Transient Arrhythmias After Aortic Valve Repair

Scenario: A 65-year-old man with a history of hypertension and hypercholesterolemia underwent an aortic valve repair (AVR). He had no prior history of atrial or ventricular arrhythmias, and his preoperative electrocardiogram (ECG) demonstrated normal sinus rhythm (NSR). The surgery and subsequent 22-hour stay in the intensive care unit were unremarkable. He was then transferred to the cardiac step-down unit, where he was hemodynamically stable with a heart rate of 72/min in NSR. Approximately 3 hours after transfer, the patient developed palpitations and shortness of breath. Bedside telemetry and a 12-lead ECG confirmed new-onset postoperative atrial flutter (AF) with rapid ventricular response. Results of a basic metabolic panel were within normal limits, and a transthoracic echocardiogram showed a well-functioning AVR with preserved left ventricular function and no significant structural abnormalities. Intravenous amiodarone and heparin infusions were started. Approximately 18 hours after the amiodarone infusion was initiated, a telemetry alarm for a pause sounded with the following ECG rhythm strip in leads II and V1.Atrial flutter at heart rate of 70/min with a 2.6-second pause, spontaneous restoration of sinus bradycardia at heart rate of 55/min.Postoperative AF is a common complication following cardiac surgery, particularly after AVR, with a reported incidence of approximately 50% in large cohorts. The development of postoperative AF is associated with increased risks of stroke, longer hospital stays, and higher rates of in-hospital mortality.The pathophysiology of postoperative AF involves multiple factors such as atrial inflammation, oxidative stress, electrolyte disturbances, and autonomic nervous system imbalance. During AVR, surgical manipulation can cause atrial tissue injury and trigger an inflammatory response, creating a vulnerable substrate for postoperative AF. It is important to recognize that postoperative AF is more prevalent following valve surgeries, such as AVR, than following coronary artery bypass grafting.In this case, a transient pause was observed before the restoration of NSR. The patient had been started on intravenous amiodarone, which is a class III antiarrhythmic agent that prolongs the cardiac action potential and refractory period by blocking potassium channels. Additionally, it exhibits β-adrenergic and calcium channel–blocking properties, which can suppress sinoatrial node automaticity and slow conduction. This suppression may lead to a transient pause and typically resolves as the sinoatrial node gradually resumes normal pacemaker activity, allowing NSR to be reestablished.Intravenous amiodarone is commonly used to manage postoperative AF due to its high efficacy in restoring NSR. Treatment typically begins with a bolus being administered followed by a continuous infusion allowing rapid attainment of therapeutic drug levels and promoting conversion to NSR. Intravenous amiodarone has the highest likelihood of success within the first 24 hours of administration. Careful monitoring is essential due to potential side effects, including the risk of extravasation. Once the patient converted to NSR, the intravenous infusion of amiodarone was stopped.Given the elevated risk of stroke, anticoagulation is an important consideration for patients with postoperative AF. Anticoagulation strategy is typically determined on the basis of a CHA2DS2-VASc score of 2 or greater (indicating a high risk of stroke). In this case, the patient’s CHA2DS2-VASc score was 2. Once the patient converted to NSR, the heparin infusion was stopped.