PARTIAL LIQUID VENTILATION COMBINED WITH INHALED NITRIC-OXIDE IN ACUTE RESPIRATORY-FAILURE WITH PULMONARY-HYPERTENSION IN PIGLETS

Citation
G. Zobel et al., PARTIAL LIQUID VENTILATION COMBINED WITH INHALED NITRIC-OXIDE IN ACUTE RESPIRATORY-FAILURE WITH PULMONARY-HYPERTENSION IN PIGLETS, Pediatric research, 41(2), 1997, pp. 172-177
Citations number
24
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
41
Issue
2
Year of publication
1997
Pages
172 - 177
Database
ISI
SICI code
0031-3998(1997)41:2<172:PLVCWI>2.0.ZU;2-1
Abstract
This study was a prospective, randomized, controlled design to evaluat e gas exchange, lung mechanics, and pulmonary hemodynamics during part ial liquid ventilation (PLV) combined with inhaled nitric oxide (NO) i n acute respiratory failure (ARF) with pulmonary hypertension (PH). AR F with PH was induced in 12 piglets weighing 9.7-13.7 kg by repeated l ung lavages and the continuous infusion of the stable endoperoxane ana log of thromboxane. Thereafter the animals were randomly assigned eith er for PLV or conventional mechanical ventilation (CMV) at a fractiona l concentration of inspired O-2 (Fio(2)) of 1.0. Perfluorocarbon (PFC) Liquid (30 mt kg(-1)) was instilled into the endotracheal tube over 5 min followed by 5 mt kg(-1)h(-1). All animals were treated with diffe rent concentrations of NO (1-10-20 ppm) inhaled in random order. Conti nuous monitoring included EGG, right atrial (Pra), mean pulmonary arte ry (Ppa), pulmonary capillary (Ppc'), and mean arterial (Pal pressures , arterial oxygen saturation, and mixed venous oxygen saturation measu rements. During PLV Pao(2)/Fio(2) increased significantly from 8.2 +/- 0.4 kPa to 34.8 +/- 5.1kPa (p < 0.01), whereas Pao(2)/FiO(2) remained constant at 9.5 +/- 0.4 kPa during CMV. The infusion of the endoperox ane analog resulted in a sudden decrease of Pao(2)/Fio(2) from 34.8 +/ - 5.1 kPa to 14.1 +/- 0.4 kPa (p < 0.01) in the PLV group and from 9.5 +/- 0.4 kPa to 6.9 +/- 0.2 kPa (p < 0.05) in the control group. Inhal ed NO significantly improved oxygenation in both groups (Pao(2)/Fio(2) : 45.7 +/- 5.3 kPa during PLV and 25.9 +/- 4.7 kPa during CMV). During inhalation of NO mean Ppa decreased significantly from 7.8 +/- 0.26 k Pa to 4.2 +/- 0.26 kPa (p < 0.01 in the PLV group and from 7.4 +/- 0.2 6 kPa to 5.1 +/- 0.13 kPa (p < 0.01) in the control group. As document ed in the literature PLV significantly improves oxygenation and lung m echanics in severe ARF. In addition, when ARF is associated with sever e PH, the combined treatment of PLV and inhaled NO improves pulmonary hemodynamics resulting in better oxygenation.