Case Presentation: A morbidly obese 61-year-old man with coronary artery disease presented for evaluation of exertional dyspnea. No chest pain was reported. Transthoracic echocardiogram and pulmonary function tests were normal, but his dyspnea persisted. Lifestyle modifications and inhaler trials failed to improve his dyspnea. Left and right coronary angiography were completed. A 90% stenosis of the left anterior descending artery was identified, and a stent was placed; however, equally concerning to his cardiologist were multiple sinus pauses of varying lengths noticed during left heart catheterization. After his procedure, telemetry detected up to 28 sinus pauses per night, the longest of which was recorded at 20 seconds. These were all associated with apneic episodes. He did not carry a diagnosis of obstructive sleep apnea (OSA), but observed apneic spells, a neck circumference of 50cm, and a BMI of 48.3 kg/m2 provided strong enough suspicion that he was granted an inpatient sleep study, which confirmed OSA. He was fitted for a BiPAP machine and his settings were titrated which resulted in resolution of bradycardia and sinus pauses. He immediately commented on the improved quality of sleep and increased daytime energy. Between coronary angiogram and treatment for OSA, dyspnea on exertion was effectively gone.
Discussion: Untreated OSA is associated with arrhythmias, both tachycardic and bradycardic. Although tachyarrhythmias such as atrial fibrillation are more commonly reported, bradycardia and sinus pauses in association with OSA have been reported. While there are case reports linking bradyarrhythmias and OSA, there is a paucity of strong objective data regarding mechanism or management. Chronic hypoxia is known to cause cardiac remodeling and resultant arrhythmias by a variety of mechanisms, but how acute hypoxia can rapidly cause bradyarrhythmia is less studied. As hypothesized in other case reports, the mechanism most likely at play in the above case is similar to that of the “diving reflex,” which has been reported in the literature for decades. It is a primitive reflex in which hypoxia from holding one’s breath under water causes bradycardia and/or pausing as a way to utilize less and conserve more oxygen. Although this is a single case, it is unique in that it was essentially an experiment in which we were able to test our hypothesis that hypoxia during apneic episodes was causing sinus bradycardia and sinus pausing. Since non-invasive positive pressure ventilation (NIPPV) rapidly and completely resolved both apneic episodes and arrhythmia, it is reasonable to infer that hypoxia did cause his arrhythmia and that NIPPV was effective monotherapy (in the short-term and in this particular patient), which is objective data and can be extrapolated to help guide management of other cases. Earlier diagnosis and treatment of OSA reduces morbidity. This was demonstrated decisively in this case as we saw immediate and complete resolution of significant sinus bradycardia and pauses in the first night during the time NIPPV was worn. The patient was never screened for OSA, likely at least partially because we do not have standardized screening guidelines for OSA. Consider OSA as a cause of arrhythmia and treat appropriately. Prompt diagnosis and treatment prevented this patient from having to take antiarrhythmic drugs or be subject to invasive procedures.
Conclusions: It is important for internists to recognize the role of early diagnosis and treatment of OSA as part of a high-value, cost-effective healthcare system.