Am Heart Hosp J. 2010;8(2):133–135


Lozenge Reference


Case Report


Progression of Low-pressure to Acute Classic Cardiac Tamponade—A Diagnostic Dilemma in the Setting of Spontaneous Left Ventricular Rupture


Vignendra Ariyarajah, MD,1 Michael Raabe, MD, FRCPC,3 Davinder S Jassal, MD, FRCPC1,2,4


Farrukh Hussain, MD, FRCPC,1 Alan Menkis, MD, FRCPC3


Robert McGregor, MD,2 and


Cardiac tamponade (CT) is a pathophysiologic continuum where hemodynamic embarrassment occurs as a result of progressive, decreased venous return that impairs diastolic ventricular filling, which in turn, when uncorrected, severely compromises cardiac output. While CT is classically associated with high intrapericardial pressures due to rapidly accumulating large pericardial effusions, low-pressure CT is a recognized entity in which a comparatively low intrapericardial pressure could result in cardiac chamber compression and subsequent cardiovascular collapse. In this article, we highlight a previously unreported scenario of rapidly re-accumulating, acute CT in the setting of left ventricular rupture in a patient who had presumably presented with low-pressure CT due to hemoperiardium.


ardiac tamponade (CT) is a pathophysiologic continuum where hemodynamic embarrassment occurs as a result of progressive, decreased venous return that impairs diastolic ventricular filling, which in turn, when uncorrected, severely compromises cardiac output.1,2


C


The overall risk for death depends on the speed of diagnosis, treatment, volume, and rate of fluid accumulation as well as the underlying pathologic process.1


While CT is classically associated with high intrapericardial pressures owing to rapidly accumulating large pericardial effusions, low-pressure CT is a recognized entity in which a comparatively low intrapericardial pressure could result in cardiac chamber compression and subsequent cardiovascular collapse.3–6


Our case highlights a


previously unreported scenario of rapidly re-accumulating, acute CT in the setting of left ventricular rupture in a patient who had presumably clinically presented with low-pressure CT due to hemopericardium.


Case


A 70-year-old physically active female with a history of paroxysmal supraventricular tachycardia on sotalol 80mg twice daily presented to the emergency room with a brief syncopal episode. Prior to experiencing syncope, she had felt slight dizziness while running on a treadmill. There was no associated pallor, cyanosis, tremors, or seizure-like activity. On regaining consciousness, she denied chest discomfort, dyspnea, palpitations, headache, leg pain, fever, or chills. She had, however, been concerned about mild to moderate epigastric discomfort for two days with some intermittent nausea. On physical examination, the patient was hypotensive with a systolic blood pressure of 60mmHg, and she had a heart rate of 60 beats per minute. Her jugular venous pressure and cardiorespiratory and abdominal examinations were unremarkable. An emergent computed tomographic scan of the abdomen ruled out an abdominal aortic aneurysmal leak or rupture. However,


• 1. Division of Cardiology, Department of Cardiac Sciences; 2. Department of Radiology; 3. Division of Cardiac Surgery, Department of Cardiac Sciences, St Boniface General Hospital, University of Manitoba; 4. Institute of Cardiovascular Sciences, St Boniface Research Center, University of Manitoba


• Correspondence: Davinder S Jassal, MD, FRCPC, FW DuVal Clinical Research Professorship, Bergen Cardiac Care Centre, Cardiology Division, Rm Y3010, Department of Cardiac Sciences, St Boniface General Hospital, 409 Tache Avenue, Winnipeg, Manitoba, Canada, R2H 2A6. E: djassal@sbgh.mb.ca


Winter 2010 Progression of Low-pressure to Acute Classic Cardiac Tamponade 133


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