Cardiac tamponade as a cause of cardiac arrest: the role of point-of-care ultrasound in prehospital care

Cardiac tamponade is most commonly caused by pericarditis, acute aortic dissection, or cardiac trauma / rupture.^1,2 Point-of-care ultrasound (POCUS) enables rapid diagnosis and treatment of cardiac tamponade, even in a prehospital setting.^2,3

An emergency medical team was dispatched after a 65-year-old man was reported to be experiencing vomiting, diarrhea, pallor, and cyanosis since morning. Upon arrival, the team found the patient sitting on the floor, leaning against the bed, and unconscious. The paramedics diagnosed cardiac arrest with pulseless electrical activity (PEA) and immediately began cardiopulmonary resuscitation (CPR). They performed manual chest compressions, endotracheal intubation, and mechanical ventilation with end-tidal carbon dioxide values of 17–22 mm Hg. A total of 6 mg of epinephrine and 1000 ml of multielectrolyte fluid were administered.

The patient had a history of anterior myocardial infarction (MI) and ischemic cardiomyopathy, with left ventricular ejection fraction of 33%. He had undergone percutaneous coronary angioplasty with drug-eluting stent implantation in the left descending artery 7 months prior. Furthermore, he suffered from alcohol use disorder, and had stopped taking antiplatelet drugs despite medical recommendations.

The paramedics performed POCUS using a handheld machine while taking 10-second pauses for pulse checks during CPR. They identified echocardiographic features of cardiac tamponade (Figure 1A), including significant pericardial effusion, systolic collapse of the right atrium, diastolic collapse of the right ventricular free wall, and a plethoric inferior vena cava. Imaging of the ascending aorta and aortic arch (Figure 1B and 1C) ruled out aortic dissection as the cause of tamponade.

The decision was made to transport the patient to the nearest emergency department while continuing CPR. Pericardiocentesis was performed in the emergency room, during which 90 ml of blood were removed. Four minutes after relieving the pericardial tamponade, return of spontaneous circulation (ROSC) occurred. Follow-up POCUS showed persistent pericardial effusion with increasing echogenicity (Figure 1D). Twelve-lead electrocardiography performed post-ROSC identified ST-elevation in leads I and aVL (Figure 1E). Arterial gases showed respiratory acidosis with a pH of 6.75–7.04. Other laboratory test results indicated myocardial ischemia with high troponin I levels (16 164 pg/l; reference range [RR] <⁠34.2 pg/l), as well as elevated aspartate aminotransferase, 5585.6 U/l (RR, 10–49 U/l) and alanine transaminase 4558.5 U/l (RR, 8–46 U/l) levels. Despite being treated for severe cardiogenic shock, the patient experienced cardiac arrest again 3 hours later with PEA and ineffective CPR, after which he died.

The resuscitation algorithm recommends using POCUS to diagnose potentially reversible causes of cardiac arrest in patients with nonshockable rhythms.⁴ This case involved cardiac tamponade caused by blood accumulation, likely due to postmyocardial free wall rupture (FWR). FWR is a fatal complication of acute MI, accounting for 0.01% of the cases, with an in-hospital mortality rate of 80%. Typical presentations include cardiac tamponade and sudden death before a diagnosis is made.⁵ In this case, paramedic-performed POCUS enabled the diagnosis of cardiac tamponade and ruled out aortic dissection, thereby guiding further management. It illustrates the essential role of POCUS in prehospital settings and underscores the importance of proper training in its use.