Interaction of sepsis and sepsis plus sympathomimetics on myocardial oxygen availability

Abstract

The ability to regulate myocardial blood flows (Q̇) in accord with changing myocardial O2 needs may be depressed in sepsis. This could be an important concern when sympathomimetics are used to augment systemic oxygen delivery (Q̇O2) in this syndrome as increased myocardial O2 needs may accompany an infusion of this class of drugs. Therefore after measuring the effect of sepsis on myocardial O2 metabolism, we then infused various sympathomimetics to evaluate the sepsis + sympathomimetic interaction on myocardial Q̇O2. We measured Q̇ to the left (LV) and right (RV) ventricles by the radioactive microsphere technique in 36 unanesthetized mature sheep, before and during the infusion of dopamine, dobutamine, dopexamine, norepinephrine, salbutamol, or placebo. Randomly selected for infusion, these drugs were titrated to augment the thermodilution-derived cardiac index (CI) by >20%. This study was repeated 24-48 h after cecal ligation and perforation had resulted in a hyperdynamic septic state [change (Δ) in CI = sepsis - baseline = +54%; P < 0.01]. During the septic study, both Q̇-LV (Δ = +80%; P < 0.01) and Q̇-RV (Δ = +84%; P < 0.01) were increased above baseline values; the augmented Q̇ to both LV and RV was directly correlated with the arterial perfusion pressure (P(A)) x CI product and the mean pulmonary artery pressure (P(PA)) x CI product, respectively. Only 23% of study animals demonstrated net transmyocardial lactate production during the septic study. When the infusion of sympathomimetics was accompanied by an increase in the P(PA) x CI and P(A) x CI products, a further increase in both Q̇-RV and Q̇- LV, respectively, occurred. Also, neither the ventricular endocardial-to- epicardial flow ratios nor transmyocardial lactate extraction were modified by the sympathomimetics infusion. We conclude that the septic response to infection in this animal model was not accompanied by significant abnormalities in the metabolic regulation of myocardial Q̇O2.