C52-20 Large Tension Pneumothorax Resulting in Stress Cardiomyopathy

Abstract Introduction Tension pneumothorax is a rare complication of pneumothoraces in which elevated pleural pressures can cause hemodynamic compromise. If not promptly recognized and treated, tension pneumothorax has high morbidity and mortality. Patients commonly present with acute dyspnea, pleuritic chest pain, and respiratory distress which can rapidly progress to cardiac arrest. Less common complications also can occur from tension pneumothorax; here, we present a case of large tension pneumothorax causing stress cardiomyopathy. Case A 76-year-old frail woman with no smoking history presented to the emergency department after several weeks of worsening dyspnea, tachypnea, and chest tightness. Vital signs were notable for hypoxemia, and the patient was placed on non-rebreather. Initial workup revealed evolving ST-segment elevations in V3-V5, high sensitivity troponins of 760 ng/L, and NT-pro BNP of 3,373 pg/mL. Chest x-ray revealed large left-sided pneumothorax associated with mediastinal shift to the right. STEMI-activation was initially called, but decision was made to first place chest tube for decompression, resulting in rapid improvement in the patient’s hypoxemia. Transthoracic echocardiogram (TTE) revealed newly reduced ejection fraction (EF) and left ventricular (LV) apical akinesis with an organized thrombus. Subsequent serial troponins eventually normalized. Cardiac MRI showed homogenous pericardial and subapical late gadolinium enhancement highly consistent with Takotsubo Syndrome. The patient underwent left heart catheterization (LHC) which showed no obstructive coronary disease. Repeat echocardiogram obtained three weeks later demonstrated complete recovery of LVEF, and subsequent EKGs also demonstrated resolution in prior ST elevations. She was discharged to rehabilitation in stable condition. Discussion Our patient’s case presented a diagnostic challenge as her EKG findings and troponin elevation suggested an acute myocardial injury. Her TTE with apical akinesis and well-organized LV thrombus could suggest an old infarct with persistent ST elevations. However, resolution of her EKG changes, cardiac biomarkers, and LV function after treating her pneumothorax, and absence of significant coronary disease on LHC point strongly towards stress cardiomyopathy. Stress cardiomyopathy after spontaneous pneumothorax has rarely been reported and is thought to be mediated by coronary vasospasm or catecholamine-mediated cardiotoxicity. While cardiac function often recovers, prompt recognition and treatment of the underlying stressor is important especially in patients with baseline debility and poor cardiopulmonary reserve who may not tolerate reduced cardiac output. Conclusion While acute coronary pathology can mimic stress cardiomyopathy and should not be missed, providers should recognize stress cardiomyopathy as a rare, but important complication of tension pneumothorax, highlighting the importance of prompt intervention. This abstract is funded by: None