Decrease in ventricular stroke volume at apnea termination is independent of oxygen desaturation

Abstract

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 O2 saturation (SaO2), changes in intrathoracic pressure, and arousal from sleep. To investigate separately the contributions of hypoxemia and of arousal from sleep to changes in cardiac function, we continuously measured left ventricular stroke volume (LVSV) and mean arterial pressure (MAP) in eight subjects with severe obstructive sleep apnea (apnea-hypopnea index > 30 events/h associated with SaO2 < or = 82%) during two experimental conditions: 1) subjects slept without intervention for 1-2 h and then supplemental O2 was administered to maintain SaO2 > or = 90% (mean SaO2 nadir 92.7%) throughout the apnea-recovery cycle and 2) upper airway obstructions were abolished using nasal continuous positive airway pressure and subjects were aroused from sleep by an auditory signal. Recovery was associated with an increase in MAP and a decrease in LVSV both with and without supplemental O2. Arousal from sleep on nasal continuous positive 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 reduction of LVSV that occurred at apnea termination may be due to different physiological mechanisms.

Ventilatory restraint of sympathetic activity during chemoreflex stress

“…As such, the restoration of blood gases (and removal of the chemoreflex stress) does not play a role in this regulation. Further, while the abrupt silencing of MSNA was simultaneous with inspiration, and the negative pressure generated by inspiration at end apnea could be expected to facilitate venous return, cardiac output is actually decreased transiently (13,14). In addition, previous research has demonstrated respiratory modulation of MSNA during both normal and positive pressure ventilation (23,33).…”

Nocturnal enuresis is associated with moderate-to-severe obstructive sleep apnea in children with snoring

“…Furthermore, upper airway obstruction is associated with exaggerated negative intrathoracic pressure swings, increased systemic venous return and preload to the right ventricle along with increased left cardiac ventricle after load (23,24). Acute overload of the cardiac ventricles could promote release of brain natriuretic peptide from ventricular myocytes which induces vasodilation and natriuresis (25).…”

Effects of Continuous Positive Airway Pressure Versus Supplemental Oxygen on 24-Hour Ambulatory Blood Pressure

“…67,68 Our findings also do not support prior human studies suggesting that oxygen desaturation, rather than frequency of arousals from sleep, is associated with higher odds ratios for systemic hypertension. 69 Prior experiments have demonstrated that BP after apneic events rises even when hypoxemia is blunted through oxygen administration 70,71 and that CPAP, but not supplemental oxygen, can lower BP variability during sleep. 72 Together, these results suggest that repeated oxyhemoglobin desaturation may be a necessary component for the development of hypertension in patients with OSA, but that improving SpO 2 alone, without treating airway obstruction and arousal, may not be enough to reverse these effects on BP.…”