允许性高碳酸血症对急性呼吸窘迫综合征绵羊全身和肠道氧代谢的影响

目的 探讨允许性高碳酸血症（ＰＨＣ）对ＡＲＤＳ肺外器官功能的影响。方法 观察不同潮气量（Ｖｒ）时,１８只ＡＲＤＳ绵羊血液动力学、氧代谢和胃粘膜ｐＨ（ｐＨｉ）的改变。结果 当ＶＴ从１６ｍｌ／ｋｇ降至４～７ｍｌ／ｋｇ,绵羊均出现ＰＨＣ;与ＶＴ１３～１６ｍｌ／ｋｇ比较,ＰＨＣ时心排指数（ＣＩ）显著降低（Ｐ〈０．０５）,体循环和肺循环阻力指数显著增高（Ｐ〈０．０５）,尽管ＰＨＣ时动脉血氧分压及氧饱和度、混     

允许性高碳酸血症在重度急性呼吸窘迫综合征治疗中的意义

目的：探讨允许性高碳酸力（ＰＨＣ）治疗重度急性呼吸窘迫综合征（ＡＲＤＳ）的治疗效应。方法：观察不同潮气量（ＶＴ）条件下，１０例重度ＡＲＤＳ患者的肺力学、血液动力学和氧动力学参数。结果：ＶＴ从常规水平降至小ＶＴ时，患者均出现ＰＨＣ，ＰａＯ２和ＳａＯ２无显著变化，但肺内分流率显著升高。气道平台压力显著降低。吸气最后２０％的顺应性与总顺应性之比明显增大。ＭＡＰ、ＰＡＰ无明显变化，但ＳＶＲＩ显著降低。ＣＩ     

急性呼吸窘迫综合征支持治疗进展

本文对机械通气、药物、体外膜氧合技术等对急性呼吸窘迫综合征的治疗作用作一综述.     

高白细胞急性白血病伴发呼吸窘迫综合征临床分析

本文报告高白细胞急性白血病７例。其周围血白细胞为１９８￣３６２×１０＾９／Ｌ，原始细胞绝对计数均〉１００×１０＾９／Ｌ。病人均发生了成人呼吸窘迫综合征，其中４例于入院后７２小时内死亡呼吸衰竭，１例死于颅内出血，另２例经吸氧、机械呼吸、化疗、抗凝、胸部放疗及抗高肿瘤细胞溶解综合征等治疗后缓解。本病伴发呼吸窘迫综合征的可能机理为：（１）高凝状态；（２）高原始细胞肺内淤滞；（３）肺血管调节的不适应性。     

急性呼吸窘迫综合征支持治疗进展

本文对机械通气、药物、体外膜氧合技术等对急性呼吸窘迫综合征的治疗作用作一 综述。     

急性呼吸窘迫综合征机械通气治疗

急性肺损伤（acute lungin jury，ALI）是以低氧血症为特征的急性呼吸衰竭，急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）是ALI病情进展的结果。机械通气是纠正ARDS低氧血症的主要手段。ARDS的病理生理特点决定了患者机械通气中必须采用特殊的通气策略。     

高压氧对兔油酸性急性呼吸窘迫综合征酏保护作用

目的：研究高压氧（HB0）是否对油酸（0A）诱导免急性呼吸窘迫综合征（ARDS）有肺保护作用。方法：成年健康新西兰大白兔36只,随机分为正常对照组（N）、ARDS组（A）、ARDs常规治疗60分钟组（M60）、ARDS常规治疗120分钟组（M120）、ARDs高压氧治疗60分钟组（O60）和ARDS高压氧治疗120分钟组（O120）。M60组和M120组为兔制备ARDs模型后接氧气吸入治疗60min和120min.     

细胞因子与急性呼吸窘迫综合征

细胞因子及其相互作用在急性呼吸窘迫综合征的炎症过程中发挥重要作用。本文综述各种细胞因子在急性呼 吸窘迫综合征发生发展中的作用机制,以期从分子水平揭示其发病机制。     

体外膜肺氧合治疗重症急性呼吸窘迫综合征的护理

目的总结体外膜肺氧合（ECMO）治疗重症急性呼吸窘迫综合征（ARDS）的临床护理策略。方法对22例机械通气效果不佳的重症ARDS患者应用ECMO治疗，同时合理调配护理人员，加强病房环境管理及各项生命指标的监测等。结果ECMO治疗24h后，患者氧代谢情况明显改善；住院治疗25～43d，治愈16例，死亡6例。结论严密监测和有效的护理是ECMt）治疗成功的重要保证。     

急性肺损伤/急性呼吸窘迫综合征液体治疗策略

背景 高通透性肺水肿是急性肺损伤/急性呼吸窘迫综合征(acute lung injury/acute respiratory distress syndrome,ALI/ARDS)的基本病理生理特征,其程度与ALI/ARDS的预后密切相关.目的 对ALI/ARDS患者合理的液体管理,有助于改善ALI/ARDS患者的肺水肿,降低该病病死率.内容 回顾了ALI/ARDS液体治疗策略探索过程中存在争议的问题(如限制性或开放性的液体治疗策略及治疗液体种类的选择),总结了该领域近年来的研究进展(如ALI/ARDS病程不同阶段的差异化治疗及液体治疗的监测指标).趋向 今后将进一步探索该病在不同的病理生理状态下特异性的液体治疗方法,寻求高效敏感的监测指标,指导液体治疗策略的选择和调整.     

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.     

Mild hypothermia attenuate kidney injury in canines with oleic acid-induced acute respiratory distress syndrome

BackgroundHypothermia may attenuate ventilator induced-lung injury in acute respiratory distress syndrome (ARDS). However, the impact of hypothermia on extra-pulmonary organ injury in ARDS remains unclear. The purpose of this study was to investigate whether hypothermia affects extra-pulmonary organ injury in a canine ARDS model induced by oleic acid.ObjectivesTwelve anesthetized canines with oleic acid-induced ARDS were randomly divided (n = 6 per group) into a hypothermia group (core temperature of 33 ± 1 °C, HT group) and a normothermia group (core temperature of 38 ± 1 °C, NT group) and treated for four hours. The liver, small intestine and kidney were assessed by evaluating biochemical parameters, plasma and tissue cytokine levels, and tissue histopathological injury scores.ResultsThe HT group showed a lower plateau pressure, lung elastance and pulmonary vascular resistance. Hypothermia was associated with lower oxygen consumption (138.4 ± 55.0 ml min⁻¹ vs. 72.0 ± 11.2 ml min⁻¹, P < 0.05) and higher oxygen saturation of mixed venous blood (62.8% ± 8.0% vs. 77.5% ± 10.1%, P < 0.05). Both groups had similar levels of tumour necrosis factor-α in the plasma and extra-pulmonary organ, however, plasma interleukin-10 (97.1 ± 25.0 pg ml⁻¹ vs. 131.4 ± 27.0 pg ml⁻¹, P < 0.05) was higher in the HT group. Further, the animals in the HT group had a lower levels of plasma creatinine (54.6 ± 19.1 U L⁻¹ vs. 29.1 ± 8.0 U L⁻¹, P < 0.05), and lower renal histopathological injury scores [4.0(3.5;7.0) vs. 1.5(0.8;3.0), P < 0.05]. Hypothermia did not affect the histopathological injury of the liver and small intestine.ConclusionsShort-term mild hypothermia can reduce lung elastance and pulmonary vascular resistance, increase the systemic anti-inflammatory response and attenuate kidney histopathological injury in a canine ARDS model induced by oleic acid.     

油酸肺损伤后肺泡液体清除功能的变化及其意义

目的观察大鼠油酸型肺损伤后肺泡上皮液体清除功能的变化。方法wistar大鼠48只,随机分为正常对照组(C组)、油酸致伤组(Ⅰ组)、阿咪洛利组(A组)、哇巴因组(O组)、阿咪洛利加哇巴因组(AO组)和特普他林组(T组)。经股静脉注入油酸0.25ml.kg-1诱导油酸型肺损伤动物模型,24h后C组和Ⅰ组经气管滴注5％白蛋白溶液5ml.kg-1。A组和O组气管内分别滴注阿咪洛利(2×10-3mol/L)和哇巴因(5×10-4mol/L)溶液5ml.kg-1;AO组则滴注阿咪洛利和哇巴因混合液;T组滴注特普他林溶液(10-4mol/L)5ml.kg-1。注药后1h测定肺泡内液体清除率(ALC)、总肺水量(TLW)、肺血管外肺水量(EVLW)和动脉血气。结果与C组相比,Ⅰ组出现严重的低氧血症,ALC降低49.2％,TLW和EVLW明显增加(P＜0.01);A组和O组ALC较I组进一步降低,TLW和EVLW进一步增加(P＜0.05);AO组ALC则降至最低点,TLW和EVLW升至最高点。而T组ALC较致伤组升高63.7％,TLW和EVLW显著减少(P＜0.01),低氧血症明显改善。ALC与TLW和EVLW之间呈显著负相关。结论肺泡上皮液体清除功能障碍是急性肺损伤后肺水肿形成的因素之一。     

Aerosolized surfactant therapy for endotoxin-induced experimental acute respiratory distress syndrome in rats

We have compared the effects of inhalation of aerosolized surfactanton experimental acute respiratory distress syndrome. Escherichiacoli endotoxin (55 (SD 20) mg kg^–1) was injected intothe tracheas of 36 adult rats anaesthetized and mechanicallyventilated with pure oxygen. When the Pa_O2 decreased to 11.3(3.3) kPa, the animals were randomly subjected to inhalationof aerosolized modified natural surfactant (MNS) for 0 min (controlgroup), 30, 60, and 120 min. In the control group, Pa_O2 remainedbelow 12 kPa for 180 min. In the groups receiving inhalationof surfactant for 30 and 60 min, Pa_O2 increased but decreasedsoon after termination of the inhalation. In contrast, Pa_O2of the group receiving inhalation of surfactant for 120 mincontinued to increase, reaching 52.1 (12.5) kPa at 180 min (P<0.05vs control). Thus, we conclude that improvement in gas exchangeas a result of inhalation of MNS depends on the duration ofinhalation. Br J Anaesth 2001; 87: 266–71     

Diagnosis and therapy of adult respiratory distress syndrome in acute pancreatitis

Acute pancreatitis has high morbidity and mortality. The treatment of these patients includes careful respiratory monitoring. Adult Respiratory Distress Syndrome could be find in 50% of patients, while 40% of these needs intensive care.     

Outcome for adults with acute respiratory distress syndrome

Acute respiratory distress syndrome in adults (ARDS) is a relatively frequent disease, the mortality of which has diminished considerably in recent years. The long-term outcome of patients who have survived ARDS has been studied extensively and should in the future be taken into account in assessing new treatment modalities. The long-term respiratory sequelae are generally minimal and moderately disabling. Secondary deterioration of respiratory function is not part of the natural history of ARDS and should suggest other diagnoses. The various studies find a clear diminution in quality of life after ARDS (compared with the general population), essentially related to neuromuscular deficiencies associated with the neuromyopathies of resuscitation or to neuropsychological damage combining cognitive disorders and symptoms of posttraumatic stress. These symptoms are not at all specific to ARDS. They are found in varying degrees in patients who have survived intensive care or resuscitation. Appropriate management for these symptoms remains to be determined. Critical care units must now work at preventing the onset of these disorders, by limiting the treatments at risk when possible and by identifying these disorders before discharge to prepare for optimal subsequent management. Patients with ARDS are only a subgroup of more severe illness among all patients in critical care departments.