Inhibition of Premature Ventricular Contractions by Desflurane.

substantial increase in the number of procedures performed in the cardiac electrophysiology (EP) laboratory. Currently, no consensus or evidence-based recommendations exist regarding the type of anesthetic or anesthetic agents and drugs used to best facilitate radiofrequency (RF) ablation of tachyarrhythmias. Additionally, little unambiguous data are available on the impact of specific anesthetics on the success of various procedures performed in the EP laboratory. Peters et al 2 reported the increase of the defibrillation threshold by adding lidocaine to propofol sedation to minimize injection pain during internal cardiac defibrillator placement, which possibly could cause unnecessary revision of the lead system. The authors present a case of premature ventricular contraction (PVC) RF ablation in which the use of desflurane led to the inhibition of the arrhythmia. CASE REPORT A 44-year-old, 188-cm, 109-kg man without significant cardiovascular history presented to his electrophysiologist’ so ffice with recurrent syncope associated with palpitations. Transthoracic echocardiography showed normal left ventricular function without significant valvular abnormalities. Subsequent Holter monitoring and treadmill stress test showed frequent monomorphic PVCs without evidence of reversible ischemia. The patient was started on metoprolol, but this failed to control his arrhythmia. Before this intervention, the patient had undergone two EP studies at another institution under conscious sedation where the earliest activation was mapped to the ventricular outflow tract region. Radiofrequency ablation in both right ventricular outflow tract (RVOT) and left ventricular outflow tract (LVOT) had temporarily suppressed the PVCs, but the arrhythmia returned once RF energy was turned off, consistent with an intramyocardial focus. Because of his continued clinical symptoms, the patient was referred for a repeat ablation. Preprocedural electrolyte laboratory values were all within normal limits (sodium 142 mEq/L, potassium 4.1 mEq/L, calcium 8.6 mg/dL, magnesium 1.8 mg/dL). The patient had taken his regular dose of metoprolol, 25 mg, on the morning of the procedure. According to institutional practice for this type of procedure, no preprocedure anxiolysis with benzodiazepines was administered because the electrophysiologists at this institution believe that benzodiazepine administration may lead to suppression of the arrhythmia. In the procedure room, the patient was sedated with propofol titrated to effect for the vascular access part of the procedure (up to 100 μg/kg/min), and monitored according to American Society of Anesthesiologists (ASA) guidelines including end-tidal CO2 measurement. No lidocaine was added to the propofol at any point during the procedure as an adjunct to decrease injection pain. Propofol was discontinued once femoral venous access was obtained and intracardiac catheters had been placed. Ten minutes after discontinuing the propofol infusion, the patient was conversant, appropriately following commands, and the neurologic status was at baseline. The electrocardiogram (ECG) showed a ventricular bigeminy with the PVC morphology of a left bundle-branch block with QRS transition in leads V2/V3 with right superior axis (Fig 1). Electrophysiologic mapping was performed using an electroanatomic mapping system (CARTO, Biosense-Webster, Diamond Bar, CA), and the arrhythmogenic focus (earliest activation) was mapped to the lateral aspect of the RVOT just below the pulmonic valve. Before commencement of RF ablation, a continuous propofol infusion was restarted at 100 μg/kg/min to deepen sedation and to prevent patient movement and discomfort during the ablation. The patient soon presented with signs of upper airway obstruction and intermittent coughing, which interfered with the RF ablation procedure. To achieve an adequate level of sedation allowing for mapping and ablation without patient movement and to relieve the airway obstruction, general anesthesia was induced with propofol (150 mg intravenous [IV] bolus) and fentanyl (100 μg IV bolus). Vecuronium (7 mg IV bolus) was administered for neuromuscular blockade and endotracheal intubation performed. General anesthesia was maintained with desflurane (targeted end-tidal concentration 5%). A few minutes after desflurane was started, the PVCs completely disappeared and electrical stimulation failed to reproduce any PVCs (Fig 2). Desflurane was discontinued and a total intravenous anesthetic technique using a continuous propofol infusion at a rate of 125 μg/kg/min was initiated. The PVCs returned as ventricular bigeminy within a few minutes after desflurane had been discontinued. When PVCs returned, no end-tidal desflurane was detected in the breathing circuit. There were no significant changes in vital signs, including arterial blood pressure, heart rate, or arterial oxygen saturation. Depth of anesthesia monitoring using the BIS monitor (Aspect Medical Systems,