Anesth Analg 2006;103:515-516
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000227219.60581.F2
LETTER TO THE EDITOR
Using Inhaled Iloprost to Wean from Cardiopulmonary Bypass After Implanting a Left Ventricular Assist Device
Michael Winterhalter, MD,
Stefan Fischer, MD MSc,
Rene Tessmann, MD,
Adelheid Goerler, MD,
Siegfried Piepenbrock, MD,
Axel Haverich, MD, and
Martin Strueber, MD
Hannover Thoracic Transplant and Cardiac Assist Program, Division of Cardiothoracic and Vascular Surgery, Department of Anaesthesiology, Hannover Medical School, Hannover, Germany, Winterhalter.Michael{at}mh-hannover.de
To the Editor:
Right ventricular function is essential when implanting a left ventricular assist device (LVAD) to avoid temporary mechanical right ventricular support. We report two cases of patients with severe acute intraoperative right ventricular failure after implantation in beating hearts with the HeartMate II LVAD. Both patients were successfully weaned from cardiopulmonary bypass with inhaled iloprost.
Patient 1: A 32 -yr-old male patient presented with recurrent left heart failure (ejection fraction = 16%) resulting from dilative cardiomyopathy. His right ventricle was also dilated (ejection fraction = 50%). The mean pulmonary arterial pressure was 28 mm Hg. He had mild mitral and tricuspid insufficiency. The patient’s condition rapidly deteriorated, requiring implantation of an LVAD. After implantation, we set the LVAD to 6500 rpm and gradually reduced bypass flows. We monitored right ventricular filling using transesophageal echocardiography (TEE). The right ventricle began to fail despite large doses of epinephrine and dobutamine. Central venous pressure increased to 20 mm Hg, and TEE showed poor right ventricular function. Inhaled nitric oxide did not improve the function of the right ventricle. Further weaning from cardiopulmonary bypass was impossible. We administered 20 µg of aerosolized iloprost (Ventavis, Schering AG, Berlin, Germany) in 2 mL of normal saline, by attaching an iloprost inhalation system with a novel ultrasonic atomizer to the ventilator circuit for 4 min (Schill multisonic®; Schill GmbH, Probstzella, Germany). Right ventricular contraction (ventricular filling and septal shifting) immediately improved. Pulmonary arterial pressure decreased from 36 to 30 mm Hg. The patient was weaned from cardiopulmonary bypass without requiring right ventricular support.
Patient 2: A 29-yr-old patient presented with decompensated heart failure New York Heart Association class IV as the result of dilative cardiomyopathy (ejection fraction = 15%). The patient had elevated serum lactate, liver enzymes, serum creatinine, and an Svo2 of 32%. He required increasing levels of catecholamine support. We implanted a LVAD to stabilize his condition. This patient also developed acute right ventricular failure, despite administration of large doses of epinephrine and dobutamine. TEE showed poor right ventricular contraction. Immediate inhalation of aerosolized iloprost (20 µg in 2 mL of normal saline) improved the patient’s right ventricular function. Mean pulmonary arterial pressure decreased from 30 to 22 mm Hg, and the patient was gradually weaned from cardiopulmonary bypass.
In both cases, patients experienced acute intraoperative right ventricular failure after implantation of a HeartMate II LVAD. Altering the speed of the LVAD did not improve right ventricular function. Increased left-sided output by the LVAD causes increased venous return to the right ventricle. Although a properly functioning LVAD will reduce right ventricular afterload and often improve right ventricular function in patients with normal pulmonary vascular resistance, patients with increased pulmonary vascular resistance may show increased right ventricular afterload (1). Right ventricular failure after LVAD implantation is life-threatening complication (2). The ability of the right ventricle to deliver an adequate volume of blood to the left ventricle and, consequently, to the LVAD, is a function of the intrinsic contractility of the right ventricular and the pulmonary vascular resistance. To improve right ventricular function, selective pulmonary vasodilatation without a decrease in mean systemic arterial blood pressure and systemic vascular resistance is essential.
Inhaled prostacyclin (PGI2) causes selective pulmonary vasodilatation, increases cardiac output (3), and improves venous and arterial oxygenation in patients with severe pulmonary hypertension (4). The acute effect on pulmonary vascular resistance seen with inhaled PGI2 is the same as that seen with IV PGI2, and avoids causing systemic hypotension and worsening of right ventricular function. Inhaled PGI2 and iloprost may be more effective at decreasing pulmonary vascular resistance than inhaled nitric oxide or oral sildenafil (5). After IV application of vasodilators, a decrease in pulmonary vascular resistance is commonly associated with systemic vasodilation and decreased systemic vascular resistance, potentially leading to reduced myocardial perfusion. Thus, application of locally acting vasodilators into the bronchial system is a promising approach. The intra and postoperative use of iloprost has been reported (6,7). This is the first report of iloprost administration for acute intraoperative right ventricular failure after LVAD implantation.
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