Section Two Diffusion of gases

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Section Two Diffusion of gases Lecture 5: Partial pressure and the composition of gasses in air. Factors affecting diffusion of gases. Ventilation perfusion ratio effect on alveolar gas concentration. Objectives: I. To explain the factors affecting O2 and CO2 diffusion across the lung. II. III. IV. To relate the clinical significance of changes in anatomical and physiological dead space. To list the factors affecting the diffusion of gases through the respiratory membrane. To analyze the partial pressure changes of O2 and CO2 in the circulation. V. Describe the effect of ventilation-perfusion on partial O2, CO2 partial pressures.

Physical Principles of Gas Exchange Partial pressure The pressure exerted by each type of gas in a mixture Dalton s law: P total = P 1 + P 2 + P 3 +... + P n Water vapor pressure Diffusion of gases through liquids Concentration of a gas in a liquid is determined by its partial pressure and its solubility coefficient

Partial pressure of gases; gas molecules undergo continuous random motion. These rapidly moving molecules exert a pressure which is increased if the rate of movement of the molecules increases. In a mixture of gases, the rate of diffusion of each gas is directly proportional to the pressure caused by this gas alone, which is called the partial pressure of the gas and is denoted by a P for e.g., PO 2, PCO 2, PN 2. The pressure that a gas exerts is proportional to: 1- The temperature. 2- Concentration of the gas (number of molecules). Net diffusion of a gas will occur from a region (area) where its partial pressure is high to a region where it is low.

Ambient air inhaled into the nasal passages and tracheobronchial tree is immediately warmed to body temperature and completely saturated with water vapor. The water vapor or water gas added to inspired air exerts a partial pressure just like the other gases comprising air.

Composition of alveolar air: If the atmospheric pressure is 760 mmhg, the total pressure within the lungs must be the same. But in alveoli there is another gas added to O 2, CO 2, N 2, which is the H 2 O vapor emitted from the moist surfaces of the respiratory tracts (humidification), H 2 O vapor exerts a pressure of about 47 mmhg at body temperature of 37 Ċ. Normal partial pressure of alveolar air at sea level: PN 2 = 569 mmhg PO 2 = 104 mmhg PCO 2 = 40 mmhg PH 2 O = 47 mmhg

Only a portion of each tidal volume is delivered to the alveoli. The total air volume of all lung alveoli before inspiration (end-expiration) is by definition the Functional Residual Capacity. For a normal adult, the FRC is about 2500 ml. So, if the volume of fresh ambient air reaching the alveoli is 300 ml, it is added to an FRC of 2500 ml. As a result, the partial pressures of alveolar gases do not fluctuate markedly with each breath since only a portion of the FRC is exchanged.

Physical Principles of Gas Exchange Factors affecting the diffusion of gases through the respiratory membrane: 1. Thickness of the membrane which is increased in cases of edema of interstitial spaces & alveoli and in fibrosis. 2. Surface area of the membrane which is reduced in case of lung resection, emphysema. 3. Diffusion coefficient of the gas in the substance of the membrane. 4. The pressure difference across the respiratory membrane, from high pressure area into lower pressure area. Relationship between ventilation and pulmonary capillary flow Increased ventilation or increased pulmonary capillary blood flow increases gas exchange.

Diffusion of Gases through the Respiratory Membrane The respiratory unit: respiratory bronchioles, alveolar ducts, atria, and alveoli. Blood flows as a sheet. Respiratory membrane is 0.2 micrometer thickness and composed of: 1) fluid (surfactant), 2) epithelium, 3) epithelial basement membrane, 4) interstitial fluid, 5) capillary basement membrane, 6) endothelial cells

Alveolar blood gas exchange: The systemic venous blood coming from the tissues enters the pulmonary capillaries. It has high PCO 2 (46 mmhg) and low PO 2 (40 mmhg). The differences in the partial pressures of O 2 & CO 2 on two sides of the alveolar-capillary membrane result in the diffusion of O 2 from alveoli (PO 2 =104 mmhg) to blood (PO 2 = 40 mmhg) and CO 2 from blood (PCO 2 = 46 mmhg) to alveoli (PCO 2 = 40 mmhg) until reaching equilibrium. Gas exchange in the tissues: The oxygenated arterial blood of the tissue capillaries is separated from interstitial fluid by only the thin capillary wall which is highly permeable to both O 2 & CO 2. The interstitial fluid is separated from the intracellular fluid by cell plasma membrane. Since metabolic reactions within the cells consuming O 2 and producing CO 2, the intracellular PO 2 is lower and PCO 2 is higher than in blood. So there is a net diffusion of O 2 from blood into cells and CO 2 from cells into blood which is now a systemic venous blood.

Diffusion of oxygen from the capillaries to the cells: O 2 is always being used by the cells. Therefore, the intracellular PO 2 remains lower than the PO 2 in the capillaries (the normal intracellular PO 2 ranges 5-40 mmhg, averaging 23 mmhg). Thus, there is again a pressure difference that causes O 2 to diffuse from the blood into the cells. Because only 1-3 mmhg of O 2 pressure is normally required for full support of the chemical processes that use O 2 in the cell. So this low cellular PO 2 of 23 mmhg is more than adequate and provides a large safety factor. Diffusion of CO 2 : Most of O 2 used by the cells becomes CO 2. This increases intracellular PCO 2. Therefore, CO 2 diffuses from the cells into the tissue capillaries and then carried by the blood into the lungs. In the lungs, it diffuses from the pulmonary capillaries into alveoli. Thus, CO 2 diffuses in a direction exactly opposite that of the diffusion of O 2, the only difference is that CO 2 can diffuse about 20 times as rapidly as O 2.

Therefore, the pressure difference that causes CO 2 diffusion, far less than the pressure difference required to cause O 2 diffusion. These pressures: 1- Intracellular PCO 2 = 46 mmhg. 2- Interstitial PCO 2 = 45 mmhg. 3- PCO 2 of arterial blood entering the tissues = 40 mmhg. 4-PCO 2 of venous blood leaving the tissues = 45 mmhg i.e., comes to equilibrium with interstitial PCO 2. PCO 2 of venous blood entering pulmonary capillaries is 45 mmhg and PCO 2 of alveoli is 40 mmhg thus, 5 mmhg pressure difference causes CO 2 diffusion out of pulmonary capillaries into alveoli.

Effect of ventilation perfusion ratio on VA/Q = 0 alveolar gas concentration O2 = 40, CO2 = 45mmHg VA/Q = infinity O2 = 149, CO2 = 0mmHg VA/Q = normal O2 = 104, CO2 = 40mmHg If less than normal then called physiological shunt If more than normal then called physiological dead space

Normally at the tip of the lung, VA/Q is (2.5) times normal (phys. dead space), while at the base, it is (0.6) times normal (phys. shunt). Normally, there are abnormal VA/Q ratios in the upper and lower portions of the lung. In the upper both ventilation and perfusion are low but VA is more than Q, so there is physiological dead space, but in the lower VA is less than Q, so there is physiological shunt.

Mismatching of V A /Q occurs in diseases when there is uneven ventilation or uneven perfusion; to cause inadequate O 2 movement between alveoli and pulmonary capillary blood i.e., there is mismatching of the air supply and blood supply in individual alveoli. The right proportion of alveolar air flow (ventilation) and capillary blood flow (perfusion) should be available to each alveolus; any mismatching is termed ventilation-perfusion inequality. The major effect of ventilation-perfusion inequality is to lower PO 2 of systemic arterial blood. Abnormally, as in smokers, bronchi obstruction (1) low ratio [no air] and (2) high ratio because of obstructed alveolar wall. emphysema

Changes in Partial Pressures