Jp. Revelly et al., EFFECT OF EPINEPHRINE ON OXYGEN-CONSUMPTION AND DELIVERY DURING PROGRESSIVE HEMORRHAGE, Critical care medicine, 23(7), 1995, pp. 1272-1278
Objective: To determine whether, during hemorrhagic shock, the effect
of epinephrine on energy metabolism could be deleterious, by enhancing
the oxygen requirement at a given level of oxygen delivery (Do(2)). D
esign: Prospective, randomized, control trial, Setting: Experimental l
aboratory, Subjects: Two groups of seven mongrel dogs were studied, Th
e epinephrine group received a continuous infusion of epinephrine (1 m
u g/min/kg) while the control group received saline, Intervention: Dog
s were anesthetized with pentobarbital, and shock was produced by step
wise hemorrhage, Measurements and Main Results: Oxygen consumption (Vo
(2)) was continuously measured by the gas exchange technique, while Do
(2) was independently calculated from cardiac output (measured by ther
modilution) and blood oxygen content, A dual-lines regression fit was
applied to the Do(2) vs. Vo(2) plot. The intersection of the two regre
ssion lines defined the critical value of Do(2). Values above critical
Do(2) belonged to phase 1, while phase 2 occurred below critical Do(2
). In the control group, Vo(2) was independent of Do(2) during phase 1
; Vo(2) was dependent on Do(2) during phase 2. In the epinephrine grou
p, the expected increase in Vo(2) (+19%) and Do(2) (+50%) occurred und
er normovolemic conditions. During hemorrhage, Vo(2) immediately decre
ased, and the slope of phase 1 was significantly (p < .01) different f
rom zero, and was significantly (p < .05) steeper than in the control
group (0.025 +/- 0.005 vs, 0.005 +/- 0.010). However, the critical Do(
2) (8.7 +/- 1.7 vs, 9.7 +/- 2.4 mL/min/kg), the critical Vo(2) (5.6 +/
- 0.5 vs, 5.5 +/- 0.9 mL/min/kg), and the slope of phase 2 (0.487 +/-
0.080 vs, 0.441 +/- 0.130) were not different from control values. Con
clusions: The administration of pharmacologic doses of epinephrine sig
nificantly increased Vo(2) under normovolemic conditions due to the ep
inephrine-induced thermogenic effect, This effect progressively decrea
sed during hemorrhage. The critical Do(2) and the relationship between
Do(2) and Vo(2) in the supply-dependent phase of shock were unaffecte
d by epinephrine infusion, These results suggest that during hemorrhag
ic shock, epinephrine administration did not exert a detrimental effec
t on the relationship between Do(2) and Vo(2).