A 43-year-old female patient with a past medical history of substance use disorder (SUD) was brought to the hospital by emergency medical services (EMS) presenting with multiple episodes of dizziness, shortness of breath, and palpitations. EMS reported ventricular tachycardia (VT) while in transit to the hospital for which she was externally defibrillated 10 times without any resolution of the ventricular arrhythmia. The patient’s past medical history was positive for depression and substance abuse of hydrocodone dating back to 2007. The patient’s husband denied any history of cardiac arrhythmias, structural heart disease, or ischemic heart disease. The patient’s husband denied using any medications, including herbal supplements, but reported drug allergies to amoxicillin and erythromycin. The patient’s social history revealed that she worked at a consignment store and had a history of alcohol and marijuana abuse. The patient’s husband also revealed recreational usage of loperamide at approximately 400 mg in the last 24 hours before the presentation. On physical exam in the emergency department, she appeared to be in moderate distress with pain from the external defibrillations. Her vital signs consisted of an elevated pulse of > 200 beats per minute (bpm), an elevated blood pressure of 157/80, and an increased respiratory rate at 24/minute. The pulmonary exam revealed decreased breath sounds bilaterally with symmetrical chest wall expansion. The cardiovascular exam revealed tachycardia with no murmurs reported. Examination of the head and neck showed moist mucous membranes with no jugular venous distension. The gastrointestinal exam was negative for distention, tenderness, rebound, guarding, hepatomegaly, or splenomegaly. The musculoskeletal exam revealed warm and well-perfused upper and lower extremities free of clubbing, cyanosis, and edema. In the processes of placing the electrocardiogram (EKG) electrodes onto the patient in the emergency room, the patient became unresponsive and the two lead EKG monitors showed polymorphic VT with a heart rate of 220 per minute and blood pressure of 84/58. The patient was immediately defibrillated once again before being sedated, intubated, and started on an amiodarone drip. The patient’s vitals were stabilized for 15 minutes before she went into another episode of polymorphic VT despite the amiodarone drip. The patient underwent synchronized cardioversion, and once her vitals stabilized, she underwent a cardiac catheterization which showed patent coronaries and a normal ejection fraction. The patient got transferred to the Medical Intensive Care Unit (MICU) for continuous monitoring and was started on a lidocaine drip in addition to the amiodarone drip. Her EKG in the MICU is shown below in Figure .\nIn the MICU, the patient continued to have polymorphic VT episodes despite medical management and went in and out of VT episodes approximately 16 times with each episode lasting between 30 seconds to two minutes. Subsequently, the patient had a transvenous cardiac pacer placed which stabilized her vital signs. After 72 hours, the pacer was removed, and the patient remained stable on amiodarone and lidocaine. Transthoracic echocardiogram in the MICU revealed a normal ejection fraction with no valvular abnormality. Serum electrolytes were within normal limits, and the urine drug screen was also negative. After the temporary pacer was removed, the patient subsequently remained in sinus rhythm with a heart rate of 70 bpm, QRS duration of 98 ms, and a QTc interval of 456 ms as seen in Figure .\nAfter five days of hospitalization, the effects of the loperamide had completely resolved, and the patient remained in normal sinus rhythm on amiodarone until discharge and followed up a month later.
A 26-year-old male, with history of heroin abuse, was brought to the ER after a transient episode of loss of consciousness. His vital signs upon arrival were heart rate of 50 beats/min, blood pressure of 125/60 mmHg, respiratory rate of 14 breaths/minute, and temperature of 98.9°F. He was lethargic and had symmetrical constricted pupil bilaterally, absent bowel sounds, and a normal neuromuscular, cardiac, and respiratory exam. His initial laboratory tests showed sodium of 142 mmol/L, potassium of 4.2 mmol/L, calcium of 9.1 mg/dL, and magnesium of 1.8 mg/dL; extended urine drug screen was positive only for opiates. Blood alcohol level was within normal limits. No abnormalities were noted on CT scan of the head. EKG showed sinus bradycardia with normal PR, QRS, and QT/QTc intervals (). Soon after presentation he developed shortness of breath, diaphoresis, and sustained ventricular tachycardia with ventricular rate of 220 beats/minute. He was defibrillated 2 times with 200 J before sinus bradycardia was attained again. After defibrillation his bradycardia worsened with heart rate of 40 beats/min; however, the patient remained symptom-free. Over the course of one hour he had 2 episodes of self-limiting Torsades de Pointes (TdP) each lasting less than 10 seconds and a third ending up in pulseless ventricular tachycardia ( shows one such episode of TdP caught on telemetric monitoring). He was defibrillated again and prompt CPR was initiated. Pulse was regained immediately and he continued to have sinus bradycardia with heart rate of 40 beats/minute. He was given 2 gm of magnesium IV and overdrive pacing was started with isoproterenol. A goal heart rate of 90 beat/minute was maintained for 48 hours. No further ventricular arrhythmias were noted; once isoproterenol was discontinued his heart rate remained between 50 and 60 beats/min. Transthoracic echocardiogram showed a normal left ventricular ejection fraction and no valvular or structural abnormalities. Cardiac angiography did not reveal any coronary pathology either. On day 3 of admission the patient admitted to taking loperamide for the past two months to relieve diarrhea associated with heroin withdrawal. Recently he had read on an internet blog that high doses of loperamide can give a similar “high” to heroin. A day prior to admission he started increasing his daily dose of the medicine to attain a euphoric state. On the day of admission his maximum ingested dose reached up to 192 mg of loperamide. At this point a serum loperamide level was sent that came back, 2 ng/mL (expected peak level after ingestion of 8 mg oral dose is 2 ng/mL or less). The patient remained hemodynamically stable and was discharged to drug rehabilitation facility on day 8 of hospitalization.