Circulation, Vol 87, 447-453, Copyright © 1993 by American Heart Association
JD Roberts Jr, P Lang, LM Bigatello, GJ Vlahakes and WM Zapol
BACKGROUND. Congenital heart lesions may be complicated by pulmonary
arterial smooth muscle hyperplasia, hypertrophy, and hypertension. We
assessed whether inhaling low levels of nitric oxide (NO), an
endothelium-derived relaxing factor, would produce selective pulmonary
vasodilation in pediatric patients with congenital heart disease and
pulmonary hypertension. We also compared the pulmonary vasodilator
potencies of inhaled NO and oxygen in these patients. METHODS AND RESULTS.
In 10 sequentially presenting, spontaneously breathing patients, we
determined whether inhaling 20-80 ppm by volume of NO at inspired oxygen
concentrations (FIO2) of 0.21-0.3 and 0.9 would reduce the pulmonary
vascular resistance index (Rp). We then compared breathing oxygen with
inhaling NO. Inhaling 80 ppm NO at FIO2 0.21-0.3 reduced mean pulmonary
artery pressure from 48 +/- 19 to 40 +/- 14 mm Hg and Rp from 658 +/- 421
to 491 +/- 417 dyne.sec.cm-5.m-2 (mean +/- SD, both p < 0.05).
Increasing the FIO2 to 0.9 without adding NO did not reduce mean pulmonary
artery pressure but reduced Rp and increased the ratio of pulmonary to
systemic blood flow (Qp/Qs), primarily by increasing Qp (p < 0.05).
Breathing 80 ppm NO at FIO2 0.9 reduced mean pulmonary artery pressure and
Rp to the lowest levels and increased Qp and Qp/Qs (all p < 0.05). While
breathing at FIO2 0.9, inhalation of 40 ppm NO reduced Rp (p < 0.05);
the maximum reduction of Rp occurred while breathing 80 ppm NO. Inhaling 80
ppm NO at FIO2 0.21-0.9 did not alter mean aortic pressure or systemic
vascular resistance. Methemoglobin levels were unchanged by breathing up to
80 ppm NO for 30 minutes. CONCLUSIONS. Inhaled NO is a potent and selective
pulmonary vasodilator in pediatric patients with congenital heart disease
complicated by pulmonary artery hypertension. Inhaling low levels of NO may
provide an important and safe means for evaluating the pulmonary
vasodilatory capacity of patients with congenital heart disease without
producing systemic vasodilation.
ARTICLES
Inhaled nitric oxide in congenital heart disease
Department of Anesthesia, Harvard Medical School, Massachusetts General Hospital, Boston 02114.
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