Hypoxemia and arousals modulate cardiac responses to respiratory events in obstructive sleep apnea.

STUDY

OBJECTIVES

Respiratory events during sleep induce immediate cardiac alterations, including increased RR intervals during events and decreased RR intervals after events. However, the extent to which related desaturations and arousals modulate these responses remains underexplored. We hypothesized that desaturations and arousals are the main contributors to respiratory event-related cardiac response, with greatest cardiac alterations expected when both are present.

METHODS

We analyzed RR, QT, and heart rate-corrected QT (QTc) intervals before, during, and after 4310 respiratory events from 129 obstructive sleep apnea patients. Mixed-effect statistical models were utilized to assess the influence of the presence and severity of desaturations and arousals on the cardiac electrical response to respiratory events.

RESULTS

There were no significant differences between pre- and post-respiratory event RR and QTc intervals in the absence of desaturation or arousal. Arousal (RR estimate = -23.9 ms; QTc estimate = 5.7 ms) or simultaneous desaturation and arousal (RR estimate = -32.8 ms; QTc estimate = 8.4 ms) modulated significantly (p < .05) mean RR and QTc intervals after respiratory events. Desaturation alone affected only RR intervals (estimate = -9.3 ms, p<.05). Greater desaturation depth (RR estimate = -0.09 ms; QTc estimate = 0.56 ms) and longer arousal duration (RR estimate = -3.52 ms; QTc estimate = 0.84 ms) were significant (p < .05) predictors of RR and QTc magnitude alterations after respiratory events.

CONCLUSIONS

Not all respiratory events have the same effects on cardiac electrophysiology; they are associated with acute alterations after events if they cause desaturations and/or arousal, with longer arousal and deeper desaturations increasing the magnitude of cardiac responses. Statement of Significance This study provides a detailed analysis of the temporal dynamics of cardiac response to respiratory events in obstructive sleep apnea patients, with a focus on the potential modulators of this response. Our observations present that not all respiratory events have the same effects on cardiac electrophysiology; they are associated with significant cardiac response if they cause desaturations and/or arousals, with longer arousal and deeper desaturations increasing the magnitude of cardiac response. Our results present evidence of possible modulators of post-event cardiac function, providing a deeper understanding of obstructive sleep apnea's impact on health as potential underlying mechanisms leading to adverse cardiovascular events.