Effects of Early Inhaled Epoprostenol Therapy on Pulmonary Artery Pressure and Blood Loss During LVAD Placement

• Published in: Journal of cardiothoracic and vascular anesthesia 2014-06, Vol.28 (3), p.652-660
• Main Authors: Groves, Danja S., MD, PhD, Blum, Franziska E., MD, Huffmyer, Julie L., MD, Kennedy, Jamie L.W., MD, Ahmad, Hasan B., BS, Durieux, Marcel E., MD, PhD, Kern, John A., MD
• Format: Article
• Language: English
• Subjects: Administration, Inhalation; Aged; Aged, 80 and over; Anesthesia & Perioperative Care; Arterial Pressure - drug effects; Blood Coagulation - drug effects; blood loss; Blood Loss, Surgical - prevention & control; Blood Transfusion - statistics & numerical data; Critical Care; Epoprostenol - administration & dosage; Epoprostenol - therapeutic use; Female; Heart-Assist Devices; Humans; inhaled epoprostenol; left ventricular assist device; Male; Middle Aged; prostacyclin; Pulmonary Artery - drug effects; pulmonary artery pressure; Retrospective Studies; Vasodilator Agents - administration & dosage; Vasodilator Agents - therapeutic use
• ISSN: 1053-0770; 1532-8422
• DOI: 10.1053/j.jvca.2013.05.028

Objective Several strategies have been used to reduce the incidence of right ventricular failure after left ventricular assist device (LVAD) placement, including pulmonary vasodilation. The inhaled prostacyclin, epoprostenol, selectively dilates the pulmonary vasculature of ventilated areas of the lung, but also has been shown to inhibit platelet aggregation.1 The authors evaluated the impact of early initiation of epoprostenol administration during LVAD placement on pulmonary artery pressures, use of vasoactive drugs, and blood loss. Design Retrospective data review. Setting Single center, university hospital. Participants A total of 37 consecutive patients undergoing LVAD (HeartMate II) placement were included. Interventions In the first group of 23 patients (group 1), inhaled epoprostenol was not initiated until weaning from cardiopulmonary bypass (CPB). In a subsequent group of 14 patients (group 2), inhaled epoprostenol was started shortly after induction of anesthesia and continued throughout and post-CPB. Measurements Mean and systolic pulmonary artery pressures (mPAP, sPAP), vasoactive drugs, as well as hemodynamic parameters, blood loss, and use of blood products were recorded at the following time points: Baseline (BL), pre-CPB, post-CPB, and during postoperative days (POD) 0, 1, and 2. Data are presented as mean±SD or median [25%, 75%]. Results Groups did not differ in demographic characteristics and comorbidities. BL sPAP (41±13 v 46±15 mmHg; p = 0.051) and mPAP (32±8 v 34±8 mmHg; p = 0.483) values were not different between the groups. Systolic and mPAP in group 1 were significantly lower in the postoperative period compared with BL (sPAP on POD 0: 34±6 mmHg; p