急性呼吸窘迫综合征静态压力-容积曲线数学模型的建立

目的论证根据压力一容积（P-V）曲线二阶导数图形寻找曲线拐点的可行性，并与逐步线性回归法测定拐点的方法进行比较。方法6只成年健康绵羊麻醉后行气管切开，纤维支气管镜温生理盐水肺泡灌洗法建立急性呼吸窘迫综合征（ARDS）模型，用低流速法描记灌洗前及灌洗后的准静态P-V曲线，利用Findgraph软件建立数学模型及分析曲线特征。结果应用多元线性回归及Boltzmann公式对正常及ARDS P—V曲线的吸气支和呼气支均能达到理想的拟合效果，利用二阶导数图形可以准确获得P—V曲线的特征点，利用此方法测定的吸气支下拐点（LIP）与逐步线性回归法所测的LIP＋2cm H2O（1cmH2O—0．098kPa）有很高的相关性。结论对于ARDS患者，P—V曲线的二阶导数图形可以准确提供曲线拐点的信息，有利于呼吸机参数的设定。     

绵羊急性呼吸窘迫综合征开放肺压力安全性的实验研究

目的观察在绵羊急性呼吸窘迫综合征（ARDS）模型上利用控制性肺膨胀法（SI）实施肺复张策略对血流动力学及肺组织结构的影响，以期找到实施SI的理想压力及时间范围。方法14只绵羊在全麻下行纤维支气管镜温生理盐水肺泡灌洗建立ARDS模型，低流速法描记准静态压力-容积（P—V）曲线，寻找P—V曲线的上拐点（UIP）以及下拐点（LIP）。以UIP下5cm H2O（1cm H2O=0．098kPa）、UIP、UIP上10cm H2O和UIP上20cm H2O将14只绵羊随机分为4组（U-5、U＋0、U＋10、U＋20组），并作为SI的峰压进行肺复张，持续时间为60s，记录每次复张过程中及复张后连续血流动力学参数和氧合指数变化，维持至2h后实验结束，行CT、肺组织病理学检查。结果U＋20组在SI过程中出现气胸，导致绵羊死亡；其余各组肺复张过程中，对血流动力学均有明显影响。U＋10组肺复张10s即出现中心静脉压（CVP）升高，心排血量（CO）、心脏指数（CI）、平均血压（MBP）明显下降，复张后CI恢复缓慢；U＋0组及U-5组可完成整个肺复张过程，CVP轻度升高，CO、CI下降，U-5组在复张结束后15s、U＋0组在复张结束后30s恢复至复张前水平。肺组织病理学观察仍见U＋0组有肺大泡形成。结论对ARDS实施肺复张，应充分考虑压力对血流动力学及肺组织的损害；肺复张压力应选择在UIP或UIP下5cm H2O，此时对血流动力学没有明显影响。     

急性呼吸窘迫综合征绵羊肺复张容积测定方法的比较

目的　比较压力容积 (P V)曲线法与等压法测定肺复张容积的差异。方法　内毒素持续静脉注射复制绵羊急性呼吸窘迫综合征模型 ,分别用 P V曲线法与等压法测定相同呼气末正压 (PEEP)的肺复张容积。结果　等压法测定肺复张容积可以立即得出结果 ;而 P V曲线法测定肺复张容积所需时间为5～ 6 min。随着 PEEP从 5 cm H2 O(1cm H2 O=0 .0 98k Pa)增至 15 cm H2 O,两种方法测定的肺复张容积均显著增加 (P均 <0 .0 5 ) ;PEEP为 5 cm H2 O时 ,等压法与 P V曲线法所测的肺复张容积分别为 (2 5 .79±2 0 .4 8) m l和 (6 3.2 6± 5 4 .5 7) m l,两组比较无明显差异 (P>0 .0 5 ) ;当 PEEP为 10和 15 cm H2 O时 ,等压法所测肺复张容积分别为 (4 8.6 4± 30 .5 1) m l、(71.5 0± 5 8.0 9) ml,P V曲线法测得肺复张容积分别为 (14 8.14±85 .4 2 ) m l、(32 2 .86± 14 8.4 2 ) m l,等压法所测值明显小于 P V曲线所测值 (P均 <0 .0 5 )。结论　虽然等压法较为简便 ,但由于准确性较差 ,因此不能代替 P V曲线法来测定肺复张容积     

急性呼吸窘迫综合征犬压力--容积曲线与肺部形态学关系的研究

目的探讨根据压力-容积(P-V)曲线选择不同水平的呼气末正压(PEEP),急性呼吸窘迫综合征(ARDS)犬肺客积的变化情况.方法用大注射器法绘制ARDS犬P-V曲线,根据曲线不同转折点的压力设定PEEP,CT扫描相应的肺部形态学变化,并且计算肺容积.结果(1)呼气相曲线曲率变化最大点(PMC,d)处的压力为10.67±0.82 cmH2O,高于吸气相低位转折点(LIP)处的压力8.77±0.88 cmH2O(P＜0.05).(2)在PEEP为O、LIP、PMC,d及UIP时,ARDS犬含气肺容积随着治疗压力的升高而增加,通气差及无通气肺组织明显减少,且均有显著差异;在PLIP及PPMC,d水平上,通气良好肺容积分别为403.16±12.6 cm3和469.96±13.7 cm3(P＜0.05),而过度充气肺组织则相似(P＞0.05);随着PEEP增加至PUIP,通气良好的肺容积进一步增加,但也引起过度通气肺容积的明显增加.结论根据P-V曲线呼气支PMC,d来确定PEEP较传统根据LIP水平更有价值.     

利用准静态压力-容积曲线呼气支评估急性呼吸窘迫综合征患者死腔的初步研究

目的 利用准静态法描记急性呼吸窘迫综合征(ARDS)患者压力-容积曲线(P-V曲线),分析其呼气支的回归点与呼气末死腔变化的关系.方法 采用前瞻性研究方法,选取本院14例接受机械通气的ARDS患者,用准静态法描记P-V曲线,描记时将潮气量表连接于流量传感器,记录呼气支呼气起始时的潮气量(VT1)和呼气结束时的潮气量(VT2),计算其差值(ΔVT=VT1-VT2);同时记录呼气过程中流量传感器显示的潮气量(VT3)和预设潮气量(VT4);并对ΔVT与VT3以及VT4与VT1进行相关性分析.结果 ΔVT为(417.40±119.68) ml,VT3为(399.29±121.36) ml;ΔVT与VT3具有很好的相关性(r=0.99,P=0.000),说明呼气支ΔVT与肺内陷闭气体量相关.VT4为(908.21±106.52) ml,VT1为(892.26±106.32) ml;VT4与VT1具有很好的相关性(r=0.99,P=0.000).结论 ARDS患者可能因呼气末部分气体陷闭,导致死腔增加,显示P-V曲线呼气支无法回到基点,且呼气支ΔVT与陷闭气体量成反比.     

控制性肺膨胀对急性呼吸窘迫综合征肺静态顺应性曲线低位转折点的影响

目的 :探讨控制性肺膨胀 (SI)对急性呼吸窘迫综合征 (ARDS)肺静态顺应性曲线低位转折点压力(Pinf)的影响。方法 :30只家兔利用肺泡灌洗法建立 ARDS模型 ,并随机分为 SI组和非 SI组 ,观察 SI后 2小时动物的 Pinf、肺气体交换和肺机械力学特征改变。结果 :SI组动物 SI前 Pinf为〔(0 .90± 0 .14 ) k Pa,1k Pa=10 .2 0 cm H2 O〕,SI 2小时后 Pinf降到 (0 .6 1± 0 .14 ) k Pa(P=0 .0 2 0 ) ;非 SI组机械通气 2小时前后 Pinf无明显改变 ,P>0 .0 5。 SI组动物机械通气 2小时后动脉血氧分压 (Pa O2 )和氧饱和度 (Sa O2 )分别为 (2 4 .2 0±8.79) k Pa(1k Pa=7.5 m m Hg)和 0 .96 7± 0 .0 2 4 ,显著高于非 SI组〔分别为 (10 .80± 1.13) k Pa和 0 .76 8±0 .0 76 ,P<0 .0 5〕。 SI组动物机械通气 2小时后动态肺顺应性 (Cydn)为 (12 .2 4± 1.5 3) ml/k Pa,显著高于非 SI组〔(9.80± 0 .82 ) ml/k Pa〕。结论 :SI具有促进肺泡复张、降低 Pinf水平的效应 ,实施 SI后应重新调整呼气末正压 (PEEP)水平。     

两种肺复张方法治疗急性呼吸窘迫综合征的效果比较

目的 探讨和比较控制性肺膨胀(sustained inflation,SI)和压力控制通气(pressure controlled ventilation,PCV)用于急性呼吸窘迫综合征(ARDS)患者肺复张的效果,及其对血流动力学和呼吸力学方面的影响.方法 对10例ARDS患者采取随机对照实验,在镇静、非肌松状态下,先后采用SI[40cmH2O(1 cmH2O=0.0981 kPa),40 s]和PCV(20 cmH2O,2 min)进行肺复张,中间间隔洗脱期.收集两种方法复张前(T0)、复张后5 min(T2)、1 h(T3)的血气分析、血流动力学指标、呼吸力学指标和复张中(T1)的呼吸力学与血流动力学指标.收集数据行单因素重复测量方差分析.结果 (1)两种方法T2和T3时点PaO2较T0均明显改善(P<0.05),方法间差异无统计学意义(P>0.05).PaCO2在各时点差异均无统计学意义(P>0.05).(2)两种方法T1时点CI均下降(P<0.05),方法间无差异(P>0.05).HR、MAP在各时点差异均无统计学意义(P>0.05).(3)两种方法T2和T3时点FRC较T0均增加(P<0.05),T1时点CS均有所改善(P<0.05),方法之间差异无统计学意义(P>0.05),Pplat在各时点差异均无统计学意义(P>0.05).结论 SI和PCV肺复张对ARDS患者PaO2、FRC、肺复张中Cs均有明显改善,肺复张对CI均有影响,两种方法效果相同.     

肺复张对肺内/外源性急性呼吸窘迫综合征模型犬呼吸生理和肺形态学影响的比较

目的 探讨以压力-容积(P-V)曲线为导向的肺复张(RM)策略对肺内/外源性急性呼吸窘迫综合征(ARDSexp/ARDSp)模型犬呼吸生理和肺形态学的影响.方法 将24只健康杂种犬按随机数字表法均分为两组,分别以静脉注射油酸0.1 ml/kg复制ARDSexp模型,以气管内注入盐酸2 ml/kg复制ARDSp模型.每种模型再随机均分为肺保护通气策略(LPVS)组和LPVS+RM组.LPVS组采用LPVS进行机械通气(MV);LPVS+RM组先进行以P-V曲线为导向的RM,RM采用压力控制通气(PCV),压力上限为高位转折点(UIP),呼气末正压(PEEP)为低位转折点(LLP)+2 cm H2O(1 cm H2O=0.098 kPa),维持60 s后再按LPVS进行MV.两组MV时间均为4 h.观察动物基础状态(成模前)及RM前后的氧合指数(PaO2/FiO2)、呼吸力学指标变化;采用低流速法记录准静态P-V曲线并计算UIP、LIP ;根据肺CT比较不同肺充气区容积占全肺容积的百分比.结果 成模前和RM前两组PaO2/FiO2及UIP、LIP比较差异均无统计学意义.RM后4 h,两种模型LPVS+RM组PaO2/FiO2和肺顺应性(Crs)均较同模型LPVS组显著升高[ARDSexp模型PaO,/FiO2(mm Hg,1 mm Hg=0.133 kPa):263.9±69.2比182.8±42.8,Crs(ml/cm H2O):11.3±4.2比9.7±3.7;ARDSp模型PaO2/FiO2(mm Hg):193.4±33.5比176.4±40.2,Crs(ml/cm H2O):10.1±3.9比9.0±3.9,P＜0.05或P＜0.01],气道压力明显低于同模型LPVS组[ARDSexp模型吸气峰压(PIP,cm H2O):24.1±7.4比30.2±8.5,气道平台压(Pplat,cm H2O):19.1±7.3比25.6±7.7;ARDSp模型PIP(cm H2O):26.6±8.4比29.6±10.3,Pplat(cm H2O):21.9±7.3比25.1±8.4,P＜0.05或P＜0.01];且ARDSexp模型改善程度较ARDSp模型更为显著(P＜0.05或P＜0.01).两种模型LPVS+RM组肺组织闭合区和充气不足区所占比例均较同模型LPVS组明显减少,正常充气区所占比例明显增加[ARDSexp模型闭合区:(9.9±3.1)%比(16.3±5.2)%,充气不足区:(10.2±4.2)%比(23.4±6.7)%,正常充气区:(76.2±12.3)%比(57.5±10.1)%;ARDSp模型闭合区:(14.3±4.8)%比(1 8.2±5.1)%,充气不足区:(17.4±6.3)%比(24.1±5.9)%,正常充气区:(63.2±10.7)%比(54.6±11.3)%,P＜0.05或P＜0.01];且ARDSexp模型各充气区所占比例改善程度均明显优于ARDSp模型(均P＜0.05).结论 对于不同原因ARDS,以P-V曲线为导向的RM均具有增加肺氧合、改善肺顺应性和肺组织通气的作用,且对ARDSexp的治疗效果明显优于ARDSp.

Abstract：

Objective To determine effects of recruitment maneuver (RM) guided by pressure-volume (P-V) curve on respiratory physiology and lung morphology in canine models of acute respiratory distress syndrome of pulmonary or extrapulmonary origin (ARDSp and ARDSexp). Methods Twenty-four healthy dogs were randomly divided into two groups with 12 dogs each: ARDSexp and ARDSp. Each dog in ARDSexp group was injected with oleic acid 0. 1 ml/kg through femoral vein, and each dog in ARDSp group received hydrochloric acid 2 ml/kg via trachea. Subsequently, dogs with both models were randomly subdivided into lung protective ventilation strategy (LPVS) group and LPVS+RM group, respectively. Dogs in LPVS group were given LPVS only without RM. RM guided by P-V curve was performed in LPVS+RM group followed by LPVS and pressure controlled ventilation (PCV) mode was selected. Phigh was set at upper inflection point (UIP) of the P-V curve, positive end-expiratory pressure (PEEP) was set at lower inflection point (LIP)+2 cm H2O (1 cm H2O=0. 098 kPa), and the duration of RM was 60 seconds. The duration of mechanical ventilation (MV) in both subgroups was 4 hours. The oxygenation index (PaO2/FiO2), relative lung mechanical indexes were measured in two ARDS models before establishment of ARDS model, and before and after RM. The UIP and LIP were calculated with P-V curve. The percentage of different volume in ventilation of lung accounting for total lung volume was compared by CT scan.Results The PaO2/FiO2, UIP and LIP did not showed significant differences among all groups before ARDSand before RM. PaO2/FiO2 and respiratory system compliance (Crs) were significantly elevated in LPVS+RM group of both models 4 hours after RM compared with corresponding LPVS group [PaO2/FiO2(mm Hg,1 mm Hg=0. 133 kPa) of ARDSexp model: 263. 9±69. 2 vs. 182.8±42. 8, Crs (ml/cm H2O) of ARDSexp model: 11.3±4. 2 vs. 9. 7±3. 7; PaO2/FiO2(mm Hg) of ARDSp model: 193. 4±33.5 vs. 176. 4±40. 2, Crs (ml/cm H2O) of ARDSp model: 10.1±3.9 vs. 9.0±3.9, P＜0. 05 or P＜0.01], and the airway pressure was significantly declined compared with corresponding LPVS group [peak inspiratory pressure (PIP),cm H2O) of ARDSexp model: 24. 1±7. 4 vs. 30. 2±8. 5, plateau pressure (Pplat, cm H2O) of ARDSexp model: 19.1±7.3 vs. 25.6±7.7; PIP (cm H2O) of ARDSp model: 26.6±8.4 vs. 29.6±10.3, Pplat (cm H2O) of ARDSp model: 21.9±7. 3 vs. 25.1±8.4, P＜0. 05 or P＜0. 01]. Moreover, PaO2/FiO2, Crs,PIP and Pplat were improved better in ARDSexp model than ARDSp model (P＜ 0. 05 or P＜ 0. 01).Compared with LPVS maneuver, RM plus LPVS maneuver could significantly decrease the proportion of closure and hypoventilation region, and increase the proportion of normal ventilation region in both models [closure region of ARDSexp model : (9.9±3.1) % vs. (16. 3± 5. 2) %, hypoventilation region of ARDSexp model: (10. 2±4.2)% vs. (23. 4±6. 7)%, normal ventilation region of ARDSexp model: (76. 2±12. 3)%vs. (57.5±10. 1)%; closure region of ARDSp model: (14.3±4. 8)% vs. (18. 2±5.1)%, hypoventilation region of ARDSp model : (17.4±6. 3) % vs. ( 24. 1 ± 5. 9) 0%, normal ventilation region of ARDSp model :(63. 2 ± 10. 7 ) % vs. ( 54. 6±11.3 ) %, P ＜ 0. 05 or P ＜ 0. 01]. All of the ventilation regions were better improved with ARDSexp model than ARDSp model (all P＜0. 05). Conclusion RM guided by P-V curve could help obtain better oxygenation, improve pulmonary compliance and lung ventilation in ARDSexp and ARDSp, and better treatment effects are seen in ARDSexp dogs than ARDSp dogs.     

急性呼吸窘迫综合征肺容积减少的机制与肺开放策略的选择

急性呼吸窘迫综合征(ARDS)是各种肺内外病因引起的肺毛细血管内皮细胞和肺泡上皮细胞损伤,由此导致的急性非心源性低氧性呼吸衰竭。肺容积减少是ARDS最重要的病理生理改变之一,也是当前ARDS机械通气治疗的主要着眼点和难点。肺组织自身重量增加导致肺泡塌陷,肺泡水肿,心脏和腹腔导致的压迫性肺不张是ARDS患者肺容积减少的原因。肺容积减少机制导向性的肺开放策略有助于达到改善氧合和减少呼吸机相关肺损伤的最佳平衡。     

密闭式吸痰对急性呼吸窘迫综合征小猪呼吸及循环系统的影响

[目的]探讨密闭式吸痰对急性呼吸窘迫综合征（ARDS）小猪动脉血气、呼吸力学和心率（HR）、血压的影响。[方法]先制作小猪ARDS模型，模型成功后将其随机分为呼气未正压（PEEP）5cmH2O组和10cmH2O组，予机械通气30min后进行密闭式吸痰。监测吸痰前1min及吸痰后1min、3min，5min、10min动脉血专、呼吸力学及HR、血压的变化。[结果]两组在密闭式吸痰后动脉血氧分压（PaO2）和动脉血氧饱和度（SaO2）均下降，直到吸痰后10min仍低于吸痰前基线水平（P〈0．05），而吸痰后舒张压（DBP）与吸痰前比较均无差异（P〉0．05）；在PEEP 5cm H2O组，吸痰后气道峰压（Ppeak）、平台压（Pplat）、平均气道压（Pmean）均升高，持续到吸痰后10min仍显著高于吸痰前基线水平（P〈0．05）；肺静态顺应性（Cs）、平均动脉压（MAP）、收缩压（SBP）均降低，持续到吸痰后10min仍低于吸痰前基线水平（P〈0.05）；在PEEP 10cm H2O组，吸痰后1min及3min Ppeak显著升高（P〈0．05），持续到吸痰后10min仍高于吸痰前基线水平但差异无统计学意义（P〉0．05）；Pplat、Pmean在吸痰后1min显著增高，在吸痰后3min、5min、10min仍高于吸痰前基线水平但无统计学差异（P〉0．05），同时在吸痰后1min及3min Cs显著下降（P〈0．05），持续到吸痰后10min仍低于吸痰前基线水平但差异无统计学意义（P〉0．05）。[结论]不论在PEEP 5cm H2O还是10cm H2O水平，密闭式吸痰可引起脑小猪较严重的低氧血症，使气道压力增高、肺顺应性降低、血压下降。但在PEEP 5cm H2O组，吸痰所引起的缺氧、气道高压及低血压持续时间较长。     

Reinterpreting the pressure-volume curve in patients with acute respiratory distress syndrome

New evidence requires a reinterpretation of the inflation pressure-volume curve and suggests that neither the lower nor the upper inflection point provides reliable information to determine safe ventilator settings in the acute respiratory distress syndrome. Recruitment probably continues throughout the inflation pressure-volume curve, and studies of the deflation pressure-volume curve, reinflations after partial deflation, or decremental positive end-expiratory pressure trials after a recruitment maneuver are probably needed to determine open-lung positive end-expiratory pressure.     

Generation of a single pulmonary pressure-volume curve does not durably affect oxygenation in patients with acute respiratory distress syndrome

Introduction  

It is possible that taking a static pressure-volume (PV) measurement could durably affect oxygenation and thus interfere with early evaluation of a therapeutic intervention delivered just after that measurement. The aim of the present study was to investigate the effects over time of a single static PV measurement on gas exchange and haemodynamics; the PV measurements were taken using a super syringe and by using the constant flow method in patients with acute respiratory distress syndrome.     

Relationship between pressure-volume curve and markers for collagen turn-over in early acute respiratory distress syndrome

Objective In acute respiratory distress syndrome, the relationships between changes in the elastic behavior of the respiratory system and biological markers of extra-cellular matrix or surfactant turn-over could give some insights into its pathophysiological determinants. Design and measurements In 17 patients with acute respiratory distress syndrome, we assessed the relationship between chord compliance measured on pressure–volume curves obtained at two levels of positive end-expiratory pressure (0 and 10 cm H₂O) and biological markers of collagen turn-over or surfactant degradation in bronchoalveolar lavage fluid obtained simultaneously in the early phase of the disease (first 4 days). Main results The compliance of the respiratory system obtained from the pressure–volume curves was significantly correlated with markers for collagen turn-over (type III procollagen peptide and matrix metalloproteinase 2) and with markers of surfactant degradation (type-IIA secretory phospholipase A2). The correlations were stronger when the curve was traced from positive end-expiratory pressure, suggesting that this condition may improve the assessment of tissue mechanics. A logarithmic relationship best described the correlation between compliance and type III procollagen peptide, in agreement with a collagen-dependent model of maximal distension. The marker for surfactant degradation was associated with ongoing alveolar inflammation (cellularity of bronchoalveolar lavage fluid and tumor necrosis factor-α concentration). Interleukin-10, an anti-inflammatory mediator, showed no correlation with compliance. Conclusion These preliminary data suggest that a severe reduction in compliance in the early phase of acute respiratory distress syndrome is associated with both collagen deposition and surfactant degradation. Presented in part at the 2003 meeting of the European Society of Intensive Care Medicine.     

Elastic pressure-volume curves in acute lung injury and acute respiratory distress syndrome

Background The principal features of elastic pressure-volume curves of lungs or the respiratory system (P_el/V curves) recorded during reexpansion of collapsed lungs and subsequent deflation have been known since the 1950s. In acute respiratory failure and acute respiratory distress syndrome such curves have recently attracted increasing interest because new knowledge can be acquired from them, and because such curves may be useful as guidelines in setting the ventilator so as to avoid ventilator-induced lung injury.Discussion This article reviews recording methods, underlying physiology and utility of P_el/V curves in research and clinical work.This work was supported by the Swedish Medical Research Council (02872) and by the Swedish Heart Lung Foundation