Effects of hypoxic and carbon monoxide (CO) hypoxia on venous return in dogs

The effects of hypoxic and CO hypoxia on venous return were studied in anesthetized dogs whose hearts were bypassed with an extracorporeal circuit that allowed control of atrial pressures (P(RA), P(LA)). During normoxia and hypoxia, venous return at P(RA) and P(LA) = O (Omax) (Qmax) mean systemic pressure (P(s)) were determined, the latter by measuring the P(RA) that occurred after turning off the bypass pumps. For equivalent decreases in arterial O₂ content (ΔCaO₂ = -11 vol %), hypoxic hypoxia increased Qmax by 65% and P(s) by 2.1 mmHg while CO hypoxia increased Qmax only 17% and decreased P(s) 2.6 mmHg. Venous capacitance was therefore decreased by hypoxic hypoxia and increased by CO hypoxia. Resistance to venous return (R(v) = P(s)/Qmax) was decreased in both types of hypoxia. If a circulatory model consisting of parallel fast and slow time constant venous circuits can be assumed, then R(v) = (F(1Q) x F(1C))R(1) + (F(2Q) x F(2C)R(2) where F(Q) = fraction of Qmax to each circuit, F(C) = fraction of total compliance in each circuit, and R the venous resistance in each circuit. The decrease in R(v) during hypoxic hypoxia may therefore not be due to a dilatation of veins but to changes in the fractional distribution of Qmax and C. However, the decrease in R(v) during CO hypoxia is probably due to venous dilatation. Arterial oxygen tension (PaO₂) may be responsible for these differences, since hypoxic, but not CO, hypoxia was associated with a decreased PaO₂.