HYPERTONIC SALINE IN STABILIZED HYPERDYNAMIC SEPSIS

Citation
L. Hannemann et al., HYPERTONIC SALINE IN STABILIZED HYPERDYNAMIC SEPSIS, Shock, 5(2), 1996, pp. 130-134
Citations number
34
Categorie Soggetti
Surgery,"Cardiac & Cardiovascular System
Journal title
ShockACNP
ISSN journal
10732322
Volume
5
Issue
2
Year of publication
1996
Pages
130 - 134
Database
ISI
SICI code
1073-2322(1996)5:2<130:HSISHS>2.0.ZU;2-P
Abstract
Hypertonic saline with or without colloidal solution has been successf ully used for treating hemorrhagic shock in animal experiments and cli nical studies. Due to its various effects at systemic, organ, and micr ocirculatory levels, the substance appears to be a promising candidate for improving tissue oxygenation in sepsis. We therefore investigated the hypothesis that infusion of hypertonic saline would further impro ve O-2 delivery, O-2 extraction, and O-2 uptake in hyperdynamic septic shock patients already stabilized by adequate volume and catecholamin e infusion. Twenty-one patients received 2-4 mL/kg body weight of hype rtonic saline in hydroxyethyl starch within 15 min. This hypertonic sa line infusion caused a rapid significant increase in O-2 delivery by 1 4% but only a marginal increase in O-2 consumption (7% by cardiovascul ar Fick [p < .05], 4% by respiratory gases [n.s.]). Hypertonic saline increased the already elevated cardiac output by 24%. The pulmonary ca pillary wedge pressure increased from 14 +/- 3 to 23 +/- 3 mmHg and pu lmonary shunt fraction increased 15%, but arterial PO2 did not fall. E xcept for the increase in pulmonary capillary wedge pressure, none of the cardiovascular changes lasted longer than 60 min. Plasma sodium le vels increased from 138 +/- 25 to 163 +/- 38 mmol/L and normalized wit hin 24 h. In these hyperdynamic septic patients, hypertonic saline inf usion produced a transient increase in circulation, but no evidence of a substantial increase in O-2 consumption. Either there was no signif icant O-2 debt due to the already elevated O-2 delivery levels at base line (700 mL/min/m(2)) or the global O-2 measurements we used were not able to detect discrete regional hypoxia.