The American Heart Association defines bradycardia as a heart rate of less than 60 beats per minute (BPM), noting however that what should be considered “too slow” for an individual patient depends on various factors such as age, physical fitness, and physiological condition. For example, during sleep the parasympathetic tone predominates (as NREM sleep occupies 80% of total sleep time), commonly resulting in bradyarrhythmias, sinus pauses greater than two seconds, and atrioventricular (AV) conduction delays. However, some cases of nocturnal bradyarrhythmias are not normal; these reflect acute bradycardia also prevalent in wakefulness and can lead to various complications. Obstructive Sleep Apnea (OSA) was found to be a promoting factor for these cases.
Numerous studies have demonstrated an increased prevalence of bradyarrhythmias in OSA patients. The classic study by Guilleminault et al looked at 400 patients with OSA.1 Of these, 48% had significant nocturnal arrhythmia with 18% bradyarrhythmia, 11% sinus arrest, and 8% AV blocks, compared to a 3% prevalence of nocturnal bradyarrhythmias in the general population.1,2 There were no important differences in age, body weight, apnea-hypopnea index (AHI), or minimum oxygen saturation between patients with and without arrhythmias. In a more recent Japanese study by Abe et al, 1,350 OSA patients and 44 control subjects were screened, and significant differences were noted in the increase in the incidence of sinus bradycardias (12.5% with OSA vs. 2.3% control, p=0.036) and sinus pause (8.7% with OSA vs. 2.3% control, p<0.001).3 Importantly, long-term monitoring with implanted pacemakers reveals an even higher incidence of bradyarrhythmias (up to 34%), suggesting that OSA can increase the risk for bradycardia dramatically.4
In addition to increasing the prevalence of bradyarrhythmias, some studies have found that OSA severity is correlated to the severity of bradyarrhythmias, with up to 3 times higher incidence of bradycardic arrhythmias in patients with severe OSA, compared to milder OSA.5 This correlation could suggest a causal relationship between the two, with OSA promoting bradycardia.
The mechanism by which OSA can reduce the heart rate is demonstrated in Figure A. During OSA, structural changes occur in the airway to obstruct airflow (Resp), and the resulting apnea activates hypoxic reflexes (SaO2%). These in turn lead to a profound elevation in sympathetic nerve activity (SNA) and subsequent elevation of atrial blood pressure (ABP) as well as a decrease of the heart rhythm (ECG). Various studies confirmed that the elevation in vagal tone is the key contributor to the bradyarrhythmias, while other factors such as sinus node anatomy or atrioventricular conduction remain largely intact in OSA patients.6 The finding that intravenous atropine administration eliminates the marked sinus arrhythmia and bradyarrhythmias observed in such patients supports this hypothesis.6 Moreover, mimicking OSA in wakefulness with Muller’s maneuver results in induced bradycardia, further confirming that the combination of prolonged negative intrathoracic pressures and the resulting hypoxemia provide the necessary underlying “mix” for this unique pathophysiology.7
The crossover between bradyarrhythmias and OSA is also made apparent by the beneficial treatment of OSA on bradycardia severity. Specifically, positive airway pressure (PAP) therapy has been shown to be highly effective in abolition and reduction of bradyarrhythmias. In the Abe study, CPAP therapy dramatically reduced sinus bradycardia (p<0.001) and sinus pauses (p=0.004).3 Thus, the current recommendation for patients with bradyarrhythmias at risk for OSA is to perform overnight polysomnography prior to pacemaker implantation, especially in younger individuals without underlying cardiac disease. Permanent pacemakers should be considered if significant bradyarrhythmia or pauses persist after an adequate treatment trial with PAP therapy.
- Guilleminault, C., Connolly, S. J., & Winkle, R. A. (1983). Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. American Journal of Cardiology, 52(5), 490-494.
- Fleg, J. L. & Kennedy, H. L. (1982). Cardiac arrhythmias in a healthy elderly population: detection by 24-hour ambulatory electrocardiography. Chest, 81, 302–307.
- Abe, H., Takahashi, M., Yaegashi, H., Eda, S., Tsunemoto, H., Kamikozawa, M., … & Ikeda, U. (2010). Effi cacy of continuous positive airway pressure on arrhythmias in obstructive sleep apnea patients. Heart and Vessels, 25(1), 63-69.
- Simantirakis, E. N., Schiza, S. I., Marketou, M. E., Chrysostomakis, S. I., Chlouverakis, G. I., Klapsinos, N. C., … & Vardas, P. E. (2004). Severe bradyarrhythmias in patients with sleep apnoea: the effect of continuous positive airway pressure treatment: a long-term evaluation using an insertable loop recorder. European Heart Journal, 25(12), 1070-1076.
- Rossi, V. A., Stradling, J. R., & Kohler, M. (2013). Effects of obstructive sleep apnoea on heart rhythm. European Respiratory Journal, 41(6), 1439-1451.
- Cutler, M. J., Hamdan, A. L., Hamdan, M. H., Ramaswamy, K., & Smith, M. L. (2002). Sleep apnea: from the nose to the heart. The Journal of the American Board of Family Practice, 15(2), 128-141.
- Huettner, M., Koehler, U., Nell, C., Kesper, K., Hildebrandt, O., & Grimm, W. (2015). Heart rate response to simulated obstructive apnea while awake predicts bradycardia during spontaneous obstructive sleep apnea.