Am. J. Respir. Crit. Care Med., Vol 154, No. 1, 07 1996, 68-75.
Serial measures of total body oxygen consumption in an awake canine model of septic shock
PQ Eichacker, WD Hoffman, RL Danner, SM Banks, S Richmond, Y Fitz and C Natanson
Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892, USA.
We examined serial changes in total body oxygen consumption (Vo2) in a
permanently tracheotomized canine sepsis model. On Day 0, beagles had an
Escherichia coli-infected (septic) or sterile (control) clot surgically
placed in the peritoneum. During the 21-d study, 10 of the 16 septic
animals and none of the six control animals died (p = 0.02). After clot
placement septic versus control animals had decreased mean arterial blood
pressure (mm Hg; Day 1: 106 versus 128, p = 0.055; Day 2: 95 versus 125, p
= 0.004, respectively) and left ventricular ejection fraction (Day 1: 0.44
versus 0.69, p = 0.0006; Day 2: 0.33 versus 0.57, p = 0.0001,
respectively). Despite significant lethality and cardiovascular
dysfunction, in the septic group on Days 1 and 2, septic versus control
animals had no significant differences in mean metabolic cart measured
(Vo2DIR, ml/kg/min; Day 1: 11.9 versus 12.4, p = 0.81; Day 2: 14.2 versus
13.5, p = 0.72, respectively) and intravascular catheter calculated
(Vo2INDIR, ml/kg/min; Day 1: 11.2 versus 11.2, p = 0.99; Day 2: 12.8 versus
15.4, p = 0.49, respectively). On Day 1 in septic and control animals,
volume infusion produced increases (p < 0.001) in oxygen delivery (Do2).
In septic and control animals these changes in Do2 were similar and were
associated with similar increases in Vo2DIR (p = 0.001), and Vo2INDIR (p =
0.001). In fact, at all time points studied (baseline, Day 1, 2, and 21),
both before and after volume infusion, levels of Do2, Vo2DIR, and Vo2INDIR
did not differ between septic and control animals, nor did they differ
between septic survivors and nonsurvivors. Because levels of Vo2DIR and
Vo2INDIR were similar in both groups, we pooled data from septic and
control animals. Throughout the study, Vo2 showed a moderate association
with Vo2INDIR (r = 0.55, p = 0.003), but mean Vo2DIR was lower at baseline
(p = 0.001) and on Day 21 (p = 0.07) and greater on Day 2 (p < 0.01). In
summary, our techniques, which detected small changes in both Vo2DIR and
Vo2INDIR occurring with volume infusion, did not demonstrate differences in
these parameters comparing control and septic animals. These results in
euvolemic septic animals suggest that total body Vo2 may not reflect
pathogenetic mechanisms during sepsis and septic shock. Furthermore, these
results suggest that although the level of total body Vo2 may reflect the
effects of therapeutic interventions such as volume loading, it should not
itself serve as a therapeutic target.
