Abstract
We infused starch microemboli (63 to 74-mu diameter) into the external jugular vein of 28 dogs, to observe the effects of continuous positive-pressure ventilation (CPPV) on gas exchange and hemodynamics during hypoxemia (PaO2 53 +/- 3 torr). CPPV at both 10 and 15 cm H2O end-tidal pressure improved PaO2. CPPV 15 returned PaO2 and pulmonary shunt to control values but reduced cardiac output, O2 transport, and O2 consumption. In spite of these changes suggesting inadequate tissue oxygenation with CPPV 15, mixed venous oxygenation was not reduced. We conclude that: (a) hypoxemia after microemboli infusion is improved by CPPV and therefore likely caused by ventilation/perfusion abnormalities; (b) the improvement in PaO2 produced by CPPV after microemboli is not beneficial if CPPV reduces perfusion and O2 transport; and (c) mixed venous oxygenation does not appear to be an adequate measure of oxygen transport to tissues when CPPV is applied in this high pulmonary vascular resistance setting.
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