Value of Volume Expansion in Cardiac Tamponade
Value of Volume Expansion in Cardiac Tamponade
Abstract & Commentary
By Michael H. Crawford, MD Professor of medicine, Chief of Clinical Cardiology, University of California, San Francisco Dr. Crawford is on the speaker's bureau for Pfizer. This article originally appeared in the May 2008 issue of Clinical Cardiology Alert. It was peer reviewed by Rakesh Mishra, MD, FACC. Dr. Mishra is Assistant Professor of Medicine, Weill Medical College, Cornell University; Assistant Attending Physician, NewYork-Presbyterian Hospital. Dr. Crawford serves on the speaker's bureau for Pfizer; he reports no financial relationships relevant to this field of study.
Source: Sagristà-Sauleda J, et al. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation. 2008;117:1545-1549.
Intravascular volume expansion has long been advised as an effective temporizing technique for patients with cardiac tamponade prior to drainage of the fluid, but there is little data supporting this practice. Thus, Sagrista-Sauleda and colleagues from Spain studied 49 patients with large pericardial effusions who were referred to the catheterization laboratory for drainage and who met hemodynamic criteria for cardiac tamponade (equalization of pericardial and right atrial pressure ± 2mmHg). Patients were excluded who were on hemodialysis, had significant valve disease, evidence of pericardial constriction, left ventricular dysfunction, pulmonary hypertension, or hyperacute cardiac tamponade due to aortic dissection or cardiac rupture. The patients ranged in age from 23-83 years, and 57% had physical signs of tamponade. Hypotension (systolic BP < 100) was noted in 20%. All were given 500 mL of normal saline over 10 minutes. Hemodynamics were repeated then and after pericardiocentesis. Volume expansion increased mean arterial pressure (from 88 to 94 mmHg, P < .003) and mean cardiac index (from 2.46 to 2.64, P = 0.13); however, cardiac index increased by 10% in 47%, was unchanged in 22%, and decreased in 31%. An increase in cardiac index was predicted by a low cardiac index and hypotension, but not with any other physical, hemodynamic, or echocardiographic findings. Also, volume expansion increased right atrial pressure (from 10-13 mmHg) and left ventricular end-diastolic pressure (from 14-19 mmHg) both P < .001. No clinical adverse effects of volume expansion were noted. Sagrista-Sauleda et al concluded that about half of patients with cardiac tamponade given volume expansion will increase their cardiac output, and this response is predicted by hypotension and a low cardiac index.
Commentary
In many ways, these results make sense. With the heart tamponaded, how could much more volume get into it? Probably only if part of the patients problem is hypovolemia. Those in this study, with low cardiac indices and hypotension, were probably hypovolemic. In the rest of the patients, volume did little except raise intracardiac pressures. With normovolemia, what little fluid gets into the cardiac chambers significantly increases diastolic pressures because the chambers are on the steep portion of a pressure volume curve due to the resistive force of the increased pericardial pressure. In this study, only 500 mL of saline was administered, and no adverse effects were noted, except that cardiac index fell in 31%. However, one can imagine a situation where more fluid is given and pulmonary edema ensues. Thus, fluids should only be given to hypotensive cardiac tamponade patients who cannot be rapidly drained.
So another medical myth bites the dust. Most critical care physicians believe fluids are indicated as a first step in almost all cases of hypotension. This would apply to cardiac tamponade, but not hypotension, due to right ventricular infarction. In this situation, the RV is on a steep pressure volume curve due to the infarction, and fluids do little unless hypovolemia is present. These patients usually require pressors to increase RV output. So the common denominator of a beneficial response to fluids is the presence of hypovolemia. Low blood pressure may be a sign of hypovolemia, but not always. Elevated jugular veins are usually a sign of adequate or high filling pressures and might be a double check in hypotensive patients. Most patients with hemodynamically significant RV infarct have elevated jugular venous pressure and don't respond to fluids. Whether this rule would apply in cardiac tamponade is unknown. In this study, only 43% had elevated jugular veins on physical examinations, but we don't know if the others were among the 47% of patients who responded to fluids. Right atrial pressure was lower in those who responded to fluids, but this was not statistically significant.
Another consideration is low pressure cardiac tamponade where the pericardial pressure is < 7mmHg with near equal right atrial pressures. In this study, these patients did not consistently respond to fluids. Thus, hypotension appears to be the best guide to which cardiac tamponade patients would benefit from a modest fluid bolus if pericardial drainage is delayed.
Intravascular volume expansion has long been advised as an effective temporizing technique for patients with cardiac tamponade prior to drainage of the fluid, but there is little data supporting this practice.Subscribe Now for Access
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