Human cardiovascular adjustments to acute hypoxaemia.

Abstract

Traditionally, cardiovascular adjustments to hypoxaemia are viewed as resultants of competing local vasodilation and vasoconstriction via arterial chemoreflexes with net effects of increased cerebral and coronary blood flows (local) and reduced flow to visceral organs and muscle (reflex). Although true in asphyxia, breathing activates lung mechanoreceptors which reduce vagal outflow and apparently, in humans, abolishes sympathetic vasomotor activity (SNA). During rest, moderate to severe hypoxaemia (PaO2 = 35 to 27 mmHg) caused no splanchnic, cutaneous or muscle vasoconstriction. Local vasodilator effects of hypoxaemia were not sufficient to overwhelm vasoconstriction; splanchnic arterioles responded normally to infused noradrenalin (NA) during hypoxaemia. Possibly, central effects of hypoxaemia blunt SNA or peripheral, prejunctional effects impair neuronal release of NA. Persistent orthostatic tolerance with normal skeletal muscle vasoconstriction and retained spinal venomotor reflexes during hypoxaemia argue against prejunctional inhibition of NA release. Results so far suggest that beyond a certain threshold, hypoxaemia centrally inhibits SNA. In contrast to rest, even moderate hypoxaemia during exercise markedly increases plasma NA concentration (and SNA), but the usual relationship among splanchnic blood flow, plasma NA and heart rate was not observed--NA and heart rate rose together, whereas the predicted splanchnic vasoconstriction was not observed. In moderate hypoxaemia, muscle blood flow and cardiac output are greater than in normoxia at a given submaximal oxygen uptake; but at maximal oxygen uptake, blood pressure, total vascular conductance and maximal cardiac output are unaffected. Given the fixed upper limit to cardiac output and the greater capacity of active muscle to vasodilate and exceed cardiac pumping capacity during hypoxaemia, we conclude that blood pressure is maintained by baroreflex- (not chemoreflex-) mediated vasoconstriction in the active muscle which must be the primary target of increased SNA and the source of NA.