Anesthetic-Electrophysiologic Interactions: How Sedatives Shape Cardiac Conduction and Arrhythmia Risk

Anesthetic and sedative agents are widely used in electrophysiology laboratories, operating rooms, and intensive care units, yet their direct effects on cardiac conduction and arrhythmia risk are often underrecognized. This review summarizes the mechanistic, experimental, and clinical evidence linking commonly used anesthetic agents to changes in myocardial excitability, autonomic tone, ion-channel activity, and perioperative arrhythmogenesis. Propofol, dexmedetomidine, volatile anesthetics, ketamine, opioids, benzodiazepines, barbiturates, etomidate, and local anesthetics demonstrate distinct electrophysiologic profiles through modulation of sodium, calcium, potassium, and pacemaker currents, as well as sympathovagal balance. These effects may manifest clinically as sinus bradycardia, atrioventricular block, atrial fibrillation, QT prolongation, torsades de pointes, or ventricular tachyarrhythmias, particularly in patients with structural heart disease, inherited channelopathies, electrolyte abnormalities, or hemodynamic instability. Continuous electrocardiographic monitoring, assessment of repolarization and conduction indices, and integration of hemodynamic and autonomic markers can support individualized anesthetic titration. Current evidence remains limited by heterogeneous study designs and a lack of standardized protocols. Future prospective studies are needed to define optimal sedation strategies that preserve procedural efficacy while minimizing arrhythmia risk.