• Hongmei Wang, Ming Gong, Bin Zhou, and Anlu Dai.
• Department of Anesthesiology, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.
• Adv Ther. 2009 Apr 1;26(4):462-8.

IntroductionIncreased pulmonary vascular resistance (PVR) is detrimental to cardiac output in postoperative cardiac-surgery patients. The aim of this study was to investigate the postoperative hemodynamic effects of milrinone inhalation, and determine whether it has a selective effect of pulmonary vasodilation in patients with pulmonary hypertension undergoing mitral valve replacement surgery.MethodsIn this study, 48 patients with pulmonary hypertension who underwent mitral valve replacement surgery were included. Patients were randomly divided into two groups with 24 patients in each: the inhaled group and the control group (intravenous [i.v.] milrinone). In the inhaled group, milrinone was administered with a jet nebulizer, and nebulized for 4 hours. In the control group, patients received a bolus of 50 microg/kg i.v. milrinone, then received a continuous milrinone infusion, 0.5 microg/kg/min, for 4 hours. A number of hemodynamic changes in all patients were evaluated.ResultsWith milrinone administration, mean pulmonary artery pressure (MPAP) and PVR showed a comparable decrease in both groups. However, after initiation of milrinone, both mean arterial pressure and systemic vascular resistance in the inhaled group were significantly higher than in the control group. MPAP and PVR returned to baseline values 60 minutes after termination of milrinone inhalation. In addition, in the inhaled group, there was a reduction in intrapulmonary shunt fraction (Qs/Qt), with an improvement in PaO(2)/FiO(2) (arterial oxygen tension/fraction of inspired oxygen).ConclusionThe major advantage of inhaled milrinone is its pulmonary selectivity, thereby avoiding systemic side effects and ventilation-perfusion mismatch. Inhaled milrinone is an effective pulmonary vasodilator and appears to be an alternative promising approach in addressing the problem of right-ventricular decompensation following cardiopulmonary bypass.

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