B52-25 Neurogenic Myocardial Stunning Leading to Cardiogenic Shock in a Young Woman: An Atypical Presentation of Suspected Pheochromocytoma

Abstract Introduction Neurogenic stunned myocardium is a reversible form of cardiac dysfunction following acute neurologic injury, most often due to subarachnoid hemorrhage, ischemic stroke, traumatic brain injury, or seizures. Excess catecholamine release is thought to cause myocardial stunning, leading to left ventricular systolic dysfunction, regional wall motion abnormalities, and cardiac biomarker elevation. Patients may present with acute heart failure or cardiogenic shock despite previously normal cardiac function. We describe a 20-year-old woman with baseline non-ischemic cardiomyopathy who developed cardiogenic shock after subacute subarachnoid hemorrhage, precipitated by a suspected pheochromocytoma. Case Presentation A 20-year-old woman with coxsackie-virus-induced cardiomyopathy (EF 20-25%) presented with acute onset dyspnea, severe hypertension, and tachycardia, concerning for sympathetic crashing acute pulmonary edema. Examination revealed cool extremities without overt volume overload. Chest radiograph showed bilateral infiltrates consistent with flash pulmonary edema. Labs demonstrated troponin 58 ng/L, BNP 20,000 pg/mL, AKI, mild transaminitis, and lactate 10 mmol/L. EKG showed extreme right axis deviation with nonspecific ST-T changes. She was initially treated with high-dose IV nitroglycerin and noninvasive ventilation. Within an hour, she developed chest and back pain, altered mental status, and hypotension concerning for aortic dissection. She was intubated, started on norepinephrine, and underwent emergent CT angiography, which excluded dissection but revealed communicating hydrocephalus and a 5.8 × 4.7 × 4.0 cm right adrenal mass suggestive of pheochromocytoma. An external ventricular drain was placed. Cerebral angiography demonstrated severe bilateral middle cerebral artery vasospasm without aneurysm or AVM. Intra-arterial verapamil was aborted due to intraoperative cardiac arrest; angioplasty achieved partial improvement. Findings were consistent with subacute subarachnoid hemorrhage likely triggered by catecholamine surge from pheochromocytoma. In the ICU, a pulmonary artery catheter revealed right atrial pressure of 16 mmHg, mean pulmonary artery pressure 24 mmHg, pulmonary capillary wedge pressure 38 mmHg, cardiac index 1.5 L/min/m², and systemic vascular resistance 2123 dynes·sec·cm⁻2, confirming cardiogenic shock. Despite multiple vasopressors, inotropes, and diuretic infusion, her neurologic status deteriorated with rising intracranial pressures (20s-30s) thought due to EVD occlusion. A decompressive craniectomy was performed, but the patient remained comatose with fixed and dilated pupils. Physical examination and cerebral perfusion imaging were consistent with brain death. Discussion This case illustrates that neurogenic stunned myocardium can present as cardiogenic shock, especially in patients with preexisting HFrEF. Prompt recognition and supportive management, including vasopressors, inotropes, or mechanical support, are crucial while evaluating reversible causes. Coordinated multidisciplinary care is essential, especially when pheochromocytoma is a potential trigger. This abstract is funded by: None