Hematocrit and metabolic changes caused by varied resuscitation strategies in a canine model of hemorrhagic shock.

The effect of acute hemorrhage on hematocrit is controversial. Our aims were to (1) define hematocrit (Hct) changes caused by acute hemorrhage and (2) to compare Hct, hemodynamic, and metabolic responses to varied resuscitation strategies. Twenty-five dogs were instrumented for hemodynamic monitoring and randomized to 4 groups: control (n = 4), large volume (n = 7), small volume (n = 7), and no fluid resuscitation (n = 7). Dogs were hemorrhaged 30% of blood volume. Large- and small-volume groups received 3 mL or 1 mL lactated ringers (LR) for every mL hemorrhaged, respectively. Data were collected over 6 hours. Mean Hct dropped by 17% in all groups posthemorrhage (P <.002) and further decreased to 50% and 24% of baseline in the large- and small-volume groups postresuscitation (P <.001). Hct changes stabilized within 1 hour. No prolonged differences in hemodynamics or metabolic parameters were observed between groups. Acute hemorrhage caused a rapid, moderate drop in Hct, which quickly stabilized. Larger decreases in Hct were caused by fluid resuscitation. Large-volume resuscitation had no advantage over small volume in this hemorrhagic shock model. Copyright 2002, Elsevier Science (USA). All rights reserved.)