Pathophysiology of Cardiac Tamponade: Vascular and Cardiac Pressure Responses1Since the systemic and pulmonary venous beds must generate sufficient pressure to fill both sides of the heart, cardiac filling is supported by a parallel rise in systemic and pulmonary venous pressures which, in tamponade, are determined primarily by pericardial rather than myocardial compliance. Secondarily, of course, cardiac chamber compliance is reduced by pericardial compression and this produces the immediate force progressively resisting filling. In response, blood volume expands (Fig 2). Indeed, part of the ability to tolerate increasing cardiac compression is the rate of venous volume expansion. This, like pericardial stretch, requires time since it occurs by fluid transfer from the tissues to the venous side of the cardiovascular system. In contrast, in rapid, hemorrhagic tamponade, eg, due to cardiac wounds, venous volume expansion is virtually inoperative. Finally, venous filling may be augmented at very low ventricular volumes by diastolic suction, the relative effectiveness of which is undetermined. buy zyrtec online

Eventually, diastolic pressure in both ventricles and the pulmonary artery equilibrate with mean right and left atrial pressures at approximately intra-pericardial pressure. Conventionally, “equilibrate” represents diastolic pressures differing by no more than 5 mm Hg. Clinically, this corresponds to “florid” tamponade, when most patients will have frank exaggeration of the respiratory fluctuation in arterial BP—pulsus paradoxus—conventionally a 10 mm Hg or greater inspiratory fall that reflects the exaggerated respiratory pressure and volume reciprocation between the right and left heart chambers. For example, during peak inspiration, left heart filling is minimal and its pressure differences from pericardial pressure are least, nil or even negative, with reversed, ie, negative, transmural pressure. In such severe tamponade, the mitral valve may only open when atrial systole occurs during expiration. With inspiration, pulmonary wedge pressure falls below pericardial pressure. In contrast, right atrial pressure, which tends to “track” pericardial pressure (Fig 3) also falls, but not below pericardial pressure, enhancing inspiratory filling of the right ventricle.

Figure 3. Cardiac tamponade. Simultaneous right atrial (RA) and pericardial (Pm) pressure curves; Insp =beginning of inspiration. Patient with atrial flutter. Top: prepericardicentesis: high atrial pressure (mean, 25 mm Ilg) tracks high pericardial pressure; in early inspiration, pericardial pressure transiently falls below RA pressure. Note QRS electric alternation and atrial flutter. Bottom-, postpericardicentesis: mean RA pressure has fallen to 15 mm Hg with little respiratory variation (pericardial restraint removed). Pericardial pressure has fallen below RA pressure with marked respiratory fluctuations: expiratory level, 8 mm Hg; inspiratory level, approximately zero. Note disappearance of electric alternation; flutter waves on atrial pressure tracing and ECG.

Figure 3. Cardiac tamponade. Simultaneous right atrial (RA) and pericardial (Pm) pressure curves; Insp =beginning of inspiration. Patient with atrial flutter. Top: prepericardicentesis: high atrial pressure (mean, 25 mm Ilg) tracks high pericardial pressure; in early inspiration, pericardial pressure transiently falls below RA pressure. Note QRS electric alternation and atrial flutter. Bottom-, postpericardicentesis: mean RA pressure has fallen to 15 mm Hg with little respiratory variation (pericardial restraint removed). Pericardial pressure has fallen below RA pressure with marked respiratory fluctuations: expiratory level, 8 mm Hg; inspiratory level, approximately zero. Note disappearance of electric alternation; flutter waves on atrial pressure tracing and ECG.