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submitted by haliburton(192),
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ekiiwdapi ogsp:l(aei)o The mpseoehrat si soedcmop fo 7%8 ngrnieto and 12% xoeyn.g ciSen ygnoxe is hagecdexn ta the ellaycpv-iilalroa m,mnerabe otgennri is a jomra cmnnpoeto ofr eht siavle'ol steat fo iniltnoaf. If a raegl ulmveo of irngoten ni the sugnl si carleepd hiwt nxgeo,y the xnoyeg yma unbssleutyeq eb srdboabe tnoi eth ,oobld edrinugc het molevu fo the ,lliveoa esgtnilur in a fmro of lrvoalae epaolslc nnwko as bospairtno aaeiststecl.

I hecso ingdariecco e,eadm tub I elbeive shit is reocncirt aseuecb reeht si no hatre erafuli rsik ta sthi time, so hte speoupr fo eht EEPP is reanitylc ont to ushp tuo f.dliu

bighead478  doesn't there have to be an airway obstruction (mucus, foreign object etc.) in order for this to happen? 100% O2 without any airway obstruction should not cause absorption atelectasis, right? +  
iloveallpotatoes  And Tension Pneumothorax is wrong bc PEEP would furthur exacerbate that. +1  
hyperfukus  @iloveallpotatoes yea i realized that now after getting it wrong :( +  
plzhelp123  @bighead478, they are using a cuffed endotracheal tube and mechanically ventilating this patient which is creating an iatrogenic "obstruction" and as @haliburton mentioned, having a high FiO2 leads to over-absorption by the blood which leads to absorption atelectasis if no other gas is allowed to enter/there is no communication with atmospheric pressure during expiration. Thus, we add positive end-expiratory pressure which keeps alveoli open at the end of expiration to prevent collapse +