What is the pathophysiology of cardiac tamponade?

What is the pathophysiology of cardiac tamponade?

The accumulation of pericardial fluid of virtually any etiology leads to cardiac tamponade when rising intra-pericardial pressure impedes atrial and ventricular filling. Rapid fluid accumulation of less than 200–250 mL in the pericardial space of an average adult will raise the central venous pressure by 10–12 cm H₂O. Increased impedance to ventricular filling results in a reduced stroke volume. The sympathetic response to rising intra-pericardial pressure leads to an increase in heart rate and constriction of the peripheral vasculature. Initially, when stroke volume is reduced and heart rate is increased, cardiac output can be maintained. With the further accumulation of peri-cardial fluid, rapid deterioration may ensue, owing to the fact that the parietal pericardium has a limited ability to stretch acutely. When the pericardial effusion is a chronic condition, the parietal pericardium can accumulate signif-icant amounts of fluid without significant rises in intra-pericardial pressures.

In order for venous return to reach the right ventricle, systemic venous pressure should be equal to or greater than intra-pericardial pressure. Since right ventricular pressure is lowest in diastole and right atrial pressure is lowest in systole, these chambers tend to collapse when intra-pericardial pressure exceeds the chamber pressure. Echocardiographic studies have illustrated these findings. Echocardiographic signs of cardiac tamponade include right ventricular diastolic collapse and right atrial late systolic collapse.

Cardiac tamponade is defined by elevation and equal-ization of all diastolic pressures within the heart. With spontaneous inspiration, blood enters the right atrium and right ventricle. This causes interventricular septal shift into the left ventricle causing a partially obliterated left ventricular cavity. The resultant reduction in left ven-tricular output and blood pressure upon inspiration is typical. When pericardial effusion makes the pericardium tense, the leftward shift of the interventricular septum is more pronounced and the reduction in blood pressure is excessive. When the systolic pressure decreases by 10 mmHg or greater, the term “pulsus paradoxus” is used.