Pathophysiology

Cardiac tamponade is a low-flow state due to increased pericardial pressure producing constriction of the cardiac chambers. It results from accumulation of blood or fluid in the pericardial sac that limits ventricular filling, stroke volume, and cardiac output. Hemopericardium and pericardial effusions are produced by a wide variety of traumatic and medical conditions (Table 1). The syndrome is uncommon, usually occurs insidiously, and carries a high mortality if unrecognized or inadequately treated. It may progress slowly with some degree of compensation, or develop rapidly into an acute tamponade syndrome with potentially lethal cardiogenic shock.

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Table 1 Causes of tamponade

The pericardial fluid confined by the relatively unyielding pericardial sac takes up space and exerts pressure. The intrapericardial pressure is transmitted across the cardiac wall to increase intracardiac pressures; this has proportionally greater effects on atrial and end-diastolic pressures than on ventricular pressures. The reduced filling pressure and the volume encroachment by the pericardial fluid limits ventricular filling and stroke volume. Thus reduced stroke volume is the major circulatory defect.

With penetrating cardiac injuries, blood that leaks into the free pericardial space is quickly decompressed into the pleural space or mediastinum. Pericardial blood accumulates and produces tamponade when bleeding is sufficiently rapid that its egress from the pericardial cavity is blocked by clots that form faster than they are lysed. A rather high incidence of clots (60 per cent) have been reported in penetrating cardiac wounds explored soon after injury; non-clotting pericardial blood, which is diagnostic of tamponade, is present because this blood has already clotted and spontaneously lysed.

Secondary compensatory circulatory responses include increases in central venous pressure, heart rate, and peripheral vascular resistance. The rise in peripheral resistance maintains blood pressure when cardiac output begins to fall. The increased heart rate improves cardiac output when the latter is limited by stroke volume, The adrenal stress response, which increases arterial blood pressure and peripheral resistance, will further increase central venous pressure, thereby augmenting the limited cardiac filling.

Decompensation occurs with progression of the disorder. When compensatory circulatory mechanisms maintaining hemodynamic stability fail, the adrenal stress response is exhausted and acidosis with low cardiac output further impairs the coronary circulation, leading to hypotension, shock, and death.

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