EXPLANATION


Cardiac tamponade is both a clinical diagnosis based on hypotension, tachycardia, and jugular venous distension and one based on echocardiographic findings. The decision to perform a pericardiocentesis may be assisted with echocardiography in determining the severity of tamponade and the potential for cardiovascular compromise during pericardiocentesis. Due to the fixed volume of the pericardial space, changes in intrapericardial pressure are transmitted to the cardiac chambers and the major systemic veins leading to core findings on echocardiogram including a pericardial effusion, diastolic right ventricle (RV) collapse, systolic right atrium (RA) collapse, plethoric IVC with minimal respiratory variation, and exaggerated respiratory changes in mitral valve (MV) and tricuspid valve (TV) inflow velocities.


Collapse of the RA is seen at early ventricular systole when the RA is relaxed with low blood volume. Brief RA collapse can be seen without tamponade, but the presence of this sign for more than one third of the cardiac cycle is more specific for tamponade. The sensitivity of RA collapse during ventricular systole is higher ranging from 50% in early tamponade to 100% with worsening tamponade physiology.


Collapse of the right ventricle (RV) is seen during early diastole when RV pressure is at its lowest. Diastolic collapse of the RV is highly specific with lower sensitivity for cardiac tamponade. It indicates very high intrapericardial pressures impeding RV filling. Longer duration of RV collapse correlates with increasing severity of tamponade.


Increased intrapericardial pressure impedes systemic venous return and this can be assessed by imaging the inferior vena cava (IVC) at its entrance into the RA. During normal spontaneous inspiration, the IVC diameter decreases by 50% or more. In tamponade physiology, the IVC remains distended (plethoric), and its diameter decreases by less than 50% during inspiration. However, even if there is minimal respiratory variation of IVC diameter with respiration, tamponade is very unlikely in the absence of chamber collapse.


Pulsus paradoxus is a normal physiologic phenomenon whereby the systolic blood pressure decreases by 10% or less during inspiration. Increased venous return to the RV during normal spontaneous inspiration occurs due to increasing negative intrathoracic pressure. This briefly shifts the ventricular septum into the left ventricle resulting in lower LV output and blood pressure. This phenomenon is exaggerated in tamponade physiology. These changes in systemic and pulmonary venous return can be characterized by measuring tricuspid and mitral inflow velocities and their changes with respiration. Under normal circumstances, these variations of inflow velocities during respiration do not exceed 20%-25%. However, during tamponade physiology, mitral inflow decreases by 25% or more and tricuspid inflow velocity increases by 40% or more. In the absence of any chamber collapse, these changes are not sensitive or specific for tamponade.


REFERENCES


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