Effects of hypercapnia, hypoxia, and rebreathing on circulatory response to apnea

Cardiovascular responses to cessation of respiration and to progressive hypoxia and hypercapnia were investigated noninvasively in eight male volunteers. A total of five 90-s breath holds (BH) with face immersion were performed by each subject. A continuous BH (BH-1) eliminated the circulatory effects of respiratory movements, BH with air (BH-3) or with O2 (BH-5) with rebreathing at 15-s intervals through a CO2 scrubber reduced the effect of hypercapnia, and BH with air (BH-2) or with O2 (BH-4) with rebreathing at 15-s intervals bypassing the CO2 scrubber produced hypercapnia with or without concomitant hypoxia. Mean arterial blood pressure rose continuously in BH-1 and BH-2 and to a much lesser degree in other BHs. Vasoconstriction was evident within 30 s of BH. Determined by impedance cardiograph, stroke volume (SV) rose by 33%, which was balanced out by a 30% reduction in heart rate (HR) from the pre-BH values, at the end of a continuous BH. A transient depression of cardiac output (CO) was observed at 30 and 60 s of BH-1. CO values were maintained at pre-BH levels throughout the BHs where progressive hypercapnia occurred (BH-2 and BH-4) but were depressed to a similar degree as BH-1 when hypercapnia was prevented (BH-3 and BH-5). Alveolar CO2 levels were found to be correlated linearly and positively with SV, HR, and CO. No such relationship existed between alveolar O2 levels and these hemodynamic parameters. Thus rebreathing and hypercapnia during BH prevented CO from falling during BH. It is reasoned that hypercapnia and consequent acidosis, through enhanced sympathoadrenal release of catecholamines, was responsible for the compensatory SV response.