Systemic and pulmonary hemodynamic responses to normal and obstructed breathing during sleep

Abstract

Schneider, H., C. D. Schaub, K. A. Andreoni, A. R. Schwartz, R. L. Smith, J. L. Robotham, and C. P. O’Donnell. Systemic and pulmonary hemodynamic responses to normal and obstructed breathing during sleep. J. Appl. Physiol. 83(5): 1671–1680, 1997.—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 postapneic 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.