肺源性与肺外源性急性呼吸窘迫综合征的再思考

急性呼吸窘迫综合征(acute respiratory distress syndrome，ARDS)是由一系列疾病损伤导致的急性呼吸衰竭，重症患者具有较高的病死率。根据危险因素的不同，ARDS可分为肺源性ARDS和肺外源性ARDS两种亚型，前者由于损伤直接作用于肺泡上皮细胞，造成肺泡膜破坏，影响气血交换；而后者通过全身性因素导致血管内皮损伤，肺血管通透性增加、肺间质渗出，进而出现肺泡塌陷、水肿，呼吸衰竭。各种肺内外危险因素在重症ARDS患者中往往同时存在，影像和呼吸力学等临床特征也未能很好区分肺源性/肺外源性ARDS，生物标志物的诊断效应还需验证，甚至病死率在肺源性/肺外源性ARDS患者中也并无明显差异。本文对肺源性ARDS和肺外源性ARDS的危险因素、临床特征、病死率进行比较，并针对ARDS的发病机制、临床表现及治疗与预后需关注之处进行梳理，为临床医生更加全面了解ARDS的发病机制、规范系统地启动ARDS的精准化评估与治疗提供借鉴，从而降低ARDS患者的病死率。     

肺复张治疗肺源性和肺外源性急性呼吸窘迫综合征的比较

急性呼吸窘迫综合征(ARDS)为多种病因导致肺部出现相似的一组症状、体征,表现为进行性、难治性低氧血症及非心源性肺水肿.根据发病机制的不同,1994年欧美共识会将其分为两大类:①原发性或肺源性ARDS,即直接损伤导致的ARDS,如严重肺部感染、胃内容物吸入、肺挫伤、吸入有毒气体、淹溺、氧中毒等;②继发性或肺外源性ARDS,即间接损伤导致的ARDS,如严重感染、严重的非胸部创伤、重症急性胰腺炎、大量输血、体外循环和弥散性血管内凝血等~([1]).以小潮气量和最佳呼气末正压(PEEP)为核心的肺保护性通气策略的实施,显著提高了ARDS患者的治疗效果.但小潮气量的缺点是不利于ARDS塌陷肺泡的膨胀,会造成低氧血症难以纠正甚至恶化.     

Ang-2与ALI/ARDS血管外肺水的关系及临床意义

急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)是由肺部和全身疾病引起的毛细血管内皮细胞和肺泡上皮细胞损伤造成弥漫性肺间质及肺泡水肿导致的急性低氧性呼吸功能不全或衰竭.血管生成素2(Ang-2)是一个前炎症细胞因子,血循环中高水平的Ang-2导致血管通透性增高,引起血管渗漏.Ang-2能够导致ALI/ARDS患者毛细血管通透性增加,与血管外肺水具有正相关性,循环中Ang-2越高氧合指数越差,是预测ALI/ARDS发展和预后的一个指标.Ang-2阻滞剂能够降低血管通透性和改善肺功能障碍程度,有针对性的以Ang-2 为靶向的干预治疗则可能为ALI/ARDS的治疗提供了一种新的思路与手段.     

急性呼吸窘迫综合征治疗的进步

急性呼吸窘迫综合征(ARDS)是临床常见的急性呼吸衰竭,病死率高达30%～40%[1-3].大量肺泡塌陷导致肺容积减少、顺应性降低和通气/血流失调是ARDS典型的病理生理改变,过度和失衡的炎症反应是导致ARDS的根本原因,肺保护性通气是近十多年来ARDS机械通气策略的重大突破,调控机体炎症反应方面进展困难,新的通气理念、间充质干细胞为ARDS治疗带来希望.     

气道压力释放通气治疗急性呼吸窘迫综合征的研究进展

急性呼吸窘迫综合征(ARDS)的早期阶段,大量肺泡塌陷导致肺容积减少,顺应性下降,所以ARDS治疗的关键是促进肺复张并保持肺开放。气道压力释放通气(APRV)是二十多年前提出的一种机械通气模式,但是直到最近它才作为一种安全有效     

ARDS与俯卧位通气

急性呼吸窘迫综合征(ARDS)是由于感染、休克、创伤及烧伤等疾病过程中,肺实质细胞损伤导致的以进行性低氧血症、呼吸窘迫为特征的临床综合征。肺顺应性降低、肺容积减少、肺内分流增加而肺毛细血管静水压不高为其病理生理特点。1976年Piehl[1] 首次报道了俯卧位通气在呼吸衰竭中的疗效。2 0世纪80年代,随着人们对急性肺损伤ALI/ARDS病理生理学的进一步认识,治疗策略不断得到改进。作为治疗ALI/ARDS的一种辅助手段,俯卧位通气开始逐渐受到重视。特别是近年来,随着人们对ALI/ARDS肺泡病变的不均一性和呼吸机相关性肺损伤认识的不断…     

急性肺损伤的诊治现状和进展

急性肺损伤(acute lung iniury,ALI)是各种直接和间接致伤因素导致的肺泡上皮细胞及毛细血管内皮细胞损伤,它造成弥漫性肺间质及肺泡水肿,导致的急性低氧性呼吸功能不全.以肺容积减少、肺顺应性降低、通气/血流比例失调为病理生理特征,临床上表现为进行性低氧血症和呼吸窘迫,肺部影像学上表现为非均一性的渗出性病变,其发展至严重阶段(氧合指数<200)被称为急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS).     

跨肺压导向急性呼吸窘迫综合征患者呼吸末正压选择的研究现状

正急性呼吸窘迫综合征(ARDS)是各种非心源性的肺内外因素致急性呼吸功能衰竭综合征,临床特点为低氧血症、弥漫性肺实质病变~([1])。ARDS病因主要有严重肺炎、脓毒血症、急性重型胰腺炎、吸入性损伤、严重创伤等~([1])。在ARDS病人的病理生理特点中,肺泡被大量破坏,表面活性物质减少,大多数肺泡呈塌陷状态,同时毛细血管通透性增加,呈现肺水肿表现,生理死腔增加、肺的容积和顺应性都下降~([2]),这也是ICU病人死亡的主要原因之一。因此,     

血管外肺水与肺血管通透性指数在急性呼吸窘迫综合征的研究进展

急性呼吸窘迫综合征（acute＆amp;respiratory＆amp;distress＆amp;syndrome,ARDS）是在严重感染、休克、创伤及烧伤等疾病的过程中,肺毛细血管内皮细胞和肺泡上皮细胞损伤,导致急性低氧性呼吸功能不全或衰竭。其病理生理特征为因肺泡膜通透性增加引起的渗出性肺水肿。 ARDS具有高患病率、高死亡率、临床预后差等特点,其死亡率高达35%～45%[1]。早期诊断ARDS非常困难,目前ARDS的临床诊断标准主要有1994年欧美联席会议标准[2]和2012年柏林定义[8],但两个标准中并没有一项直接体现ARDS病理生理过程中的肺水量化标准,这一缺陷可能会影响ARDS诊断的敏感性和特异性。随着脉搏指示剂连续心排血量监测（pulseC indicator＆amp;continous＆amp;output, PiCCO）技术的进步,用经肺热稀释法测得的血管外肺水指数（extravascularClungCwaterCindex,EVLWI）和肺血管通透性指数（pulmonaryCvascularCpermeabilityC index,PVPI）能较好地反映ARDS毛细血管通透性改变的特征性病理生理过程,对ARDS的早期诊断、早期干预及鉴别诊断等方面有重要意义。本次研究就血管外肺水（extravascularClungCwaterC,EVLW）和PVPI在ARDS的研究进展作一综述。     

控制性肺膨胀对急性呼吸窘迫综合征绵羊肺力学和肺损伤的影响

目的：探讨控制性肺膨胀（SI）与肺保护性通气策略联合应用时，对急性呼吸窘迫综合征（ARDS）的肺泡复张作用及其安全性。方法：利用内毒秀导的绵羊ARDS模型，观察实施SI[2.94kPa(1kPa=10.20cmH2O)，屏气时间20秒]后绵羊的肺力学和组织病理学改变。结果：实施SI后，绵羊的动态肺顺应性和肺容积显著增加，气道峰值压、平台压和平均气道压均显著降低（P均＜0．05），并可维持3－4小时。与未应用SI的绵羊比较，实施SI后的绵羊肺损伤减轻，肺不张改善。结论：SI具有肺复张和肺保护作用，是肺保护性通气策略的重要补充。     

Mesenchymal stem cells and acute lung injury

Acute respiratory distress syndrome (ARDS) is a clinical syndrome of acute respiratory failure presenting with hypoxemia and bilateral pulmonary infiltrates, most often in the setting of pneumonia, sepsis, or major trauma. The pathogenesis of ARDS involves lung endothelial injury, alveolar epithelial injury, and the accumulation of protein-rich fluid and cellular debris in the alveolar space. No pharmacologic therapy has so far proved effective. A potential strategy involves cell-based therapies, including mesenchymal stem cells (MSCs). Herein we review basic properties of MSCs, their use in preclinical models of lung injury and ARDS, and potential therapeutic mechanisms.     

Ventilator-induced lung injury

The clinical relevance of experimental ventilator-induced lung injury has recently received a resounding illustration by the Acute Respiratory Distress Syndrome Network trial that showed a 22% reduction of mortality in patients with acute respiratory disease syndrome when lung mechanical stress was lessened by tidal volume reduction during mechanical ventilation. This clinical confirmation of the concept of ventilator-induced lung injury has also undisputedly substantiated the experimental observation that excessive tidal volume and/or end-inspiratory lung volume is the main determinant of ventilator-induced lung injury. More recently, attention has focused on the roles and implication in the pathogenesis of ventilator-induced lung injury of inflammatory cells and mediators that may be activated and released either in the alveolar space or in the systemic circulation because of the rupture of the alveolar-capillary barrier and on the cellular response to mechanical stress.     

内科胸腔镜肺活检对弥漫性间质性肺疾病诊断价值及安全性分析

目的探讨内科胸腔镜肺活检对弥漫性间质性肺疾病患者的诊断价值及安全性。方法回顾性分析35例内科胸腔镜肺活检的弥漫性间质性肺疾病患者临床及病理诊断资料。结果 31例患者获病理确诊,确诊率88.6%(31/35),其中普通型间质性肺炎(UIP)10例,肺结核6例,肺泡细胞癌4例,非特异性间质性肺炎(NSIP)、隐源性机化性肺炎(COP)各3例,肺泡蛋白沉着症(PAP)2例,韦格纳肉芽肿病(WG)、急性间质性肺炎(AIP)和淋巴管肌瘤病(LAM)各1例。术后并发症3例(8.6%),其中肺部感染合并呼吸衰竭2例,特发性肺间质纤维化急性加重1例,导致死亡2例(5.7%)。结论内科胸腔镜肺活检是诊断弥漫性间质性肺疾病安全有效的方法。     

Recruitment and retention of lung volume

Both a reduction in tidal volume and alveolar recruitment may be necessary to prevent ventilator-induced lung injury in the management of patients with acute respiratory distress syndrome. The lung collapse associated with endotracheal suctioning produces hypoxaemia, but it also causes de-recruitment, potentially aggravating lung injury. A study conducted by Dyhr and colleagues demonstrates the benefit of lung recruitment manoeuvres after suctioning, which help to improve oxygenation and restore lung volume more rapidly. Although this intervention appears safe and beneficial, the precise role of lung volume recruitment manoeuvres remains to be elucidated.     

Clinical review: The implications of experimental and clinical studies of recruitment maneuvers in acute lung injury

Mechanical ventilation can cause and perpetuate lung injury if alveolar overdistension, cyclic collapse, and reopening of alveolar units occur. The use of low tidal volume and limited airway pressure has improved survival in patients with acute lung injury or acute respiratory distress syndrome. The use of recruitment maneuvers has been proposed as an adjunct to mechanical ventilation to re-expand collapsed lung tissue. Many investigators have studied the benefits of recruitment maneuvers in healthy anesthetized patients and in patients ventilated with low positive end-expiratory pressure. However, it is unclear whether recruitment maneuvers are useful when patients with acute lung injury or acute respiratory distress syndrome are ventilated with high positive end-expiratory pressure, and in the presence of lung fibrosis or a stiff chest wall. Moreover, it is unclear whether the use of high airway pressures during recruitment maneuvers can cause bacterial translocation. This article reviews the intrinsic mechanisms of mechanical stress, the controversy regarding clinical use of recruitment maneuvers, and the interactions between lung infection and application of high intrathoracic pressures.     

机械通气对急性肺损伤大鼠细胞凋亡的影响

目的 研究不同潮气量及不同呼气末正压(PEEP)水平对急性肺损伤(AU)大鼠支气管和肺组织细胞凋亡的影响,并初步探讨细胞凋亡在呼吸机相关性肺损伤(VILI)中的作用机制.方法 选用40只SD大鼠,制作ALI模型,随机(随机数字法)分为:(1)小潮气量组(LV组),潮气量8 mL/kg,不加PEEP;(2)大潮气量组,潮气量30 mL./kg,不加PEEP;(3)小潮气量+ 2PEEP组(LV2P组),潮气量8 mL/kg,同时给PEEP 2 cmH2O(1 crnH2O =0.098 kPa);(4)小潮气量+5PEEP组(LV5P组),潮气量8 mL/kg,同时给PEEP 5 cmH2O;(5)小潮气量+8PEEP组(LV8P组),潮气量8 mL/kg,同时给PEEP 8 cmH2O.通气2h后处死动物,留取肺标本.用脱氧核糖核苷酸末端转移酶介导的末端标记法(TUNEL)分析肺组织中的细胞凋亡情况,用免疫组化法检测肺组织中caspase-3蛋白的表达及分布.结果 大潮气量组支气管和肺组织细胞凋亡的明显增加(P＜0.01),caspase-3蛋白酶表达最强.采用PEEP后,支气管和肺组织细胞凋亡减少,capase-3蛋白酶表达弱阳性,以LV5P组最为显著(P＜0.01).结论 小潮气量对肺组织有保护作用,采用PEEP后保护作用更加明显,细胞凋亡在VILI的发生中有重要作用.     

促红细胞生成素在急性肺损伤与急性呼吸窘迫综合征中作用的研究进展

急性肺损伤（ALI）或急性呼吸窘迫综合征（ARDS）是临床常见急危重症。各种病因包括严重感染、创伤、休克、急性胰腺炎、肺炎等肺内或肺外因素均可导致ALI/ARDS,发病机制主要包括炎症反应、细胞凋亡、氧化应激和肺泡毛细血管膜的损害等,目前尚无特殊有效的治疗方法,临床上也无修复肺损伤的有效药物。促红细胞生成素（EPO）作为一种多功能的内源性调节因子对各种组织损伤有一定的细胞保护作用,尤其是肺组织〔1〕,成为治疗ALI/ARDS的研究热点,     

Unilateral lung injury

Mechanical ventilation is a supportive lifesaving therapy that can potentially cause lung injury if periodic alveolar overdistension, or cyclic collapse, and reopening occur. The use of a low tidal volume with moderate to high positive end-expiratory pressure improves the survival of patients with acute lung injury and acute respiratory distress syndrome. Positioning the patient with the "good lung down" and using differential ventilation with selective positive end-expiratory pressure are the two currently accepted ventilatory strategies to be applied in patients with severe unilateral lung injury. However, both have serious limitations in clinical practice. Lung injury may be rather inhomogeneous-confined to one lung or preferentially distributed toward the dependent lung areas. In unilateral lung injury, ventilatory strategies that allow recruitment of injured lung and that avoid overdistension of uninjured lung parenchyma should be applied. Experimental studies have shown that the use of selective tracheal gas insufflation and partial liquid ventilation facilitates low tidal volume with appropriate gas exchange while reducing cyclic lung stretch and shear stresses. Further studies are needed to determine future applications of these therapies in humans.