Case Series:
Case 1: A 48-year-old Hispanic male with a past medical history of type 2 diabetes mellitus, morbid obesity (BMI 39.5 kg/m²), with normal cardiac function and a known small pericardial effusion (not amenable to pericardiocentesis), presented with complaints of dyspnea and fatigue for one month, and acute deterioration for the past 24 hours. Nasopharyngeal swab was positive for COVID-19, serum troponins were within normal range, and arterial blood gas (ABG) analysis showed a pH of 7.26, partial pressure of carbon dioxide (pCO2) of 83 mmHg, and partial pressure of oxygen (pO2) of 187 mmHg. Chest x-ray demonstrated clear lung fields and a large cardiac silhouette. Echocardiogram showed a moderate-to-large pericardial effusion with tamponade physiology (Figure 1).
He underwent emergent percutaneous drainage of 1,500 mL of clear pericardial fluid using a pigtail catheter. On post-operative day (POD) 8, the patient developed acute cardiovascular decompensation. An echocardiogram showed a large pericardial fluid collection with signs of obstructive shock (Figure 2). He underwent a sub-xyphoid pericardial drainage of 900 mL of sanguineous fluid. Postoperative course was unremarkable, and patient was discharged 10 days after the second procedure in stable condition with drop in his inflammatory markers after Pericardiocentesis (Table 2).
Case 2: A 56-year-old Hispanic overweight (BMI of 27.1 kg/m²) male with no significant medical history presented with a one-week history of cough, chest pain, fever and chills. Laboratory investigations showed a serum troponin-I level of 1.2 ng/dl and nasopharyngeal swab confirmed COVID-19 infection. Over the next few hours, the patient developed progressive hypotension. Echocardiogram showed a large pericardial effusion with tamponade physiology (No images recorded in system, as it was an emergent bedside ECHO), and a left ventricular ejection fraction of 20%. He underwent emergent sub-xyphoid drainage of 400 mL of serous pericardial fluid. On POD0, the patient experienced cardio-pulmonary arrest and expired. Inflammatory markers can be seen in (Table 2)
Case 3: A 55-year-old African American male with a past medical history of hypertension and obesity (BMI of 30.5 kg/m²) presented with two weeks of dyspnea, productive cough, myalgias, headaches, fatigue, fever, and chills. Upon initial evaluation, patient was placed on 15 liters/min of oxygen via a non-rebreather mask for hypoxia. ABG showed a pH of 7.46, pCO2 of 32 mmHg, and pO2 of 67 mmHg. Serum troponin-I was within normal range, serum creatinine was 2.3 mg/d, and nasopharyngeal swab was positive for COVID-19. CXR showed bilateral lung opacities and a mildly enlarged cardiac silhouette. On hospital day two, the patient required endotracheal intubation and mechanical ventilation for progressive hypoxia, and subsequently, on hospital day 5, required Veno-Venous Extra Corporeal Membrane Oxygenation (ECMO). Laboratory investigations during hospitalization are seen in (Table 3). On hospital day 7, the patient developed pulseless electrical activity (PEA) cardiac arrest. A bedside echocardiogram revealed a large pericardial effusion with tamponade physiology, and 800 mL of sanguineous fluid was drained percutaneously, with return of spontaneous circulation. On hospital day 8, due to increasing vasopressor and inotropic requirements, a repeat echocardiogram was performed which demonstrated biventricular failure, likely from COVID-related myocarditis (Figure 3). Further aggressive management was deemed futile, and all interventions were withdrawn per family’s wishes; the patient underwent ECMO decannulation and was pronounced dead.