肺保护性通气策略在急性呼吸窘迫综合征中的作用

机械通气是急性呼吸窘迫综合征（ARDS）的重要支持手段,为减少或避免机械通气所致的肺损伤,近年来逐步形成ARDS肺保护性通气策略。深刻认识ARDS病理生理特点,合理评价肺保护性通气策略,对于提高ARDS患机械通气效果,改善ARDS预后,具有十分重要的临床意义。     

BIPAP通气对ARDS病人肺保护性作用的观察

目的 探计对ARDS实施保护性通气方法。方法 对比观察BIPAP（双相气正压通气）和常规容量辅助/控制模式（A/C）通气方法对ARDS病人氧合指数、肺顺性、血液动力学及死亡率和并发症的影响。结果 BIPAP通气方式与传统通气方式A/C相比，血氧饱和度和氧合指数明显改善，血液动力不稳定，肺顺应性增加，带机时间缩短，死亡率和并发症减少。结论 BIPAP通气方式可从限压、小潮气量方面实施保护性肺通气；BIPAP通气的另一个重要特点是保持病人在高低压两个水平的自主呼吸，人机配合良好，符合生理要求。     

急性肺损伤急性呼吸窘迫综合征保护性肺通气的研究进展

急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）于1967年首次在文献中描述，至今已有30多年了。既往ARDS患者的抢救成功率非常低，病死率高达50％-70％。自从1990年一种创新的机械通气策略发表后，ARDS患者的病死率明显下降。这种策略称为“保护性肺通气策略”，1993年The American College of Chest Physicians Consensus Conference发表的指南再次强调了它的重要性。保护性肺通气策略的实质是限制机械通气时的潮气量（TV）和气道压力，以减轻肺过度充气；     

保护性肺通气策略在单肺通气中的应用

在胸外科手术麻醉中,单肺通气(one-lung ventilation,OLV)是一种很重要的通气方式。它既可防止术侧肺的血液及分泌物溢入健侧肺,保证呼吸道通畅,避免交叉感染,同时也利于手术操作。但是在开胸手术OLV中一些肺部并发症,如肺炎、脓胸、肺不张等不断有报道,目前认为这些症状都是开胸术后肺损伤(lung injury after thoracotomy,LIAT)的表现形式。其中不同的OLV模式可直接影响LIAT的发生。     

肺保护性通气策略在急性呼吸窘迫综合征中的作用

机械通气是急性呼吸窘迫综合征(ARDS)的重要支持手段,为减少或避免机械通气所致的肺损伤,近年来逐步形成ARDS肺保护-性通气策略。深刻认识ARDS病理生理特点,合理评价肺保护性通气策略,对于提高ARDS患者机械通气效果,改善ARDS预后,具有十分重要的临床意义。     

急性呼吸窘迫综合征肺保护性通气

急性呼吸窘迫综合征（ARDS）基础和临床研究虽然近年来取得了显著进步,但到目前为止,机械通气仍然是ARDS治疗的基石。众所周知,机械通气是一把双刃剑,ARDS肺部病变不均一的特点使得机械通气更容易在这些患者中导致呼吸机相关性肺损伤。为了减轻这些损伤,产生了小潮气量、高呼气末正压（PEEP）、允许性高二氧化碳血症的肺保护性通气策略。随着对病理生理认识逐步加深,关于传统肺保护性通气策略的争议也逐渐增加。肺超保护性通气策略、右心保护性的通气策略、肺-膈肌保护通气策略等理念被提出,文章综述了这些策略组成的历史沿革和进展,为促进肺保护性通气策略在ARDS治疗的应用提供思考。     

肺保护性通气对严重胸外伤致急性呼吸窘迫综合征疗效的影响研究

目的探讨小潮气量（LTV）加呼气末正压（PEEP）机械通气（MV）治疗严重胸外伤致急性呼吸窘迫综合征（ARDS）的疗效。方法以28例常规潮气量（8～12ml/kg）MV为对照组,30例小潮气量（5～7ml/kg）加用PEEP的MV模式为观察组,比较两组血气,RR、HR、MAP、CVP、呼吸机所致肺损伤（VILI）、多脏器功能不全（MODS）发生率及ARDS病死率。结果两组PaO2差异无显著性意义;观察组PaCO2高于对照组;观察组出现6例VILI、4例MODS及死亡3例,对照组13例VILI、7例MODS、死亡5例。结论在ARDS治疗中采用小潮气量加PEEP及允许范围内高碳酸血症（PHC）的肺保护性通气策略,可明显改善缺氧,减少VILI发生,从而降低病死率。     

早期应用保护性肺通气治疗急性肺损伤

急性肺损伤的常规机械通气治疗尽管取得了一定的效果 ,但在治疗期间病情进展程度和死亡率没有得到很好的控制 ,究其原因 ,机械通气造成的肺再损伤是一个重要因素。我们对 8例急性肺损伤患者早期行保护性肺通气治疗 ,取得了较好效果。现报告如下。1　资料与方法1 .1　临床资料　本文急性肺损伤患者 1 0例 ,男 4例 ,女 6例 ,年龄 2 6～ 6 5岁 ,平均 3 8.8岁。神经源性肺损伤 4例 (颅内出血 3例 ,脑外伤 1例 ) ,感染性肺损伤 4例 (肺部感染 2例 ,腹部感染和盆腔感染各 1例 ) ,药物中毒性肺损伤 2例 (均为有机磷农药中毒 )。均按中华医学会呼吸…     

通气机所致肺损伤和通气策略的改变

通气机所致肺损伤和通气策略的改变俞森洋朱元珏通气机所致肺损伤（ＶＩＬＩ）是机械通气最重要的并发症，近年对其研究的深入，导致了某些通气策略的改变和通气新方法的不断涌现。一、ＶＩＬＩ的类型［１～３］ＶＩＬＩ包括４种类型：（１）肺泡外气体；（２）系统性气栓...     

P-V曲线与保护性肺通气

机械通气造成的肺再损伤的主要原因是损伤肺病理生理的不均一性和大通气量、高通气压造成的区域性肺泡过张以及呼气末塌陷的肺泡随呼吸周期性张闭所产生的剪切应力性损伤。因此,个体化选择PEEP和Vt将减轻通气性肺损伤,有利于肺功能的保护和肺病理的恢复。P-V曲线反映肺的病理生理状况,依其下、上曲点个体化选择PEEP和下调Vt符合病理生理状况,有利于肺保护。     

Molecular mechanisms underlying inflammatory lung diseases in the elderly: Development of a novel therapeutic strategy for acute lung injury and pulmonary fibrosis

In the elderly, inflammatory lung diseases, including acute lung injury and pulmonary fibrosis, are significant in terms of both mortality and difficulty in management. Acute respiratory distress syndrome (ARDS) is an acute lung injury and the mortality rate for ARDS ranges from 40 to 70% despite intensive care. Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disorder of the lung parenchyma. No useful drugs are currently available to treat IPF. However, molecular mechanisms underlying these lung diseases are little understood and the development of a novel therapeutic strategy is urgently needed. Platelet‐activating factor (PAF) and metabolites of arachidonic acid, i.e. eicosanoids, are lipid mediators that have various biological effects. A key enzyme for the production of these inflammatory mediators, including eicosanoids and PAF, is phospholipase A₂. In particular, cytosolic PLA₂ (cPLA₂) is especially important. The purpose of this article is to report novel findings regarding the role of PAF and cPLA₂ in lung inflammatory diseases, especially, acute lung injury and pulmonary fibrosis. To address this question, we used mutant mice, i.e. PAFR transgenic mice, PAFR gene‐disrupted mice and cPLA₂ gene‐disrupted mice. We have shown that PAF and eicosanoids, downstream mediators of cPLA₂, may be involved in the pathogenesis of ARDS and IPF, which are important diseases in the elderly. Although there exist extreme differences in clinical features between ARDS and IPF, both diseases are fatal disorders for which no useful drugs are currently available. On the basis of recent reports using mutant mice, cPLA₂ might be a potential target to intervene in the development of pulmonary fibrosis and acute lung injury in the elderly.     

Oxygen and resolution of lung injury

We investigated the effects of varying inspired oxygen concentrations on the resolution of oleic acid-induced lung injury in rabbits. Rabbits were injected intravenously with oleic acid and maintained in room air, or exposed to 60, 70, or 80% oxygen for periods of 7 or 10 days. Oleic acid caused hemorrhagic pulmonary edema with hypoxemia. Hypoxemia was more profound in the oxygen-treated animals, a difference that was significant after 7 days' exposure to 60 and 70% oxygen, and after 4 days to 80% oxygen. Mortality was increased in the animals maintained in 80% oxygen. The data suggest that environmental oxygen concentrations greater than 60% interfere with the return to normal lung function following oleic acid injury in rabbits. The hypoxemia may be due to either mismatching of ventilation and perfusion or to a diffusion block resulting from the increased septal width. There was no evidence of massive pulmonary edema as a cause of the hypoxemia. It was not possible to distinguish between injury primarily caused by oxygen and its interference with the healing process.     

The protective effects of glutamine in a rat model of ventilator-induced lung injury

Background

The mortality rate of patients with acute respiratory distress syndrome (ARDS) is still high despite the use of protective ventilatory strategies. We sought to examine the pharmacological effects of glutamine (GLN) in a two-hit model of endotoxin-induced inflammation followed by ventilator-induced lung injury (VILI). We hypothesized that the administration of GLN ameliorates the VILI.

Methods

Sprague-Dawley rats were anesthetized and given lipopolysaccharide (LPS) intratracheally as a first hit to induce lung inflammation, followed 24 h later by a second hit of mechanical ventilation (MV) with either low tidal volume (6 mL/kg) with 5 cmH₂O of positive end-expiratory pressure (PEEP) or high tidal volume (22 mL/kg) with zero PEEP for 4 h. GLN or lactated Ringer’s solution as the placebo was administered intravenously 15 min prior to MV.

Results

In the LPS-challenged rats ventilated with high tidal volume, the treatment with GLN improved lung injury indices, lung mechanics and cytokine responses compared with the placebo group.

Conclusions

The administration of GLN given immediately prior to MV may be beneficial in the context of reducing VILI.     

肺保护性通气对急性呼吸窘迫综合征兔肺部炎症反应的影响

目的　观察肺保护性通气对急性呼吸窘迫综合征 (ARDS)家兔肺部炎症反应的影响。方法　生理盐水肺泡灌洗法复制ARDS家兔模型 ,将 36只家兔随机分为 6组 :(1)正常对照组 (N组 ) ,(2 )ARDS模型组 (M组 ) ,(3)小潮气量 (VT) 最佳呼气末正压 (PEEP)组 (A组 ) ,(4)常规VT 最佳PEEP组 (B组 ) ,(5 )小VT 高PEEP组 (C组 ) ,(6 )高VT 零PEEP组 (D组 )。机械通气 4h后测定肺组织湿/干重比 (W/D) ,迁移率改变电泳法 (EMSA)测定肺组织核因子κB(NF κB)活性 ,逆转录 聚合酶链反应(RT PCR)检测肺组织中肿瘤坏死因子α(TNF α)和白细胞介素 10 (IL 10 )mRNA表达 ,酶联免疫吸附测定 (ELISA)检测肺组织TNF α及IL 10浓度。结果　A组肺组织W/D为 5 6± 1 1,不但显著低于B组(6 6± 0 8)和D组 (6 9± 1 0 ) ,而且也显著低于C组 (6 6± 1 0 ,P均 <0 0 5 ) ,但与M组 (5 8± 0 5 )比较差异无显著性 (P >0 0 5 )。A组肺组织NF κB活性 (331± 113)显著低于B组 (45 5± 6 3)、C组 (478±74 )和D组 (6 4 5± 16 2 ,P均 <0 0 5 ) ,其中D组NF κB活性最高。与A组比较 ,B、C和D组肺组织TNF α及IL 10mRNA表达及浓度显著增高 ,其中D组TNF α和IL 10mRNA表达及其浓度在各组中最高。肺组织髓过氧化物酶 (MPO)及丙二醛 (MDA)含     

Vaping‐associated lung injury caused by inhalation of cannabis oil

Vaping is a growing concern in adolescents, and a growing proportion is using electronic devices to inhale cannabis oil. The short‐term and long‐term effects of cannabis oil inhalation are not well understood. We report on a case of severe acute lung injury secondary to inhalation of cannabis oil via a vape pen, and propose a new term that describes lung injury related to vaping.     

保护性肺通气对肺功能正常患者呼吸力学的影响

目的 探讨保护性肺通气对肺功能正常的患者呼吸力学的影响.方法 将我院2010年6月至2011年3月收治的100例腹部手术的患者分为研究组和对照组,每组50例,对照组采用常规机械通气,研究组采用保护性肺通气模式,比较两组患者的呼吸力学参数的改变.结果 研究组气道峰压(Ppeak)、气道平均压(Pmean),呼气末二氧化碳分压(PETCO2),呼吸系统总顺应性(Crs)显著高于对照组,P<0.05.呼吸系统总阻力(Rrs)显著低于对照组,P<0.05.结论 与常规机械通气模式对比,采用保护性肺通气,患者的Ppeak、Pmean,PETCO2、Crs显著提高,Rrs显著降低.     

肺保护与肺开放通气策略对急性呼吸窘迫综合征家兔血管外肺水的影响

目的探讨肺保护与肺开放通气策略对急性呼吸窘迫综合征(ARDS)血管外肺水(EVLWI)的影响。方法以肺泡灌洗法复制家兔ARDS模型,分为中等潮气量(VT)零呼气末正压(PEEP)组(MVZP组)、小VT零PEEP组(LVZP组)、小VT最佳PEEP组(LVBP组)和小VT最佳PEEP+控制性肺膨胀(SI)组(LVBP+SI组)。采用单指示剂热稀释法测定EVLWI。观察在不同通气条件下0、1、2和3h EVLWI的变化。结果MVZP组、LVZP组、LVBP组和LVBP+SI组EVLWI在基础时分别为(11.3±2.4)、(10.2±2.4)、(10.3±4.6)和(9.7±2.3)ml/kg,达到ARDS模型(0h)时显著升高[(22.3±5.6)、(20.0±3.8)、(25.7±9.7)和(22.5±6.2)ml/kg,P均<0.05]。在实验观察3h中,MVZP组在2、3h EVLWI[(32.0±12.2)、(36.2±12.4)ml/kg]显著高于0h[(22.3±5.6)ml/kg,P均<0.05]。LVZP组在2、3h EVLWI[(27.8±12.9)、(30.3±13.0)ml/kg]也显著高于0h[(20.0±3.8)ml/kg,P均<0.05];LVBP组1h时EVLWI为(18.5±8.1)ml/kg,与0h[(25.7±9.7)ml/kg]比较差异有统计学意义(P=0.027)。LVBP+SI组在1、2、3h各时点EVLWI分别为(16.8±6.5)、(18.0±7.1)、(15.7±2.7)ml/kg,与0h[(22.5±6.2)ml/kg]比较显著降低(P均<0.05)。与MVZP组比较,1、3h时LVBP组与LVBP+SI组EVLWI显著降低(P均<0.05)。3hLVBP+SI组EVLWI显著低于LVZP组(P<0.05)。结论肺保护与肺开放通气策略可降低EVLWI,增加肺水清除。     

不同体位保护性通气模式对误吸性急性肺损伤的影响及机制研究

目的 研究采用俯卧位和仰卧位保护性通气模式对误吸性急性肺损伤患者的影响,并探讨其机制.方法 2009年1月至2012年12月的误吸性急性肺损伤患者60例,随机分为A组和B组,每组30例.两组均采用急诊经纤维支气管镜治疗和保护性通气模式(小潮气量+呼气末正压通气)辅助通气.A组采取俯卧位,B组仰卧位.检测两组患者治疗前和治疗后24 h的呼吸功能、血流动力学指标及血清白介素6(IL 6)、肿瘤坏死因子α(TNF-α)的水平,并随访4周时两组的临床预后.结果 A组患者治疗后24 h时的动脉血氧分压、氧合指数、脉搏血氧饱和度和心率改善优于B组(P＜0.01),A组患者血清IL-6和TNF-α的水平显著低于B组(P＜0.01).治疗后4周A组的病死率(3.33％)低于B组(20.00％)(P＜0.05).结论 俯卧位保护性通气可改善误吸性急性肺损伤患者的临床预后,其机制可能与改善患者呼吸功能和抑制炎症介质有关.