The Comparative Pathobiology of Stress-induced and Sepsis-induced Cardiomyopathy

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Abstract

One of the primary treatments of septic shock to maintain blood pressure is with fluids (colloids and crystalloids), and catecholamines. Paradoxically, catecholamines administered to treat sepsis-induced low blood pressure, and released within the vasculature as part of the stress response to shock, could be responsible for or contribute to, the worsening of cardiac dysfunction during sepsis (i.e. stress-induced cardiomyopathy). Consistent with the notion that sepsis is at least in part a stress-induced cardiomyopathy, we have shown in our large animal septic shock model that epinephrine can worsen cardiac function during sepsis. In this protocol, we tested this hypothesis directly in a 2 by 2 factorial design using animals randomized to receive a bacterial inoculation to develop a pneumonia model of septic shock (or not) and then further randomized to receive a 40 h epinephrine infusion (or not). Hemodynamic parameters included serial echocardiograms, central and peripheral pressures and cardiac output. Unexpectedly, the epinephrine infusion was found to mitigate the myocardial depression of septic shock and promote a quicker functional recovery. We are currently investigating whether this new finding can provide novel insights about underlying causes of myocardial depression in septic shock and if there are beneficial effects associated with epinephrine in sepsis.