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致病因素所导致的急性进行性缺氧性呼吸衰竭，它们具有性质相同的病理生理改变，严重的ALI或ALI的最终严重阶段被定义为ARDS，临床表现以呼吸窘迫、顽固性低氧血症和非心源性肺水肿为特征，采用常规的治疗难以纠正其低氧血症，死亡率高达60%。目前，有关ALI/ARDS的研究取得较多进展，其中，能有效评估ALI病情和预测死亡率的临床参数和生化指标一直是研究热点。
Objective To compare the effects of high and low positive end-expiratory pressure( PEEP) levels on mortality and risk of barotrauma in patients with acute respiratory distress syndrome ( ARDS) . Methods Randomized controlled trials ( RCTs) were recruited from PubMed( 1966-2008. 9) ,EMBASE( 1980-2008. 9) , Cochrane Database ( Issue 2, 2008) , Chinese Cochrane Centre Database and CBMdisc ( 1978-2008. 9) . Related published and unpublished data and attached references were hand searched. All RCTs about ventilation with PEEP for patients with ARDS were included, then a systematic review were performed. Results Five eligible trials were enrolled in the systematic review. According to ventilation strategy, all trials were divided into subgroup A( low tidal volumes + high PEEP vs traditional tidal volumes + low PEEP) and subgroup B( low tidal volumes + high PEEP vs low tidal volumes + low PEEP) . In subgroup A, high PEEP was associated with a lower mortality[ RR 0. 59, 95%CI( 0. 43, 0. 82) ] and a lower prevalence of barotraumas [ RR 0. 24, 95% CI( 0. 09, 0. 70) ] in patients with ARDS. In subgroup B, the difference in mortality[ RR 0. 97, 95%CI( 0. 83, 1. 13) ] and barotraumas[ RR 1. 13, 95% CI( 0. 78, 1. 63) ]were not significant. Conclusions As compared with conventional ventilation, low tidal volumes and high PEEP ventilation strategy is associated with improved survival and a lower prevalence of barotraumas in patients with ARDS. It is necessary to further confirm the role of sole high PEEP in the ventilation strategy.
Objective To explore the effects of different humidification and heating strategies during non-invasive positive pressure ventilation( NIPPV) in patients with ALI/ARDS. Methods A total of 45 patients with ALI/ARDS were randomly divided into three groups to receive NIPPV with different humidification and heating strategies, ie. Group A ( humidification with a 370 Humidifier without heating) ,group B ( humidification with a 370 Humidifier along with a MR410 Heater) , and group C ( humidification and heating with aMR850 Humidifier, and a RT308 circuit heater) . The changes of air temperature, absolute humidity, relative humidity, sputum thickness and patient comfort were compared between the three groups. Sputum thickness was evaluated with AWSS scoring system. Results After humidification and heating, the air temperature, absolute humidity and AWSS score improved significantly in group B [ elevated from ( 23. 9 ±1. 0) ℃, (9.8 ±1. 3) mg/L and 2. 0 ±0. 7 respectively to ( 30. 3 ±1. 7) ℃, ( 31. 0 ±2. 3)mg/L and ( 3. 0 ±0. 9) respectively, P lt; 0. 001] and group C [ elevated from( 23. 8 ±1. 0) , ( 9. 8 ±1. 5)mg/L and ( 2. 1 ±0. 7) respectively to ( 34. 0 ±1. 1) ℃, ( 43.8 ±2. 5) mg /L and 3. 5 ±1. 0 respectively,P lt; 0. 001] . Air temperature and absolute humidity were significantly higher in group C than those in group B( P lt; 0. 001) . Of all the parameters, only absolute humidity showed a significant improvment in group A [ elevated from( 9. 9 ±1. 6) mg/L to ( 11. 9 ±0. 9) mg/L, P lt; 0. 001] . The degree of comfort in group C was significantly higher than that in group A and B [ 8. 0 ±1. 7 vs 5. 0 ±1. 2 and 3. 0 ±0. 4, respectively, P lt;0. 001] . In group A seven patients were switched to group C because of discomfort, four accepted NIPPV continuously, and two avoided invasive mechanical ventilation eventually. In group B three patients were switched to group C because of intolerance of too much condensed water in the breathing circuit, all of them accepted NIPPV continuously, and one avoided invasive mechanical ventilation eventually. Conclusions Compared with mere humidification or humidification with heating humidifier, humidification with heating humidifier and circuit heating during NIPPV can improve the absolute humidity, air temperature and patient comfort,meanwhile decreasing the sputumthickness of patients with ALI/ARDS.
Objective To explore the effects of lateral position ventilation on lung volume and oxygenation in patients with acute respiratory distress syndrome ( ARDS) . Methods Fourteen patients with ARDS were enrolled. Supine position, lateral position and supine position were successively adopted and continued for one hour respectively. End-expiratory lung volume ( EELV) was measured at the end of each epoch. Effects of different position on gas exchange, lung mechanics and hemodynamics were monitored.Results EELV was increased from ( 1109 ±321) mL to ( 1376 ±381) mL after lateral ventilation ( P lt;0. 05) , and decreased to ( 1143 ±376) mL after the second supine ventilation ( P lt;0. 05) . Compared with initial supine ventilation, there was no significant difference in EELV after the second supine ventilation( P gt;0. 05) . PaO2 /FiO2 was increased from ( 154. 3 ±35. 0) mm Hg to ( 189. 9 ±60. 1) mm Hg after lateral ventilation ( P lt;0. 05) , and increased to ( 209. 2 ±75. 4) mm Hg after the second supine ventilation ( P lt; 0. 05) . Compared with initial supine ventilation, PaO2 /FiO2 was increased greatly after the secondsupine ventilation ( P lt; 0. 01) . There was no significant difference in PaCO2 , lung mechanics and hemodynamics after changing different position. Conclusion Lateral position ventilation can increase EELV and improve oxygenation in patients with ARDS.
Objective To investigate whether the new oxygenation index [ PaO2 /( FiO2 ×Paw ) ]which including mean airway pressure ( Paw ) for assessing intrapulmonary shunting of acute respiratory distress syndrome( ARDS) could be more accurate than the conventional oxygenation ratio ( PaO2 /FiO2 ) .Methods Twelve patients with ARDS were recruited. All patients received mechanical ventilation under lung ventilation protective strategy ( VT 6 mL/kg, f 16 bpm, FiO2 60% ) , and had a Swan-Ganz catheter inserted. Then, pressure/ volume curves were determined by low-flow method and the lower inflection point pressure was surveyed. Subsequently, parameters of respiratory mechanics and haemodynamics were recorded while periphery and pulmonary artery blood gas analysis were performed when positive end expiratory pressure ( PEEP) were changed. PaO2 /FiO2 and Qsp/Qt were calculated through special formula respectively. Results The progressive PEEP could not change Cst, PaO2 /FiO2 , and PaO2 / ( FiO2 ×Paw) in patients with ARDS significantly ( P gt; 0. 05) . The progressive PEEP did not change Qsp/Qt significantly ( P gt;0. 05) . The Δz which was used to test the difference between the correlation coefficient of Qsp/Qt and PaO2 / ( FiO2 ×Paw) and the correlation coefficient of Qsp/Qt and PaO2 /FiO2 was 0. 571, and there was no difference between the two correlation coefficients ( P gt; 0. 05) . It was not Paw but Cst which impacted on Qsp/Qt and PaO2 /FiO2 . Conclusion PaO2 / ( FiO2 × Paw ) is equal to PaO2 /FiO2 in assessing intrapulmonary shunting of ARDS.
Objective To explore the role of renin-angiotensin system( RAS) in acute lung injury( ALI) /acute respiratory dysfunction syndrome( ARDS) by using amouse cecal ligation and puncture ( CLP)model.Methods The ALI/ARDS animal models were assessed bymeasuring blood gas, wet/dry lung weight ratio( W/D) , and lung tissue histology 18 hours after CLP operation. After the ALI/ARDS models was successfully established, immunohistochemistry, western blotting and radioimmunity were used to investigate the changes of several key enzymes of RAS, such as ACE, ACE2 and Ang Ⅱ. In addition, two groups of animals received a separate intraperitoneal injection of angiotensin-converting enzyme ( ACE) inhibitor captopril or recombinant mouse ACE2 ( rmACE2) after CLP, then the changes of RAS in ALI/ARDS modelswere observed. Results The extensive lung injuries can be observed in the lung tissues from CLP-treated animals 18 hours after operation. The CLP-induced ALI/ARDS led to an increase in the wet/dry weight ratio of the lung tissues, and a decrease in the PaO2 /FiO2 [ ( 194. 3 ±23. 9) mm Hg vs ( 346. 7 ±20. 5) mm Hg,P lt;0. 01] . Immunohistochemistry and western blotting tests of the lung tissues from CLP-treated animals showed a decrease in the ACE2 protein level. However, in both the CLP and sham mice there were no significant differences between the two groups. CLP markedly increased Ang Ⅱ level in lungs and plasma of mice, and RAS drugs significantly impacted the Ang Ⅱ levels of mice. Compared with the CLP group,captopril or rmACE2 led to a decrease of the Ang Ⅱ level in mice [ Lung: ( 1. 58 ±0. 16) fmol /mg,( 1. 65 ±0. 21) fmol /mg vs ( 2. 38 ±0. 41) fmol /mg; Plasma: ( 178. 04 ±17. 87) fmol /mL, ( 153. 74 ±10. 24) fmol /mL vs ( 213. 38 ± 25. 44) fmol /mL] . Conclusions RAS activation is one of the characteristics of CLP-induced ALI/ARDS in mice models. ACE and ACE2 in RAS have a different role in the regulation of AngⅡ synthesis, while ACE has a positive effect in generating AngⅡ, and ACE2 shows a negative effect.
Objective To investigate the role of angiotensin-II type 1 receptor ( AT1) antagonist in treatment of acute lung injury/acute respiratory distress syndrome ( ALI/ARDS) . Methods Animal model of ALI/ARDS was induced by cecal ligation and perforation ( CLP) . ALI/ARDS animals received a separate intraperitoneal injection of several concentrations( 5, 10, 15, 20, 25 mg/kg) of AT1 inhibitor losartan after CLP, then the changes of lung injury and 7-day survival were measured. Results Oxygenation index and lung wet to dry weight ratio ( W/D) showed an improving trend when losartan was administered at doses of 5 to 15 mg/kg in ALI/ARDS rats, but aggravated above the dose of 15 mg/kg. Losartan ( 15 mg/kg) treatment significantly alleviated pulmonary edema after CLP operation, and decreased serumlevels of TNF-α, IL-6, andIL-1β [ TNF-α: ( 554. 1 ±62. 7 ) pg/mL vs. ( 759. 2 ±21. 5 ) pg/mL, P lt; 0. 01; IL-6: ( 1227. 3 ±130. 0) pg/mL vs. ( 2670. 4 ±174. 1) pg/mL, P lt; 0. 01; IL-1β: ( 444. 0 ±38. 6) pg/mL vs. ( 486. 6 ±61. 7)pg/mL, P lt; 0. 05] . 7-day survival rate also increased in losartan treatment group at a dose of 15 mg/kg( 6. 7% vs. 0 ) . Conclusions The AT1 inhibitor, losartan, can significantly prevent lung injury in ALI/ARDS after CLP, and improve the 7-day survival rate.
Objective To investigate the effects of noninvasive ventilation for the treatment of acute respiratory failure secondary to severe acute respiratory syndrome ( SARS) . Methods 127 patients with complete information were collected from the database of SARS in Guangdong province, who were all consistent with the ALI/ARDS diagnostic criteria. The patients were divided into three groups depending on ventilation status, ie. a no-ventilation group, a noninvasive ventilation group, and a mechanical ventilation group. The outcome of ventilation treatmentwas followed up.Multi-factor regression analysis was conducted to analyze the relations of ventilation treatment with ARDS and mortality, and factors associated with success of noninvasive ventilation. Results As soon as the patients met the diagnostic criteria of ALI/ARDS, the patients in the noninvasive ventilation group were in more serious condition and had a higher proportion of ARDS compared with the no-ventilation group ( P lt;0. 01) . The patients in the mechanical ventilation group had a higher mortality rate ( P lt;0.01) . 6 and 7 patients in the no-ventilation group had noninvasive ventilation and invasive ventilation thereafter, respectively. 15 patients in the noninvasive group switched to invasive ventilation. Compared with the patients without ventilation ( n =45) , the patients receiving noninvasive ventilation ( n = 61) were in more serious condition and at higher risk of developing ARDS ( P lt;0. 01) , but the mortality was not different between them ( P gt; 0. 05) . The patients who continued to receive noninvasive ventilation ( n = 40) were in more serious condition, and at higher risk of developing ARDS compared with the patients without ventilation ( n = 45) ( P lt; 0. 01) . 15 patients in the noninvasive group who switched to invasive ventilation were older than those patients continuing noninvasive ventilation.Conclusions For SARS patients fulfilling the ALI/ARDS criteria, the patients underwent noninvasive ventilation are more severe, run a higher probability of developing ARDS from ALI. But earlier initiation of noninvasive ventilation has no impact on mortality. The patients who tolerate noninvasive ventilation can avoid intubation, especially for young patients. However, the time and indication of shifting from noninvasive ventilation to invasive ventilation should be emphasized.