What is the primary effect of inhaled nitric oxide in respiratory therapy?

Inhaled nitric oxide is primarily used in respiratory therapy because it causes vasodilation in the pulmonary vasculature. This effect is particularly beneficial in conditions such as pulmonary hypertension or acute respiratory distress syndrome (ARDS) where elevated pulmonary artery pressures can lead to compromised oxygenation and impaired blood flow. By selectively dilating the pulmonary blood vessels, inhaled nitric oxide helps improve perfusion in well-ventilated areas of the lungs, enhancing oxygen uptake and reducing the shunting of blood away from well-ventilated regions.

The use of inhaled nitric oxide does not necessarily result in significant changes to airway resistance, nor does it function as a traditional bronchodilator that would widen the airways themselves. Additionally, while increased lung compliance might be a result of improved lung function in some patients, the primary mechanism of inhaled nitric oxide relates directly to pulmonary vasodilation rather than factors affecting lung compliance. This distinct action underscores its therapeutic role in managing specific pulmonary conditions.