Alcohol-Induced Syncope in a Healthy Young Adult: A Case of Transient Nodal Dysfunction
A. El Bouazizi *
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
D. Bennani
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
L. Afendi
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
S. Essadqi
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
M. Haboub
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
M. Bouziane
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
S. Arous
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
G. Benouna
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
A. Drighil
Department of Cardiology, CHU Ibn Rochd, Casablanca, Morocco.
*Author to whom correspondence should be addressed.
Abstract
Aims: To emphasize that acute alcohol consumption may provoke transient sinoatrial or atrioventricular conduction disturbances leading to syncope in otherwise healthy young adults, and to advocate for prolonged electrocardiographic monitoring in such settings.
Presentation of Case: A 35-year-old man with no prior medical history presented to the emergency department following a witnessed episode of transient loss of consciousness after consuming six to seven beers the previous evening. Clinical examination, vital signs, standard 12-lead electrocardiogram (ECG), and routine laboratory tests—including cardiac biomarkers and electrolytes—were unremarkable. In-hospital continuous telemetry monitoring over 24 hours revealed no arrhythmias, pauses, or conduction abnormalities. Despite features suggestive of reflex syncope, the temporal association with heavy alcohol intake prompted concern for transient electrophysiological dysfunction. A 72-hour Holter ECG was therefore prescribed for further evaluation.
Discussion: Ethanol exerts multiple cardiovascular effects, including vasodilation, autonomic imbalance (increased vagal tone, reduced sympathetic activity), and direct electrophysiological actions on cardiac ion channels. These can transiently depress sinoatrial and atrioventricular nodal function, even in structurally normal hearts. Prior case reports and experimental studies have documented reversible sinoatrial block, sinus bradycardia, and second-degree AV block after acute alcohol ingestion. Such disturbances often resolve within 24 hours and may escape detection on standard ECG or short-term monitoring.
Conclusion: Syncope after acute alcohol intake in young adults may result from transient conduction abnormalities not captured during initial workup. Clinicians should consider alcohol as a potential trigger of electrophysiological instability and employ prolonged Holter monitoring to avoid misattribution to benign reflex mechanisms alone.
Keywords: Alcohol-induced syncope, transient sinoatrial dysfunction, atrioventricular conduction block, holiday heart syndrome, vagally-mediated bradycardia, young adult, prolonged ECG monitoring, reversible conduction disorder