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Large increase in cardiac output in a patient with ARDS and acute right heart failure during inhalation of nitric oxide
Author(s) -
BENZING A.,
MOLS G.,
BEYER U.,
GEIGER K.
Publication year - 1997
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1997.tb04758.x
Subject(s) - medicine , ards , inhalation , cardiac output , nitric oxide , anesthesia , cardiology , heart failure , afterload , pulmonary artery , cardiac function curve , lung , hemodynamics
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.