BASICS of RESPIRATORY FUNCTION

Mee Wah Ng RSO Dubai 2002

Ventilation:
The moving of Oxygen and Carbon Dioxide in and out of our body. Commonly termed breathing

Respiration:
Metabolic process that occurs in the lungs and cells of the body breaking down organic substances to simpler products to release energy

Mee Wah Ng RSO Dubai 2002

VENTILATION

Moving of gas from the atmosphere to the lung alveoli

by convection or bulk flow through conducting airways

due to a pressure gradient

Mee Wah Ng RSO Dubai 2002

Air enters the RESPIRATORY SYSTEM through

2. then passes down the throat (pharynx)
(Tiny hairs called cilia help remove dirt and microbes. )

1.The nose and mouth

( filtrated, warmed and moistened )

and through the voice box (larynx).

( The entrance to the larynx is covered by a small flap of muscular tissue (epiglottis) that closes when swallowing, thus preventing food from entering the airways.

3.The largest airway is the windpipe (trachea), which branches into 4. Two smaller airways (bronchi) to supply the two lungs. 6. At the end of each bronchiole are dozens of bubble-shaped, air-filled cavities (alveoli) that is surrounded by a dense network of capillaries. The extremely thin walls of the alveoli allow oxygen to move from the alveoli to the capillaries and carbon dioxide to move from the capillaries into the alveoli.
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5. The bronchi themselves divide many times before evolving into smaller airways (bronchioles).
These are the narrowest airways--one fiftieth of an inch across.

Mee Wah Ng RSO Dubai 2002

Breathing in and out is known as inhalation and exhalation (inspiration and expiration) Due to changes in the volume of the thoracic cavity. Leads to pressure changes which cause air to enter or leave the lungs.

The main components facilitating the lung volume change are:

The diaphragm which is a sheet of muscle under the lungs The intercostal muscles which connect the ribs. There are two sets. The internal intercostal muscles and the external intercostal muscles.

Mee Wah Ng RSO Dubai 2002

Air will flow from an area of higher pressure to one of lower pressure ( pressure gradient )
Inspiration Diaphragm contracts The external intercostal muscles contract moving the ribs upwards and outwards. Chest expands Lungs are pulled outwards Alveolar pressure decreases Expiration Diaphragm relaxes The external intercostal muscles relax allowing the ribs to drop back down Lungs recoil inwards Air is forced out Alveolar pressure equals atmospheric pressure
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Mee Wah Ng RSO Dubai 2002

PRESSURE AND FLOW

Three pressures determine airflow and volume of the lungs

ATMOSPHERIC PRESSURE (PATM) Barometric pressure

ALVEOLAR PRESSURE (PALV) The pressure in the lung.

PLEURAL PRESSURE (PPLU) The pressure in the pleura, between the lung and thoracic wall.

Mee Wah Ng RSO Dubai 2002

PRESSURE AND FLOW

(PATM - PALV) = TRANSAIRFLOW PRESSURE The pressure difference between the atmosphere and alveoli which determines airflow. DeltaP = (PATM - PALV) = (Airflow) x (Resistance) The higher the flow, the higher the pressure; the higher the resistance for an equivalent flow, the higher the pressure required to overcome that resistance.

(PALV - PPLU) = TRANSPULMONARY PRESSURE Transpulmonary pressure determines the volume of the lung and is therefore dependent on the compliance of the lung.

The lower the compliance of the lung, the higher the transpulmonary pressure necessary to achieve an equivalent tidal volume.
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Mee Wah Ng RSO Dubai 2002

PRESSURE AND FLOW

BEGINNING OF INSPIRATION: no movement of air. alveolar pressure is 0 (the same as atmospheric pressure) Pleural Pressure is -5 cm H2O
During INSPIRATION pleural pressure changes from -5 to about -8 cm H2O Air flows into the lungs and lung volume increases Amount of pressure changes is dependent on the compliance of the lung.
FORCED INSPIRATION Rapid or forced inspiration causes pleural pressure to become much more negative than usual. EXPIRATION Normal expiration is simple relaxation of the diaphragm ------> lungvolume decreases due to its natural elasticity. FORCED EXPIRATION The pleural pressure can actually become positive as air is forced out of lungs
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Mee Wah Ng RSO Dubai 2002

Compliance
This relationship between lung volume and pressure determine

compliance of the lung.

Compliance is a measure of

change in volume in response to a change in pressure.

Compliance is related to 1. the elasticity 2. Surface tension

Affects: Chest wall Lungs - alveoli Diaphragm

High compliance thoracic wall and lungs expand easily Low compliance thoracic wall and lungs resist expansion

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Mee Wah Ng RSO Dubai 2002

Compliance
La PLACE relationship PRESSURE required to keep alveoli inflated = (2 Surface Tension) / r The higher the surface tension, the more pressure required to inflate alveolus. The lower the radius (size) of the alveolus, the more pressure required to inflate alveolus.
the

bigger (r), the less pressure is needed to hold them open the smaller (r) , the more pressure will be needed

Compliance decreases with lung volume. an empty lung has a higher compliance than a filled lung. This is consistent with the P/V curve leveling off as it approaches Total Lung Capacity.
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Mee Wah Ng RSO Dubai 2002

ELASTANCE
Refers to the tendency of an object to resist deformation and the ability to return to its original shape after deformation

( elastic recoil. )

Two factors explain the lung's desire to return to end expiration volume. 1. elastic fibres located throughout lung parenchyma which, when stretched by lung inflation, attempts to recoil. 2. A very thin coating of fluid lines the inner surface of alveoli which serves to enhance recoil properties of the lung. 3. This fluid, called surfactant encourages lung recoil when fully inflated yet serves to prevent collapse of alveoli when the lungs are near end expiration.

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Mee Wah Ng RSO Dubai 2002

Static Recoil Pressure or Pst

the elastic like tendency of the lung to return to its end expiration volume is due to

static recoil pressure

Which unlike pleural pressure, is positive relative to atmospheric pressure. Static recoil pressure is in direct opposition to pleural pressure

Elastance is Relative to Compliance As Compliance ; Elastance

As Compliance

: Elastance

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Mee Wah Ng RSO Dubai 2002

Compliance
Lung volume measurements reflect the stiffness or elasticity of the lungs and the rib cage.

Disorders that cause stiff lungs or that reduce the movement of the rib cage are called restrictive disorders.

Compliance decreases with conditions that Destroys lung tissues Causes it to become fluid filled Produces a deficiency in surfactant In any way impedes lung expansion or contraction

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Mee Wah Ng RSO Dubai 2002

Compliance
HIGH COMPLIANCE as in Obstructive Lung Disease

The lungs have trouble deflating because they have lost their elasticity
destruction of elastic fibers in lung great difficulty in exhaling but not inhaling.

LOW COMPLIANCE As in Restrictive Lung Disease. great difficulty in inhaling, expanding the lung. lack of surfactant as in Infant Respiratory Distress Syndrome ( IRDS )

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Mee Wah Ng RSO Dubai 2002

Compliance
"Static" Compliance is a measure of the "stiffness" or elasticity of lung and chest wall "Dynamic" compliance includes the extra pressure needed to overcome resistance to airflow, inertia of chest wall, and viscoelasticity of tissues. Total compliance varies from person to person and from time to time.

Lung compliance is an important consideration for many therapeutics routinely carried out in the critical care setting.

influences how best to ventilate critically ill patients

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Mee Wah Ng RSO Dubai 2002

RESISTANCE
Defined as the Force ( Pressure ) necessary to maintain a specific flow in a particular system It is a measure of the change in pressure per unit change in flow

R=

PA-PB V

mbar L/s

Resistance in a system is affected by Lumen of system Length of system Type of flow in system Branching of system
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Mee Wah Ng RSO Dubai 2002

Law of Hagen - Poiseulle

1 R~ r
4

The most important determinant of airway resistance in a single tube system is the radius of the tube Under laminar conditions, resistance is a function of length divided by radius to the fourth power Reduction in radius by one half would require a sixteenfold driving pressure to maintain the same flowrate of gas per unit time

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Mee Wah Ng RSO Dubai 2002

RESISTANCE
Resistance to gas flow arises because of: airway resistance friction between gas molecules and the walls of airway viscous tissue resistance friction between the tissues of the lung and the chest wall Resistance is inversely proportional to lung volume. airway resistance is lower during inspiration due to effects of changes in intrapleural pressure on airway diameter. During inspiration, pleural pressure becomes negative, a distending pressure is applied across the lung. which increases airway diameter as well as alveolar diameter decreases the resistance to gas flow. During expiration, pleural pressure increases and airways are compressed. When intrapleural pressure is high during active expiration, airways may collapse and gas may be trapped in the lung.
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Mee Wah Ng RSO Dubai 2002

AIRWAY RESISTANCE
the region of greatest resistance Highest resistance always occurs in the nose and nasopharynx..

The terminal bronchioles have low resistance because they have

the highest total cross-sectional area.

Rtotal can be partitioned into two components Rperipheral (gen. 7 - gen. 23): low resistance (laminar & diffusive zones) Rcentral (nose - gen. 6): high resistance (turbulent flow zone) Rcentral >>> Rperipheral (50% of resistance in nasal passages alone)

Airway resistance represents approximately 80% of the total resistance of the respiratory system.

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Mee Wah Ng RSO Dubai 2002

AIRWAY RESISTANCE
The higher the pressure difference required to maintain flow, the higher the airway resistance.

Flow rate measurements reflect the degree of narrowing or obstruction of the airways. This type of disorder is called an

obstructive disorder.

Chronic obstructive pulmonary disease such as bronchitis, asthma and emphysema have some degree of obstruction of the airway which increases airway resistance

Normal response to increased resistance is increased effort

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Mee Wah Ng RSO Dubai 2002

Work of Breathing
Components of Work elastic work - work to overcome: lung elastic recoil thoracic cage displacement abdominal organ displacement frictional work - work to overcome: air-flow resistance (major) viscous resistance (lobe friction, minor ) inertial work - work to overcome: acceleration and deceleration of air (negligible due to low mass of air) acceleration and deceleration of chest wall and lungs (negligible due to overdamping)
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Mee Wah Ng RSO Dubai 2002

Graphical Representation of the Major Components of Work

work = force * distance pressure * volume / 2

elastic work - area a-b-c-a inspiratory flow-resistive work - area a-i-b-a expiratory flow-resistive work - area a-b-e-a

passive recoil of lungs overcomes the work of expiratory flow-resistance

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Mee Wah Ng RSO Dubai 2002

RESPIRATION

External Respiration
Exchange of oxygen and carbon dioxide between the alveoli of the lung and pulmonary blood capillaries

Internal Respiration
Exchange of oxygen and carbon dioxide between tissue blood capillaries and tissue cells

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Mee Wah Ng RSO Dubai 2002

External Respiration
Gas exchange by "diffusion due to partial pressure gradient 1. to supply oxygen to the blood for distribution to the cells of the body,

2.

to remove carbon dioxide from the blood that has been collected from the cells of the body.

Gas exchange in the lungs occurs only in the smallest airways and the alveoli.

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Mee Wah Ng RSO Dubai 2002

Factors that influence external respiration

Partial pressure difference

alveolar pO2 is 105 mm Hg whilst systemic vein pO2 is only 40
mm Hg. O2 thus diffuses from alveoli to the surrounding blood supply

Surface area for gas exchange

Any pulmonary disorder that decreases the functional surface
area formed by the alveolar-capillary membranes decreases the rate of external respiration

Diffusion Distance
Total thickness of the alveolar-capillary membranes is only 0.5
micrometer. Thicker membranes will slow the rate of diffusion The narrow internal diameter of the capillaries also minimizes the difusion distance from alveolar airspace to the haemoglobin in the red blood cells In the presence of pulmonary oedema the build up of fluid increases diffusion distance slowing the rate of gas exchange
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Mee Wah Ng RSO Dubai 2002

Partial pressure difference

Physiologic Region inspired air trachea alveolus pulmonary vein pulmonary artery

PO2 (mm Hg) 159 149 100 95 40

PCO2 (mm Hg) 0.23 0.21 40 40 46

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Mee Wah Ng RSO Dubai 2002

DEAD SPACE
inspired air that is not perfused by blood thus "wasted" as it does not contribute to gas exchange. ANATOMICAL DEAD SPACE The volume of air occupying the upper airways where there are no alveoli. ALVEOLAR DEAD SPACE The volume of air that reaches the alveoli but doesn't get perfused by blood.

ANATOMICAL DEAD SPACE + ALVEOLAR DEAD SPACE = PHYSIOLOGICAL DEAD SPACE

In HEALTHY Individuals Alveolar Dead Space should be virtually zero, so physiological dead space = anatomical dead space.
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Mee Wah Ng RSO Dubai 2002

DEAD SPACE: VA/Q TOO HIGH. Normally dead space should only be anatomical dead space (20- 30% of tidal volume). Any dead space in excess is physiological. Alveolar air that is not perfused has the same O2 concentration as atmospheric air, 147 mm Hg So, an alveolar PAO2 of close to 147 is indicative of too much dead space.
. .

SHUNTED BLOOD: VA/Q TOO LOW. Shunted blood is defined as blood that goes through pulmonary circulation without getting ventilated (i.e. without taking up O2). This occurs when there is too little ventilation (hypoventilation) relative to perfusion. More shunted blood ------> lower PCapO2 ------> arterial gas composition (both CO2 and O2) approaches the levels of venous blood.
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Mee Wah Ng RSO Dubai 2002

Concept of Ventilation/Perfusion Matching

ideally, ventilation and perfusion must be exactly matched ventilation must be distributed to perfused areas perfusion must be distributed to. ventilated areas . the ratio of ventilation to perfusion (V A/Q ) is the critical factor governing gas exchange regions of high ventilation should have high blood flows (base of lung) regions of low ventilation should have low blood flows (apex of lung) one lung is represented by many regional V A/Q ratios, not a single V A/Q value
. . . .

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Mee Wah Ng RSO Dubai 2002

Regional Variation in Lung Ventilation

Ventilation within the lungs is greatest near the bases, in the upright position. This is probably mainly due to variation in intra-pleural pressure As we move from apex to base - pressure is more negative near the apex. Effectively, this probably causes more expansion of the apices at FRC. During inhalation, it is easier to expand the bases, as these are less distended than the apices!

EFFECTS OF GRAVITY ON FRC

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Mee Wah Ng RSO Dubai 2002

Regional Variations in Ventilation, Perfusion and Vent/Perf Ratio

APEX OF LUNG: Relatively less air and less blood go to the apex. low V A, lower Q , high V A/Q > 1 (wasted . ventilation) high PAO2 & low PACO2 due to high V A/Q.> 1 BASE OF LUNG: Relatively more air and more blood go to the base of the lung, primarily due to gravity. . . . . high V A, higher Q , low V A/Q < 1 (wasted perfusion) . . A/Q Low PAO2 & High PACO2 due to low V <1

MIDDLE . . OF LUNG: the VA/Q ratio most closely approximates 1. . . moderate V A, moderate Q , . . ideal V A/Q = 1 average PAO2 . &. average PACO2 due to ideal V A/Q = 1 Wests Lung Zones
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Mee Wah Ng RSO Dubai 2002

shunt unit: :VA/Q = 0, PAO2 = 40 mm Hg, PACO2 = 46 mm Hg . . alveolar Q >> V A (wasted perfusion) . . dead . space . alveolar unit: V A/Q = infinity, PAO2 = 150 mm Hg, PACO2 = 0 mm Hg Q << V A (wasted ventilation) . . ideal alveolar unit: V A/Q . = 1, . PAO2 = 100 mm Hg, PACO2 = 40 mm Hg . . . Q = V A (idealized matching) . . . . ventilation/perfusion inequality is the most common

. .

clinical . . cause of arterial hypoxemia

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Mee Wah Ng RSO Dubai 2002

. . VA/Q Balance Compensatory Mechanisms

HYPOXIC PULMONARY VASOCONSTRICTION Low PO2 in the pulmonary circulation indicates poor ventilation. If we have poor ventilation, we don't want blood to flow to that region. Thus Poor ventilation ------> Low PO2 locally ------> local vasoconstriction diverts blood elsewhere. This is the exact opposite of the systemic circulation, where low PO2 in tissues leads to vasodilation to increase local flow.

COMPENSATORY BRONCHOCONSTRICTION The converse of above.

If there is low blood flow to a region of lung, the corresponding bronchioles will bronchoconstrict. Local low blood flow ------> local low PCO2 ------> Regional bronchoconstriction ------> decreased ventilation to region
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Mee Wah Ng RSO Dubai 2002

Gravity and Positioning

Supine
Mee Wah Ng RSO Dubai 2002

Prone
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Raised Position
90 Healthy subject FRC reduction of approx. 1 Ltr.

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Diseased subject FRC improved Reduce WOB spontaneous breathing is encouraged

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Mee Wah Ng RSO Dubai 2002

Internal Respiration
Transport of gases between the lungs and body tissues
is a function of blood and cardiac output

How much pO2 blood can hold depends on:

the amount of haemoglobin 1 gm Hb can hold 1.34 mls of O2 type of haemoglobin Temperature Acidity

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Mee Wah Ng RSO Dubai 2002

HYPOXIA Differential causes of hypoxia Hypoxic hypoxia - low pO2 in arterial blood due to:
Intrinsic lung problems Fluid in the lungs High altitude

Anaemic Hypoxia - Low level of haemoglobin as aresult of:

Haemorrhage Anaemia Failure of Hb to carry its normal complement of O2 as in carbon monoxide poisoning Stagnant Hypoxia inability of blood to carry O2 to tissues fast enough for their needs Heart failure Circulatory shock

Histotoxic hypoxia
Although there is adequate delivery of oxygen to tissues, the tissues are unable to utilise it properly eg as in cyanide poisoning
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Mee Wah Ng RSO Dubai 2002

Control of Breathing
Breathing is usually automatic, controlled subconsciously by the respiratory center at the base of the brain known as the respiratory centre. The respiratory centre is functionally divided into three areas: Medullary rythmicity area
controls the basic rhythm of breathing Normal inspiration time 2 secs Expiration 3 seconds

Pnuemotaxic area co-ordinate transition between inspiration and expiration Inhibits inspiratory phase ( as to prevent overinflation )

Apneustic Area

Another part that co-ordinates transition between inspiration and expiration Prolongs inspiration when pneumotaxic area is inactive

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Mee Wah Ng RSO Dubai 2002

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Mee Wah Ng RSO Dubai 2002

Regulation of Respiratory Centre Activity

Controlled by 3 main factors: Cortical Influences: Cerebral cortex connects with respiratory centre allowing voluntary control of pattern of breathing.
Emotional stimuli such as crying

Inflation reflex: Stretch receptors send messages along the vagus nerves to inspiratory
area
Located in walls of bronchi and bronchioles Stimulates the start of expiration Known as the inflation ( Hering - Breur ) reflex Evidence that this reflex is mainly a protective mechanism for preventing overinflation of the lungs

Chemical Regulation:
The brain and small sensory organs in the aorta and carotid arteries sense when oxygen levels are too low or carbon dioxide levels are too high, and the brain increases the speed and depth of breathing. Hypercapnia ( High pCO2 ) results in increased respiratory rate Hypocapnia ( Low pCO2 ) results in decreased respiratory rate
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Mee Wah Ng RSO Dubai 2002

Summary of stimuli that affect ventilation rate and depth

Stimuli that Increase Rate and Depth of Ventilation Increase in arterial blood H+ level or pCO2 > 40 mm Hg Decrease in arterial blood pO2 from 105 to 50 mm Hg Decrease in blood pressure Increase in body temperature Prolonged pain Stimuli that Decrease Rate and Depth of Ventilation Decrease in arterial blood H+ level or pCO2< 40 mm Hg Decrease in arterial blood pO2 > 50 mm Hg Increase in blood pressure Decrease in body temperature Severe pain causes apnoea Irritation of pharyns or larynx by touch or chemicals causes apnoea

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Mee Wah Ng RSO Dubai 2002

Normal Respiratory Mechanics Values

Parameter
Respiratory Rate Tidal Volume Minute Ventilation Dynamic Compliance

Adult Range
10-15 breaths/minute 7-10 ml/kg 5-10 liters/minute 25-50 ml/cmH2O

Neonatal Range
30-40 breaths/minute 5-7 ml/kg
200-300 ml/kg/min

1-2 ml/cmH2O/kg

Airway Resistance Work of Breathing (Insp.)

Intrinsic PEEP Respiratory Drive P0.1

2-5 cmH2O/L/S
0.3-0.6 joules/liter 0 cmH2O 2-4 cmH2O

25-50 cmH2O/L/S

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Mee Wah Ng RSO Dubai 2002