Submitted on August 12, 2004
Accepted on October 29, 2004
CARDIOVAGAL REGULATION DURING COMBINED HYPOXIC AND ORTHOSTATIC STRESS: FAINTERS VS NON-FAINTERS
John R Halliwill1* and Christopher T Minson1
1 Department of Human Physiology, University of Oregon, Eugene, OR, USA
* To whom correspondence should be addressed. E-mail: halliwil{at}uoregon.edu.
We tested the hypothesis that individual differences in the effect of acute hypoxia on the cardiovagal arterial baroreflex would determine individual susceptibility to hypoxic syncope. In 16 healthy, non-smoking, normotensive subjects (8 women, 8 men, 20 - 33 yrs), we assessed orthostatic tolerance with a 20-min 60 ° head upright tilt during both normoxia and hypoxia (breathing 12 % O2). On a separate occasion, we assessed baroreflex control of heart rate (cardiovagal baroreflex gain) using the modified Oxford technique during both normoxia and hypoxia. When subjects were tilted under hypoxic conditions, 5 of the 16 developed pre-syncopal signs or symptoms and the 20-min tilt had to be terminated. These "fainters" had comparable cardiovagal baroreflex gain to "non-fainters" under both normoxic and hypoxic conditions (normoxia, fainters: -1.2 ± 0.2, non-fainters: -1.0 ± 0.2 beats/min/mmHg, P = 0.252; hypoxia, fainters: -1.3 ± 0.2, non-fainters: -1.0 ± 0.1 beats/min/mmHg, all P = 0.208). Furthermore, hypoxia did not alter cardiovagal baroreflex gain in either group (both P > 0.8). It appears from these observations that hypoxic syncope results from the superimposed vasodilator effects of hypoxia on the cardiovascular system and not from a hypoxia-induced maladjustment in baroreflex control of heart rate.
