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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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too long, only ask help for the sentences that you really can't understand,ok?
2Â¥2012-08-20 16:03:31
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СºËÌÒС: ½ð±Ò+5, ¡ïÓаïÖú, ÒѾ­ºÜºÃÀ² 2012-08-20 22:16:25
Conclusions
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The current pathophysiologic scenario of ARDS includes ventilator-induced lung injury as a factor that can worsen the severity of the syndrome.
Ŀǰ¼±ÐÔºôÎü¾½ÆÈ×ÛºÏÕ÷(ARDS)µÄ²¡ÀíÇé¿ö°üÀ¨ºôÎü»úÏà¹ØÐÔ·ÎËðÉË£¬ÕâÖÖËðʧÄÜÔì³É²¢·¢Ö¢×´µÄ¶ñ»¯¡£
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.  
»Ø¹ËÉÏÊöÎÄÏ׵óö£¬Õý³£·ÎµÄ×Ô·¢»òÕß»úеͨ·çÄܸıä·Î±íÃæ»îÐÔÎïÖÊ»òÕ߸ıä±íÃæÕÅÁ¦£¬·Î±íÃæÕÅÁ¦µÄÔöÇ¿×ãÒÔµ¼Ö·β»ÕÅ£¬ÑöÎÔλ»òÕßÕò¾²×´Ì¬·Î²»ÕÅÖ¢×´¼Ó¾ç£¬³ÖÐøµÄ³±ÆøÁ¿ÏÞÖÆÁ˱íÃæ»îÐÔÎïÖÊ´Ó·ÎÅݵĶþÐÍ·Îϸ°ûÖÐÊÍ·Å£¬ÒÔ¼°·Î±íÃæ»îÐÔÎïÖʵĸıäͨ³£·¢ÉúÔÚARDS·¢×÷֮ǰ¡£
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.
ÕâЩ·¢ÏÖ¸øARDSÌṩÁËÒ»ÖÖеIJ¡Àí¿ÉÄÜÇé¿ö£¬¼´ÓÉÓÚ×Ô·¢»ò»úеͨ·çÒý·¢µÄ·Î±íÃæ»îÐÔÎïÖʵļõÉÙÒÔ¼°ÎÒÃÇĿǰÕýÔÚÑо¿µÄ²¡ÈËλÖúÍÕò¾²×´Ì¬£¬Ê¹µÃ·Î±íÃæÕÅÁ¦Ôö´ó£¬×îÖÕµ¼ÖÂÕý³£·Î²¿ÇøÓòµÄÅòÕͲ»È«¡£
Spontaneous or mechanical ventilation of these atelectatic regions then causes the initial lung injury via atelectrauma.
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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.  
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Although these ideas are supported by considerable literature, they remain hypotheses that require testing in patients at risk for ARDS.
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