STUDY OBJECTIVES: Heart rate increases after obstructive events in patients with obstructive sleep apnea (OSA). This response is generally attributed to arousal from sleep. Opening of the obstructed airway, however, is associated with ventilatory and hemodynamic changes that could result in physiologic responses unrelated to arousal. Our objective was to determine the contribution of these physiologic responses to postevent tachycardia. DESIGN: Analysis of data obtained during previous research protocols. SETTING: Academic sleep laboratory. PARTICIPANTS: Twenty patients with severe OSA. INTERVENTIONS: Patients were placed on a continuous positive airway pressure (CPAP) device. CPAP was reduced during sleep to different levels (dial-downs), producing obstructive events of varying severity. Some dial-downs with severe obstruction were maintained until spontaneous airway opening. In others, CPAP was increased after three obstructed breaths, terminating the events approximately 10 sec before spontaneous termination in long dial-downs. MEASUREMENT AND RESULTS: Beat-by-beat heart rate (HR) was measured for 20 sec following airway opening. Spontaneous opening during sustained dial-downs occurred 21.9 ± 8.4 sec after dial-down, was associated with arousal, and resulted in the greatest postevent tachycardia (7.8 ± 4.0 min(-1)). However, deliberate termination of events (12.2 ± 2.6 sec after dial-down) was also followed by tachycardia that, in the absence of cortical arousal, showed a dose-response behavior, increasing with severity of obstruction and without apparent threshold. ΔHR following deliberately brief, severe obstruction (3.8 ± 3.0 min(-1)) was approximately half the ΔHR that followed spontaneous opening of equally severe obstructions despite the shorter duration and absence of cortical arousal. CONCLUSIONS: Postevent tachycardia is due in large part to physiologic (arousal-unrelated) responses that occur upon relief of obstruction.
STUDY OBJECTIVES: Heart rate increases after obstructive events in patients with obstructive sleep apnea (OSA). This response is generally attributed to arousal from sleep. Opening of the obstructed airway, however, is associated with ventilatory and hemodynamic changes that could result in physiologic responses unrelated to arousal. Our objective was to determine the contribution of these physiologic responses to postevent tachycardia. DESIGN: Analysis of data obtained during previous research protocols. SETTING: Academic sleep laboratory. PARTICIPANTS: Twenty patients with severe OSA. INTERVENTIONS:Patients were placed on a continuous positive airway pressure (CPAP) device. CPAP was reduced during sleep to different levels (dial-downs), producing obstructive events of varying severity. Some dial-downs with severe obstruction were maintained until spontaneous airway opening. In others, CPAP was increased after three obstructed breaths, terminating the events approximately 10 sec before spontaneous termination in long dial-downs. MEASUREMENT AND RESULTS: Beat-by-beat heart rate (HR) was measured for 20 sec following airway opening. Spontaneous opening during sustained dial-downs occurred 21.9 ± 8.4 sec after dial-down, was associated with arousal, and resulted in the greatest postevent tachycardia (7.8 ± 4.0 min(-1)). However, deliberate termination of events (12.2 ± 2.6 sec after dial-down) was also followed by tachycardia that, in the absence of cortical arousal, showed a dose-response behavior, increasing with severity of obstruction and without apparent threshold. ΔHR following deliberately brief, severe obstruction (3.8 ± 3.0 min(-1)) was approximately half the ΔHR that followed spontaneous opening of equally severe obstructions despite the shorter duration and absence of cortical arousal. CONCLUSIONS: Postevent tachycardia is due in large part to physiologic (arousal-unrelated) responses that occur upon relief of obstruction.
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