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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. |

榮譽(yù)版主 (文壇精英)
有愛(ài)的二哥
| 目前ARDS的生理病理情況包括人工呼吸器造成的肺部損傷,肺部損傷又能進(jìn)一步加重綜合癥病情。根據(jù)以上文獻(xiàn)報(bào)道,正常肺部的自發(fā)呼吸以及機(jī)械通氣可改變肺部表面作用劑并增加表面張力,當(dāng)表面張力存在并到達(dá)一定程度后就會(huì)引起肺萎縮,同時(shí),在仰臥定位狀態(tài)下注射鎮(zhèn)定劑也可引起肺萎縮。 保持空氣持續(xù)流通可減、蛐头闻菁(xì)胞表面作用劑的釋放并在ARDS發(fā)病前使表面作用劑發(fā)生變化。綜合以上結(jié)果,再結(jié)合我們目前的研究思路——即對(duì)病人在仰臥定位下注射鎮(zhèn)定劑,揭示了ARDS一種新的病理生理情況,自發(fā)呼吸或機(jī)械呼吸可導(dǎo)致肺泡細(xì)胞表面作用劑的減少,表面作用劑的減少導(dǎo)致表面張力的增加,表面張力的增加導(dǎo)致正常肺區(qū)的萎縮。 對(duì)肺不張區(qū)域進(jìn)行自發(fā)或機(jī)械通氣引起的剪切力作用是造成肺損傷的最初原因。如上述情況在某種程度上正確,除了采用低速VTs和最低速PEEP使空氣流動(dòng)外,通過(guò)采用呼吸方式也可能預(yù)防ARDS,如避免仰臥,增加復(fù)位頻率并采用俯臥或半俯臥方式、補(bǔ)充減少鎮(zhèn)定劑的使用,補(bǔ)充經(jīng)確診的或和開(kāi)始進(jìn)行機(jī)械呼吸的病人的臨床變化情況,而不是坐等ARDS的發(fā)生。盡管以上觀點(diǎn)有文獻(xiàn)支持,但仍為猜測(cè),需進(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(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(kāi)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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