Cardiovascular drugs play a major role in pre-, and postoperative care in neonates with congenital heart disease (CHD), however systematic aproach to the hemodynamic effects of these therapies in the neonatal population is scarce. Management strategies aim to optimize contractility, improve diastolic function, maintain adequate preload, and reduce afterload. Thus, inodilators are standard treatment in these patients. Levosimendan, a novel inodilator, enhances myocardial contractility mainly through myofilament calcium sensitization, and causes peripheral and coronary vasodilation via opening ATP-dependent K-channels in vascular smooth muscle cells.
Aims Systematic approach to evaluate the acute hemodynamic effects of levosimendan in neonates with CHD treated for low cardiac output syndrome (LCOS).
Methods Observational study. Intervention: 48 hours continuous i.v. levosimendan (0.1–0.2 microg/k/min) infusion. Outcomes: continuous monitoring of mean blood pressure (MBP), heart rate (HR), central and peripheral temperature, transcutaneous CO2. Two near-infrared units (frontal-parietal = C; thigh = P) were used to assess changes in cerebral blood volume, cerebral (C-dDHb) and peripheral (P-dDHb) blood flow, and C and P tissue oxygenation index. Baseline and end-of-study pH and lactate were determined.
Results 7 dosis of levosimendan were investigated. Mean study time was 13.3 (7–19) hours. Levosimendan produced an increase in blood flow (C-dDHb, p<0.05; P-dDHb, NS) and a decrease in HR (p<0.001) and lactate (p<0.05). Trends showed an increase in MBP (NS). These effects were independent of time. Multiple regression analysis identified MBP and levosimendan as factors significantly associated with C-dDHb and P-dDHb changes.
Conclusions Levosimendan improves cerebral and systemic perfusion in neonates with LCOS.
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