Tachycardia and Anxiety in a 14-year-old Boy

A 14-year-old boy with a history of generalized anxiety disorder and attention-deficit/hyperactivity disorder presents to the emergency department (ED) with increasing anxiety and palpitations. He reports that he was riding his bicycle when he suddenly felt his heart racing, which continued when he arrived home. His mother checked his heart rate and noted persistent elevation at approximately 180 beats/min. She called her neighbor, a pediatric cardiologist, who advised attempting vagal maneuvers. The maneuvers were ineffective in lowering his heart rate. The neighbor then recommended bringing the patient to the ED for evaluation.On presentation to the ED, the patient denies chest pain, dizziness, lightheadedness, syncope, nausea, or shortness of breath. He reveals that the night before presentation he took 75 mg of sertraline instead of his prescribed 25 mg because he was feeling more anxious than usual. He denies any other co-ingestions, vaping, excessive caffeine or energy drink consumption, exercise supplements, or intentional overdose. He denies any acute stressors at home or school.ED vital signs are as follows: temperature, 97.9°F (36.6°C); heart rate, 170 beats/min; respirations, 24 breaths/min; blood pressure, 125/89 mm Hg; and oxygen saturation, 100% on room air. On physical examination, the patient is anxious but in no acute distress. His pupils are equal, round, and reactive to light. His airway is clear. His trachea is midline, and there is no appreciable jugular venous distention. His respirations are unlabored, and his lungs are clear. Cardiac examination demonstrates persistent tachycardia with little heart rate variability and normal heart sounds without murmur, rub, or gallop. His abdomen is soft, nontender, and without masses or organomegaly. Capillary refill is less than 2 seconds. Neurologic examination reveals normal mental status, muscle tone, and reflexes, and no appreciable clonus. His skin examination reveals no diaphoresis, rashes, or signs of self-injury.The patient is placed on a cardiac monitor, and wide complex tachycardia with a rate of 170 beats/min is noted. A peripheral venous catheter is placed, basic laboratory tests (including electrolytes and troponin) are sent, chest radiography is performed, and an electrocardiogram (ECG) is obtained (Fig 1).The differential diagnosis for wide complex tachycardia in children is broad and includes both life-threatening and relatively benign conditions. For patients who present with hemodynamic instability, stabilization and resuscitation, including acute termination of the arrhythmia, must be initiated to prevent serious morbidity and mortality.The diagnostic possibilities of wide complex tachycardia can be grouped into genetic, acquired, and idiopathic causes.Genetic disorders, such as channelopathies and inherited cardiomyopathies that affect the structure or function of the cardiac myocyte can be associated with ventricular tachycardia, although in these settings the tachyarrhythmia is usually unstable. (1) These inherited causes include long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, hypertrophic and dilated cardiomyopathies, and arrhythmogenic right ventricular cardiomyopathy. (1) Inquiring about a family history of sudden, unexplained death in young individuals and other early cardiac disease should be included in the history of any patient with cardiac illness. Although rare, congenital structural coronary anomalies, such as late-presenting anomalous left coronary artery from the pulmonary artery or origin of the left coronary artery arising from the right carotid sinus, may predispose an individual to life-threatening tachyarrhythmias. (2) It is important to note that in a previously healthy patient without a family history of cardiac illness and with a stable monomorphic wide complex tachycardia, congenital etiologies are unlikely.Acquired heart diseases such as infectious or inflammatory myocarditis may also cause ventricular tachycardia. (3) Patients who have undergone ventriculotomy for repair of congenital heart disease (eg, tetralogy of Fallot), especially those with continued abnormal hemodynamic values after repair, are at increased risk for ventricular tachycardia and sudden death as a late complication. (4) A more common acquired cause of tachyarrhythmia, especially in adolescents, is an intentional drug ingestion. Ingestion of amphetamines, cocaine, excess caffeine, nicotine, exogenous thyroid hormone, and a variety of cardiac medications such as digoxin can lead to ventricular tachycardia. (5) A comprehensive ingestion history, including illicit substances, and prescription and nonprescription medications available at home is paramount in these patients.Idiopathic causes tend to be relatively benign and include right ventricular outflow tract ventricular tachycardia (RVOT VT) and idiopathic left ventricular tachycardia (ILVT), also referred to as left ventricular fascicular tachycardia, Belhassen syndrome, or verapamil-sensitive tachycardia. (6)(7) Although RVOT VT has a benign course and is often an incidental finding, if excessively fast or incessant, ablation is sometimes necessary. In addition, arrhythmogenic right ventricular cardiomyopathy needs to be considered with any right ventricular outflow tract ectopy. This rare cardiomyopathy predisposes individuals to unstable ventricular tachycardia and sudden cardiac death. (8)It is important to consider aberrantly conducted supraventricular tachycardia (SVT) in the differential diagnosis of stable wide complex tachycardia. SVT typically presents as narrow complex tachycardia, but it can result in a wide QRS complex in the presence of aberrant ventricular conduction (eg, a bundle branch block) or rarely in Wolff-Parkinson-White syndrome with atrioventricular reentrant tachycardia using antegrade conduction across the accessory pathway (so-called antidromic reciprocating tachycardia). (9) These idiopathic (RVOT VT and ILVT) causes of ventricular tachycardia and aberrantly conducted SVT are the most likely etiologies in a previously healthy adolescent with stable monomorphic wide complex tachycardia.An ECG is obtained and demonstrates a regular wide complex tachycardia with a rate of 180 beats/min, QRS duration of 130 milliseconds, left axis deviation (with a counterclockwise vector loop), and a right bundle branch block. Venous blood gas with electrolytes, urine toxicology screen, troponin level, complete blood cell count, comprehensive metabolic panel, and chest radiography are all normal. Pediatric cardiology is consulted. The patient’s ECG is noted by the cardiologist as “classic” for ILVT/Belhassen syndrome. In retrospect, the laboratory work and imaging performed in this patient were not necessary to make the final diagnosis.ILVT or Belhassen syndrome is a morphologically unique and identifiable tachyarrhythmia that usually occurs in individuals aged 20 to 40 years with a structurally normal heart. ILVT most commonly presents with palpitations and presyncopal symptoms but is not typically associated with syncope or incited by exercise. (10) Cardiac arrest and cardiomyopathy are rarely associated. ILVT is not sensitive to vagal maneuvers compared with reentrant atrioventricular tachycardia but is exquisitely sensitive to verapamil. The mechanism of ILVT is assumed to be reentry near the left posterior fascicle in the presence of abnormal Purkinje tissue (Fig 2). (6)(7) On ECG, ILVT presents as a right bundle branch block with left axis deviation. QRS duration is minimally prolonged, ranging from 120 to 140 milliseconds. (7) In the electrophysiology laboratory, ILVT may be induced by atrial or ventricular pacing. (11) The diagnosis of ILVT may be made on clinical presentation and ECG alone and requires no additional testing. Treatment and prevention of ILVT is achieved with verapamil and in resistant cases with catheter-based ablation. (7)(10)(11) To acutely terminate an ILVT episode, verapamil should be administered as a slow intravenous push (0.1 mg/kg per dose, with a maximum of 5 mg) while the patient’s rhythm is continuously monitored with close observation of blood pressures. Epinephrine, calcium gluconate, and cardioversion pads should be available during verapamil administration in case of cardiovascular collapse. Patients are then usually maintained on oral verapamil with close cardiology follow-up.With cardiology present, our patient received a slow push of a total of 3 mg of intravenous verapamil with initial slowing of the ventricular tachycardia rate and then conversion to normal sinus rhythm. The patient was admitted to the PICU for telemetry overnight without recurrence of tachyarrhythmia. His increased dose of sertraline was not felt to have contributed to his presentation as selective serotonin reuptake inhibitors, except for citalopram, are rarely associated with arrhythmias and cardiac toxicity. (12) The patient’s anxiety was discussed during his hospitalization to ensure he had appropriate ongoing outpatient treatment. The patient was ultimately discharged home on long-acting verapamil with cardiology follow-up. Of note, the patient presented to the ED 3 weeks later with a second episode of ILVT responsive to intravenous verapamil. He was discharged home from the ED on an increased dose of oral verapamil and has remained asymptomatic since.