Nonsustained Ventricular Tachycardia Resolving Under General Anesthesia

To the Editor Asymptomatic nonsustained ventricular tachycardia (NSVT) without presence of coronary artery disease, as described in the case presentation below, is typical for outflow tract tachycardia seen in patients with structurally normal hearts. In most of these cases (85%), the source is in the right ventricular outflow tract under the pulmonic valve.1 Treatment with β-blockers and calcium-channel blockers is used when the arrhythmia is symptomatic, but otherwise is not necessary because these arrhythmias are typically not life threatening.1 A 14-year-old 50 kg competitive female gymnast, ASA Physical Status II, presented for a right distal femoral osteotomy. She had a history of asymptomatic NSVT for 2 years diagnosed immediately before a prior anesthetic, and the arrhythmia resolved during general anesthesia. In review of her cardiology testing, a Holter monitor recording showed normal sinus rhythm with frequent uniform ventricular ectopy in singles, couplets, and triplets occurring 30% of the time and followed a diurnal pattern with a nadir between the hours of 3:00 AM and 5:00 AM. Echocardiography revealed a structurally normal heart with normal ventricular function. Exercise testing showed no increase in arrhythmia with exertion; ventricular ectopy was suppressed when her sinus rate exceeded 115 bpm. During the present surgery, after induction with 200 mg propofol and 40 mg lidocaine, anesthesia was maintained with 1.3% to 1.6% isoflurane (and a femoral nerve block) during which NSVT improved to sinus rhythm with rare premature ventricular contractions after induction. After a 2½-hour surgery, within 5 minutes after emergence and tracheal extubation, her NSVT returned to baseline with much more ventricular ectopy. Irrespective of her cardiac rhythm, vital signs remained stable and she remained otherwise asymptomatic. This case presents repeated temporary resolution of NSVT under general anesthesia followed by NSVT with a short-term increase in ventricular tachycardia from baseline frequency of 30% to 80% with normal hemodynamics. Her NSVT decreased immediately after induction, before initiation of isoflurane. The etiology of this is likely due to the antiarrhythmic effect of lidocaine initially2 or decrease in sympathetic outflow. However, the effect greatly outlasted the half-life of lidocaine. Isoflurane itself may exhibit proarrhythmic and antiarrhythmic effects via multiple cardiac ion channel effects.3,4 Specifically, its effects on sodium channels may extend “recovery” time of the channels, and thus produce a class 1c antiarrhythmic effect, which may have specific utility for ventricular ectopy.2 In animal models, volatile anesthetics decreased ventricular ectopy caused by a previous myocardial infarction.5 Of the possible etiologies, given the diurnal ectopy pattern noted on the Holter recording, resolution of her NSVT may have been influenced by changes in the central nervous system or sympathetic nervous system outflow during the state of general anesthesia but termination of her NSVT throughout her anesthetic was likely due to the antiarrhythmic effect of volatile isoflurane.3–5 In the presence of a structurally normal heart and a negative exercise test, patients with asymptomatic NSVT have low perioperative morbidity as compared with those with catecholamine-inducible arrhythmias or structural abnormalities.1 When a patient presents in the preoperative setting with asymptomatic monomorphic NSVT, an echocardiogram excluding cardiac structural abnormalities, a 12-lead electrocardiogram, and cardiac consult should be obtained before proceeding. Consent: The patient’s mother consented for this patient’s information to be used in publication. No identifiers are provided. Lance S. Patak, MD, MBA Bishr Haydar, MD Department of Anesthesiology University of Michigan Medical School Ann Arbor, Michigan [email protected]