Research report: Reflex‐Mediated Bradycardia and Asystole During Skull Base and Parapharyngeal Surgery: A Three‐Case Series Highlighting Anatomical Predictability

During an operation to remove a recurrent nasopharyngeal tumor from a 54-year-old man, surgeons and anesthesiologists watched the patient's heart rate fall, recover, fall again, and then stop entirely. Six hours after incision, the monitor showed abrupt asystole during deep dissection at the skull base. Chest compressions, atropine, and epinephrine restored spontaneous circulation after roughly five minutes, the operation was abandoned, and the patient later completed a second procedure uneventfully under temporary cardiac pacing.

The case is one of three reported in a new case series describing reflex-mediated bradycardia and asystole during skull base and parapharyngeal surgery. The other two patients—a 24-year-old man with a paraganglioma centered on the right jugular foramen and a 53-year-old woman with a parapharyngeal space mass displacing the carotid sheath—experienced sudden sinus arrest and abrupt bradycardia, respectively, at the precise moments their surgeons manipulated tumor tissue in cranial nerve-rich territory. The physiological logic behind these events begins with the cranial nerves that crowd the skull base and parapharyngeal space.

The glossopharyngeal nerve, or cranial nerve IX, and the vagus nerve, or cranial nerve X, carry sensory fibers from the pharynx, carotid region, and surrounding structures into the brainstem. Mechanical stimulation of these fibers—whether by tumor traction, dissection near the jugular foramen, or manipulation of the carotid sheath—can generate afferent signals that relay through the nucleus tractus solitarius, the brainstem's principal visceral sensory hub. From there, connections project to cardiac vagal motor neurons in the nucleus ambiguus and the dorsal motor nucleus of the vagus, which fire parasympathetic output that slows the sinus node and, in severe cases, halts it altogether.

In some circumstances the reflex can bypass this central relay entirely. Direct mechanical traction on the vagal nerve trunk within the carotid sheath can trigger a peripheral vagal reflex in which the same nerve carries both the afferent signal and the efferent braking command to the heart. A third variant involves the carotid sinus, the baroreceptor-rich dilatation at the base of the internal carotid artery, where pressure or chemical stimulation sends glossopharyngeal afferents to the brainstem and provokes vagal efferent slowing.

Each pattern carries a distinct clinical signature, and distinguishing among them shapes how the surgical and anesthesia teams should respond. The three cases illustrate the spectrum of severity such reflexes can produce. In the second patient, sudden sinus arrest occurred during dissection inferior to the internal carotid artery and around the jugular foramen, structures intimately associated with lower cranial nerve rootlets.

The surgeon stopped immediately, the anesthesiologist gave 0.5 milligrams of intravenous atropine, brief chest compressions were initiated, and spontaneous cardiac activity returned within approximately ten seconds. Surgery resumed with gentler manipulation and no further episodes occurred. The third patient's bradycardia arose during mobilization of a 4.4 by 3.1 by 4.5 centimeter mass suspected to be a schwannoma; stopping the manipulation and giving 0.3 milligrams of atropine restored the baseline heart rate, and the procedure was completed without further instability.

The first patient's course was far more dramatic. His recurrent nonkeratinizing nasopharyngeal carcinoma, previously treated with chemoradiotherapy, involved the left nasopharynx, skull base, deep parapharyngeal tissues, and the pericarotid region, including the left internal carotid artery itself. Because of the hemorrhage risk, the artery had been deliberately occluded by endovascular means before surgery.

Recurrent bradycardia episodes began about two hours after incision, and the terminal asystolic event followed at six hours. Notably, the operative record did not identify which structure was being manipulated at the onset of either event, so the authors can only offer an anatomy-based hypothesis—vagal or glossopharyngeal-vagal activation—rather than a confirmed trigger. That honest uncertainty is itself instructive: even when a reflex mechanism is the most plausible explanation, causal attribution requires documentation of what the surgeon's instruments were touching at the critical moment.

Establishing that a reflex, rather than something more mundane, caused the cardiac arrest requires systematic exclusion. The authors emphasize that in all three patients there was no hypoxemia, no hypercapnia, no anesthetic overdose, no electrolyte or metabolic disturbance, no hemorrhage-related instability, no evidence of myocardial ischemia, and no baseline hypotension or progressive hemodynamic deterioration preceding the events. In the second and third cases, the tight temporal coupling between tumor manipulation and the cardioinhibitory event in cranial nerve-rich regions strengthened the reflex interpretation.

In the first case, the deep skull base and pericarotid location of the dissection provided the anatomical context, even without a documented trigger structure. This differential process—ruling out ventilatory, metabolic, pharmacologic, and hemodynamic causes before invoking a reflex—is the diagnostic backbone of managing these events. What distinguishes this report from earlier literature, the authors argue, is its emphasis on anticipation rather than reaction.

Similar reflex-mediated events have been described during skull base, transsphenoidal, and posterior fossa procedures, with trigeminocardiac and glossopharyngeal-vagal pathways implicated, but previous accounts have focused largely on pathophysiology or isolated cases. Generic bradycardia algorithms, meanwhile, emphasize treatment after hemodynamic deterioration has already occurred and seldom incorporate procedure-specific anatomical risk regions. The proposed alternative is to treat the anatomy itself as a warning label: before entering the jugular foramen, the parapharyngeal space, or the pericarotid region, the surgeon should identify the relevant neurovascular structures on preoperative imaging and alert the anesthesiologist before any traction, coagulation, or deep dissection begins.

The management framework that follows is deliberately stepwise and shared between teams. The anesthesiologist ensures adequate oxygenation, ventilation, and anesthetic depth, with atropine, epinephrine, resuscitation drugs, and pacing or defibrillation equipment immediately at hand. When bradycardia or sinus arrest occurs, the surgeon stops stimulation and releases traction while the anesthesiologist excludes hypoxemia, hypercapnia, anesthetic overdose, hemorrhage, and metabolic causes.

Bradycardia with a pulse and hemodynamic compromise that does not promptly resolve is treated with atropine; refractory cases may require an adrenergic agent such as epinephrine or temporary pacing. A pulseless rhythm demands immediate chest compressions and advanced life support. If dissection must continue in the same region, options include gentler manipulation, local anesthetic infiltration or topical application where anatomically appropriate, prophylactic anticholinergic treatment in selected cases, and temporary pacing for recurrent or severe bradycardia with a preserved pulse.

The authors are candid about the limits of their evidence. Three cases constitute a small sample, and the proposed reflex mechanisms rest on clinical observation, anatomical reasoning, and literature-supported pathways rather than direct neurophysiologic recording. The exact triggering structure could not be confirmed in every patient.

Nevertheless, the convergence of anatomical context, temporal association, and the exclusion of alternative causes supports reflex-mediated cardioinhibition as the most plausible explanation in all three patients.

Subject of Research: Reflex-mediated bradycardia and asystole during skull base and parapharyngeal surgery

Article Title: Reflex‐Mediated Bradycardia and Asystole During Skull Base and Parapharyngeal Surgery: A Three‐Case Series Highlighting Anatomical Predictability

Article References: Chi, S., Wang, Y., & Shen, X. (2026). Reflex‐Mediated Bradycardia and Asystole During Skull Base and Parapharyngeal Surgery: A Three‐Case Series Highlighting Anatomical Predictability. Clinical Case Reports, 14(10), Article e73752. https://doi.org/10.1002/ccr3.73752

Image Credits: AI Generated

DOI: 10.1002/ccr3.73752

Keywords: skull base surgery, parapharyngeal space, bradycardia, asystole, vagal reflex, glossopharyngeal nerve, jugular foramen, carotid sheath, anesthesia, paraganglioma, nasopharyngeal carcinoma, intraoperative crisis