背景：高强度无创正压通气（NPPV）是一种新颖的通气方法，可以通过逐步增加压力支持来最大程度地降低动脉二氧化碳张力（PaCO2）升高，使其达到正常碳酸血症。我们测试了高强度NPPV是否比低强度NPPV在降低PaCO2，减少吸气量方面更有效，缓解呼吸困难，提高意识，改善慢性阻塞性肺疾病急性加重期（AECOPD）患者的NPPV耐受性。
方法：在这种生理上，随机对照试验，我们将24例AECOPD患者分为高强度NPPV(n=12)或低强度NPPV(n=12).主要结果是随机分组后24小时PaCO2。次要结果包括随机分组后24小时除PaCO2以外的气体交换，吸气的努力，呼吸困难,意识,NPPV公差,病人-呼吸机异步,心功能,呼吸机相关性肺损伤（VILI），和NPPV相关的不良事件。
结果：随机分组后24小时吸气气道正压显著高于对照组（28.0[26.0-28.0]vs.15.5[15.0-17.5]cmH2O；p=0.000），前24小时内的NPPV持续时间明显更长（21.8±2.1vs.15.3±4.7h；p=0.001）在高强度NPPV组中。随机分组24小时后，高强度NPPV组的PaCO2降至54.0±11.6mmHg，而低强度NPPV组仅降至67.4±10.6mmHg（p=0.008）。吸气食管压力摆动，食管压力-时间乘积（PTPes）/呼吸，PTPes/min,高强度组PTPes/L明显降低。随机分组后24小时的副肌使用和呼吸困难评分在该组中也显著较低。在意识方面没有观察到显著的组间差异,NPPV公差,病人-呼吸机异步,心功能,VILI,或NPPV相关不良事件。
结论：高强度NPPV比低强度NPPV在降低PaCO2升高，减少吸气努力方面更有效，缓解AECOPD患者的呼吸困难。
背景：ClinicalTrials.gov（NCT04044625；2019年8月5日注册）。
BACKGROUND: High-intensity noninvasive positive pressure ventilation (NPPV) is a novel ventilatory approach to maximally decreasing elevated arterial carbon dioxide tension (PaCO2) toward
normocapnia with stepwise up-titration of pressure support. We tested whether high-intensity NPPV is more effective than low-intensity NPPV at decreasing PaCO2, reducing inspiratory effort, alleviating dyspnoea, improving consciousness, and improving NPPV tolerance in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).
METHODS: In this physiological, randomised controlled trial, we assigned 24 AECOPD patients to undergo either high-intensity NPPV (n = 12) or low-intensity NPPV (n = 12). The primary outcome was PaCO2 24 h after randomisation. Secondary outcomes included gas exchange other than PaCO2 24 h after randomisation, inspiratory effort, dyspnoea, consciousness, NPPV tolerance, patient-ventilator asynchrony, cardiac function, ventilator-induced lung injury (VILI), and NPPV-related adverse events.
RESULTS: Inspiratory positive airway pressure 24 h after randomisation was significantly higher (28.0 [26.0-28.0] vs. 15.5 [15.0-17.5] cmH2O; p = 0.000) and NPPV duration within the first 24 h was significantly longer (21.8 ± 2.1 vs. 15.3 ± 4.7 h; p = 0.001) in the high-intensity NPPV group. PaCO2 24 h after randomisation decreased to 54.0 ± 11.6 mmHg in the high-intensity NPPV group but only decreased to 67.4 ± 10.6 mmHg in the low-intensity NPPV group (p = 0.008). Inspiratory oesophageal pressure swing, oesophageal pressure-time product (PTPes)/breath, PTPes/min, and PTPes/L were significantly lower in the high-intensity group. Accessory muscle use and dyspnoea score 24 h after randomisation were also significantly lower in that group. No significant between-groups differences were observed in consciousness, NPPV tolerance, patient-ventilator asynchrony, cardiac function, VILI, or NPPV-related adverse events.
CONCLUSIONS: High-intensity NPPV is more effective than low-intensity NPPV at decreasing elevated PaCO2, reducing inspiratory effort, and alleviating dyspnoea in AECOPD patients.
BACKGROUND: ClinicalTrials.gov (NCT04044625; registered 5 August 2019).
