Incessant Ventricular Tachycardia Terminated by Extracorporeal Life Support

Incessant ventricular arrhythmia, whether tachycardia or fibrillation, is defined as a continuous sustained rhythm with prompt recurrence despite repeated intervention and termination. Electrical storm (ES) or incessant ventricular tachycardia (VT) is further characterized as >3 separate episodes of ventricular tachycardia or ventricular fibrillation requiring termination within 24 hours. Most cases are related to underlying structural heart disease; however, approximately 10% of patients with tachyarrhythmias leading to ES have structurally normal hearts. Several treatment modalities consisting of pharmacologic and non-pharmacologic have been shown to be efficacious; however, in the setting of persistent arrhythmia, additional salvage therapies such as extracorporeal membrane oxygenation (ECMO) have been indicated. We describe a case of incessant ventricular tachycardia terminated by ECMO in the setting of pharmacologic refractoriness.

Case Presentation

A 29-year-old male with no known past medical history presented to the emergency department via emergency medical services (EMS) following a witnessed cardiac arrest. The patient was of his usual state of health and preparing to leave for work the morning of the incident. He was accompanied by his wife, who witnessed him collapse without warning. Immediately following a call to 911, she began performing hands-only cardiopulmonary resuscitation (CPR) for approximately 5-7 minutes prior to EMS arrival.

Initial rhythm evaluation in the field demonstrated a wide complex monomorphic tachycardia, prompting emergent defibrillation. He was intubated and administered a 300 mg amiodarone bolus; however, en route to the hospital, he sustained an additional arrest requiring 3 rounds of CPR and 2 defibrillations with achievement of return of spontaneous circulation (ROSC). Given his labile state, lidocaine bolus and infusion were started prior to his arrival to the hospital.

Initial workup included a negative drug screen, a troponin level of 0.93, potassium of 3, and magnesium of 1.8. A 12-lead electrocardiogram showed sinus tachycardia, anterolateral ST depressions, and a QTc of 477 (Figure 1). Aggressive electrolyte repletion was instituted and a bedside echocardiogram was performed, which revealed severely depressed left ventricular (LV) systolic function (ejection fraction 15-20%) without significant wall motion or valvular abnormalities. He subsequently underwent coronary angiography, which did not reveal any significant epicardial coronary artery disease, but demonstrated an elevated left ventricular end diastolic pressure of 25 mmHg. Upon completion of the procedure, the patient developed VT, requiring 4 consecutive unsynchronized cardioversions with return to sinus rhythm. In the intensive care unit (ICU), an EKG was obtained demonstrating premature ventricular complexes with left bundle morphology (Figure 2). Further analysis of telemetry monitoring highlighted associated PVCs with the onset of witnessed ventricular tachycardia.

Electrophysiology was consulted in the hope of pursuing 2 potential treatment strategies, including the placement of an atrial pacemaker lead for possible overdrive pacing versus an emergent electrophysiologic study (EPS) and VT ablation. Unfortunately, the patient continued to degrade into VT despite antiarrhythmic therapy, deep sedation, paralytics, and repetitive cardioversions. A formal echocardiogram continued to demonstrate severely reduced LV function, and despite adequate ventilatory strategies, the patient developed significant hypoxia and acidemia. Cardiothoracic surgery was consulted and a multidisciplinary decision was made to pursue ECMO, in which successful cannulation was performed at bedside. Shortly thereafter, telemetry and EKG analysis exhibited complete resolution of ventricular ectopy, and over the course of recovery, the patient ceased to have additional ventricular arrhythmias. The patient was weaned off of infusion therapies and transitioned to an oral amiodarone regimen. Paralytics and sedatives were weaned, and he was successfully liberated from ECMO on hospital day 12. An implantable cardioverter-defibrillator (ICD) was implanted for secondary prevention, and follow-up echocardiography demonstrated significantly improved LV function and an EF of 55-60%.

Discussion

This case describes an unusual presentation of incessant ventricular tachycardia thought to be mediated by PVCs in the setting of no underlying preexisting medical condition or current state of acute illness. Workup of reversible causes such as infection and toxicity were unremarkable, and despite medical therapy, salvage ECMO support was necessary and resulted in complete resolution of ventricular ectopy and the development of ventricular tachycardia.

Management options for VT commonly include both medicinal and mechanical approaches consisting of antiarrhythmic therapies, ICDs, ablations, and surgery.¹ As demonstrated in our case, the aforementioned therapies may be suboptimal or unobtainable, and could lead to the continuation of incessant VT leading to low cardiac output and hemodynamic collapse, further necessitating salvage therapies such as ECMO.²

Hemodynamic collapse is a fear during planned VT catheter ablation; thus, ECMO in addition to a left ventricular assist device has been successfully utilized to accomplish mapping and ablation.^2,3 In emergent situations, ECMO has been a staple of therapies for neonates and infants, with more recent utilization in the adult population, especially in the setting of cardiogenic shock.^4-7 The process of ECMO cannulation and support has not only demonstrated adequate support for failing organs, but also showcased significant reduction in catecholamines, resulting in adequate suppression of ventricular ectopy and VT.^8–10 Though algorithmic approaches to VT should be conducted as demonstrated in the 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death, several studies have suggested that the institution of ECMO be strongly considered in hemodynamically unstable patients with refractory unstable arrhythmias.^11,12 By providing adequate stability and hemodynamic support, further treatment options such as EPS and ablation can be safely pursued in hopes of providing definitive therapy.

Summary

We demonstrate the potential utility of salvage ECMO therapy in patients with refractory ventricular arrhythmias and hemodynamic instability despite adequate medical therapy. ECMO has provided significant stability in patients needing further evaluation for definitive ventricular ectopy and tachyarrhythmias therapy by means of EPS and ablation.

Key Teaching Points

–Incessant VT can be difficult to treat with standard guideline therapy.

–ECMO therapy has been shown to decrease catecholaminergic surges responsible for ventricular ectopy and VT.

–The use of ECMO can provide lifesaving stabilization in hemodynamically compromised patients with refractory VT. 

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