Contribution of arousal from sleep to postevent tachycardia in patients with obstructive sleep apnea

Abstract

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.

Keywords: CPAP dial-down; OSA; heart rate.

Figure 1

Top panel: Tracings showing a mild, brief (10 sec) hypopnea produced by decreasing continuous positive airway pressure (CPAP) from 13 cm H₂O to 10 cm H₂O for three breaths (dial-down). C3/A2 and C4/O1 are two electroencephalogram leads; SpO₂, oxyhemoglobin saturation; EKG, electrocardiogram. Time 0 is the time of upper airway opening. Note the increase in flow and in heart rate (numerals above EKG) following the increase in CPAP in the absence of cortical arousal. Bottom panel: Tracings from the same patient showing a long dial- down at 2 cm H₂O, producing severe obstruction, which was maintained until the airway opened spontaneously, with intense arousal, at 20 sec. Note that in the brief obstruction (top), peak tachycardia occurred about 10 sec after opening and 18 sec after the onset of the hypopnea (vertical dotted line). At 18 sec following the onset of apnea in the long dial-down (dotted line) there was still no appreciable increase in HR even though the obstruction was much more severe and had lasted longer at this point. Thus, the timing of tachycardia is linked to the end of obstruction and not to the severity of arousal stimuli.

Figure 2

Sec-by-sec averages (19 patients) of the change in heart rate after upper airway opening with five different interventions (see insert and Table 2). Brief events (no hypopnea, minimal, mild/moderage, and severe) were terminated deliberately by increasing continuous positive airway pressure (CPAP) after three breaths and were not associated with arousal. Long events terminated spontaneously with an associated arousal. Note that the response increases with event severity in observations without cortical arousal and that the pattern of increase is very similar. Response after severe long events (with arousal) was greater than after brief severe events and extended beyond 12 sec. Bars are standard error of the mean. Asterisks in brief dial-downs denote significant difference from heart rate just before increasing CPAP. Asterisks in the long dial-downs denote significant difference from heart rate just before airway opening. *P < 0.05; **P < 0.005; ***P < 0.0005.

Figure 3

Comparison of average heart rate responses after brief severe obstructive events not associated with arousal, brief severe events that were followed by cortical arousal, and long obstructive events with spontaneous opening and arousals in 14 patients who demonstrated all three types of response. Error bars are standard error of the mean. There were significant differences by repeated-measures analysis of variance (ANOVA) at all time points following airway opening. Asterisk denotes significantly different from brief events without arousals. Plus sign denotes significantly different from both types of brief events (repeated-measures ANOVA).

Figure 4

Left panel: Sec-by-sec averages (19 patients) of heart rate in individual patients in the interval dial-down onset (time 0) ± 10 sec. Right panel: Sec-by-sec averages (19 patients) of heart rate in individual patients in the 10-sec interval preceding upper airway opening. Data pertain to long dial-downs associated with severe obstruction. The heavy lines in the two panels are the overall averages.