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小核桃小銀蟲 (初入文壇)
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[求助]
重金求助！急啊
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Conclusions The current pathophysiologic scenario of ARDS includes ventilator-induced lung injury as a factor that can worsen the severity of the syndrome. The literature reviewed above documents that spontaneous or mechanical ventilation of normal lungs alters surfactant and increases surface tension, that increased surface tension is necessary and sufficient to cause atelectasis, that atelectasis is augmented by supine positioning and sedation, that constant VT ventilation limits surfactant release from type II pneumocytes and that changes in surfactant occur prior to the onset of ARDS. These findings suggest a new pathophysiologic scenario for ARDS, one in which normal lung regions become atelectatic from the increase in surface tension resulting from spontaneous or mechanical ventilation-induced decreases in surfactant, together with our current approaches to patient positioning and sedation. Spontaneous or mechanical ventilation of these atelectatic regions then causes the initial lung injury via atelectrauma. If the proposed scenario were correct at least some instances of ARDS might be prevented by routinely administering sigh breaths in addition to ventilating with low VTs and at least low levels of PEEP, by avoiding supine positioning, by increasinthe frequency of repositioning and the use of prone or semi-prone positioning, by limiting the use of sedation, and by implementing these changes in practice from the time patients are admitted and/or mechanical ventilation is initiated rather than waiti until ARDS has developed. Although these ideas are supported by considerable literature, they remain hypotheses that require testing in patients at risk for ARDS. |
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【答案】應(yīng)助回帖
★ ★ ★ ★ ★ ★ ★
sltmac: 金幣+2 2012-08-20 21:46:54
小核桃小: 金幣+5, ★有幫助, 已經(jīng)很好啦 2012-08-20 22:16:25
sltmac: 金幣+2 2012-08-20 21:46:54
小核桃小: 金幣+5, ★有幫助, 已經(jīng)很好啦 2012-08-20 22:16:25
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Conclusions 結(jié)論 The current pathophysiologic scenario of ARDS includes ventilator-induced lung injury as a factor that can worsen the severity of the syndrome. 目前急性呼吸窘迫綜合征(ARDS)的病理情況包括呼吸機(jī)相關(guān)性肺損傷，這種損失能造成并發(fā)癥狀的惡化。 The literature reviewed above documents that spontaneous or mechanical ventilation of normal lungs alters surfactant and increases surface tension, that increased surface tension is necessary and sufficient to cause atelectasis, that atelectasis is augmented by supine positioning and sedation, that constant VT ventilation limits surfactant release from type II pneumocytes and that changes in surfactant occur prior to the onset of ARDS. 回顧上述文獻(xiàn)得出，正常肺的自發(fā)或者機(jī)械通風(fēng)能改變肺表面活性物質(zhì)或者改變表面張力，肺表面張力的增強(qiáng)足以導(dǎo)致肺不張，仰臥位或者鎮(zhèn)靜狀態(tài)肺不張癥狀加劇，持續(xù)的潮氣量限制了表面活性物質(zhì)從肺泡的二型肺細(xì)胞中釋放，以及肺表面活性物質(zhì)的改變通常發(fā)生在ARDS發(fā)作之前。 These findings suggest a new pathophysiologic scenario for ARDS, one in which normal lung regions become atelectatic from the increase in surface tension resulting from spontaneous or mechanical ventilation-induced decreases in surfactant, together with our current approaches to patient positioning and sedation. 這些發(fā)現(xiàn)給ARDS提供了一種新的病理可能情況，即由于自發(fā)或機(jī)械通風(fēng)引發(fā)的肺表面活性物質(zhì)的減少以及我們目前正在研究的病人位置和鎮(zhèn)靜狀態(tài)，使得肺表面張力增大，最終導(dǎo)致正常肺部區(qū)域的膨脹不全。 Spontaneous or mechanical ventilation of these atelectatic regions then causes the initial lung injury via atelectrauma. 之后，這些肺不張區(qū)域自發(fā)的或者機(jī)械通風(fēng)經(jīng)由“肺萎陷傷”（不張傷）導(dǎo)致最初的肺損傷。 If the proposed scenario were correct at least some instances of ARDS might be prevented by routinely administering sigh breaths in addition to ventilating with low VTs and at least low levels of PEEP, by avoiding supine positioning, by increasing the frequency of repositioning and the use of prone or semi-prone positioning, by limiting the use of sedation, and by implementing these changes in practice from the time patients are admitted and/or mechanical ventilation is initiated rather than waiting until ARDS has developed. 如果上述提出的病例場(chǎng)景是正確的，除了通過(guò)低潮氣量通風(fēng)和低呼氣末正壓，通過(guò)定期的管理嘆吸氣頻率，通過(guò)避免仰臥位，增加換位頻率和俯臥或半俯臥的置位，通過(guò)限制出現(xiàn)鎮(zhèn)靜狀況，以及在病人確診之后或者機(jī)械通風(fēng)已經(jīng)引起時(shí)而不是在等到ARDS發(fā)作之時(shí)，實(shí)施這些改變， 那么至少一些ARDS的實(shí)例可以得到阻止 Although these ideas are supported by considerable literature, they remain hypotheses that require testing in patients at risk for ARDS. 盡管這些想法得到很多文獻(xiàn)支持，但仍屬于臆測(cè)，需要通過(guò)在出于ARDS狀況的病人身上進(jìn)行測(cè)試驗(yàn)證。 |
6樓2012-08-20 18:44:57
8814402
至尊木蟲 (職業(yè)作家)
- 翻譯EPI: 509
- 應(yīng)助: 18 (小學(xué)生)
- 貴賓: 0.381
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- 蟲號(hào): 1184404
- 注冊(cè): 2011-01-06
- 專業(yè): 藥物學(xué)其他科學(xué)問(wèn)題
2樓2012-08-20 16:03:31
xxx3612
金蟲 (正式寫手)
- 翻譯EPI: 1
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- 金幣: 2791.6
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- 注冊(cè): 2012-05-12
- 性別: GG
- 專業(yè): 運(yùn)籌與管理
【答案】應(yīng)助回帖
sltmac: 金幣-5, 本版禁止機(jī)器翻譯，請(qǐng)應(yīng)助前仔細(xì)閱讀版規(guī) 2012-08-20 21:46:43
sltmac: 違規(guī)存檔 2012-08-20 21:47:02
小核桃小: 金幣+5, 翻譯EPI+1, ★有幫助, 還是不夠好，謝謝 2012-08-20 22:15:43
sltmac: 違規(guī)存檔 2012-08-20 21:47:02
小核桃小: 金幣+5, 翻譯EPI+1, ★有幫助, 還是不夠好，謝謝 2012-08-20 22:15:43
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用有道翻譯，雖然不太標(biāo)準(zhǔn)，但是你稍微改一下就好了 結(jié)論 當(dāng)前的病理生理的場(chǎng)景包括通風(fēng)機(jī)誘導(dǎo)肺的ARDS 受傷是一個(gè)因素,可以進(jìn)一步惡化的嚴(yán)重性綜合癥。一文獻(xiàn)回顧上述文件,自發(fā)或機(jī)械通風(fēng)的正常肺改變表面活性劑和增加表面張力,提高表面張力是必要的,足以引起肺不張、肺不張,增強(qiáng)了懶散的定位和鎮(zhèn)靜,常數(shù)VT通風(fēng)限制表面活性劑從II型pneumocytes釋放,改變發(fā)生在表面活性劑爆發(fā)之前,ARDS。這些發(fā)現(xiàn)提出了一個(gè)新的ARDS病理生理的場(chǎng)景,一個(gè)正常的肺萎陷地區(qū)成為從增加的表面張力源于自發(fā)或機(jī)械通氣誘導(dǎo)減少表面活性劑,連同我們當(dāng)前的方法來(lái)定位和鎮(zhèn)靜病人。自發(fā)或機(jī)械通風(fēng)的這些萎陷地區(qū)然后導(dǎo)致最初通過(guò)atelectrauma肺損傷。如果提出的場(chǎng)景是正確的,至少一些實(shí)例可以預(yù)防的ARDS通過(guò)定期 管理嘆息呼吸除了通風(fēng)與低變形機(jī)和至少低水平的窺視,通過(guò)避免仰臥的定位,通過(guò)increasinthe頻率的重新定位和使用容易或半容易定位,通過(guò)限制使用鎮(zhèn)靜,通過(guò)實(shí)現(xiàn)這些變化實(shí)際上從病人承認(rèn)和/或機(jī)械通風(fēng)啟動(dòng)而不是waiti直到ARDS已經(jīng)開發(fā)了。雖然這些想法都支持相當(dāng)大的文學(xué),他們?nèi)匀恍枰獪y(cè)試假設(shè)在危險(xiǎn)的患者ARDS。 |
3樓2012-08-20 17:11:58
4樓2012-08-20 17:40:27
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