Inhaled nitric oxide as therapy for pulmonary hypertension in postoperative cases of congenital heart defects.

This is a prospective study using inhaled nitric oxide (NO) as a selective pulmonary vasodilator in postoperative cases of CHD. From February 1995 to December 1995, NO was used selectively in 10 patients postoperatively in whom conventional management of PAH crisis failed and PA pressures were more than half the systemic pressure. The age of the patients varied from 2 months to 3 years and duration of NO inhalation ranged from 1 day to 13 days. Of 10 patients, 8 patients responded well with 5-20 ppm and 2 did not respond, even after increasing the NO to 120 ppm. The preoperative mean pulmonary systolic pressure was 83 +/- 17.1 mm Hg against mean systemic systolic pressure of 84 +/- 9.2 mm Hg. Postoperatively, their PA pressure reduced to 54 +/- 16.1 mm Hg (mean systolic) with systemic pressure of 85 +/- 15.9 mm Hg (mean systolic). After using inhaled NO, PA pressure dropped to 19 +/- 2.5 mm Hg mean systolic (p < 0.0078), after excluding the nonresponders. The two nonresponders died postoperatively. Our study shows that NO selectively reduces the PA pressure unlike conventional vasodilators. This helps to decrease the incidence of postoperative PAH crisis, thereby reducing the morbidity and mortality. However, long-term beneficial effects are yet to be studied.