Abstract
The use of epinephrine in septic shock remains controversial. Nevertheless, epinephrine is widely used around the world and the reported morbidity and mortality rates with it are no different from those observed with other vasopressors. In volunteers, epinephrine increases heart rate, mean arterial pressure and cardiac output. Epinephrine also induces hyperglycemia and hyperlactatemia. In hyperkinetic septic shock, epinephrine consistently increases arterial pressure and cardiac output in a dose dependent manner. Epinephrine transiently increases lactate levels through an increase in aerobic glycolysis. Epinephrine has no effect on splanchnic circulation in dopamine-sensitive septic shock. On the other hand, in dopamine-resistant septic shock, epinephrine has no effect on tonometric parameters but decreases fractional splanchnic blood flow with an increase in the gradient of mixed venous oxygen saturation (SVO2) and hepatic venous oxygen saturation (SHO2). In conclusion, epinephrine has predictable effects on systemic hemodynamics and is as efficient as norepinephrine in correcting hemodynamic disturbances of septic shock. Moreover, epinephrine is cheaper than other commonly used catecholamine regimens in septic shock. The clinical impact of the transient hyperlactatemia and of the splanchnic effects are not established.
Highlights
Goal directed therapy [1] is considered as a gold standard in the early phase of septic shock
Epinephrine when used in septic shock increases lactate level together with a slightly enhanced lactate/pyruvate (L/P) ratio, decreases global splanchnic flow and elevates the tonometric mucosal partial CO2 tension (PCO2) gap, a surrogate marker of gastric mucosal metabolism and/or perfusion
We found that epinephrine increased lactate level without any increase in the L/P ratio when the latter was normalized to pH (H+ = 10–pH)
Summary
Goal directed therapy [1] is considered as a gold standard in the early phase of septic shock. The addition of dobutamine to epinephrine-treated patients has been shown to improve gastric mucosal perfusion, as assessed by improvements in intramucosal pH, arterial lactate concentration and the PCO2 gap [20] It is not clear whether a transient decrease in hepatosplanchnic blood flow in septic shock is deleterious [20]. In nine of ten cases of dopamine-resistant septic shock, epinephrine, when associated with dobutamine, decreased hepatosplanchnic blood flow, increased the SVO2-SHO2 gradient and increased arterial lactate and hepatic lactate consumption without any net effect on the PCO2 gap, which may indicate a constant blood flow in the mucosa. Seguin et al [21] demonstrated in patients with septic shock that epinephrine at doses that induced the same mean arterial pressure did not modify ICG clearance and enhanced more gastric mucosal blood flow than the combination of dobutamine at 5 μg/kg per minute and norepinephrine. The clinical impact remains to be demonstrated during septic conditions, epinephrine modulates the inflammatory state and decreases the 564 hypercoagulation state
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