Effective control of pulmonary vascular resistance with inhaled nitric oxide after cardiac operation

• Published in: The Journal of thoracic and cardiovascular surgery Vol. 111; no. 4; pp. 753 - 763
• Main Authors: Fullerton, David A., Jones, Stephen D., Jaggers, James, Piedalue, Fran, Grover, Frederick L., McIntyre, Robert C.
• Format: Journal Article
• Language: English
• Published: United States Mosby, Inc 01.04.1996; AATS/WTSA
• Subjects: Administration, Inhalation; Coronary Artery Bypass; Coronary Disease - physiopathology; Coronary Disease - surgery; Hemodynamics - drug effects; Humans; Lung - drug effects; Lung - physiology; Male; Middle Aged; Nitric Oxide - administration & dosage; Nitric Oxide - pharmacology; Pulmonary Circulation - drug effects; Vascular Resistance - drug effects; Vasodilator Agents - administration & dosage; Vasodilator Agents - pharmacology
• ISSN: 0022-5223; 1097-685X
• DOI: 10.1016/S0022-5223(96)70335-5

Increased pulmonary vascular resistance may greatly complicate the perioperative management of cardiac surgical patients. Inhaled nitric oxide may be a promising new therapy to selectively lower pulmonary vascular resistance. The purpose of this study was to examine the effects of inhaled nitric oxide on pulmonary and systemic hemodynamics in cardiac surgical patients. Twenty patients (age 57 ± 6 years) were studied in the operating room after weaning from cardiopulmonary bypass. Mean pulmonary artery pressure, pulmonary vascular resistance, systemic vascular resistance, and mean aortic pressure were determined at four points of data collection: before nitric oxide, with 20 ppm nitric oxide, with 40 ppm nitric oxide, and after nitric oxide. Statistical analysis was by analysis of variance; significance was accepted for p < 0.05. Inhaled nitric oxide produced selective pulmonary vasorelaxation. Pulmonary vascular resistance was lowered from 343 ± 30 before nitric oxide to 233 ± 25 dynes · sec -1 · cm -5 with 20 ppm nitric oxide. Pulmonary vascular resistance was not further lowered by 40 ppm nitric oxide ( p < 0.05). Mean pulmonary arterial pressure was 29 ± 1 mm Hg before nitric oxide and was lowered to 22 ± 1 mm Hg by 20 ppm nitric oxide and 21 ± 1 mm Hg by 40 ppm nitric oxide ( p < 0.05). Both pulmonary vascular resistance and mean pulmonary arterial pressure returned to baseline after withdrawal of inhaled nitric oxide. Inhaled nitric oxide produced no changes in either systemic vascular resistance or mean aortic pressure. We conclude that nitric oxide may be used as an effective pulmonary vasodilator after cardiac operations. It may be particularly valuable for selectively lowering right ventricular afterload in patients with right ventricular dysfunction. (J T HORAC C ARDIOVASC S URG 1996;111:753-63)