McIntyre R C, Moore F A, Moore E E, Piedalue F, Haenel J S, Fullerton D A
Department of Surgery, University of Colorado Health Sciences Center, Denver 80262, USA.
J Trauma. 1995 Sep;39(3):418-25. doi: 10.1097/00005373-199509000-00004.
The purpose of this study was to determine the effect of inhaled nitric oxide (NO) on oxygenation, hemodynamics, and ventilation in patients with adult respiratory distress syndrome (ARDS).
Sixteen trials of inhaled NO were performed in 14 ARDS patients (age 42.9 +/- 6) who had significant pulmonary hypertension (mean pulmonary artery pressure > 30 mm Hg). Patients were monitored with arterial and pulmonary artery catheters. Volume ventilation was performed by a strict protocol. Data were collected at baseline and 30 minutes after 20 and 40 ppm NO.
Overall, the Pao2/FIO2 ratio increased from 69.5 +/- 3.9 to 100.8 +/- 9.5 at 20 ppm, a 42.9 +/- 8.7% increase, and to 97.7 +/- 13.1 at 40 ppm, a 44.1 +/- 14.2% increase over baseline (p = 0.001). However, 5/16 trials demonstrated minimal improvement (Pao2/FIO2 ratio increase < 20%), 5 moderate improvement (20-50%), and 6 marked improvement (> 50%). Overall the mean pulmonary artery pressure (MPAP) decreased from 41.1 +/- 1.8 mm Hg to 34.3 +/- 1.3 at 20 ppm and 33.5 +/- 1.8 mm Hg at 40 ppm, a 15.0 +/- 3.7% decrease, p = 0.002. However, 5/16 trials demonstrated minimal improvement (MPAP decrease < 10%), 7 moderate improvement (10-20%), and 4 marked improvement (> 20%). At 40 ppm NO, 4 patients with moderate improvement in MPAP at 20 ppm NO had marked improvement. There were no changes in systemic oxygen delivery and consumption, intrapulmonary shunt, or lung compliance at 20 or 40 ppm (p > 0.05). Following collection of these data, prolonged NO inhalation (2-20 ppm) was done in 10 of 14 patients for 4.5 +/- 0.7 days (range 1-10 days). Overall, there were 7 deaths (mortality 50%). In patients receiving prolonged NO, there were 3 deaths (mortality 30%). All 4 patients who failed to respond to inhaled NO subsequently died (mortality 100%).
Inhaled NO improves oxygenation and pulmonary hemodynamics in patients with ARDS. However, the improvement to NO is variable.
本研究旨在确定吸入一氧化氮（NO）对成人呼吸窘迫综合征（ARDS）患者氧合、血流动力学及通气的影响。
对14例（年龄42.9±6岁）患有严重肺动脉高压（平均肺动脉压>30 mmHg）的ARDS患者进行了16次吸入NO试验。通过动脉和肺动脉导管对患者进行监测。按照严格方案进行容量通气。在基线以及吸入20 ppm和40 ppm NO后30分钟收集数据。
总体而言，吸入20 ppm NO时，动脉血氧分压/吸氧浓度（Pao2/FIO2）比值从69.5±3.9升至100.8±9.5，较基线升高42.9±8.7%；吸入40 ppm NO时，该比值升至97.7±13.1，较基线升高44.1±14.2%（p = 0.001）。然而，16次试验中有5次显示改善极小（Pao2/FIO2比值升高<20%），5次为中度改善（20 - 50%），6次为显著改善（>50%）。总体而言，平均肺动脉压（MPAP）在吸入20 ppm NO时从41.1±1.8 mmHg降至34.3±1.3 mmHg，在吸入40 ppm NO时降至33.5±1.8 mmHg，降低了15.0±3.7%，p = 0.002。然而，16次试验中有5次显示改善极小（MPAP降低<10%），7次为中度改善（10 - 20%），4次为显著改善（>20%）。在吸入40 ppm NO时，4例在吸入20 ppm NO时MPAP中度改善的患者有显著改善。吸入20 ppm或40 ppm NO时，全身氧输送和消耗、肺内分流或肺顺应性均无变化（p>0.05）。收集这些数据后，14例患者中的10例进行了持续NO吸入（2 - 20 ppm），持续4.5±0.7天（范围1 - 10天）。总体共有7例死亡（死亡率50%）。在接受持续NO吸入的患者中，有3例死亡（死亡率30%）。所有4例对吸入NO无反应的患者随后均死亡（死亡率100%）。
吸入NO可改善ARDS患者的氧合及肺血流动力学。然而，对NO的反应存在个体差异。
