Lundin S, Westfelt U N, Stenqvist O, Blomqvist H, Lindh A, Berggren L, Arvidsson S, Rudberg U, Frostell C G
Department of Anaesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Intensive Care Med. 1996 Aug;22(8):728-34. doi: 10.1007/BF01709513.
To evaluate the dose response of inhaled nitric oxide (NO) on gas exchange and central haemodynamics in patients with early acute lung injury (ALI).
Prospective, multicentre clinical study.
General ICUs in university and regional hospitals.
18 Patients with early ALI according to specified criteria.
During controlled ventilation an inhalation system was used to deliver NO (1000 ppm in N2) and O2/air to the low pressure fresh gas inlet of a Siemens 900C ventilator. Haemodynamics and pulmonary gas exchange variables were measured at baseline and at stepwise increased inspiratory NO concentrations of 0.1, 0.3, 1, 3, 10, 30 and 100 ppm, each dose being maintained for 15 min. Dose testing was repeated the next day, and the response to prolonged (2 h) NO inhalation at 1 and 10 ppm was also tested.
Inhalation of NO produced a significant increase in PaO2 (P < 0.0025). The degree of response, as well as the optimal NO dose varied in individual patients and between different days. Venous admixture (QVA/QT) was reduced (P < 0.02) from 38% (31-46%) to 33% (26-41%). In our patients with early acute lung injury and only a moderate elevation in pulmonary arterial pressure NO inhalation did not reduce mean pulmonary artery pressure significantly, being 27.0 (21-30) mmHg at baseline and 26.0 (21-30) mm Hg at 100 ppm.
This study shows that improvements in arterial oxygenation in response to inhaled NO may show great inter- as well as intraindividual variability, and that improvements in arterial oxygenation occur without any measurable lowering of the pulmonary artery pressure.
评估吸入一氧化氮(NO)对早期急性肺损伤(ALI)患者气体交换及中心血流动力学的剂量反应。
前瞻性多中心临床研究。
大学及地区医院的普通重症监护病房。
18例符合特定标准的早期ALI患者。
在控制通气期间,使用吸入系统将NO(氮气中浓度为1000 ppm)和氧气/空气输送至西门子900C呼吸机的低压新鲜气体入口。在基线时以及逐步增加吸入NO浓度至0.1、0.3、1、3、10、30和100 ppm时测量血流动力学和肺气体交换变量,每个剂量维持15分钟。次日重复剂量测试,并测试1和10 ppm的NO延长吸入(2小时)的反应。
吸入NO使动脉血氧分压(PaO2)显著升高(P < 0.0025)。反应程度以及最佳NO剂量在个体患者之间和不同日期有所不同。静脉混合血(QVA/QT)从38%(31 - 46%)降至33%(26 - 41%)(P < 0.02)。在我们这些早期急性肺损伤且肺动脉压仅中度升高的患者中,吸入NO并未显著降低平均肺动脉压,基线时为27.0(21 - 30)mmHg,100 ppm时为26.0(21 - 30)mmHg。
本研究表明,吸入NO后动脉氧合的改善可能存在较大的个体间及个体内变异性,并且动脉氧合改善时肺动脉压无任何可测量的降低。