Altered distribution of pulmonary ventilation and blood flow following induction of inhalational anesthesia

Abstract

The development of impairment of pulmonary gas exchange during inhalational anesthesia was studied in ten patients (ages 52-75 years) by use of the multiple-inert-gas elimination method. Preoperative pulmonary function tests indicated a wide range of abnormal pulmonary function. Control gas-exchange studies with the subjects awake (supine position) demonstrated modest increases in pulmonary ventilation-blood flow (V(A)/Q distribution in all subjects (mean log SD=0.96), but the shunt was minimal (mean 1.3%). Inhalational anesthesia was either 1) halothane, 0.4% (end-tidal) in N2O, 50-60%, balance oxygen, for eight subjects, or 2) halothane, 0.6%, in nitrogen, 50-60%, balance oxygen, for two subjects. Striking increases in retention of the least soluble tracer gases (SF6 and ethane) were seen in all patients after a minimum of 35 min of anesthesia, during mechanical ventilation with both anesthetic regimens. This was due to one of three different patterns of responses. Three subjects showed primarily increased intrapulmonary shunt (mean shunt = 23% of cardiac output). Three subjects showed primarily increases in low-V(A)/Q units (mean=32% of cardiac output), with little or no shunt, while the remaining four had both intrapulmonary shunt and units of low V(A)/Q. Arterial blood P(O2) measurements suggested substantially greater impairment of oxygenation when the pattern of response was primarily an increase in shunt. This difference was accentuated by the concentrating effect of N2O uptake on alveolar P(O2) in low-V(A)/Q units. As a consequence, arterial blood P(O2) values grossly underestimated the V(A)/Q inequality in patients in whom low-V(A)/Q regions developed. An alternative index, the development of CO2 retention at constant alveolar ventilation, more reliably identified patients in whom severe V(A)/Q inequality developed during inhalational anesthesia.