Case Presentation: A 38 year-old female presented after collapsing in a parking lot. Initial rhythm was unknown but return of spontaneous circulation was achieved after cardiopulmonary resuscitation and 2 rounds of defibrillation. The patient’s EKG found no QT prolongation but there was a concern for inferior wall ischemia. Telemetry found many premature ventricular contractions (PVC’s) occurring near the R-T interval. While a bedside echocardiography was being obtained, the patient went into polymorphic ventricular tachycardia (PVT) and was rushed to the cath lab. She was found to have non-significant coronary artery disease. Initial echocardiography found severe global hypokinesis but repeat echocardiography found no abnormalities. The patient was placed on the hypothermia protocol with no cardiac events. Soon after extubation the patient was found unresponsive in PVT. She was shocked and converted back to normal sinus rhythm and lidocaine and amiodarone drips were started. Over the next couple hours she required multiple shocks as frequent PVC’s were near the R-T interval which continually transitioned into PVT. This transition seemed to be exacerbated while central and arterial lines were being placed. Eventually the patient was stabilized. Lidocaine was stopped, amiodarone was transitioned to oral, mexiletine and nadolol were added and a single chamber ICD was placed. The patient recovered quite well and was discharged home with outpatient follow-up to determine the cause of her PVT.
Discussion: Polymorphic ventricular tachycardia (PVT) is a serious ventricular arrhythmia that can progress into ventricular fibrillation and ultimately death. This arrhythmia is usually categorized based on the presence of a normal or prolonged QT interval. While PVT with normal QT interval usually occurs in the background of ischemia, cardiomyopathy or structural heart disease, some patients can present with PVT from catecholamine release (1). While many patients with catecholamine-induced PVT usually present at a young age, some patients present in their 30’s (2). Workup usually includes an EKG, Holter monitoring, Echo/MRI, exercise stress testing and/or genetic testing (1). While our patient did meet some of the diagnostic criteria for catecholaminergic polymorphic ventricular tachycardia (CPVT), the diagnosis was never confirmed. Exercise stress testing to induce PVT would not be done as an inpatient and there is no role for electrophysiologic testing as CPVT is not electrically inducible (1). Confirmatory diagnosis could also be established with genomic testing but this would not be ordered as an inpatient (1). Even though the diagnosis was not confirmed, the patient was discharged with the mainstays of treatment for CPVT (exercise avoidance, ICD placement, and long acting beta-blockers) (1). Antiarrhythmics such as flecainide can be added if beta-blockers are insufficient. Given that our patient’s PVT was not confirmed to be catecholamine-induced, she was discharged on amiodarone and mexiletine (1).
Conclusions: We report a case of a young female who presented after collapsing and was subsequently diagnosed with cardiac arrest from polymorphic ventricular tachycardia (PVT) that was possibly catecholamine-induced. This case represents how difficult it can be to establish an etiology in PVT in the absence of a prolonged QT interval, ischemia, or structural heart disease.