The ventilation/perfusion ratio in a normal lung is approximately 0.8, but it can vary widely in different lung units. When ventilation is greater than perfusion, the ratio is greater than 1 (V̇ /Q̇ > 1), and when perfusion exceeds ventilation, the ratio is less than 1 (V̇ /Q̇ < 1). Mismatching of pulmonary blood flow and ventilation impairs the transfer of O2 and CO2. In individuals with cardiopulmonary disease, mismatching of pulmonary blood flow and alveolar ventilation is the most common cause of reduced arterial oxygen levels (PaO2). V̇ /Q̇ ratios greater than 1 are generally not associated with hypoxemia.

A normal ventilation/perfusion ratio does not necessarily mean that the ventilation and perfusion of a lung unit are normal. It simply indicates that the relationship between ventilation and perfusion is normal. For instance, in lobar pneumonia, ventilation to the affected lobe is reduced. If perfusion to this area remains unchanged, perfusion would exceed ventilation, resulting in a ratio less than 1 (V̇ /Q̇ < 1). However, the decrease in ventilation triggers hypoxic vasoconstriction in the pulmonary arteries supplying this lobe. This reduces perfusion to the affected area and brings the ventilation/perfusion ratio closer to normal. However, neither the ventilation nor the perfusion to this area is normal, as both are decreased.

The ventilation/perfusion ratio varies across different areas of the lung. In an upright individual, although both ventilation and perfusion increase from the top to the bottom of the lung, the increase in ventilation is smaller than the increase in blood flow. Therefore, the V̇ /Q̇ ratio at the top of the lung is significantly greater than 1 (ventilation exceeds perfusion), while the ratio at the bottom of the lung is much less than 1 (perfusion exceeds ventilation).

PACO2 and PaCO2 are equal due to the solubility properties of CO2. However, this is not the case for alveolar and arterial oxygen. Even in individuals with normal lungs, PAO2 is slightly higher than PaO2. The difference between PAO2 and PaO2 is referred to as the alveolar-arterial difference for oxygen (AaDO2). An increased AaDO2 indicates abnormal oxygen exchange. In healthy individuals, this small difference is not caused by imperfect gas exchange, but by the small number of veins that bypass the lungs and directly empty into the arterial circulation. For example, the thebesian vessels of the left ventricular myocardium drain directly into the left ventricle instead of the coronary sinus in the right atrium, and some bronchial and mediastinal veins drain into the pulmonary veins. This results in venous admixture and a decrease in PaO2. Approximately 2% to 3% of the cardiac output is shunted in this manner.

To assess the clinical effectiveness of gas exchange in the lung, PaO2 and PaCO2 are measured. PAO2 is calculated using the alveolar air equation.
in a normal lung, the overall ventilation/perfusion ratio is approximately 0.8, but the range of V̇ /Q̇ ratios varies widely in different lung units. When ventilation exceeds perfusion, the ventilation/perfusion ratio is greater than 1 (V̇ /Q̇ > 1), and when perfusion exceeds ventilation, the ventilation/ perfusion ratio is less than 1 (V̇ /Q̇ < 1). Mismatching of pulmonary blood flow and ventilation results in impaired O2 and CO2 transfer. In individuals with cardiopulmonary disease, mismatching of pulmonary blood flow and alveolar ventilation is the most frequent cause of systemic arterial hypoxemia (reduced PaO2). In general, V̇ /Q̇ ratios greater than 1 are not associated with hypoxemia.
A normal ventilation/perfusion ratio does not mean that ventilation and perfusion of that lung unit are normal; it simply means that the relationship between ventilation and perfusion is normal. For example, in lobar pneumonia, ventilation to the affected lobe is decreased. If perfusion to this area remains unchanged, perfusion would exceed ventilation; that is, the ventilation/perfusion ratio would be less than 1 (V̇ /Q̇ < 1). However, the decrease in ventilation to this area produces hypoxic vasoconstriction in the pulmonary arterial bed supplying this lobe. This results in a decrease in perfusion to the affected area and a more “normal” ventilation/perfusion ratio. Nonetheless, neither the ventilation nor the perfusion to this area is normal (both are decreased), but the relationship between the two could approach the normal range.
The ventilation/perfusion ratio varies in different areas of the lung. In an upright individual, although both ventilation and perfusion increase from the apex to the base of the lung, the increase in ventilation is less than the increase in blood flow. As a result, the normal V̇ /Q̇ ratio at the apex of the lung is much greater than 1 (ventilation exceeds perfusion), whereas the V̇ /Q̇ ratio at the base of the lung is much less than 1 (perfusion exceeds ventilation). The relationship between ventilation and perfusion from the apex to the base of the lung is depicted in
Fig. 23.7 • Fig. 23.7 Ventilation/Perfusion Relationships in a Normal Lung in the Upright Position. Only the apical and basal values are shown for clarity. In each column, the number on top represents values at the apex of the lung, and the number on the bottom represents values at the base. PCO2, partial pressure of carbon dioxide; PN2, partial pressure of nitrogen; PO2, partial pressure of oxygen; Q̇ , perfusion per minute; VA, alveolar ventilation per minute.
PACO2 and PaCO2 are equal because of the solubility properties of CO2 (see ). The same is not true for alveolar and arterial O2. Even in individuals with normal lungs, PAO2 is slightly greater than PaO2. The difference between PAO2 and PaO2 is called the alveolar-arterial difference for oxygen (AaDO2). An increase in the AaDO2 is a hallmark of abnormal O2 exchange. This small difference in healthy individuals is not caused by “imperfect” gas exchange, but by the small number of veins that bypass the lung and empty directly into the arterial circulation. The thebesian vessels of the left ventricular myocardium drain directly into the left ventricle (rather than into the coronary sinus in the right atrium), and some bronchial and mediastinal veins drain into the pulmonary veins. This results in venous admixture and a decrease in PaO2. (This is an example of an anatomical shunt; see the section .”) Approximately 2% to 3% of the cardiac output is shunted in this way.
To measure the clinical effectiveness of gas exchange in the lung, PaO2 and PaCO2 are measured. PAO2 is calculated from the alveolar air equation (