B52-34 Beyond the S1q3t3: A Deadly Decompression in Pulmonary Hypertension

Abstract Introduction Acute right ventricular (RV) failure after pericardial drainage in chronic pulmonary hypertension (PH) is an underappreciated phenomenon. Limited case-based literature suggests that pericardial effusion may paradoxically support interventricular balance in the pressure-overloaded RV, with its removal precipitating collapse. The absence of standardized guidelines makes management of recurrent effusions challenging. We highlight fatal RV failure following pericardial decompression, emphasizing the need for pericardial effusion management in severe, chronic PH. Case Description A 57-year-old woman with COPD on home oxygen, HFpEF, prior PE on Eliquis, likely mixed PH, presented with chest pain and dyspnea. Evaluation revealed mild RV dilation with pericardial effusion demonstrating early tamponade physiology, which was thought to be the cause of her symptoms (Figure 1A). She underwent a subxiphoid window, draining 550 mL of serous fluid with a post-surgical transthoracic echocardiogram (TEE) revealing complete resolution of the pericardial effusion (Figure 1B). Over the next 48 hours, she developed altered mentation and profound metabolic acidosis, with a lactate of 10 mmol/L, necessitating vasopressor support. ​​Repeat EKG demonstrated an S1Q3T3 pattern indicative of acute RV strain, and transthoracic echocardiography showed a severely dilated, hypertrophied RV with reduced wall motion (Figure 1C, D), consistent with acute-on-chronic RV failure. Inotropic support with milrinone and afterload reduction using inhaled epoprostenol were initiated.The patient was taken for emergent right heart catheterization (RHC), which demonstrated severe pre-capillary PH with RA pressures 20/20/18 mmHg, RV 73/11/21 mmHg, PA 79/36/51 mmHg (PA sat 49%), PCWP 9 mmHg, PVR 10.1 Wood units, PAPI 2.1, and Fick cardiac output 4.17 L/min (CI 1.98 L/min/m²). These findings were consistent with acute right ventricular failure.The patient developed severe metabolic derangements with worsening cardiogenic shock. Although the presentation could mimic a new PE, CT angiography was precluded by hemodynamic instability, and the diagnosis was less likely given ongoing apixaban use. Findings were most consistent with acute-on-chronic right heart failure triggered by pericardial decompression. Despite aggressive medical management by ICU and cardiology teams, the patient remained critically ill and passed away. Conclusion This case underscores the paradoxical risk of pericardial decompression in chronic pulmonary hypertension, where relief of effusion can trigger acute-on-chronic RV failure and refractory shock. This case emphasizes the urgent need for standardized approaches to pericardial effusion management in severe, chronic PH, whether that be via gradual drainage or preemptive RV support strategies. This abstract is funded by: None