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.