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该前瞻性研究的目的在于确定吸入一氧化氮(NO)是否可以逆转急性呼吸窘迫综合征(ARDS)患者因高碳酸血症(代偿期)所致的肺动脉压力和肺血管阻力的增加。 对11例ARDS的危重患者进行研究,其中有9例男性,2例女性;3例为外伤后发生ARDS,8例为外科术后引起;平均年龄在59±22岁。Murray评分≥2.5。对上述患者持续静脉给予镇静镇痛药物,并进行连续正压机械通气。调整每分通气量使PaCO_2在4.7～6kPa以造成常碳酸血症,使通气量减少一半而造成代偿性高碳酸血症。分别于常碳酸血症期和高碳酸血症期采用含NO(浓度为2ppm)的气体进行机械性肺通气,并进行四个时相的研究:①常碳酸血症期(PaCO_25.1±0.8kPa,潮气量65±132ml)。此期为1小时。②常碳酸血症期+NO(2ppm)吸入,为时30分钟。⑧高碳酸血症期(PaCO_2 8.7±2kPa,潮气量330±93ml),为时60～
The purpose of this prospective study was to determine whether inhaled nitric oxide (NO) reverses pulmonary artery pressure and pulmonary vascular resistance in patients with acute respiratory distress syndrome (ARDS) due to hypercapnia (compensatory phase). Eleven patients with critically ill ARDS were studied, including 9 males and 2 females; 3 developed ARDS after trauma and 8 resulted in surgery; mean age was 59 ± 22 years. Murray score ≥2.5. The above patients continued intravenous sedative and analgesic drugs, and continuous positive pressure mechanical ventilation. Adjust the ventilation rate per minute to make PaCO_2 at 4.7 ~ 6kPa to cause hypercapnia, ventilation reduced by half and cause compensatory hypercapnia. Mechanical ventilation was performed in patients with hypercapnia and hypercapnia using NO (2ppm concentration) respectively, and four phases were studied: (1) hypercapnia (PaCO_25.1 ± 0.8 kPa, tidal volume of 65 ± 132ml). This period is 1 hour. ② hypercapnia + NO (2ppm) inhalation, for 30 minutes. ⑧ hypercapnia (PaCO_2 8.7 ± 2kPa, tidal volume 330 ± 93ml), the time of 60 ~