Ventilation-Perfusion Ratio Abnormalities

Until this point, I have assumed equality of alveolar and arterial anesthetic partial pressures (i.e., that the alveolar gases completely equilibrate with the blood passing through the lungs). For normal patients, this assumption is approximately correct, but diseases such as emphysema, pneumonia, and atelectasis, as well as congenital cardiac defects, produce substantial deviations from equilibration. The associated ventilation-perfusion ratio abnormality increases the alveolar (end-tidal) anesthetic partial pressure and decreases the arterial anesthetic partial pressure (i.e., a partial pressure difference appears between alveolar gas and arterial blood). The relative change depends on the solubility of the anesthetic. With a poorly soluble agent, the end-tidal concentration is slightly increased, but the arterial partial pressure is significantly reduced. The opposite occurs with a highly soluble anesthetic.^[52]

The considerable decrease in the arterial anesthetic partial pressure that occurs with poorly soluble agents may be explained as follows. Ventilation-perfusion ratio abnormalities increase ventilation relative to perfusion of some alveoli, whereas in other alveoli, the reverse occurs. With a poorly soluble anesthetic, an increase in ventilation relative to perfusion does not appreciably increase the alveolar or arterial anesthetic partial pressure issuing from those alveoli (see Fig. 5-5 for nitrous oxide effect). However, when ventilation decreases relative to perfusion (e.g., with atelectasis), blood emerges from that segment with no additional anesthetic. Such anesthetic-deficient blood then mixes with the blood from the ventilated segments containing a normal complement of anesthetic. The mixture produces an arterial anesthetic partial pressure considerably below normal.

Figure 5-9 Proportional increases in alveolar ventilation (VA) and cardiac output (Q) increase the rate at which the alveolar concentration of anesthetic/concentration of inspired anesthetic (FA/FI ratio) rises. The effect is relatively small if the increase in cardiac output is distributed proportionately to all tissues (i.e., if cardiac output is doubled, all tissue blood flows are doubled). The greatest effect occurs with the most soluble anesthetic. (Adapted from Eger EI II, Bahlman SH, Munson ES: Effect of age on the rate of increase of alveolar anesthetic concentration. Anesthesiology 35:365–372, 1971.)

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Figure 5-10 The alveolar rate of rise of halothane concentration is more rapid in children (dashed lines) than in adults (solid lines). The difference probably results from the greater ventilation and perfusion per kilogram of tissue in children and the fact that a disproportionate amount of the increased perfusion is devoted to the vessel-rich tissues. FA/FI is the alveolar concentration of anesthetic/concentration of inspired anesthetic. (Data from references ^{[6] [49] [50]} and ^[51] .)

With highly soluble agents, a different situation results from the same ventilation-perfusion ratio abnormalities. In alveoli receiving more ventilation relative to perfusion, the anesthetic partial pressure increases nearly in proportion to the increase in ventilation (see Fig. 5-5 for effect with diethyl ether). Blood issuing from these alveoli has an increased anesthetic content almost proportional to the increased ventilation. Assuming that overall (total) ventilation remains normal, this increase in the anesthetic contained by blood from the relatively hyperventilated alveoli compensates for the lack of anesthetic uptake in unventilated alveoli.

These effects are illustrated in Figure 5-11 for endobronchial intubation. Direction of all ventilation to one lung produces hyperventilation relative to perfusion. FA/FI for this lung is slightly increased (above that obtained in the absence of endobronchial intubation) with the poorly soluble cyclopropane and greatly increased with the highly soluble ether. The increase with ether compensates for the absence of uptake from the unventilated lung, a compensation that is not available with cyclopropane. The result is that the cyclopropane arterial partial pressure is well below normal, whereas the ether arterial partial pressure is scarcely changed.

These concepts have been confirmed experimentally by comparing the rate of arterial anesthetic rise with

Figure 5-11 When no ventilation-perfusion abnormalities exist, the alveolar (PA) and arterial (Pa) anesthetic partial pressures rise together (solid lines) toward the inspired partial pressure (PI). When 50% of the cardiac output is shunted through the lungs, the rate of rise of the end-tidal partial pressure (dashed lines) is accelerated, and the rate of rise of the arterial partial pressure (dotted or dashed lines) is retarded. The greatest retardation occurs with the least soluble anesthetic, cyclopropane. FA/FI is the alveolar concentration of anesthetic/concentration of inspired anesthetic. (Adapted from Eger EI II, Severinghaus JW: Effect of uneven pulmonary distribution of blood and gas on induction with inhalation anesthetics. Anesthesiology 25:620–626, 1964.)