Inhaled vasodilators have been hypothesized to provide benefit in the setting of pulmonary embolism via their ability to modulate the production of cyclic guanosine monophosphate leading to decreased pulmonary arterial pressure. Studies have shown that inhaled nitric oxide may be beneficial in providing afterload reduction to the right ventricle in patients with acute pulmonary embolism; however, there are no recommendations for its use in current practice guidelines. Join Dr. Cody Craven in reviewing the existing literature surrounding this topic and learn new guidance on the potential use of inhaled nitric oxide for patients with acute pulmonary embolism.
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Acute pulmonary embolism (PE) is characterized by direct thrombotic occlusion of the pulmonary vasculature. However, the associated mortality risk is driven by an increase in pulmonary vascular resistance and afterload resulting in decompensated right ventricular failure. Right ventricular dysfunction also contributes to ventilation-perfusion abnormalities that further exacerbate dyspnea and hypoxemia. Inhaled vasodilators have been hypothesized to provide benefit in the setting of PE via their ability to modulate the production of cyclic guanosine monophosphate leading to decreased pulmonary arterial pressure. Nitric oxide, in particular, is an intriguing agent given the relative deficiency of nitric oxide in patients with PE. In this seminar, we will discuss the current perspective on the use of inhaled nitric oxide in patients with PE as well as the clinical challenges that may arise with its use. Finally, the available literature will be critiqued and recommendations for use provided.
- Describe the underlying pathophysiologic mechanisms of acute pulmonary embolism.
- Identify the mechanism of action of inhaled nitric oxide in reducing pulmonary vascular resistance.
- Explain the potential role of inhaled nitric oxide in patients with acute pulmonary embolism.
Dr. Cody Craven
Release Date: Feb 12, 2021
Credit Expiration Date: Feb 12, 2024