Cardiac Tamponade - Pathophysiology

on 24.8.07 with 0 comments



The pericardium, which is the membrane surrounding the heart, is composed of 2 layers. The parietal pericardium is the outer fibrous layer; the visceral pericardium is the inner serous layer. The pericardial space normally contains 20-50 mL of fluid. Pericardial effusions can be serous, serosanguineous, hemorrhagic, or chylous.

Reddy et al describe 3 phases of hemodynamic changes in tamponade.

  • Phase I: The accumulation of pericardial fluid causes increased stiffness of the ventricle, requiring a higher filling pressure. During this phase, the left and right ventricular filling pressures are higher than the intrapericardial pressure.

  • Phase II: With further fluid accumulation, the pericardial pressure increases above the ventricular filling pressure, resulting in reduced cardiac output.

  • Phase III: A further decrease in cardiac output occurs, which is due to equilibration of pericardial and left ventricular (LV) filling pressures.

The underlying pathophysiologic process for the development of tamponade is markedly diminished diastolic filling because transmural distending pressures are insufficient to overcome the increased intrapericardial pressures.

Systemic venous return is also altered during tamponade. Because the heart is compressed throughout the cardiac cycle due to the increased intrapericardial pressure, systemic venous return is impaired and right atrial collapse occurs. During inspiration, intrapericardial and right atrial pressures decrease because of negative intrathoracic pressure. This results in augmented systemic venous return to right-sided chambers and a marked increase in the right ventricular volume. Because the pulmonary vascular bed is a vast and compliant circuit, blood preferentially accumulates in the venous circulation, at the expense of LV filling. This results in a reduced cardiac output.

The amount of pericardial fluid needed to impair the diastolic filling of the heart depends on the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output, whereas 1000 mL of fluid may accumulate over a longer period without any significant effect on diastolic filling of the heart. This is due to adaptive stretching of the pericardium over time. A more compliant pericardium can allow considerable fluid accumulation over a longer period without hemodynamic insult.

Category: Medicine Notes

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