The Gas Exchanger: Matching Ventilation and Perfusion

Summary Points

• Alveolar ventilation is the sum of air that enters or exits the alveolus each minute and is one of the key determinants of the P_aCO₂.
• Dead space refers to regions of the lung that receive air but do not participate in gas exchange.
• Physiologic dead space is the sum of anatomic dead space (airways) and alveolar dead space (alveoli that receive air but are not perfused).
• Total ventilation is the sum of alveolar and dead space ventilation.
• Physiological dead space can be measured with determination of the dead space to tidal volume ratio using the Bohr method, which makes use of the principle that gas coming from dead space contains no carbon dioxide, while gas coming from perfused alveoli has a PCO₂ equivalent to the P_aCO₂.
• The carbon dioxide elimination relationship, or clearance equation for the lung, indicates that alveolar PCO₂ is inversely proportional to arterial PCO₂, and is directly proportional to carbon dioxide production.
• At FRC in an upright person, the alveoli at the apex of the lung are larger than at the base because of the distribution of the pleural pressure over the lung; the pleural pressure is more negative at the apex of the lung.
• During a normal tidal volume breath from FRC, the bases of the lung receive a greater proportion of the breath than the apices of the lung.
• The pulmonary circulation is a high-compliance, low-resistance system and can accommodate significant increases in blood flow with relatively small changes in pressure.
• In a normal person in the upright position, more blood flow goes to the bases than the apices of the lungs as a result of the effects of gravity.
• In the most superior (opposite gravity) portions of the lung, there may be no blood flow to some alveoli (alveolar dead space; zone 1 of the lung). In these regions of the lung, alveolar pressure may exceed pulmonary capillary pressure.
• The three zones of the lung describe the relative amounts of perfusion to different regions of the lung. These zones are derived from the relationships between alveolar, pulmonary arterial, and pulmonary venous pressures.
• The pulmonary arterioles respond to local hypoxia by vasoconstricting. This results in the redirection of blood flow to lung units with higher PO₂.
• Optimal efficiency of gas exchange depends on matching of ventilation and perfusion within the lung. mismatch is a major cause of hypoxemia in patients with cardiopulmonary diseases.
• The carbon dioxide–hemoglobin dissociation curve is relatively linear. This relationship allows hyperventilation of normal alveoli to compensate for hypoventilation of diseased lung units.
• The Haldane effect describes the shift to the right of the carbon dioxide–hemoglobin dissociation curve in the presence of oxygen. Carbon dioxide is displaced from hemoglobin and enters the blood as a dissolved gas. Thus, for a given CO₂ content, PCO₂ is higher.
• The physiological causes of hypoxemia include reduced alveolar ventilation (because of a decrease in total ventilation, a change in breathing pattern, or mismatch) and increased carbon dioxide production in the setting of minimal ventilatory reserve.
• The oxygen–hemoglobin dissociation curve has a sigmoid shape. This relationship ensures that a mild decrease in alveolar PO₂ does not significantly affect hemoglobin saturation and the oxygen content of the blood and that oxygen is readily released when blood reaches peripheral tissue.
• The majority of oxygen carried in blood is bound to hemoglobin.
• Anemia leads to reduced oxygen content in the blood but does not affect the P_aO₂.
• The oxygen–hemoglobin dissociation curve may shift to the right or the left based on body temperature, blood pH, and P_aCO₂.
• The alveolar gas equation allows one to calculate the P_AO₂. Using this value and the P_aO₂ obtained from an ABG, one can calculate the A-aDO₂, a number that is essential in analyzing the physiological cause of hypoxemia. An abnormal A-aDO₂ indicates that there is a problem with the gas exchanger.
• The five physiological causes of hypoxemia are decreased P_IO₂, alveolar hypoventilation, mismatch, shunt, and abnormal diffusion. The physiological cause of hypoxemia can often be determined with knowledge of the A-aDO₂ and the response of the P_aO₂ to supplemental oxygen and with information whether the hypoxemia is present at rest or only with exercise.
• mismatch is the most common physiological cause of hypoxemia. Mild to moderate mismatch is much more likely to produce hypoxemia than hypercapnia because of the different shapes of the oxygen-hemoglobin and carbon dioxide–hemoglobin dissociation curves.