Question

50分那翻译 在追加30分

INTRODUCTION
Only in recent years has the significance of ventilator-induced lung injury (VILI) been appreciated. This is largely because the pathology of VILI is inseparable from that of acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). VILI must be studied in animal experiments to view its pathophysiology and progression in isolation.It is now apparent that the “natural history” of acute respiratory failure is greatly influenced by the manner in which the lung is ventilated and that VILI contributes to the pathology of respiratory failure.

AVOIDANCE OF VENTILATOR-INDUCED LUNG INJURY
The pressure volume curve of the lung has both upper and lower inflection points. The lower inflection point is the pressure at which lung volume begins to decline sharply with falling airway pressure. This represents the pressure below which atelectasis rapidly accumulates during deflation. The upper inflection point is the pressure at which lung volume ceases to increase sharply with rising airway pressure. This represents the pressure at which the lung begins to stiffen and over distend during inflation. Lung injury might be avoided by ventilating the lung at a PEEP above the lower inflection point, to prevent opening and closure of alveoli, while restricting
tidal volume so that end-inspiratory pressure does not exceed the upper inflection point. This regimen has been shown to reduce mortality in a small clinical trial published by Amato et al . Prevention of “barotrauma” by restricting peak inspiratory pressure was suggested by Hickling as early as 1984. His strategy, permissive hypercapnia , entailed limiting peak pressure, which directly reduced tidal volume. It was, in fact, a “volutrauma” prevention regimen. He simply ignored PaCO2 to the extent that was tolerated by the patient. Roupie et al subsequently showed that, as tidal volume increased, the percent of patients with acute respiratory distress syndrome who had peak inspiratory pressure in excess of the upper inflection point also increased . In 1999, the NIH ARDS Network Trial showed that, by decreasing tidal volume from 12 ml/kg to 6 mL/kg, the mortality rate of the acute respiratory distress syndrome was reduced from 40 % to 30 % . This study has been interpreted to support the importance of ventilating at airway pressures below the upper inflection point.
通顺点 一起给80分哈
机器翻译 能搞通顺也算你本事
我从PDF上下的 。。。
美国一个医院的医生写的一篇论文中的一部分

Answer 1

元照英美法来了！

引言

只有在最近几年，呼吸机所致肺损伤(VILI)的严重性才引起了人们的高度重视。这主要是因为呼吸机所致肺损伤的病症与急性呼吸窘迫综合征（ARDS）和急性肺损伤（ALI）的病症具有不可分性。VILI的研究必须使用动物实验，去观察病理生理学机理和其独立的病理发展进程。如今，已经明确的是，急性呼吸衰竭的发展过程主要受肺的呼吸方式，并且呼吸机所致肺损伤（VILI）对呼吸衰竭的病理有一定的影响。

避免呼吸机所致肺损伤
肺的压力容积曲线有上下两个拐点。下拐点是肺活量与气道压力同时开始急速下降时，气道所产生的压力。这显示的是肺在不扩张的状态下积聚在通道的压力；上拐点是肺活量与气道压力突然停止上升所产生的压力，这显示的是肺在扩展状态下变硬和扩张的压力。通过小孔于下拐点之上对肺充气，防止肺泡张开和关闭，同时限制呼气量，以致最终呼吸压力不超过上拐点，这样也许能防止肺损伤。阿玛托等人公开的小型临床试验显示，该种治疗法能减少肺损伤的死亡率。

早在1984年，赫克林已提出，通过阻止吸气到达峰值能防止气压性损伤。赫克林有关容许性高碳酸血症的方法是，必须限制峰值，其能直接减少正常呼气量。此方法其实也是容积伤的防治法。他只是在一定程度上忽略了病人所能容忍的动脉血。鲁皮等人后来发现，随着正常呼气量的提高，患急性呼吸窘迫综合症的比例也提高了，这些病人呼吸超过了上拐点，同时呼吸压力到达了峰值。

在1999年，美国国家卫生院的有关急性呼吸窘迫综合症的网络实验显示，通过把正常呼吸量从12毫升/千克降到6毫升/千克，急性呼吸窘迫综合症的死亡率从40%降到了30%。该项研究被解读为支持了这样一种观点，即在气道之上拐点以下呼吸的重要性。

Answer 2

the first friend has given good understanding and translation. he did a good job. i have no time to do the long translation.

Answer 3

我晕，这是英文吗？我没法翻译。全不通顺。

Answer 4

导言

只是在近几年的意义呼吸机所致肺损伤（损伤）的赞赏。这主要是因为病理损伤是分不开的急性呼吸窘迫综合征（ ARDS ）和急性肺损伤（ ALI ） 。损伤必须研究在动物实验中，以检视其病理生理和进展isolation.It现在明显的是， “自然历史”急性呼吸衰竭是很大影响的方式，是肺通气和损伤有助于病理呼吸衰竭。
避免呼吸机所致肺损伤

压力容积曲线肺既有上下拐点。低拐点的压力是在肺容积的衰落就开始了大幅下降气道压力。这是压力，低于这个迅速积聚在肺不张通货紧缩。拐点上的压力是在肺容积不再急剧增加与气道压力上升。这是压力，其中肺癌开始变硬和扩张过程中的通货膨胀。急性肺损伤可能避免通风肺偷看以上的低拐点，以防止开放和关闭肺泡，同时限制
潮气量，以便最终吸气压力不超过上拐点。这个方案已经显示出，以减少死亡率的一个小型的临床试验发表的达马托等人。防止“压伤”限制吸气峰压建议希克林早在1984年。他的策略，允许性高碳酸血症，需要限制峰值压力，这直接降低潮气量。事实上，一个“ volutrauma ”预防方案。他完全忽视动脉血的范围是不能容忍的病人。 Roupie等人随后表明，作为潮气量增加，患者的百分之急性呼吸窘迫综合征谁了吸气峰压超过上拐点也有所增加。 1999年，美国国立卫生研究院ARDS的网络测试表明，通过降低潮气量从12毫升/公斤至6毫升/公斤，死亡率的急性呼吸窘迫综合征减少40 ％至30 ％ 。这项研究已被解释为支持的重要性，通风在气道压力低于上拐点。

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