INTRODUCTION: Levosimendan is a new inotropic vasodilator for the treatment of decompensated heart failure. Compared to other inotropic agents, it has been shown to improve myocardial contractility without increasing oxygen requirements. However, experience with levosimendan in patients with low cardiac output after cardiopulmonary bypass is limited. In this case series we present the short-term haemodynamic effects of levosimendan added to dobutamine for the management of low cardiac output syndrome after cardiac surgery. METHODS: Twelve patients with low cardiac output during the first 6 hours after completion of cardiopulmonary bypass, who were already receiving dobutamine at a mean dose of 6.7 microg/kg/min, were treated with levosimendan at a loading dose of 6 microg/kg, followed by a 24-hour infusion of 0.2 microg/kg/min. During a 24-hour observation period the following haemodynamic parameters were measured: arterial, central venous, pulmonary arterial and pulmonary capillary wedge pressure, heart rate, cardiac index, stroke volume, systemic and pulmonary vascular resistance, as well as mixed venous oxygen saturation, oxygen delivery and oxygen extraction ratio. RESULTS: Levosimendan significantly improved cardiac index (from 2.1 +/- 0.1 L/min/m2 at baseline to 3.2 +/- 0.3 L/min/m2 at 24 hrs, p < 0.001) as well as mixed venous oxygen saturation, oxygen delivery and oxygen extraction ratio (p < 0.001) and caused a significant reduction in systemic and pulmonary vascular resistance (p < 0.001). At the same time, a significant decrease in central venous, pulmonary arterial and pulmonary capillary wedge pressure was noted (p < 0.001). These beneficial haemodynamic effects resulted in significantly decreased catecholamine requirements. CONCLUSIONS: In this group of cardiac surgical patients with postoperative myocardial dysfunction resistant to dobutamine, levosimendan added to dobutamine was effective in reversing low cardiac output syndrome.
INTRODUCTION:Levosimendan is a new inotropic vasodilator for the treatment of decompensated heart failure. Compared to other inotropic agents, it has been shown to improve myocardial contractility without increasing oxygen requirements. However, experience with levosimendan in patients with low cardiac output after cardiopulmonary bypass is limited. In this case series we present the short-term haemodynamic effects of levosimendan added to dobutamine for the management of low cardiac output syndrome after cardiac surgery. METHODS: Twelve patients with low cardiac output during the first 6 hours after completion of cardiopulmonary bypass, who were already receiving dobutamine at a mean dose of 6.7 microg/kg/min, were treated with levosimendan at a loading dose of 6 microg/kg, followed by a 24-hour infusion of 0.2 microg/kg/min. During a 24-hour observation period the following haemodynamic parameters were measured: arterial, central venous, pulmonary arterial and pulmonary capillary wedge pressure, heart rate, cardiac index, stroke volume, systemic and pulmonary vascular resistance, as well as mixed venous oxygen saturation, oxygen delivery and oxygen extraction ratio. RESULTS:Levosimendan significantly improved cardiac index (from 2.1 +/- 0.1 L/min/m2 at baseline to 3.2 +/- 0.3 L/min/m2 at 24 hrs, p < 0.001) as well as mixed venous oxygen saturation, oxygen delivery and oxygen extraction ratio (p < 0.001) and caused a significant reduction in systemic and pulmonary vascular resistance (p < 0.001). At the same time, a significant decrease in central venous, pulmonary arterial and pulmonary capillary wedge pressure was noted (p < 0.001). These beneficial haemodynamic effects resulted in significantly decreased catecholamine requirements. CONCLUSIONS: In this group of cardiac surgical patients with postoperative myocardial dysfunction resistant to dobutamine, levosimendan added to dobutamine was effective in reversing low cardiac output syndrome.