肺保护性通气治疗急性呼吸窘迫综合征的疗效观察

目的探讨肺保护性通气治疗急性呼吸窘迫综合征(ARDS)的临床疗效。方法将62例ARDS患者随机分为两组,其中对照组30例给予常规机械通气治疗,观察组32例给予肺保护性通气治疗,比较两组患者血氧分压(Pa O2)、二氧化碳分压(Pa CO2)、氧合指数(Pa O2/Fi O2)的变化情况以及带机时间、住院时间、呼吸机相关肺损伤(VALI)的发生率等。结果观察组患者经通气后8 h、24 h、48 h的Pa O2、Pa CO2、Pa O2/Fi O2均明显高于对照组(P0.05),带机时间和住院时间均明显短于对照组(P0.05),VALI发生率也明显低于对照组(P0.05)。结论肺保护性通气能明显改善氧合,缩短带机时间和住院时间,减少VALI发生,对ARDS的临床救治具有重要意义。     

肺保护性通气改善急性呼吸窘迫综合征预后的机制

肺保护性通气策略（lung protective ventilation strategy,LPVS）的提出是近年来在急性呼吸窘迫综合征（ARDS）治疗方面的最主要进展,LPVS在临床的应用是ARDS病死率降低的重要原因。最初认为LPVS是通过降低ARDS机械通气过程中的机械性损伤而改善ARDS预后的,但目前研究显示LPVS还可通过降低肺和全身炎症反应、改善肺氧化一抗氧化失衡和细胞凋亡异常等多个机制改善ARDS预后。     

Lung protective mechanical ventilation in acute respiratory distress syndrome

The evidence supports the idea that mechanical ventilation can potentially cause further lung injury. The only ventilator manipulation that so far has been shown definitively to reduce injury and improve mortality is the reduction of VT to 6 mL/kg PBW or lower and targeting Pplat to 30 cm H2O or lower. Much research is needed to provide further guidance in applying ventilatory support techniques.     

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 syn-drome,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 ofChest 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;同时允许动脉血二氧化碳分压(PaCO2)升高到一个较高的水平;同时给予…     

Lung recruitment maneuvers in acute respiratory distress syndrome

In the experimental setting, repeated derecruitments of the lungs of ARDS models accentuate lung injury during mechanical ventilation, whereas open lung concept strategies can attenuate the injury. In the clinical setting, recruitment manuevers that use a continuous positive airway pressure of 40 cmH2O for 40 secs improve oxygenation in patients with early ARDS who do not have an impairment in the chest wall. High intermittent positive end-expiratory pressure (PEEP), intermitent sighs, or high-pressure controlled ventilation improves short-term oxygenation in ARDS patients. Both conventional and electrical impedance thoracictomography studies at the clinical setting indicate that high PEEP associated with low levels of pressure control ventilation recruit the collapsed portions of the ARDS lungs and that adequate PEEP levels are necessary to keep the ARDS lungs opened allowing a more homogenous ventilation. High PEEP/low tidal volume ventilation was seen to reduce inflammatory mediators in both bronchoalveolar lavage and plasma, compared to low PEEP/high tidal volume ventilation, after 36 hours of mechanical ventilation in ARDS patients. Recruitment maneuvers that used continuous positive airway pressure levels of 35-40 cmH2O for 40 secs, with PEEP set at 2 cmH2O above the lower inflection point of the pressure-volume curve, and tidal volume < 6 mL/kg were associated with a 28-day intensive care unit survival rate of 62%. This contrasted with a survival rate of only 29% with conventional ventilation (defined as the lowest PEEP for acceptable oxygenation without hemodynamic impairment with a tidal volume of 12 mL/kg), without recruitment manuevers (number needed to treat = 3; p < 0.001). In the near future, thoracic computed tomography associated with high-performance monitoring of regional ventilation may be used at the bedside to determine the optimal mechanical ventilation of the ARDS keeping an opened lung with a homogenous ventilation.     

Mechanical ventilation in acute lung injury and acute respiratory distress syndrome

Mechanical ventilation provides life-sustaining support for most patients with acute lung injury and acute respiratory distress syndrome; however, traditional approaches to mechanical ventilation may cause ventilator-associated lung injury, which could exacerbate or perpetuate respiratory failure caused initially by conditions such as pneumonia, sepsis, and trauma. This article reviews the theory, laboratory data, and results of recent clinical trials that suggest that modified ventilator strategies can reduce ventilator-associated lung injury and improve clinical outcomes.     

Conventional mechanical ventilation in acute lung injury and acute respiratory distress syndrome

Acute lung injury and acute respiratory distress syndrome are inflammatory conditions involving a broad spectrum of lung injury from mild respiratory abnormality to severe respiratory derangement. Regardless of cause (direct or indirect lung injury), pulmonary physiology and mechanics are altered, leading to hypoxemic respiratory failure. the use of positive pressure ventilation itself may cause lung injury (ventilator-induced lung injury, or VILI). VILI may amplify preexisting injury, delay lung recovery, and result in adverse outcomes. This article examines the evidence supporting lung-protective ventilation strategies and addresses the methods, outcomes, and potential obstacles to implementation of such approaches.     

Recruitment maneuvers in acute lung injury

Maintaining optimal lung recruitment has a marked effect on the outcome of patients who suffer from ARDS. RMs superimposed on mechanical ventilation have the potential to recruit atelectatic lungs in the course of general anesthesia; however, the physiologic benefits are less evident in ARDS patients who are ventilated at low VT values and high PEEP levels. Currently, the following technical aspects warrant further investigation: optimal time (the first hours after intubation or the first days of ARDS), duration (from 15 seconds to 2 minutes), mode (continuous positive end-expiratory pressure or pressure controlled ventilation with high PEEP), and type of patients (pulmonary versus extrapulmonary ARDS). Before the routine implementation of RMs to recruit the lungs fully in ARDS patients, clinicians also need more information on side effects and contraindications. Although RMs are transient, they may be associated with complications such as hypotension, bradycardia, and barotrauma. Moreover, further studies are needed to compare the efficacy of periodic high-pressure RMs that are superimposed on mechanical ventilation with ventilation using high PEEP levels and low VT values without RMs in patients who have early ARDS after initial hemodynamic stabilization.     

���Ժ��������ۺ����dz����еͨ��

??Abstract??Mechanical ventilation is still one of the main treatment measures of acute respiratory distress syndrome (ARDS).From the traditional high tidal volume ventilation (10 ~ 15 mL/kg) to the current use of lung protective ventilation strategies??low tidal volume ventilation (VT)??positive end-expiratory pressure (PEEP)??airway pressure release ventilation (APRV)??bilevel positive airway pressure(BIPAP)??considerable progress has been made.In addition to the well-known conventional mechanical ventilation modes and methods??there are many non-standard mechanical ventilation modes and methods??such as prone position ventilation??neurally adjusted ventilatory assist (NAVA)??extracorporeal membrane oxygenation (ECMO)??high-frequency ventilation and etc.All these measures produce unique effects on the treatment of ARDS.     

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。     

Tidal hyperinflation during low tidal volume ventilation in acute respiratory distress syndrome.

RATIONALE: Tidal volume and plateau pressure limitation decreases mortality in acute respiratory distress syndrome. Computed tomography demonstrated a small, normally aerated compartment on the top of poorly aerated and nonaerated compartments that may be hyperinflated by tidal inflation. OBJECTIVES: We hypothesized that despite tidal volume and plateau pressure limitation, patients with a larger nonaerated compartment are exposed to tidal hyperinflation of the normally aerated compartment. MEASUREMENTS AND MAIN RESULTS: Pulmonary computed tomography at end-expiration and end-inspiration was obtained in 30 patients ventilated with a low tidal volume (6 ml/kg predicted body weight). Cluster analysis identified 20 patients in whom tidal inflation occurred largely in the normally aerated compartment (69.9 +/- 6.9%; "more protected"), and 10 patients in whom tidal inflation occurred largely within the hyperinflated compartments (63.0 +/- 12.7%; "less protected"). The nonaerated compartment was smaller and the normally aerated compartment was larger in the more protected patients than in the less protected patients (p = 0.01). Pulmonary cytokines were lower in the more protected patients than in the less protected patients (p < 0.05). Ventilator-free days were 7 +/- 8 and 1 +/- 2 d in the more protected and less protected patients, respectively (p = 0.01). Plateau pressure ranged between 25 and 26 cm H(2)O in the more protected patients and between 28 and 30 cm H(2)O in the less protected patients (p = 0.006). CONCLUSIONS: Limiting tidal volume to 6 ml/kg predicted body weight and plateau pressure to 30 cm H(2)O may not be sufficient in patients characterized by a larger nonaerated compartment.     

Management of acidosis during lung-protective ventilation in acute respiratory distress syndrome

In ARDS, when acidosis complicates LPV, the goal of alkali therapy is to maintain arterial pH at a safe level (> or = 7.20). A pure respiratory acidosis generally does not require alkali therapy. If the Pplat is greater than 30 cm H2O, and the respiratory rate equals the upper limit (35-40 breaths/minute), then V(E) is slowly titrated down by approximately 1 L/hour, so that PaCO2 increases by 10 mm Hg/hour or less. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics. Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. Using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation. Under these circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. When renal failure is present, CRRT is indicated to manage acidosis. When ARDS is complicated by traumatic or hemorrhagic shock, overresuscitation with Cl(-)-rich solutions should be avoided to prevent metabolic acidosis.     

急性呼吸窘迫综合征小潮气量肺保护通气策略的预后分析

目的：探讨急性呼吸窘迫综合征应用小潮气量肺保护性通气策略的预后情况。方法：急性呼吸窘迫综合征患者80例根据入住病床单双号分为治疗组40例与对照组40例,两组都给予常规治疗,治疗组采用小潮气量辅助/控制机械通气治疗,对照组采用肺复张/机械通气治疗。结果：两组治疗前Pa02、Pa02/Fi02和PaC02对比无明显差异,治疗后各时间点Pa02和Pa02/Fi02值明显上升,PaC02值显下降(P<0.05),同时组间对比无统计学差异。治疗组的机械通气时间与住院时间都明显少于对照组,差异有统计学意义(P<0.05)。两组都无死亡患者,治疗组呼吸机相关肺炎、恶心呕吐和肺出血并发症发生率明显低于对照组(P<0.05)。结论：小潮气量肺保护性通气策略应用于呼吸窘迫综合征的治疗能有效保持动脉血气的稳定,加快患者的恢复,减少并发症,值得推广应用。     

俯卧位通气与急性呼吸窘迫综合征

急性呼吸窘迫综合征 (ＡＲＤＳ)是一种严重的疾病 ,每年威胁全世界近一百万人的生命。自从三千年前这种疾病被描述以来 ,由于它的高病死率、难以治疗以及独特的病理生理过程 ,引起临床医生和基础研究者们的广泛关注[1] 。对于俯卧位的研究则是在 2 0世纪 2 0年代开始的。最初Ｂｅａｍｓ及Ｈｕｒｔａｄｏ等人的注意力集中在俯卧位与仰卧位比较对正常人或动物肺活量[2 ] 、残气量[3] 等肺容量的影响。直到 1976年 ,Ｄｏｕｇｌａｓ等首次报道俯卧位通气可以提高ＡＲＤＳ患者的氧合 ,之后的 2 0多年间 ,临床上逐渐将其应用于ＡＲＤＳ患者治疗 ,…     

呼气末正压递增法肺复张在急性呼吸窘迫综合征治疗中的应用研究

基于对急性呼吸窘迫综合征(ARDS)病理和对机械通气相关性肺损伤(VILI)认识的加深以及对VILI高度重视,近年来不再主张以前以追求正常血气为目的采用大潮气量(VT)、低呼气末正压(PEEP)的通气策略,发展到提倡能限制肺泡跨肇压和尽量减少呼吸周期中肺泡内压和容积变化的保护肺的通气策略,以及保证达到合适血气值前提下,避免VILI或减少其程度,但肺保护性策略通气不可避免地引起肺泡塌陷,不能使塌陷的肺泡重新复张.     

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     

Acute lung injury and acute respiratory distress syndrome: extracorporeal life support and liquid ventilation for severe acute respiratory distress syndrome in adults

Acute respiratory distress syndrome (ARDS) has many underlying causes and carries an overall mortality of 40 to 60%. For those patients with severe ARDS who have a predicted mortality of 80 to 100%, extracorporeal life support (ECLS) can provide an extraordinary means of support. We recently demonstrated a survival to hospital discharge of 52% in this subset of patients. ECLS is capable of providing full respiratory and cardiac support, allowing time for the patient to recover from the underlying disease process. Additionally, ventilator settings are reduced to "rest" settings, avoiding the consequences of ventilator-induced lung injury that can contribute to a worse outcome. Systemic heparinization is a mainstay of ECLS therapy because of platelet activation in the circuit. Mechanical complications and significant bleeding can occur in up to one quarter of patients, requiring close attention and prompt intervention should they occur. Although not currently in clinical practice, liquid ventilation using perfluorocarbons to provide gas exchange in the lungs is a potentially useful adjunct in the management of severe respiratory failure.     

老年肺损伤的机械通气治疗

急性肺损伤（acutelunginjury,ALI）和急性呼吸窘迫综合征（acuterespiratorydistresssyndrome,ARDS）多发生于原心肺功能正常的患者,是由于心源性以外的各种肺内、肺外致病因素引起的以肺泡一毛细血管炎症损伤为主的急性I型呼吸衰竭,为临床上常见的危重症之一。     

Personalizing mechanical ventilation for acute respiratory distress syndrome

Lung-protective ventilation with low tidal volumes remains the cornerstone for treating patient with acute respiratory distress syndrome (ARDS). Personalizing such an approach to each patient’s unique physiology may improve outcomes further. Many factors should be considered when mechanically ventilating a critically ill patient with ARDS. Estimations of transpulmonary pressures as well as individual’s hemodynamics and respiratory mechanics should influence PEEP decisions as well as response to therapy (recruitability). This summary will emphasize the potential role of personalized therapy in mechanical ventilation.