Why the study?
Does levosimendan improve hemodynamics and survival in patients with septic shock and decompensated myocardial failure?
Does levosimendan improve hemodynamics and survival in patients with septic shock and decompensated myocardial failure?
Levosimendan may be an alternative strategy to improve hemodynamics and reduce the need for conventional inotropes in patients with septic shock and decompensated myocardial failure.
Should not yet change practice; leaves open levosimendan's role in septic shock with myocardial failure.
Decreased global contractility is relatively common in patients with septic shock. Levosimendan is a novel inodilator that improves cardiac contractility by sensitizing troponin C to calcium. Calcium desensitization plays an important role in the pathophysiology of septic myocardial depression. For these reasons, we thought that levosimendan might be beneficial to the patients with sepsis-induced cardiac dysfunction. We infused levosimendan for 24 hours to 15 septic shock patients after 24 hour of conventional treatment (dopamine or adrenaline) and observed mean urine output, mean arterial pressure, changes of conventional inotropic agents' dose, central venous pressure and outcome. In nine (%70) of the fifteen patients, infusion of conventional inotrops have been decreased or ceased. Nine patients (%70) were died, but others (%30) were recovered from shock. Nine patients died and 3 of them died at 96 hours after levosimendan infusion. Urine outputs of all patients have been adequate. In only six (%40) patients, no urine output has been observed. Our series precede that levosimendan can be used in hopeless and unsuccessfully treated decompensate myocardial failure of septic shock. Therefore, we suggested that levosimendan, removes the symptoms of acute cardiac failure in septic shock and improves the hemodynamic function, in addition to slow down or stop the progressive ventricle dysfunction and to form a hemodynamic balance and improve the survival. As our impression, levosimendan may be an alternative to the strategy of increasing the dose of conventional inotrops and unsuccessfully treated decompensate myocardial failure under septic shock status.
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A 2007 study studied this question.
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