Postresuscitative hypertension: a reappraisal.

New concepts of cause and therapy for postresuscitative hypertension (PRH) were evaluated in four patients with PRH. Each patient had severe injury and shock, and received an average of 28.3 transfusions, 15.4 L of electrolyte solution, and 1.4 L of plasma by the end of surgery for control of bleeding. Near the end of the sequestration phase, PRH developed. In two patients, PRH (190/100 mm Hg and 180/90 mm Hg) responded to previously recommended therapy; blood pressure fell to about 135/90 mm Hg. Shortly thereafter, bradycardia developed and both patients died. In the latter two patients, PRH (205/115 mm Hg and 150/120 mmHg) was treated less aggressively, maintaining intravenous fluids to keep urine output at a minimum of 50 mL/hr. Postresuscitative hypertension persisted for five and six days as both patients improved, continued to mobilize sequestered fluid, and maintained good organ perfusion. Postresuscitative hypertension may be a cell-mediated protective response to a need for increased capillary hydrostatic pressure to facilitate mitochondrial oxygenation. Fluid replacement should be guided by careful monitoring of cardiac, pulmonary, and renal function.