Role of inhaled nitric oxide as a selective pulmonary vasodilator in pediatric cardiac surgical practice.

Our aim was to assess the role of inhaled nitric oxide (NO) therapy in post operative cases of congenital heart defects who developed pulmonary arterial hypertensive (PAH) crisis and had no response with conventional management. From February '95 to January '97, inhaled NO therapy was used in 21 children. Age ranged from 2 months to 9 years (mean 5.6 years) and duration of therapy ranged from 1 to 13 days. Of 21 patients, 17 responded well with 5-20 ppm while 4 did not. The preoperative mean pulmonary systolic pressure was 88 mm Hg against mean systemic pressure of 96 mm Hg. Post operatively, their PA pressure reduced to 62 mm Hg, with systemic pressure of 98 mm Hg. After using inhaled NO, PA pressure dropped to 24 mm Hg (mean systolic) (p < 0.007), after excluding the non responders. Of 4 non responders, two died due to irreversible pulmonary vascular disease and remaining two died due to residual defects. The study shows that inhaled NO is a selective pulmonary vasodilator, which is useful in postoperative PAH crisis and also reduces the transpulmonary gradient in single ventricle repair cases. It is safe and effective for prolonged use. It is very useful in Indian perspective, when more number of cases with congenital heart defects (CHD) along with severe PAH are encountered routinely.

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.