IMPROVED OUTCOME WITH EARLY BLOOD ADMINISTRATION IN A NEAR-FATAL MODEL OF PORCINE HEMORRHAGIC-SHOCK

Current recommendations for the preoperative management of hemorrhagic shock include the initial infusion of 2 L of isotonic crystalloid regardless of the severity of hemorrhage. While this approach may be adequate for patients who experience only mild to moderate hemorrhagic insults, it has never been tested in a clinically relevant model of severe life-threatening hemorrhage. The authors used a porcine model of rapidly fatal hemorrhage with a reproducible and relevant physiologic end-point, the absence of vital signs, to test the hypothesis that even brief delays in blood replacement may result in higher mortality rates and worsen hemodynamic and metabolic responses to hemorrhage. Twenty-four immature swine (11-17 kg) were bled continuously at a decelerating rate until the following criteria were met: (1) respiratory arrest, (2) a pulse pressure of 0 and, (3) a slowing of cardiac electrical activity of 15% or more. Resuscitation was begun 1 minute later. The animals were randomly assigned to one of three resuscitation regimens. Group A (n = 8) received shed blood at a rate of 3 mL/kg/min for 10 minutes followed by normal saline (NS) at a rate of 3 mL/kg/min for 10 minutes. Group B (n = 8) received NS at a rate of 3 mL/kg/min for 10 minutes followed by shed blood at a rate of 3 mL/kg/min for 10 minutes. Group C, controls, (n = 8) received NS at a rate of 3 mL/kg/min for 20 minutes. Animals were observed for 30 minutes after resuscitation or until death. Mortality was 25%, 37.5%, and 100% for groups A, B, and C, respectively (P < .05 for group C versus group A or B). The group A animals demonstrated better hemodynamic and metabolic profiles throughout the resuscitation and observation periods as compared with the animals in groups B and C. The authors conclude that in the near-fatal hemorrhagic shock model, crystalloids are not the ideal initial resuscitation agent; even brief delays in blood replacement result in worse biochemical and hemodynamic response to the hemorrhagic insult. © 1992.