B26-20 Refractory Ventricular Fibrillation and Multiorgan Failure Following Cannabis Exposure: A Critical Care Management Challenge

Abstract Background Prolonged ventricular fibrillation (VF) arrest can result in cardiogenic shock, multiorgan failure, and challenging ICU management. Although the cardiovascular effects of cannabis are often underestimated, emerging data suggest a possible link between tetrahydrocannabinol (THC) exposure and malignant ventricular arrhythmias. We present a case of recurrent VF and torsades de pointes (TdP) temporally associated with cannabis use, resulting in refractory cardiac arrest, cardiogenic shock, renal failure, and hypoxic-ischemic brain injury. Case Report A 31-year-old man with untreated hypertension smoked marijuana less than one hour before experiencing sudden out-of-hospital cardiac arrest. Emergency medical services documented VF; return of spontaneous circulation (ROSC) was achieved after 45 minutes, requiring 12 defibrillation shocks and an amiodarone infusion. At an outside hospital, he suffered recurrent TdP and another cardiac arrest, with ROSC after 25 minutes. On transfer to our ICU, he was profoundly acidotic (pH 6.9, lactate 8.4 mmol/L) with troponin 29,787 ng/L and creatinine 2.5 mg/dL. Urine toxicology was positive for THC and negative for cocaine, amphetamines, opiates, and phencyclidine. ECG showed ST-segment depression in leads V4-V6, and echocardiography demonstrated severe biventricular dysfunction with a left ventricular ejection fraction of 15-20%. During brain MRI, he experienced a third cardiac arrest with ROSC after two CPR cycles. Right-heart catheterization revealed a cardiac index of 1.2 L/min/m², prompting Impella placement. He developed oliguric renal failure requiring hemodialysis. Brain MRI revealed punctate cerebellar infarcts and subtle cortical ribbon diffusion restriction in the parietal lobes, consistent with early hypoxic-ischemic injury. ECMO was deferred due to neurologic findings and subsequent hemodynamic stabilization. Conclusion This case illustrates a potential association between cannabis exposure and malignant ventricular arrhythmias. The temporal relationship, absence of other intoxicants, and lack of structural heart disease suggest THC as a plausible arrhythmogenic trigger. Proposed mechanisms include sympathetic surge, increased myocardial oxygen demand, coronary vasospasm, and ion-channel modulation. Severe acidosis and catecholamine excess likely intensified these effects. Clinicians should maintain vigilance for THC-induced arrhythmias, obtain urine toxicology in unexplained cardiac arrests, and avoid QT-prolonging agents. As cannabis use becomes moreprevalent, greater awareness and public health evaluation of its cardiovascular risks are warranted. This abstract is funded by: None