Johannigman J A, Davis K, Campbell R S, Luchette F, Hurst J M, Branson R D
Department of Surgery, University of Cincinnati Medical Center, Ohio 45267-0558, USA.
J Trauma. 1997 Dec;43(6):904-9; discussion 909-10. doi: 10.1097/00005373-199712000-00006.
Inhaled nitric oxide has been shown to improve oxygenation in select patients with acute respiratory distress syndrome (ARDS).
The purpose of this study was to evaluate the clinical response to four concentrations of inhaled nitric oxide (NO) in 20 patients with ARDS.
All patients with ARDS were eligible for the study. ARDS was defined as (1) the presence of a predisposing factor; (2) a PaO2/FiO2 ratio < 200; (3) bilateral infiltrates on chest radiograph; and (4) absence of evidence of congestive heart failure and pulmonary artery wedge pressure < 18 mm Hg. Patients received each of four doses (1, 15, 30, and 60 ppm) in random order, each for a 3-hour period. Cardiovascular variables were continuously monitored, and arterial and mixed venous blood gas measurements were obtained at 30 minutes and 3 hours.
Thirteen of the 20 patients demonstrated a significant increase in their PaO2/FiO2 (> 20% increase) when treated with inhaled NO. The administration of inhaled NO was associated with an increase in oxygenation at doses of 1, 15, and 30 ppm, but not 60 ppm. Increasing NO dose to more than 1 ppm did not significantly improve response. Mean pulmonary artery pressure decreased with increasing NO concentration, but this did not reach statistical significance. Nine of the 13 responding patients and 2 of the 7 nonresponding patients survived.
Inhaled NO was successful in increasing PaO2/FiO2 by > 20% in 65% of the surgical patients in this trial. Response to NO could not be predicted by initial PaO2/FiO2 or pulmonary artery pressures. A trial of inhaled NO at a dose of < 10 ppm may be helpful in ARDS patients requiring increasing FiO2 and positive end-expiratory pressure.
吸入一氧化氮已被证明可改善部分急性呼吸窘迫综合征（ARDS）患者的氧合情况。
本研究旨在评估20例ARDS患者对四种浓度吸入一氧化氮（NO）的临床反应。
所有ARDS患者均符合研究条件。ARDS定义为：（1）存在诱发因素；（2）动脉血氧分压/吸入氧分数值（PaO2/FiO2）比值<200；（3）胸部X线片显示双侧浸润影；（4）无充血性心力衰竭证据且肺动脉楔压<18 mmHg。患者按随机顺序接受四种剂量（1、15、30和60 ppm）中的每一种，每种剂量持续3小时。持续监测心血管变量，并在30分钟和3小时时获取动脉血和混合静脉血气测量值。
20例患者中有13例在接受吸入NO治疗时其PaO2/FiO2显著升高（升高>20%）。吸入NO在1、15和30 ppm剂量时与氧合增加相关，但60 ppm剂量时并非如此。将NO剂量增加至超过1 ppm并未显著改善反应。平均肺动脉压随NO浓度增加而降低，但未达到统计学显著性。13例有反应的患者中有9例存活，7例无反应的患者中有2例存活。
在本试验中，吸入NO成功使65%的外科患者的PaO2/FiO2升高>20%。无法通过初始PaO2/FiO2或肺动脉压预测对NO的反应。对于需要增加FiO2和呼气末正压的ARDS患者，试用<10 ppm剂量的吸入NO可能会有帮助。
