Mismatching between ventilation and perfusion is the most frequent cause of arterial hypoxemia in individuals with respiratory disorders. In the most common example, the composition of mixed venous blood, total blood flow (cardiac output), and the distribution of blood flow are normal. However, when alveolar ventilation is distributed unevenly between the two gas-exchange units (
Fig. 23.11 ) and blood flow is equally distributed, the unit with decreased ventilation has a V̇ /Q̇ ratio of less than 1, whereas the unit with the increased ventilation has a V̇ /Q̇ of greater than 1. This causes the alveolar and end-capillary gas compositions to vary. Both the arterial O2 content and CO2 content are abnormal in the blood that has come from the unit with the decreased ventilation (V̇ /Q̇ , <1). The unit with the increased ventilation (V̇ /Q̇ , >1) has a lower CO2 content and a higher O2 content because it is being overventilated. The actual PaO2 and PaCO2 vary, depending on the relative contribution of each of these units to arterial blood. The alveolar-arterial O2 gradient (AaDO2) is increased because the relative overventilation of one unit does not fully
PlO2 = 150 PlCO2 = 0 PAO2 = 77 PACO2 = 45 PCO2= 45PO2= 77 PAO2 = 105 PACO2 = 36 PpvO2 = 89 PpvCO2 = 40.5 Pulmonary vein Pulmonary artery PvO2 = 40 PvCO2 = 46 – – Anatomic dead space • Fig. 23.11 Effects of Ventilation/Perfusion Mismatching on Gas Exchange. The decrease in ventilation to the one lung unit could be due to mucus obstruction, airway edema, bronchospasm, a foreign body, or a tumor. PACO2, partial pressure of alveolar carbon dioxide; PAO2, partial pressure of alveolar oxygen; PiCO2, partial pressure of inspired carbon dioxide; PiO2, partial pressure of inspired oxygen; PpvCO2, partial pressure of carbon dioxide in portal venous blood; PpvO2, partial pressure of oxygen in portal venous blood; PvCO2, partial pressure of carbon dioxide in mixed venous blood; PvO2, partial pressure of oxygen in mixed venous blood.
compensate (either by the addition of extra O2 or by the removal of extra CO2) for underventilation of the other unit. The failure to compensate is greater for O2 than for CO2, as indicated by the flatness of the upper part of the oxyhemoglobin dissociation curve, in contrast to the slope of the CO2 dissociation curve (see
Chapter 24).
In other words, increased ventilation increases PAO2, but it adds little extra O2 content to the blood because hemoglobin is close to being 100% saturated in the overventilated areas. This is not the case for CO2, for which the steeper slope of the CO2 curve indicates removal of more CO2 when ventilation increases. Thus inasmuch as CO2 moves by diffusion, then as long as a CO2 gradient is maintained, CO2 diffusion will occur.
The PAO2 is determined by a balance between the rate of O2 uptake and the rate of O2 replenishment by ventilation. Oxygen uptake depends on blood flow through the lung and the metabolic demands of the tissues. If ventilation decreases, PAO2 decreases, and PaO2 subsequently decreases. In addition, VA and PACO2 are directly but inversely related. When ventilation is halved, the PACO2 doubles and thus so does the PaCO2 (see
Eq. 23.16 ). Ventilation insufficient to maintain normal levels of CO2 is called hypoventilation. Hypoventilation always decreases PaO2 and increases PaCO2.