Large increase in cardiac output in a patient with ARDS and acute right heart failure during inhalation of nitric oxide

• Published in: Acta anaesthesiologica Scandinavica Vol. 41; no. 5; pp. 643 - 646
• Main Authors: BENZING, A., MOLS, G., BEYER, U., GEIGER, K.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.1997; Blackwell
• Subjects: Acute Disease; Acute respiratory distress syndrome; Administration, Inhalation; Biological and medical sciences; Cardiac Output - drug effects; Cardiovascular system; Echocardiography; Electrocardiography; Heart Failure - drug therapy; Heart Failure - physiopathology; Hemodynamics - drug effects; Humans; Male; Medical sciences; Middle Aged; nitric oxide; Nitric Oxide - administration & dosage; Nitric Oxide - pharmacology; Pharmacology. Drug treatments; Pulmonary Gas Exchange - drug effects; Pulmonary Gas Exchange - physiology; Respiratory Distress Syndrome, Adult - drug therapy; Respiratory Distress Syndrome, Adult - physiopathology; right heart failure; therapeutic use; Vasodilator Agents - administration & dosage; Vasodilator Agents - pharmacology; Vasodilator agents. Cerebral vasodilators; Ventricular Dysfunction, Right - drug therapy; Ventricular Dysfunction, Right - physiopathology; Heart; Human; Heart failure; Vasodilator agent; Cardiovascular disease; Blood flow; Inhalation; Case study; Chemotherapy; Treatment; Adult respiratory distress syndrome; Heart disease; Nitric oxide; Hemodynamics
• ISSN: 0001-5172; 1399-6576
• DOI: 10.1111/j.1399-6576.1997.tb04758.x

Background Inhaled nitric oxide (NO), a selective pulmonary vasodilator, reduces pulmonary artery pressure in patients with acute respiratory distress syndrome (ARDS). In spite of the reduction of right ventricular afterload, the effect of NO on cardiac output remains unclear. Methods:A patient with ARDS and echocardiographically determined severe acute right heart failure was treated with increasing concentrations of inhaled nitric oxide (NO). Haemo‐dynamic and gas exchange variables were determined for each concentration of NO. NO treatment was continued for 3 days. Results:During initial right heart failure, administration of NO: resulted in a large increase (32%) in cardiac output in a dose‐dependent manner. When right ventricular function had improved, inhalation of NO did not increase cardiac output. Conclusion: Our observations suggest that inhalation of NO is likely to increase cardiac output in ARE when severe acute right heart failure is present.