Pathophysiology of Cardiac TamponadeCardiac tamponade is always life threatening and nearly always requires urgent and precise therapeutic intervention. It is perhaps unique in that appreciation of its pathophysiologic state is essential to precise diagnosis and rational treatment. Since the 19th centuiy, investigations in experimental animals provided a basic understanding that has been continually refined by recent investigators to the point where an integrated picture of its macrophysiologic condition emerges. This review covers the resultant concepts. Procedural details of investigations can be found in the references (thus, for example, the text omits the relative merits of catheters vs flat balloons for intrapericardial pressure determination). canadian family pharmacy online

General Considerations
Cardiac tamponade is defined as significant compression of the heart by accumulating pericardial contents, including effusion fluids, blood, clots, pus, and gas, singly or in combinations. “Significant compression” depends on whether tamponade is approached from a purely physiologic or clinical standpoint. Since tamponade is a pathophysiologic continuum, hearts can be said to be mildly to floridly tamponaded, the latter being a life-threatening emergency and the former a stage that can progress in that direction. “Life threatening” is a result of progressive, ultimately critical, reduction in cardiac output that can occur from as little as 150 mL of blood flooding the pericardium after a cardiac wound to much more than 1 L of fluid in slowly accumulating pericardial effusions. The “continuum” concept, formulated by Reddy et al, involves stages seen in intact, unanesthetized animals, fully recovered from operations to implant instrumentation (with responses quantitatively different from open chest, anesthetized animals undergoing short-term experiments) and also in human tamponade as measured by cardiac catheterization. However, the continuum begins before catheterization is clinically justified when small, medium, and large asymptomatic, “nontamponading” effusions couple the parietal pericardium to the heart, thereby exaggerating ventricular interaction and the consequent respiratory responses, as measured by sensitive noninvasive techniques in patients without pulsus paradoxus, the classic respiratory response of critical cardiac tamponade.