以跨肺压为导向的肺保护通气策略对犬急性呼吸窘迫综合征模型呼吸生理及肺损伤的影响
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摘要
目的:比较以跨肺压(PL)为导向的肺保护通气策略(控制PL)和传统肺保护通气策略(控制Pplat)分别在机控通气和保留自主呼吸模式下对犬急性呼吸窘迫综合征(ARDS)模型呼吸生理的影响,并探讨其机制。方法:18只比格犬采用静注油酸复制ARDS模型,随机分为3组,每组6只:A组(镇静组):充分镇静肌松,呼吸机控制通气,控制Pplat=30cmH_2O(即相当于控制吸气末PL=20cmH2O);B组(控制PL组):保留自主呼吸,控制吸气末PL=20cmH_2O;C组(控制Pplat组):保留自主呼吸,控制Pplat=30cmH_2O。观察动物基础状态(成模前)及肺保护通气前后的氧合功能、呼吸力学指标变化,胸活检取肺组织,HE染色进行病理学评分。结果:与A、B两组相比,C组动态肺顺应性(CL-dyn)、静态肺顺应性(CL-stat)明显低于A组和B组(P<0.05),潮气量(VT)高于A组和B组(P<0.05);C组氧输送(DO_2)明显低于A组和B组,肺内分流比例(Qs/Qt)高于A组和B组(P<0.05);C组的肺损伤总分高于A组和B组(P<0.05);肺损伤分类评分中,C组中性白细胞浸润评分和间质水肿高于A组和B组(P<0.05),C组肺不张评分均低于A组和B组(P<0.05);结论:监控PL无论在自主呼吸或机控呼吸状态下,均能够有效地调控肺容量,改善肺顺应性和氧输送,减轻呼吸机相关性肺损伤(VILI);在保留自主呼吸时,单纯监控Pplat不能有效的调控肺容量,可加重VILI。
Objective:To compare the effect of lung protective ventilation strategy(LPVS)guided by respiratory physiology(PL)and traditional LPVS on respiratory physiology and lung injury in a canine model of ARDS under the modes of controlled mechanical ventilation or spontaneous breath.Methods:Eighteen dogs were recruited to induct ARDS models by venous injection ofoleic acid and divided into Groups A,B and C.After 4 hours of LPVS,pneumodynamic indexes and oxygenation indexes of blood gas were monitored.Lung tissues were obtained by thoracotomy,then HE staining and pathological scores were performed.Results:Four hours after LPVS,CL,sta and CL,dyn of groups A and B were higher than those of group C(P<0.05),while VT of groups A and B were lower than that of group C(P<0.05);DO_2 of groups A and B were also higher than that of group C(P<0.05);The total lung injury score of group C was higher than those of groups A and B(P<0.05).In the classification score of lung injury,neutrophilic infiltration and interstitial edema scores of group C were higher but atelectasis score was lower than those of groups A and B(P<0.05).Conclusion:No matter under spontaneous breath or controlled mechanical ventilation,monitoring PL can effectively regulate lung volume,improve lung compliance and alleviate VILI;Under spontaneous breath,simply controlled Pplat can not regulate lung volume effectively,and it may induce VILI.
Objective:To compare the effect of lung protective ventilation strategy(LPVS)guided by respiratory physiology(PL)and traditional LPVS on respiratory physiology and lung injury in a canine model of ARDS under the modes of controlled mechanical ventilation or spontaneous breath.Methods:Eighteen dogs were recruited to induct ARDS models by venous injection ofoleic acid and divided into Groups A,B and C.After 4 hours of LPVS,pneumodynamic indexes and oxygenation indexes of blood gas were monitored.Lung tissues were obtained by thoracotomy,then HE staining and pathological scores were performed.Results:Four hours after LPVS,CL,sta and CL,dyn of groups A and B were higher than those of group C(P<0.05),while VT of groups A and B were lower than that of group C(P<0.05);DO_2 of groups A and B were also higher than that of group C(P<0.05);The total lung injury score of group C was higher than those of groups A and B(P<0.05).In the classification score of lung injury,neutrophilic infiltration and interstitial edema scores of group C were higher but atelectasis score was lower than those of groups A and B(P<0.05).Conclusion:No matter under spontaneous breath or controlled mechanical ventilation,monitoring PL can effectively regulate lung volume,improve lung compliance and alleviate VILI;Under spontaneous breath,simply controlled Pplat can not regulate lung volume effectively,and it may induce VILI.
引文
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[9]Chiumello D,Cressoni M,Colombo A,et al.The assessment of transpulmonary pressure in mechanically ventilated ARDS patients[J].Intensive Care Med,2014,40(11):1 670-1 678.
[10]Gattinoni L,Carlesso E,Cadringher P,et al.Physical and biological triggers of ventilator-induced lung injury and its prevention[J].Eur Respir J,2003,47(Suppl):15-25.
[11]Crotti S,Mascheroni D,Cairomi P,et al.Recruitment and derecruiment during acute respiratory failure:A clinical study[J].Am J Respir Crit Care Med,2001,164(1):131-140.
[12]Luecke T,Meinhardt JP,Herrmann P,et al.Oleic acid vs saline solution lung lavage-induced lung injury:effects on lung morphology,pressure-volume relationships,and response to positive end-expiratory pressure[J].Chest,2006,130(2):392-401.
[13]Suki B,Hubmayr R.Epithelial and endothelial damage induced by mechanical ventilation modes[J].Curr Opin Crit Care.2014;20(1):17-24.
[2]Wang JT,Chang SC.Severe acute respiratory syndrome[J].Curr Opin Infect Dis,2004,17(2):143-148.
[3]Sarge T,Talmor D.Targeting transpulmonary pressure to prevent ventilator lung injury[J].Minerva Anestesiol,2009,75(5):293-299.
[4]Talmor D,Sarge T,Malhotra A,et al.Mechanical Ventilation Guided by Esophageal Pressure in Acute Lung Injury[J].N Engl J Med,2008,389(20):2 095-2 014.
[5]Talmor D,Sarge T,O’Donnell CR,et al.Esophageal and transpulmonary pressures in acute respiratory failure[J].Critical Care Medicine,2006,34(5):1 389-1 394.
[6]Smith KM,Mrozek JD,Simonton SC,et al.Prolonged partial liquid ventilation using conventional and highfrequency ventilatory techniques:gas exchange andl ung pathology in animal model of respiratory distress syndrome[J].Crit Care Med,1997,25(11):1 888-1 897.
[7]Suki B,Hubmayr R.Epithelial and endothelial damage induced by mechanical ventilation modes[J].Curr Opin Crit Care.2014,20(1):17-24.
[8]Talmor D,Sarge T,O’Donnell CR,et al.Esophageal and transpulmonary pressures in acute respiratory failure[J].Crit Care Med,2006,34(5):1 389-1 394.
[9]Chiumello D,Cressoni M,Colombo A,et al.The assessment of transpulmonary pressure in mechanically ventilated ARDS patients[J].Intensive Care Med,2014,40(11):1 670-1 678.
[10]Gattinoni L,Carlesso E,Cadringher P,et al.Physical and biological triggers of ventilator-induced lung injury and its prevention[J].Eur Respir J,2003,47(Suppl):15-25.
[11]Crotti S,Mascheroni D,Cairomi P,et al.Recruitment and derecruiment during acute respiratory failure:A clinical study[J].Am J Respir Crit Care Med,2001,164(1):131-140.
[12]Luecke T,Meinhardt JP,Herrmann P,et al.Oleic acid vs saline solution lung lavage-induced lung injury:effects on lung morphology,pressure-volume relationships,and response to positive end-expiratory pressure[J].Chest,2006,130(2):392-401.
[13]Suki B,Hubmayr R.Epithelial and endothelial damage induced by mechanical ventilation modes[J].Curr Opin Crit Care.2014;20(1):17-24.