Impact of inhaled nitric oxide on pulmonary capillary pressure in ARDS patients

Introduction

Inhaled nitric oxide (NO) causes selective pulmonary vasodilation. In experiment, pulmonary arteries were shown to be primary site of NO effect. Our aim was to study the effect of inhaled NO on pulmonary vasculature in ARDS patients.

Materials and methods

Inhaled NO was tested in 8 ARDS patients (PaO₂/FiO₂ = 71 ± 26 mmHg, LIS >2.5). One hour test of 20 ppm NO was performed and in 3 patients NO was additionally increased to 40 ppm with the primary aim to improve oxygenation. Positive pressure response was defined as a decrease of mean pulmonary artery pressure (mPAP) >2 mmHg. Pressure curves during pulmonary artery occlusion were recorded in duplicate before and with NO and the more representative one was used for pulmonary capillary pressure (PCP) estimation [1]. Positive response in oxygenation was defined as PaO₂/FiO₂ increase >20%. Statistics: non-parametrical Wilcoxon test for two related samples and simple correlation when appropriate. Data are presented as means ± SD. P < 0.05 was considered significant.

Results

In 1 patient a marked decrease in mPAP was measured (l5 mmHg), in other 4 patients the drop was marginal (3-4 mmHg). Three patients did not respond to NO inhalation by any significant change in mPAP. In five responders PCP and PCWP pressure did not change before and after the NO test (25.0 ± 4.5 and 24.2 ± 5.3 mmHg for PCP; P = 0.18 and 18.0 ± 3.3 and l7.8 ± 3.9 mmHg for PCWP; P = 0.59). Transpulmonary pressure difference (dPAP-PCWP) decreased significantly (14.6 ± 1.4 and 11.0 ± 3.7 mmHg, respectively: P = 0.04) which corresponded with trend to decrease the arterial component of the transpulmonary pressure difference (dPAP-PCP) (7.6 ± 3.0 and 4.5 ± 2.6 mmHg, respectively; P = 0.11 i.e. decrease in 4 cases).

Conclusion

When effective in lowering pulmonary pressures, inhaled NO seems to act primarily on the arterial component of transpulmonal vascular resistance.