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.