New Approaches to Modifying Inotropy in Sepsis-Induced Myocardial Dysfunction*

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Excerpt

Sepsis and septic shock are accompanied by myocardial dysfunction (1). The underlying cause of sepsis-induced myocardial dysfunction is the development of a complex intramyocardial inflammatory response but also includes a potential contribution from demand ischemia (2). This pathophysiology is quite distinct from decreased ventricular contractility from other primary cardiac etiologies. So how should sepsis-induced myocardial dysfunction be treated in the ICU? Current Surviving Sepsis Campaign guidelines recommend dobutamine as a first-line agent to treat decreased ventricular contractility during sepsis (3). But β-adrenergic stimulation has a number of adverse features, particularly during sepsis. Accordingly, Chagnon et al (4) test the hypothesis that alternative signaling pathways may be helpful. They find that apelin-13, an inotropic agent that signals via pathways distinct from adrenergic agonists, may have features that are superior to dobutamine.

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