The American Heart Hospital Journal perfusion and, ultimately, shock.8 Classic clinical diagnosis


therefore often relies on ‘textbook’ clinical findings, such as the presence of pulsus paradoxus, elevated jugular veins with a rapid ‘x’ descent, and/or an attenuated or abolished ‘y’ (diastolic) descent, Ewart’s sign, Beck’s triad (a combination of jugular venous distension, hypotension, and muffled heart sounds), or electrical alternans on the electrocardiogram.1,2


However, with rapidly accumulating


pericardial effusions such as occur with spontaneous left ventricular rupture, time is crucial and pathognomonic signs as well as symptoms may understandably be overlooked or even masked.


in 1979. It is a poorly characterized syndrome in which the typical manifestations of CT such as jugular venous distention or pulsus paradoxus are absent.6


Low-pressure CT was first described clinically by Antman et al.3


As such, not


only does it often predispose to a diagnostic dilemma, but it could perhaps also account for both the low reported prevalence and the limited available clinical information to guide diagnosis. In a retrospective series of 1,429 patients with pericarditis, of whom 279 had undergone combined pericardiocentesis and cardiac catheterization between 1986 and 2004, Sagristà-Sauleda et al.6


found that


only 29 patients had cardiac catheterization-based criteria of low-pressure CT (intrapericardial pressure <7mmHg pre-pericardiocentesis and right atrial pressure <4mmHg after intrapericardial pressure had been lowered to near 0mmHg post-pericardiocentesis). The authors noted that these patients less frequently demonstrated clinical signs of CT, although the rate of constitutional symptoms, use of diuretic medications, and echocardiographic findings of CT were somewhat similar to those seen in patients with classic CT.


Although infrequently cited, low-pressure CT has been well described in experimental situations.6,9


By altering


intravascular volume before CT to a hypovolemic, euvolemic, or hypervolemic state using saline solution and dextran infusion or hemorrhaging to achieve the prescribed mean right atrial blood pressure, Klopfenstein et


1. Spodick DH, Acute cardiac tamponade, N Engl J Med, 2003;349:684–90.


2. Braunwald E, Pericardial disease. In: Fauci AS, Braunwald E, Isselbacker KJ, et al. (eds), Harrison’s principles of internal medicine (13th ed.), New York: McGraw-Hill, 1998:1334–41.


3. Antman EM, Cargill V, Grossman W, Low-pressure cardiac tamponade, Ann Intern Med, 1979;91:403–6.


4. Boltwood CM, Lee PY, Tei C, Shah PM, Low pressure cardiac tamponade, N Engl J Med, 1983;309:667–8.


5. Labib SB, Udelson JE, Pandian NG, Echocardiography in low pressure cardiac tamponade, Am J Cardiol, 1989;63:1156–7. 6. Sagrista-Sauleda J, Angel J, Sambola A, et al., Low-pressure


Winter 2010 al.9


Case Report


studied five unanesthetized, chronically instrumented dogs using 2D echocardiography during 41 episodes of induced CT. These authors successfully demonstrated that, compared with the euvolemic state, the onset of right ventricular diastolic collapse in volume contraction occurred at a lower intrapericardial pressure (with lower aortic blood pressure and cardiac output). Therefore, while some clinical findings could certainly be suggestive, diagnosing low-pressure CT, unlike its acute counterpart, could remain challenging.


The clinical presentation of our patient did not support that of an acute myocardial infarction. There were no changes on the electrocardiogram to suggest this and creatine kinase was normal, although, disproportionately, troponin was elevated. The transthoracic echocardiogram confirmed the absence of any wall-motion abnormalities and did not reveal thinned or aneurysmal myocardial segments to suggest previous myocardial injury or scar. Thus, her hypotension was perhaps less likely to have been caused by a myocardial infarction that was large, with left ventricular rupture, or at least considerable enough to cause the symptom. However, it is unclear if our patient could have later suffered a myocardial infarction during resuscitation or when subject to emergent surgery. In any case, her overall compromised state may certainly have made her most susceptible throughout the course of her presentation. Indeed, intrapericardial pressures were not determined in our patient to confirm low-pressure CT. However, owing to the rapid progression of the sequence of events that ultimately led to her death, such measurements were neither conducive nor appropriate. Moreover, a precise definition to describe low-pressure CT remains undetermined. As such, this patient’s potential diagnosis could perhaps have been missed or overlooked clinically, despite the small pericardial effusion, if she had not progressed to classic CT. Clinicians should therefore always be aware of the varied spectrum of presentations that may be associated with CT to be better prepared for similar, atypical as well as unexpected challenges. n


cardiac tamponade: clinical and hemodynamic profile, Circulation, 2006;114:945–52.


7. Spodick DH, Congenital abnormalities of the pericardium. in: Spodick DH (ed.), The pericardium: a comprehensive textbook, New York: Marcel Dekker, 1997:65–70.


8. Reddy PS, Curtiss EI, O’Toole JD, Shaver JA, Cardiac tamponade: Hemodynamic observation in man, Circulation, 1978;58:265–72.


9. Klopfenstein HS, Cogswell TL, Bernarth GA, et al., Alterations in intravascular volume affect the relation between right ventricular diastolic collapse and the hemodynamic severity of cardiac tamponade, J Am Coll Cardiol, 1985;6:1057–63.


Progression of Low-pressure to Acute Classic Cardiac Tamponade 135


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