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 35-year-old male with a history of AICD placement for long QT syndrome by a local cardiologist six months ago presented to the ED by ambulance for altered mental status and frequent shocks from AICD secondary to a loperamide overdose. He was unable to provide a history of more than “yes" or "no” because of his agitation, so the most history was obtained from emergency medical services (EMS), with confirmation by the patient. EMS stated that the patient was having dinner with his spouse when the spouse noticed that he had a brief loss of consciousness for several seconds. The spouse stated that when the patient awoke, he became very anxious, diaphoretic, and irritable; it was unclear if the defibrillator had fired at that time. On arrival, EMS gave the patient 2 mg of naloxone IV without any effect. They stated that en route to the facility, they noted that the AICD had fired several times, causing the patient much anxiety and pain. EMS also stated that they found a bag full of loperamide tablets inside a purse-string bag near the patient, which they brought into the department for identification. They stated that the patient had a history of IV drug abuse and had overdosed on loperamide in the past when he had been unable to obtain opiate medications. In the ED, the patient was anxious and diaphoretic and was shocked by his defibrillator every three to four minutes for runs of polymorphic ventricular tachycardia (Torsades). A review of symptoms was negative, except for tachycardia, anxiety, and diaphoresis. Initial vital signs were a heart rate of 120, respiratory rate of 24, oxygen saturation 99% on room air, and blood pressure 138/64. Physical exam showed that the patient could not hold an extended conversation; he was anxious, had reactive mydriasis, and an AICD in place in the left chest, without signs of infection; otherwise, the physical was normal.\nPotassium was found to be 2.7 so IV potassium, magnesium, bicarbonate, and saline were started with lidocaine chosen as an antiarrhythmic (with which cardiology and poison control had agreed). The remaining basic labs, as well as toxicology and cardiac enzymes, were normal. Lorazepam was also used to control agitation. The electrocardiogram (ECG) showed tachycardia, which was different from the patient’s baseline atrial-paced rhythm. This ECG (Figure ) was obtained when the patient was not in polymorphic ventricular tachycardia, which was only shown on the monitor for several seconds before being detected and electrically cardioverted by the AICD. Chest X-ray was normal. After treatment in the ED and intensive care unit (ICU), the shocks eventually became less frequent as electrolytes normalized. The patient was eventually removed from the lidocaine drip and discharged home five days later with the normalization of ECG over time (Figures -).