Determinants of the circulatory response to hypoxia and hypercapnia

Abstract

1. 1. Mechanisms responsible for circulatory changes in hypoxia and hypercapnia have been studied with an “aperiodic” ballistocardiograph, teeterboard, and ancillary techniques. The results emphasize the necessity for measuring cardiac function in evaluating the effects of drugs or autonomic discharges, for both the vasomotor center and chemoreceptors altered ventricular contractility as well as vasomotor tone. 2. 2. In man, no significant change in thoracic blood volume was demonstrable in response to 10 per cent O 2 or 6 per cent CO 2. 3. 3. Contractility increased on 10 per cent O 2 but decreased steadily when reflex compensation was prevented by spinal transection. Peripheral chemoreceptors constituted the afferent limb and epinephrine the chief effector of this reflex. Cardiac depression occurred on return to 100 per cent O 2 and may be important in the circulatory collapse which sometimes follows abrupt reoxygenation in man. Neither adrenalectomy nor adrenergic “blockade” prevented the positive inotropic response to hypoxia, and hexamethonium paradoxically sensitized the heart to epinephrine. The significance of these observations is discussed. 4. 4. In cats, an epinephrine discharge occurred regularly with inspired CO 2 concentrations in excess of 15 per cent in O 2, and in dogs epinephrine was demonstrable in venous blood at peak ballistic response to 30 per cent CO 2. Though mild hypercapnia (6 per cent) increased ballistic amplitude in both dog and man, severe hypercapnia (15 to 30 per cent) markedly depressed the heart until reflex epinephrine discharge restored contractility toward normal. Chemoreceptors were not uniformly necessary, but adaptation seemed facilitated by their presence. 5. 5. Circulatory performance in hypoxia and hypercapnia represents the resultant of direct cardiac depressant effects and opposing reflexly mediated alterations in contractility and vascular tone.