Pulseless Electrical Activity Arrest in End-Stage Heart Failure Complicated by Cocaine-Associated Cardiotoxicity and Cerebellar Infarction: A Post-resuscitation Diagnostic Pitfall

Pulseless electrical activity (PEA) arrest in patients with end-stage heart failure with reduced ejection fraction (HFrEF) most commonly reflects profound circulatory collapse rather than a primary arrhythmogenic event. Although post-resuscitation encephalopathy often prompts early neurologic prognostication, myocardial dysfunction and refractory shock frequently dominate outcomes in this population. We report the case of a 59-year-old woman with end-stage HFrEF, severe multivessel coronary artery disease, chronic lung disease, HIV infection, and active cocaine use who presented with acute hypoxic respiratory failure and decompensated heart failure and subsequently developed prolonged PEA arrest. Her post-arrest course was complicated by refractory cardiogenic shock, focal cerebellar infarction with delayed MRI due to hemodynamic instability and vasopressor dependence, and multisystem organ failure. Taken together, these findings underscore an important post-resuscitation diagnostic pitfall: neurologic abnormalities may coexist; however, refractory hemodynamic collapse often predominates. An integrated framework incorporating shock physiology, substance-associated cardiotoxicity, and competing neurologic injury is essential for accurate clinical assessment and informed goals-of-care discussions.