应用肺动态压力-容积曲线低位转折点选择最佳呼气末正压的研究

目的探讨根据动态肺压力-容积曲线低位转折点压力(Pinf)选择急性呼吸窘迫综合征(ARDS)患者最佳呼气末正压(PEEP)的可行性.方法以8例早期ARDS患者为研究对象,测定动态肺压力-容积曲线及Pinfd.采用低流速法测定准静态肺压力-容积曲线,并确定静态肺压力-容积曲线低位转折点压力(Pinfs).调整PEEP水平,观察患者血流动力学、肺机械力学和氧代谢的变化.结果当PEEP从Pinfd-6cmH2O水平增加到Pinfd+6cmH2O时,动脉血氧分压、动脉血氧饱和度、气道平均压和气道峰压均显著增加.与Pinfd+6cmH2O比较,Pinfd-4cmH2O时的动态肺顺应性显著增高.Pinfd+6cmH2O时的心脏指数有降低趋势,Pinfd-4cmH2O时的氧输送有升高趋势.当Pinfd为(12.8±3.2)cmH2O,Pinfs为(11.0±3.2)cmH2O,两者具有正相关性(r=0.99,P《0.05).回归方程为Pinfd=1.66+1.01×Pinfs.结论当ARDS患者行机械通气治疗时,Pinfd-4cmH2O或Pinfs-2cmH2O为最佳PEEP,可获得最大氧输送.     

静态压力-容积曲线在急性呼吸窘迫综合征肺复张和肺塌陷中的应用

目的在新西兰兔肺泡灌洗的急性呼吸窘迫综合征(ARDS)机械通气过程中,使用静态压力-容积(P-V)曲线描述肺复张及肺塌陷的特征,寻找复张肺泡并减少呼吸机相关性肺损伤的方法。方法在10例新西兰兔肺泡灌洗ARDS模型中,动态CT扫描肺泡逐步复张及逐步塌陷时肺内气体压力、容积及分布,同时测量静态P-V曲线,评估肺复张和肺塌陷的特征。结果吸气时各充气区域容积比例随气道压力的变化而变化(t=2．477-9．794,P均<0．05)。肺复张不仅包括闭合区域开放过程即肺开放,还包括充气不良区域肺泡张大的过程;肺塌陷也不只是闭合区域的产生即肺闭合,还包括充气不良区域的产生。肺开放与肺吸气频数分布不一致(r=0．219,P=0．220);肺闭合与肺呼气频数分布也不一致(r=0．094,P=0．593);静态P-V曲线顺应性仅与充气不良区域容积相关(吸气相r=0．827,P=0．006;呼气相r=0．792,P=0．011);吸气相曲线最大顺应性点压力[(16．2±3．5)cm H2O,1 cm H2O=0．098 kPa]与肺开放压[(16．4±3．4)em H2O]接近(r=0．900,P=0．002),而呼气相曲线最大顺应性点压力[(11．9±2．4)cm H2O]与肺闭合压[(11．3±2．5)cm H2O]接近(r= 0．887,P=0．003)。结论吸气时肺复张和肺泡过度膨胀同时发生。静态P-V曲线顺应性可反映肺增大潜能,并可预测肺开放压和闭合压。     

氮气洗入/洗出法测定急性肺损伤患者肺复张容积的研究

  目的 探讨氮气洗入/洗出法测急性肺损伤(ALI)患者肺复张容积的准确性及可行性。方法 将15例有创机械通气的ALI患者纳入本研究,根据ARDSnet法和跨肺压法滴定2种呼气末正压(PEEP) 水平,分别通气30 min,记录各PEEP水平下潮气量(Vt)、气道平台压等呼吸力学及血流动力学指标,并利用氮气洗入/洗出法测2种PEEP水平的呼气末肺容积(EELV),根据公式推算氮气洗入/洗出法测的肺复张容积,同时根据低流速压力-容积(P-V)曲线法获得肺复张容积,比较2种方法获得的肺复张容积的相关性及一致性。结果 (1)ARDSnet法滴定的PEEP为（7±2） cm H₂O（1 cm H₂O=0.098 kPa）,气道峰压为（23±5） cm H₂O,气道平台压为(17±4） cm H₂O;跨肺压法滴定的PEEP为（14±5 )cm H₂O,气道峰压为（28±6） cm H₂O,气道平台压为（22±6） cm H₂O,2种方法比较差异有统计学意义(P<0.05)。(2) 低流速P-V曲线法测的肺复张容积为100（-25~185）ml,氮气洗入/洗出法测的肺复张容积为180（-19~255）ml,两者具有较好的相关性,R²=0.755,P<0.0001,且测量误差为46（8~80）ml。结论 氮气洗入/洗出法可测定ALI患者的肺复张容积。        

允许性高碳酸血症治疗ARDS对肺力学的影响

目的探讨允许性高碳酸血症(PHC)对重度急性呼吸窘迫综合征(ARDS)肺力学及血流动力学的影响。方法观察不同潮气量(VT)时,30例重度ARDS患者肺气体交换、肺力学的改变。结果当VT从15ml/kg降至6ml/kg时,病人均出现PHC,动脉血氧分压、氧饱和度和混合静脉血氧饱和度显著降低(P<0.05)。PHC时,气道压力显著降低,气道阻力明显增高(P<0.05)。静态肺压力-容积曲线高位转折点对应的压力为(22.2±1.9)cmH2O,容积为10ml/kg。结论在实施PHC时,只有当气道平台压<20~25cmH2O时才有可能避免肺泡过度膨胀,减少呼吸机相关性肺损伤。     

急性呼吸窘迫综合征犬肺牵张指数与肺复张及氧合的关系

目的探讨以不同肺牵张指数(lung stress index)选择的呼气末正压(PEEP)与急性呼吸窘迫综合征(ARDS)肺复张容积与氧合的关系。方法油酸静脉注射复制犬ARDS模型,容量控制通气,流速恒定的压力-时间(P-t)曲线吸气支,回归法计算得方程P=a×timeb+c,b为肺牵张指数。调整PEEP水平使b=1。采用控制性肺膨胀实施肺复张手法,复张后再次调整PEEP水平分别达到b=1、0．60．05)。在呼吸力学方面,与复张后b=1相比, 1．1相似文献   

控制性肺膨胀治疗急性呼吸窘迫综合征后最佳PEEP选择

目的探讨控制性肺膨胀（SI）治疗急性呼吸窘迫综合征（ARDS）后最佳呼气末正压（PEEP）。方法利用肺泡灌洗法建立家兔ARDS模型,测定静态肺顺应性（P—V）曲线,确定曲线低位转折点（Pinf）,实施SI后,分别以Pinf-6 cmH2O、Pinf-4 cmH2O、Pinf-2 cmH2O、Pinf、Pinf＋2 cmH2O、Pinf＋4 cmH2O、Pinf＋6 cmH2O的PEEP进行机械通气,监测家兔血流动力学、肺力学、肺气体交换。结果随着PEEP增加,PaO2和SaO2逐渐增加,气道峰值压、平台压、Pm逐渐升高。与Pinf、Pinf＋6 cmH2O相比,Pinf-4 cmH2O时动态肺顺应性（Cdyn）最高。结论ARDS进行机械通气时,在实施SI后以静态P—V曲线Pinf-4 cmH2O为ARDS早期最佳PEEP。     

)反比通气对急性呼吸窘迫综合征绵羊血流动力学及氧代谢的影响

目的探讨反比通气(IRV)对急性呼吸窘迫综合征(ARDS)绵羊血流动力学及氧代谢的影响。方法总呼气末正压(PEEPt)相同条件下,观察压力控制(PC)/容量控制(VC)正比和反比通气(IRV)对血流动力学及氧代谢的影响。结果与VC及VC-IRV比较,PC及PC-IRV时的气道峰值压力明显降低。但IRV时的平均气道压力明显高于正比通气(P<0.05)。VC-IRV与VC及PC-IRV与PC比较,血流动力学及氧代谢均无明显差异。实施PC-IRV时,内源性呼气末正压为(3.0±1.0)cmH2O,显著高于VC(2.1±0.8)cmH2O(P<0.05)。PEEPt相同的前提下,PC-IRV时动脉血氧饱和度(SaO2)为90%,显著低于VC(96%)(P<0.05)。结论在PEEPt相同的前提下,无论是VC-IRV还是PC-IRV,均不优于常规正比通气。PEEPt是影响氧合的主要因素。     

缓激肽B2受体拮抗剂对致敏豚鼠模型咳嗽反应性的影响

目的研究缓激肽受体B2拮抗剂FR173657对卵蛋白致敏和激发豚鼠咳嗽反应性的影响.方法正常和卵蛋白致敏豚鼠各40只,卵蛋白雾化吸入激发.24 h后,再各自分成对照组、小剂量FR173657组、中剂量FR173657组和大剂量FR173657组.每组10只,分别腹腔注射生理盐水、FR173657溶液0.03 mg/kg、0.3 mg/kg和3 mg/kg,观察吸入辣椒素溶液诱导的咳嗽反应.用非侵入性方法测量正常对照组、致敏对照组和致敏中剂量FR173657组豚鼠的特异性气道阻力.结果不同剂量的FR173657不影响正常豚鼠的咳嗽反应和气道阻力.致敏对照组豚鼠吸入10-4 mol/L辣椒素溶液诱导的咳嗽次数和特异性气道阻力分别为[(21.7±3.0)次/3 min]和[(9.4±0.5) cm H2O/s]与正常对照组[(8.3±1.4)次/3 min,(7.9±0.9) cm H2O/s] 比较,差异有显著性(P<0.05),中剂量FR173657能抑制这些改变,咳嗽次数和特异性气道阻力分别为[(12.2±1.3)次/3 min,(7.5±0.9) cm H2O/s],两组比较差异有显著性(P<0.05).结论缓激肽B2受体拮抗剂抑制致敏豚鼠卵蛋白激发后增高的咳嗽反应和气道阻力.因此,缓激肽可能是嗜酸细胞性气道炎症所致咳嗽的重要介质.     

过氧化氢上调白细胞介素1β诱导人肺上皮细胞表达环氧合酶2

目的探讨过氧化氢(H2O2)对白细胞介素1β(IL-1β)诱导人肺上皮细胞(HPEC)环氧合酶2(COX-2)表达的影响.方法应用逆转录-聚合酶链反应(RT-PCR)半定量法和酶联免疫吸附试验 (ELISA)测定IL-1β、H2O2或二者联合干预后HPEC COX-2 mRNA表达量及前列腺素E2(PGE2)释放量的变化, 以不加任何试剂的细胞为对照组.结果 (1)COX-2 mRNA表达量1、5、10 mg/L 的IL-1β处理组COX-2 mRNA表达量分别为(143.1±7.2)%、(179.9±9.0)%、(190.0±9.5)%,对照组为(32.9±1.7)%,1、5、10 mg/L 的IL-1β处理组与对照组比较差异有显著性(P均<0.05); (2)培养基上清液PGE2浓度5、10 mg/L 的IL-1β处理组培养基上清液PGE2浓度分别为 (20.86±5.23)×10-6 g/L、(31.16±2.64)×10-6 g/L,对照组为(10.49±0.36)×10-6 g/L, 5、10 mg/L 的IL-1β处理组与对照组比较差异有显著性(P<0.05);(3) COX-2 mRNA表达量 0.10、0.25、0.50 mmol/L 的H2O2和IL-1β共处理组COX-2 mRNA表达量分别为 (149.2±7.5)%、(189.6±9.5)%、(239.1±12.0)%, IL-1β单独处理组为(66.1±3.7)%, 对照组为(41.6±2.1)%, 0.10、0.25、0.50 mmol/L 的H2O2和IL-1β共处理组与IL-1β单独处理组比较,差异有显著性 (P<0.05); (4)培养基上清液PGE2浓度0.10、0.25、0.50 mmol/L的H2O2和IL-1β共处理组,培养基上清液PGE2浓度分别为 (27.01±5.16)×10-6 g/L、(32.79±3.01)×10-6 g/L、(41.13±3.41)×10-6 g/L,对照组为(10.49±0.36)×10-6 g/L,0.10、0.25、0.50 mmol/L的H2O2和IL-1β共处理组与对照组比较差异有显著性(P<0.05).0.25、0.50 mmol/L的 H2O2和IL-1β共处理组PGE2浓度均与IL-1β单独处理组[(20.86±5.23)×10-6 g/L]比较差异有显著性 (P<0.05). 结论过氧化氢上调IL-1β对HPEC COX-2的诱导表达,其调节机制可能发生在转录水平.     

控制性肺膨胀治疗急性呼吸窘迫综合征家兔的最佳压力选择

目的　探讨实施控制性肺膨胀 (SI)治疗急性呼吸窘迫综合征 (ARDS)的最佳复张压力。方法　采用肺泡灌洗法建立重度ARDS家兔模型 ,以 1～ 6倍的平均气道压 (Pm)作为实施SI的压力 ,屏气时间 2 0s。在SI前、SI期间及SI后 2min和 5min监测家兔血流动力学、肺力学、肺气体交换和肺损伤指标。以改善氧合和肺容积最显著、不加重肺损伤、同时对血流动力学影响最小的压力为最佳压力。结果　SI的压力达到 3Pm 以上时 ,家兔动脉血氧分压 (PaO2 )和动脉血氧饱和度明显提高。 5Pm 和6Pm 时SI前后的PaO2 差值 (ΔPaO2 )分别为 (6 5± 40 )mmHg(1mmHg =0 133kPa)和 (5 2± 2 5 )mmHg ,显著高于 1Pm[(- 5± 4)mmHg ,P <0 0 5 ]。 5Pm SI时的动态肺顺应性增加最明显 ,达 (3 0 6± 0 2 4)ml/cmH2 O ,明显高于SI前的水平 [(1 0 9± 0 18)ml/cmH2 O ,P <0 0 5 ]。 5Pm 时SI前后肺容积改变最显著 ,达到 (4 4 0± 3 1)ml/kg,明显高于 1Pm[(8 3± 0 7)ml/kg ,P <0 0 5 ]。未实施SI的ARDS家兔肺损伤评分为 6 10± 0 77,5Pm 时的肺损伤评分显著降低 (4 4 0± 1 6 6 ,P <0 0 1)。 6Pm 时则导致肺泡过度膨胀 ,加重肺损伤。随着SI的压力增加 ,家兔的平均动脉血压显著降低。结论　重度ARDS家兔实施SI的最佳压力是 5Pm(2 5～     

压力—容量曲线对急性肺损伤家兔实行个体化保护性通气？…

OBJECTIVE: To explore the lung-protective effect of ventilation with tidal volume and PEEP determined on pressure-volume curve in oleic acid rabbit models of acute lung injury. METHODS: 24 New Zealand rabbits were randomly divided into 4 groups (V1P1, V1P2, V2P1, V2P2). After inducing lung injury, the P-V curves were measured and drawn. The low and upper inflection point pressure (Pinf and Pdef respectively) were manually determined. Two levels of tidal volume (V1 = 15 ml/kg, V2 reduced for Pplat < Pdef) and two levels of PEEP (P1 = Pinf, P2 = Pinf - 3 cm H2O) were selected. The peak airway pressure (PIP), plateau pressure (Pplat), mean pressure (PAW), static compliance (Cst), heart rate, arterial blood pressure and blood-gas analysis were measured. The lung tissues were pathologically analyzed with light microscope. RESULTS: The oxygenation was not significantly different among 4 groups. The reduced VT significantly raised PaCO2 and lowered pH. Larger VT reduced arterial blood pressure. VT and PEEP synergetically raised airway pressure. Larger PEEP improved Cst, which was counteracted by larger VT. Reduced VT significantly lessened alveolar barotrauma. Larger PEEP lightened alveolar hyaline membrane formation and hemorrhage. CONCLUSION: The ventilation with VT and PEEP determined on P-V curve has significant protective effect on the acutely injured lung.     

Effects of PEEP on respiratory mechanics after open heart surgery.

Respiratory dysfunction, particularly atelectasis, is common after open heart surgery. Routine use of PEEP (5 to 10 cm H2O) in these patients has been advocated. We studied the effects of different levels of PEEP on respiratory mechanics in ten mechanically ventilated open heart surgery patients in the immediate postoperative period. PEEP was studied in increasing increments and decreasing decrements. This procedure was repeated three times. Flow, tidal volume, and airway pressure were measured. We used the rapid airway occlusion technique to determine static compliance of the respiratory system (Cst,rs) and intrinsic PEEP (PEEPi). The changes in end-expiratory lung volume (delta EELV) were measured with respiratory inductive plethysmography. Recruitment of lung units (Vrec) was estimated as the difference in lung volume between PEEP and zero end-expiratory (ZEEP) for the same static inflation pressure (15 cm H2O). We found that (1) Cst,rs at ZEEP was significantly reduced (60 +/- 2 ml/cm H2O); (2) while PEEP of 5 cm H2O did not cause significant recruitment, higher levels of PEEP (10 to 15 cm H2O) were effective; (3) Cst,rs, Vrec, and delta EELV were higher during stepwise PEEP decrease; (4) after the first and second stepwise PEEP increase-decrease run, there was a small persistent increase in EELV and Cst,rs at ZEEP. No further changes were found after the third run. We conclude that after open heart surgery, PEEP less than 10 cm H2O is not effective to reopen atelectatic lung units.     

压力-容量曲线对急性肺损伤家兔实行个体化保护性通气的应用

目的研究以压力容量（P-V）曲线确定通气参数对急性肺损伤家兔肺的保护作用。方法新西兰家兔24只,随机分为4组（V1P1、V1P2、V2P1、V2P2）,每组4只。用油酸复制急性肺损伤模型,测定P-V曲线,以下曲点压力（Pinf）和上曲点压力（Pdef）分别选择呼气末正压（PEEP）的两水平：P1＝PinfP2＝Pinf－3cmH2O,潮气量（VT）两水平：V1＝15ml／kg,V2下调使平台压小于上曲点压力（Pplat＜Pdef）。观察肺力学、血气、血循环及肺病理改变。结果4组氧合效果基本相同,动脉血二氧化碳分压（PaCO2）和pH主要受VT影响。平均动脉压在大PEEP和（或）大VT时有所下降。呼吸系统静态顺应性（Cst）则以PEEP为Pinf时改善最明显,但大VT抵消了其作用且对肺泡有明显的损伤。小PEEP组肺泡透明膜变加重。结论以呼吸系统P-V曲线选择PEEP和VT进行个体化通气,对肺的力学特性和肺的病理性损伤有明显的保护作用,可能有利于改善急性肺损伤的预后。     

呼气末压力为零时的静态压力容积曲线在急性呼吸窘迫综合征患者控制性肺膨胀中的应用

目的　评价呼气末压力为零 (ZEEP)时静态压力 容积 (P V)曲线在预测急性呼吸窘迫综合征 (ARDS)患者对控制性肺膨胀 (SI)反应性的作用。方法　 2 0例ARDS患者进行机械通气并测量ZEEP时的静态P V曲线 ,在使用呼气末正压通气 (PEEP) 2h后进行SI。根据 2 0例患者使用SI后改良氧合指数 (PaO2 /FiO2 )进行分组 ,增加≥ 2 0 %为SI反应组 (A组 ) ,<2 0 %为SI无反应组 (B组 )。结果　(1)A组ZEEP时静态P V曲线参数c - 2d≥ 0cmH2 O(1cmH2 O =0 0 98kPa) ,且c≥ 18cmH2 O ,呈向上凹的形态 ;而B组c - 2d <0cmH2 O或c <18cmH2 O ,呈向上凸的形态或一直线。 (2 )使用SI后 ,A组患者可减少肺内分流 (P =0 0 0 6 ) ,而B组不减少肺内分流 (P =0 339)。相同吸气压下的肺容积增加 ,A、B组间比较差异有显著性 [(2 4 1± 111)ml,(2 9± 4 6 )ml,P =0 0 36 ]。结论ARDS患者在ZEEP时静态P V曲线具有不同的形态 ,使用曲线参数的c - 2d及c值可迅速判断静态P V曲线形态 ,对指导预测ARDS患者中SI治疗具有一定的意义。     

Static and dynamic upper airway obstruction in sleep apnea: role of the breathing gas properties

Increased upper airway collapsibility in the sleep apnea/hypopnea syndrome (SAHS) is usually interpreted by a collapsible resistor model characterized by a critical pressure (Pcrit) and an upstream resistance (Rup). To investigate the role played by the upstream segment of the upper airway, we tested the hypothesis that breathing different gases would modify Rup but not Pcrit. The study was performed on 10 patients with severe SAHS (apnea-hypopnea index: 59 +/- 14 events/hour) when breathing air and helium-oxygen (He-O2) during non-REM sleep. The continuous positive airway pressure that normalized flow (CPAPopt) was measured. Rup and Pcrit were determined from the linear relationship between maximal inspiratory flow VImax and nasal pressure (PN):VImax = (PN - Pcrit)/Rup. Changing the breathing gas selectively modified the severity of dynamic (CPAPopt, Rup) and static (Pcrit) obstructions. CPAPopt was significantly (p = 0.0013) lower when breathing He-O2 (8.44 +/- 1.66 cm H2O; mean +/- SD) than air (10.18 +/- 2.34 cm H2O). Rup was markedly lower (p = 0.0001) when breathing He-O2 (9.21 +/- 3.93 cm H2O x s/L) than air (15.92 +/- 6.27 cm H2O x s/L). Pcrit was similar (p = 0.039) when breathing He-O2 (4.89 +/- 2.37 cm H2O) and air (4.19 +/- 2.93 cm H2O). The data demonstrate the role played by the upstream segment of the upper airway and suggest that different mechanisms determine static (Pcrit) and dynamic (Rup) upper airway obstructions in SAHS.     

Effect of tidal volume and positive end-expiratory pressure on compliance during mechanical ventilation.

In 12 patients requiring therapy with mechanical ventilation for acute respiratory failure, total static compliance (Cst) increased from 29 +/- 4 ml/cm H2O at a tidal volume (TV) of 5 ml/kg to 42 +/- 7 ml/cm H2O at a TV of 15 ml/kg. Similarly, Cst increased from 42 +/- 7 ml/cm H2O to 52 +/- 8 ml/cm H2O between 0 and 6 cm H2O of positive end-expiratory pressure (PEEP). At high levels of pulmonary inflation (ie, high PEEP and large TV) compliance decreased. The changes of total respiratory compliance with TV were mainly due to changes in pulmonary compliance. With PEEP, the functional residual capacity increased, and specific compliance did not change. Two mechanisms may be responsible for the changes in compliance. First, varying TV or PEEP will alter the position of tidal ventilation on the pressure-volume curve, resulting in an increase in compliance with increasing TV and PEEP up to a point, where overdistention occurs and compliance decreases. Secondly, the function of the surface-lowering substance may be altered in acute pulmonary parenchymal disease, thus disturbing the regulation of surface tension over the range of pulmonary inflation studied.     

肺泡复张后不同呼气末正压和潮气量调节策略对防止肺泡再萎陷效果的实验研究

目的探讨肺泡复张(RM)后再萎陷的机制以及呼气末正压(PEEP)和潮气量(VT)的调节策略。方法健康杂种犬18只,建立油酸所致急性呼吸窘迫综合征(ARDS),行容量控制通气(VCV)、PEEP 16 cm H2O、VT10 m l/kg、通气频率(RR)30次/m in,稳定后作为基础状态(0 m in)。以压力控制通气[气道峰压(PIP)50 cm H2O,PEEP 35 cm H2O,持续60 s]行RM,然后随机分为小VT中等PEEP组(LVMP组,VT10 m l/kg、PEEP 16 cm H2O、RR 30次/m in),小VT低PEEP组(LVLP组,VT10 m l/kg、PEEP 10 cm H2O、RR 30次/m in)和中等VT低PEEP组(MVLP组,VT15 m l/kg、PEEP 10cm H2O、RR 20次/m in)。观察4 h后处死动物,行支气管肺泡灌冼。监测氧合、呼吸力学、血流动力学及肺损伤指标。结果(1)LVMP、LVLP、MVLP组低位拐点(LIP)分别为(16.0±1.3)、(15.8±3.0)、(16.3±1.9)cm H2O。(2)在RM后30、60 m in,LVMP组动脉血氧分压(PaO2)[(371±64)、(365±51)mm Hg]显著高于LVLP组[(243±112)、(240±108)mm Hg]及MVLP组[(242±97)、(232±87)mm Hg,P均<0.05],但直至RM后4 h 3组比较差异无统计学意义;LVLP与MVLP组在RM后各个时间点的PaO2与基础状态比较差异均无统计学意义;MVLP组的通气功能较其他两组显著改善。(3)与基础状态比较,RM后LVMP组平均动脉压(mABP)显著降低,平均肺动脉压(mPAP)显著增加,而其他两组mABP保持稳定,mPAP降低。(4)与基础状态比较,3组PIP和气道平台压(Pp lat)在RM后均显著降低,呼吸系统静态顺应性(Cst)显著改善。在RM后同一时间点比较,MVLP组PIP、Pp lat和Cst均显著好于LVMP组。MVLP组与LVLP组相比,Cst有增加趋势。(5)在相同部位的支气管肺泡灌冼液中,肺损伤指标在各组之间无显著差异。结论与LIP相近的高PEEP有助于防止复张肺泡的再萎陷,但对血流动力学和呼吸力学产生不利影响;早期应用RM能有效“节约”PEEP,并为上调VT提供了较肺泡复张之前更大的空间。     

Improved arterial oxygenation with biologically variable or fractal ventilation using low tidal volumes in a porcine model of acute respiratory distress syndrome

We compared biologically variable ventilation (V (bv); n = 9) with control mode ventilation (V (c); n = 8) at low tidal volume (VT)--initial 6 ml/kg--in a porcine model of acute respiratory distress syndrome (ARDS). Hemodynamics, respiratory gases, airway pressures, and VT data were measured. Static P-V curves were generated at 5 h. Interleukin (IL)-8 and IL-10 were measured in serum and tracheal aspirate. By 5 h, higher Pa(O(2)) (173 +/- 30 mm Hg versus 119 +/- 23 mm Hg; mean +/- SD; p < 0.0001 group x time interaction [G x T]), lower shunt fraction (6 +/- 1% versus 9 +/- 3%; p = 0.0026, G x T) at lower peak airway pressure (21 +/- 2 versus 24 +/- 1 cm H(2)O; p = 0.0342; G x T) occurred with V (bv). IL-8 concentrations in tracheal aspirate and wet:dry weight ratios were inversely related; p = 0.011. With V (c), IL-8 concentrations were 3.75-fold greater at wet:dry weight ratio of 10. IL-10 concentrations did not differ between groups. In both groups, ventilation was on the linear portion of the P-V curve. With V (bv), VT variability demonstrated an inverse power law indicating fractal behavior. In this model of ARDS, V (bv) improved Pa(O(2)) at lower peak airway pressure and IL-8 levels compared with V (c).