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

Acta Anaesthesiol Scand. 1997 May;41(5):643-6. 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). Haemodynamic 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 ARDS when severe acute right heart failure is present.

Publication types

  • Case Reports

MeSH terms

  • Acute Disease
  • Administration, Inhalation
  • Cardiac Output / drug effects*
  • Echocardiography
  • Electrocardiography
  • Heart Failure / drug therapy
  • Heart Failure / physiopathology*
  • Hemodynamics / drug effects
  • Humans
  • Male
  • Middle Aged
  • Nitric Oxide / administration & dosage
  • Nitric Oxide / pharmacology*
  • Pulmonary Gas Exchange / drug effects
  • Pulmonary Gas Exchange / physiology
  • Respiratory Distress Syndrome / drug therapy
  • Respiratory Distress Syndrome / physiopathology*
  • Vasodilator Agents / administration & dosage
  • Vasodilator Agents / pharmacology*
  • Ventricular Dysfunction, Right / drug therapy
  • Ventricular Dysfunction, Right / physiopathology*


  • Vasodilator Agents
  • Nitric Oxide