急性呼吸窘迫综合征家兔肺不同区域有效血流灌注变化及肺保护性通气对其的影响

目的 通过观察家兔急性呼吸窘迫综合征(ARDS)模型肺不同区域有效血流灌注变化及肺保护性通气对其的影响,探讨ARDS所致严重低氧血症的发生机制。方法 采用静脉注射油酸的方法建立家兔ARDS模型,应用PIM-Ⅱ激光多普勒血流灌注扫描仪观察不同肺通气模式[(大潮气、小潮气 外源性呼气末正压(PEEP)、大潮气 俯卧位、俯卧位 小潮气 PEEP]下肺不同区域(肺上区、肺下区腹侧和肺下区背侧)局部有效血流灌注及动脉血气指标的变化。结果 家兔静脉注射油酸后,(1)肺不同区域氧合指数明显下降,应用肺保护性通气(小潮气 PEEP,俯卧位 小潮气 PEEP)后氧合指数明显改善;(2)肺不同区域局部有效血流灌注均有不同程度的下降,以肺下区背侧最为明显,肺下区腹侧次之,肺上区变化最小,应用肺保护性通气后,小潮气 PEEP对改善肺下区背侧胸膜下肺局部有效血流灌注的效果不如俯卧位 小潮气 PEEP。结论小潮气 PEEP、俯卧位 小潮气 PEEP均可良好改善肺局部有效血流灌注,其中俯卧位 小潮气 PEEP效果尤为明显;右-左分流导致的肺内分流可能是ARDS发生严重进行性低氧血症的主要原因之一。     

死腔分数导向急性呼吸窘迫综合征呼气末正压选择的临床研究

目的 探讨早期急性呼吸窘迫综合征( ARDS)患者采用死腔分数法选择呼气末正压(PEEP)的可行性.方法 选23例机械通气的早期ARDS患者行持续肺膨胀手法充分肺复张,PEEP递减过程中分别采用最小死腔分数法、最大顺应性法、最佳氧合法选择最佳PEEP,观察不同方法选择的PEEP对患者氧合、解剖死腔容积(VD)/潮气容积(VT)、静态肺顺应性(CLst)和功能残气量(FRC)等的影响.结果 最小死腔分数法[(10.1±2.8)cm H2O(1 cm H2O =0.098 kPa)]和最大顺应性法[(11.3±2.5) cmH2O]选择的最佳PEEP间差异无统计学意义(P＞0.05),均明显低于最佳氧合法[(15.0±3.4) cm H2O,P＜0.05].最小死腔分数法选择PEEP机械通气时患者VD/VT(0.53±0.09)较基础状态(0.59±0.09)明显下降,但最大顺应性法和最佳氧合法选择的PEEP机械通气时VD/VT较基础状态未见明显变化.最小死腔分数法选择的PEEP,其氧合指数明显低于最佳氧合法[(288±123) mm Hg(1 mm Hg=0.133 kPa)比(356±119)mm Hg,P＜0.05],与最大顺应性法相比差异无统计学意义(P＞0.05),均高于基础状态.最小死腔分数法选择PEEP机械通气时气道平台压[(24±4) cm H2O]明显低于最大氧合法[(31±9) cm H2O].最佳氧合法选择的PEEP机械通气时的FRC明显高于最小死腔分数法和最大顺应性法.结论 采用最小死腔分数法选择的最佳PEEP,可改善ARDS患者氧合和CLst,减少死腔通气、降低气道平台压,是床边选择最佳PEEP的可行方法.     

分侧肺通气时不同呼气末正压和潮气量对单侧肺损伤犬循环的影响

目的 观察不同步分侧肺通气和同步分侧肺通气对单侧急性肺损伤(ALI)犬循环的影响.方法 取健康杂种犬12只,建立盐酸所致单侧肺损伤动物模型,行容积控制通气,将犬按随机数字表法分为不同步分侧肺通气组(NS组)和同步分侧肺通气组(S组).参数:患侧潮气量3.5 ml/kg保持不变,呼气末正压(PEEP)选择15、20、25 cm H2O(1 cm H2O=0.098 kPa);患侧PEEP 10 cm H2O不变,潮气量用随机数字表法选择5、7.5、10 ml/kg.健侧通气参数始终不变,检测不同通气条件下两组犬血流动力学和氧动力学指标.结果 (1)患侧潮气量3.5 ml/kg不变,PEEP为15、20 cm H2O时,两组血流动力学和氧动力学参数差异无统计学意义.当患侧PEEP为25 cm H2O时,NS组心率、体循环平均压(mABP)、心输出量、氧合指数和混合静脉血氧饱和度(SvO2)分别为(98±8)次/min、(84±6)mm Hg(1 mm Hg=0.133 kPa)、(1.10±0.13)L/min、(199±14)mm Hg和(55±6)%,明显低于S组[分别为(124±9)次/min、(103±7)mm Hg、(1.52±0.28)L/min、(221±15)mm Hg和(62±4)%,t值分别为-7.852、-16.561、-15.043、-13.314和-5.653,均P＜0.01].(2)患侧PEEP 10 cm H2O不变,潮气量分别为5、7.5 ml/kg时,两组的血流动力学和氧动力学参数比较差异无统计学意义.当患侧潮气量为10 ml/kg时,NS组HR、mABP、心输出量、氧合指数和SvO2均低于S组(均P＜0.01).结论 在本实验动物模型中,患侧与健侧所用PEEP水平相差≤20 cm H2O或患侧潮气量≤7.5 ml/kg时,同步和非同步分侧肺通气均能保持循环稳定.若需要更高水平PEEP时,建议选用同步分侧肺通气.     

床旁超声指导下肺保护通气对ARDS患者氧合指数的影响研究

目的探讨床旁超声指导下肺保护通气对急性呼吸窘迫综合征(acute respiratory distress syndrome, ARDS)患者氧合指数的影响。方法将125例ARDS患者分为床旁超声指导组(n=63)和最大氧合法组(n=62)。床旁超声指导组通过连续两次超声再气化评分增加幅度30%则将肺复张后PEEP值增加2cmH_2O,以此值作为肺复张后最佳PEEP值;最大氧合法组在氧合指数原基础上降低幅度10%,则重新将PEEEP增加22cmH_2O,以此值作为肺复张后最佳PEEP值。结果床旁超声指导组最佳PEEP值明显高于最大氧合法组,APACHEⅡ评分明显低于最大氧合法组,ICU留院时间明显短于最大氧合法组,P0.05。肺复张0.5、1h后,床旁超声指导组氧合指数明显低于最大氧合法组,但肺复张2h后,床旁超声指导组氧合指数明显高于最大氧合法组,P0.05,随着肺复张时间的延长,氧合指数呈逐渐增高的倾向P0.05。床旁超声指导组PVPI、ELWI明显低于最大氧合法组,P0.05。结论床旁超声指导下肺保护通气,有助于明显改善ARDS患者肺复苏后氧合指数,且不影响血流动力学参数。     

肺泡复张手法治疗急性呼吸窘迫综合征

急性肺损伤／急性呼吸窘迫综合征(ALI／ARDS)具有正常通气功能肺泡的明显减少和病变的不均一性，使其在应用机械通气时容易发生呼吸机相关肺损伤(ventilator associated lung injury，VALI)。对VALI的深入认识和研究是对ALI／ARDS患者合理应用机械通气的基础。大量研究表明，过大的潮气量使肺泡的过度牵拉和过小的呼气末肺容积致终末气道和肺泡的反复开闭都会产生VALI，因而给予小潮气量通气(6-8ml／kg)与合适的呼气末正压(PEEP)以避免吸气末肺容积过大和呼气末肺容积过低，是实施肺保护通气策略的主要内容和防止VALI的关键。尽管最近由美国国立卫生研究院(NIH)组织的由11家医学中心参加完成的多中心随机对照研究(RCT)表明，     

短暂高水平PEEP对压力控制通气ARDS患者氧合和血液动力学的影响

目的观察短暂高水平呼气末正压通气(PEEP)对急性呼吸窘迫综合征(ARDS)患者氧合情况及血流动力学的影响。方法 40例ARDS患者,随机分为实验组22例和对照组18例。实验组给予压力控制通气+短暂高水平PEEP促进肺复张,对照组仅给予压力控制通气。观察并比较两组患者的氧合及血流动力学变化。结果通气13、7、d后实验组患者PaO2/FiO2明显优于对照组(P均<0.05);通气17、d时实验组患者动脉血pH、PaCO2明显低于对照组(P均<0.05);通气1 d时实验组患者PaO2明显低于对照组(P<0.05)。两组患者通气1、2、3 d时HR、MAP、CVP相比,P均>0.05。结论短暂高水平PEEP可改善ARDS患者的氧合,对血流动力学无明显影响。     

俯卧位通气联合控制性肺膨胀对肺内、外源性急性呼吸窘迫综合征犬气体交换的影响

目的探讨俯卧位通气联合控制性肺膨胀(sustained inflation,SI)对肺内源性急性呼吸窘迫综合征(ARDSp)和肺外源性急性呼吸窘迫综合征(ARDSexp)犬的气体交换的影响。方法健康杂种犬48只,随机分为ARDSexp和ARDSp组,每组24只,静脉注射油酸复制ARDSexp模型,盐酸灌肺复制ARDSp模型,再随机各分为4组,每组6只,分别应用俯卧位通气(PC)、俯卧位通气联合SI(PS)、仰卧位通气(SC)、仰卧位通气联合SI(SS)。观察造模前基础状态,ARDS0、2、5h时氧合指数(PaO2/Fi O2)、动脉血二氧化碳分压(PaCO2)的变化,同时监测呼吸力学、平均动脉压(MAP)和心率的变化。结果对于ARDSexp和ARDSp犬SC组、PC组、SS组及PS组的PaO2/Fi O2在基础状态分别为(419±19)、(357±23)、(476±57)、(449±23)、(535±26)、(532±27)、(529±35)、(520±50)mmHg;在0h为(123±27)、(117±44)、(141±38)、(101±35)、(123±58)、(136±61)、(117±45)、(116±21)mmHg,各组间差异无统计学意义(P>0.05),但均显著低于基础值(P<0.05)。PS对于ARDSexp和ARDSp均能显著改善氧合(378±78/117±45;209±65/116±21,P<0.05),但对ARDSexp氧合改善作用更明显(378±78/209±65,P<0.05)。同时点,对于不同原因的ARDS,PS比单独PC及单独应用SI能更好地改善氧合(P<0.05)。在氧合改善的同时降低了气道阻力,增加了肺顺应性,并且对MAP、心率和PaCO2无明显影响。结论对于不同原因ARDS,PS较单应用PC及单应用SI能更好地改善氧合,且对于ARDSexp氧合改善作用更明显,氧合改善的时间更早。     

肺泡复张手法治疗急性呼吸窘迫综合征

急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)具有正常通气功能肺泡的明显减少和病变的不均一性,使其在应用机械通气时容易发生呼吸机相关肺损伤(ventilator associated lung injury,VALI)。对VALI的深入认识和研究是对ALI/ARDS患者合理应用机械通气的基础。大量研究表明,过大的潮气量使肺泡的过度牵拉和过小的呼气末肺容积致终末气道和肺泡的反复开闭都会产生VALI,因而给予小潮气量通气(6~8ml/kg)与合适的呼气末正压(PEEP)以避免吸气末肺容积过大和呼气末肺容积过低,是实施肺保护通气策略的主要内容和防止VALI的关键。尽管最近…     

纳络酮对油酸型ARDS大鼠的治疗作用

将30只健康的Wistar大鼠随机分为对照组、油酸组、纳络酮组,由股静脉注入油酸0.1 ml/kg建立急性呼吸窘迫综合征(ARDS)模型,测定血清肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、内皮素-1(ET-1)和肺组织丙二醛(MDA),并计算左肺湿/干重比值,并行肺组织病理学观察.结果 显示,油酸组与对照组比较,左肺湿/干重比值、血清中TNF-α、IL-1β及血浆ET-1含量明显升高,肺组织中MDA含量明显升高,肺组织出现明显病理损害,纳络酮组动物肺损伤轻于油酸组.认为纳络酮可抑制TNF-α、IL-1β、ET-1、MDA升高,对实验性大鼠油酸ARDS有一定的治疗作用.     

高水平呼气末正压治疗严重ARDS对患者预后的影响

目前,ARDS患者的死亡率居高不下,探索有效的治疗手段特别重要。呼气末正压(PEEP)是治疗ARDS的常用手段。与传统通气方式相比,使用PEEP,特别是高水平PEEP对ARDS的疗效及患者死亡率的影响尚不清楚。作者通过回顾性研究,探讨高PEEP对多病因的严重ARDS患者死亡率的影响。 34个月期间收住外科ICU的严重ARDS患者,PEEP大于15cmH_2O者纳入观察组。严重ARDS诊断标准:存在明显诱因,吸入氧浓度(FiO_2)>50%时,PaO_2<70mmHg,X线胸片显示斑片状阴影,肺顺应性     

ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure

RATIONALE: In patients with acute respiratory distress syndrome (ARDS), a focal distribution of loss of aeration in lung computed tomography predicts low potential for alveolar recruitment and susceptibility to alveolar hyperinflation with high levels of positive end-expiratory pressure (PEEP). OBJECTIVES: We tested the hypothesis that, in this cohort of patients, the table-based PEEP setting criteria of the National Heart, Lung, and Blood Institute's ARDS Network (ARDSnet) low tidal volume ventilatory protocol could induce tidal alveolar hyperinflation. METHODS: In 15 patients, physiologic parameters and plasma inflammatory mediators were measured during two ventilatory strategies, applied randomly: the ARDSnet and the stress index strategy. The latter used the same ARDSnet ventilatory pattern except for the PEEP level, which was adjusted based on the stress index, a monitoring tool intended to quantify tidal alveolar hyperinflation and/or recruiting/derecruiting that occurs during constant-flow ventilation, on a breath-by-breath basis. MEASUREMENTS AND MAIN RESULTS: In all patients, the stress index revealed alveolar hyperinflation during application of the ARDSnet strategy, and consequently, PEEP was significantly decreased (P < 0.01) to normalize the stress index value. Static lung elastance (P = 0.01), plasma concentrations of interleukin-6 (P < 0.01), interleukin-8 (P = 0.031), and soluble tumor necrosis factor receptor I (P = 0.013) were significantly lower during the stress index as compared with the ARDSnet strategy-guided ventilation. CONCLUSIONS: Alveolar hyperinflation in patients with focal ARDS ventilated with the ARDSnet protocol is attenuated by a physiologic approach to PEEP setting based on the stress index measurement.     

八肽胆囊收缩素对大肠杆菌致急性肺损伤大鼠的抗炎作用

目的 探讨八肽胆囊收缩素(CCK-8)对大肠杆菌致急性肺损伤(ALI)大鼠肺水肿及炎症反应的抑制作用.方法 将45只雄性SD大鼠按随机数字表法分为3组,ALI/急性呼吸窘迫综合征(ARDS)组、ALI/ARDS+ CCK-8组和对照组.ALI/ARDS组气管注射大肠杆菌制作ALI/ARDS模型;ALI/ARDS+ CC...     

Respiratory system mechanics in acute respiratory distress syndrome

Respiratory mechanics research is important to the advancement of ARDS management. Twenty-eight years ago, research on the effects of PEEP and VT indicated that the lungs of ARDS patients did not behave in a manner consistent with homogenously distributed lung injury. Both Suter and colleagues] and Katz and colleagues reported that oxygenation continued to improve as PEEP increased (suggesting lung recruitment), even though static Crs decreased and dead-space ventilation increased (suggesting concurrent lung overdistension). This research strongly suggested that without VT reduction, the favorable effects of PEEP on lung recruitment are offset by lung overdistension at end-inspiration. The implications of these studies were not fully appreciated at that time, in part because the concept of ventilator-associated lung injury was in its nascent state. Ten years later. Gattinoni and colleagues compared measurements of static pressure-volume curves with FRC and CT scans of the chest in ARDS. They found that although PEEP recruits collapsed (primarily dorsal) lung segments, it simultaneously causes overdistension of non-dependent, inflated lung regions. Furthermore, the specific compliance of the aerated, residually healthy lung tissue is essentially normal. The main implication of these findings is that traditional mechanical ventilation practice was injecting excessive volumes of gas into functionally small lungs. Therefore, the emblematic low static Crs measured in ARDS reflects not only surface tension phenomena and recruitment of collapsed airspaces but also overdistension of the remaining healthy lung. The studies reviewed in this article support the concept that lung injury in ARDS is heterogeneously distributed, with resulting disparate mechanical stresses, and indicate the additional complexity from alterations in chest wall mechanics. Most of these studies, however, were published before lung-protective ventilation. Therefore, further studies are needed to refine the understanding of the mechanical effects of lung-protective ventilation. Although low-VT ventilation is becoming a standard of care for ARDS patients, many issues remain unresolved; among them are the role of PEEP and recruitment maneuvers in either preventing or promoting lung injury and the effects of respiratory rate and graded VT reduction on mechanical stress in the lungs. The authors believe that advances in mechanical ventilation that may further improve patient outcomes are likely to come from more sophisticated monitoring capabilities (ie, the ability to measure P1 or perhaps Cslice) than from the creation of new modes of ventilatory support.     

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     

Montelukast versus inhaled corticosteroids in the management of pediatric mild persistent asthma

Background

Lung tissue of patients with acute respiratory distress syndrome (ARDS) is heterogeneously damaged and prone to develop atelectasis. During inflation, atelectatic regions may exhibit alveolar recruitment accompanied by prolonged filling with air in contrast to regions with already open alveoli with a fast increase in regional aeration. During deflation, derecruitment of injured regions is possible with ongoing loss in regional aeration. The aim of our study was to assess the dynamics of regional lung aeration in mechanically ventilated patients with ARDS and its dependency on positive end-expiratory pressure (PEEP) using electrical impedance tomography (EIT).

Methods

Twelve lung healthy and twenty ARDS patients were examined by EIT during sustained step increases in airway pressure from 0, 8 and 15 cm H₂O to 35 cm H₂O and during subsequent step decrease to the corresponding PEEP. Regional EIT waveforms in the ventral and dorsal lung regions were fitted to bi-exponential equations. Regional fast and slow respiratory time constants and the sizes of the fast and slow compartments were subsequently calculated.

Results

ARDS patients exhibited significantly lower fast and slow time constants than the lung healthy patients in ventral and dorsal regions. The time constants were significantly affected by PEEP and differed between the regions. The size of the fast compartment was significantly lower in ARDS patients than in patients with healthy lung under all studied conditions.

Conclusion

These results show that regional lung mechanics can be assessed by EIT. They reflect the lower respiratory system compliance of injured lungs and imply more pronounced regional recruitment and derecruitment in ARDS patients.     

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.     

双重打击急性肺损伤大鼠激素受体mRNA水平及激素干预效果研究

目的 探讨尾静脉注射脂多糖(lipopolysaccharide,LPS)的一次打击及LPS尾静脉注射后盐酸(HCI)气管内滴入双重打击致急性肺损伤(acute lung injury,ALI)的炎症机制、激素干预效果的差异及潜在机制.方法 健康雄性SD大鼠48只,随机分为6组(每组8只):生理盐水(NS)组、LPS组、LPS-HCl组、NS+地塞米松(Dex)组、LPS+Dex组和LPS-HCl+Dex组.检测各组支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中细胞总数、蛋白含量,肺湿/干重比(W/D),肺组织病理评分,血清和BALF中TNF-α、IL-1β、IL-4、IL-10的含量及肺组织中糖皮质激素受体(GR)mRNA水平.结果 ①LPS-HCl组BALF中蛋白含量高于LPS组(P＜0.05),LPS+Dex组BALF中细胞总数、蛋白含量以及肺W/D均低于LPS组(P值均＜0.05),而LPS-HCl+Dex组只有肺W/D比LPS-HCl组降低(P＜0.05);②LPS+Dex组和LPS-HCl+Dex组的病理评分均较激素干预之前显著降低(P值均＜0.01),且LPS-HCl+Dex组评分明显高于LPS+Dex组(P＜0.01);③LPS-HCl组BALF中IL-1β、IL-4水平明显高于LPS组(P值均＜0.05),LPS+Dex组和LPS-HCl+Dex组血清和BALF中TNF-α的含量较激素干预之前降低(P值均＜0.01),IL-10的含量升高(P值均＜0.05),同时LPS+Dex组BALF中IL-1β的含量下降(P＜0.05);④LPS+Dex组和LPS-HCl+Dex组肺组织中GR mRNA水平均较激素干预之前升高(P值均＜0.05),而NS+Dex组肺组织中GR mRNA水平较NS组显著降低(P＜0.01).结论 一次打击及双重打击所致ALI/急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)在蛋白渗漏、细胞因子水平方面存在一定差异,说明ALI/ARDS的炎症反应与致病因素是紧密相连的;LPS组的激素干预效果优于LPS-HCl组,这可能与两种模型的GR表达水平、功能状态及病理损伤特点不同有关.     

Recruitment maneuvers in three experimental models of acute lung injury. Effect on lung volume and gas exchange

Recruitment maneuvers (RM), consisting of sustained inflations at high airway pressures, have been advocated as an adjunct to mechanical ventilation in acute respiratory distress syndrome (ARDS). We studied the effect of baseline ventilatory strategy and RM on end-expiratory lung volume (EELV) and oxygenation in 18 dogs, using three models of acute lung injury (ALI; n = 6 in each group): saline lavage (LAV), oleic acid injury (OAI), and intratracheal instillation of Escherichia coli (pneumonia; PNM). All three models exhibited similar degrees of lung injury. The PNM model was less responsive to positive end-expiratory pressure (PEEP) than was the LAV or OAI model. Only the LAV model showed an oxygenation response to increasing tidal volume (VT). After RM, there were transient increases in Pa(O(2)) and EELV when ventilating with PEEP = 10 cm H(2)O. At PEEP = 20 cm H(2)O the lungs were probably fully recruited, since the plateau airway pressures were relatively high ( approximately 45 cm H(2)O) and the oxygenation was similar to preinjury values, thus making the system unresponsive to RM. Sustained improvement in oxygenation after RM was seen in the LAV model when ventilating with PEEP = 10 cm H(2)O and VT = 15 ml/kg. Changes in EELV correlated with changes in Pa(O(2)) only in the OAI model with PEEP = 10 cm H(2)O. We conclude that responses to PEEP, VT, and RM differ among these models of ALI. RM may have a role in some patients with ARDS who are ventilated with low PEEP and low VT.