Neurocirculatory consequences of intermittent asphyxia in humans

Abstract

We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O(2) saturation = 79-85%, end-tidal PCO(2) =3-5 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 +/- 2.0 l/min in the final 5 min of asphyxia vs. 7.5 +/- 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 +/- 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 +/- 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 +/- 4 beats/min in the final 5 min of asphyxia vs. 61 +/- 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.

Blood pressure increase detected by ambulatory monitoring correlates with hypoxemia reflecting sleep apnea severity

“…Six groups of subjects were examined in the study: (1) healthy controls, (2) patients with AH alone, (3,4,5) those with mild, moderate and severe SAHS, and (6) those with SAHS treated by CPAP. The study was designed to determine the secondary hypertensive effect of SAHS and the BP-lowering effect of CPAP therapy by comparisons of approximately 30 variables obtained during parallel ABPM and whole-night polysomnography, with the informed consent of all subjects.…”

“…Hypoxemia and hypercapnia resulting mainly from apneahypopnea episodes initiate progressive activation of the sympathetic nervous system, involving the carotid sinus and aortal baroreceptors [3,4,6,34,35]. Arousal reactions induced by repeated apnea episodes also provoke sympatho-adrenergic activation, despite interruption of hypoxic-hypercapnic stimuli, and they could lead to the elevation of heart rate and BP [3,4]. In addition, the upper-airway stimulation induced by pressure changes caused by snoring, or post-apnea sighs and gasps may evoke reflex tachycardia and vasoconstriction already present in the early stages of SAHS.…”

“…Sleepdisordered breathing has been found to occur in 24% of men and 9% of women in the general population [1,2]. Frequent apnea-hypopnea episodes in patients with SAHS trigger various hemodynamic effects that are in direct contrast to the relaxation effects of physiological sleep; these include arterial hypertension (AH) resulting from hypoxia, hypercapnia, arousal, and sympathetic stimulation [3][4][5][6][7]. Several studies have established that patients with SAHS have a higher prevalence of AH than the general population, even after adjusting for such confounding variables as body mass index, age, and sex [5,[8][9][10][11][12].…”

“…Previously unrecognized AH has also been found by clinical BP measurement in 39% of patients with newly diagnosed SAHS and by ambulatory blood pressure monitoring (ABPM) in as many as 62% [13,14]. SAHS is also an independent risk factor for AH and various cardiovascular diseases, such as coronary artery disease, myocardial infarction, stroke, and atherosclerosis [2,4,10,[15][16][17][18][19][20][21].…”

Sleep apnoea, hypertension and vascular disease: where are we now?

“…In a study by XIE et al [43], a hypercapnic hypoxic gas mixture was administered intermittently (20 s of the gas mixture, 40 s normoxia) in healthy subjects during 20 min. Muscle SNA was found to follow a cyclic crescendo-decrescendo pattern in conjunction with asphyxic periods.…”