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Ann Thorac Surg 1996;61:710-711
© 1996 The Society of Thoracic Surgeons
Departments of Cardiothoracic Surgery, Cardiology, and Thoracic Physiology, Karolinska Hospital, Stockholm, Sweden
Accepted for publication August 2, 1995.
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| Introduction |
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The patient was admitted to a neurology ward for observation. During the time of observation the blood pressure dropped twice to an unmeasurable level while the patient was straining, but was otherwise approximately 100 mm Hg systolic. The heart rate increased to 120 beats/min. Physical examination revealed rhales of the lungs and edema of the legs. The blood tests showed elevated liver enzyme levels. Ultrasonography of the liver and pancreas was performed and found to be normal. The patient was treated with fluids and intravenous diuretics. A roentgenogram of the chest 36 hours after admission showed signs of congestion and an enlarged heart. After 42 hours of observation the patient exhibited no focal neurologic signs but manifestations of cardiac failure despite aggressive treatment.
On arrival in the cardiac intensive care the patient had a systolic blood pressure of 110 mm Hg, sinus rhythm of 100 beats/min, and rhales of the lungs. To investigate the cause of biventricular failure in a patient without a history of cardiac failure we immediately performed transthoracic echocardiography, which revealed cardiac tamponade with the echogenic character of liquid and coagulated blood. An attempt to aspirate from the pericardium was unsuccessful. The aortography was normal. Out of fear of further compromising the patient's already precarious situation, we then took the patient to the operating room, where he was dressed and anesthetized before transesophageal echocardiography was performed. The systolic blood pressure was 125 mm Hg and the heart rate was 110 beats/min. The examination revealed a discontinuity of the left atrial wall (Fig 1
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Our case illustrates that tamponade of the heart is not immediately fatal in all cases. However, the importance of rapid diagnosis and treatment is stressed in all publications. With the aid of echocardiography the cardiac tamponade could have been discovered in the emergency room. The diagnosis of cardiac failure was based on signs of congestion on the chest film compunded with rhales and edema of the legs. Congestion of the systemic circulation was caused by the cardiac tamponade and reduced return of blood to the heart. Congestion of the pulmonary circulation could be a result of the tamponade of the left atrium created by a clot at the rupture site, which impeded the return of blood from the lungs.
Although uncommon, the material discussed demonstrates the possibility of cardiac rupture as a complication of external cardiac massage. More extensive use of echocardiography in the evaluation of sudden onset of heart failure or of the resuscitated patient by experienced physicians could be of great value.
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