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Inhaled nitric oxide versus intravenous vasodilators in severe pulmonary hypertension after cardiac surgery


Schmid, E R; Bürki, C; Engel, M H; Schmidlin, D; Tornic, M; Seifert, Burkhardt (1999). Inhaled nitric oxide versus intravenous vasodilators in severe pulmonary hypertension after cardiac surgery. Anesthesia and Analgesia, 89(5):1108-1115.

Abstract

UNLABELLED Inhaled nitric oxide (iNO) is superior to i.v. vasodilators for treatment of pulmonary hypertension (PH) after cardiac surgery, but iNO is a potentially toxic gas, and patient subsets who benefit from iNO are not yet clearly defined. We administered iNO 40 ppm, prostaglandin E1 (PGE1) 0.1 microg x kg(-1) min(-1), and nitroglycerin (NTG) 3 to 5 microg x kg(-1) min(-1), in a randomized crossover study to 14 adult patients with severe PH after cardiac surgery. iNO, PGE1, and NTG were of similar efficacy in reducing pulmonary vascular resistance (P = 0.003). iNO induced selective pulmonary vasodilation, while PGE1 and NTG had significant concomitant systemic vasodilatory effects. iNO led to an increase in cardiac index (CI) (P = 0.012), and PGE1 increased CI (P = 0.006) and right ventricular (RV) ejection fraction (P = 0.015), while NTG had no effect on CI and RV performance. After study completion, patients continued with PGE1 administration with favorable in-hospital outcome. We conclude that PH per se, even if severe, does not necessarily imply postoperative RV dysfunction, and selective pulmonary vasodilation with iNO may not be superior to PGE1 with regard to CI and RV performance.
IMPLICATIONS In a prospective, randomized crossover study of inhaled nitric oxide (iNO) versus IV vasodilators, performed in adult patients with severe pulmonary hypertension but preserved right ventricular function after cardiac surgery, iNO was not superior to IV prostaglandin E1 with regard to cardiac index and right ventricular performance. Considering the potential toxicity of iNO, better definition of patient subsets with a positive benefit/risk ratio is warranted.

Abstract

UNLABELLED Inhaled nitric oxide (iNO) is superior to i.v. vasodilators for treatment of pulmonary hypertension (PH) after cardiac surgery, but iNO is a potentially toxic gas, and patient subsets who benefit from iNO are not yet clearly defined. We administered iNO 40 ppm, prostaglandin E1 (PGE1) 0.1 microg x kg(-1) min(-1), and nitroglycerin (NTG) 3 to 5 microg x kg(-1) min(-1), in a randomized crossover study to 14 adult patients with severe PH after cardiac surgery. iNO, PGE1, and NTG were of similar efficacy in reducing pulmonary vascular resistance (P = 0.003). iNO induced selective pulmonary vasodilation, while PGE1 and NTG had significant concomitant systemic vasodilatory effects. iNO led to an increase in cardiac index (CI) (P = 0.012), and PGE1 increased CI (P = 0.006) and right ventricular (RV) ejection fraction (P = 0.015), while NTG had no effect on CI and RV performance. After study completion, patients continued with PGE1 administration with favorable in-hospital outcome. We conclude that PH per se, even if severe, does not necessarily imply postoperative RV dysfunction, and selective pulmonary vasodilation with iNO may not be superior to PGE1 with regard to CI and RV performance.
IMPLICATIONS In a prospective, randomized crossover study of inhaled nitric oxide (iNO) versus IV vasodilators, performed in adult patients with severe pulmonary hypertension but preserved right ventricular function after cardiac surgery, iNO was not superior to IV prostaglandin E1 with regard to cardiac index and right ventricular performance. Considering the potential toxicity of iNO, better definition of patient subsets with a positive benefit/risk ratio is warranted.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Epidemiology, Biostatistics and Prevention Institute (EBPI)
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:November 1999
Deposited On:15 Oct 2015 08:11
Last Modified:05 Apr 2016 19:26
Publisher:Lippincott Williams & Wilkins
ISSN:0003-2999
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1213/00000539-199911000-00007
PubMed ID:10553820

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