肺保护性通气策略治疗急性呼吸窘迫综合征的临床探讨

目的探讨肺保护性通气策略治疗急性呼吸窘迫综合征（ARDS）的临床疗效。方法 36例ARDS患者采用肺保护性通气策略,给予适当的呼气末正压（PEEP）,小潮气量（6～8 ml/kg）,平台压控制于30～35 cm H2O以下,观察抢救成功率、机械通气时间、病死率及机械通气并发症。结果 36例患者中成功脱机30例,病情平稳后转出ICU,抢救成功率83.3%。出现呼吸机相关性肺炎2例。6例患者死亡,病死率16.7%。结论对于ARDS患者应用肺保护性策略进行机械通气,能够改善氧合,降低呼吸机相关肺损伤的发生率,提高抢救成功率,改善预后。     

改良叹气法肺复张在急性呼吸窘迫综合征治疗中的应用进展

在急性呼吸窘迫综合征患者机械通气中,肺复张策略越来越受到重视.改良叹气法是肺复张的一种方法 .本文主要就改良叹气法肺复张的实施方法 、呼气末正压的选择、复张效果、耐受性以及与其他肺复张方法 的比较做一综述,究竟哪一种肺复张方法 联合肺保护性通气策略疗效会更好,尚无定论.     

肺保护性通气策略治疗急性呼吸窘迫综合征29例

机械通气是临床上常用的治疗急性呼吸窘迫综合征（ARDS）的手段，但有可能因呼吸机相关性肺损伤（VILI）而影响到患的预后。目前提倡采取肺保护性通气策略（LPVS）来减轻呼吸机相关性肺损伤。作对机械通气成功治疗的29例ARDS患报告如下。     

急性呼吸窘迫综合征机械通气中的自主呼吸：兴利除弊

急性呼吸窘迫综合征（ARDS）是重症医学科（ICU）常见危重症。尽管人们不断地探索其诊疗方法,但病死率仍高达40%。肺保护性通气策略指导的机械通气仍是ARDS治疗的基石。ARDS患者接受机械通气时保留适度的自主呼吸有助于塌陷肺泡的复张、改善氧合、预防膈肌功能障碍等。联合有效的监测技术,设置恰当的机械通气模式及参数等措施使患者保持耐受性良好的自主呼吸状态,预防患者自身诱发性肺损伤（P-SILI）,可能是肺保护性通气策略的又一重要组成部分。     

肺复张策略在急性呼吸窘迫综合征治疗中的应用

目的:探讨肺复张策略在急性呼吸窘迫综合征(ARDS)治疗中的应用效果。方法:将40例ARDS患者随机分为A组和B组各20例,A组采用保护性通气策略,B组采用肺复张策略,观察两组的疗效和并发症发生情况。结果:两组治疗3 d后PaO2/FiO2、SaO2及PaO2较治疗前有明显改善(P<0.05);B组与A组治疗3 d后PaO2/FiO2、SaO2及PaO2比较差异有统计学意义(P<0.05);B组机械通气时间I、CU住院时间少于A组(P<0.05)。结论:肺复张策略可改善ARDS患者的血氧饱和度,对血流动力学影响短暂,安全有效。     

保护性通气策略治疗海水淹溺急性肺损伤兔的实验研究

目的 观察保护性肺通气策略在海水淹溺急性肺损伤应用时的治疗作用和安全性.方法 应用保护性机械通气策略对SWD-ALI兔进行分组救治,在不同时间点观察血气分析、呼吸动力学、血液动力学、肺损伤指标,并进行肺组织学检查,以评价治疗效果和安全性.结果 采用6～8 mL/kg小潮气量机械通气不仅能改善SWD-ALI时的氧合(P＜0.05),而且能有效控制气道峰压和平台压,从而避免呼吸机相关肺损伤.结论 肺保护性通气策略联合应用治疗SWD-ALI,能够明显改善氧和,避免继发肺损伤,是一种安全有效的治疗SWD-ALI的机械通气手段.     

急性呼吸窘迫综合征患者机械通气策略新进展

机械通气是治疗急性呼吸窘迫综合征(ARDS)最主要的手段之一.由于对ARDS病理生理认识的改变,通气策略由过去大潮气量、低呼气末正压(PEEP)发展为肺保护性通气策略,容许性高碳酸血症策略,但肺保护性通气策略势必引起肺泡萎陷,采用肺复张方法(RM)成为必要,但复张后应选用最佳PEEP,防止肺泡再度塌陷.本文综述ARDS患者机械通气策略的新进展.     

反复肺复张联合肺保护性通气对急性呼吸窘迫综合征患者肺损伤的作用

目的评价反复肺复张联合肺保护性通气对急性呼吸窘迫综合征(ARDS)患者肺损伤的作用。方法选择30例ARDS机械通气的患者,采用双水平正压通气模式(BIPAP)实施肺复张(RM),高水平和低水平压力分别为40和20cmH2O,呼吸14次/min,吸:呼=1:1.5,时间持续2min;每2h复张1次,共复张3次(RM1、RM2、RM3)。监测肺复张前、每次肺复张后10min和反复复张后4h的血流动力学和肺气体交换及血管外肺水(EVLW)的指标;肺复张前、反复肺复张后10min和4h采集血清,采用酶联免疫吸附法(ELISA)测定TNF-α、IL-6和IL-10浓度。结果每次肺复张后10min和反复肺复张后4h与肺复张前比较,心率、平均动脉压(MAP)、中心静脉压(CVP)、心脏指数(CI)变化没有统计学意义(P>0.05);而每次肺复张后10min和反复肺复张后4h与肺复张前比较,PaO2/FiO2明显增加,血管外肺水指数(EVLWI)明显减少,变化有统计学意义(P<0.05);RM3后10min与RM1后10min比较,PaO2/FiO2明显增加,变化有统计学差异(P<0.05);RM3后10min和反复肺复张后4h与RM1后10min比较,EVLWI减少有统计学意义(P<0.05)。反复肺复张后10min和4h与肺复张前比较,细胞因子TNF-α、IL-6、IL-10均有降低,但无统计学意义(P>0.05)。结论反复肺复张联合肺保护性通气可提高ARDS患者PaO2/FiO2,减少EVLW,且不加重ARDS的肺损伤。     

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。     

肺表面活性物质联合肺保护通气策略治疗新生儿重型胎粪吸入综合征合并急性肺损伤的疗效观察

目的探讨肺表面活性物质联合肺保护性通气策略治疗重症胎粪吸入综合征合并急性肺损伤新生儿的临床效果。方法选取50例重症胎粪吸入综合征合并急性肺损伤患儿,随机分成治疗组和对照组各25例。治疗组采取肺表面活性物质联合肺保护性通气策略,而对照组仅采取肺保护性通气策略治疗。比较通气前及通气2、12、24 h以及治疗后2组患儿的呼吸机相关指数、氧合指数、肺顺应性指标,同时比较2组患儿通气时间和住院时间。结果 (1)呼吸机相关参数比较,治疗组患儿吸入氧浓度24 h内显著下降,动脉血氧分压显著上升,平均气道分压也在24 h内迅速下降,2组比较有显著差异(P0.05)。(2)肺氧合指数比较上,治疗组患儿显著低于对照组患儿,在肺顺应性比较上,治疗组患儿显著高于对照组患儿。(3)治疗组患儿的通气时间和住院时间短于对照组患儿。讨论肺表面活性物质联合肺保护性通气策略对于治疗新生儿重型胎粪吸入综合征合并急性肺损伤的临床疗效优于单纯采用肺保护性通气策略。     

肺复张后不同潮气量对急性肺损伤大鼠肺血管内皮舒张功能的影响

目的 观察肺复张与肺复张后不同潮气量对ALI大鼠肺内皮舒张功能的影响.方法 内毒素(LPS)静脉注射复制大鼠ALI模型.25只清洁级SD大鼠随机(随机数字法)分成5组,每组5只:对照组、ALI组、小潮气量(VT)组(LV组,VT 6 mL/kg)、SI+小VT组(SI+LV组,VT 6 mL/kg)、SI+常规VT组(SI+MV组,VT12mL/kg),SI(30 cmH2O)维持30 s,进行肺复张.应用不同潮气量联合肺复张监测呼吸功能和血流动力学,实验5 h后放血处死动物.观察肺组织病理形态改变和湿/干重比(W/D);放射免疫法检测肺组织中ET-1;免疫组织化学法半定量分析肺动脉内皮细胞内皮型一氧化氮合酶(eNOS)蛋白表达水平;血管张力实验检测离体肺动脉环对乙酰胆碱(Ach)和硝普钠(SNP)介导的舒张功能的影响;ELISA检测肿瘤坏死因子-α(TNF-α)炎症反应指标.结果 与CON组比较,LPS增加各组内肺水肿,加重肺损伤,增加TNF-α含量,增加ET-1含量,减少肺动脉内皮细胞eNOS蛋白表达,减弱Ach介导的内皮依赖的舒张功能,最终影响内皮功能.SI+LV组ET-1含量为(109.18±15.62)pg/mL,SI+MV组和LV组肺组织ET-1含量分别为(158.78±30.40)pg/mL和(152.35±8.21)pr/mL,较SI+LV组升高(P＜0.05);SI+LV组肺组织eNOS蛋白表达的iOD值为(12663.83±1348.93),SI+MV组和LV组肺组织eNOS蛋白表达的iOD值分别为(9208.12±2773.68)和(9339.53±3366.40),较SI+LV组无统计学差异,但有降低趋势(P＞0.05);与SI+LV组比较,ALI组和SI+MV组在不同浓度Ach作用下内皮依赖的舒张功能降低(P＜0.05),LV组虽然与SI+LV组比较差异无统计学意义,但Ach介导舒张功能有下降的趋势;SI+LV组肺组织TNF-α含量(2374.53±410.60)ng/L,较SI+MV组(3468.86±659.25)ng/L和LV组(3370.75±314.17)ng/L降低(P＜0.05).结论 肺复张联合大潮气量和小潮气量机械通气能够改善ALI大鼠肺血管内皮舒张功能,肺复张联合小潮气量可进一步减轻ALI大鼠肺血管内皮舒张功能的损伤.     

肺复张对急性呼吸窘迫综合征患者血管外肺水的影响

目的 探讨肺复张(RM)策略对急性呼吸窘迫综合征(ARDS)患者血管外肺水(EVLW)的影响.方法 采用随机对照病例研究方法,将20例ARDS患者随机分为RM组和对照组.按肺保护性通气策略的原则给患者进行机械通气;用双水平气道正压(BIPAP)通气模式进行RM,每8 h重复1次,连续7 d或至脱机前;除RM外,其余治疗两组相同.记录患者的基线资料和每日RM结束后的EVLW、血管外肺水指数(EVLWI)、呼吸力学参数、氧合指数(PaO2/FiO2)、中心静脉压(CVP)、血浆胶体渗透压(COP)以及糖皮质激素、肾上腺素能药物用量和24 h液体出入量平衡等影响EVLW各因素的数值.结果 RM组和对照组EVLW、EVLWI随时间延长呈逐渐降低趋势,但两组间比较差异无统计学意义(P均>0.05).两组间CVP、COP和去甲肾上腺素、氢化可的松用量比较差异均无统计学意义(P均>0.05);RM组多巴胺用量在4 d时明显少于对照组(P<0.05);液体出入量平衡RM组7 d时为负平衡,对照组则为正平衡(P<0.05).RM组平均气道压(Pmean)的均值[(18.8±3.2)cm H2O(1 cm H2O=0.098 kPa)]和肺准静态顺应性(Cstat)的均值[(36.5±14.5)ml/cm H2O]均明显高于对照组[(16.6±3.9)cm H2O和(29.3±12.0)ml/cm H2O,P均<0.05];其中RM组5 d时Cstat大于2 d和3 d时(P均<0.05).两组间PaO2/FiO2比较则未见明显差异(P均>0.05).结论 针对ARDS患者实施的RM治疗并没有明显影响EVLW,而仅起到了改善肺呼吸力学特征的作用.本研究中所涉及的影响肺水的因素并未影响肺水的形成和清除.     

俯卧位通气加肺复张对急性呼吸窘迫综合征的作用

目的 评价俯卧位通气(PPV)联合肺复张(RM)对急性呼吸窘迫综合征(ARDS)犬的肺保护作用及机制.方法 经股静脉快速注入油酸建立犬ARDS模型,容积控制通气,在小潮气量(VT,10 ml/kg)+高呼气末正压(PEEP,16 cm H2O,1 cm H2O=0.098 kPa)通气基础上,按随机数字表法分为仰卧位组、俯卧位组、仰卧+RM组、俯卧+RM组,每组6只.测定通气后0.5、2和4 h血清细胞因子.4 h后经股动脉放血处死动物,开胸取肺;取左肺组织制备匀浆,测定细胞因子;取右肺测定湿/干重(W/D)比值及制备病理切片,行病理评分.结果 ①通气4 h时仰卧+RM组血清白细胞介素-8(IL-8)浓度明显高于其他3组(P均<0.05),且仰卧+RM组血清肿瘤坏死因子-α(TNF-α)浓度明显高于俯卧位组及俯卧+RM组(P均<0.05).②俯卧位组及俯卧+RM组背侧肺组织匀浆中IL-8浓度明显低于仰卧位组(P均<0.05),TNF-α浓度明显低于仰卧+RM组(P均<0.05).③俯卧位组、俯卧+RM组右肺W/D比值明显低于仰卧位组及仰卧+RM组(P均<0.05).④俯卧位组及俯卧+RM组背侧病理评分显著低于仰卧位组及仰卧+RM组(P均<0.05).结论 在犬ARDS模型中,予以小VT+PEEP的肺保护性通气时,在俯卧位实施RM可以减轻肺损伤.     

Effect of post recruitment maneuver ventilation by different tidal volume on lung vascular endothelial diastole function in rats with acute lung injury

BACKGROUND: This study aimed to observe the effect of recruitment maneuver (RM) and post-RM ventilation at different tidal volume on lung vascular diastole endothelial function in rats with acute lung injury (ALI).METHODS: A ALI rat model was produced by intravenous infusion of lipopolysaccharide (6 mg/kg). Twenty-five rats were randomly divided into five groups: control group (n=5), ALI group (n=5), low tidal volume group (LV group, VT 6 mL/kg, n=5), sustained inflation (SI) with low tidal volume group (SI+LV group, VT 6 mL/kg, n=5), and SI with moderate tidal volume group (SI+MV group, VT 12 mL/kg, n=5). RM was performed with SI, airway pressure 30 cmH₂O for 30 seconds, and positive end-expiratory pressure (PEEP) was set to 5 cmH₂O. Lung tissue was taken after 5 hours of mechanical ventilation. Mean arterial blood pressure (MAP) was monitored during the experiment. Endothelin-1 (ET-1), endothelial nitricoxide synthase (eNOS), Ach-induced endothelium-dependent relaxation response of isolated pulmonary artery rings were determined at 5 hours.RESULTS: LPS increased ET-1 level, decreased the expression of eNOS in lung tissue, impaired the Ach-induced endothelium-dependent relaxation response in the pulmonary artery, without obvious effect on systemic hemodynamics. SI+LV significantly reduced LPS-induced elevation of ET-1 level, increased the expression of eNOS, significantly improved endothelial dysfunction, and improved the dysfunction of endothelium-dependent relaxation in the pulmonary artery.CONCLUSIONS: RM with a high or low tidal volume ventilation could improve the lung vascular endothelial function of rats with acute lung injury, and RM with low tidal volume ventilation could lower significantly the injury of lung vascular endothelial diastole function in rats with acute lung injury.     

Intercomparison of recruitment maneuver efficacy in three models of acute lung injury

OBJECTIVE: To compare the relative efficacy of three forms of recruitment maneuvers in diverse models of acute lung injury characterized by differing pathoanatomy. DESIGN: We compared three recruiting maneuver (RM) techniques at three levels of post-RM positive end-expiratory pressure in three distinct porcine models of acute lung injury: oleic acid injury; injury induced purely by the mechanical stress of high-tidal airway pressures; and pneumococcal pneumonia. SETTING: Laboratory in a clinical research facility. SUBJECTS: Twenty-eight anesthetized mixed-breed pigs (23.8 +/- 2.6 kg). INTERVENTIONS: The RM techniques tested were sustained inflation, extended sigh or incremental positive end-expiratory pressure, and pressure-controlled ventilation. PRIMARY MEASUREMENTS: Oxygenation and end-expiratory lung volume. MAIN RESULTS: The post-RM positive end-expiratory pressure level was the major determinant of post-maneuver PaO2, independent of the RM technique. The pressure-controlled ventilation RM caused a lasting increase of PaO2 in the ventilator-induced lung injury model, but in oleic acid injury and pneumococcal pneumonia, there were no sustained oxygenation differences for any RM technique (sustained inflation, incremental positive end-expiratory pressure, or pressure-controlled ventilation) that differed from raising positive end-expiratory pressure without RM. CONCLUSIONS: Recruitment by pressure-controlled ventilation is equivalent or superior to sustained inflation, with the same peak pressure in all tested models of acute lung injury, despite its lower mean airway pressure and reduced risk for hemodynamic compromise. Although RM may improve PaO2 in certain injury settings when traditional tidal volumes are used, sustained improvement depends on the post-RM positive end-expiratory pressure value.     

肺保护性通气对肺内外源性急性呼吸窘迫综合征外周血和肺泡灌洗液中炎性介质影响的比较

目的　观察在肺保护性通气条件下急性呼吸窘迫综合征 (ARDS)模型犬氧合指数以及外周血和肺不同部位 (肺上区、肺下区腹侧和肺下区背侧 )支气管肺泡灌洗液 (BAL F)中炎性介质的变化。方法　健康雄性杂种犬 2 4只 ,随机分为肺内源性 ARDS(ARDSp)实验组、ARDSp 对照组、肺外源性 ARDS(ARDSexp)实验组和 ARDSexp对照组 ,每组 6只。采用静脉注射油酸形成 ARDSexp模型 ,应用十六烷磺基丁二酸钠盐气管内吸入形成 ARDSp模型。实验组肺损伤后进行肺保护性通气〔潮气量 8ml/ kg,呼气末正压(PEEP) 10 cm H2 O(1cm H2 O=0 .0 98k Pa)〕;对照组则继续进行大潮气量通气。动态观察肺保护性通气条件下 ARDS模型犬外周血和肺不同部位 (如肺尖叶、肺心叶和肺膈叶 ) BAL F中的炎性介质 ,如肿瘤坏死因子α(TNFα)、白细胞介素 (IL 1β,IL 6 )的变化。结果　肺损伤后 ARDS模型犬氧合指数均显著恶化 ,外周血中炎性介质明显升高 (P均 <0 .0 5 ) ,ARDSp模型犬肺尖叶和心叶 BAL F中炎性介质水平明显高于 ARDSexp模型犬 (P均 <0 .0 5 )。应用肺保护性通气治疗后 ,实验组犬氧合指数有不同程度改善 ,炎性介质水平有不同程度下降 ;但 ARDSp实验组的治疗效果不如 ARDSexp实验组。结论　 ARDSexp和 ARDSp的肺不同部位炎性介质释放和氧合     

Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury

OBJECTIVE: Elevated lung volumes and increased pleural pressures associated with recruitment maneuvers (RM) may adversely affect pulmonary vascular resistance and cardiac filling or performance. We investigated the hemodynamic consequences of three RM techniques after inducing acute lung injury. DESIGN: Prospective, randomized, controlled experimental study. SETTING: Hospital research laboratory. SUBJECTS: Thirteen anesthetized, mechanically ventilated pigs. INTERVENTIONS: We induced three types of acute lung injury: oleic acid injury (n = 4); ventilator-induced lung injury (n = 4); and pneumonia (n = 5). All three models were designed to initiate a similar severity of oxygenation impairment. RM methods tested were sustained inflation, incremental positive end-expiratory pressure (PEEP) with a limited peak pressure, and pressure-controlled ventilation with increased PEEP and a fixed driving pressure. From a baseline PEEP of 8 cm H2O, all interventions were tested using post-RM PEEP levels of 8, 12, and 16 cm H2O. Cardiac output by thermodilution and systemic and pulmonary artery pressures were measured frequently during the RM and for 15 mins after its completion. MEASUREMENTS AND MAIN RESULTS: During the RM, cardiac output decreased to a greater extent in the pneumonia model (0.49 of baseline cardiac output) than in the oleic acid injury (0.67 of baseline) or ventilator-induced lung injury (0.79 of baseline) models. Cardiac output recovered to the baseline value by 5 mins post-RM in oleic acid injury and ventilator-induced lung injury models. However, cardiac output remained decreased 15 mins post-RM in the pneumonia model. There were no differences in hemodynamic parameters among RM methods in oleic acid injury and ventilator-induced lung injury models. In the pneumonia model, however, cardiac output decreased to a greater extent during the RM with sustained inflation (to 0.33 of baseline cardiac output) compared with pressure-controlled ventilation (to 0.68 of baseline). CONCLUSIONS: We conclude that RM transiently but profoundly depressed cardiac output in three models of acute lung injury. The results imply that a lung recruiting maneuver should be used with caution, especially when using sustained inflation in the setting of pneumonia.     

Lung recruitment maneuver effects on respiratory mechanics and extravascular lung water index in patients with acute respiratory distress syndrome

BACKGROUND:

Animal experiments showed that recruitment maneuver (RM) and protective ventilation strategy of the lung could improve oxygenation and reduce extravascular lung water. This study was to investigate the effects of RM on respiratory mechanics and extravascular lung water index (EVLWI) in patients with acute respiratory distress syndrome (ARDS).

METHODS:

Thirty patients with ARDS were randomized into a RM group and a non-RM group. In the RM group, after basic mechanical ventilation stabilized for 30 minutes, RM was performed and repeated once every 12 hours for 3 days. In the non-RM group, lung protective strategy was conducted without RM. Oxygenation index (PaO₂/FiO₂), peak inspiratory pressure (PIP), Plateau pressure (Pplat), static pulmonary compliance (Cst) and EVLWI of patients before treatment and at 12, 24, 48, 72 hours after the treatment were measured and compared between the groups. Hemodynamic changes were observed before and after RM. One-way ANOVA, Student''s t test and Fisher''s exact test were used to process the data.

RESULTS:

The levels of PaO₂/FiO₂ and Cst increased after treatment in the two groups, but they were higher in the RM group than in the non-RM group (P<0.05). The PIP and Pplat decreased after treatment in the two groups, but they were lower in the RM group than in the non-RM group (P<0.05). The EVLWI in the two groups showed downward trend after treatment (P<0.05), and the differences were signifcant at all time points (P<0.01); the EVLWI in the RM group was lower than that in the non-RM group at 12, 24, 48 and 72 hours (P<0.05 or P<0.01). Compared with pre-RM, hemodynamics changes during RM were significantly different (P<0.01); compared with pre-RM, the changes were not significantly different at 120 seconds after the end of RM (P>0.05).

CONCLUSIONS:

RM could reduce EVLWI, increase oxygenation and lung compliance. The effect of RM on hemodynamics was transient.KEY WORDS: Lung recruitment maneuver, Acute respiratory distress syndrome, Respiratory mechanics, Extravascular lung water index, Hemodynamics, Lung protective ventilation, Oxygenation index     

氯氮平中毒继发急性肺损伤/急性呼吸窘迫综合征的抢救体会

目的:探讨氯氮平中毒继发急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)有效的治疗方法。方法:总结分析16例氯氮平中毒继发ALI/ARDS患者的临床表现和治疗方法。患者在中毒后6～144h出现ALI/ARDS表现,予气管插管、机械通气,抗胆碱药物治疗及血液灌流等综合治疗。结果:本组患者均治愈,平均住院时间(14±1.6)d;机械通气时间平均(134±12)h,中毒后(48～96)h意识转清。结论:氯氮平中毒继发的急性肺损伤/急性呼吸窘迫综合征主要与肺水肿、吸入性肺炎及氯氮平对肺组织的直接损伤作用有关。早期进行机械通气联合血液灌流和合理抗胆碱药物的,是治疗重度氯氮平重度并发急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)的有效方法。     

不同呼气末正压水平对肺复张患者脑灌注压及血流动力学的影响

目的 观察肺复张(RM)对颅内压(ICP)、脑灌注压(CPP)及平均动脉压(MAP)的影响.方法 选择因严重颅脑疾患伴肺损伤需要进行机械通气的6例患者,在进行RM的同时进行持续ICP、MAP、中心静脉压(CVP)、脉搏血氧饱和度(SpO2)等监测.RM采用压力控制通气模式,逐步提升呼气末正压(PEEP)的方法.结果 6例患者共进行22例次RM,2例次分别在3 cm H2O(1 cm H2O=0.098 kPa)和6 cm H2O PEEP水平出现MAP、CPP显著降低而终止.其余20例次RM中不同PEEP水平相应的MAP、CVP、ICP、CPP平均值与基础值相比差异均无统计学意义(P均>0.05);MAP与CPP呈高度相关性(r=0.706,P=0.000).20例次RM中,单次RM内参数间呈高度相关性的比例:MAP与CPP占85%(17/20);PEEP与CVP占75%(15/20);PEEP与ICP占75%(15/20);PEEP与CPP占40%(8/20).22例次RM中MAP随PEEP变化有6种趋势:8例次相对稳定;6例次随PEEP增加而降低,然后随PEEP降低而逐渐回升;2例次随PEEP增加而升高,随PEEP降低逐渐回到基础值;2例次随PEEP增加而降低,PEEP降低后MAP不能相应升高;2例次随PEEP增加而增加,在PEEP降到基础值后MAP仍维持在高水平;2例次随PEEP增加MAP急剧降低而终止RM.11例次RM中ICP随PEEP升高而升高,随PEEP降低而降低;6例次在RM过程中无明显变化;3例次RM后ICP处于高值末回到基线.12例次RM中CPP随PEEP升高而降低,随PEEP降低而增加,并随PEEP回到基线时恢复到基础值;6例次无明显变化;2例次CPP维持在低值,分别在PEEP回到基线后10 min、20 min恢复到基础值.结论 RM对MAP、ICP、CPP的影响存在明显的个体差异.ICP监测有助于保障脑部疾患合并肺损伤患者RM实施的安全性.