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Welcome to noselex’s page.
Contributor score: 5

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 +1  (nbme22#38)
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I dannsedrut seepl aeapn lwduo eucsa hypaixo nad ansierce in SNS ia.ityvct oS trmtnteae wuold eurced PB adn etrHa etRa. I asw tkcus ebwetne teh two to.pnsio hyW asw eht srwane dolbo erseurps adn tno H?R I eooggld udoanr a tbi dan nufod stuesid hatt wsho prdo ni htbo HR and P.B I suges PB srdpo more? naC omensoe seeapl iaplen.x

madeforupvoting2  CPAP increases intrapleural pressure as the elevated airway pressure is transmitted to other things in the cavity (lung pushes on pleural space/cavity which can then push on other structures). This can lead to compression of veins, including the vena cava -> decreased venous return -> decreased bp (from decreased preload). This is similar to what happens during valsalva (exertion phases) though the positive pressure is provided by a machine pump instead of abdominal muscles/diaphragm. I think heart rate likely increases instead of decrease as a compensatory response. Here’s one site that explains it well (the “free” content is enough and probably already exceeds the depth one might need to know) +3
apolla24  I guess since changes in HR are such a transient phenomenon and you only have sustained increase in HR when exercising or like acutely experiencing some medical emergency vs BP that can be elevated for long periods of times with no effects. Therefore an improvement in BP is more important. That’s my take. +

 +3  (nbme22#45)
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xeotrD vs od:Ciene tBho era nttusisiav,se tub xretod is remo fo NMAD atisnog htta oals ahs odioip gsinato vciaityt. tDoexr is enoft dsubea ot egt a imalris uto fo byod lfgenie edu ot its ANDM soigatn .fectef iedeoCn on teh other hreto is a ullnf-o oiiopd nisa.tgo It’s lsao deus as ai,n-tlrdhiraae so siaopnintoct si eryv mnoocm adevres ectef.f

moiroipTut is owrgn suebaec ’tsi tno na atnsiuevsti. l,sAo ’its an tlinaircingheco hiwch is (1) naddoirneitcatc in eyldelr snuels larely catn,ieddi (2) a ducwlne-lmdotee cnlitrcoinhaeig feetfc si ionoatt.ncips

pparalpha  According to Sketchy and Amboss: dextromethorphan is a weak opioid receptor AGONIST and NMDA receptor ANTAGONIST (it's not an agonist). +5

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submitted by gribear(0),
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aCn nooseme xenpail hwy nwhe uoy tscrntea eth aplsni cdor epurisro ot the lelev of ciastpmyeht lfuoowt -- nad yuo etg a mcsstyei iofitcenn -- eht neproses is atreoltain fo hte ohitrtetmsac set ?ontip

its_raining_jimbos  So I chose that one because set point is controlled by the hypothalamus (PGE2 and IL-1 mediate fever in the hypothalamus) and the rest of the answer choices involved something below the level that has been transected. Not 100% sure if that’s accurate though. +3  
noselex  Agreed with @its_raining_jimbos -- Fever is mediated by altering set point in hypothalamus. All the other choices, as far as I can tell, involve sympathetic nerves and their effects at target organs. +1