Heart rate during obstructive sleep apnea depends on individual hypoxic chemosensitivity of the carotid body.

The intersubject variation of the HR changes during sleep apnea can be explained in large part by individual hypoxic chemosensitivity of the carotid body regardless of the type of apnea.

Abstract

BACKGROUND: In patients with obstructive sleep apnea syndrome (OSAS), there are cyclic fluctuations in heart rate (HR), that is, bradycardia during apnea followed by abrupt tachycardia on resumption of ventilation. Although a previous study suggested that the degree of bradycardia observed during central apnea at high altitude was determined by individual hypoxic chemosensitivity of the carotid body, it is not known whether this is true for subjects with obstructive sleep apnea syndrome. METHODS AND RESULTS: First, we examined apnea-associated HR changes in II subjects with OSAS and analyzed the relationship of the HR change during apnea (delta HR, defined as the difference between the values at the beginning and the end of apnea) and apnea-induced nadir SaO2 in each subject. Second, we conducted an apnea-simulation study in 7 subjects to examine whether the individual pattern of delta HR could be simulated while they held their breath under different levels of arterial oxygenation. The delta HR was highly variable among subjects: 2 showed an increase in HR during apnea, 6 a decrease, and the other 3 a borderline-type response. The slope factor of the nadir of the SaO2-delta HR line obtained from each subject had a significant correlation with the HR change during breath-holding conducted under normoxia (Spearman's rank correlation coefficient, rs = 69, P < .05) or hypoxia (rs = .81, P < .05) but not under hyperoxia. Finally, we evaluated hypoxic chemosensitivity of the carotid body by measuring the ventilatory response to isocapnic progressive hypoxia in all subjects. The magnitude of the ventilatory response ranged from 0.05 to 1.89 L.min-1.%SaO2 fall-1 and showed a significant correlation with the slope factor of the nadir of the SaO2-delta HR line (rs = -.64, P < .05). CONCLUSIONS: The intersubject variation of the HR changes during sleep apnea can be explained in large part by individual hypoxic chemosensitivity of the carotid body regardless of the type of apnea.