Cardiac tamponade

With cardiac tamponade, a rapid, unchecked rise in intrapericardial pressure impairs diastolic filling of the heart. The rise in pressure usually results from blood or fluid accumulation in the pericardial sac.
If fluid accumulates rapidly, the condition can be fatal, thus necessitating emergency lifesaving measures. Slow accumulation and rise in pressure, as with pericardial effusion associated with cancer, may not produce immediate symptoms because the fibrous wall of the pericardial sac can gradually stretch to accommodate 1 to 2 L of fluid.
Causes
Increased intrapericardial pressure and cardiac tamponade may be idiopathic (Dressler’s syndrome) or may result from any of the following conditions:
effusion (in patients with cancer, a bacterial infection, tuberculosis or, rarely, acute rheumatic fever)
hemorrhage from trauma (such as gunshot or stab wounds of the chest and perforation by a catheter during cardiac or central venous catheterization or after cardiac surgery)
hemorrhage from nontraumatic causes (such as rupture of the heart or great vessels or anticoagulant therapy in a patient with pericarditis)
acute myocardial infarction (MI)
uremia.
Signs and symptoms
Cardiac tamponade typically produces increased venous pressure with neck vein distention, reduced arterial blood pressure, muffled heart sounds on auscultation, and paradoxical pulse (an abnormal inspiratory drop in systemic blood pressure greater than 15 mm Hg). These classic signs represent failure of physiologic compensatory mechanisms to override the effects of rapidly rising pericardial pressure, which limits diastolic filling of the ventricles and reduces stroke volume to a critically low level.

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