An 80-year-old man with paroxysmal atrial fibrillation and symptomatic bradycardia underwent successful pacemaker placement as an outpatient. The patient was restarted on his warfarin therapy and returned home with no complaints.
A week later, the patient developed new diffuse chest discomfort that progressed over the ensuing 24 hours to include associated dyspnea and nausea. He presented to the emergency department (ED) for evaluation where he was noted to be afebrile with a blood pressure of 113/66, heart rate of 95, and an oxygen saturation of 99% on room air. On physical examination, he appeared comfortable and in no distress. His cardiac exam was notable only for flat neck veins, an irregularly irregular rhythm, a well-healed pacer site, and no peripheral edema. Laboratory studies revealed a stable hemoglobin level, a negative troponin, and an INR of 2.6 (within the therapeutic range), but a slightly elevated creatinine and a new transaminitis (elevated liver tests) compared to a week ago. An electrocardiogram showed atrial fibrillation but no evidence of ischemia. Imaging studies included a chest x-ray, which was normal, and a computed tomography (CT) scan of the abdomen, which revealed a pericardial effusion but no hepatobiliary pathology.
The ED physician discussed the case and CT findings with the on-call cardiologist who recommended admission but no need for an urgent echocardiogram given the normal vital signs and the patient's clinical stability. The following day, the patient's echocardiogram confirmed a large pericardial effusion "without tamponade" physiology. Providers continued to remark about the patient's clinical stability based on vital signs and appearance. Later that day, the patient became acutely hypotensive, developed ventricular tachycardia and pulseless electrical activity, and required emergent resuscitative measures, including large drainage of a pericardial effusion to relieve his cardiac tamponade. While surviving the emergent resuscitation, the patient ultimately suffered additional complications and passed away after a prolonged hospital course.
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Figure. Normal cardiac anatomy with a progression from a moderate pericardial effusion to one with tamponade physiology due to ventricular collapse.
(Illustration © 2011 by Chris Gralapp.)