Hickling K G, Walsh J, Henderson S, Jackson R
Department of Intensive Care, Christchurch Hospital, New Zealand.
Crit Care Med. 1994 Oct;22(10):1568-78. doi: 10.1097/00003246-199422100-00011.
To evaluate the outcome in patients with severe adult respiratory distress syndrome (ARDS) managed with limitation of peak inspiratory pressure to 30 to 40 cm H2O, low tidal volumes (4 to 7 mL/kg), spontaneous breathing using synchronized intermittent mandatory ventilation from the start of ventilation, and permissive hypercapnia without the use of bicarbonate to buffer acidosis. Also, to compare hospital mortality rate with that predicted by the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system and the "ventilator score."
A ten-bed general intensive care unit in a university hospital.
Prospective, descriptive study.
Fifty-three patients with severe ARDS having a lung injury score of > or = 2.5.
Data recording.
The hospital mortality rate was significantly lower than that predicted by the APACHE II scores (26.4% vs. 53.3%, p = .004), even after correcting the latter for the effect of hypercapnic acidosis (26.4% vs. 51.1%, p = .008). The mortality rate increased with increasing number of organ failures, but was only 43% in patients with > or = 4 organ failures, 20.5% with < or = 3 organ failures, and 6.6% with only respiratory failure. The mean maximum PaCO2 was 66.5 torr (range 38 to 158 torr [8.87 kPa, range 5.07 to 21.07]), and the mean arterial pH at the same time was 7.23 (range 6.79 to 7.45). There was no correlation between the maximum PaCO2 or the corresponding pH and the total respiratory rate at the same time. No pneumothoraces developed during mechanical ventilation.
These results lend further support to the hypothesis that limitation of peak inspiratory pressure and reduction of regional lung overdistention by the use of low tidal volumes with permissive hypercapnia may reduce ventilator-induced lung injury and improve outcome in severe ARDS. This hypothesis is supported by a large body of experimental evidence, which also suggests that ventilator-induced lung injury may result in the release of inflammatory mediators, and thus may have the potential to augment the development of multiple organ dysfunction. However, the hypothesis requires testing in a randomized trial as acute hypercapnia could potentially have some adverse as well as beneficial effects.
评估对重症成人呼吸窘迫综合征（ARDS）患者采用以下治疗方法的效果：将吸气峰压限制在30至40 cm H₂O，采用低潮气量（4至7 mL/kg），从通气开始即使用同步间歇指令通气进行自主呼吸，以及允许高碳酸血症且不使用碳酸氢盐缓冲酸中毒。此外，将医院死亡率与急性生理与慢性健康状况评估（APACHE）II评分系统和“通气评分”预测的死亡率进行比较。
一所大学医院的一间拥有十张床位的综合重症监护病房。
前瞻性描述性研究。
53例重症ARDS患者，肺损伤评分≥2.5。
数据记录。
医院死亡率显著低于APACHE II评分预测的死亡率（26.4%对53.3%，p = 0.004），即使在对后者校正高碳酸血症酸中毒的影响后也是如此（26.4%对51.1%，p = 0.008）。死亡率随器官衰竭数量的增加而升高，但在器官衰竭≥4个的患者中仅为43%，在器官衰竭≤3个的患者中为20.5%，在仅呼吸衰竭的患者中为6.6%。平均最高PaCO₂为66.5 torr（范围38至158 torr [8.87 kPa，范围5.07至21.07]），同时的平均动脉pH值为7.23（范围6.79至7.45）。最高PaCO₂或相应的pH值与同时的总呼吸频率之间无相关性。机械通气期间未发生气胸。
这些结果进一步支持了以下假设：通过使用低潮气量并允许高碳酸血症来限制吸气峰压和减少局部肺过度膨胀，可能会减少呼吸机诱发的肺损伤并改善重症ARDS的预后。这一假设得到了大量实验证据的支持，这些证据还表明呼吸机诱发的肺损伤可能导致炎症介质的释放，因此可能有加剧多器官功能障碍发展的潜力。然而，这一假设需要在随机试验中进行验证，因为急性高碳酸血症可能既有潜在的不良影响，也有有益影响。
