Previous work in our laboratory has demonstrated that HSD is an effective small-volume
resuscitation fluid for the treatment of hemorrhagic
hypotension, but limitations to its usefulness in severe
hemorrhage have not been explored. In the present study, animals (N = 12) were bled from an
arterial line at a rate of 1 mL/kg/min until continuously monitored aortic blood flow was reduced to one-half its baseline value, and then they were immediately resuscitated with 7.5% NaCl/6%
dextran 70 (hypertonic saline
dextran, 4 mL/kg) administered intravenously over 3 min. After recording the maximum improvement in blood pressure, blood samples were obtained and the
hemorrhage-
resuscitation sequence was repeated until no further measurable increase in cardiac index or blood pressure could be elicited by
resuscitation. In the majority of the animals, cardiac index and right and left ventricular
stroke work could be improved at least through two bleedings and
resuscitation. These improvements sufficed to increase
oxygen delivery and consumption, despite the decreases in hematocrit induced by
bleeding, transcapillary refill, and asanguinous fluid administration. Under these severe
hemorrhage conditions, the
acid-base imbalance was not improved by hypertonic saline
dextran, and the rate of increase in
acidosis was not affected by its administration. We observed a progressive decrease in base excess from +1.35+/-3.19 (mean +/- standard error) to -12.9+/-2.1 mEq/L even when
resuscitation improved oxygen consumption significantly by 95+/-20%. In animals that survived as many as three bleedings and
resuscitation, the depletion of buffering capacity of the blood was most predominant, and
bicarbonate reached a nadir of 7.62 mEq/L with a base excess of -22.4 mEq/L. It is evident that restoration of perfusion in
shock treats only a portion of the physiologic dysfunction, leaving major metabolic derangements uncorrected.