气管内吹气对机械通气相关性急性肺损伤保护作用的实验研究

目的：探讨气管内吹气（ＴＧＩ）对机械通气相关性急性肺损伤（ＡＬＩ）家兔实施容许性高碳酸血症（ＰＨＣ）时二氧化碳清除效果及其在维持二氧化碳分压（ＰａＣＯ２）大致正常时降氏潮气量（ＶＴ）、气道峰压（Ｐｐｅａｋ）和平台压（Ｐｐｌａｔｃ）的作用。方法：用自行设计的ＴＧＩ装置对常规机械通气（ＣＭＶ）组和小ＶＴ爱气致ＰＨＣ时ＡＬＩ家兔行ＴＧＩ,观察２组动物在不同吹气流量（）．２Ｌ／ｍｉｎ和０．４Ｌ／ｍｉｎ）时     

高频喷射通气联合气管内吹气对急性肺损伤的治疗作用

目的　探讨高频喷射通气联合气管内吹气对急性肺损伤的治疗作用。方法　杂种犬 12条 ,随机分为两组 ,用大剂量生理盐水灌洗肺造成急性肺损伤。各组分别给予高频喷射通气 ,调整呼吸机参数使第一组实验犬PaCO2 维持在 35～ 5 0mmHg,第二组实验犬PaCO2 维持在 6 0～ 80mmHg。然后进行 4L/min和 8L/min氧气流量的气管内吹气 ,每阶段进行 30min ,观察血流动力学指标和血气指标的变化。结果　①联合通气后 ,两组PaCO2 及PetCO2 均明显下降 ,且随着吹入气氧流量的增加下降更明显。②联合通气后 ,动脉血氧分压在两组中明显上升 ,但随着吹入气氧流量的增加 ,动脉血氧分压变化无明显差异 (P >0 0 5 )。③联合通气后使各组气道压明显上升。④联合通气对各组犬血流动力学无显著影响 (P >0 0 5 )。结论　高频喷射通气联合气管内吹气能有效地降低肺损伤犬PaCO2 ,促进二氧化碳的排除 ,提高肺损伤犬的氧合且不影响实验犬的血流动力学     

高频喷射通气联合气管内吹气对急性肺损伤的影响

目的观察高频喷射通气（HFJV）联合气管内吹气（TGI）对急性肺损伤（ALI）患者的影响。方法将24例ALI患者随机分为观察组（HFJV联合TGI组）及对照组（HFJV组）,每组12例。2组均采用常规药物及HFJV治疗。在此基础上,观察组加用TGI治疗。同时检测2组治疗前,治疗后1、48h血气[pH值、动脉血氧分压（PaO2）、动脉血氧饱和度（SaO2）、动脉血二氧化碳分压（PaCO2）]、血流动力学[平均动脉压（MAP）、中心静脉压（CVP）、心率（HR）]、呼气末二氧化碳分压（PETCO2）及治疗前、治疗后48h血清肺表面活性蛋A（SP-A）灰度值,并对2组进行急性生理功能和慢性健康状况评分（APACHE-Ⅱ）、肺损伤评分（LIS）。结果观察组治疗后48hPaCO2、PETCO2值均较对照组明显下降,差异均有统计学意义（均P〈0.05）,而PaO2明显升高（P〈0.05）。观察组治疗后48hHR、MAP、CVP值、APACHE-Ⅱ评分值与对照组比较,差异均无统计学意义（均P〉0.05）。观察组治疗后48h血清SP-A灰度值、LIS评分值均较对照组明显下降,差异均有统计学意义（均P〈0.05）。结论联合通气可明显降低PaCO2水平,促进CO2排出,提高PaO2、SaO2,但不影响血流动力学,并且还可减少肺表面活性蛋白A（SP-A）流失,减低LIS评分。     

气管内肺通气对急性肺损伤羊通气功能的影响

气管内肺通气（ＩＴＰＶ）是一种新的持续正压通气方式。本研究应用直流和反流两种气管插管内导管进行ＩＴＰＶ，并与压力控制通气（ＰＣＶ）进行比较。结果显示：直流ＩＴＰＶ的ＰａＣＯ２下降０．６９～０．９３ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ，Ｐ＜０．０５），生理死腔（ＶＤ）减少０．８ｍｌ／ｋｇ；反流ＩＴＰＶ的ＰａＣＯ２下降１．０７～１．３３ｋＰａ（Ｐ＜０．０１），ＶＤ减少１．０ｍｌ／ｋｇ；在维持ＰａＣＯ２５．０７±０．４４ｋＰａ条件下，反流ＩＴＰＶ气管内吸气压峰压（ＰＩＰ）下降３３％，平均气道压（Ｐａｗ）下降约５０％；ＰａＯ２和血流动力学参数均无显著变化（Ｐ＞０．０５）。提示：ＩＴＰＶ通过减少生理死腔使通气效率提高，可以用较低的ＰＩＰ和Ｐａｗ维持肺的正常气体交换；反流ＩＴＰＶ比直流ＩＴＰＶ显示更有效的通气效率     

机械通气相关肺损伤与肺保护性通气策略

近年来发现,对某些急性呼吸窘迫综合征(ARDS)患者进行机械通气治疗时,反而加重原本存在的肺损伤和炎症。因此,有些学者对高压高容通气、高压低容通气和低压高容通气进行比较,结果表明,潮气量过大对肺泡的牵拉作用是机械通气相关肺损伤的最重要原因。因而,提出了“容积损伤”(volutrauma)的概念。急性肺损伤(ALI)/ARDS患者多同时存在多种可致肺损伤的危险因素。这些因素的存在不仅使ARDS患者对机械通气所致肺损伤的易感性增加,而且降低机体对肺损伤的修复能力。ALI/ARDS患者广泛存在的肺不张和肺水肿使肺脏的有效充气容积明显减少,…     

机械通气在急性肺损伤治疗中的作用和地位

所谓“肺损伤”，并非仅指对肺的直接损伤，也包括其他脏器发生的炎症和病损引起的继发性肺部损害。根据2000年中华医学会呼吸病学分会提出的标准，急性肺损伤（ALI）和急性呼吸窘迫综合征（ARDs）是指由心源性以外的各种肺内、外因素所导致的急性、进行性缺氧性呼吸衰竭。ALI和ARDS的病理、生理学发展过程基本是一致的，严重的ALI或ALI的严重阶段即为ARDS。ALI和ARDS的临床特征均为进行性呼吸困难和顽固性低氧血症。自1967年Ashbaugh等首先报道ARDS以来，随着机械通气，尤其是呼气末正压（PEEP）等治疗手段的大量应用，虽然也有报道ALI／ARDS的病死率在30％～60％之间，但近年来大部分的临床资料显示其死亡率在30％～40％左右，呈下降趋势。     

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.     

肺复张和保护性肺通气在急性肺损伤救治中的护理

目的探讨肺复张联合保护性肺通气策略治疗急性肺损伤患者的疗效及护理。方法对42例急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)患者均采用保护性机械通气,并联合肺复张手法,给予35 cmH2O的气道压力,持续30 s后,恢复原通气模式及条件。结果 31例患者成功撤机,临床症状明显好转,治愈出院,成功率73.8%。死亡11例,病死率26.2%。结论肺复张和保护性肺通气策略是治疗急性肺损伤的主要手段。做好保护性机械通气期间的护理及严密监测是治疗成功的关键。     

气管内吹气在急性呼吸窘迫综合征患者中的应用

目的 观察在小潮气量机械通气基础上应用气管内吹气(tracheal gas insufflation,TGI)对实施允许性高碳酸血症(PHC)的急性呼吸窘迫综合征(ARDS)患者的疗效,并探讨其机制.方法 对我院两年来诊断明确的ARDS患者在小潮气量机械通气、PHC基础上应用我院自行设计的气管内吹气装置持续TGI,低流量(2 L/min)吹入新鲜气体治疗2 h,每30min记录动脉血气(PaCO2、PaO2)、潮气量、血氧饱和度(SaO2)、吸气峰压(PIP)、平台压(Plat)、呼气末正压(PEEP)、心率和平均动脉压(MAP).结果 在各时间段气管内吹气后PaCO2较吹气前下降,120 min 组差异有统计学意义.结论 应用自行设计的气管内通气装置在ARDS患者中短期实施气管内吹气,可以改善PHC,降低呼吸机的支持条件.     

机械通气治疗急性呼吸窘迫综合征中的肺开放通气策略

机械通气是治疗急性呼吸窘迫综合征的关键性措施，肺开放通气策略是肺保护通气策略的重要补充，其最终日的是为了实现肺保护。实施肺开放通气策略我们主要是围绕以下两方面来进行：一方面是采用何种方式及压力水平使更多萎陷肺泡开放（open up the lung）。另一方面是打开肺后如何设法使已开放的肺泡尽量维持于开放状态（keep the lung open）。肺开放性通气策略实施的方法有多种，最佳PEEP是维持肺开放的核心，多种因素影响肺开放通气实施效果和检测。     

Continuous tracheal gas insufflation during protective mechanical ventilation in juvenile piglets with acute lung injury induced by endotoxin

BACKGROUND:

Low tidal volume mechanical ventilation is difficult to correct hypoxemia, and prolonged inhalation of pure oxygen can lead to oxygen poisoning. We suggest that continuous tracheal gas insufflation (TGI) during protective mechanical ventilation could improve cardiopulmonary function in acute lung injury.

METHODS:

Totally 12 healthy juvenile piglets were anesthetized and mechanically ventilated at PEEP of 2 cmH₂O with a peak inspiratory pressure of 10 cmH₂O. The piglets were challenged with lipopolysaccharide and randomly assigned into two groups (n=6 each group): mechanical ventilation (MV) alone and TGI with continuous airway flow 2 l/min. FIO₂ was set at 0.4 to avoid oxygen toxicity and continuously monitored with an oxygen analyzer.

RESULTS:

Tidal volume, ventilation efficacy index and mean airway resistant pressure were significantly improved in the TGI group (P<0.01 or P<0.05). At 4 hours post ALI, pH decreased to below 7.20 in the MV group, and improved in the TGI group (P<0.01). Similarly, PaCO₂ was stable and was significantly lower in the TGI group than in the MV group (P<0.01). PaO₂ and PaO₂/FIO₂ increased also in the TGI group (P<0.05). There was no significant difference in heart rate, respiratory rate, mean artery pressure, central venous pressure, dynamic lung compliance and mean resistance of airway between the two groups. Lung histological examination showed reduced inflammation, reduced intra-alveolar and interstitial patchy hemorrhage, and homogenously expanded lungs in the TGI group.

CONCLUSION:

Continuous TGI during MV can significantly improve gas exchange and ventilation efficacy and may provide a better treatment for acute lung injury.KEY WORDS: Acute lung injury, Tracheal gas insufflation, Lung protective strategy, Mechanical ventilation     

Effects of expiratory tracheal gas insufflation in patients with severe head trauma and acute lung injury

Objective This study analyzed the effect of phasic tracheal gas insufflation at mid- to end-expiration in patients with severe head trauma and acute lung injury (ALI)/acute respiratory distress syndrome (ARDS).Design and setting A prospective interventional study in a 16-bed intensive care unit.Patients Seven patients with severe head trauma (Glasgow Coma Scale <9) and ALI/ARDS.Interventions Patients were ventilated in assist/control mode with a ventilatory strategy providing adequate oxygenation (PaO₂ >70 mmHg) and normocapnia (PaCO₂ between 35–40 mmHg). Mid to end expiratory tracheal gas insufflation at 8 l/min flow rate was delivered for 90 min while normocapnia was maintained by simultaneous reductions in tidal volume. We measured (hemodynamics, oxygenation, lung mechanics, and cerebral parameters) in basal situation and during and after tracheal insufflation.Measurements and results Tracheal gas insufflation allowed a significant decrease in tidal volume from 9.1 to 7.2 ml/kg, with associated reduction in driving pressure (plateau pressure minus positive end-expiratory pressure, PEEP) from 18.1 to 13.2 cmH₂O. Total PEEP increased from 9.3 to 12.7 cmH₂O due to the generation of lung hyperinflation. Oxygenation improved slightly during tracheal gas insufflation, and this improvement remained after stopping tracheal insufflation. No changes in hemodynamic or cerebral parameters were observed during the study.Conclusions In patients with severe head trauma and ALI receiving mechanical ventilation, expiratory tracheal gas insufflation allowed the targeted arterial PCO₂ level to be maintained together with a substantial reduction in tidal volume.This work was supported by Fondo de Investigaciones Sanitarias (expedient 01/1036), Ministry of Health, and Fundació Parc Taulí.     

Preemptive mechanical ventilation can block progressive acute lung injury

Mortality from acute respiratory distress syndrome (ARDS) remains unacceptable, approaching 45% in certain high-risk patient populations. Treating fulminant ARDS is currently relegated to supportive care measures only. Thus, the best treatment for ARDS may lie with preventing this syndrome from ever occurring. Clinical studies were examined to determine why ARDS has remained resistant to treatment over the past several decades. In addition, both basic science and clinical studies were examined to determine the impact that early, protective mechanical ventilation may have on preventing the development of ARDS in at-risk patients. Fulminant ARDS is highly resistant to both pharmacologic treatment and methods of mechanical ventilation. However, ARDS is a progressive disease with an early treatment window that can be exploited. In particular, protective mechanical ventilation initiated before the onset of lung injury can prevent the progression to ARDS. Airway pressure release ventilation (APRV) is a novel mechanical ventilation strategy for delivering a protective breath that has been shown to block progressive acute lung injury (ALI) and prevent ALI from progressing to ARDS. ARDS mortality currently remains as high as 45% in some studies. As ARDS is a progressive disease, the key to treatment lies with preventing the disease from ever occurring while it remains subclinical. Early protective mechanical ventilation with APRV appears to offer substantial benefit in this regard and may be the prophylactic treatment of choice for preventing ARDS.     

Theoretical interactions between ventilator settings and proximal deadspace ventilation during tracheal gas insufflation

Objective To investigate the theoretical interactions between ventilator settings, tracheal gas insufflation (TGI), and alveolar ventilation.Design We derived differential equations governing compartmental volume changes in a one-compartment model of TGI-assisted ventilation and equations governing gas dilution in the airway proximal to the TGI catheter and the additional CO₂ clearing ventilation arising from this dilution. This additional ventilation was called proximal ventilation. Validation was conducted in a mechanical lung analog. Model predictions for proximal ventilation were then generated over wide ranges of frequency, duty cycle, and tidal volume.Results Significant interactions were identified between ventilator settings and proximal ventilation. The persistence of end-expiratory flow from the lung decreased proximal dilution by fresh gas and thereby reduced TGI-aided proximal ventilation. Changes in end-expiratory lung flow resulting from alterations in ventilator settings were correlated inversely with proximal ventilation.Conclusions During TGI with constant catheter flow, ventilator settings that promote end-expiratory flow of gas from the lung diminish proximal ventilation. When frequency increases, the decrease in dilution efficiency of the individual breath is partially offset by the increase in cycle number, an effect which is magnified by any concomitant decrease in inspired tidal volume. Prolongation of the duty cycle tends to decrease proximal ventilation. Increases in expiratory resistance, including those arising from the external ventilator circuit or the endotracheal tube, also impair proximal ventilation.     

呼吸机致大鼠急性肺损伤的实验研究

目的探讨不同潮气量机械通气在大鼠急性肺损伤发生中的作用。方法32只Wistar大鼠随机分为对照组、小潮气量组、常规潮气量组和大潮气量组。分别在肉眼、光镜和电镜下观察各组大鼠肺组织病理学改变,测定动脉血气和BALF中性粒细胞计数(PMN)、蛋白含量和髓过氧化物酶(MPO)活性。结果小潮气量组肺组织在肉眼、光镜和电镜下观察与对照组比较差异无显著性;常规潮气量和大潮气量组肺组织在光镜和电镜下可观察到具有不同程度损伤改变,其BALF中PMN、MPO活性和蛋白含量均明显高于对照组和小潮气量组,而动脉血氧分压(PaO_2)明显低于对照组和小潮气量组(P＜0．01,P＜0．05);大潮气量组BALF中MPO活性和蛋白含量与常规潮气量组比较差异也有显著性(P＜0．01);小潮气量组各项指标与对照组比较差异均无统计学意义(P＞0．05)。结论小潮气量通气对正常肺组织无明显影响,但没有任何肺保护措施的常规潮气量通气对正常肺组织具有一定损伤作用,其损伤作用与中性粒细胞在肺内募集和活化有密切关系。     

部分液体通气减轻油酸诱导乳猪重度肺损伤炎症反应的实验研究

目的:探讨以全氟化碳为载体的部分液体通气对油酸诱导乳猪炎症反应后气体交换及炎症反应的影响。方法:油酸间断注射诱导乳猪急性肺损伤,随机分为部分液体通气组(实验组)和传统机械通气组(对照组),每组各6只。分别于模型建立前、肺损伤后每隔60min行动脉血气分析。通气4h后,取动脉血离心,监测血浆肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6;取左下肺组织,监测组织肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6含量。结果:实验组动物动脉血氧分压、二氧化碳分压,pH较对照组均明显改善,血浆肿瘤坏死因子-α,白细胞介素-6,白细胞介素-1β均较对照组降低(P<0.05),组织肿瘤坏死因子-α,白细胞介素-6,白细胞介素-1β均较对照组降低(P<0.05)。光镜检验显示部分液体通气组肺组织损伤明显减轻。结论:部分液体通气可以改善油酸诱导乳猪肺损伤模型气体交换功能,明显减轻乳猪肺部炎症反应和组织学损伤。     

高二氧化碳通气对急性肺损伤兔病理生理指标的影响

目的　探求急性肺损伤 (ALI)动物模型在高CO2 通气时病理生理指标的改变机制。方法　 2 2只新西兰大白兔随机分为对照组 (C组 )、非高CO2 通气组 (N组 )、高CO2 (8% )通气组 (H组 )。N组和H组通过静脉注射油酸 (0 1ml/kg)复制ALI模型。 3组均机械通气至 3h ,观察生理及病理指标的变化。结果　H组气道峰压显著低于N组 ,动态胸肺顺应性显著高于N组。动脉血氧分压H组明显高于N组 ;H组与N组BALF细胞数、BALF中蛋白含量、肺组织湿重 /干重比差异均有显著性 (P <0 0 5 ) ;肺组织中髓过氧化物酶的含量H组明显低于N组 (P <0 0 5 ) ;H组病理组织学改变较N组明显减轻 (P <0 0 5 ) ;PaCO2 与pH密切相关 ,与PaO2 、动态顺应性均呈正相关 ,与气道峰压呈负相关。结论　机械通气时吸入8%的CO2 所致高碳酸血症对ALI动物模型有保护作用 ,其机制可能与改善了肺力学、减少肺泡中蛋白质渗出 ,减轻多形核白细胞在肺内的扣押及抑制其活性有关。