Clinically significant cardiac compression by pericardial fluids depends on three interrelated conditions. The pericardial contents must do the following: (1) fill the relatively small pericardial reserve volume (Fig 1)—the volume which, added to the normal 15 to 35 mL of pericardial fluid, will just distend the parietal pericardium by filling its numerous recesses and sinuses; (2) thereafter increase at a rate exceeding the stretch rate of the parietal pericardium; and (3) exceed the rate at which venous blood volume expands to support the small normal pressure gradient for right heart filling. Because at any instant the pericardium is relatively inextensible, the heart and the pericardial contents compete continuously for the relatively fixed intrapericardial volume. Therefore, unless the abnormal pericardial contents increase veiy slowly, permitting progressive “give” of the parietal pericardium, their increase is at the expense of cardiac chamber volume. The key operational defect is reduced cardiac inflow due to compression of all cardiac chambers, progressively reducing their diastolic compliance and ultimately equalizing the mean diastolic pressures in each of them.
Pericardial stiffness determines the fluid increments causing tamponade. Despite elastic tissue and initially wavy collagen, the initial elements of pericardial relaxation, even the normal parietal pericardium is relatively noncompliant so that after the initial give, the pericardial pressure-volume curve angulates and becomes vertical (Fig 1). Thus, patients with critical tamponade function on the steep vertical portion of the pericardial pressure-volume curve with progressively smaller fluid increments provoking progressively large pressure increments. If unchecked by compensatory mechanisms (Fig 2) or effective treatment, the heart becomes critically compressed, because cardiac filling, ie, maximum diastolic volume, competes unsuccessfully with pathologic pericardial filling for the relatively fixed space within the parietal pericardium. This results in progressive reduction in cardiac chamber volumes. diabetes amaryl
Figure 1. Dimensionless schematic pericardial pressure-volume (and also stress-strain) curve also indicating the pericardial reserve volume (see text). Dimensions omitted because of wide individual variations in principal determinants of the curve: rate of fluid increase and parietal pericardial compliance. From Spodick DH. In: Spodick DH, ed. The pericardium: a comprehensive textbook. New York: Dekker, 1997; 19 (with permission).
Figure 2. Cardiac tamponade: relationships among major hemodynamic events and major compensatory mechanisms (see text). Simple arrows = tamponade sequences; pointed arrowheads = stimulatory compensatory actions; blunt arrowheads — oppositional compensatory actions. Modified from Spodick DH. In: Spodick DH, ed. The pericardium: a comprehensive textbook. New York: Dekker, 1997; 182 (with permission).
Category: Heart disease
Tags: cardiac compression, pericardium, tamponade physiology