Treatment of supraventricular arrhythmias in critical care patients with sepsis.

Supraventricular arrhythmias, especially new-onset atrial fibrillation, occur in approximately 8-46% of critically ill patients with sepsis, depending on the population and monitoring intensity. New-onset atrial fibrillation is independently associated with increased mortality, prolonged intensive care unit stay, and elevated thromboembolic risk. Sepsis-associated atrial fibrillation arises from the interplay of pre-existing patient risk factors, systemic inflammation, sepsis-induced atrial and ventricular remodeling, catecholamine exposure, mechanical ventilation, and electrolyte disturbances. Fluid loading further augments arrhythmia risk in the context of diastolic dysfunction and increased right-ventricular afterload in acute respiratory distress syndrome. Evidence regarding antiarrhythmic drug choice remains limited. The Propafenone vs. Amiodarone for Supraventricular Arrhythmias in Septic Shock trial, the only double-blind randomized comparison of these agents, showed similar 24-hour cardioversion rates but faster cardioversion and fewer recurrences with propafenone, with treatment effects strongly modified by left atrial volume index. Trials of ultra-short acting beta-blockers demonstrated reliable heart-rate control but heterogeneous and fragile mortality signals, with the suggested benefit largely driven by single-center esmolol data and not consistently reproduced in multicenter landiolol studies. Evidence for digoxin and magnesium supports primarily adjunctive roles rather than first-line rate- or rhythm-control strategies. No study has evaluated vernakalant specifically in sepsis, limiting the evidence for its use in hemodynamically unstable patients. Anticoagulation decisions in sepsis-associated new-onset atrial fibrillation are complicated by high bleeding risk, potential changes in stroke risk over time, and limited data on long-term thromboembolic outcomes, underscoring the need for individualized assessment. Overall, current evidence supports prioritizing correction of triggers and individualized selection of a rate- vs. rhythm-control strategy based on hemodynamic status, ventricular function, left atrial size, and arrhythmia characteristics. Future multicenter randomized trials are required to refine antiarrhythmic and anticoagulation strategies in this high-risk population.