Abstract Body (Do not enter title and authors here): Introduction:
Cardiac tamponade typically results from pericardial fluid accumulation that impairs diastolic filling. Rarely, extracardiac structures can cause similar physiologic compromise. We report a case of extracardiac tamponade caused by a large paraesophageal hernia, emphasizing the need to maintain a broad differential diagnosis of causes in patients with hemodynamic instability.

Case:
An 87-year-old male with stage IV chronic kidney disease, prior stroke with expressive aphasia, paroxysmal atrial fibrillation, and poor functional status became hypoxic during an outpatient echocardiogram. On arrival to the ED, he was alert, oriented, and denied chest pain, palpitations, or dyspnea. Vitals showed BP 125/61 mmHg and oxygen saturation of 88% on room air, improved with 2L nasal cannula. ECG revealed a normal sinus rhythm with first-degree AV block. Chest CT showed a large paraesophageal hernia, fluid-filled esophagus, and bilateral pleural effusions (Figure 1). Transthoracic echocardiogram (TTE) showed preserved LV ejection fraction but significant diastolic compression of the inferior and inferolateral walls, with increased mitral and tricuspid inflow variability—findings consistent with tamponade physiology (Figure 2). Notably, no pericardial effusion was seen. He was deemed too high risk for any surgical or endoscopic intervention. A nasogastric (NG) tube was placed, and 500 cc of gastric contents were aspirated. Repeat TTE still showed tamponade physiology, prompting continued NG decompression for 48 hours. Follow-up imaging demonstrated resolution of LV compression and improvement in inflow variability (Figure 3).

Discussion:
While cardiac tamponade is most often due to pericardial effusion, external cardiac compression from adjacent thoracic structures can produce a similar pathophysiology. Large hernias can compress cardiac structures, particularly the posterior LV, leading to hemodynamic compromise. This case emphasizes the importance of considering extracardiac causes when tamponade features are present without pericardial effusion. Extracardiac tamponade should be suspected in patients with tamponade physiology and no effusion. Cross-sectional imaging and interdisciplinary management are essential. Conservative decompression may be effective in high-risk patients.