specialists are termed Respiratory Therapists in most places internationally but may also be referred to as Respiratory Scientists or Respiratory Care Practitioners. Respiratory therapy clinicians are also sometimes referred

to as cardio-pulmonary therapists or respiratory care practitioners. Respiratory therapists work independently and as part of a team to plan, integrate, and evaluate cardiac and pulmonary care.

Contents
[hide]

1 Clinical practice 2 History 3 Treatment 4 Respiratory therapy as a career o 4.1 Credentialing in the United States 5 Scientific research 6 Specialty areas o 6.1 Asthma o 6.2 Cystic fibrosis o 6.3 Extracorporeal Membrane Oxygenation (ECMO) o 6.4 Intensive care o 6.5 Neonatal & Pediatric Intensive Care o 6.6 Sleep Disorder Specialist o 6.7 Case Management o 6.8 Surface & Air Transport 7 See also 8 References

[edit] Clinical practice

Respiratory therapists are found in various sectors of health care. In the hospital setting, respiratory therapists evaluate, treat and assist with diagnosis of respiratory/pulmonary diseases. In the United States, Registered Respiratory Therapists evaluate and treat patients with a great deal of autonomy under the direction of a pulmonologist[1], and in specialty facilities respiratory therapists are a preferred addition to surface or air transport[2]. In other settings respiratory therapists are found in schools as asthma educators, working with teachers and coachs about childhood symptoms of asthma and how to spot an emergency. In the United States, legislation has been introduced several times to allow asthma specialist registered respiratory therapists to

prescribe and manage previously diagnosed respiratory patients in physician clinics.[3][4]. In sleep clinics respiratory therapists work with physicians in diagnosis of sleep-related illnesses.

[edit] History
Main article: Timeline of respiratory therapy

Respiratory therapy is a young practice in the field of medicine, beginning in the United States around 1950 and in its current form beginning around 1990. In 2004 Vermont became the 48th state in the United States to enact a Respiratory Care Act, allowing for the practice and licensure of respiratory care clinicians in that state. The Roman physician Galen may have been the first to describe mechanical ventilation: "If you take a dead animal and blow air through its larynx [through a reed], you will fill its bronchi and watch its lungs attain the greatest distention."[5] Vesalius too describes ventilation by inserting a reed or cane into the trachea of animals.[6] In 1908 George Poe demonstrated his mechanical respirator by asphyxiating dogs and seemingly bringing them back to life.[7] Respiratory therapy has grown considerably through the past four decades. There was a time when respiratory therapists were on-the-job trained technicians, with little formal education. Their main function was to ensure safe oxygen use, to administer intermittent positive pressure breathing (IPPB) treatments, to perform cardiopulmonary resuscitation (CPR), and to operate negative pressure (iron lung) ventilators. They were initially titled inhalation therapists. With the advent of positive pressure mechanical ventilators, the more widespread hospital provision of Neonatal and Pediatric care, more sophisticated pulmonary function testing (PFT), a need for thoroughly trained clinical practitioners presented itself. Over the years respiratory therapists have evolved to being college and university trained clinicians who work in a variety of settings.

[edit] Treatment
See also: Pulmonary rehabilitation and Pulmonary hygiene

Medication Medication is the most important treatment of most diseases of pulmonology, usually by inhalation (bronchodilators and steroids) or also by mouth or IV (antibiotics, leukotriene antagonists). A common example being the usage of inhalers in the treatment of inflammatory lung conditions such as Asthma or Chronic obstructive pulmonary disease (Emphysema. Oxygen therapy is often necessary in severe respiratory disease such as pulmonary fibrosis. Intensive Care Mechanical ventilation may be required in instances of rapidly advancing disease or difficulty after surgery. Different modes of mechanical ventilation are used for various instances depending on the patients need.

Pulmonary Rehabilitation Pulmonary rehabilitation may be initiated as a treatment as a source for continuity of improvement after a hospital stay or as a therapeutic way to increase quality of life. Pulmonary rehabilitation is intended to educate the patient, the family, and improve the overall quality of life and prognosis for the patient. Pulmonary Rehabilitation involves therapies and evaluations by Respiratory Therapists, Occupational Therapists and Physical Therapists.

[edit] Respiratory therapy as a career

In the United States and Canada, Respiratory Therapists are therapists who, after receiving a degree in cardiopulmonary science or respiratory science complete a credentialing process. After satisfactorily completing the required examinations and added to a registry, the therapist is then eligible to apply for a license to practice in their respective state or territory. In the United States, specialist respiratory therapists are clinicians who hold specialized credentials in a specific field of study, such as a Asthma Educator or a Neonatal & Pediatric Transport Specialist.
[edit] Credentialing in the United States

In the United States there are two separate credentialing bodies. One is the State Board of Respiratory Care in the state in which a respiratory therapist is licensed to practice and the other is the National Board for Respiratory Care (NBRC) which regulates two levels of certification. The Certified Respiratory Therapist (CRT) and the Registered Respiratory Therapist (RRT). The CRT is the certification given after successfully passing the entry-level examination NBRCELE; The RRT certification is given after first becoming a CRT and then passing the NBRCWRE and NBRC-CSE. Most state boards of respiratory care require proof of the appropriate NBRC credential and award various license titles; including (but not limited to) Respiratory Care Practitioner, Licensed Registered Respiratory Therapist, and Licensed Certified Respiratory Therapist. There has been a substantial push to standardize the state licensure by the American Association for Respiratory Care[8]. The NBRC credential is renewed every 5 years for a fee in addition to fees assessed by the state boards of respiratory care.

[edit] Scientific research

Respiratory scientists are specialists in pulmonary function. Respiratory therapists work with Pulmonologists in both clinical and general research of the respiratory system, ranging from the anatomy of the respiratory epithelium to the most effective treatment of pulmonary hypertension in pediatrics. Scientific research also takes place to look for causes and possible treatment in diseases such as asthma and lung cancer.

[edit] Specialty areas

[edit] Asthma

Asthma specialist's work with clinics, hospitals and schools as an educator for teachers and practitioners on asthma and allergies. Respiratory Therapists in the role as an Asthma Educator additionally help diagnose and treat asthma and other respiratory illness.[9] An Asthma Educator is the resource clinician in inpatient and outpatient environments for evaluating and advising physicians on treatment plans and helping facilitate patient understanding and compliance with the plan. In the United States, Certified Asthma Educators (AE-C) are credentialed by the National Asthma Educator Certification Board (NAECB).[10]
[edit] Cystic fibrosis

Respiratory Therapists work with people suffering from cystic fibrosis in clinics and hospitals[11] by educating them about their disease and working with them on a treatment plan. While admitted to a hospital, patients with cystic fibrosis have their treatment schedule modified and maintained by respiratory therapists. Maintaining a healthy schedule for pharmokonetic and physical therapeutic airway clearance typically more frequent than home treatment plans because admissions are usually due to an increased need for therapy during the stay.
[edit] Extracorporeal Membrane Oxygenation (ECMO)

Extracorporeal membrane oxygenation (ECMO) is a modified cardiopulmonary bypass technique used for the treatment of life threatening cardiac or respiratory failure. An ECMO Specialist is the technical specialist educated to manage the ECMO system including blood pump, tubing, artificial oxygenator, and related equipment. The ECMO Specialist, under qualified medical direction and supervision, is also responsible for the clinical needs of the patient on ECMO which can include maintenance of normal acid-base balance, oxygenation, and ventilation, administration of blood and blood by-products, medication delivery, and maintenance of appropriate anticoagulation therapies for the blood.[12] The ECMO Specialist is either a registered respiratory therapist a registered nurse or a (Certified Clinical Perfusionist).
[edit] Intensive care

Intensive Care is one of the mainstays of respiratory therapy. Respiratory Therapists are taking an increased clinical role in recent years related to intensive care. Ventilatory support is usually the largest criteria for being placed into an intensive care setting which is maintained entirely by Respiratory Therapists and Cardiopulmonary specialists. Mechanical Ventilation is a rapidly expanding science and has been recognized as a complex technology by the respiratory therapy credentialing agency (NBRC) who in 2011 added the speciality credential called the "Adult Critical Care Specialist", available only to the registered respiratory therapist (RRT-ACCS).[13]
[edit] Neonatal & Pediatric Intensive Care

Much like adult intensivist therapists neonatal and pediatric specialists deal primarily with monitoring ventilation and perfusion[14]. The NPS practitioner is trained extensively in antenatal and intrapartum patients and family. Neonatal assessment and laboratory studies. The

practitioner is also a specialist in ventilatory support and cardio-pulmonary therapy of neonatal and pediatric patients[14]. In the United States NPS credentialing is available to both the certified respiratory therapist (CRT-NPS) and the registered respiratory therapist (RRT-NPS) however the registered respiratory therapist (RRT-NPS) is preferred by most organizations[14][15].
[edit] Sleep Disorder Specialist Main article: Sleep disorder specialist

The Sleep Disorder Specialist is a Registered Respiratory Therapist (RRT-SDS) whom performs sleep disorders testing and therapeutic intervention along with diagnosis of sleep related disease such as Obstructive Sleep Apnea or Central Apnea. The role is very similar to the Polysomnographic Technologist.
[edit] Case Management Main article: Certified Case Manager

Case management is a collaborative process that assesses, plans, implements, coordinates, monitors, and evaluates the options and services required to meet the client's health and human services needs. It is characterized by advocacy, communication, and resource management and promotes quality and cost-effective interventions and outcomes. Eligibility and certification is maintained by the Commission for Case Management Certification, a body certifying healthcare professionals in the United States.[16]
[edit] Surface & Air Transport Main article: Air medical services

Respiratory therapists work with nurses, physicians, and paramedics in emergency flight and ground transport.[17] They are a vital practitioner delivering care inside helicopters, air ambulance or ground ambulance working to pick up a patient and move them to a facility that has what they need. In the United States certification for transport (C-NPT) is currently awarded by The National Certification Corporation.[18] The NREMT has included respiratory therapists as qualifing for the advanced credentialing as a critical care paramedic CCEMT-P.

Breathing gases Breathing gas

From Wikipedia, the free encyclopedia Jump to: navigation, search

Breathing gas is a mixture of gaseous chemical elements and compounds used for respiration. Air is the most common and only natural breathing gas. Other artificial gases, either pure gases or mixtures of gases, are used in breathing equipment and enclosed habitats such as SCUBA

equipment, surface supplied diving equipment, recompression chambers, submarines, space suits, spacecraft and anaesthetic machines.[1][2][3] Most breathing gases are a mixture of oxygen and one or more inert gases.[1][3] Other breathing gases have been developed to improve on the performance of air by reducing the risk of decompression sickness, reducing the duration of decompression stops, reducing nitrogen narcosis or allowing safer deep diving.[1][3] A safe breathing gas has three essential features:

it must contain sufficient oxygen to support the life, consciousness and work rate of the breather.[1][2][3] it must not contain harmful gases. Carbon monoxide and carbon dioxide are common poisons in breathing gases. There are many others.[1][2][3] it must not become toxic when being breathed at high pressure such as when underwater. Oxygen and nitrogen are examples of gases that become toxic under pressure.[1][2][3]

The techniques used to fill diving cylinders with gases other than air are called gas blending.[4][5]

Contents
[hide]

1 Common diving breathing gases 2 Individual component gases o 2.1 Oxygen 2.1.1 Fraction of oxygen 2.1.2 Partial pressure of oxygen 2.1.3 Divox o 2.2 Nitrogen o 2.3 Helium o 2.4 Neon o 2.5 Hydrogen 3 Unwelcome components of breathing gases o 3.1 Argon o 3.2 Carbon dioxide o 3.3 Carbon monoxide o 3.4 Hydrocarbons 4 Moisture content 5 Gas detection and measurement 6 References 7 External links

[edit] Common diving breathing gases

Common diving breathing gases are:

Air is a mixture of 21% oxygen, 78% nitrogen, and approximately 1% other trace gases; to simplify calculations this last 1% is usually treated as if it were nitrogen. Being cheap and simple to use, it is the most common diving gas.[1][2][3] As its nitrogen component causes nitrogen narcosis it is considered to have a safe depth limit of about 40 metres (130 feet) for most divers, although the maximum operating depth of air is 66.2 metres (218 feet).[1][3][6] Pure oxygen is mainly used to speed the shallow decompression stops at the end of a military, commercial or technical dive and is only safe down to a depth of 6 meters (maximum operating depth) before oxygen toxicity steps in.[1][2][3][6] It was much used in frogmen's rebreathers.[2][6][7][8] Nitrox is a mixture of oxygen and air, and generally refers to mixtures which are more than 21% oxygen. It can be used as a tool to accelerate in-water decompression stops or to decrease the risk of decompression sickness and thus prolong a dive (a common misconception is that the diver can go deeper, this is not true owing to a shallower maximum operating depth than on conventional air).[1][2][3][9] Trimix is a mixture of oxygen, nitrogen and helium and is often used at depth in technical diving and commercial diving instead of air to reduce nitrogen narcosis and to avoid the dangers of oxygen toxicity.[1][2][3] Heliox is a mixture of oxygen and helium and is often used in the deep phase of a commercial deep dive to eliminate nitrogen narcosis.[1][2][3][10] Heliair is a form of trimix that is easily blended from helium and air without using pure oxygen. It always has a 21:79 ratio of oxygen to nitrogen; the balance of the mix is helium.[3][11] Hydreliox is a mixture of oxygen, helium, and hydrogen and is used for dives below 130 metres in commercial diving.[1][3][10][12][13] Hydrox, a gas mixture of hydrogen and oxygen is used as a breathing gas in very deep diving.[1][3][10][12][14] Neox (also called neonox) is a mixture of oxygen and neon sometimes employed for in deep commercial diving. It is rarely used due to its cost. Also, DCS symptoms produced by neon ("neox bends") have a poor reputation, being widely reported to be more severe than those produced by an exactly equivalent dive-table and mix with helium.[1][3][10][15]

[edit] Individual component gases

NEDU gas analysis lab [edit] Oxygen For the main article on the Medical use of Oxygen see Oxygen therapy

Oxygen (O2) must be present in every breathing gas.[1][2][3] This is because it is essential to the human body's metabolic process, which sustains life. The human body cannot store oxygen for later use as it does with food. If the body is deprived of oxygen for more than a few minutes, unconsciousness and death result. The tissues and organs within the body (notably the heart and brain) are damaged if deprived of oxygen for much longer than four minutes. Filling a diving cylinder with pure oxygen costs around five times more than filling it with compressed air. As oxygen supports combustion and causes rust in diving cylinders, it should be handled with caution when gas blending.[4][5] Oxygen has historically been obtained by fractional distillation of liquid air, but is increasingly obtained by non cryogenic technologies such as pressure swing adsorption (PSA) and vacuumpressure swing adsorption (VPSA) technologies.[16] [edit] Fraction of oxygen The fraction of the oxygen component of a breathing gas mixture is sometimes used when naming the mix:

hypoxic mixes, strictly, contain less than 21% oxygen, although often a boundary of 16% is used, and are designed only to be breathed at depth as a "bottom gas" where the higher pressure increases the partial pressure of oxygen to a safe level.[1][2][3] Trimix, Heliox and Heliair create typical hypoxic mixes and are used in technical diving as deep breathing gases.[1][3] normoxic mixes have the same proportion of oxygen as air, 21%.[1][3] The maximum operating depth of a normoxic mix could be as shallow as 47 metres (155 feet). Trimix with between 17% and 21% oxygen is often described as normoxic because it contains a high enough proportion of oxygen to be safe to breathe at the surface. hyperoxic mixes have more than 21% oxygen. Enriched Air Nitrox (EANx) is a typical hyperoxic breathing gas.[1][3][9] Hyperoxic mixtures, when compared to air, cause oxygen toxicity at shallower depths but can be used to shorten decompression stops by drawing dissolved inert gases out of the body more quickly.[6][9]

The fraction of the oxygen determines the deepest the mixture gas can safely be used to avoid oxygen toxicity. This depth is called the maximum operating depth.[1][3][6][9] [edit] Partial pressure of oxygen The concentration of oxygen in a gas mix depends on both the fraction and the pressure of the mixture. It is expressed by the partial pressure of oxygen (ppO2).[1][3][6][9] The partial pressure of any component gas in a mixture is calculated as:
partial pressure = total absolute pressure x volume fraction of gas component

For the oxygen component:

ppO2 = P x FO2

where: ppO2 = partial pressure of oxygen P = total pressure FO2 = volume fraction of oxygen

The minimum safe partial pressure of oxygen in a breathing gas is commonly held to be 16 kPa (0.16 bar). Below this partial pressure the diver may be at risk of unconsciousness and death due to hypoxia, depending on factors including individual physiology and level of exertion. When a hypoxic mix is breathed in shallow water it may not have a high enough ppO2 to keep the diver conscious. For this reason normoxic or hyperoxic "travel gases" are used at medium depth between the "bottom" and "decompression" phases of the dive. The maximum safe ppO2 in a breathing gas depends on exposure time, the level of exercise and the security of the breathing equipment being used. It is typically between 100 kPa (1 bar) and 160 kPa (1.6 bar) but for dives of less than three hours is commonly considered to be 140 kPa (1.4 bar), although the U.S. Navy has been known to authorize dives with a ppO2 of as much as 180 kPa (1.8 bar).[1][2][3][6][9] At high ppO2 or longer exposures, the diver risks oxygen toxicity including a seizure.[1][2] Each breathing gas has a maximum operating depth that is determined by its oxygen content.[1][2][3][6][9] Oxygen analysers measure the ppO2 in the gas mix.[4] [edit] Divox "Divox" is oxygen. In the Netherlands, pure oxygen for breathing purposes is regarded as medicinal as opposed to industrial oxygen, such as that used in welding, and is only available on medical prescription. The diving industry "created" Divox and registered it as a trademark to circumvent the strict rules concerning medicinal oxygen thus making it easier for (recreational) scuba divers to obtain oxygen for blending their breathing gas. In most countries, there is no difference in purity in medical oxygen and industrial oxygen, as they are produced by exactly the same methods and manufacturers, but labeled and tanked differently. The chief difference between them is that the paper record-keeping trail is much more extensive for medical oxygen, in order to more easily identify the exact manufacturing trail of a "lot" of oxygen, in case problems are later found with its purity.

[edit] Nitrogen

Nitrogen (N2) is a diatomic gas and the main component of air, the cheapest and most common breathing gas used for diving. It causes nitrogen narcosis in the diver, so its use is limited to shallower dives. Nitrogen can cause decompression sickness.[1][2][3][17] Equivalent air depth is used to estimate the decompression requirements of a nitrox (oxygen/nitrogen) mixture. Equivalent narcotic depth is used to estimate the narcotic potency of trimix (oxygen/helium/nitrogen mixture). Many divers find that the level of narcosis caused by a 30 m (100 ft) dive, whilst breathing air, is a comfortable maximum.[1][2][3][18][19] Nitrogen in a gas mix is almost always obtained by adding air to the mix.
[edit] Helium

Helium (He) is an inert gas that is less narcotic than nitrogen at equivalent pressure (in fact there is no evidence for any narcosis from helium at all), so it is more suitable for deeper dives than nitrogen.[1][3] Helium is equally able to cause decompression sickness. At high pressures, helium also causes High Pressure Nervous Syndrome, which is a CNS irritation syndrome which is in some ways opposite to narcosis.[1][2][3][20] Helium fills typically cost ten times more than an equivalent air fill. Helium is not very suitable for dry suit inflation due to its poor thermal insulation properties helium is a very good conductor of heat (compared to air which is a rather poor, making it more of an insulator).[1][3] Helium's low molecular weight (monatomic MW=4, compared with diatomic nitrogen MW=28) increases the timbre of the breather's voice, which may impede communication.[1][3][21] This is because the speed of sound is faster in a lower molecular weight gas, which increases the resonance frequency of the vocal cords.[1][21] Helium leaks from damaged or faulty valves more readily than other gases because atoms of helium are smaller allowing them to pass through smaller gaps in seals. Helium is found in significant amounts only in natural gas, from which it is extracted at low temperatures by fractional distillation.
[edit] Neon

Neon (Ne) is an inert gas sometimes used in deep commercial diving but is very expensive.[1][3][10][15] Like helium, it is less narcotic than nitrogen, but unlike helium, it does not distort the diver's voice.

[edit] Hydrogen

Hydrogen (H2) has been used in deep diving gas mixes but is very explosive when mixed with more than about 4 to 5% oxygen (such as the oxygen found in breathing gas).[1][3][10][12] This limits use of hydrogen to deep dives and imposes complicated protocols to ensure that oxygen is cleared from the lungs, the blood stream and the breathing equipment before breathing hydrogen starts. Like helium, it increases the timbre of the diver's voice. The hydrogen-oxygen mix when used as a diving gas is sometimes referred to as Hydrox.

[edit] Unwelcome components of breathing gases

Many gases are not suitable for use in diving breathing gases.[5][22] Here is an incomplete list of gases commonly present in a diving environment:
[edit] Argon

Argon (Ar) is an inert gas that is more narcotic than nitrogen, so is not generally suitable as a diving breathing gas.[23] Argox is used for decompression research.[1][3][24][25] It is sometimes used for dry suit inflation by divers whose primary breathing gas is heliumbased, because of argon's good thermal insulation properties. Argon is more expensive than air or oxygen, but considerably less expensive than helium.
[edit] Carbon dioxide

Carbon dioxide (CO2) is produced by the metabolism in the human body and can cause carbon dioxide poisoning.[22][26][27]
[edit] Carbon monoxide

Carbon monoxide (CO) is produced by incomplete combustion.[1][2][5][22] See carbon monoxide poisoning. Four common sources are:

Internal combustion engine exhaust gas containing CO in the air being drawn into a diving air compressor. CO in the intake air cannot be stopped by any filter. The exhausts of all internal combustion engines running on petroleum fuels contain some CO, and this is a particular problem on boats, where the intake of the compressor cannot be arbitrarily moved as far as desired from the engine and compressor exhausts. Heating of lubricants inside the compressor may vaporize them sufficiently to be available to a compressor intake or intake system line. In some cases hydrocarbon lubricating oil may be drawn into the compressor's cylinder directly through damaged or worn seals, and the oil may (and usually will) then undergo combustion, being ignited by the immense compression ratio and subsequent temperature rise. Since heavy oils don't burn well - especially when not atomized properly - incomplete combustion will result in carbon monoxide production.

A similar process is thought to potentially happen to any particulate material, which contains "organic" (carbon-containing) matter, especially in cylinders which are used for hyperoxic gas mixtures. If the compressor air filter(s) fail, ordinary dust will be introduced to the cylinder, which contains organic matter (since it usually contains humus). A more severe danger is that air particulates on boats and industrial areas, where cylinders are filled, often contain carbon-particulate combustion products (these are what makes a dirt rag black), and these represent a more severe CO danger when introduced into a cylinder.

[edit] Hydrocarbons

Hydrocarbons (CxHy) are present in compressor lubricants and fuels. They can enter diving cylinders as a result of contamination, leaks, or due to incomplete combustion near the air intake.[2][4][5][22][28]

They can act as a fuel in combustion increasing the risk of explosion, especially in highoxygen gas mixtures. Inhaling oil mist can damage the lungs and ultimately cause the lungs to degenerate with severe lipid pneumonia or emphysema.

[edit] Moisture content

The process of compressing gas into a diving cylinder removes moisture from the gas.[5][22] This is good for corrosion prevention in the cylinder but means that the diver inhales very dry gas. The dry gas extracts moisture from the diver's lungs while underwater contributing to dehydration, which is also thought to be a predisposing risk factor of decompression sickness. It is also uncomfortable, causing a dry mouth and throat and making the diver thirsty. This problem is reduced in rebreathers because the soda lime reaction to remove carbon dioxide puts moisture back into the breathing gas.[8] In hot climates, open circuit diving can accelerate heat exhaustion because of dehydration. Another concern with regard to moisture content is the tendency of moisture to condense as the gas is decompressed while passing through the regulator; this coupled with the extreme reduction in temperature, also due to the decompression can cause the moisture to solidify as ice. This icing up in a regulator can cause moving parts to seize and the regulator to fail or free flow. It is for this reason that SCUBA regulators are generally constructed from brass, and chrome plated (for protection). Brass, with its good thermal conductive properties, quickly conducts heat from the surrounding water to the cold, newly decompressed air, helping to prevent icing up.

[edit] Gas detection and measurement

Divers find it difficult to detect most gases that are likely to be present in diving cylinders because they are colourless, odourless and tasteless. Electronic sensors exist for some gases, such as oxygen analysers, helium analyser, carbon monoxide detectors and carbon dioxide detectors.[2][4][5] Oxygen analysers are commonly found underwater in rebreathers.[8] Oxygen and helium analysers are often used on the surface during gas blending to determine the percentage of oxygen or helium in a breathing gas mix.[4]

Chemical and other types of gas detection methods are not often used in recreational diving.

Hyperbaric oxygen therapy Hyperbaric medicine

From Wikipedia, the free encyclopedia (Redirected from Hyperbaric oxygen therapy) Jump to: navigation, search

Hyperbaric medicine
Intervention

A Sechrist Monoplace hyperbaric chamber at the Moose Jaw Union Hospital, Saskatchewan, Canada

ICD-9-CM

93.95

MeSH

D006931

OPS-301 code:

8-721

Hyperbaric medicine, also known as hyperbaric oxygen therapy (HBOT), is the medical use of oxygen at a level higher than atmospheric pressure. The equipment required consists of a

pressure chamber, which may be of rigid or flexible construction, and a means of delivering 100% oxygen. Operation is performed to a predetermined schedule by trained personnel who monitor the patient and may adjust the schedule as required. HBOT found early use in the treatment of decompression sickness, but has shown great effectiveness in treating conditions such as gas gangrene and carbon monoxide poisoning. More recent research has examined the possibility that it may also have value for other conditions such as cerebral palsy and multiple sclerosis, but no significant evidence has been found.

Contents
[hide]

1 Therapeutic principles 2 Indications 3 Hyperbaric chambers o 3.1 Construction o 3.2 Oxygen supply 4 Treatments o 4.1 Protocol o 4.2 Home and out-patient clinic treatment o 4.3 Possible complications and concerns o 4.4 Effects of Pressure o 4.5 Contraindications o 4.6 Neuro-rehabilitation 5 See also 6 References 7 Further reading 8 External links

[edit] Therapeutic principles

Several therapeutic principles are made use of in HBOT:[1]

The increased overall pressure is of therapeutic value when HBOT is used in the treatment of decompression sickness and air embolism;[2] For many other conditions, the therapeutic principle of HBOT lies in its ability to drastically increase partial pressure of oxygen in the tissues of the body. The oxygen partial pressures achievable using HBOT are much higher than those achievable while breathing pure oxygen at normobaric conditions (i.e. at normal atmospheric pressure); A related effect is the increased oxygen transport capacity of the blood. Under normal atmospheric pressure, oxygen transport is limited by the oxygen binding capacity of hemoglobin in red blood cells and very little oxygen is transported by blood plasma. Because the hemoglobin of the red blood cells is almost saturated with oxygen under atmospheric pressure, this route of transport cannot be exploited any further. Oxygen transport by plasma, however is significantly increased using HBOT as the stimulus.

Recent evidence notes that exposure to hyperbaric oxygen (HBOT) mobilizes stem/progenitor cells from the bone marrow by a nitric oxide (NO) -dependent mechanism.[2] This mechanism may account for the patient cases that suggest recovery of damaged organs and tissues with HBOT.

[edit] Indications
In the United States the Undersea and Hyperbaric Medical Society, known as UHMS, lists approvals for reimbursement for certain diagnoses in hospitals and clinics. The following indications are approved (for reimbursement) uses of hyperbaric oxygen therapy as defined by the UHMS Hyperbaric Oxygen Therapy Committee:[1][3] However, these are reimbursement decisions based on cost of medical treatments vs HBOT at the average U.S. hospital charge of $1,800.00 per 90 minute HBOT treatment. China and Russia treat more than 80 maladies, conditions and trauma with HBOT, since dollar costs are insignificant in those countries.[4]

Air or gas embolism;[5] Carbon monoxide poisoning;[6][7] [8][9][10] o Carbon monoxide poisoning complicated by cyanide poisoning; Clostridal myositis and myonecrosis (gas gangrene);[11][12][13] Crush injury, compartment syndrome, and other acute traumatic ischemias;[14][15] Decompression sickness;[16][17][18] Enhancement of healing in selected problem wounds;[19][20][21] [22][23] o Diabetically derived illness, such as diabetic foot, diabetic retinopathy,[24][25] diabetic nephropathy;[26] Exceptional blood loss (anemia);[27][28] Intracranial abscess;[29][30] Necrotizing soft tissue infections (necrotizing fasciitis);[31][32] Osteomyelitis (refractory);[33][34][35] Delayed radiation injury (soft tissue and bony necrosis);[36][37][38] Skin grafts and flaps (compromised);[39][40] Thermal burns.[41][42]

HBOT is recognized by Medicare in the United States as a reimbursable treatment for 14 UHMS "approved" conditions. A 1-hour HBOT session may cost between $108 and $250 in private clinics, and over $1,000 in hospitals. U.S. physicians (either M.D. or D.O.) may lawfully prescribe HBOT for "off-label" conditions such as Lyme Disease,[43] stroke,[44][45][46] and migraines.[47][48][49] Such patients are treated in outpatient clinics. In the United Kingdom most chambers are financed by the National Health Service, although some, such as those run by Multiple Sclerosis Therapy Centres, are non-profit. Other reported applications include:

Autism. A small 2009 double-blind study of autistic children found that 40 hourly treatments of 24% oxygen at 1.3 atm provided significant improvement in the children's behavior immediately after treatment sessions.[50] The study's effect has not been independently confirmed. Research conducted by the Center for Autism and Related Disorders (CARD) found that hyperbaric oxygen therapy does not have a significant effect on symptoms of autism.[51] Cerebral Palsy;[52]

Epidural abscesses;[53] Certain kind of hearing loss;[54] multiple sclerosis[55] Radiation-induced hemorrhagic cystitis;[56] Inflammatory bowel disease.[57][58] Psoriasis.[59]

The toxicology of the treatment has recently been reviewed by Ustundag et al.[60] and its risk management is discussed by Christian R. Mortensen.[61]

[edit] Hyperbaric chambers

Multiplace hyperbaric chambers, showing control panel, monitoring facilities, and different chamber sizes in Spanish facilities [edit] Construction

The traditional type of hyperbaric chamber used for HBOT is a hard shelled pressure vessel. Such chambers can be run at absolute pressures as much as 6 bars (87 psi), 600,000 Pa. Navies, diving organizations, hospitals, and dedicated recompression facilities typically operate these. They range in size from semi-portable, one-patient units to room-sized units that can treat eight or more patients. Recent advances in materials technology have resulted in the manufacture of portable, "soft" chambers that can operate at between 0.3 and 0.5 bar (4.4 and 7.3 psi) above atmospheric pressure.[62] Hard chambers and soft chambers should not be considered equivalent in regards to efficacy and safety as they are different in many aspects.

A hard chamber may consist of

a pressure vessel that is generally made of steel, aluminium with the view ports (windows) made of acrylic; one or more human entry hatchessmall and circular or wheel-in type hatches for patients on gurneys; the airlock that allows human entrya separate chamber with two hatches, one to the outside and one to the main chamber, which can be independently pressurized to allow patients to enter or exit the main chamber while it is still pressurized and a small airlock for medicines, instruments, and food; glass ports or closed-circuit television that allows technicians and medical staff outside the chamber to monitor the patient inside the chamber; an intercom or walkie-talkie allowing two-way communication; a carbon dioxide scrubberconsisting of a fan that passes the gas inside the chamber through a soda lime canister; a control panel outside the chamber to open and close valves that control air flow to and from the chamber, and regulate oxygen to helmets or masks.

A soft chamber may consist of

a urethane-coated, nylon-bonded flexible acrylic pressure vessel with steel-weld technology; a full-length dual zipper-sealed opening; an over-pressure valve, if oxygen is fed into a small mask and expired gas has to be circulated toward the end of the chamber and out through the pressure regulators.

[edit] Oxygen supply

A recompression chamber for a single diving casualty

In today's larger multiplace chambers, both patients and medical staff inside the chamber breathe from either "oxygen hoods" flexible, transparent soft plastic hoods with a seal around the neck similar to a space suit helmet or tightly fitting oxygen masks, which supply pure oxygen and may be designed to directly exhaust the exhaled gas from the chamber. During treatment patients breathe 100% oxygen most of the time to maximise the effectiveness of their treatment, but have periodic "air breaks" during which they breathe room air (21% oxygen) to minimize the risk of

oxygen toxicity. The exhaled gas must be removed from the chamber to prevent the build up of oxygen, which could present a fire risk. Attendants may also breathe oxygen to reduce their risk of decompression sickness. The pressure inside a hard chamber is increased by opening valves allowing high-pressure air to enter from storage cylinders, which are filled by an air compressor. A soft chamber may be pressurised directly from a compressor. Smaller "monoplace" chambers can only accommodate the patient, and no medical staff can enter. The chamber may be pressurised with pure oxygen or compressed air. If pure oxygen is used, no oxygen breathing mask or helmet is needed, but the cost of using pure oxygen is much higher than that of using compressed air. If compressed air is used then an oxygen mask or hood is needed as in a multiplace, hard chamber. In monoplace chambers that are compressed with pure oxygen a mask is available to provide the patient with "air breaks," periods of breathing normal air (21% oxygen), in order to reduce the risk of hyperoxic seizures. In soft chambers, using compressed air and a mask supplying 96% oxygen, no air breaks are necessary as there is negligible risk of oxygen toxicity because of relatively low oxygen partial pressures and the short duration of treatment.

[edit] Treatments
Initially, HBOT was developed as a treatment for diving disorders involving bubbles of gas in the tissues, such as decompression sickness and gas embolism. The chamber cures decompression sickness and gas embolism by increasing pressure, reducing the size of the gas bubbles and improving the transport of blood to downstream tissues. The high concentrations of oxygen in the tissues are beneficial in keeping oxygen-starved tissues alive, and have the effect of removing the nitrogen from the bubble, making it smaller until it consists only of oxygen, which is re-absorbed into the body. After elimination of bubbles, the pressure is gradually reduced back to atmospheric levels.
[edit] Protocol

The slang term, at some facilities, for a cycle of pressurization inside the HBOT chamber is "a dive". An HBOT treatment for longer-term conditions is often a series of 20 to 40 dives, or compressions. Again, these dives last for about an hour and can be administered via a hard, highpressure chamber or a soft, low-pressure chamber - the major difference being per-dive "dose" of oxygen. Many conditions do quite well with the lower dose, lower cost-per-hour, soft chambers. Emergency HBOT for decompression illness follows treatment schedules laid out in treatment tables. Most cases employ a recompression to 2.8 bars (41 psi) absolute, the equivalent of 18 metres (60 ft) of water, for 4.5 to 5.5 hours with the casualty breathing pure oxygen, but taking air breaks every 20 minutes to reduce oxygen toxicity. For extremely serious cases resulting from very deep dives, the treatment may require a chamber capable of a maximum pressure of 8 bars (120 psi), the equivalent of 70 metres (230 ft) of water, and the ability to supply heliox as a breathing gas.[63]

U.S. Navy treatment charts are used in Canada and the United States to determine the duration, pressure, and breathing gas of the therapy. The most frequently used tables are Table 5 and Table 6. In the UK the Royal Navy 62 and 67 tables are used. The Undersea and Hyperbaric Medical Society (UHMS) publishes a report that compiles the latest research findings and contains information regarding the recommended duration and pressure of the longer-term conditions.[64]
[edit] Home and out-patient clinic treatment This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed.
(December 2009)

An example of mild portable hyperbaric chamber. This 40-inch-diameter (1,000 mm) chamber is one of the larger chambers available for home.

There are several sizes of portable chambers, which are used for home treatment. These are usually referred to as "mild personal hyperbaric chambers", which is a reference to the lower pressure (compared to hard chambers) of soft-sided chambers. Food and Drug Administration (FDA) approved chambers for use with room air are available in the USA and may go up to 4.4 pounds per square inch (psi) above atmospheric pressure,[citation needed] which equals 1.3 atmospheres absolute (ATA), equivalent to a depth of 10 feet of sea water. In the US, these "mild personal hyperbaric chambers" are categorized by the FDA as CLASS II medical devices and requires a prescription in order to purchase one or take treatments.[65] Personal hyperbaric chambers are only FDA approved to reach 1.3 ATA.[citation needed] While hyperbaric chamber distributors and manufacturers cannot supply a chamber in the US with any form of elevated oxygen delivery system, a physician can write a prescription to combine the two modalities, as long as there is a prescription for both hyperbarics and oxygen.[citation needed] The most common option (but not approved by FDA) some patients choose is to acquire an oxygen concentrator which typically delivers 8596% oxygen as the breathing gas. Due to the high circulation of air through the chamber, the total concentration of oxygen in the chamber never exceeds 25% as this can increase the risk of fire.[citation needed] Oxygen is never fed directly into soft chambers but is rather introduced via a line and mask directly to the patient. FDA approved oxygen concentrators for human consumption in confined areas used for HBOT are regularly monitored for purity (+/1%) and flow (10 to 15 liters per minute outflow pressure). An audible alarm will sound if the

purity ever drops below 80%. Personal hyperbaric chambers use 120 volt or 220 volt outlets. Ranging in size from 21 inches up to 40 inches in diameter these chambers measure between 84 in (7 ft) to 120 in (10 ft) in length.[citation needed] The soft chambers are approved by the FDA for the treatment of altitude sickness, but are commonly used for other "off-label" purposes.[citation
needed]

[edit] Possible complications and concerns

There are risks associated with HBOT, similar to some diving disorders. Pressure changes can cause a "squeeze" or barotrauma in the tissues surrounding trapped air inside the body, such as the lungs,[66] behind the eardrum,[67][68] inside paranasal sinuses,[67] or trapped underneath dental fillings.[69] Breathing high-pressure oxygen may cause oxygen toxicity.[70] Temporarily blurred vision can be caused by swelling of the lens, which usually resolves in two to four weeks.[71][72] There are reports that cataract may progress following HBOT.[73] Also a rare side effect has been blindness secondary to optic neuritis (inflammation of the optic nerve).[citation needed]
[edit] Effects of Pressure

Patients inside the chamber may notice discomfort inside their ears as a pressure difference develops between their middle ear and the chamber atmosphere.[74] This can be relieved by the Valsalva maneuver or by "jaw wiggling". As the pressure increases further, mist may form in the air inside the chamber and the air may become warm. Increased pressure may also cause ear drums to rupture, resulting in severe pain. To reduce the pressure, a valve is opened to allow air out of the chamber. As the pressure falls, the patients ears may "squeak" as the pressure inside the ear equalizes with the chamber. The temperature in the chamber will fall. The speed of pressurization and de-pressurization can be adjusted to each patient's needs.
[edit] Contraindications

The only absolute contraindication to hyperbaric oxygen therapy is untreated pneumothorax.[66] Also, the treatment may raise the issue of Occupational health and safety (OHS), which has been encountered by the therapist.[75][clarification needed] Patients should not undergo HBO therapy if they are taking or have recently taken the following drugs:

Doxorubicin (Adriamycin) A chemotherapeutic drug. Cisplatin Also a chemotherapeutic drug. Disulfiram (Antabuse) Used in the treatment of alcoholism. Mafenide acetate (Sulfamylon) Suppresses bacterial infections in burn wounds

The following are relative contraindications -- meaning that special consideration must be made by specialist physicians before HBO treatments begin:

Upper respiratory infections These conditions can make it difficult for the patient to equalise their ears or sinuses, which can result in what is termed ear or sinus squeeze. High fevers In most cases the fever should be lowered before HBO treatment begins. Emphysema with CO2 retention This condition can lead to pneumothorax during HBO treatment. History of thoracic (chest) surgery This is rarely a problem and usually not considered a contraindication. However, there is concern that air may be trapped in lesions that were created by surgical scarring. These conditions need to be evaluated prior to considering HBO therapy. Malignant disease: Cancers thrive in blood rich environments but may be suppressed by high oxygen levels. HBO treatment of individuals who have cancer presents a problem, since HBO both increases blood flow via angiogenesis and also raises oxygen levels. Taking an anti-angiogenic supplement may provide a solution.[76][77] A study by Feldemier, et al. and recent NIH funded study on Stem Cells by Thom, et al., indicate that HBO is actually beneficial in producing stem/progenitor cells and the malignant process is not accelerated.[78] Middle ear barotrauma is always a consideration in treating both children and adults in a hyperbaric environment because of the necessity to equalise pressure in the ears. Pregnancy is a relative contraindication to both SCUBA diving and hyperbaric oxygen treatments. In cases where a pregnant woman has carbon monoxide poisoning there is evidence that lower pressure (2.0 ATA) HBOT treatments are not harmful to the fetus, and that the risk involved is outweighed by the greater risk of the untreated effects of CO on the fetus (neurologic abnormalities or death.)[79][80]

[edit] Neuro-rehabilitation

A father and his son inside a hyperbaric oxygen chamber.

A 2004 systematic review of HBOT in traumatic brain injury identified 2 randomized controlled trials and 5 observational studies that met evaluated functional health outcomes. The studies ranged from fair to poor in quality. None adequately reported adverse events, the most serious reported being seizures, pulmonary symptoms, and neurologic deterioration. The review concluded that was insufficient evidence to prove the effectiveness or ineffectiveness, including risks and benefits of HBOT for TBI. In one RCT, the HBOT group had reduced mortality compared to the control group but much higher levels of disability. Another, smaller, study found no difference in mortality. The observational studies were weak in quality and did not provide enough evidence of clinical improvement following HBOT treatment.[81]

Evidence in a 2005 systematic review of the evidence for HBOT in the treatment of stroke showed no benefit to the treatment, though the generalizability of the finding was limited due to the wide variety in stage and type of stroke, and the treatment given. Good quality studies were recommended to determine if HBOT provides any benefit in stroke.[82] Another review that examined the effectiveness of HBOT in acute stroke. It found no evidence that HBOT improved clinical outcomes at 6 months, but further study was recommended.[44] A systematic review of HBOT for cerebral palsy was published in 2007. Two randomized controlled trials and four observational studies were identified.[83] The best evidence from a randomized controlled trial (the Collet study) found that HBOT and slightly pressurized room air resulted in similar improvements in motor function of about 56% compared to baseline.[83][84] Neuropsychological tests also showed no difference between HBOT and room air. Based on caregiver report, those who received room air had significantly better mobility and social functioning.[83][84] Several methodological concerns about the study were raised. Another trial found no difference between a HBOT and a no treatment group.[83] Some low quality observational studies of HBOT reported similar improvements in motor function. Children receiving HBOT were reported to experience seizures and the need for tympanostomy tubes to equalize ear pressure, though the incidence was not clear. Future research was recommended to determine the efficacy of pressurized room air and non-pressurized oxygen compared with standard treatments.[83] A review of 12 randomized studies using HBOT with multiple sclerosis suggested that there is no clinically significant benefit from the administration of HBOT. The review proposed that more trials for selected subgroups of MS and for prolonged treatments may be worthwhile, but that routine use of HBOT in the treatment of MS was not recommended.[85] The 2004 Cochrane review concluded that further "trials are not, in our view, justified".[55]

Hypoxia Hypoxia (medical)

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Hypoxia
ICD-9 799.02

MeSH

D000860

Hypoxia, or hypoxiation, is a pathological condition in which the body as a whole (generalized hypoxia) or a region of the body (tissue hypoxia) is deprived of adequate oxygen supply. Variations in arterial oxygen concentrations can be part of the normal physiology, for example, during strenuous physical exercise. A mismatch between oxygen supply and its demand at the cellular level may result in a hypoxic condition. Hypoxia in which there is complete deprivation of oxygen supply is referred to as anoxia. Hypoxia differs from hypoxemia in that, in the latter, the oxygen concentration within the arterial blood is abnormally low.[1] It is possible to experience hypoxia and have a low oxygen content (e.g., due to anemia) but maintain high oxygen partial pressure (pO2). Incorrect use of these terms can lead to confusion, especially as hypoxemia is among the causes of hypoxia (in hypoxemic hypoxia). Generalized hypoxia occurs in healthy people when they ascend to high altitude, where it causes altitude sickness leading to potentially fatal complications: high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE).[2] Hypoxia also occurs in healthy individuals when breathing mixtures of gases with a low oxygen content, e.g. while diving underwater especially when using closed-circuit rebreather systems that control the amount of oxygen in the supplied air. A mild and non-damaging intermittent hypoxia is used intentionally during altitude trainings to develop an athletic performance adaptation at both the systemic and cellular level.[3] Hypoxia is also a serious consequence of preterm birth in the neonate. The main cause for this is that the lungs of the human foetus are among the last organs to develop during pregnancy. To assist the lungs to distribute oxygenated blood throughout the body, infants at risk of hypoxia are often placed inside an incubator capable of providing continuous positive airway pressure (also known as a humidicrib).

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Pathophysiology o 3.1 Vasoconstriction and vasodilation 4 Treatment 5 See also 6 References 7 Bibliography

[edit] Classification

Hypoxemic hypoxia is a generalized hypoxia, an inadequate supply of oxygen to the body as a whole. The term "hypoxemic hypoxia" specifies hypoxia caused by low partial pressure of oxygen in

arterial blood. In the other causes of hypoxia that follow, the partial pressure of oxygen in arterial blood is normal. Hypoxemic hypoxia may be due to: o Hypoventilation. Inadequate pulmonary minute ventilation (e.g., respiratory arrest or by drugs such as opiates) o Shunts in the pulmonary circulation or a right-to-left shunt in the heart. Shunts can be caused by collapsed alveoli that are still perfused or a block in ventilation to an area of the lung. Whatever the mechanism, blood meant for the pulmonary system is not ventilated and so no gas exchange occurs (the ventilation/perfusion ratio is decreased). Normal anatomical shunt occur due to Thebesian veins which empty into the left ventricle and the bronchial circulation which supplies the bronchi with oxygen. Normal physiological shunts occur due to the effect of gravity. The highest concentration of blood in the pulmonary circulation occurs in the bases of the pulmonary tree compared to the highest pressure of gas in the apices of the lungs. o V/Q mismatch. When the ventilation does not match the perfusion through the paranchyema of the lung. This can occur for a variety of reasons, the commonest being a Pulmonary embolism o Diffusing defects such as pulmonary fibrosis where the Aa gradient has increased. o Decreased concentration of oxygen in inspired air. Low partial pressure of atmospheric oxygen such as found at high altitude[4] or by reduced replacement of oxygen in the breathing mix. Low partial pressure of oxygen in the lungs when switching from inhaled anaesthesia to atmospheric air, due to the Fink effect, or diffusion hypoxia. Anaemia in which arterial oxygen pressure is normal, but total oxygen content of the blood is reduced. This is due to a decreased total carrying capacity.[5] Hypoxia when the blood fails to deliver oxygen to target tissues. o Carbon monoxide poisoning which inhibits the ability of hemoglobin to release the oxygen bound to it. o Methaemoglobinaemia in which an abnormal version of hemoglobin accumulates in the blood Histotoxic hypoxia in which quantity of oxygen reaching the cells is normal, but the cells are unable to use the oxygen effectively, due to disabled oxidative phosphorylation enzymes. Cyanide toxicity is one example.

[edit] Signs and symptoms

The symptoms of generalized hypoxia depend on its severity and acceleration of onset. In the case of altitude sickness, where hypoxia develops gradually, the symptoms include headaches, fatigue, shortness of breath, a feeling of euphoria and nausea. In severe hypoxia, or hypoxia of very rapid onset, changes in levels of consciousness, seizures, coma, priapism, and death occur. Severe hypoxia induces a blue discolouration of the skin, called cyanosis. Because hemoglobin is a darker red when it is not bound to oxygen (deoxyhemoglobin), as opposed to the rich red colour that it has when bound to oxygen (oxyhemoglobin), when seen through the skin it has an increased tendency to reflect blue light back to the eye. In cases where the oxygen is displaced by another molecule, such as carbon monoxide, the skin may appear 'cherry red' instead of cyanotic.

[edit] Pathophysiology

After mixing with water vapour and expired CO2 in the lungs, oxygen diffuses down a pressure gradient to enter arterial blood where its partial pressure is around 100 mmHg (13.3 kPa).[4] Arterial blood flow delivers oxygen to the peripheral tissues, where it again diffuses down a pressure gradient into the cells and into their mitochondria. These bacteria-like cytoplasmic structures strip hydrogen from fuels (glucose, fats and some amino acids) to burn with oxygen to form water. The fuel's carbon is oxidized to CO2, which diffuses down its partial pressure gradient out of the cells into venous blood to be exhaled finally by the lungs. Experimentally, oxygen diffusion becomes rate limiting (and lethal) when arterial oxygen partial pressure falls to 40 mmHg (5.3 kPa) or below. If oxygen delivery to cells is insufficient for the demand (hypoxia), hydrogen will be shifted to pyruvic acid converting it to lactic acid. This temporary measure (anaerobic metabolism) allows small amounts of energy to be released. Lactic acid build up (in tissues and blood) is a sign of inadequate mitochondrial oxygenation, which may be due to hypoxemia, poor blood flow (e.g., shock) or a combination of both.[6] If severe or prolonged it could lead to cell death.
[edit] Vasoconstriction and vasodilation

In most tissues of the body, the response to hypoxia is vasodilation. By widening the blood vessels, the tissue allows greater perfusion. By contrast, in the lungs, the response to hypoxia is vasoconstriction. This is known as "Hypoxic pulmonary vasoconstriction", or "HPV".

[edit] Treatment
To counter the effects of high-altitude diseases, the body must return arterial pO2 toward normal. Acclimatization, the means by which the body adapts to higher altitudes, only partially restores pO2 to standard levels. Hyperventilation, the bodys most common response to high-altitude conditions, increases alveolar pO2 by raising the depth and rate of breathing. However, while pO2 does improve with hyperventilation, it does not return to normal. Studies of miners and astronomers working at 3000 meters and above show improved alveolar pO2 with full acclimatization, yet the pO2 level remains equal to or even below the threshold for continuous oxygen therapy for patients with chronic obstructive pulmonary disease (COPD).[7] In addition, there are complications involved with acclimatization. Polycythemia, in which the body increases the number of red blood cells in circulation, thickens the blood, raising the danger that the heart cant pump it. In high-altitude conditions, only oxygen enrichment can counteract the effects of hypoxia. By increasing the concentration of oxygen in the air, the effects of lower barometric pressure are countered and the level of arterial pO2 is restored toward normal capacity. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At 4000 m, raising the oxygen concentration level by 5 percent via an oxygen concentrator and an existing ventilation system provides an altitude equivalent of 3000 m, which is much more tolerable for the increasing number of low-landers who work in high altitude.[8] In a study of astronomers working in Chile at 5050 m, oxygen concentrators increased the level of oxygen concentration

by almost 30 percent (that is, from 21 percent to 27 percent). This resulted in increased worker productivity, less fatigue, and improved sleep.[9] Oxygen concentrators are uniquely suited for this purpose. They require little maintenance and electricity, provide a constant source of oxygen, and eliminate the expensive, and often dangerous, task of transporting oxygen cylinders to remote areas. Offices and housing already have climate-controlled rooms, in which temperature and humidity are kept at a constant level. Oxygen can be added to this system easily and relatively cheaply.

Gas embolism Air embolism

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(August 2010)

Air embolism
Classification and external resources

ICD-9

673.0, 999.1

eMedicine

emerg/787

MeSH

D004618

An air embolism, or more generally gas embolism, is a pathological condition caused by gas bubbles in a vascular system. The most common context is a human body, in which case it refers to gas bubbles in the bloodstream (embolism in a medical context refers to any large moving mass or defect in the blood stream). However air embolisms may also occur in the xylem of vascular plants, especially when suffering from water stress.

Contents
[hide]

1 In humans and animals o 1.1 Pathogenesis o 1.2 Gas embolism in diving o 1.3 Prevention o 1.4 Treatment 2 In vascular plants 3 See also 4 References 5 External links

[edit] In humans and animals

Small amounts of air often get into the blood circulation accidentally during surgery and other medical procedures (for example a bubble entering an intravenous fluid line), but most of these air emboli enter the veins and are stopped at the lungs, and thus a venous air embolism that shows any symptoms is very rare.[citation needed] For venous air embolisms, death may occur if a large bubble of gas becomes lodged in the heart, stopping blood from flowing from the right ventricle to the lungs (this is similar to vapor lock in engine fuel systems).[1] [2]However, experiments in animals[where?] show that the amount of gas necessary for this to happen is quite variable, and also depends on several other factors, such as body position.[citation needed] Very large and symptomatic amounts of venous air emboli may also occur in rapid decompression in severe diving or decompression accidents, where they may interfere with circulation in the lungs and result in respiratory distress and hypoxia.[3] Gas embolism into an artery, termed arterial gas embolism (AGE), is a more serious matter than in a vein, because a gas bubble in an artery may directly stop blood flow to an area fed by the artery. The symptoms of 'AGE' depend on the area of blood flow, and may be those of stroke or heart attack if the brain or heart, respectively, is affected.[3] The amount of arterial gas embolism that causes symptoms depends on location, but in the brain may be a bubble with a volume only a fraction of a milliliter.[citation needed]
[edit] Pathogenesis

Air embolism can occur whenever a blood vessel is open and a pressure gradient exists favoring entry of gas. Because the circulatory pressure in most arteries and veins is greater than atmospheric pressure, an air embolus does not always happen when a blood vessel is injured. In the veins above the heart, such as in the head and neck, the pressure is less than atmospheric and an injury may let air in.[citation needed] This is one reason why surgeons must be particularly careful

when operating on the brain, and why the head of the bed is tilted down when inserting or removing a central venous catheter from the jugular or subclavian veins.[citation needed] When air enters the veins, it travels to the right side of the heart, and then to the lungs. [4] This can cause the vessels of the lung to constrict, raising the pressure in the right side of the heart[citation needed]. If the pressure rises high enough in a patient who is one of the 20% to 30% of the population with a patent foramen ovale, the gas bubble can then travel to the left side of the heart, and on to the brain or coronary arteries.[citation needed] Such bubbles are responsible for the most serious of gas embolic symptoms. Trauma to the lung can also cause an air embolism. This may happen after a patient is placed on a ventilator and air is forced into an injured vein or artery, causing sudden death.[citation needed] Breath-holding while ascending from scuba diving may also force lung air into pulmonary arteries or veins in a similar manner, due to the pressure difference[3]. Air can be injected directly into the veins either accidentally or as a deliberate act. Examples include misuse of a syringe, and industrial injury resulting from use of compressed air.[citation needed] However, the amount of air that would be administered by a single small syringe is, in most cases, not enough to suddenly stop the heart, nor cause instant death.[citation needed] However, such bubbles may occasionally reach the arterial system through a patent foramen ovale, as noted above, and cause random ischemic damage, depending on their route of arterial travel.[citation
needed]

There have been rare cases of air embolism being caused by air entering the bloodstream from the uterus or tears in female genitalia.[5][6] The risk appears to be greater during pregnancy.[5] Cases have been reported that resulted from attempts to perform an abortion by syringing.[6] These appear to have been due to damage to the placenta allowing air to enter the bloodstream.[6] Oral sex during pregnancy has also resulted in cases of air embolism.[6] Outside of pregnancy there is at least one case where an air embolism resulted from the insertion of an object into the vagina during masturbation.[6]
[edit] Gas embolism in diving

Gas embolism is a diving disorder suffered by compressed air divers and can happen in two distinct ways:

Pulmonary barotrauma: Air bubbles enter the bloodstream as a result of gross trauma to the lining of the lung following a rapid ascent while holding the breath; the air held within the lung expands to the point where the lungs burst (pulmonary barotrauma). This is easy to do as the lungs give little warning through pain until they do burst. The diver will arrive at the surface in pain and distress and may froth or spit blood. A pulmonary barotrauma is very obvious and presents quite differently from the decompression sickness below. Decompression sickness (DCS): Air bubbles precipitate out into the bloodstream if the gas dissolved in the blood at pressure is not allowed sufficient time to out-gas on ascent. The symptoms may be subtle and not immediately noticeable.

Bubbles in the bloodstream from any source are dangerous as they can form clots and precipitate stroke or thrombosis. Pulmonary barotrauma, although more dramatic, is less likely to affect oxygen supply to the brain because bubbles tend to be introduced into the venous system and are trapped and managed at the lung. Gas embolism arising from decompression sickness are potentially more dangerous as they can form in the arterial system, the bubbles are smaller and they can travel to and lodge in the brain where they can cause stroke. The first aid treatment for both is to administer oxygen, treat for shock and get to hospital; at the hospital both may use a hyperbaric chamber but otherwise treatment is different.
[edit] Prevention

If an arterial gas embolism resulting from patent foramen ovale is suspected, an exam by echocardiography may be performed to diagnose the defect. In this test, very fine (microscopic) bubbles are introduced into a patient's vein by agitating saline in a syringe to produce the bubbles, then injecting them into an arm vein. A few seconds later, these bubbles may be clearly seen in the ultrasound image, as they travel through the patient's right atrium and ventricle. At this time, bubbles may be observed directly crossing a septal defect, or else a patent foramen ovale may be opened temporarily by asking the patient to perform the Valsalva maneuver while the bubbles are crossing through the right heart an action which will open the foramen flap and show bubbles passing into the left heart. Such bubbles are too small to cause harm in the test, but such a diagnosis may alert the patient to possible problems which may occur from larger bubbles, formed during activities like scuba diving.
[edit] Treatment

Recompression is the most effective treatment of an air embolism.[2] Normally this is carried out in a recompression chamber. This is because as pressure increases, the solubility of a gas increases. Additionally, owing to Boyle's law, the size of the gas bubble or bubbles decreases in proportion to the increase in atmospheric pressure. In the hyperbaric chamber the patient breathes 100% oxygen. Under hyperbaric conditions, oxygen diffuses into the bubbles, displacing the nitrogen from the bubble and into solution in the blood. Oxygen bubbles are more easily tolerated[1]. Air is composed of 21% oxygen and 78% nitrogen with trace amounts of other gases. Additionally, diffusion of oxygen into the blood and tissues under hyperbaric conditions supports areas of the body which are deprived of blood flow when arteries are blocked by gas bubbles. This helps to reduce ischemic injury. Finally, the effects of hyperbaric oxygen antagonize leukocyte-mediated ischemic-reperfusion injury. It is also important to promptly place the patient in Trendelenburg position (head down) and on their left side (left lateral decubitus position). This positioning helps to trap air in the apex of the ventricle and prevent it from reaching the lung circulation.[1][7][dubious discuss] Oxygen first aid treatment is useful for suspected gas embolism casualties or divers who have made fast ascents or missed decompression stops.[8] Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators. However pure oxygen from an oxygen tank

through a Non-rebreather mask is always the most optimal way to deliver needed oxygen to a decompression sickness patient[3].

[edit] In vascular plants

Air embolisms generally occur in the xylem of vascular plants because a fall in hydraulic conductivity results in cavitation. Possible causes of falling hydraulic conductivity include water stress and the freeze-thaw cycle. A number of physiological adaptations serve to prevent embolisms. These include variations in the length and diameter of vessel elements in different parts of the plant; and the ability to reduce transpiration by closing off leaf stomata.

Decompression sickness Decompression sickness

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Caisson disease [decompression sickness]

Classification and external resources

Two United States Navy sailors prepare for training inside a decompression chamber.

ICD-10

T70.3

ICD-9

993.3

DiseasesDB

3491

eMedicine

emerg/121

MeSH

C21.866.120.248

Decompression sickness (DCS; also known as divers' disease, the bends or caisson disease) describes a condition arising from dissolved gases coming out of solution into bubbles inside the body on depressurization. DCS most commonly refers to a specific type of scuba diving hazard but may be experienced in other depressurisation events such as caisson working, flying in unpressurised aircraft, and extra-vehicular activity from spacecraft. Since bubbles can form in or migrate to any part of the body, DCS can produce many symptoms, and its effects may vary from joint pain and rashes to paralysis and death. Individual susceptibility can vary from day to day, and different individuals under the same conditions may be affected differently or not at all. The classification of types of DCS by its symptoms has evolved since its original description over a hundred years ago. Although DCS is not a common event, its potential severity is such that much research has gone into preventing it, and scuba divers use dive tables or dive computers to set limits on their exposure to pressure and their ascent speed. Treatment is by hyperbaric oxygen therapy in a recompression chamber. If treated early, there is a significantly higher chance of successful recovery.

Contents
[hide]

1 Classification o 1.1 Decompression illness and dysbarism 2 Signs and symptoms o 2.1 Frequency o 2.2 Onset 3 Causes o 3.1 Ascent from depth o 3.2 Leaving a high-pressure environment o 3.3 Ascent to altitude 4 Predisposing factors o 4.1 Environmental

o 4.2 Individual 5 Mechanism o 5.1 Inert gases o 5.2 Isobaric counterdiffusion 6 Diagnosis 7 Prevention o 7.1 Underwater diving o 7.2 Exposure to altitude 8 Treatment 9 Prognosis 10 Epidemiology 11 History 12 Society and culture o 12.1 Economics 13 Footnotes 14 References 15 Bibliography 16 External links

[edit] Classification
DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems.[1] In 1960, Golding et al. introduced a simpler classification using the term "Type I ('simple')" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II ('serious')" for symptoms where other organs (such as the central nervous system) are involved.[1] Type II DCS is considered more serious and usually has worse outcomes.[2] This system, with minor modifications, may still be used today.[3] Following changes to treatment methods, this classification is now much less useful in diagnosis,[4] since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management.[5]
[edit] Decompression illness and dysbarism

The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made.[6] DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body.[5] The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism.[7] Their spectra of symptoms also overlap, although those from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death).

[edit] Signs and symptoms

While bubbles can form anywhere in the body, DCS is most frequently observed in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for about 60% to 70% of all altitude DCS cases, with the shoulder being the most common site. Neurological symptoms are present in 10% to 15% of DCS cases with headache and visual disturbances the most common symptom. Skin manifestations are present in about 10% to 15% of cases. Pulmonary DCS ("the chokes") is very rare in divers and has been observed much less frequently in aviators since the introduction of oxygen pre-breathing protocols.[8] The table below shows symptoms for different DCS types.[9]
Signs and symptoms of decompression sickness DCS type Bubble location

Signs & symptoms (clinical manifestations) Localized deep pain, ranging from mild to excruciating. Sometimes a dull ache, but rarely a sharp pain. Active and passive motion of the joint aggravates the pain. The pain may be reduced by bending the joint to find a more comfortable position. If caused by altitude, pain can occur immediately or up to many hours later. Itching, usually around the ears, face, neck, arms, and upper torso Sensation of tiny insects crawling over the skin (formication) Mottled or marbled skin usually around the shoulders, upper chest and abdomen, with itching Swelling of the skin, accompanied by tiny scar-like skin depressions (pitting edema) Altered sensation, tingling or numbness paresthesia, increased sensitivity hyperesthesia Confusion or memory loss (amnesia) Visual abnormalities Unexplained mood or behaviour changes Seizures, unconsciousness Ascending weakness or paralysis in the legs Girdling abdominal or chest pain Urinary incontinence and fecal incontinence Headache Unexplained fatigue

Mostly large joints Musculoskeletal

(elbows, shoulders, hip, wrists, knees, ankles)

Cutaneous

Skin

Neurologic

Brain

Neurologic

Spinal cord

Constitutional Whole body

Generalised malaise, poorly localised aches Loss of balance Dizziness, vertigo, nausea, vomiting Hearing loss Dry persistent cough Burning chest pain under the sternum, aggravated by breathing Shortness of breath

Audiovestibular Inner ear

[10][note 1]

Pulmonary

Lungs

[edit] Frequency Symptoms by frequency Symptoms local joint pain arm symptoms leg symptoms dizziness paralysis shortness of breath extreme fatigue collapse/unconsciousness Frequency 89% 70% 30% 5.3% 2.3% 1.6% 1.3% 0.5%

[edit] Onset Onset of DCS symptoms Time to onset Percentage of cases within 1 hour within 3 hours within 8 hours within 24 hours within 48 hours 42% 60% 83% 98% 100%

The distribution of symptoms of DCS observed by the U.S. Navy are as follows:[11]

Although onset of DCS can occur rapidly after a dive, in more than half of all cases symptoms do not begin to appear for at least an hour. In extreme cases, symptoms may occur before the dive has been completed. The U.S. Navy and Technical Diving International, a leading technical diver training organization, have published a table that indicates onset of first symptoms. The table does not differentiate between types of DCS, or types of symptom.[12][13]

[edit] Causes
DCS is caused by a reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body. It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude.

[edit] Ascent from depth

DCS is best known as a diving disorder that affects divers having breathed gas that is at a higher pressure than the surface pressure, owing to the pressure of the surrounding water. The risk of DCS increases when diving for extended periods or at greater depth, without ascending gradually and making the decompression stops needed to slowly reduce the excess pressure of inert gases dissolved in the body. The specific risk factors are not well understood and some divers may be more susceptible than others under identical conditions.[14][15] DCS has been confirmed in rare cases of breath-holding divers who have made a sequence of many deep dives with short surface intervals; and it may be the cause of the disease called taravana by South Pacific island natives who for centuries have dived by breath-holding for food and pearls.[16] Two principal factors control the risk of a diver suffering DCS:
1. the rate and duration of gas absorption under pressure the deeper or longer the dive the more gas is absorbed into body tissue in higher concentrations than normal (Henry's Law); 2. the rate and duration of outgassing on depressurization the faster the ascent and the shorter the interval between dives the less time there is for absorbed gas to be offloaded safely through the lungs, causing these gases to come out of solution and form "micro bubbles" in the blood.[17]

Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON). DON can develop from a single exposure to rapid decompression.[18]
[edit] Leaving a high-pressure environment

The principal features of a caisson are the workspace, pressurised by an external air supply, and the access tube with an airlock

When a worker comes out of a pressurized caisson or out of a mine that has been pressurized to keep water out, they will experience a significant reduction in ambient pressure.[14][19] A similar pressure reduction occurs when an astronaut exits a space vehicle to perform a space-walk or extra-vehicular activity, where the pressure in his spacesuit is lower than the pressure in the vehicle.[14][20][21][22] The original name for DCS was "caisson disease"; this term was used in the 19th century, in large engineering excavations below the water table, such as bridge supports and tunnels, where caissons under pressure were used to keep water from flooding the excavations. Workers spending time in high-pressure atmospheric pressure conditions are at risk when they return to the lower pressure outside the caisson if the pressure surrounding them was not reduced slowly. DCS was a major factor during construction of Eads Bridge, when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling.[23]
[edit] Ascent to altitude

Passengers may be at risk of DCS when an unpressurized aircraft ascends to high altitude.[14][20][21][24] Likewise, there is increased risk for divers flying in any aircraft shortly after diving, since even in a pressurized aircraft the cabin pressure is not maintained at sea-level pressure but may drop to as low as 73% of sea level pressure.[14][20][25] Altitude DCS became a common problem in the 1930s with the development of high-altitude balloon and aircraft flights. Today, cabin pressurization systems maintain commercial aircraft cabin pressure at the equivalent altitude of 2,400 m (7,900 ft) or less, allowing safe flights at 12,000 m (39,000 ft) or more. DCS is very rare in healthy individuals who experience pressures equivalent to this altitude. However, since the pressure in the cabin is not actually maintained at sea-level pressure, there is still a risk of DCS in individuals having dived recently. Also, cabin pressurization systems still fail occasionally, and some people may be predisposed to the drop in pressure that occurs even in pressurized aircraft.[26][27] There is no specific altitude threshold that can be considered safe for everyone and below which no one will develop altitude DCS. Nevertheless, there is very little evidence of altitude DCS occurring among healthy individuals who have not been scuba diving at pressure altitudes below 5,500 m (18,000 ft). The higher the altitude of exposure the greater is the risk of developing altitude DCS. Although exposures to incremental altitudes above 5,500 m (18,000 ft) show an incremental risk of altitude DCS, they do not show a direct relationship with the severity of the various types of DCS. Individual exposures to pressure altitudes between 5,500 m (18,000 ft) and 7,500 m (24,600 ft) have shown a low occurrence of altitude DCS. A US Air Force study of altitude DCS cases reported that 87% of incidents occurred at 7,500 m (24,600 ft) or higher.[28] High altitude parachutists performing a HALO jump may develop altitude DCS if they do not flush nitrogen from the body by pre-breathing pure oxygen.[29]

[edit] Predisposing factors

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual.
[edit] Environmental

The following environmental factors have been shown to increase the risk of DCS:

the magnitude of the pressure reduction ratio a large pressure reduction ratio is more likely to cause DCS than a small one.[20][25][30] repetitive exposures repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above 5,500 metres (18,000 ft) within similar short periods increase the risk of developing altitude DCS.[20][30] the rate of ascent the faster the ascent the greater the risk of developing DCS. The US Navy Dive Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS, while recreational dive tables such as the Bhlmann tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute.[31] An individual exposed to a rapid decompression (high rate of ascent) above 5,500 metres (18,000 ft) has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.[20][30] the duration of exposure the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of 5,500 m (18,000 ft) and above, carry a greater risk of altitude DCS.[20] scuba diving before flying divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of 2,400 m (7,900 ft) above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits.[32][33][34] diving before travelling to altitude DCS can occur without flying if the person moves to a highaltitude location on land immediately after scuba diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at 2,400 m (7,900 ft) increase their risk of DCS.[35] diving at altitude diving in water whose surface altitude is above 300 m (980 ft) for example, Lake Titicaca is at 3,800 m (12,500 ft) without using versions of decompression tables or dive computers that are modified for high-altitude.[32][36]

[edit] Individual

Atrial septal defect (PFO) showing left-to-right shunt. A right-to-left shunt may allow bubbles to pass into the arterial circulation.

The following individual factors have been identified as possibly contributing to increased risk of DCS:

a person's age there are some reports indicating a higher risk of altitude DCS with increasing age.[14][30] previous injury there is some indication that recent joint or limb injuries may predispose individuals to developing decompression-related bubbles.[14][37] ambient temperature there is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS.[14][30] Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.[38] body type typically, a person who has a high body fat content is at greater risk of DCS.[14][30] This is due to nitrogen's five times greater solubility in fat than in water, leading to greater amounts of total body dissolved nitrogen during time at pressure. Fat represents about 1525 percent of a healthy adult's body, but stores about half of the total amount of nitrogen (about 1 litre) at normal pressures.[39] alcohol consumption and dehydration although alcohol consumption increases dehydration and therefore may increase susceptibility to DCS,[30] a 2005 study concluded that alcohol consumption did not increase the risk of DCS.[40] Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline,[41] and the high surface tension of water is generally regarded as helpful in controlling bubble size.[30] Maintaining proper hydration is recommended.[42] patent foramen ovale a hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In about 20% of adults the flap does not completely seal, however, allowing blood through the hole when coughing or during activities that raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to the arterial system (including arteries to the brain, spinal cord and heart).[43] In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, infarction results in stroke, and in the spinal cord it may result in paralysis.[44]

[edit] Mechanism

This surfacing diver must enter a decompression chamber to avoid decompression sickness.

Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness.[14][45] Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DCS.[46] The amount of gas dissolved in a liquid is described by Henry's Law, which indicates that, when the pressure of a gas in contact with a liquid is decreased, the amount of that gas dissolved in the liquid will also decrease proportionately. On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs.[47][48] If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood or within the solid tissues of the body. The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage. The most severe types of DCS interrupt and ultimately damage spinal cord function, leading to paralysis, sensory dysfunction, or death. In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism.[5][49] A similar effect, known as ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure.[50]

[edit] Inert gases

The main inert gas in air is nitrogen, but nitrogen is not the only gas that can cause DCS. Breathing gas mixtures such as trimix and heliox include helium, which can also cause decompression sickness. Helium both enters and leaves the body faster than nitrogen, so different decompression schedules are required, but, since helium does not cause narcosis, it is preferred over nitrogen in gas mixtures for deep diving.[51] There is some debate as to the decompression requirements for helium during short-duration dives. Most divers do longer decompressions, however some groups like the WKPP have been pioneering the use of shorter decompression times by including deep stops.[52] Any inert gas that is breathed under pressure can form bubbles when the ambient pressure decreases. Very deep dives have been made using hydrogen-oxygen mixtures (hydrox),[53] but controlled decompression is still required to avoid DCS.[54]
[edit] Isobaric counterdiffusion Further information: Isobaric counterdiffusion

DCS can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives.[55] For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium, but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect.[56]

[edit] Diagnosis
Decompression sickness should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving.[57] In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours.[58] An alternative diagnosis should be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing.[59] The diagnosis is confirmed if the symptoms are relieved by recompression.[59][60] Although MRI or CT can frequently identify bubbles in DCS, they are not as good at determining the diagnosis as a proper history of the event and description of the symptoms.[3]

[edit] Prevention

[edit] Underwater diving

The display of a basic personal dive computer shows depth, dive time, and decompression information.

To prevent the excess formation of bubbles that can lead to decompression sickness, divers limit their ascent rate to about 10 metres (33 ft) per minute, and carry out a decompression schedule as necessary.[61] This schedule requires the diver to ascend to a particular depth, and remain at that depth until sufficient gas has been eliminated from the body to allow further ascent.[62] Each of these is termed a "decompression stop", and a schedule for a given bottom time and depth may contain one or more stops, or none at all. Dives that contain no decompression stops are called "no-stop dives", but divers usually schedule a short "safety stop" at 3 metres (10 ft), 4.6 metres (15 ft), or 6 metres (20 ft), depending on the training agency.[61][note 2] The decompression schedule may be derived from decompression tables, decompression software, or from dive computers, and these are commonly based upon a mathematical model of the body's uptake and release of inert gas as pressure changes. These models, such as the Bhlmann decompression algorithm, are designed to fit empirical data and provide a decompression schedule for a given depth and dive duration.[63] Since divers on the surface after a dive still have excess inert gas in their bodies, any subsequent dive before this excess is fully eliminated needs to modify the schedule to take account of the residual gas load from the previous dive. This will result in a shorter available time under water or an increased decompression time during the subsequent dive. The total elimination of excess gas may take many hours, and tables will indicate the time at normal pressures that is required, which may be up to 18 hours.[64] Decompression time can be significantly shortened by breathing mixtures containing much less inert gas during the decompression phase of the dive (or pure oxygen at stops in 6 metres (20 ft) of water or less). The reason is that the inert gas outgases at a rate proportional to the difference between the partial pressure of inert gas in the diver's body and its partial pressure in the breathing gas; whereas the likelihood of bubble formation depends on the difference between the

inert gas partial pressure in the diver's body and the ambient pressure. Reduction in decompression requirements can also be gained by breathing a nitrox mix during the dive, since less nitrogen will be taken into the body than during the same dive done on air.[65] Following a decompression schedule does not completely protect against DCS. The algorithms used are designed to reduce the probability of DCS to a very low level, but do not reduce it to zero.[66]
[edit] Exposure to altitude

One of the most significant breakthroughs in the prevention of altitude DCS is oxygen prebreathing. Breathing pure oxygen significantly reduces the nitrogen loads in body tissues and, if continued without interruption, provides effective protection upon exposure to low-barometric pressure environments.[20][21] However, breathing pure oxygen during flight alone (ascent, en route, descent) does not decrease the risk of altitude DCS.[20][21] Although pure oxygen pre-breathing is an effective method to protect against altitude DCS, it is logistically complicated and expensive for the protection of civil aviation flyers, either commercial or private. Therefore, it is currently used only by military flight crews and astronauts for protection during high-altitude and space operations. It is also used by flight test crews involved with certifying aircraft. Astronauts aboard the International Space Station preparing for extra-vehicular activity (EVA) "camp out" at low atmospheric pressure, 10.2 psi (0.70 bar), spending eight sleeping hours in the Quest airlock chamber before their spacewalk. During the EVA they breathe 100% oxygen in their spacesuits, which operate at 4.3 psi (0.30 bar),[67] although research has examined the possibility of using 100% O2 at 9.5 psi (0.66 bar) in the suits to lessen the pressure reduction, and hence the risk of DCS.[68]

[edit] Treatment

The recompression chamber at the Neutral Buoyancy Lab. Further information: Hyperbaric medicine

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided.[69] Mild cases of the "bends" and some skin symptoms may disappear during descent from high altitude; however, it is recommended that these cases still be evaluated. Neurological symptoms, pulmonary symptoms, and mottled or marbled skin lesions should be treated with hyperbaric oxygen therapy if seen within 10 to 14 days of development.[70] Recompression on room air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909.[71] Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke,[72] and has since become the standard of care for treatment of DCS.[73] Recompression is normally carried out in a recompression chamber. At a dive site, a riskier alternative is in-water recompression.[74][75][76] Oxygen first aid has been used as an emergency treatment for diving injuries for years.[77] If given within the first four hours of surfacing, it increases the success of recompression therapy as well as a decrease the number of recompression treatments required.[78] Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as a means of supplying oxygen if dedicated equipment is not available.[79] It is beneficial to give fluids, as this helps reduce dehydration. It is no longer recommended to administer aspirin, unless advised to do so by medical personnel, as analgesics may mask symptoms. People should be made comfortable and placed in the supine position (horizontal), or the recovery position if vomiting occurs.[57] In the past, both the Trendelenburg position and the left lateral decubitus position (Durant's maneuver) have been suggested as beneficial where air emboli are suspected,[80] but are no longer recommended for extended periods, owing to concerns regarding cerebral edema.[77][81]

[edit] Prognosis
Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long term effects. However, permanent long-term injury from DCS is possible. Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed "still had residual signs and symptoms from Type II DCS and 7% from Type I DCS".[82][83] Long-term follow-ups showed similar results, with 16% having permanent neurological sequelae.[84]

Barotrauma

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Barotrauma
From Wikipedia, the free encyclopedia

Jump to: navigation, search

Barotrauma, otitic & Barotrauma, sinus

Classification and external resources

ICD-10

T70.0, T70.1

ICD-9

993.0, 993.1

DiseasesDB

3491

eMedicine

emerg/53

MeSH

D001469

Barotrauma is physical damage to body tissues caused by a difference in pressure between an air space inside or beside the body and the surrounding fluid.[1][2] In addition to humans, and in contrast with Avian lungs, bats suffer fatal barotrauma around wind farms.[3] Barotrauma typically occurs to air spaces within a body when that body moves to or from a higher pressure environment, such as when a SCUBA diver, a free-diving diver or an airplane passenger ascends or descends, or during uncontrolled decompression of a pressure vessel. Boyle's law defines the relationship between the volume of the air space and the ambient pressure. Damage occurs in the tissues around the body's air spaces because gases are compressible and the tissues are not. During increases in ambient pressure, the internal air space provides the surrounding tissues with little support to resist the higher external pressure. During decreases in ambient pressure, the higher pressure of the gas inside the air spaces causes damage to the surrounding tissues if that gas becomes trapped.

Contents
[hide]

1 Types of injury 2 Diving barotrauma o 2.1 Ear barotrauma

2.2 Barosinusitis 2.3 Mask squeeze 2.4 Pulmonary barotrauma 2.5 Causes 2.6 Avoidance and treatment 3 Blast induced barotrauma 4 Ventilator induced barotrauma 5 See also 6 References

o o o o o

[edit] Types of injury

Examples of organs or tissues easily damaged by barotrauma are:

middle ear (barotitis or aerotitis)[1][2][4][5][6][7] paranasal sinuses[1][2][5] (causing Aerosinusitis) lungs[1][2][8][9] eyes[1][2] (the unsupportive air space is inside the diving mask[10]) skin[1][2] (when wearing a diving suit which creates an air space) bone (bone necrosis and temporal lobe injury)[11] Teeth (causing Barodontalgia, i.e. barometric pressure related dental pain,[12][13][14][15][16] or dental fractures[17][18][19])

[edit] Diving barotrauma

[edit] Ear barotrauma

Barotrauma can affect the external, middle, or inner ear. Middle ear barotrauma (MEBT) is the most common being experienced by between 10% and 30% of divers and is due to insufficient equilibration of the middle ear. External ear barotrauma may occur on ascent if high pressure air is trapped in the external auditory canal either by tight fitting SCUBA equipment or ear wax. Inner ear barotrauma (IEBT) though much less common than MEBT shares a similar mechanism. Mechanical trauma to the inner ear can lead to varying degrees of conductive and sensorineural hearing loss as well as vertigo.[20]
[edit] Barosinusitis

The sinuses similar to other air filled cavities are susceptible to barotrauma if their openings become obstructed. This can result in pain as well as epistaxis.[21]

[edit] Mask squeeze

If a diver's mask is not equalized during descent the relative negative pressure can produce petechial hemorrhages in the area covered by the mask along with subconjunctival hemorrhages.[21]
[edit] Pulmonary barotrauma

Pulmonary (lung) pressure damage in scuba divers is usually caused by breath-holding on ascent. The compressed gas in the lungs expands as the ambient pressure decreases causing the lungs to over expand and rupture unless the diver breathes out. The lungs do not sense pain when overexpanded giving the diver little warning to prevent the injury. This does not affect breath-hold skin divers as they bring a lungfull of air with them from the surface, which merely re-expands safely to near its original volume on ascent. The problem only arises if a breath of compressed gas is taken at depth, which will then expand on ascent to more than the lung volume. Pulmonary barotrauma may also be caused by explosive decompression of a pressurised aircraft.
[edit] Causes

When diving, the pressure differences needed to cause the barotrauma come from two sources:

descending and ascending in water. There are two components to the surrounding pressure acting on the diver: the atmospheric pressure and the water pressure. A descent of 10 metres (33 feet) in water increases the ambient pressure by approximately the pressure of the atmosphere at sea level. So, a descent from the surface to 10 metres (33 feet) underwater results in a doubling of the pressure on the diver. breathing gas at depth from SCUBA equipment results in the lungs containing gas at a higher pressure than atmospheric pressure. So a free-diving diver can dive to 10 metres (33 feet) and safely ascend without exhaling, because the gas in the lungs had been inhaled at atmospheric pressure, whereas a SCUBA diver who breathes at 10 metres and ascends without exhaling has lungs containing gas at twice atmospheric pressure and is very likely to suffer life-threatening lung damage.

[edit] Avoidance and treatment

Diving barotrauma can be avoided by eliminating any pressure differences acting on the tissue or organ by equalizing the pressure. There are a variety of techniques:

The air spaces in the ears, and the sinuses. The risk is burst eardrum. Here, the diver can use the Valsalva manoeuvre, to let air into the middle ears via the Eustachian tubes. Sometimes swallowing will open the Eustachian tubes and equalise the ears. See ear clearing. The lungs. The risk is pneumothorax. which is commonly called burst lung by divers. To equalise, always breathe normally and never hold the breath. This risk does not arise when snorkel diving from the surface, unless the snorkeller breathes from a high pressure gas source underwater, or from submerged air pockets. The air inside the usual eyes-and-nose diving mask. The main risk is bleeding around the eyes from the negative pressure[10] or orbital emphysema from higher pressures.[22] Here, let air into the mask

through the nose. Do not dive in eyes-only goggles as sometimes seen on land with industrial breathing sets. Air spaces inside a dry suit. The main risk is folds of skin getting pinched inside folds of the drysuit. Most modern drysuits have a tube connection to feed air in from the cylinder. Air must be injected on the descent and vented on the ascent.

Following barotrauma of the ears or lungs from diving the diver should not dive again until thoroughly cleared by a doctor, which can take many months. [23] Use of a hyperbaric chamber. Patients undergoing hyperbaric oxygen therapy must learn to equalize in order to avoid barotrauma.[24] Some patients may be at greater risk of otic barotrauma than others.[24]

[edit] Blast induced barotrauma

An explosive blast and explosive decompression create a pressure wave that can induce barotrauma. The difference in pressure between internal organs and the outer surface of the body causes injuries to internal organs that contain gas, such as the lungs, gastrointestinal tract, and ear.[25] Lung injuries can also occur during rapid decompression, although the risk of injury is lower than with explosive decompression.[26][27]

[edit] Ventilator induced barotrauma

Mechanical ventilation can lead to barotrauma of the lungs. This can be due to either:

absolute pressures used in order to ventilate non-compliant lungs. shearing forces, particularly associated with rapid changes in gas velocity.

The resultant alveolar rupture can lead to pneumothorax, pulmonary interstitial emphysema (PIE) and pneumomediastinum

Oxygen toxicity

Nitrogen narcosis Nitrogen narcosis

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Inert gas narcosis [Nitrogen narcosis]

Classification and external resources

Divers breathe a mixture of oxygen, helium and nitrogen for deep dives to avoid the effects of narcosis. A cylinder label shows the maximum operating depth and mixture (oxygen/helium).

DiseasesDB

30088

MeSH

C21.613.455.571

Some components of breathing gases, and their relative narcotic potentcies[1]

Gas Ne H2 N2 O2 Ar Kr CO2 Xe

Relative narcotic potency 0.3 0.6 1.0 1.7 2.3 7.1 20.0 25.6

Narcosis while diving (also known as nitrogen narcosis, inert gas narcosis, raptures of the deep, Martini effect), is a reversible alteration in consciousness that occurs while scuba diving

at depth. The Greek word (narcosis) is derived from narke, "temporary decline or loss of senses and movement, numbness", a term used by Homer and Hippocrates.[2] Narcosis produces a state similar to alcohol intoxication or nitrous oxide inhalation, and can occur during shallow dives, but usually does not become noticeable until greater depths, beyond 30 meters (100 ft). Apart from helium, and probably neon, all gases that can be breathed have a narcotic effect, which is greater as the lipid solubility of the gas increases.[3] As depth increases, the effects may become hazardous as the diver is increasingly impaired. Although divers can learn to cope with the effects, it is not possible to develop a tolerance. While narcosis affects all divers, predicting the depth at which narcosis will affect a diver is difficult, as susceptibility varies widely from dive to dive and amongst individuals. The condition is completely reversed by ascending to a shallower depth with no long-term effects. For this reason, narcosis while diving in open water rarely develops into a serious problem as long as the divers are aware of its symptoms and ascend to manage it. Diving beyond 40 m (130 ft) is considered outside the scope of recreational diving: as narcosis and oxygen toxicity become critical factors, specialist training is required in the use of various gas mixtures such as trimix or heliox.

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Causes 4 Mechanism 5 Diagnosis and management 6 Prevention 7 Prognosis and epidemiology 8 History 9 See also 10 Footnotes 11 References 12 External links

[edit] Classification
Narcosis results from breathing gases under elevated pressure and may be classified by the principal gas involved. The noble gases, except helium and probably neon,[3] as well as nitrogen, oxygen and hydrogen cause a decrement in mental function, but their effect on psychomotor function (processes affecting the coordination of sensory or cognitive processes and motor activity) varies widely. The effects of carbon dioxide consistently result in a decrease of both

mental and psychomotor function.[4] The noble gases argon, krypton, and xenon are more narcotic than nitrogen at a given pressure, and xenon has so much anesthetic activity that it is actually a usable anesthetic at 80% concentration and normal atmospheric pressure. Xenon has historically been too expensive to be used very much in practice, but it has been successfully used for surgical operations, and xenon anesthesia systems are still being proposed and designed.[5]

[edit] Signs and symptoms

Narcosis can produce tunnel vision, making it difficult to read multiple gauges Due to its perception-altering effects, the onset of narcosis may be hard to recognize.[6][7] At its most benign, narcosis results in relief of anxiety - a feeling of tranquility and mastery of the environment. These effects are essentially identical to various concentrations of nitrous oxide. They also resemble (though not as closely) the effects of alcohol and the familiar benzodiazepine drugs such as diazepam and alprazolam.[8] Such effects are not harmful unless they cause some immediate danger not to be recognized and addressed. Once stabilized, the effects generally remain the same at a given depth, only worsening if the diver ventures deeper.[9] The most dangerous aspects of narcosis are the loss of decision-making ability and focus, and impaired judgement, multi-tasking and coordination. Other effects include vertigo, and visual or auditory disturbances. The syndrome may cause exhilaration, giddiness, extreme anxiety, depression, or paranoia, depending on the individual diver and the diver's medical or personal history. When more serious, the diver may feel overconfident, disregarding normal safe diving practices.[10] The relation of depth to narcosis is sometimes informally known as "Martini's law". This is the idea that narcosis results in the feeling of one martini for every 10 m (33 ft) below 20 m (66 ft) depth. This is a very rough guide, and not a substitute for an individual diver's known susceptibility, or for standard diving safety guides. Professional divers use such a calculation only as a rough guide to give new divers a metaphor, comparing a situation they may be more familiar with.[11] Reported signs and symptoms are summarized against typical depths in meters and feet of sea water in the following table:[10]

Signs and symptoms of narcosis (breathing air)

Pressure Depth Depth (bar) (m) (ft) 12 010

Comments

0-33 Unnoticeable small symptoms, or no symptoms at all.

24

Mild impairment of performance of unpracticed tasks. 1030 33100 Mildly impaired reasoning. Mild euphoria possible.

46

3050

Delayed response to visual and auditory stimuli. Reasoning and immediate memory affected more than motor coordination. Calculation errors and wrong choices. 100 Idea fixation. 165 Over-confidence and sense of well-being. Laughter and loquacity (in chambers) which may be overcome by self control. Anxiety (common in cold murky water).

68

5070

Sleepiness, impaired judgment, confusion. Hallucinations. 165 Severe delay in response to signals, instructions and other stimuli. 230 Occasional dizziness. Uncontrolled laughter, hysteria (in chamber). Terror in some. Poor concentration and mental confusion. 230 Stupefaction with some decrease in dexterity and judgment. 300 Loss of memory, increased excitability. Hallucinations. Increased intensity of vision and hearing. Sense of impending blackout, euphoria, dizziness, manic or 300+ depressive states, a sense of levitation, disorganization of the sense of time, changes in facial appearance. Unconsciousness. Death.

810

7090

10+

90+

[edit] Causes
The cause of narcosis is related to the increased solubility of gases in body tissues, as a result of the elevated pressures at depth (Henry's law).[12] Modern theories have suggested that inert gases dissolving in the lipid bilayer of cell membranes cause narcosis.[13] More recently, researchers have been looking at neurotransmitter receptor protein mechanisms as a possible cause of the narcosis.[14] The breathing gas mix entering the diver's lungs will have the same pressure as the surrounding water, known as the ambient pressure. For any given depth, the pressure of gases in the blood passing through the brain catches up with ambient pressure within a minute or two and this produces a delay in narcotic effect after coming to a new depth.[6][15] Rapid compression potentiates narcosis, owing to carbon dioxide retention.[16][17] A divers' cognition may be affected on dives as shallow as 10 m (33 ft), but the changes are not usually noticeable.[18] However there is no reliable method to predict the depth at which narcosis becomes noticeable, or the severity of the effect on an individual diver, as the effect may vary from dive to dive (even on the same day).[6][17] Significant impairment due to narcosis is an increasing risk below depths of about 30 m (100 ft), corresponding to an ambient pressure of about 4 bar (400 kPa).[6] Most sport scuba training organizations recommend depths of no more than 40 m (130 ft) because of risk of narcosis.[11] When breathing air at depths of 90 m (300 ft)an ambient pressure of about 10 bar (1,000 kPa)narcosis in most divers leads to hallucinations, loss of memory, and unconsciousness.[16][19] A number of divers have died in attempts to set air depth records below 120 m (400 ft). Because of these incidents, the Guinness Book of World Records no longer reports on this figure.[20] Narcosis has been compared with altitude sickness insofar as its variability (though not its symptoms); its effects depend on many factors, with variations between individuals. Thermal cold, stress, heavy work, fatigue, and carbon dioxide retention all increase the risk and severity of narcosis.[4][6] Carbon dioxide has a high narcotic potential and also causes increased blood flood to the brain, increasing the effects of other gases.[21] Increased risk of narcosis results from increasing the amount of carbon dioxide retained through heavy exercise, shallow or skip breathing, or because of poor gas exchange in the lungs.[22] Narcosis is known to be additive to even minimal alcohol intoxication,[23][24] and also to the effects of other drugs such as marijuana (which is more likely than alcohol to have effects which last into a day of abstinence from use).[25] Other sedative and analgesic drugs, such as opiate narcotics and benzodiazepines, add to narcosis.[23]

[edit] Mechanism

Illustration of a lipid bilayer, typical of a cell membrane, showing the hydrophilic heads on the outside and hydrophobic tails inside The precise mechanism is not well understood, but it appears to be the direct effect of gas dissolving into nerve membranes and causing temporary disruption in nerve transmissions. While the effect was first observed with air, other gases including argon, krypton and hydrogen cause very similar effects at higher than atmospheric pressure.[26] Some of these effects may be due to antagonism at NMDA receptors and potentiation of GABAA receptors,[27] similar to the mechanism of nonpolar anesthetics such diethyl ether or ethylene.[28] However, their reproduction by the very chemically inactive gas argon makes them unlikely to be a strictly chemical bonding to receptors in the usual sense of a chemical bond. An indirect physical effectsuch as a change in membrane volumewould therefore be needed to affect the ligandgated ion channels of nerve cells.[29] Trudell et al. have suggested non-chemical binding due to the attractive van der Waals force between proteins and inert gases.[30] Similar to the mechanism of ethanol's effect, the increase of gas dissolved in nerve cell membranes may cause altered ion permeability properties of the neural cells' lipid bilayers. The partial pressure of a gas required to cause a measured degree of impairment correlates well with the lipid solubility of the gas: the greater the solubility, the less partial pressure is needed.[29] An early theory, the Meyer-Overton hypothesis suggested that narcosis happens when the gas penetrates the lipids of the brain's nerve cells, causing direct mechanical interference with the transmission of signals from one nerve cell to another.[12][13][17] More recently, specific types of chemically-gated receptors in nerve cells have been identified as being involved with anesthesia and narcosis. However, the basic and most general underlying idea, that nerve transmission is altered in many diffuse areas of the brain as a result of gas molecules dissolved in the nerve cells' fatty membranes, remains largely unchallenged.[14][31]

[edit] Diagnosis and management

The symptoms described may be caused by other factors during a dive: ear problems causing disorientation or nausea;[32] early signs of oxygen toxicity causing visual disturbances;[33] or hypothermia causing rapid breathing and shivering.[34] Nevertheless the presence of any of these symptoms should imply narcosis. Alleviation of the effects upon ascending to a shallower depth will confirm the diagnosis. Given the setting, other likely conditions do not produce reversible effects. In the rare event of misdiagnosis when another condition is causing the symptoms, the initial managementascending closer to the surfaceis still essential.[7]

The management of narcosis is simply to ascend to shallower depths; the effects then disappear within minutes.[35] In the event of complications or other conditions being present, ascending is always the correct initial response. Should problems remain, then it is necessary to abort the dive. The decompression schedule can still be followed unless other conditions require emergency assistance.[36]

[edit] Prevention

Narcosis while deep diving is prevented by filling dive cylinders with a gas mixture containing helium. Helium is stored in brown cylinders. The most straightforward way to avoid nitrogen narcosis is for a diver to limit the depth of dives. If narcosis does occur, the effects disappear almost immediately upon ascending to a shallower depth. Since narcosis becomes more severe as depth increases, a diver keeping to shallower depths can avoid serious narcosis. Most recreational dive schools will only certify basic divers to depths of 18 m (60 ft), and at these depths narcosis does not present a large risk. Further training is normally required for certification up to 30 m (100 ft) on air, and this training should include a discussion of narcosis, its effects, and cure. Some diver training agencies offer specialty training to prepare recreational divers to go to depths of 40 m (130 ft), often consisting of further theory and some practice in deep dives with close supervision.[37][nb 1] Scuba organizations which train for diving beyond recreational depths,[nb 2] may forbid diving with gases that cause too much narcosis at depth in the average diver, and strongly encourage the use of other breathing gas mixes containing helium in place of some or all of the nitrogen in airsuch as trimix and helioxbecause helium has no narcotic potential.[3][38] The use of these gases forms part of technical diving and requires further training and certification.[11] While the individual diver cannot predict exactly at what depth the onset of narcosis will occur on a given day, the first symptoms of narcosis for any given diver are often more predictable and personal. For example, one diver may have trouble with eye focus (close accommodation for middle-aged divers), another may experience feelings of euphoria, and another feelings of claustrophobia. Some divers report that they have hearing changes, and that the sound which

their exhaled bubbles make becomes different. Specialist training may help divers in identifying these personal onset signs, and these may then be used as a signal to ascend to shallower depths. Although severe narcosis may interfere with the judgment necessary to take preventive action, a diver who remains calm and is alert to the danger will be capable of resolving these problems at an earlier stage.[35] Deep dives should be made only after a gradual training to gradually test the individual diver's sensitivity to increasing depths, with careful supervision and logging of reactions. Diving organizations such as Global Underwater Explorers (GUE) emphasize that such sessions are for the purpose of gaining experience in recognizing the onset symptoms of narcosis for an individual, which are somewhat more repeatable than for the average group of divers. Scientific evidence does not show that a diver can train to overcome any measure of narcosis at a given depth or become tolerant of it.[39] Equivalent narcotic depth (END) is a commonly used way of expressing the narcotic effect of different breathing gases.[40] The National Oceanic and Atmospheric Administration (NOAA) Diving Manual now states that both oxygen and nitrogen should be considered equally narcotic.[41] Standard tables, based on relative lipid solubilities, list conversion factors for narcotic effect of other gases.[42] For example, neon at a given pressure has a narcotic effect equivalent to nitrogen at 0.28 times that pressure, so in principle it should be usable at nearly four times the depth. Argon, however, has 2.33 times the narcotic effect of nitrogen, and is not suitable as a breathing gas for diving (it is used as a drysuit inflation gas, owing to its low thermal conductivity). Some gases have other dangerous effects when breathed at pressure; for example, high-pressure oxygen can lead to oxygen toxicity. Although helium is the least intoxicating of the breathing gases, at greater depths it can cause high pressure nervous syndrome, a still-mysterious but apparently unrelated phenomenon.[43] Inert gas narcosis is only one factor which influences the choice of gas mixture; the risks of decompression sickness and oxygen toxicity, cost, and other factors are also important.[44] Because of similar and additive effects, divers should avoid sedating medications and drugs, such as marijuana and alcohol before any dive. A hangover, combined with the reduced physical capacity that goes with it, makes nitrogen narcosis more likely.[23] Experts recommend total abstinence from alcohol at least 12 hours before diving, and longer for other drugs.[45] Abstinence time needed for marijuana is unknown, but due to the much longer half-life of the active agent of this drug in the body, it is likely to be longer than for alcohol.[25]

[edit] Prognosis and epidemiology

Narcosis is potentially one of the most dangerous conditions to affect the scuba diver below about 30 m (100 ft). Except for occasional amnesia of events at depth, the effects of narcosis are entirely reversible by ascending and therefore pose no problem in themselves, even for repeated, chronic or acute exposure.[6][17] Nevertheless, the severity of narcosis is unpredictable and it can be fatal while diving, as the result of illogical behavior in a dangerous environment.[17] Tests have shown that all divers are affected by nitrogen narcosis, though some are less affected than others. Even though it is possible that some divers can manage better than others because of

learning to cope with the subjective impairment, the underlying behavioral effects remain.[28][46][47] These effects are particularly dangerous because a diver may feel they are not experiencing narcosis, yet still be affected by it.[6]

[edit] History

Both Meyer and Overton discovered that the narcotic potency of an anesthetic can generally be predicted from its solubility in oil See also: Theories of general anesthetic action French researcher Victor T. Junod was the first to describe symptoms of narcosis in 1834, noting "the functions of the brain are activated, imagination is lively, thoughts have a peculiar charm and, in some persons, symptoms of intoxication are present."[48][49] Junod suggested that narcosis resulted from pressure causing increased blood flow and hence stimulating nerve centers.[50] Walter Moxon (18361886), a prominent Victorian physician, hypothesized in 1881 that pressure forced blood to inaccessible parts of the body and the stagnant blood then resulted in emotional changes.[51] The first report of anesthetic potency being related to lipid solubility was published by Hans H. Meyer in 1899, entitled Zur Theorie der Alkoholnarkose. Two years later a similar theory was published independently by Charles Ernest Overton.[52] What became known as the Meyer-Overton Hypothesis is illustrated in the diagram to the right. In 1939, Albert R. Behnke and O. D. Yarborough demonstrated that gases other than nitrogen also could cause narcosis.[53] For an inert gas the narcotic potency was found to be proportional to its lipid solubility. As hydrogen has only 0.55 the solubility of nitrogen, deep diving experiments using hydrox were conducted by Arne Zetterstrm between 1943 and 1945.[54] Jacques-Yves Cousteau in 1953 famously described it as "livresse des grandes profondeurs" or the "rapture of the deep".[55]

Further research into the possible mechanisms of narcosis by anesthetic action led to the "minimum alveolar concentration" concept in 1965. This measures the relative concentration of different gases required to prevent motor response in 50% of subjects in response to stimulus, and shows similar results for anesthetic potency as the measurements of lipid solubility.[56] The (NOAA) Diving Manual was revised to recommend treating oxygen as if it were as narcotic as nitrogen, following research by Christian J. Lambertsen et al. in 1977 and 1978.[57]

Carbon dioxide poisoning Hypercapnia

From Wikipedia, the free encyclopedia (Redirected from Carbon dioxide poisoning) Jump to: navigation, search

Hypercapnia
Classification and external resources

Carbon dioxide

ICD-10

R06.8

ICD-9

786.09

DiseasesDB

95

MeSH

D006935

Hypercapnia or hypercapnea (from the Greek hyper = "above" and kapnos = "smoke"), also known as hypercarbia, is a condition where there is too much carbon dioxide (CO2) in the blood. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs. Hypercapnia normally triggers a reflex which increases breathing and access to oxygen, such as arousal and turning the head during sleep. A failure of this reflex can be fatal, as in sudden infant death syndrome.[1] Hypercapnia is the opposite of hypocapnia.

Contents
[hide]

1 Causes 2 Symptoms and signs 3 Laboratory values 4 During diving o 4.1 Additional sources of carbon dioxide in diving o 4.2 Skip breathing o 4.3 Rebreathers 5 See also 6 References

[edit] Causes
Hypercapnia is generally caused by hypoventilation, lung disease, or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide (usually due to volcanic or geothermal causes), or by rebreathing exhaled carbon dioxide. It can also be an initial effect of administering supplemental oxygen on a patient with sleep apnea. In this situation the hypercapnia can also be accompanied by respiratory acidosis.[2]

[edit] Symptoms and signs

Main symptoms of Carbon dioxide toxicity, by increasing volume percent in air.[3][4]

Symptoms and signs of early hypercapnia include flushed skin, full pulse, tachypnea, dyspnoea, extrasystoles, muscle twitches, hand flaps, reduced neural activity, and possibly a raised blood pressure. According to other sources, symptoms of mild hypercapnia might include headache, confusion and lethargy. Hypercapnia can induce increased cardiac output, an elevation in arterial blood pressure, and a propensity toward arrhythmias.[5][6] In severe hypercapnia (generally PaCO2 greater than 10 kPa or 75 mmHg), symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death.[7][8]

[edit] Laboratory values

Hypercapnia is generally defined as a blood gas carbon dioxide level over 45 mmHg. Since carbon dioxide is in equilibrium with bicarbonate in the blood, hypercapnia can also result in a high serum bicarbonate (HCO3) concentration. Normal bicarbonate concentrations vary from 22 to 28 milligrams per deciliter.

[edit] During diving

Normal respiration in divers results in alveolar hypoventilation resulting in inadequate CO2 elimination or hypercapnia. Lanphier's work at the US Navy Experimental Diving Unit answered the question "why don't divers breathe enough?":[9]

Higher Inspired Oxygen (PiO2) at 4 atm (404 kPa) accounted for not more than 25% of the elevation in End Tidal CO2 (etCO2) above values found at the same work rate when breathing air just below the surface.[10][11][12][13] Increased Work of Breathing accounted for most of the elevation of PACO2 (alveolar gas equation) in exposures above 1 atm (101 kPa), as indicated by the results when helium was substituted for nitrogen at 4 atm (404 kPa).[10][11][12][13]

Inadequate ventilatory response to exertion was indicated by the fact that, despite resting values in the normal range, PetCO2 rose markedly with exertion even when the divers breathed air at a depth of only a few feet.[10][11][12][13]

[edit] Additional sources of carbon dioxide in diving

There is a variety of reasons for carbon dioxide not being expelled completely when the diver exhales:

The diver is exhaling into a vessel that does not allow all the CO2 to escape to the environment, such as a long snorkel, full face diving mask, or diving helmet, and the diver then re-inhales from that vessel, causing increased deadspace.[13] The carbon dioxide scrubber in the diver's rebreather is failing to remove sufficient carbon dioxide from the loop (Higher inspired CO2). The diver is over-exercising, producing excess carbon dioxide due to elevated metabolic activity. The density of the breathing gas is higher at depth, so the effort required to fully inhale and exhale has increased, making breathing more difficult and less efficient (Work of breathing).[9] The higher gas density also causes gas mixing within the lung to be less efficient, thus increasing the deadspace (wasted breathing).[13] The diver is deliberately hypoventilating, known as "skip breathing" (see below).

[edit] Skip breathing

Skip breathing is a controversial technique to conserve breathing gas when using open-circuit scuba, which consists of briefly holding one's breath between inhalation and exhalation (i.e., "skipping" a breath). It leads to CO2 not being exhaled efficiently. There is also an increased risk of burst lung from holding the breath while ascending. It is counterproductive with a rebreather, where the act of breathing pumps the gas around the "loop", pushing carbon dioxide through the scrubber and mixing freshly injected oxygen.
[edit] Rebreathers

In closed circuit SCUBA (rebreather) diving, exhaled carbon dioxide must be removed from the breathing system, usually by a scrubber containing a solid chemical compound with a high affinity for CO2, such as soda lime.[14] If not removed from the system, it may be re-inhaled, causing an increase in the inhaled concentration.

Carbon monoxide poisoning Carbon monoxide poisoning

From Wikipedia, the free encyclopedia Jump to: navigation, search

This article is about carbon monoxide poisoning. For general information on carbon monoxide, see carbon monoxide.

Carbon monoxide poisoning

Classification and external resources

Spacefilling model of a carbon monoxide molecule

ICD-10

T58.

ICD-9

986

DiseasesDB

2020

MedlinePlus

002804

eMedicine

emerg/817

MeSH

C21.613.455.245

Carbon monoxide poisoning occurs after enough inhalation of carbon monoxide (CO). Carbon monoxide is a toxic gas, but, being colorless, odorless, tasteless, and initially non-irritating, it is very difficult for people to detect. Carbon monoxide is a product of incomplete combustion of organic matter due to insufficient oxygen supply to enable complete oxidation to carbon dioxide (CO2). It is often produced in domestic or industrial settings by older motor vehicles and other gasoline-powered tools, heaters, and cooking equipment. Exposures at 100 ppm or greater can be dangerous to human health.[1]

Symptoms of mild acute poisoning include lightheadedness, confusion, headaches, vertigo, and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart, and even death. Following acute poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman. Chronic exposure to low levels of carbon monoxide can lead to depression, confusion, and memory loss. Carbon monoxide mainly causes adverse effects in humans by combining with hemoglobin to form carboxyhemoglobin (HbCO) in the blood. This prevents oxygen binding to hemoglobin, reducing the oxygen-carrying capacity of the blood, leading to hypoxia. Additionally, myoglobin and mitochondrial cytochrome oxidase are thought to be adversely affected. Carboxyhemoglobin can revert to hemoglobin, but the recovery takes time because the HbCO complex is fairly stable. Treatment of poisoning largely consists of administering 100% oxygen or providing hyperbaric oxygen therapy, although the optimum treatment remains controversial.[2] Oxygen works as an antidote as it increases the removal of carbon monoxide from hemoglobin, in turn providing the body with normal levels of oxygen. The prevention of poisoning is a significant public health issue. Domestic carbon monoxide poisoning can be prevented by early detection with the use of household carbon monoxide detectors. Carbon monoxide poisoning is the most common type of fatal poisoning in many countries.[3] Historically, it was also commonly used as a method to commit suicide, usually by deliberately inhaling the exhaust fumes of a running car engine. Modern cars with electronically controlled combustion and catalytic converters produce so little carbon monoxide that this is much less viable. Carbon monoxide poisoning has also been implicated as the cause of apparent haunted houses. Symptoms such as delirium and hallucinations have led people suffering poisoning to think they have seen ghosts or to believe their house is haunted.[4]

Contents
[hide]

1 Signs and symptoms o 1.1 Acute poisoning o 1.2 Chronic poisoning 2 Causes 3 Pathophysiology o 3.1 Hemoglobin o 3.2 Myoglobin o 3.3 Cytochrome oxidase o 3.4 Central nervous system effects o 3.5 Pregnancy 4 Diagnosis o 4.1 Differential diagnosis o 4.2 Detection in biological specimens 5 Prevention o 5.1 Carbon monoxide detection o 5.2 Standardization 6 Treatment

6.1 Hyperbaric oxygen 6.2 Other 7 Epidemiology o 7.1 Suicide 8 Society and culture o 8.1 Haunted houses 9 References 10 See also

o o

[edit] Signs and symptoms

Carbon monoxide is toxic to all aerobic forms of life. It is easily absorbed through the lungs.[5] Carbon monoxide is colorless, odorless, tasteless, and non-irritating, which makes it difficult for humans to detect.[5] Inhaling even relatively small amounts of the gas can lead to hypoxic injury, neurological damage, and even death. Different people and populations may have a different carbon monoxide tolerance level.[6] On average, exposures at 100 ppm or greater is dangerous to human health.[1] In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm averaged over an 8-hour period;[7][8] in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached.[9] Carbon monoxide exposure may lead to a significantly shorter life span due to heart damage.[10] The carbon monoxide tolerance level for any person is altered by several factors, including activity level, rate of ventilation, a pre-existing cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease and other hematological disorders, barometric pressure, and metabolic rate.[11][12][13] The acute effects produced by carbon monoxide in relation to ambient concentration in parts per million are listed below:[14][15]
Concentration Symptoms

35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure 100 ppm (0.01%) Slight headache in two to three hours 200 ppm (0.02%) Slight headache within two to three hours; loss of judgment 400 ppm (0.04%) Frontal headache within one to two hours 800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 min; insensible within 2 hours 1,600 ppm (0.16%) Headache, tachycardia, dizziness, and nausea within 20 min; death in less than 2 hours

3,200 ppm (0.32%) 6,400 ppm (0.64%) 12,800 ppm (1.28%)

Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes. Headache and dizziness in one to two minutes. Convulsions, respiratory arrest, and death in less than 20 minutes. Unconsciousness after 2-3 breaths. Death in less than three minutes.

[edit] Acute poisoning

The main manifestations of poisoning develop in the organ systems most dependent on oxygen use, the central nervous system and the heart.[7] The initial symptoms of acute carbon monoxide poisoning include headache, nausea, malaise, and fatigue.[16] These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis.[17] Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous.[18] Increasing exposure produces cardiac abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia;[19][20] central nervous system symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and even death.[21][22] Less common symptoms of acute carbon monoxide poisoning include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute kidney failure, skin lesions, and visual and auditory problems.[19][23][24][25] One of the major concerns following acute carbon monoxide poisoning is the severe delayed neurological manifestations that may occur. Problems may include difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia, psychosis, irritability, a strange gait, speech disturbances, Parkinson's disease-like syndromes, cortical blindness, and a depressed mood.[17][26] Depression may even occur in those who did not have pre-existing depression.[27] These delayed neurological sequelae may occur in up to 50% of poisoned patients after 2 to 40 days.[17] It is difficult to predict who will develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms.[28]
[edit] Chronic poisoning

Chronic exposure to relatively low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, nausea and vomiting.[29] It is unknown whether low-level chronic exposure may cause permanent neurological damage.[17] Typically, upon removal from exposure to carbon monoxide, symptoms usually resolve themselves, unless there has been an episode of severe acute poisoning.[29] However, one case noted permanent memory loss and learning problems after a 3-year exposure to relatively low levels of carbon monoxide from a faulty furnace.[30] Chronic exposure may worsen cardiovascular symptoms in some people.[29] Long-term exposures to carbon monoxide present the greatest risk to persons with coronary heart disease and in females who are pregnant.[31]

[edit] Causes
Concentration 0.1 ppm 0.5 to 5 ppm 5 to 15 ppm Source Natural atmosphere level (MOPITT)[32] Average level in homes[33] Near properly adjusted gas stoves in homes[33]

100 to 200 ppm Exhaust from automobiles in the Mexico City central area[34] 5,000 ppm 7,000 ppm Exhaust from a home wood fire[35] Undiluted warm car exhaust without a catalytic converter[35]

Carbon monoxide is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Sources of carbon monoxide include cigarette smoke, house fires, faulty furnaces, heaters, wood-burning stoves, internal combustion vehicle exhaust, electrical generators, propane-fueled equipment such as portable stoves, and gasoline-powered tools such as leaf blowers, lawn mowers, high-pressure washers, concrete cutting saws, power trowels, and welders.[17][29][36][37][38][39] Exposure typically occurs when equipment is used in buildings or semi-enclosed spaces.[17] Poisoning may also occur following the use of a self-contained underwater breathing apparatus (SCUBA) due to faulty diving air compressors.[40] Riding in pickup trucks has led to poisoning in children.[41] Idling automobiles with the exhaust pipe blocked by snow has led to the poisoning of car occupants.[42] Generators and propulsion engines on boats, especially houseboats, has resulted in fatal carbon monoxide exposures.[43][44] Another source of poisoning is exposure to the organic solvent dichloromethane, found in some paint strippers. Dichloromethane is converted into carbon monoxide by the body.[45][46][47] In some caves carbon monoxide can build up in enclosed chambers due to decomposing organic matter.[48]

[edit] Pathophysiology
The precise mechanisms by which the effects of carbon monoxide are induced upon bodily systems, are complex and not yet fully understood.[16] Known mechanisms include carbon monoxide binding to hemoglobin, myoglobin and mitochondrial cytochrome oxidase, and carbon monoxide causing brain lipid peroxidation.[21][49][50]

[edit] Hemoglobin

Carbon monoxide shifts the oxygen-dissociation curve to the left.

Following absorption, carbon monoxide binds to hemoglobin, which is the principal oxygencarrying compound in blood; this produces a compound known as carboxyhemoglobin. The traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood and inhibits the transport, delivery, and utilization of oxygen by the body. The affinity between hemoglobin and carbon monoxide is approximately 230 times stronger than the affinity between hemoglobin and oxygen so hemoglobin binds to carbon monoxide in preference to oxygen.[50][51][52] Hemoglobin is a tetramer with four oxygen binding sites. The binding of carbon monoxide at one of these sites increases the oxygen affinity of the remaining three sites, which causes the hemoglobin molecule to retain oxygen that would otherwise be delivered to the tissue.[49] This situation is described as carbon monoxide shifting the oxygen dissociation curve to the left.[50] Because of the increased affinity between hemoglobin and oxygen during carbon monoxide poisoning, the blood oxygen content is increased. But because all the oxygen stays in the hemoglobin, none is delivered to the tissues. This causes hypoxic tissue injury.[17] Hemoglobin acquires a bright red color when converted into carboxyhemoglobin, so poisoned patients have been described as looking pink-cheeked and healthy. However, this cherry-red appearance is rarely seen in living patients so is not considered a reliable diagnostic sign.[50][53][54]
[edit] Myoglobin

Carbon monoxide also binds to the hemeprotein myoglobin. It has a high affinity for myoglobin, about 60 times greater than that of oxygen.[17] Carbon monoxide bound to myoglobin may impair its ability to utilize oxygen.[50] This causes reduced cardiac output and hypotension, which may result in brain ischemia.[17] A delayed return of symptoms have been reported. This results following a recurrence of increased carboxyhemoglobin levels; this effect may be due to a late release of carbon monoxide from myoglobin, which subsequently binds to hemoglobin.[3]

[edit] Cytochrome oxidase

Another mechanism involves effects on the mitochondrial respiratory enzyme chain that is responsible for effective tissue utilization of oxygen. Carbon monoxide binds to cytochrome oxidase with less affinity than oxygen, so it is possible that it requires significant intracellular hypoxia before binding.[55] This binding interferes with aerobic metabolism and efficient adenosine triphosphate synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death.[56] The rate of dissociation between carbon monoxide and cytochrome oxidase is slow, causing a relatively prolonged impairment of oxidative metabolism.[16]
[edit] Central nervous system effects

The mechanism that is thought to have a significant influence on delayed effects involves formed blood cells and chemical mediators, which cause brain lipid peroxidation (degradation of unsaturated fatty acids). Carbon monoxide causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals including peroxynitrite.[16] In the brain this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis.[57] The result of these effects is lipid peroxidation, which causes delayed reversible demyelinization of white matter in the central nervous system known as Grinker myelinopathy, which can lead to edema and necrosis within the brain.[49] This brain damage occurs mainly during the recovery period. This may result in cognitive defects, especially affecting memory and learning, and movement disorders. These disorders are typically related to damage to the cerebral white matter and basal ganglia.[57][58] Hallmark pathological changes following poisoning are bilateral necrosis of the white matter, globus pallidus, cerebellum, hippocampus and the cerebral cortex.[1][17][59]
[edit] Pregnancy

Carbon monoxide poisoning in pregnant women may cause severe adverse fetal effects. Poisoning causes fetal tissue hypoxia by decreasing the release of maternal oxygen to the fetus. Carbon monoxide also crosses the placenta and combines with fetal hemoglobin, causing more direct fetal tissue hypoxia. Additionally, fetal hemoglobin has a 10 to 15% higher affinity for carbon monoxide than adult hemoglobin, causing more severe poisoning in the fetus than in the adult.[3] Elimination of carbon monoxide is slower in the fetus, leading to an accumulation of the toxic chemical.[60] The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so despite mild maternal poisoning or following maternal recovery, severe fetal poisoning or death may still occur.[61]

[edit] Diagnosis

Finger tip Carboxyhemoglobin saturation monitor (SpCO%). Note: This is not the same as a pulse oximeter (SpO2%), although some models (such as this one) do measure both the oxygen and carbon monoxide saturation.

As many symptoms of carbon monoxide poisoning also occur with many other types of poisonings and infections (such as the flu), the diagnosis is often difficult.[47][62] A history of potential carbon monoxide exposure, such as being exposed to a residential fire, may suggest poisoning, but the diagnosis is confirmed by measuring the levels of carbon monoxide in the blood. This can be determined by measuring the amount of carboxyhemoglobin compared to the amount of hemoglobin in the blood.[17] Carbon monoxide is produced naturally by the body as a byproduct of converting protoporphyrin into bilirubin. This carbon monoxide also combines with hemoglobin to make carbooxyhemoglobin, but not at toxic levels.[17] The ratio of carboxyhemoglobin to hemoglobin molecules in an average person may be up to 5%, although cigarette smokers who smoke two packs/day may have levels up to 9%.[63] Serious toxicity occurs with the carboxyhemoglobin to hemoglobin ratio above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects.[16] Carboxyhemoglobin levels should be considered as guides to exposure levels rather than guides to effects, as they do not reliably predict clinical course of action or short- and long-term consequences.[64] Patients may continue to experience significant symptoms of CO poisoning long after their blood carboxyhemoglobin concentration has returned to normal.[65] Because of this, for late arriving patients a normal carboxyhemoglobin level does not rule out poisoning.[66] A CO-oximeter is used to determine carboxyhemoglobin levels.[67][68] Pulse CO-oximeters estimate carboxyhemoglobin with a non-invasive finger clip similar to a pulse oximeter.[69]

These devices function by passing various wavelengths of light through the fingertip and measuring the light absorption of the different types of hemoglobin in the capillaries.[70] A 2010 study was undertaken to address concerns over the differences in concentration measurements between CO-oximeter results and the results of a standard laboratory blood test. Smaller previous studies had been conducted, however because of specific issues with their study design, the clinical application of CO-oximetry was called into question.[71][72][73][74] In the 2010 study, differences between CO-oximeter results and standard laboratory tests fell outside of the clinically acceptable limits of +/- 5% carboxyhemoglobin in 33.3% of tests. When compared to the laboratory test results, the discrepancies between CO-oximetry tests ranged from -11.6% to +14.4%. Sensitivity in this study was determined to be 48%, while specificity was determined to be 99%.[72] Additionally, because these devices function based on measuring absorbance of light wavelengths, a patients skin-tone can affect results, which is specifically of concern when these devices are used on black or Hispanic patients.[71] The researchers concluded, based on their results and a lack of peer-reviewed research on the subject, that CO-oximetry cannot replace standard laboratory analysis in clinical care. CO-oximeters were also not recommended for use as an out-of-hospital triage tool. The use of a regular pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning as patients suffering from carbon monoxide poisoning may have a normal oxygen saturation level on a pulse oximeter.[75] This is due to the carboxyhemoglobin being misrepresented as oxyhemoglobin.[76]

Breath CO monitor displaying carbon monoxide concentration of an exhaled breath sample (in ppm) with its corresponding percent concentration of carboxyhemoglobin.

Breath CO monitoring offers a viable alternative to pulse CO-oximetry. Carboxyhemoglobin levels have been shown to have a strong correlation with breath CO concentration[77] .[78] Because of this, monitoring CO in an exhaled sample allows for a non-invasive means to determine carboxyhemoglobin concentrations and to help diagnose patients experiencing symptoms of CO poisoning. Several models of Breath CO monitors are available commercially, which function based on the use of an electrochemical gas sensor to detect CO.[79] These devices are not susceptible to misrepresenting carboxyhemoglobin as oxyhemoglobin. Monitoring CO via exhaled breath has been demonstrated to be useful in emergency medical services when determining the blood CO levels of individuals who are known or suspected to have received exposure.[80]
[edit] Differential diagnosis

There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning.[7][22] The earliest symptoms, especially from low level exposures, are often nonspecific and readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue syndrome, chest pain, and migraine or other headaches.[81] Carbon monoxide has been called a great mimicker due to the presentation of poisoning being diverse and nonspecific.[7] Other conditions included in the differential diagnosis include acute respiratory distress syndrome, altitude sickness, lactic acidosis, diabetic ketoacidosis, meningitis, methemoglobinemia, or opioid or toxic alcohol poisoning.[22]
[edit] Detection in biological specimens

Carbon monoxide may be quantitated in blood using spectrophotometric methods or chromatographic techniques in order to confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation of a case of fatal exposure. Carboxyhemoglobin blood saturations may range up to 8-10% in heavy smokers or persons extensively exposed to automotive exhaust gases. In symptomatic poisoned patients they are often in the 10-30% range, while persons who succumb may have postmortem blood levels of 30-90%.[82][83]

[edit] Prevention

Carbon Monoxide detector connected to a North American power outlet [edit] Carbon monoxide detection

Prevention remains a vital public health issue, requiring public education on the safe operation of appliances, heaters, fireplaces, and internal-combustion engines, as well as increased emphasis on the installation of carbon monoxide detectors.[5] In buildings, carbon monoxide detectors are usually installed around heaters and other equipment. If a relatively high level of carbon monoxide is detected, the device sounds an alarm, giving people the chance to evacuate and ventilate the building.[84][85] Unlike smoke detectors, carbon monoxide detectors do not need to be placed near ceiling level.[86] The United States Consumer Product Safety Commission has stated, "carbon monoxide detectors are as important to home safety as smoke detectors are," and recommends each home have at least one carbon monoxide detector, and preferably one on each level of the building.[87] These devices, which are relatively inexpensive[85] and widely available, are either battery- or AC-powered, with or without battery backup.[88]
[edit] Standardization

The use of carbon monoxide detectors has been standardized in many areas. In the USA, NFPA 720-2009,[89] the carbon monoxide detector guidelines published by the National Fire Protection Association, mandates the placement of carbon monoxide detectors/alarms on every level of the residence, including the basement, in addition to outside sleeping areas. In new homes, ACpowered detectors must have battery backup and be interconnected to ensure early warning of occupants at all levels.[89] NFPA 720-2009 is the first national carbon monoxide standard to

address devices in non-residential buildings. These guidelines, which now pertain to schools, healthcare centers, nursing homes and other non-residential buildings, includes three main points:[89]
1. A secondary power supply (battery backup) must operate all carbon monoxide notification appliances for at least 12 hours, 2. Detectors must be on the ceiling in the same room as permanently installed fuel-burning appliances, and 3. Detectors must be located on every habitable level and in every HVAC zone of the building.

[edit] Treatment
Initial treatment for carbon monoxide poisoning is to immediately remove the person from the exposure without endangering further people. Those who are unconscious may require CPR on site.[50] Administering oxygen via non-rebreather mask shortens the half life of carbon monoxide to 80 minutes from 320 minutes on normal air.[21] Oxygen hastens the dissociation of carbon monoxide from carboxyhemoglobin, thus turning it back into hemoglobin.[6][90] Due to the possible severe effects in the fetus, pregnant women are treated with oxygen for longer periods of time than nonpregnant patients.[91]
[edit] Hyperbaric oxygen

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin[6] and cytochrome oxidase[92] to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 minutes, compared to 80 minutes for regular oxygen.[6] It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin.[90] However it is controversial whether hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen, in terms of increased survival or improved long-term outcomes.[2][93][94][95][96][97] There have been randomized controlled trials in which the two treatment options have been compared;[64][98][99][100][101][102] of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen.[2] Some of these trials have been criticized for apparent flaws in their implementation.[103][104][105] A review of all the literature on carbon monoxide poisoning treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a medically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.[2]

[edit] Other

Further treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support.[50] Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression.[106] Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols.[17] If severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability.[107] Treatment of acidosis may only need to consist of oxygen therapy.[17][22] The delayed development of neuropsychiatric impairment is one of the most serious complications of carbon monoxide poisoning. Brain damage is confirmed following MRI or CAT scans.[16][108][109] Extensive follow up and supportive treatment is often required for delayed neurological damage.[21] Outcomes are often difficult to predict following poisoning,[110] especially patients who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels.[22] One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome.[47]

[edit] Epidemiology
The true number of incidents of carbon monoxide poisoning is unknown, since many non-lethal exposures go undetected.[16][47] From the available data, carbon monoxide poisoning is the most common cause of injury and death due to poisoning worldwide.[111] Poisoning is typically more common during the winter months.[7][112][113][114] This thought to be due increased domestic use of gas furnaces, gas or kerosene space heaters, and kitchen stoves during the winter months, which if faulty and/or are used without adequate ventilation, may produce excessive carbon monoxide.[7][115] It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[116] In many industrialized countries carbon monoxide is the cause of more than 50% of fatal poisonings.[3] In the United States, approximately 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[87] Carbon monoxide poisoning contributes to the approximately 5613 smoke inhalation deaths each year in the United States.[117] The CDC reports, "Each year, more than 500 Americans die from unintentional carbon monoxide poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."[118] For the 10-year period from 1979 to 1988, 56,133 deaths from carbon monoxide poisoning occurred in the United States, with 25,889 of those being suicides, leaving 30,244 unintentional deaths.[117] A report from New Zealand showed that 206 people died from carbon monoxide poisoning in the years of 2001 and 2002. In total carbon monoxide poisoning was responsible for 43.9% of deaths by poisoning in that country.[119] In South Korea, 1,950 people had been poisoned by carbon monoxide with 254 deaths

from 2001 through 2003.[120] A report from Jerusalem showed 3.53 per 100,000 people were poisoned annually from 2001 through 2006.[121] in Hubei, China, 218 deaths from poisoning were reported over a 10 year period with 16.5% being from carbon monoxide exposure.[122]
[edit] Suicide

Before the 1960s most domestic gas supply in the United Kingdom was coal gas (alternatively known as town gas), which in its unburned form contained high levels of carbon monoxide. Carbon monoxide poisoning by intentionally inhaling coal gas was a common suicide method, accounting for nearly half of all suicides in the United Kingdom in the late 1950s.[123] After the British government phased out coal gas in favor of natural gas in the 1960s, the suicide rate in Britain fell by almost a third and has not risen since.[123] The use of coal gas as a suicide method has declined as most domestic gas supply worldwide is now natural gas, which lacks carbon monoxide.[124][125] Until the invention of catalytic converters, suicide has been committed by inhaling the exhaust fumes of a running car engine, particularly in an enclosed space such as a garage.[126][127] Before 1975, motor car exhaust contained 410% carbon monoxide, but newer cars have catalytic converters that eliminate over 99% of the carbon monoxide produced.[128] However even cars with catalytic converters can produce substantial amounts of carbon monoxide if an idling car is left in an enclosed space such as a closed garage.[129] As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or fossil fuels within a confined space.[130] Such incidents have occurred mostly in connection with group suicide pacts in Asian countries such as Japan, Taiwan, and Hong Kong,[131][132][133][134] but are starting to occur in western countries as well,[135][136][137] such as the 2007 suicide of Boston lead singer Brad Delp.[138]

[edit] Society and culture

[edit] Haunted houses

Many of the phenomena generally associated with haunted houses, including strange visions and sounds and feelings of dread, can be attributed to carbon monoxide poisoning, as its symptoms include confusion, delirium, emotional disturbances, and hallucinations.[22][139] In one famous case, carbon monoxide poisoning was clearly identified as the cause of an alleged haunting. Dr. William Wilmer, an ophthalmologist, described the experiences of one of his patients in a 1921 article published in the American Journal of Ophthalmology. "Mr. and Mrs. H." moved into a new home, but soon began to complain of headaches and fatigue. They began to think they were hearing bells and footsteps during the night, accompanied by strange physical sensations and sightings of mysterious figures. When they began to investigate the symptoms, they discovered the previous residents of the house had

similar experiences. An examination of their furnace found it to be severely damaged, resulting in incomplete combustion and forcing most of the fumes, including carbon monoxide, into the house rather than up the chimney.[4] A report published in 2005 described a 23-year old female victim of carbon monoxide poisoning, found delirious and hyperventilating, who thought she saw a ghost while in the shower. A new gas water heater had just been improperly installed in her home, which flooded the house with carbon monoxide when the victim closed all the exterior windows and doors and took a shower.[139]

HPNS High-pressure nervous syndrome

From Wikipedia, the free encyclopedia (Redirected from HPNS) Jump to: navigation, search

High-pressure nervous syndrome (HPNS also known as high-pressure neurological syndrome) is a neurological and physiological diving disorder that results when a commercial diver or scuba diver descends below about 500 feet (150 m) while breathing a heliumoxygen mixture. The effects depend on the rate of descent and the depth.[1] HPNS is a limiting factor in future deep diving. "Helium tremors" were first widely described in 1965 by Royal Navy physiologist Peter B. Bennett, who also founded the Divers Alert Network.[1][2] Russian scientist G. L. Zal'tsman also reported on helium tremors in his experiments from 1961. Unfortunately these reports were not available in the West until 1967.[3] The term high pressure nervous syndrome was first used by Brauer to describe the combined symptoms of tremor, electroencephalography (EEG) changes, and somnolence that appeared during a 1,189-foot (362 m) chamber dive in Marseilles.[4]

Contents
[hide]

1 Symptoms 2 Causes 3 Prevention o 3.1 Rate of Compression o 3.2 Breathing Mixture o 3.3 Drugs

4 See also 5 References 6 External links

[edit] Symptoms
Symptoms of HPNS include tremors, myoclonic jerking, somnolence, EEG changes,[5] visual disturbance, nausea, dizziness, and decreased mental performance.[1][2]

[edit] Causes
HPNS has two components, one resulting from the speed of compression and the other from the absolute pressure. The compression effects may occur when descending below 500 feet (150 m) at rates greater than a few metres per minute, but reduce within a few hours once the pressure has stabilised. The effects from depth become significant at depths exceeding 1,000 feet (300 m) and remain regardless of the time spent at that depth.[1] The susceptibility of divers and animals to HPNS varies over a wide range depending on the individual, but has little variation between different dives by the same diver.[1]

[edit] Prevention
It is likely that HPNS can not be entirely prevented but there are effective methods to delay or change the development of the symptoms.[1][6]
[edit] Rate of Compression

Utilizing slow rates of compression or adding stops to the compression have been found to prevent large initial decrements in performance.[1][7]
[edit] Breathing Mixture

Including other gases in the mix, such as nitrogen (creating trimix) or hydrogen (hydreliox) suppresses the neurological effects.[8][9][10]
[edit] Drugs

Alcohol, anesthetics and anticonvulsant drugs have had varying results in suppressing HPNS with animals.[1] None are currently in use for humans.

Salt water aspiration syndrome Salt water aspiration syndrome

From Wikipedia, the free encyclopedia

Jump to: navigation, search Salt water aspiration syndrome is a rare diving disorder suffered by SCUBA divers who inhale a mist of seawater from a faulty demand valve causing irritation of the lungs.[1][2] It can be treated by rest for several hours. If severe, medical assessment is required.

Contents
[hide]

1 Symptoms 2 See also 3 References 4 External links

[edit] Symptoms
Symptoms of salt water aspiration syndrome include:

Aches and pains Cyanosis Mild fever Shortness of breath

Respiratory physiology
Respiratory physiology is the branch of human physiology focusing upon respiration.

Gaseous exchange in the lung.

Lung volumes
Lung volumes and lung capacities refer to the volume of air associated with different phases of the respiratory cycle. Lung volumes are directly measured. Lung capacities are inferred from lung volumes. The average total lung capacity of an adult human male is about 6 litres of air, but only a small amount of this capacity is used during normal breathing. Tidal breathing is normal, resting breathing; the tidal volume is the volume of air that is inhaled or exhaled in a single such breath.

TLC

Total lung capacity: the volume in the lungs at maximal inflation

RV

Residual volume: the volume of air remaining in the lungs after a maximal exhalation

ERV

Expiratory reserve volume: the maximal volume of air that can be exhaled from the end-expiratory position

IRV

Inspiratory reserve volume: the maximal volume that can be inhaled from the endinspiratory level

IC

Inspiratory capacity: the sum of IRV and TV

IVC

Inspiratory vital capacity: the maximum volume of air inhaled from the point of maximum expiration

VC

Vital capacity: the volume equal to TLC R

VT

Tidal volume: that volume of air moved into or out of the lungs during quiet breathing

(VT indicates a subdivision of the lung; when tidal volume is precisely measured, as in gas exchange calculation, the symbol VT or VT is used.)

FRC

Functional residual capacity: the volume in the lungs at the end-expiratory position

RV/TLC% Residual volume expressed as percent of TLC

VA

Alveolar gas volume

VL

Actual volume of the lung including the volume of the conducting airway.

FVC

Forced vital capacity: the determination of the vital capacity from a maximally forced expiratory effort

FEV1

Volume that has been exhaled at the end of the first second of forced expiration

FEFx

Forced expiratory flow related to some portion of the FVC curve; modifiers refer to amount of FVC already exhaled

FEFmax

The maximum instantaneous flow achieved during a FVC maneuver

FIF

Forced inspiratory flow: (Specific measurement of the forced inspiratory curve is denoted by nomenclature analogous to that for the forced expiratory curve. For example,

maximum inspiratory flow is denoted FIFmax. Unless otherwise specified, volume qualifiers indicate the volume inspired from RV at the point of measurement.)

PEF

The highest forced expiratory flow measured with a peak flow meter

MVV

Maximal voluntary ventilation: volume of air expired in a specified period during repetitive maximal effort

vde

An average human breathes some 12-20 times per minute.

Factors affecting volumes

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(December 2010)

Several factors affect lung volumes; some can be controlled and some cannot. Lung volumes can be measured using the following terms: Larger volumes taller people non-smokers people who live at higher altitudes Smaller volumes shorter people smokers people who live at lower altitudes

A person who is born and lives at sea level will develop a slightly smaller lung capacity than a person who spends their life at a high altitude. This is because the partial pressure of oxygen is lower at higher altitude which, as a result means that oxygen less readily diffuses into the

bloodstream. In response to higher altitude, the body's diffusing capacity increases in order to process more air. When someone living at or near sea level travels to locations at high altitudes (e.g., the Andes, Denver, Colorado, Tibet, the Himalayas, etc.) that person can develop a condition called altitude sickness because their lungs remove adequate amounts of carbon dioxide but they do not take in enough oxygen. (In normal individuals, carbon dioxide is the primary determinant of respiratory drive.) Specific changes in lung volumes occur also during pregnancy. Decreased functional residual capacity is seen, typically falling from 1.7 to 1.35 litres,[citation needed] due to the compression of the diaphragm by the uterus. The compression also causes a decreased total lung capacity (TLC) by 5% and decreased expiratory reserve volume. Tidal volume increases with 30-40%, from 0.45 to 0.65 litres,[citation needed] and minute ventilation by 30-40%[1] giving an increase in pulmonary ventilation. This is necessary to meet the increased oxygen requirement of the body, which reaches 50 mL/min, 20 mL of which goes to reproductive tissues. Overall, the net change in maximum breathing capacity is zero.[2]

Values
Average lung volumes in healthy adults[3] Volume Inspiratory reserve volume Tidal volume Expiratory reserve volume Residual volume Value (litres) In men In women 3.3 0.5 1.0 1.2 1.9 0.5 0.7 1.1

Lung capacities in healthy adults[3] Volume Vital capacity Inspiratory capacity Functional residual capacity Total lung capacity Average value (litres) In men 4.8 3.8 2.2 6.0 In women 3.1 2.4 1.8 4.2 Derivation IRV plus TV plus ERV IRV plus TV ERV plus RV IRV plus TV plus ERV plus RV

The tidal volume, vital capacity, inspiratory capacity and expiratory reserve volume can be measured directly with a spirometer. These are the basic elements of a ventilatory pulmonary function test. Determination of the residual volume can be done by radiographic planimetry, body plethysmography, closed circuit dilution and nitrogen washout.

In absence of such , estimates of residual volume have been prepared as a proportion of body mass for infants (18.1ml/kg),[4] or as a proportion of vital capacity (0.24 for men and 0.28 for women)[5] or in relation to height and age ((0.0275*AgeInYears+0.0189*HeightInCentimetres2.6139) litres for normal-weight individuals and (0.0277*AgeInYears+0.0138*HeightInCentimeters-2.3967) litres for overweight individuals).[6] Standard errors in prediction equations for residual volume have been measured at 579ml for men and 355ml for women, while the use of 0.24*FVC gave a standard error of 318ml.[7]

Restrictive and obstructive

The results (in particular FEV1/FVC and FRC) can be used to distinguish between restrictive and obstructive pulmonary diseases: Type Examples Description pulmonary fibrosis, Infant restrictive Respiratory Distress Syndrome, volumes are diseases weak respiratory muscles, decreased pneumothorax volumes are obstructive essentially normal asthma or COPD diseases but flow rates are impeded FEV1/FVC often in a normal range (0.8 - 1.0) often low (Asthma can reduce the ratio to 0.6, Emphysema can reduce the ratio to 0.78 - 0.45)

Vital capacity
Vital capacity is the maximum amount of air a person can expel from the lungs after a maximum inspiration. It is equal to the inspiratory reserve volume plus the tidal volume plus the expiratory reserve volume. A person's vital capacity can be measured by a spirometer which can be a wet or regular spirometer. In combination with other physiological measurements, the vital capacity can help make a diagnosis of underlying lung disease. The unit that is used to determine this vital capacity is the millilitre (ml). A normal adult has a vital capacity between 3 and 5 litres. Predicted normal values for VC can be calculated online and depend on age, sex, height, weight and ethnicity as well as the research study that they are based upon.

Functional residual capacity

Functional Residual Capacity (FRC) is the volume of air present in the lungs, specifically the parenchyma tissues, at the end of passive expiration. At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles. FRC is the sum of Expiratory Reserve Volume (ERV) and Residual Volume (RV) and measures approximately 2400 ml in a 70 kg, average-sized male. It can not be estimated through spirometry, since it includes the residual volume. In order to measure RV precisely, one would need to perform a test such as nitrogen washout, helium dilution or body plethysmography. A lowered or elevated FRC is often an indication of some form of respiratory disease. For instance, in emphysema, the lungs are more compliant and therefore are more susceptible to the outward recoil forces of the chest wall. Emphysema patients often have noticeably broader chests because they are breathing at larger volumes. The helium dilution technique is a common way of measuring the functional residual capacity of the lungs.

Dead space (physiology)

Blood gas, acid-base, & gas exchange terms
Pa O 2 Arterial oxygen tension, or partial pressure

PAO2

Alveolar oxygen tension, or partial pressure

PACO2

Arterial carbon dioxide tension, or partial pressure

PaCO2

Alveolar carbon dioxide tension, or partial pressure

PvO2

Oxygen tension of mixed venous blood

P(A-a)O2 Alveolar-arterial oxygen tension difference. The term formerly used (A-a DO2) is discouraged.

P(a/A)O2 Alveolar-arterial tension ratio; PaO2:PAO2 The term oxygen exchange index describes this ratio.

C(a-v)O2 Arteriovenous oxygen content difference

SaO2

Oxygen saturation of the hemoglobin of arterial blood

SpO2

Oxygen saturation as measured by pulse oximetry

CaO2

Oxygen content of arterial blood

pH

Symbol relating the hydrogen ion concentration or activity of a solution to that of a standard solution; approximately equal to the negative logarithm of the hydrogen ion concentration. pH is an indicator of the relative acidity or alkalinity of a solution

vde

It has been suggested that Deadspace (in breathing apparatus) be merged into this article or section. (Discuss) Proposed since November 2010.

In physiology, dead space is air that is inhaled by the body in breathing, but does not take part in gas exchange. Not all the air in each breath is able to be used for the exchange of oxygen and carbon dioxide. About a third of every resting breath has no change in O2 and CO2 levels. In adults, it is usually in the range of 150 mL.[1] Because of dead space, taking deep breaths more slowly (e.g. ten 500 mL breaths per minute) is more effective than taking shallow breaths quickly (e.g. twenty 250 mL breaths per minute). Although the amount of gas per minute is the same (5 L/min), a large proportion of the shallow breaths is dead space, and does not allow oxygen to get into the blood. Dead space can be enlarged (and better envisaged) by breathing into a long tube. Even though one end of the tube is open to the air, when one inhales, it is mostly the carbon dioxide from expiration. Using a snorkel increases a diver's dead space in the airways.

Components
Total dead space (also known as "physiological" dead space) can be divided into anatomical dead space and alveolar dead space.
Anatomical dead space

Anatomical dead space is the gas in the conducting areas of the respiratory system, such as the mouth and trachea, where air does not come into contact with the alveoli of the lungs. Birds, which, relatively, have a far longer and wider trachea than mammals, have a higher proportion of dead space.

It is normally equal in milliliters to your body weight in pounds. A 150 lb (68 kg) male would have an anatomical dead space of about 150 mL. 1 mL per lb or 2.2 mL per kilogram of body weight. This is the same conversion of kilograms to pounds, except the final unit is in mL. This is about a third of the resting tidal volume (450-500 mL). Anatomic dead space is the volume of the conducting airways. It may be measured by Fowler's method, a nitrogen washout technique.[2][3][4]
Alveolar dead space

Alveolar dead space is caused by air contacting alveoli without bloodflow in their adjacent pulmonary capillaries, i.e. ventilation without perfusion. As a result, no gas exchange can occur.[5] Alveolar dead space is negligible in healthy individuals, but can increase dramatically in some lung diseases.

Calculating the dead space

Overview

Anatomical and alveolar dead space can both be measured using the Bohr equation.[6][7] Formally, Bohr's method is used to calculate the former. In practice, it is more commonly used to calculate the latter. The Bohr equation states that the dead space (Vd) is calculated as follows:

where Vd is dead space volume, Vt is tidal volume, PaCO2 is the partial pressure of carbon dioxide in the arterial blood, and PeCO2 is the partial pressure of carbon dioxide in the expired air. Depending on how the expired CO2 is measured, this equation gives the physiological or alveolar dead space. When calculating the:

physiological dead space, a large plastic bag (that is, a Douglas bag) is used to collect all of the patients expired gas, and the total expired CO2 is measured as a fraction of total expired gas. This gives PeCO2, which is then substituted into the Bohr equation. alveolar dead space, the end-tidal CO2 in capnography is used as a surrogate for the expired CO2. PetCO2 is then used instead of PeCO2 in the Bohr equation.

Example

If a patient's tidal volume is 500 mL, their arterial carbon dioxide (PaCO2) is 42 mmHg (5.6 kPa), and their end-expired carbon dioxide (ETCO2) on capnography is 40 mmHg (5.3 kPa), the alveolar dead space can be calculated as follows:

Spirometry
From Wikipedia, the free encyclopedia Jump to: navigation, search

TLC

Total lung capacity: the volume in the lungs at maximal inflation Residual volume: the volume of air remaining in the lungs after a maximal exhalation Expiratory reserve volume: the maximal volume of air that can be exhaled from the end-expiratory position Inspiratory reserve volume: the maximal volume that can be inhaled from the endinspiratory level

RV

ERV

IRV

IC

Inspiratory capacity: the sum of IRV and TV Inspiratory vital capacity: the maximum volume of air inhaled from the point of maximum expiration Vital capacity: the volume equal to TLC R Tidal volume: that volume of air moved into or out of the lungs during quiet breathing (VT indicates a subdivision of the lung; when tidal volume is precisely measured, as in gas exchange calculation, the symbol VT or VT is used.) Functional residual capacity: the volume in the lungs at the end-expiratory position

IVC

VC

VT

FRC

RV/TLC% Residual volume expressed as percent of TLC VA VL Alveolar gas volume Actual volume of the lung including the volume of the conducting airway. Forced vital capacity: the determination of the vital capacity from a maximally forced expiratory effort Volume that has been exhaled at the end of the first second of forced expiration Forced expiratory flow related to some portion of the FVC curve; modifiers refer to amount of FVC already exhaled The maximum instantaneous flow achieved during a FVC maneuver Forced inspiratory flow: (Specific measurement of the forced inspiratory curve

FVC

FEV1

FEFx

FEFmax

FIF

is denoted by nomenclature analogous to that for the forced expiratory curve. For example, maximum inspiratory flow is denoted FIFmax. Unless otherwise specified, volume qualifiers indicate the volume inspired from RV at the point of measurement.) PEF The highest forced expiratory flow measured with a peak flow meter Maximal voluntary ventilation: volume of air expired in a specified period during repetitive maximal effort vde

MVV

Spirometry
Diagnostics

Flow-Volume loop showing successful FVC maneuver. Positive values represent expiration, negative values represent inspiration. The trace moves clockwise for expiration followed by inspiration. (Note the FEV1 value is arbitrary in this graph and just shown for illustrative purposes; these values must be calculated as part of the procedure).

MeSH OPS-301 code

D013147 1-712

Spirometry (meaning the measuring of breath) is the most common of the pulmonary function tests (PFTs), measuring lung function, specifically the measurement of the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled. Spirometry is an important tool used for generating pneumotachographs which are helpful in assessing conditions such as asthma, pulmonary fibrosis, cystic fibrosis, and COPD.

Contents
[hide]

1 Spirometry testing o 1.1 Procedure o 1.2 Limitations of test o 1.3 Related tests 2 Parameters o 2.1 Forced vital capacity (FVC) o 2.2 Forced expiratory volume in 1 second (FEV1) o 2.3 FEV1/FVC ratio (FEV1%) o 2.4 Forced expiratory flow (FEF) o 2.5 Forced inspiratory flow 2575% or 2550% o 2.6 Peak expiratory flow (PEF) o 2.7 Tidal volume (TV) o 2.8 Total lung capacity (TLC) o 2.9 Diffusion capacity (DLCO) o 2.10 Maximum voluntary ventilation (MVV) o 2.11 Static lung compliance (Cst) o 2.12 Others 3 Technologies used in spirometers 4 See also 5 References 6 Further reading 7 External links

Spirometry testing

Device for spirometry. The patient places his or her lips around the blue mouthpiece. The teeth go between the nubs and the shield, and the lips go over the shield. A noseclip guarantees that breath will flow only through the mouth.

A modern USB PC-based spirometer.

Screen for spirometry readouts at right. The chamber can also be used for body plethysmography.

The spirometry test is performed using a device called a spirometer, which comes in several different varieties. Most spirometers display the following graphs, called spirograms:

a volume-time curve, showing volume (liters) along the Y-axis and time (seconds) along the Xaxis a flow-volume loop, which graphically depicts the rate of airflow on the Y-axis and the total volume inspired or expired on the X-axis

Procedure

The basic forced volume vital capacity (FVC) test varies slightly depending on the equipment used. Generally, the patient is asked to take the deepest breath they can, and then exhale into the sensor as hard as possible, for as long as possible, preferably at least 6 seconds. It is sometimes directly followed by a rapid inhalation (inspiration), in particular when assessing possible upper airway obstruction. Sometimes, the test will be preceded by a period of quiet breathing in and out from the sensor (tidal volume), or the rapid breath in (forced inspiratory part) will come before the forced exhalation. During the test, soft nose clips may be used to prevent air escaping through the nose. Filter mouthpieces may be used to prevent the spread of microorganisms.
Limitations of test

The maneuver is highly dependent on patient cooperation and effort, and is normally repeated at least three times to ensure reproducibility. Since results are dependent on patient cooperation, FVC can only be underestimated, never overestimated. FEV1 may sometimes be overestimated in people with some diseases - a softer blow can reduce the spasm or collapse of lung tissue to elevate the measure. Due to the patient cooperation required, spirometry can only be used on children old enough to comprehend and follow the instructions given (6 years old or more), and only on patients who are able to understand and follow instructions - thus, this test is not suitable for patients who are unconscious, heavily sedated, or have limitations that would interfere with vigorous respiratory efforts. Other types of lung function tests are available for infants and unconscious persons. Another major limitation is the fact that many intermittent or mild asthmatics have normal spirometry between acute exacerbation, limiting spirometry's usefulness as a diagnostic. It is more useful as a monitoring tool: a sudden decrease in FEV1 or other spirometric measure in the same patient can signal worsening control, even if the raw value is still normal. Patients are encouraged to record their personal best measures.

Related tests

Spirometry can also be part of a bronchial challenge test, used to determine bronchial hyperresponsiveness to either rigorous exercise, inhalation of cold/dry air, or with a pharmaceutical agent such as methacholine or histamine. Sometimes, to assess the reversibility of a particular condition, a bronchodilator is administered before performing another round of tests for comparison. This is commonly referred to as a reversibility test, or a post bronchodilator test (Post BD), and is an important part in diagnosing asthma versus COPD. Other complementary lung functions tests include plethysmography and nitrogen washout.

Parameters

Example of a modern PC based spirometer printout.

The most common parameters measured in Approximate value spirometry are Vital capacity (VC), Forced vital Measurement capacity (FVC), Forced expiratory volume (FEV) at Male Female timed intervals of 0.5, 1.0 (FEV1), 2.0, and 3.0 seconds, Forced expiratory flow 2575% (FEF 25 Forced vital capacity (FVC) 4.8 L 3.7 L 75) and Maximal voluntary ventilation (MVV),[1] also known as Maximum breathing capacity.[2] Tidal volume (Vt) 500mL 390mL Other tests may be performed in certain situations. Results are usually given in both raw data (litres, litres per second) and percent predicted - the test result as a percent of the "predicted values" for the patients of similar characteristics (height, age, sex, and sometimes race and weight). The interpretation of the results can vary depending on the physician and the source of the predicted values. Generally speaking, results nearest to 100% predicted are the most normal, and results over 80% are often considered normal. Multiple publications of predicted values have been published and may be calculated online based on age, sex, weight and ethnicity. However, review by a doctor is necessary for accurate diagnosis of any individual situation. A bronchodilator is also given in certain circumstances and a pre/post graph comparison is done to assess the effectiveness of the bronchodilator. See the example printout. Functional residual capacity (FRC) cannot be measured via spirometry, but it can be measured with a plethysmograph or dilution tests (for example, helium dilution test).
Total lung capacity (TLC) 6.0 L 4.7 L

Average values for Forced Vital Capacity (FVC), Forced Expiratory Volume in 1 Second (FEV1) and Forced Expiratory Flow 2575% (FEF2575%), according to a study in the United States 2007 of 3,600 subjects aged 480 years.[3] Y-axis is expressed in litres for FVC and FEV1, and in litres/second for FEF2575%.

Forced vital capacity (FVC)

Forced vital capacity (FVC) is the volume of air that can forcibly be blown out after full inspiration, measured in liters. FVC is the most basic maneuver in spirometry tests.

Forced expiratory volume in 1 second (FEV1)

Average values for FEV1 in healthy people depend mainly on sex and age, according to the diagram at left. Values of between 80% and 120% of the average value are considered normal.[4] Predicted normal values for FEV1 can be calculated online and depend on age, sex, height, weight and ethnicity as well as the research study that they are based upon.
FEV1/FVC ratio (FEV1%)

FEV1/FVC (FEV1%) is the ratio of FEV1 to FVC. In healthy adults this should be approximately 7580%. In obstructive diseases (asthma, COPD, chronic bronchitis, emphysema) FEV1 is diminished because of increased airway resistance to expiratory flow; the FVC may be decreased as well, due to the premature closure of airway in expiration, just not in the same proportion as FEV1 (for instance, both FEV1 and FVC are reduced, but the former is more affected because of the increased airway resistance). This generates a reduced value (<80%, often ~45%). In restrictive diseases (such as pulmonary fibrosis) the FEV1 and FVC are both reduced proportionally and the value may be normal or even increased as a result of decreased lung compliance. A derived value of FEV1% is FEV1% predicted, which is defined as FEV1% of the patient divided by the average FEV1% in the population for any person of similar age, sex and body composition.
Forced expiratory flow (FEF)

Forced expiratory flow (FEF) is the flow (or speed) of air coming out of the lung during the middle portion of a forced expiration. It can be given at discrete times, generally defined by what fraction remains of the functional vital capacity (FVC). The usual intervals are 25%, 50% and 75% (FEF25, FEF50 and FEF75), or 25% and 50% of FVC. It can also be given as a mean of the flow during an interval, also generally delimited by when specific fractions remain of FVC, usually 2575% (FEF2575%). Average ranges in the healthy population depend mainly on sex and age, with FEF2575% shown in diagram at left. Values ranging from 50-60% and up to 130% of the average are considered normal.[4] Predicted normal values for FEF can be calculated online and depend on age, sex, height, weight and ethnicity as well as the research study that they are based upon. MMEF or MEF stands for maximal (mid-)expiratory flow and is the peak of expiratory flow as taken from the flow-volume curve and measured in liters per second. It should theoretically be identical to peak expiratory flow (PEF), which is, however, generally measured by a peak flow meter and given in liters per minute.[5] Recent research suggests that FEF25-75% or FEF25-50% may be a more sensitive parameter than FEV1 in the detection of obstructive small airway disease.[6][7] However, in the absence of concomitant changes in the standard markers, discrepancies in mid-range expiratory flow may not be specific enough to be useful, and current practice guidelines recommend continuing to use FEV1, VC, and FEV1/VC as indicators of obstructive disease.[8][9]

More rarely, forced expiratory flow may be given at intervals defined by how much remains of total lung capacity. In such cases, it is usually designated as e.g. FEF70%TLC, FEF60%TLC and FEF50%TLC.[5]
Forced inspiratory flow 2575% or 2550%

Forced inspiratory flow 2575% or 2550% (FIF 2575% or 2550%) is similar to FEF 2575% or 2550% except the measurement is taken during inspiration.
Peak expiratory flow (PEF)

Normal values for Peak Expiratory Flow (PEF), shown on EU scale.[10]

Peak expiratory flow (PEF) is the maximal flow (or speed) achieved during the maximally forced expiration initiated at full expiration, measured in liters per minute.
Tidal volume (TV)

Tidal volume (TV) is the volume of air inspired or expired in a single breath at rest.
Total lung capacity (TLC)

Total lung capacity (TLC) is the maximum volume of air present in the lungs
Diffusion capacity (DLCO)

Diffusing capacity (DLCO)is the carbon monoxide uptake from a single inspiration in a standard time (usually 10 sec). Since air consists of very minute or trace quantities of CO, 10 seconds is considered to be the standard time for inhalation, then rapidly blow it out (exhale). The exhaled

gas is tested to determine how much of the tracer gas was absorbed during the breath. This will pick up diffusion impairments, for instance in pulmonary fibrosis.[11] This must be corrected for anemia (because rapid CO diffusion is dependent on hemoglobin in RBC's; a low hemoglobin concentration, anemia, will reduce DLCO) and pulmonary hemorrhage (excess RBC's in the interstitium or alveoli can absorb CO and artificially increase the DLCO capacity). Atmospheric pressure and/or altitude will also affect measured DLCO, and so a correction factor is needed to adjust for standard pressure. Online calculators are available to correct for hemoglobin levels and altitude and/or pressure where the measurement was taken.
Maximum voluntary ventilation (MVV)

Maximum voluntary ventilation (MVV) is a measure of the maximum amount of air that can be inhaled and exhaled within one minute. For the comfort of the patient this is done over a 15 second time period before being extrapolated to a value for one minute expressed as liters/minute. Average values for males and females are 140-180 and 80-120 liters per minute respectively.
Static lung compliance (Cst)

When estimating static lung compliance, volume measurements by the spirometer needs to be complemented by pressure transducers in order to simultaneously measure the transpulmonary pressure. When having drawn a curve with the relations between changes in volume to changes in transpulmonary pressure, Cst is the slope of the curve during any given volume, or, mathematically, V/P.[12] Static lung compliance is perhaps the most sensitive parameter for the detection of abnormal pulmonary mechanics.[13] It is considered normal if it is 60% to 140% of the average value in the population for any person of similar age, sex and body composition.[4] In those with acute respiratory failure on mechanical ventilation, "the static compliance of the total respiratory system is conventionally obtained by dividing the tidal volume by the difference between the "plateau" pressure measured at the airway opening (PaO) during an occlusion at end-inspiration and positive end-expiratory pressure (PEEP) set by the ventilator".[14]
Others

Forced Expiratory Time (FET) Forced Expiratory Time (FET) measures the length of the expiration in seconds. Slow vital capacity (SVC) Slow vital capacity (SVC) is the maximum volume of air that can be exhaled slowly after slow maximum inhalation. Maximal pressure (Pmax and Pi) Pmax is the asymptotically maximal pressure that can be developed by the respiratory muscles at any lung volume and Pi is the maximum inspiratory pressure that can be developed at specific lung volumes.[15] This measurement also requires pressure transducers in addition. It is considered normal if it is 60% to 140% of the average value in the population for any person of

similar age, sex and body composition.[4] A derived parameter is the coefficient of retraction (CR) which is Pmax/TLC .<hedenstrom2009/> Mean transit time (MTT) Mean transit time is the area under the flow-volume curve divided by the forced vital capacity.[16]

Technologies used in spirometers

Volumetric Spirometers o Water bell o Bellows wedge Flow measuring Spirometers o Fleisch-pneumotach o Lilly (screen) pneumotach o Turbine (actually a rotating vane which spins because of the air flow generated by the subject. The revolutions of the vane are counted as they break a light beam) o Pitot tube o Hot-wire anemometer o Ultrasound

Body plethysmography
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Body plethysmography
Diagnostics

A whole body plethysmography. A person is entirely enclosed within the body box space, the door sealed, pressure equilibrated, and measurements taken. With high visibility and intercom communication with the pulmonary function technologist, the subject has less risk of fearing the test.

MeSH

D010993

OPS-301 code

1-710

Body plethysmography or "Body Box" for short, is a very sensitive lung measurement used to detect lung pathology that might be missed with conventional pulmonary function tests. This method of obtaining the absolute volume of air within one's lungs may also be used in situations where several repeated trials are required or where the patient is unable to perform the multibreath tests. The technique requires moderately complex coaching and instruction for the subject. In the USA, such tests are usually performed by Certified or Registered Pulmonary Function Technologists (CPFT or RPFT) who are credentialed by the National Board for Respiratory Care NBRC [1]. More specifically, the test is done by enclosing the subject in an airtight chamber often referred to as a body box; a pneumotachometer is used to measure airflow while a mouth pressure transducer with a shutter measures the alveolar pressure. The most common measurements made using body plethysmographs are thoracic gas volume (VTG) and airway resistance (RAW). This test is used mainly in the Pulmonary Function Testing laboratories.

Using body plethysmography, doctors can examine the lungs' resistance to airflow, distinguish between restrictive and obstructive lung diseases, determine the response to bronchodilators, and determine bronchial hyperreactivity in response to methacholine[2], histamine, or isocapnic hyperventilation.

Flow and Pressure Plethysmographs

There are two types of plethysmographs: flow and pressure. In flow plethysmography, airway resistance is measured by two maneuvers. The patient first pants while the mouth shutter is open to allow flow changes to be measured. Then, the mouth shutter closes at the patient's end expiratory or FRC level and the patient continues panting while maintaining an open glottis. This provides a measure of the driving pressure used to move air into the lungs. Pressure plethysmographs are usually measured at the end-expiratory level and are then equal to FRC. The patient sits in the box, which has the pressure transducer in the wall of the device, and breathes through a mouthpiece connected to a device that contains an electronic shutter and a differential pressure pneumotachometer. The mouth pressure and box pressure changes that are measured during tidal breathing and panting maneuvers which are performed during the test by the patient at the end of expiration are sent to a microprocessor unit that calculates thoracic gas volume.

Preclinical research
Preclinical researchers studying pulmonary function measure respiratory parameters from conscious restrained and freely moving animals, as well as resistance/compliance from sedated animals using different models of body plethysmographs.

Peak expiratory flow

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Peak expiratory flow

Diagnostics

A peak flow meter issued in the UK.

MeSH

D010366

The peak expiratory flow (PEF), also called peak expiratory flow rate (PEFR) is a person's maximum speed of expiration, as measured with a peak flow meter, a small, hand-held device used to monitor a person's ability to breathe out air. It measures the airflow through the bronchi and thus the degree of obstruction in the airways.

Contents
[hide]

1 Function 2 Scales 3 Measurement 4 History 5 See also 6 References

Function
Peak flow readings are higher when patients are well, and lower when the airways are constricted. From changes in recorded values, patients and doctors may determine lung functionality, severity of asthma symptoms, and treatment options. First measure of precaution would be to check patient for signs and symptoms of asthmatic hypervolemia. This would indicate whether or not to even continue with the Peak Flow Meter procedure. Measurement of PEFR requires training to correctly use a meter and the normal expected value depends on a patient's sex, age and height. It is classically reduced in obstructive lung disorders such as asthma.

Due to the wide range of normal' values and high degree of variability, peak flow is not the recommended test to identify asthma. However, it can be useful in some circumstances. A small proportion of people with asthma may benefit from regular peak flow monitoring. When monitoring is recommended, it is usually done in addition to reviewing asthma symptoms and frequency of reliever medication use.[1] When peak flow is being monitored regularly, the results may be recorded on a peak flow chart. It is important to use the same peak flow meter every time.

Scales

Normal values, shown on EU scale.[2]

This peak flow meter uses the EU scale. There are a number of non-equivalent scales used in the measurement of Peak Flow.[3] Graphs or tables are available of predicted normal values based on a person's sex, age and height, and online calculators are available. There is a wide natural variation in results from healthy test subjects.

Wright scale[4][5] EN 13826 or EU scale[6] A.T.S. (American Thoracic Society) scale

In 2004 the UK switched from the original Wright scale to the newer, more accurate European scale. Wright values may be converted to the EU scale using the following formula[7]:

The reverse calculation is:

Measurement
The highest of three readings is used as the recorded value of the Peak Expiratory Flow Rate. It may be plotted out on graph paper charts together with a record of symptoms or using peak flow charting software. This allows patients to self-monitor and pass information back to their doctor or nurse.[8] Peak flow readings are often classified into 3 zones of measurement according to the American Lung Association[9]; green, yellow, and red. Doctors and health practitioners can develop an asthma management plan based on the green-yellow-red zones.

Reading 80 to 100 percent of the Green usual or normal peak Zone flow readings are clear. 50 to 79 percent of the Yellow usual or normal peak Zone flow readings Red Zone

Zone

Description A peak flow reading in the green zone indicates that the asthma is under good control. Indicates caution. It may mean respiratory airways are narrowing and additional medication may be required.

Indicates a medical emergency. Severe airway Less than 50 percent of narrowing may be occurring and immediate action the usual or normal needs to be taken. This would usually involve peak flow readings contacting a doctor or hospital.

History
The measurement of peak expiratory flow was pioneered by Martin Wright, who produced the first meter specifically designed to measure this index of lung function. Since the original design of instrument was introduced in the late 1950s, and the subsequent development of a more portable, lower cost version (the "Mini-Wright" peak flow meter), other designs and copies have become available across the world.