Cardiac Tamponade

Overview

Cardiac Tamponade results from excessive fluid within the pericardial sac to a degree sufficient to place pressure on the heart and thus interfere with ventricular diastolic filling. Cardiac tamponade can be a serious complication of a variety of etiologies and can result in life-threatening hemodynamic derangements if not treated promptly.

Etiologies

Any of the etiologies mentioned in pericardial effusion can result in cardiac tamponade if fluid accumulation occurs rapidly. acute pericarditis caused by uremia, metastasis, or Viruses such as Group B Coxsackie Viruses are the most common etiologies. However, direct hemorrhage of high pressure blood into the pericardial sac, known as hemopericardium, can also be a source of tamponade. This can occur due to post-Myocardial Infarction left ventricular wall rupture, aortic dissection, or during traumatic chest wounds.

Pathophysiology

The pericardium is a relatively stiff sac, similar to a plastic grocery bag, surrounding the heart. Consequently, the compliance curve of the pericardial sac follows two patterns: At low volumes the sac has a high compliance and can accommodate fluid volume without much increase in pressure; however, at a certain threshold the compliance suddenly decreases and even small additions of fluid volume cause large increases in intra-pericardial pressure. Again, this is similar to a plastic shopping bag which can easily accommodate fluid volumes until it becomes tense, at which point addition of further fluid requires enormous pressures. Cardiac tamponade then, occurs when fluid volume is added above that threshold, resulting in large increases in fluid pressure surrounding the heart.

Fluid flow into the ventricles during diastole depends on the pressure gradient between the intra-atrial pressure and the intra-pericardial pressure pushing against the outer ventricular wall. In normal individuals, intra-pericardial pressure is nearly zero, allowing even low diastolic atrial pressures to push large volumes of blood into the ventricle. However, if intra-pericardial pressures increase significantly, then large increases in atrial pressures are required to achieve sufficient diastolic ventricular filling and maintain cardiac output. Consequently, the primary pathophysiological sequelae of cardiac tamponade are significant increases in left and right atrial pressures.
These increased atrial pressures are transmitted retrogradely into the pulmonary circulation and systemic veins, resulting in significant clinical consequences described below. As intra-pericardial pressure increases with significant tamponade, then even these compensatory increases in intra-atrial pressure are frequently not sufficient to maintain cardiac output and hypotension develops

Clinical Consequences

The volume of fluid required to generate tamponade varies depending on the rate at which fluid accumulates. Given rapid accumulation, volumes of 200-300 mL may result in symptomology, whereas slowly developing accumulations may require more than 2L of fluid due to progressive remodeling of the pericadial sac. Whatever the case, cardiac tamponade is heralded by signs and symptomology akin to bi-ventricular Heart Failure due to the reduced capacity of the heart to generate cardiac output along with increased atrial pressures. When fluid accumulates rapidly, symptomology associated with reduced cardiac output is most prominent whereas in cases of slow fluid accumulation symptomology of heart failure is most prominent.

Reduced Cardiac Output: Results in hypotension and reactive tachycardia
Left Heart Failure: Results in pulmonary edema and resultant dyspnea
Right Heart Failure: Results in prominent increases in jugular venous pressure along with peripheral edema, ascites, and hepatomegaly

The most prominent sign of cardiac tamponade is "Pulsus Paradoxus" referring to an abnormal decline (<10 mm Hg) in the systemic arterial pressure during inspiration. When tamponade is severe the peripheral pulses may completely disappear upon inspiration. Inspiration reduces intra-thoracic pressure resulting in increased filling of the right ventricle and thus higher right ventricular volumes. Because of the limited space in the pericardial sac during contexts of tamponade, the increased right ventricular volume comes at the cost of left ventricular filling. Thus, inspiration reduces left ventricular volume and cardiac output, resulting in reductions in systemic arterial pressure. In addition to Pulsus Paradoxus, patients with cardiac tamponade display fainter heart sounds due to the auscultory insulation by pericardial fluid.

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