Sensory inputs from glossopharyngeal and vagal afferents converge on the nucleus tractus solitarius (NTS) of the medulla, where baroreceptor signals from the carotid sinus, aortic arch, and cardiopulmonary receptors are integrated (6). Parasympathetic efferents arising from the dorsal motor nucleus of the vagus nerve and nucleus ambiguus then project to the sinoatrial and atrioventricular nodes, exerting inhibitory effects on cardiac conduction. Experimental research has further demonstrated that the disruption of NTS neuronal activity directly induces bradycardia and hypotension (7), underscoring the central role of this reflex arc in cardiovascular regulation.

During throat pack placement, the stimulation of the laryngopharyngeal mucosa, particularly the epiglottic surface innervated by the internal branch of the superior laryngeal nerve, has been reported to trigger vagal reflexes that may culminate in profound bradyarrhythmia or asystole (3). In addition, the activation of the Bezold-Jarisch reflex, mediated by cardiac receptors with non-myelinated vagal C-fiber afferents, produces a characteristic triad of bradycardia, hypotension and peripheral vasodilation (8). These reflex mechanisms collectively provide a plausible physiologic explanation for the abrupt vagally mediated cardiac arrest observed in the case presented herein (Fig. 3).

Reflex-mediated cardiovascular responses may progress stepwise. Campagna and Carter (8) described how vagal reflexes can evolve from initial bradycardia and hypotension to sinus arrest and high-grade atrioventricular block, and ultimately to asystole and pulseless electrical activity. Clinically, such events have been observed during airway manipulation: Redmann et al (3) reported asystole during suspension microlaryngoscopy, attributed to direct vagal stimulation, while Chung et al (9) documented transient asystole immediately after balloon dilation of the Eustachian tube.

In contrast to these reports of vigorous stimuli, cardiac arrest from throat pack insertion alone remains uncommon. Its occurrence in the case described herein, despite the minimally invasive nature of the intervention, may reflect high baseline vagal tone or a lowered reflex threshold under light anesthesia.

Under light anesthesia, the suppression of sympathetic activity predisposes patients to parasympathetic dominance. Propofol and suxamethonium can produce profound bradycardia without anticholinergic premedication (10), while hypercapnia enhances cardiac vagal responsiveness (11). Fluctuations in autonomic balance have also been implicated in vagally mediated bradycardia and circulatory collapse in patients with syncope (12). Adequate anesthetic depth and ventilation before pharyngeal manipulation are therefore essential, and prophylactic atropine may be warranted when vagal predominance is anticipated.

In the patient described in the present case report, spontaneous cardiac rhythm resumed within ~20 sec without chest compressions after cessation of the stimulus and the administration of 8 mg ephedrine. This rapid recovery is consistent with vasovagal cardiac arrest, in which vagal dominance and sympathetic inhibition predominate (8,12). The prompt return of spontaneous circulation suggests that pharmacologic intervention effectively interrupted the reflex arc. Clinically, the key measures are to discontinue the provoking stimulus immediately and administer anticholinergic or vasopressor agents without delay.

While the temporal association and clinical course strongly suggest a vagally mediated mechanism, definitive confirmation would require comprehensive exclusion of alternative factors including anesthetic depth, ventilation status and baseline autonomic tone, data not completely documented in real-time during this event.

The present case report has several limitations which should be mentioned. First, as a single case report, the findings cannot be generalized to all patients undergoing throat pack insertion. Second, although coronary computed tomography angiography was performed, the original axial and multiplanar reconstructed imaging data were unavailable for publication, which limits independent visual assessment of coronary anatomy. Nevertheless, the cardiology report, normal transthoracic echocardiographic findings and the uneventful postoperative course support the absence of clinically significant structural heart disease. Third, other potential contributing factors that may have predisposed this patient to vagal reflex, such as individual variations in autonomic tone or unrecognized cardiovascular sensitivity, cannot be definitively excluded.

In conclusion, the exact mechanism of reflex activation remains speculative, as direct neurophysiological monitoring was not performed during the procedure, and long-term follow-up data are limited, although no immediate complications were observed.