Inhaled Nitric Oxide in Pulmonary Embolism

The early phase of severe pulmonary embolism is associated with high mortality. Right ventricular failure induced by the increase in right ventricular afterload is the final cause of deterioration leading to circulatory failure in patients who die from severe pulmonary embolism. Therefore, reduction of right ventricular afterload remains the central therapeutic strategy. In acute pulmonary embolism, the increase in pulmonary vascular resistance is caused by reduction in the cross-sectional area of the pulmonary vascular bed from obstructing emboli. Pulmonary arterial constriction further increases pulmonary vascular resistance, whereby vasoactive humoral factors may be contributing, which are released from activated platelets accumulating at the site of the clot. Consequently, administration of vasodilators of the pulmonary circulation may be regarded as a therapeutic option to antagonize increased pulmonary vasoconstriction or compensate for impaired vasodilation. Inhaled nitric oxide (NO) acts as a powerful selective pulmonary vasodilator. The aim of the study is to determine, if short-term inhalation of NO is beneficial in respiratory compromised patients with right ventricular dysfunction after acute pulmonary embolism.

Inclusion criteria

• Patients with acute pulmonary embolism within 24 hours after onset of symptoms.
• Patients with hypoxaemia not present before pulmonary embolism and acute right ventricular dysfunction.

Exclusion criteria

• Age < 18 years.
• Chronic lung disease, left heart failure, suspected or documented intracranial bleeding.
• Pregnancy, Methaemoglobinaemia.
• Patients who previously needed thrombolysis or surgical embolectomy.
• Negative D-Dimer test.