60 100 Po2 mmHg

FIGURE 9 A three-compartment model showing how Va/Q differences between lung units can increase the difference between mixed-alveolar Po2 (Pao2 = 116 mm Hg) and mixed-arterial Po2 (Pao2 = 55 mm Hg). Inspired Po2 is assumed normal (150 mmHg). Alveolar Po2 in any individual unit is assumed equal to the Po2 in end-capillary blood from that unit (open circles on O2 dissociation curve in lower panel). However, Po2 in mixed arterial blood is weighted toward Po2 in the low Va/Q units, and Po2 in mixed alveolar gas is weighted toward Po2 in the high Va/Q units. The shape of the O2 dissociation curve also contributes to the large alveolar-arterial Po2 difference as described in the text. (After West, Ventilation/blood flow and gas exchange. New York: Blackwell Scientific, 1990.)

the high Va/Q unit contributes more volume to mixed alveolar gas.

Therefore, Va/Q heterogeneity decreases Pao2, and increases PAo2 from ideal values, so the alveolar-arterial Po2 is increased. This mechanism increases the alveolar-arterial partial pressure difference for any gas, including C02 and anesthetic gases. However, Va/Q affects 02 more than other gases because the shape of the blood-02 equilibrium curve depresses Pao2. High and low Va/Q regions can offset the effects of each other more effectively for Co2 and anesthetic gases because the blood-equilibrium curves are relatively linear for these gases. Consequently, increasing overall ventilation is effective at overcoming Paco2 increases from Va/Q heterogeneity, and the ventilatory control reflexes are quite effective at maintaining normal PaCO2 by this mechanism (see Carbon Dioxide Exchange and Chapter 22).

Va/Q heterogeneity occurs in normal lungs and explains the normal alveolar-arterial Po2 in healthy young individuals. However, only half the Va/Q heterogeneity necessary to explain the normal alveolar-arterial Po2 difference is caused by gravitational-dependent differences in Va and Q at different heights in the lung. Significant intraregional Va/Q heterogeneity occurs between functional units of gas exchange (acini; see Chapter 18) at any given height in the lung. Va/Q heterogeneity is also the most common cause of hypoxemia in lung disease (see Clinical Note later in this chapter).

Several methods are available for measuring the exact nature of Va/Q heterogeneity, but they are generally restricted to the research laboratory and not useful clinically. Va/Q heterogeneity can be diagnosed clinically by eliminating other causes of hypoxemia. Hypoventilation can be ruled out if the measured alveolar-arterial Po2 difference is greater than the normal predicted value. Diffusion limitation can be ruled out if the measured Dlco is at least 50% of normal, or if breathing high inspired o2 relieves hypoxemia and decreases the alveolar-arterial Po2 difference. However, 100% o2 breathing will also eliminate hypoxemia from Va/Q heterogeneity if all of the alveoli equilibrate with inspired Po2. With pure O2 breathing, only O2 and CO2 (plus water vapor) are in the alveolar gas, so PAo2 is at least 600 mm Hg in all alveoli. In practice, Va/Q heterogeneity includes poorly ventilated lung units, so it may take up to 30 min to wash nitrogen out of all the alveoli during o2 breathing. Consequently, o2 breathing improves hypoxemia from Va/Q heterogeneity, but not nearly as quickly as it does with a pure diffusion limitation (which requires < 1 min). If shunt is present, 100% O2 breathing will never resolve the hypoxemia or decrease the alveolar-arterial Po2 difference.

Other clinical measures of Va/Q heterogeneity include physiologic shunt and dead space. Low Va/Q gas exchange units and shunt have similar effects on Pao2. This means that physiologic shunt (or venous admixture) can be used to quantify Va/Q heterogeneity. Physiologic shunt is measured with the Berggren shunt equation in an individual breathing less than 100% o2, and usually room air (see Shunts section). Va/Q heterogeneity causes hypoxemia "as if" there were an increase in shunt, so it increases physiologic shunt. Similarly, the effects of high Va/Q units on Pao2 resemble the effects of dead space. Therefore, physiologic dead space (see Physiologic Dead Space section) can be used to quantify the effects of Va/Q heterogeneity on Pao2 and Paco2 "as if" there were an increase in anatomic dead space. Note that both physiologic shunt and dead space will be less than the actual amounts of blood flow or ventilation going to abnormal Va/Q units. This is because shunt and dead space represent the extremes of the Va/Q ratio, and actual Va/Q ratios between 0 and infinity will have smaller effects on alveolar and arterial Po2 and Pco2 (see Fig. 7).

Note that the alveolar ventilation equation introduced earlier does not accurately quantify Va when arterial Pco2 is substituted for alveolar Pco2 if Va/Q heterogeneity is present. Va/Q heterogeneity causes alveolar Pco2 to be less than arterial Pco2. Hence, the total ventilation to all alveoli is underestimated if arterial Pco2 is used in the alveolar ventilation equation. Because it is difficult to measure mixed alveolar Pco2, the alveolar ventilation equation is not used on people with lung disease.

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