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Physiology. Guyton Ch 42. Respiratory Insufficiency.

[Alycia]
So there are 4 traditional objs. for this chapter but the last objective states Overall, you should be able to discuss ALL the topics outlined in this chapter! I think it will be more beneficial if I essentially outline the chapter while making sure Dr. Raymonds ppts points are included. Here are the topics that the 4 traditional objs. focused on Pulmonary Function Test: normal vs disease states like emphysema. Pathophysiologic conditions of atelectasis, pneumonia, asthma, and TB. Oxygen Therapy for various diseases. 1. Blood gases and pH are important to determining the appropriate therapy for acute respiratory distress or acute acid-base imbalance (pg. 524- 525) a. Only a few drops of blood are required to give quick and accurate gases and pH b. pH is determined by a voltmeter scale where the voltage generated by a miniature glass electrode is a direct measure of pH c. Blood CO2 can also be determined by the same electrode because the pH is a function of the CO and bicarbonate ion concentrations pH = 6.1 = log(HCO3- / CO2) The pH electrode is surrounded by a plastic membrane that contains a known concentration of sodium bicarbonate, through which the drop of blood is able to diffuse, allowing for the Henderson-Hasslebach equation to give both the pH and Blood CO2 d. Blood O2 is determined by polarography A negative electrode (usually platinum) is surrounded by a plastic membrane through which only oxygen can diffuse which then mixes with a solution. A voltage is created due to the movement 1) rate of flow is directly proportional to the concentration of O2. e. These two electrodes are usually built into the same apparatus and can give measurements within a minute or so. 2. Measurement of Max. Expiratory Flow (MEF) (pg. 525 & PPT!) a. When a person expires their Total Lung Capacity (TLC) with great force, the expiratory airflow reaches a maximum flow at which the flow cannot be increased anymore even with greatly increased additional force. MEF is much greater when the lungs are filled with air than when they are nearly empty 1) Try exhaling completely. It gets really difficult at the end when there is less air in there This occurs because the increased pressure forces air from the alveoli to the bronchioles but it also collapses the bronchioles so that air cannot move out. These forces are equal so that a further increase in flow is prevented A.) shows the collapsing forces on the airway during MEF B.) shows the effect of lung volume on the MEF of a normal healthy person. They quickly reach 400 L/min and it decreases as the lung volume decreases. This curve will not change for this healthy individual no matter how hard they try to blow out.

3. Abnormalities of MEF (pg. 526 & PPT) a. Constricted lungs have TLC and Residual Volume (RV) AKA Restrictive lung disease Blue curve Since the lung cant expand to normal max volume, it can never reach the MEF of a normal lung. These diseases include fibrotic lung diseases: 1) TB, silicosis, and pneumoconioses(inhaled particles like sand and coal dust) Also, kyphosis, scoliosis, and fibrotic pleurisy, because they constrict the chest cage b. Airway obstruction cause TLC and RV to Green curve Usually much more difficult to expire than inspire 1) Extra negative pressure usually pulls the airways open at the same time it expands the alveoli Classic disease is asthma and COPD chronic bronchitis, emphysema) 4. Forced Expiratory Vital Capacity (FVC) and Forced Expiratory Volume (FEV) (pg 526 & PPT) a. Person takes a maximum inspiration to TLC then exhales into spirometer with maximum effort as fast and completely as possible. b. Total downslope of the lung volume = FVC Use the first second of expiration to be FEV1 c. Use these measurements to ID Obstructive disease FEV1/FVC > 70% - 85% = normal 1) Ex. Normal FEV1 = 4 L, FVC = 5 L FEV1/FVC <70% = obstructive 1) Ex. Obstructive FEV1 = 1.3 L, FVC = 3.1 L 2) Acute asthma can decrease to less than 20% FEV1/FVC > 85% = restrictive 1) Ex. Restrictive FEV1= 2.8L, FVC = 3.1 L d. These are the ranges I figured out, Will ask to clarify. 5. Flow Volume Loop (PPT) a. The book does not discuss these but they are in Dr. Raymonds PPT. b. It seems as though plotting the volume changes during inspiration and expiration produces different kinds of shapes that are indicative of different kinds of respiratory diseases.

6. Physiological effects of Chronic Emphysema (pg 526 527 & PPT) Emphysema a. Pulmonary Emphysema means excess air in the lungs b. But usually used to describe the effect of long term smoking on the lungs: Chronic infection 1) Nicotine partially paralysizes cilia 2) Excess mucus secretion exacerbates the condition 3) Inhibit pulmonary macrophages Chronic infection + inflammatory edema = Chronic Obstruction 1) Traps air in the alveoli Causes overstretching This + chronic infection destroys 50 80% of the alveolar walls a) PVR leads to pulmonary hypertension Can cause R sided Heart Failure b) compliance because elastin is destroyed too 2) airway resistance Normal Must work hard to breathe a) Expiration is especially difficult because the outside compressive forces act on the alveioli and bronchioles 3) gas exchange Lungs cant oxygenate and remove carbon dioxide well Disease progresses over years causing hypoxia and hypercapnia until death 4) Abnormal alveolare ventilation-perfusion ratio (Va/Q) Obstruction is worse in some parts a) Some areas have reallyVa/Q Creates physiological shunts in these parts of lung b) Some areas have really Va/Q Causes physiological dead space when ventilation is wasted 7. Physiological effects of Pneumonia (pg 527 528 & PPT) a. Any inflammatory process with alveolar fluid and blood cells 1) consolidation b. Often caused by bacteria MCC pneumococci membrane permeability to allow fluid, RBC and WBC in the alveioli Spreads by extension c. Early Stage More likely to be localized to only one lung 1) alveolar ventilation 2) BUT blood flow to lung = Causes in total available surface area of respiratory membrane Va/Q 1) Causes hypoxemia and hypercapnia 2) Blood thru aerated lung is 97% oxygenated while the blood thru the pneumonic lung only becomes 60% oxygenated. The mean is what ends up in the Aorta and available to all the tissues 78% is quite a bit below normal.

8. Physiological effect of Atelectasis (pg 528 -529 & PPT) a. Atelectasis means collapse of alveoli Due to lack of surfactant like in respiratory distress syndrome (hyaline membrane disease) 1) Surface Tension is crazy Lungs tend to collapse or fill with fluid Infants can die when large portions of the lung tissue become atelectatic Due to total obstruction of airway 1) Caused by mucus plug or tumor 2) If pliable enough, alveoli will collapse once the trapped air is absorbed into the surrounding capillaries 3) If the lung is too rigid, the alveoli will not collapse when the air is absorbed so negative pressure is created Negative pressure pulls fluid into the alveoli causing edema a) When this happens to an entire lung its called massive collapse Can be localized or the entire lung b. PVR due to the collapse Causes hypoxia and therefore vasoconstriction 1) Blood flow thru the atelectatic lung significantly c. This is NOT the same as the effects of pneumonia because here the blood flow to the effected lung and therefore the effect of less saturated blood coming from the atelectatic lung is not so detrimental to the saturation within the aorta 9. Physiological effect of Asthma (pg 529 &PPT) a. Causes contraction of bronchial smooth muscle An obstructive disease b. Contraction can be because of a hypersensitivity reaction IgE antibodies which are attached to mast cells are activated when the antigen is presented 1) The mast cells release histamine, slow-reacting substance of anaphylaxis, eosinophilic chemotactic factor, and bradykinin Causes edema and smooth muscle constriction a) Which causes increased PVR c. Especially severe obstruction during expiration Max respiratory rate and timed expiratory volume 1) Causes dyspnea functional residual capacity and residual volume 1) Over time will be come barrel-chested to compensate and these values will be permanently elevated 10. Physiological effect of TB (pg 530) a. Tubercle bacilli cause: Invasion of infected tissue my macrophages Walling off of the lesion by fibrous tissue 1) Called the tubercle 2) Helps to limit further transmission 3) If walling off doesnt work (~3% pts) Tubercle bacilli spread throughout and destroy the lungs creating abscess cavities b. Total amount of functional lung is

Respiratory muscles have to work extra hard 1) Because of Reduced Vital Capacity and Breathing capacity Diminished Pulmonary diffusing capacity 1) Because Total Respiratory membrane Surface Area and thickness of respiratory membrane Abnormal ventilation-perfusion ratio

11. Causes of Hypoxia (pg 530 531 & PPT) a. Inadequate oxygenation of blood atmospheric oxygen Hypoventilation (neuromuscular disorders) b. Pulmonary disease Hypoventilation because airways resistance or pulmonary compliance Abnormal Va/Q 1) shunts or dead space c. Venous - arterial shunts in the heart d. Inadequate oxygen transport to the tissues by the blood Anemia or abnormal hemoglobin General or Localized Circulatory Deficiency Tissue edema e. Inadequate oxygen usage by tissues Poisons hurting oxidative enzymes 1) Ex. Cyanide poisoning blocks cytochrome oxidase metabolism for using oxygen 1) Ex. Vitamin B deficiency by BeriBeri 12. Hypoxia A-a gradient (PPT) a. Used to differentiate location of hypoxia/cyanosis Pulmonary or extrapulmonary? Based on Alveolar arteriolar PO2 1) If A-a >30mmHg, then pulmonary cause Ventilation defects Perfusion defects Diffusion defects 2) If A-a < 30mmHg AKA Normal, then extra-pulmonary cause Upper respiratory obstruction respiratory drive a) Ex barbiturates 13. Hypoxia causes flow chart (PPT) a. If A-a gradient Normal BUT Low PaO2, then Hypoventilation b. If A-a gradient >30mmHg Give 100% 02 1) If PaO2 , then Va/Q Imbalance MCC arterial hypoxemia 2) If NO Change in PaO2, then Shunt Perfusion without ventilation

14. Oxygen therapy for different types of hypoxia (pg 530 531 & PPT)

a. Oxygen can be administered by placing head in tent of air fortified with oxygen, pure or high oxygen mask, or intranasal tube b. It is beneficial for atmospheric, hypoventilation and decrease alveolar diffusion (edema) c. Its of low benefit when oxygen is already available in the alveoli but there is a problem with transporting it into the tissues. But still give it! Anemia induced hypoxia Shunts Circulatory deficiency d. NO benefit when tissues are unable to use oxygen 15. Cyanosis (pg 531) a. amounts of deoxygenated hemoglobin, especially in the capillaries Has dark blue-purle color which is transmitted thru the skin b. Definite cyanosis appears when arterial blood >5 g deoxygenated hemoglobin/100mL blood Anemic pts rarely have cyanosis because there is not enough hemoglobin for it to be deoxygenated However, Polycythemia vera pts have increased amounts of hemoglobin and can therefore appear cyanotic even when everything is honky dory c. Therefore cyanosis is not always indicative of hypoxia but its a good clue! 16. Hypercapnia (pg 531 532 & PPT) a. carbon dioxide in the body b. Occurs with hypoxia in hypoventilation and ischemia (circulatory deficiency) ONLY Hypercapnia usually doesnt occur when poor oxygen diffusion is the cause of hypoxia because carbon dioxide actually diffuses 20% more rapidly 1) If it does, ventilation can usually correct the hypercapnia but not the hypoxia c. PCO2 ~ 60 80 mmHg Normal person will be breathing rapidly and deeply Will have dyspnea sensation d. PCO2 ~ 80 100 mmHg Normal person will become lethargic and semicomatose e. PCO2 ~ 120 150 mmHg Anesthesia and death Excess CO2 at this point ill slow respiration instead which creates a vicious cycle of increasing CO2 and depressing respiration 17. Dyspnea (pg 532 & PPT) a. The mental anguish of having difficulty breathing The ominous..AIR HUNGERRRRR b. Three factors that are often causative Abnormal blood gases 1) Especailly Hypercapnia! amount of work done by the respiratory muscles in order to keep ventilation adequate State of mind 1) Neurogenic dyspnea when the blood gases and respiratory functions are normal but the sensation of dyspnea is still felt 18. Artificial Respiration (pg 532 & PPT)

a. Resuscitator CPAP or tracheal intubation b. Iron Lung Tank respirator Motor increases and decreases pressure within the tank 1) Leather diaphragm moves in to create positive pressure Causes Expiration 2) Leather diaphragm moves out to create negative pressure Causes Inspiration 3) Same directions and results as our own diaphragm c. Can cause decrease in Cardiac Output if the pressures are too high The pressure in the lungs is greater than everywhere else in the body so the flow into the chest from the peripheral veins is impeded 1) Decreased Venous return causes decrease CO Exposure to >30mmHg for more than a few minutes can cause death 1) And on that note, youre done with Ch. 42!

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