Despite progressively falling cardiac output, increased peripheral resistance supports arterial BP until relatively late, partly by an a-adrenergic mechanism. Thus, increased peripheral resistance is not affected by |3-blockade, but is opposed by a-block-ade. Ultimately BP tends to decline precipitously—the “last drop” phenomenon. (In experimental animals that are anesthetized or not recovered from surgery, BP falls relatively slowly in contrast to intact animals that more closely resemble human responses.) The critical BP fall is also influenced by an opioid-dependent mechanism, demonstrated by naloxone-induced BP increase during tamponade. This increase occurs without increasing cardiac output, so that this mechanism must act through increased systemic vascular resistance. (Further evidence that systolic function does not limit cardiac output in uncomplicated tamponade.) Naloxone-induced BP increase further suggests a “peripheral resistance reserve,” despite the already high peripheral resistance that is a principal compensatory response (Fig 2).
Further Neurohormonal Activation
BP is augmented by further neurohormonal activation associated with arterial and atrial baroreceptor unloading, resembling neurohormonal activation in cardiac failure (but much less investigated). The renin-angiotensin-aldosterone system contributes renin, angiotensin II, arginine vasopressin, and aldosterone, with consequent sympathetic nervous system stimulation, vasoconstriction, decreased urine flow, decreased renal sodium and potassium excretion, and water retention. These effects are mainly relatively late, during decompensating tamponade, after aortic BP decreases by about 30%2> and are followed by increased production of adrenocorticotropic hormone. They are preceded by neurogenic reduction in renal sodium output. However, unlike cardiac failure at comparably high central pressures, serum atrial natriuretic factor does not increase, because tamponade prevents myocardial stretch. This is associated with the external compression of the heart and the critically reduced trans mural filling pressures of tamponade that prevent atrial distention. (In contrast, transmural pressures are preserved in cardiac failure, permitting myocardial stretch with consequent atrial natriuretic factor production). Thus, tamponade prevents this mechanism for increasing renal natriuresis. This, with the neurogenic renal sodium retention, contributes to increased blood volume, tending to support the compensatorily increased venous pressures (Fig 2). cialis professional 20 mg

Tamponade in Summary
Figure 2 summarizes the principal elements of tamponade dynamics and the main compensatory mechanisms. The discussion emphasizes the complexity of each of these, adding the important neu-rohormonal elements that resemble those of congestive heart failure. The pathophysiologic continuum of the tamponade state— not all or none”—is fundamental to its appreciation.