丙泊酚镇静对急性肺损伤/急性呼吸窘迫综合征患者血液动力学及氧合的影响

目的观察丙泊酚镇静对急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)患者行机械通气时血液动力学和肺氧合功能的影响。方法18例实施机械通气的ALI/ARDS患者随机分为丙泊酚组(P组,镇静诱导和维持用丙泊酚)和咪唑安定组(M组,镇静诱导和维持用咪唑安定)。根据Ramsay分级标准调整两组用药量。记录两组患者镇静诱导前即刻(T0)、镇静诱导后1h(T1)、5h(T2)、9h(T3)和12h(T4)血液动力学变化,同时采集上述各时点中心静脉血、股动脉血测定血气,计算肺内动静脉分流率(Qs/Qt)和氧合指数(OI)。结果(1)与T0时比较,T1～T4时两组患者MAP、HR下降(P<0.05);(2)与M组比较,T2～T4时P组Qs/Qt下降、OI升高(P<0.05)。结论丙泊酚镇静有利于改善机械通气时ALI/ARDS患者氧合,可为其病因治疗和肺损伤的修复赢得时间。     

联合应用肺表面活性物质和保护性机械通气策略治疗婴幼儿体外循环后急性肺损伤

目的　探讨联合应用外源性肺表面活性物质 (PS)和保护性肺通气策略对体外循环后急性肺损伤 (ALI) /急性呼吸窘迫综合征 (ARDS)的治疗效应。方法　婴幼儿体外循环术后ALI/ARDS患者 16例 ,随机分为A和B两组 ,A组 9例采用保护性肺机械通气治疗 ;B组 7例在保护性肺通气治疗基础上经气管插管联合应用外源性PS(15 0mg/kg体重 )。观察两组患儿的临床转归 ,并监测 48h内肺动态顺应性 (Cdyn)、氧合指数 (OI)、血浆肿瘤坏死因子 (TNF α)的水平。结果与以往同类病例的治疗结果相比 ,本组患儿死亡率 (6.2 5 % )和并发症显著降低。在治疗后 48h内的各个时点 ,B组Cdyn显著高于A组 (P <0 .0 5 ) ,OI和TNF α的水平显著低于A组 (P <0 .0 5～0 .0 1)。结论　外源性PS与保护性肺通气具有协同作用 ,二者联合应用可明显提高体外循环后ALI/ARDS的治疗效应     

部分液体通气与吸入NO对急性肺损伤动物疗效的对比研究

目的对肺灌洗(Lavage)诱导的急性肺损伤(ALI)家猪实施以氟碳(PFC)为媒介的部分液体通气(PLV)及吸入20ppm的一氧化氮(NO),比较二者对肺气体交换及血液动力学的影响.方法24头健康家猪,麻醉后经气管导管肺内以生理盐水反复灌洗,直至动脉氧分压(PaO2)<100mmHg达1h,记录气体交换及血液动力学各参数作为急性肺损伤的基础值.随机分为PLV组、NO组及对照组,PLV组肺内灌以相当于肺功能余气量(30ml/kg)的PFC,然后以普通呼吸机行常规气体通气,补充PFC4ml·kg-1·h-1以弥补蒸发损失;NO组吸入20ppmNO,对照组不给予其它治疗,各组每小时记录气体交换及血液动力学各参数的变化.结果PLV组实施PLV1h后,PaO2即从ALI时的(53±11)mmHg升高至(142±133)mmHg,4h后达(318±109)mmHg,与ALI时比较差异有显著性(P＜0.01),亦显著高于对照组(P＜0.05).实施PLV1h后Qs/Qt从ALI时的(57±9)%降至(42±13)%,4h后降至(26±10)%,较ALI时差异有显著性(P＜0.01),并于2h后显著低于对照组(P＜0.05).NO组的MPAP在整个实验过程中显著低于对照组(P＜0.01).NO组吸入NO1h后,PaO2即呈上升趋势,4h后从ALI时的65±14升至(114±36)mmHg,与对照组比较差异有显著性(P＜0.05).同时肺内分流(Qs/Qt)及肺泡-动脉氧压差(AaDO2)降低.MAP及体循环血管阻力(SVR)与对照组比较无显著性改变.结论以氟碳为媒介的部分液体通气及吸入20ppm的NO均能有效的改善ALI动物肺气体交换.吸入NO能显著降低MPAP,而PLV更能显著的升高PaO2.     

俯卧位通气下急性呼吸窘迫综合征患者氧合的变化

目的探讨俯卧位通气下急性呼吸窘迫综合征(ARDS)患者氧合的变化及其机制。方法23例早期ARDS患者(病程<72 h),在镇静、肌松下持续俯卧位通气2 h。呼吸机参数设定为潮气量6-8 ml/kg,吸气时间1.0-1.2 s,吸气流速40 L/min,呼吸频率12-20次/min。吸入氧浓度0.4- 1.0,呼气末正压6-18 cm H2O。观察俯卧位前即刻、俯卧位0.5、2 h及恢复仰卧位2 h的氧合指数(PaO2/FiO2)、呼吸系统静态顺应性(Cst)、心率(HR)、平均动脉压(MAP)、中心静脉压(CVP)、平均肺动脉压(MPAP)。肺动脉楔压(PAWP)、心脏指数(CI)、气道峰压(PIP)及气道阻力(Paw)。俯卧位后PaO2/FiO2比俯卧位前上升超过20%作为氧合改善的判断标准。结果与俯卧位前比较,87%患者俯卧位0.5、2 h、恢复仰卧位2 h时PaO2/FiO2和PaO2升高(P<0.01);Cst HR、MAP、CVP、MPAP、PAWP、CI、Raw、PaCO2、PIP差异无统计学意义;87%氧合改善的患者在俯卧位0.5、2 h时Cst差异无统计学意义, 恢复仰卧位2 h时Cst升高(P<0.05)。结论俯卧位通气可改善早期ARDS患者的氧合,且恢复仰卧位后氧合改善持续存在。     

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目的　探讨适应性支持通气(ASV)对术后恢复期急性肺损伤(ALI)呼吸力学的影响。方法　采用自身对照方法,对广东省人民医院2 0 0 3年1～9月2 3例术后ALI病人序贯应用同步间歇指令 压力支持通气模式(SIMV PS)和ASV模式进行机械通气(MV) ,记录两种模式下的各项呼吸力学参数。结果　全部病人均成功脱机,总呼吸频率明显降低(P <0 . 0 5 ) ,自主呼吸频率增加(P >0 . 0 5 ) ,潮气量(VT)明显升高(P <0 . 0 5 ) ,平台压(Pplat)和平均气道压(Pawm)有所升高(P <0 .0 5 ) ,顺应性(Cst)有所下降,P0. 1(0. 1s的口腔闭合压)稍有下降(P >0 .0 5 ) ,生命体征、血气分析和血流动力学指标无明显变化。结论　ASV对术后ALI病人,可根据病人的呼吸力学状况自动调整吸气压力支持水平,提高潮气量、降低呼吸频率,而对血流动力学和生命体征没有影响。     

ALI/ARDS患者俯卧位与仰卧位通气的Meta分析

目的比较俯卧位通气与仰卧位通气在急性肺损伤或急性呼吸窘迫综合征(ALI/ARDS)患者中的有效性及安全性。方法计算机检索Pubmed、EMBASE、Cochrane图书馆、CINAHL、CBM、VIP、CNKI和万方数据库,查找所有比较俯卧位通气与仰卧位通气治疗ALI/ARDS患者的随机对照试验(RCT),检索时限均为建库至2015年6月31日。同时手动检索纳入文献的参考文献和灰色文献。由两人独立按照纳入和排除标准进行文献筛选、质量评价、资料提取后,使用RevMan5.0软件进行数据分析。结果共纳入11篇RCT文献,纳入的研究对象共2 268例。Meta分析结果显示,在病死率方面,当俯卧位通气时间大于12h/d时,患者30d病死率较仰卧位通气低(RR=0.70,95%CI 0.58~0.85,P0.01);对于氧合指数(PaO2/FiO2)≤100mmHg组和100mmHgPaO2/FiO2≤200mmHg组的患者,使用俯卧位通气的患者病死率低于使用仰卧位通气的患者(RR=0.70,95%CI0.56~0.89,P0.01)、(RR=0.69,95%CI0.50~0.94,P0.05);当呼气末正压通气(PEEP)≥10cmH2O时,俯卧位通气患者的60d病死率较仰卧位通气低(RR=0.81,95%CI0.67~0.97,P0.05),10cmH2OPEEP≤13cmH2O时,俯卧位通气患者90d病死率较仰卧位低(RR=0.57,95%CI0.43~0.74,P0.01);在并发症的发生方面,俯卧位通气患者的压疮新发病率和静脉通路脱出发生率高于仰卧位通气患者(RR=1.26,95%CI1.11~1.42,P0.01),(RR=1.70,95%CI1.01~2.86,P0.05);而其他并发症如心血管意外、气管内插管移位、呼吸机相关性肺炎、静脉通路脱落、气胸发生率无统计学意义。结论俯卧位通气与仰卧位通气相比,可以降低重症患者的病死率,且俯卧位时间越长,生存率越高;但俯卧位通气可能会增加压疮和静脉通路脱出的发生率,临床上应注意预防。     

比较地氟醚、丙泊酚在单肺通气时对肺内分流的影响

目的　探讨地氟醚与丙泊酚在单肺通气期间对肺内分流、动脉氧分压的影响。方法　30例胸科手术病人 ,随机分为地氟醚组 (D组 ,1MAC)和丙泊酚组 (P组 ,6mg·kg 1·h 1)行循环紧闭麻醉。在手术前分别于平卧位双肺通气 30min、平卧位单肺通气 30min、侧卧位单肺通气 30min ,采集动脉血和混合静脉血行血气分析 ,计算肺内分流率。结果　在单肺通气后 ,D组和P组肺内分流增加明显 (P <0 0 1)。但平卧位分别增加 14 1%和 13 3% (P >0 0 5 ) ,侧卧位分别增加 13 2 %和12 7% (P >0 0 5 ) ,两组间无显著性差异。D组和P组动脉氧分压明显下降 (P <0 0 1) ,且平卧位比侧卧位下降更为明显。结论　 1MAC地氟醚在循环紧闭麻醉单肺通气期间对肺内分流和动脉氧合无明显的抑制。     

早期持续性高容量血液滤过对重症急性胰腺炎急性肺损伤影响研究

目的研究早期持续性高容量血液滤过（HVHF）对重症急性胰腺炎（SAP）急性肺损伤（ALI）的影响。方法自2006年1月到2007年12月间,前瞻性随机将南京军区南京总医院普通外科研究所ICU 收治的59例入院时合并ALI/ARDS的SAP病人分为HVHF组和对照组,比较两组病人的氧合指数、ALI/ARDS的发生率、机械通气的例数及时间。结果（1）氧合指数：HVHF组入院第3、10天均较入院时明显改善（P<005）,而对照组至入院第10天才较入院时有所改善（P<005）;并且在入院第3、10天,HVHF组均优于对照组病人（P<005）。（2）ALI、ARDS的发生率：HVHF组入院第10天较入院时明显降低（P<005）;对照组入院第10天较入院时降低不明显（P＞005）;入院第10天HVHF组均明显低于对照组（P<005）。（3）机械通气：两组病人急性期机械通气的例数差异无统计学意义（P＞005）,但HVHF组机械通气时间明显较对照组缩短（P<005）。结论早期持续性HVHF治疗能有效促进合并ALI/ARDS的SAP病人肺功能的恢复,是一项重要的辅助治疗措施。     

经皮氧分压监测在急性呼吸窘迫综合征治疗中的应用

目的 观察经皮氧分压(PtcO2)在急性呼吸窘迫综合征(ARDS)患者中的变化特点,了解其在ARDS治疗中的作用.方法 采用经皮氧分压监测仪对49例ARDS患者实施连续动态监测PtcO2,记录通气前和通气后4、8、16、24 hPtcO2值,同期抽取动脉血检测PaO2、SaO2,记录心率(HR)和平均动脉压(MAP).并比较存活组与死亡组不同时间PtcO2的差异.结果 SaO2、HR、MAP随时间变化的程度不明显(均P＞0.05),PtcO2和PaO2随时间变化显著(均P＜0.05);存活组(35例)与死亡组(14例)PtcO2比较,差异有显著性意义(P＜0.05).结论 PtcO2监测对ARDS治疗能提供连续、可靠的指导作用,PtcO2早期的变化对判断预后有一定帮助.     

气道压力释放通气对急性肺损伤或急性呼吸窘迫综合征患者呼吸功能的影响

目的评价气道压力释放通气（APRV）对急性肺损伤（ALI）或急性呼吸窘迫综合征（ARDS）患者呼吸功能的影响。方法ALI患者42例、ARDS患者33例，随机分2组，APRV组（n=37）、同步间歇指令通气（SIMV）组（n=38）；两组均用SIMV加用呼气末正压通气30min后，APRV组采用APRV模式通气，SIMV组仍用初始参数，分别于APRV前（基础值）、APRV1、8、16、24h测定动脉血气、气道峰压（Ppeak）、气道平均压（Pmean）、中心静脉压（CVP）、氧合指数（PaO2／FiO2）、心率（HR），并记录芬太尼、咪达唑仑、多巴胺用量及尿量。结果与SIMV组比较，APRV组APRV1～24h各时点Ppeak、Pmean降低，APRV16、24h时动脉血PaCO2降低，PaO2／FiO2升高，APRV1—24h时CVP和HR降低，芬太尼用量和咪达唑仑用量明显减少，APRV8—24h各时点尿量升高，多巴胺用量减少（P〈0．05或0．01）。结论APRV用于ARDS或ALI患者的机械通气治疗，不仅能提供更好的通气，而且血液动力学平稳，减少镇静剂和麻醉药用量。     

Der Einfluß des kontinuierlichen axialen Lagewechsels bei der Behandlung des posttraumatischen Lungenversagens (ARDS)

In the treatment of posttraumatic adult respiratory distress syndrome (ARDS) so far no breakthrough has been achieved. In several cases of severe ARDS we have seen improvements of lung function by means of continuous body positioning. We therefore compared the effect of kinetic positioning (KIN) on lung function and hemodynamics in ARDS patients to conventional (KON) supine positioning. 22 ARDS patiens with multiple trauma treated by supportive continuous body positioning (KIN) (KCI-Mediscus) and without continuous positioning (KON) were investigated daily. Pulmonary and systemic hemodynamics were determined on the basis of pulmonary artery catheter measurements. Oxygenation ratio (PaO₂/FiO₂) and pulmonary shunt (Qs/Qt, %) were calculated. Extravascular lung water (EVLW, ml/kg body weight) was determined by double indicator thermodilution technique. Total injury severity by injury severity score (ISS) was 29.6±6 points (KIN) and 31.6±5 points (KON). The oxygenation ratio (PaO₂/FiO₂) increased significantly from 140±45 (day 0) to 237±40 (p<0.05) [day 5] (KIN), in KON patients no improvement (143±48 [day 0], 133±44 [day 5]) was seen (p<0.05 between groups). There were no significant changes of systemic hemodynamics between the groups or compared to day 0. Pulmonary shunt decreased significantly from 26.6±4% (day0) to12.5±2% (day5) (p<0.05) in KIN patients and was 36.6±6% at day 0 and 31.4±2% at day 5 in KON patients (p<0.05 between groups). EVLW was 11.1±2 ml/kg body weight at day 0 and 9.4±1 ml/kg body weight at day 5 (KIN)-EVLW was 12.9±2 ml/kg body weight at day 0 and 17.4±3 ml/kg body weight at day 5 (KON) (not significant). We found no hemodynamic side effects from continuous body positioning. In ARDS-patients submitted to body positioning oxygenation and pulmonary shunt improved significantly and were significantly better compared to those with conventional supine positioning. Continuous body positioning appears to represent a promising supportive treatment regimen in posttraumatic ARDS.     

Effect of bronchial drainage on the improvement in gas exchange observed in ventral decubitus in ARDS

OBJECTIVES: A bronchial secretion draining effect is frequently suggested as a mechanism for oxygenation improvement during prone positioning (PP) in patients with acute respiratory distress syndrome (ARDS). Nevertheless, it has never really been evaluated. The aim of this study was to search for an interrelationship between the volume of the bronchial secretion and the improvement of the PaO2/FIO2 ratio during prone positioning, with NO inhalation or not. STUDY DESIGN: Open prospective clinical study. PATIENTS: The study included 15 consecutive patients with severe ARDS (PaO2/FIO2 < 200 after alveolar recruitment, Murray score > 2.5). METHODS: They were returned to the prone position for 4 hours (h0-h4) combined with an inhalation of 5 ppm NO during 1 hour (h2-h3). Tracheal suction were performed hourly between h-2 and h6 and weighed on a precision scale from h-1 to h6. Haemodynamic, blood gas and respiratory compliance were recorded at h0, h2, h3, h4 and h6. RESULTS: No significant haemodynamic changes were observed in the various phases. Compared with the baseline condition at h0, PP and PP + NO respectively improved PaO2/FIO2 by 102 +/- 62% at h2 (P < 0.005) and 156 +/- 79% at h3 (P < 0.005/h0 and < 0.01/h2). 14/15 patients responded to PP and 15/15 to PP + NO (gain in PaO2/FIO2 > 10%). Concerning secretions, we collected 3.0 +/- 7.5 g, 4.4 +/- 6.1 g, 1.7 +/- 1.4 g and 1.7 +/- 1.6 between h-2 and h0, h0 and h2, h2 and h4, h4 and h6. Individual assessments showed no relationship between the PaO2/FIO2 evolution at any time and the quantity of secretions obtained during the first 2 hours in the prone position. Six patients presented secretions of less than 1 g between h0 and h2, and for whom the improvement in oxygenation was higher than average (115 +/- 53% at h2). CONCLUSION: In patients with little or moderate secretions, the improvement observed in oxygenation, with or without NO, does not depend on their volume.     

Methylprednisolone and the adult respiratory distress syndrome

Total hip replacement was carried out on 22 patients under general anaesthesia. Of these, 10 were pretreated with methylprednisolone (30 mg/kg); 1 of these developed the adult respiratory distress syndrome (ARDS) and had high levels of thromboxane B2 (TXB2) 5 minutes after fixation of the femoral prosthesis and at the end of the operation. The other 12 patients served as controls; 5 of them developed ARDS and had statistically significant higher TXB2 levels than the other 7 control patients who remained well. All patients who did not develop ARDS had low TXB2 levels. TXB2 and beta-thromboglobulin levels followed the same trend and there was good correlation (r=0,6806; P less than 0,01) at the end of the operation in the control group patients who developed ARDS. There was no statistical difference in 6-keto-PGF1 alpha levels between the patients who developed ARDS and those in the control group who remained well. Steroids reduce arachidonic acid metabolism by inhibiting the release of substrate for cyclo-oxygenase and lipoxygenase activity. Patients prone to ARDS thus benefit from methylprednisolone administration.     

Effects of ibuprofen on a pig Pseudomonas ARDS model

The effects of ibuprofen (I) were studied in the Pseudomonas (P) porcine ARDS model. Pigs, 14-26 kg (5 in each group), were anesthetized and ventilated with 0.5 FiO2 and 5 cm H2O PEEP. A control (C) group received saline only, a second group was given P, 1 X 10(8) org/ml at 0.3 cc/20 kg/min, and a third group was given P followed by 12.5 mg I at 20 and 120 min. Pulmonary arterial (PAP), wedge (PWP) and systemic arterial pressures, cardiac output (CO), and thermal-cardiogreen extravascular lung water (EVLW), thromboxane (TxB2), 6-keto-PGF1 alpha, PaO2, PaCO2 were determined every 30 min. Albumin flux was measured with scintigraphic determination of lung:heart radioactivity ratios versus time, called slope index (SI). At 3 hr, P produced marked (P less than 0.05) increases in PAP (18 +/- 7 to 37 +/- 2 mm Hg), TxB2 (471 +/- 513 to 9216 +/- 3615 pg/ml), 6-keto-PGF1 alpha, EVLW (6.4 +/- 1.4 to 14.6 +/- 5.7 mg/kg), and SI (0.4 +/- 0.2 to 1.7 +/- 0.5 X 10(-3) U/min) with decreases in PaO2 (214 +/- 47 to 101 +/- 41 torr), CO and SAP. Ibuprofen caused a rapid clearing of TxB2 and 6-keto-PGF1 alpha associated with a transient decrease in PAP; PaO2 was considerably improved compared to P; however, CO, SAP, EVLW, and SI were unaffected. Prostaglandin blockage temporarily ameliorated the pulmonary hypertension and markedly improved oxygenation in this porcine septic ARDS model, but failed to alter increased permeability, confirming other studies that the increased pulmonary shunt in ARDS is not only dependent upon capillary leak.     

Are corticosteroids salvage therapy for refractory acute respiratory distress syndrome?

: Late acute respiratory distress syndrome (ARDS), characterized by progressive pulmonary interstitial fibroproliferation, is associated with mortality >80%. Although previous large prospective trials failed to show a benefit of steroids in early ARDS, recent small reports describe improved survival in patients with late ARDS. Recognizing the pathogenetic differences between early and late ARDS, we employed steroid therapy in patients with refractory late ARDS. : Over a 5-year period, we treated 6 patients who were dying of isolated refractory ARDS with methylprednisolone sodium succinate (1 to 2 mg/kg every 6 hours). Ventilatory parameters and lung injury scores were serially recorded, and steroids were weaned based on clinical response. : Steroids were instituted after 16 days of advanced mechanical ventilatory support. By day 7 of steroid therapy, there was clinically significant improvement in PaO₂/FiO₂ ratios (84 to 172) and lung injury scores (3.6 to 2.9); 5 patients (83%) survived. : Steroid therapy appears to be effective in patients with refractory late ARDS. Prospective trials are needed to define the indications, timing of intervention, dose and duration, and precautions of steroid therapy.     

Lung protective ventilation strategies: have we applied them in trauma patients at risk for acute lung injury and acute respiratory distress syndrome?

Lung protective ventilation strategies for patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are well documented, and many medical centers fail to apply these strategies in ALI/ARDS. The objective of this study was to determine if we apply these strategies in trauma patients at risk for ALI/ARDS. We undertook a retrospective review of trauma patients mechanically ventilated for > or = 4 days with an ICD-9 for traumatic pneumothorax, hemothorax, lung contusion, and/or fractured ribs admitted from May 1, 1999 through April 30, 2000 (Group 1), the pre-ARDS Network study, and from May 1, 2003 through April 30, 2004 (Group 2), the post-ARDS Network study. Tidal volume (VT)/kg admission body weight, VT/kg ideal body weight (IBW), and plateau and peak pressures were analyzed with respect to mortality. VT/Kg admission body weight and IBW were significantly reduced when comparing Group 1 with Group 2 (9.27 to 8.03 and 11.67 to 10.04, respectively). VT/kg IBW was greater (P < 0.01) for patients who died in Group 1 (13.81) compared with patients who lived (10.29) or died (9.89) in Group 2. Peak and plateau pressures were greater (P < 0.01) in patients who died in Group 1 than patients who lived or died in Group 2. A strict ARDS Network ventilation strategy (VT < 6 mL/kg) is not followed, rather a low plateau/peak pressure strategy is used, which is a form of lung protective ventilation.     

Extracorporeal life support for severe acute respiratory distress syndrome in adults

OBJECTIVE: Severe acute respiratory distress syndrome (ARDS) is associated with a high level of mortality. Extracorporeal life support (ECLS) during severe ARDS maintains oxygen and carbon dioxide gas exchange while providing an optimal environment for recovery of pulmonary function. Since 1989, we have used a protocol-driven algorithm for treatment of severe ARDS, which includes the use of ECLS when standard therapy fails. The objective of this study was to evaluate our experience with ECLS in adult patients with severe ARDS with respect to mortality and morbidity. METHODS: We reviewed our complete experience with ELCS in adults from January 1, 1989, through December 31, 2003. Severe ARDS was defined as acute onset pulmonary failure, with bilateral infiltrates on chest x-ray, and PaO2/fraction of inspired oxygen (FiO2) ratio < or =100 or A-aDO2 >600 mm Hg despite maximal ventilator settings. The indication for ECLS was acute severe ARDS unresponsive to optimal conventional treatment. The technique of ECLS included veno-venous or veno-arterial vascular access, lung "rest" at low FiO2 and inspiratory pressure, minimal anticoagulation, and optimization of systemic oxygen delivery. RESULTS: During the study period, ECLS was used for 405 adult patients age 17 or older. Of these 405 patients, 255 were placed on ECLS for severe ARDS refractory to all other treatment. Sixty-seven percent were weaned off ECLS, and 52% survived to hospital discharge. Multivariate logistic regression analysis identified the following pre-ELCS variables as significant independent predictors of survival: (1) age (P = 0.01); (2) gender (P = 0.048); (3) pH < or =7.10 (P = 0.01); (4) PaO2/FiO2 ratio (P = 0.03); and (5) days of mechanical ventilation (P < 0.001). None of the patients who survived required permanent mechanical ventilation or supplemental oxygen therapy. CONCLUSION: Extracorporeal life support for severe ARDS in adults is a successful therapeutic option in those patients who do not respond to conventional mechanical ventilator strategies.     

双相正压通气与持续正压通气对急性呼吸窘迫综合征患者肺复张效果的比较

目的 比较双相正压通气(BIPAP)与持续正压通气(CPAP)对急性呼吸窘迫综合征(ARDS)患者肺复张的效果.方法 选择ARDS患者44例,ASA Ⅲ或Ⅳ级,性别不限,年龄35～63岁,体重52～74 kg,肺复张前基础通气模式为同步间歇指令通气联合压力支持通气,随机分为2组(n=22):CPAP组和BIPAP组.CPAP组10 s内逐渐上升呼气末正压(PEEP)至30 cm H2O,持续30 s,然后在5～10 8内恢复肺复张前通气模式.BIPAP组高水平和低水平压力分别为40、20 cm H2O,持续90 s,然后在5～10 s内恢复肺复张前通气模式.记录肺复张通气前即刻(T1),肺复张通气结束后即刻(T2)、2 min(T3)、5 min(T4)、15 min(T5)、30 min(T6)时HR、MAP、CVP、SpO2和肺动态顺应性(Cdyn).分别于T1、T5、肺复张通气结束后1 h(T7)、2 h(T8)、4 h(T9)时采集桡动脉血样,测定pH值、PaO2和PaCO2,计算PaO2/FiO2比值.结果 与CPAP组比较,BIPAP组SpO2、Cdyn、PaO2和PaO2/FiO2升高,CVP降低(P<0.05),HR和MAP比较差异无统计学意义(P>0.05).与T1时比较,CPAP组T3时MAP升高,T2时CVP升高,Cdyn降低,T3～6时SpO2和Cdyn升高,T7,8时PaO2升高,T5,7,8时PaO2/FiO2升高,BIPAP组T2～6时SpO2升高,T3～6时Cdyn升高,T5,7,8时PaO2和PaO2/FiO2升高(P<0.05).结论 与CPAP比较,BIPAP对ARDS患者行肺复张通气时血液动力学影响小,可进一步提高氧合和肺顺应性,是一种安全有效的肺复张方法 .     

Acute respiratory distress syndrome secondary to inhalation of chlorine gas in sheep

BACKGROUND: Toxic industrial chemicals (TICs) are potential terrorist weapons. Several TICs, such as chlorine, act primarily on the respiratory tract, but knowledge of the pathophysiology and treatment of these injuries is inadequate. This study aims to characterize the acute respiratory distress syndrome (ARDS) caused by chlorine gas (Cl2) inhalation in a large-animal model. METHODS: Anesthetized female sheep were ventilated with 300 L of a Cl2/air/oxygen mixture for 30 minutes. In phase 1 (n = 35), doses were 0 ppm (Group 1, n = 6); 120 ppm (Group 2, n = 6); 240 to 350 ppm (Group 3, n = 11); and 400 to 500 ppm (Group 4, n = 12). In phase 2 (n = 17), doses were 0 ppm (Group 5, n = 5); 60 ppm (Group 6, n = 5); and 90 ppm (Group 7, n = 7), and the multiple inert gas elimination technique (MIGET) was used to characterize the etiology of hypoxemia. Computed tomography (CT) scans were performed daily for all animals. RESULTS: In Phase 1, lung function was well maintained in Group 1; Cl2 caused immediate and sustained acute lung injury (PaO2-to-FiO2 ratio, PFR<3.0) in Group 2 and ARDS (PFR<2.0) in Groups 3 and 4. All animals in Groups 1 and 2 survived 96 hours. Kaplan-Meier analysis showed dose-related differences in survival (log-rank test, p < 0.0001). Logistic regression identified 280 ppm as the lethal dose 50%. CT and histopathology demonstrated lesions of both small airways and alveoli. In Phase 2, MIGET showed diversion of blood flow from normal to true-shunt lung compartments and, transiently, to poorly ventilated compartments. CONCLUSIONS: Cl2 causes severe, dose-related lung injury, with features seen in both smoke inhalation and in ARDS secondary to systemic disease. This model will be used to test new therapeutic modalities.     

Early alveolar and systemic mediator release in patients at different risks for ARDS after multiple trauma

Alveolar IL-8 has been reported to early identify patients at-risk to develop ARDS. However, it remains unknown how alveolar IL-8 is related to pulmonary and systemic inflammation in patients predisposed for ARDS. We studied 24 patients 2-6h after multiple trauma. Patients with IL-8 >200 pg/ml in bronchoalveolar lavage (BAL) were assigned to the group at high risk for ARDS (H, n = 8) and patients with BAL IL-8 <200 pg/ml to the group at low risk for ARDS (L, n = 16). ARDS developed within 24h after trauma in 5 patients at high and at least after 1 week in 2 patients at low risk for ARDS (p = 0.003). High-risk patients had also increased BAL IL-6, TNF-α, IL-1β, IL-10 and IL-1ra levels (p<0.05). BAL neutrophil counts did not differ between patient groups (H vs. L, 12% (3-73%) vs. 6% (2-32%), p = 0.1) but correlated significantly with BAL IL-8, IL-6 and IL-1ra. High-risk patients had increased plasma levels of pro- but not anti-inflammatory mediators. The enhanced alveolar and systemic inflammation associated with alveolar IL-8 release should be considered to identify high-risk patients for pulmonary complications after multiple trauma to adjust surgical and other treatment strategies to the individual risk profile.