1Hedenstierna Laboratory, Department of Surgical Sciences, Section of Anaesthesiology & Critical Care, Uppsala University, Uppsala, Sweden. 2CIBER de enfermedades respiratorias (CIBERES), Madrid, Spain. 3Centro Nacional de Investigaciones Cardiovasculares Carlos III, CNIC, Madrid, Spain. 4Intensive Care Unit, Hospital General de Villalba, Villalba, Spain. 5Intensive Care Unit, Hospital del SAS, Jerez de la Frontera, Spain. 6Departamento de Medicina Intensiva, Pontificia Universidad Católica de Chile, Santiago, Chile. 7Division of Pulmonary, Heart Institute (InCor), Hospital das Clinicas, University of São Paulo, São Paulo, Brazil. 8Department of Anesthesia, Hospital Privado de Comunidad, Mar del Plata, Argentina. 9Department of Medical Sciences, Clinical Physiology, Uppsala University, Uppsala, Sweden.
Crit Care Med. 2017 Nov;45(11):e1157-e1164. doi: 10.1097/CCM.0000000000002701.
To compare the effects of two lung-protective ventilation strategies on pulmonary vascular mechanics in early acute respiratory distress syndrome.
Experimental study.
University animal research laboratory.
Twelve pigs (30.8 ± 2.5 kg).
Acute respiratory distress syndrome was induced by repeated lung lavages and injurious mechanical ventilation. Thereafter, animals were randomized to 4 hours ventilation according to the Acute Respiratory Distress Syndrome Network protocol or to an open lung approach strategy. Pressure and flow sensors placed at the pulmonary artery trunk allowed continuous assessment of pulmonary artery resistance, effective elastance, compliance, and reflected pressure waves. Respiratory mechanics and gas exchange data were collected.
Acute respiratory distress syndrome led to pulmonary vascular mechanics deterioration. Four hours after randomization, pulmonary vascular mechanics was similar in Acute Respiratory Distress Syndrome Network and open lung approach: resistance (578 ± 252 vs 626 ± 153 dyn.s/cm; p = 0.714), effective elastance, (0.63 ± 0.22 vs 0.58 ± 0.17 mm Hg/mL; p = 0.710), compliance (1.19 ± 0.8 vs 1.50 ± 0.27 mL/mm Hg; p = 0.437), and reflection index (0.36 ± 0.04 vs 0.34 ± 0.09; p = 0.680). Open lung approach as compared to Acute Respiratory Distress Syndrome Network was associated with improved dynamic respiratory compliance (17.3 ± 2.6 vs 10.5 ± 1.3 mL/cm H2O; p < 0.001), driving pressure (9.6 ± 1.3 vs 19.3 ± 2.7 cm H2O; p < 0.001), and venous admixture (0.05 ± 0.01 vs 0.22 ± 0.03, p < 0.001) and lower mean pulmonary artery pressure (26 ± 3 vs 34 ± 7 mm Hg; p = 0.045) despite of using a higher positive end-expiratory pressure (17.4 ± 0.7 vs 9.5 ± 2.4 cm H2O; p < 0.001). Cardiac index, however, was lower in open lung approach (1.42 ± 0.16 vs 2.27 ± 0.48 L/min; p = 0.005).
In this experimental model, Acute Respiratory Distress Syndrome Network and open lung approach affected pulmonary vascular mechanics similarly. The use of higher positive end-expiratory pressures in the open lung approach strategy did not worsen pulmonary vascular mechanics, improved lung mechanics, and gas exchange but at the expense of a lower cardiac index.
比较两种肺保护性通气策略对急性呼吸窘迫综合征早期肺血管力学的影响。
实验研究。
大学动物研究实验室。
12 头猪（30.8±2.5kg）。
通过反复肺灌洗和损伤性机械通气诱导急性呼吸窘迫综合征。此后，动物随机分为 4 小时通气，根据急性呼吸窘迫综合征网络协议或开放肺方法策略进行通气。肺动脉干上放置的压力和流量传感器可连续评估肺动脉阻力、有效弹性、顺应性和反射压力波。收集呼吸力学和气体交换数据。
急性呼吸窘迫综合征导致肺血管力学恶化。随机分组 4 小时后，急性呼吸窘迫综合征网络和开放肺方法的肺血管力学相似：阻力（578±252 对 626±153 dyn.s/cm；p=0.714）、有效弹性（0.63±0.22 对 0.58±0.17 mm Hg/mL；p=0.710）、顺应性（1.19±0.8 对 1.50±0.27 mm Hg；p=0.437）和反射指数（0.36±0.04 对 0.34±0.09；p=0.680）。与急性呼吸窘迫综合征网络相比，开放肺方法与改善的动态呼吸顺应性（17.3±2.6 对 10.5±1.3 mL/cm H2O；p<0.001）、驱动压（9.6±1.3 对 19.3±2.7 cm H2O；p<0.001）和静脉混合（0.05±0.01 对 0.22±0.03，p<0.001）和较低的平均肺动脉压（26±3 对 34±7 mm Hg；p=0.045）相关，尽管使用了较高的呼气末正压（17.4±0.7 对 9.5±2.4 cm H2O；p<0.001）。然而，开放肺方法的心脏指数较低（1.42±0.16 对 2.27±0.48 L/min；p=0.005）。
在这个实验模型中，急性呼吸窘迫综合征网络和开放肺方法对肺血管力学的影响相似。在开放肺方法策略中使用更高的呼气末正压并没有使肺血管力学恶化，改善了肺力学和气体交换，但以较低的心脏指数为代价。
