doc08
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1) UW says in adults in aspirin toxicity after the respiratory alkalosis in the acute stage, later stage will show mixed primary metabolic acidosis and primary resp alkalosis !!!!!
as far as i know, metabolic acidosis and resp alkalosis cannot coexist am i right? is UW wrong?
(step 1 kaplan says high therapeutic dose causes respiratory alkalosis and toxic doses will cause respiratory acidosis and metabolic acidosis)
2) also to diagnose a mixed disorder the CO2 and HCO3 must change in opposite directions right ???
can anyone please explain?
thanks in advance
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| dr in trouble
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Resp alkalosis is compensation for metabolic acidosis, so u can see both together.
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| doyoudig
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Asprirn Toxicity:
In Adults - Primary Metabolic Acidosis + Primary Resp Alkalosis -- Mixed
In Child - Primary Metabolic Acidosis + Compenation w/ Resp Alkalosis -- Compensated
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| doc08
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i understand that as a compensation for metabolic acidosis , respiratory alkalosis can occur, but UW words it as primary alkalosis and not compensated alkalosis????
though in high therapuetic doses aspirin causes resp alkalosis , IN toxic doses aspirin will inhibit respiarory center and it should cause respiratory acidosis and not resp alkalosis, any thoughts on this?
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| dr in trouble
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ASPIRIN causes uncoupling of oxidative phosphorylation. More oxygen is consumed and more CO2 is produced which leads to activation of resp rester cause Resp alkalosis. Then metabolic acidosis develops due to build up of acid which leads to metabolic acidosis and finally compensated resp alkalosis develops in response to metabolic acidosis.
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| ssrpk
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well if you read the explanation in UW it gives very interesting explanation which can be understood by taking into consideration winter's formula which gives approximate values of PCO2 as a result of compensation in metabolic acidosis
for eg: if HCO3 level falls to 16, expected compensatory PCO2 level should be 32mmHg as calculated by winter's formula [HCO3X1.5 + 8], now in case of aspirin toxicity with HCO3 level opf 16 if PCO2 is 32, we''ll call it compensated resp.alkalosis which is typically the case with peds group, however if the level of PCO2 is far below 32mmHg then its obvious that all the decrease is not attributable to a compensatory response, rather there is a primary factor playing a role too.
Be careful
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| doc08
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thanks guys !!!!!!! makes sense
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