HEMODYNAMIC AND METABOLIC RESPONSES TO REPEATED HEMORRHAGE AND RESUSCITATION WITH HYPERTONIC SALINE DEXTRAN IN CONSCIOUS SWINE

Citation
Jd. Obenar et al., HEMODYNAMIC AND METABOLIC RESPONSES TO REPEATED HEMORRHAGE AND RESUSCITATION WITH HYPERTONIC SALINE DEXTRAN IN CONSCIOUS SWINE, Shock, 10(3), 1998, pp. 223-228
Citations number
33
Categorie Soggetti
Peripheal Vascular Diseas","Emergency Medicine & Critical Care",Hematology,Surgery
Journal title
ShockACNP
ISSN journal
10732322
Volume
10
Issue
3
Year of publication
1998
Pages
223 - 228
Database
ISI
SICI code
1073-2322(1998)10:3<223:HAMRTR>2.0.ZU;2-Q
Abstract
Previous work in our laboratory has demonstrated that HSD is an effect ive small-volume resuscitation fluid for the treatment of hemorrhagic hypotension, but limitations to its usefulness in severe hemorrhage ha ve 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 mon itored aortic blood flow was reduced to one-half its baseline value, a nd then they were immediately resuscitated with 7.5% NaCl/6% dextran 7 0 (hypertonic saline dextran, 4 mL/kg) administered intravenously over 3 min. After recording the maximum improvement in blood pressure, blo od samples were obtained and the hemorrhage-resuscitation sequence was repeated until no further measurable increase in cardiac index or blo od pressure could be elicited by resuscitation. In the majority of the animals, cardiac index and right and left ventricular stroke work cou ld be improved at least through two bleedings and resuscitation. These improvements sufficed to increase oxygen delivery and consumption, de spite the decreases in hematocrit induced by bleeding, transcapillary refill, and asanguineous fluid administration. Under these severe hemo rrhage conditions, the acid-base imbalance was not improved by hyperto nic saline dextran, and the rate of increase in acidosis was not affec ted 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 significantl y by 95 +/- 20%. In animals that survived as many as three bleedings a nd 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 perfus ion in shock treats only a portion of the physiologic dysfunction, lea ving major metabolic derangements uncorrected.