A.4. What is the pathophysiology of acute pericardial tamponade?
Answer:
Acute pericardial tamponade represents a rapid increase in intrapericardial pressure exceeding intracardiac pressures, resulting in impaired venous return and diastolic filling. If pericardial pressure is high enough, cardiac chamber collapse can occur, leading to decreased cardiac output and systemic hypoperfusion, which can result in cardiopulmonary arrest. Physical exam findings associated with pericardial tamponade include Beck triad (hypotension, distended neck veins, and muffled heart sounds), tachycardia, and pulsus paradoxus (decrease in systolic blood pressure [SBP] >10 mm Hg during inspiration). Some of these signs can be easily missed in a hypovolemic trauma patient who could be in a low-pressure tamponade state with low central venous pressure. Diagnosis of cardiac tamponade can be aided with transthoracic echocardiography, demonstrating key findings including the presence of a pericardial effusion, dilated inferior vena cava (IVC), right-sided chamber collapse during diastole, exaggerated respirophasic transvalvular flow velocities (pulse wave pulsus paradoxus), respirophasic septal shift, and a swinging heart. The hemodynamic effects of pericardial effusion depend on the change in ventricular diastolic function in response to increased intracardiac pressure and not the size of the effusion per se. If a diagnosis of acute pericardial tamponade is made and the patient is unstable, immediate evacuation of the pericardium by pericardiocentesis or pericardial window is required (see Chapter 12: Cardiac Tamponade).