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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. |

木蟲 (正式寫手)
| 目前ARDS的生理病理機(jī)制涵蓋了呼吸機(jī)相關(guān)性肺損傷,肺損傷又能進(jìn)一步加重ARDS。自主或者機(jī)械通氣可改變正常肺的表面活性物質(zhì)并增加肺泡表面張力,當(dāng)肺泡表面張力存在并到達(dá)一定程度后就會(huì)引起肺萎陷;在仰臥位狀態(tài)下注射鎮(zhèn)定劑也可引起肺萎陷;恒定的潮氣量限制了表面活性物質(zhì)從Ⅱ型肺泡細(xì)胞釋放,并且在ARDS之前就已發(fā)生此種改變。綜合以上結(jié)果,再結(jié)合我們目前的研究思路,揭示了ARDS一種新的病理生理情況,由于ICU或EICU對(duì)于病人的體位的限制及鎮(zhèn)靜藥物的使用,增加了肺泡表面張力,繼而導(dǎo)致了正常的肺萎陷。在這些肺萎陷的區(qū)域,自主或者機(jī)械通氣導(dǎo)致的不張傷是造成肺損傷的最初原因。如果現(xiàn)實(shí)中的情況正如Albert RK等人預(yù)測(cè)的那樣,除了采用常規(guī)的嘆息方式,低潮氣量和低水平PEEP使空氣流動(dòng)外,患者應(yīng)避免仰臥,增加翻身的頻率并采用俯臥或半俯臥方式,減少鎮(zhèn)定劑的使用,一經(jīng)確診的和/或開始進(jìn)行機(jī)械通氣的病人應(yīng)立即采用以上措施,而不是坐以待斃。該設(shè)想的與臨床呼吸機(jī)應(yīng)用患者的實(shí)際情況的一致性仍有待進(jìn)一步進(jìn)行臨床實(shí)驗(yàn)證明。 |
至尊木蟲 (職業(yè)作家)
金蟲 (正式寫手)
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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,通過避免仰臥的定位,通過increasinthe頻率的重新定位和使用容易或半容易定位,通過限制使用鎮(zhèn)靜,通過實(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。 |

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