Introduction: Brainstem strokes can disrupt autonomic regulation of breathing and heart rate. While medullary infarcts are well-known to cause central apnea and arrhythmias, similar effects from pontine strokes are less commonly reported. The pons contains key centers involved in respiration and autonomic control, but its role in cardiorespiratory instability remains underrecognized. Description: A 70-year-old woman with history of hypertension, diabetes mellitus, chronic kidney disease, hypothyroidism, and a left-sided pontine stroke five weeks earlier resulting in incomplete Wallenberg syndrome with right hemiplegia, dysarthria, and dysphagia, was admitted from a long-term acute care hospital to the ICU for evaluation of intermittent apneic episodes with associated brady-tachy arrhythmia. Just prior to admission, telemetry had revealed episodic bradycardia, unresponsive to beta-blocker discontinuation. On arrival, she was hemodynamically stable (BP 139/76 mmHg, HR 87 bpm) with SpO2 of 100% on 4 L oxygen via nasal cannula. Laboratory results were unremarkable, and 12-lead EKG showed normal sinus rhythm. Telemetry in the ICU demonstrated repeated intermittent apneic episodes followed by transient bradycardia (HR in the 30–40s) lasting several seconds, followed by reactive tachycardia reaching 95 bpm. Blood pressure and oxygen saturation remained stable on supplemental oxygen. Given the consistent cardiorespiratory coupling, an electrophysiology consultation was obtained, and the patient underwent dual-chamber pacemaker implantation. Discussion: Although medullary strokes are known to cause central apnea and autonomic instability, pontine infarcts are rarely associated with these effects, especially when symptoms appear in a delayed fashion. Our patient developed central apnea with bradycardia and reactive tachycardia likely reflecting evolving injury to pontine autonomic centers such as the parabrachial complex and Kölliker-Fuse nucleus, which are integral to respiratory rhythm and heart rate regulation. Similar physiology is seen in central sleep apnea, where apnea-induced hypercapnia triggers vagal bradycardia, followed by sympathetic rebound tachycardia. Recognizing this delayed autonomic pattern is critical, as early electrophysiologic evaluation and pacemaker placement may be lifesaving.
Chesterman et al. (Sun,) studied this question.