E. Garpestad et al., DECREASE IN VENTRICULAR STROKE VOLUME AT APNEA TERMINATION IS INDEPENDENT OF OXYGEN DESATURATION, Journal of applied physiology, 77(4), 1994, pp. 1602-1608
Patients with obstructive sleep apnea experience nocturnal hemodynamic
oscillations in association with repetitive respiratory events. Apnea
termination (recovery) is accompanied by the nadir of arterial O-2 sa
turation (Sa(o2)), changes in intrathoracic pressure, and arousal from
sleep. To investigate separately the contributions of hypoxemia and o
f arousal from sleep to changes in cardiac function, we continuously m
easured left ventricular stroke volume (LVSV) and mean arterial pressu
re (MAP) in eight subjects with severe obstructive sleep apnea (apnea-
hypopnea index > 30 events/h associated with Sa(o2) less than or equal
to 82%) during two experimental conditions: 1) subjects slept without
intervention for 1-2 h and then supplemental O-2 was administered to
maintain Sa(o2) greater than or equal to 90% (mean Sa(o2) nadir 92.7%)
throughout the apnea-recovery cycle and 2) upper airway obstructions
were abolished using nasal continuous positive airway pressure and sub
jects were aroused from sleep by an auditory signal. Recovery was asso
ciated with an increase in MAP and a decrease in LVSV both with and wi
thout supplemental O-2. Arousal from sleep on nasal continuous positiv
e airway pressure reproduced the postapneic elevation of MAP but not a
decrease in cardiac function of the magnitude that occurred at apnea
termination. We conclude that elevation of blood pressure and reductio
n of LVSV that occurred at apnea termination may be due to different p
hysiological mechanisms.