IMPROVEMENT OF PERIOPERATIVE HEMODYNAMICS AND GAS-EXCHANGE BY INHALEDNITRIC-OXIDE IN CHILDREN WITH CONGENITAL CARDIOPULMONARY DEFECTS

Objectives: In critically ill infants and children before or after sur gery for congenital cardiopulmonary disease it was evaluated whether c ontinuous NO inhalation can reduce pulmonary artery pressure (PAP) and improve arterial oxygen saturation (SaO(2)). Methods: All patients (n = 24; age 1 day-6.5 years) were intubated and artificially ventilated . They had either secondary pulmonary hypertension (n = 16), acute res piratory distress syndrome (n = 3), or reduced SaO(2) (n = 5) due to p ulmonary hypoperfusion. NO was introduced into the afferent limb of th e ventilator circuit close to the endotracheal tube, while continuousl y measuring the inspired NO and O-2 concentrations. The initially appl ied concentration of NO was 20 +/- 2.0 ppm. Results: The hemodynamic c ondition and/or oxygen saturation was significantly improved by NO in 23 patients (95 %). Mean PAP declined significantly from 45 +/- 7 to 2 8 +/- 3.7 mm Hg, while mean systemic arterial pressure remained consta nt (56 +/- 2.1 vs. 58 +/- 2.5 mm Hg). This was related to a selective reduction in pulmonary vascular resistance by 48 +/- 8.5 %. SaO(2) inc reased significantly (p < 0.05) from 83 +/- 2.5 % to 93 +/- 1.5 % due to a decreased intrapulmonary right-to-left shunt. NO therapy was appl ied with a median of 6 days (range 1.5-36 days). During NO inhalation methemoglobin concentration was significantly increased (0.77 +/- .0.0 5 % vs. 1.46 +/- 0.15 %), but neither was oxygen transport capacity af fected, nor was any evidence for accumulation observed. Using a model ventilatory circuit, a nitric dioxide (NO2) formation of 1.14 +/- 0.11 % of the applied NO concentration was measured, i.e. approximately 0. 5 ppm NO2 at 40 ppm NO. This amount of NO2 in the inspired gas is well be low toxicologically relevant concentrations . Conclusions: Low-dos e NO inhalation selectively reduces PAP and improves SaO(2) in childre n with congenital cardiopulmonary disease during perioperative intensi ve care. It is expected that the overall hemodynamic improvement is re lated to a reduced afterload of the subpulmonary ventricle without cha nges in coronary perfusion pressure, as is often observed with other v asodilators applied intravenously. We recommend an upper dose limit of 40 ppm NO for continuous NO inhalation to avoid possible toxicologica lly relevant NO2 concentrations.