Schneider H, Schaub C D, Andreoni K A, Schwartz A R, Smith P L, Robotham J L, O'Donnell C P
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland 21224, USA.
J Appl Physiol (1985). 1997 Nov;83(5):1671-80. doi: 10.1152/jappl.1997.83.5.1671.
We examined the hemodynamic responses to normal breathing and induced upper airway obstructions during sleep in a canine model of obstructive sleep apnea. During normal breathing, cardiac output decreased (12.9 +/- 3.5%, P < 0.025) from wakefulness to non-rapid-eye-movement sleep (NREM) but did not change from NREM to rapid-eye-movement (REM) sleep. There was a decrease (P < 0.05) in systemic (7.2 +/- 2.1 mmHg) and pulmonary (2.0 +/- 0.6 mmHg) arterial pressures from wakefulness to NREM sleep. In contrast, systemic (8.1 +/- 1.0 mmHg, P < 0.025), but not pulmonary, arterial pressures decreased from NREM to REM sleep. During repetitive airway obstructions (56.0 +/- 4.7 events/h) in NREM sleep, cardiac output (17.9 +/- 3.1%) and heart rate (16.2 +/- 2.5%) increased (P < 0.05), without a change in stroke volume, compared with normal breathing during NREM sleep. During single obstructive events, left (7.8 +/- 3.0%, P < 0.05) and right (7.1 +/- 0.7%, P < 0.01) ventricular outputs decreased during the apneic period. However, left (20.7 +/- 1.6%, P < 0.01) and right (24.0 +/- 4.2%, P < 0.05) ventricular outputs increased in the post-apneic period because of an increase in heart rate. Thus 1) the systemic, but not the pulmonary, circulation vasodilates during REM sleep with normal breathing; 2) heart rate, rather than stroke volume, is the dominant factor modulating ventricular output in response to apnea; and 3) left and right ventricular outputs oscillate markedly and in phase throughout the apnea cycle.
