Aspirin; Respiratory Acidosis or Respiratory Alkalosis? - USMLE Forums
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Old 09-22-2012
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Drug Aspirin; Respiratory Acidosis or Respiratory Alkalosis?

A 26 yr old woman brought to emergency depratment 3 hr after ingesting 50 aspirin tablets in suicide attempt. She is nauseated, confused and sleepy. Pulse 130/min, respiration 30/min, BP 100/60 mmHg. Which following lab value is most likely on evaluation of blood obtained before treatment?

Serum HCO3 -- PH -- PCO2
A in -- de -- in
B de -- de -- de
C in -- in -- de
D de -- de -- in
E in -- in -- in

Answer is B. What I know is that in acute aspirin poisoning, at first, respiratory center is depressed, so PCO2 should be increased. But why decreased here?
Thank for explanation
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Old 09-22-2012
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Aspirin poisoning --> metab acidosis w/ increase anion gap-->LOW pH_---> H stimulate-->respiratory center--> increase respiratory frequency-->decrease CO2
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Old 09-22-2012
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Quote:
Originally Posted by Fuser00 View Post
Aspiriin poisoning --> metab acidosis w/ increase anion gap-->LOW pH_---> H stimulate-->respiratory center--> increase respiratory frencuency-->decrease CO2
Thank,yes, its right. but in some question, at very first, the respiratory center is depress that lead to reduce Co2 and then low pH , H stimulate respiratory center. I found two questions regarding this, how can I differentiate between two? because in first question, i chose decrease CO 2 and then it false and 2nd is this question.
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Old 09-22-2012
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aspirin overdose---- metabolic acidosis--- pH decrease---- compensatory respiratory alkalosis (pCO2- decrease)
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Old 09-22-2012
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Quote:
Originally Posted by koolkiller88 View Post
aspirin overdose---- metabolic acidosis--- pH decrease---- compensatory respiratory alkalosis (pCO2- decrease)
i don't think so....coz from many sources i came to know that it's initial resp.alkalosis(hyperventilation) is seen..which eventually lead to met. acidosis(as aspirin is acid)...
i myself got this doubt when i did this question.......thanks for asking.....im eagerly waiting for the explanation
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Old 09-22-2012
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Originally Posted by venky2600 View Post
i don't think so....coz from many sources i came to know that it's initial resp.alkalosis(hyperventilation) is seen..which eventually lead to met. acidosis(as aspirin is acid)...
i myself got this doubt when i did this question.......thanks for asking.....im eagerly waiting for the explanation
Ya just now I also read this reasoning in wiki.
And I think this makes more sense.
But in both way HCo3- will be dec. pH will be dec and pCo2 will be dec too.


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Quote:
Originally Posted by koolkiller88 View Post
Ya just now I also read this reasoning in wiki.
And I think this makes more sense.
But in both way HCo3- will be dec. pH will be dec and pCo2 will be dec too.


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then how come it's called resp. alkalosis...?
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Old 09-22-2012
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What Kaplan says

Aspirin in high Rx dose--- mild uncoupling of Oxidative phosphorylayion -- increased RR -- respiratory alkalosis -- usually compensated

Aspirin at toxic dose - 1) respiratory depression-- resp acidosis; and 2) severe uncoupling of Oxidative phosphorylayion --- metabolic acidosis

In this case respiration is not suppressed RR is 30/min
Pco2 will decrease so left with B n C

Toxic dose likely to cause Met acidosis so I ll go with B

wonder why resp is not suppressed at toxic dose!!,??
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Old 09-23-2012
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to distinguish between the two case i suggest u to look to the RR....

if RR low it is respiratory acidosis so pH will be decreased and because kidneys need at least a couple of hours to compensate , HCO3 would still the same. so it is acute aspirin intoxication.

if RR high it is respiratory alkalosis so pH will be increased. and because it is long lasting, kidneys can compensate so HCO3 would be decreased. so it is not acute.

so the RR is your key for aspirin intoxication.
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Old 09-23-2012
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I think here is the timing after ingestion very important. If the presentation was the same but 1h after ingestion, I would go with:

Serum HCO3 -- PH -- PCO2
de -- in -- de

due to respiratory alkalosis.

As the amount of absorbed acetylsalicyc acid* increases, metabolic acidosis developes instead.
* it's acid, that's why metabolic acidos with increased anion gap.

Rookie: Do you think that the mechanism for met. acidosis is severe uncoupling of Oxidative phosphorylayion?
Aspirin is an uncoupler, but with decreased H+ gradient, thus increased NADH ->NAD + H, thus decreased NADH/NAD ratio, I would expect decreased lactate, and I don't see the point for metabolic acidosis. Can you explain it a bit please?
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Old 09-23-2012
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[QUOTE=Rookie;149362]What Kaplan says

Aspirin in high Rx dose--- mild uncoupling of Oxidative phosphorylayion -- increased RR -- respiratory alkalosis -- usually compensated

Aspirin at toxic dose - 1) respiratory depression-- resp acidosis; and 2) severe uncoupling of Oxidative phosphorylayion --- metabolic acidosis

In this case respiration is not suppressed RR is 30/min
Pco2 will decrease so left with B n C

Toxic dose likely to cause Met acidosis so I ll go with B


nice explanation but this patient took toxic dose(50 tabs is toxic dose,10 tabs can be consudered high dose)
this pxt should therfore have respiratory depression--->respiratory acidosion,high co2,low ph.
at presention,HCO3 should still be normal in acute state,it takes the kidney 3-5days to compensate.
something is wrong somewhere with the question/answer
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[QUOTE=chux;149452]
Quote:
Originally Posted by Rookie View Post
What Kaplan says

Aspirin in high Rx dose--- mild uncoupling of Oxidative phosphorylayion -- increased RR -- respiratory alkalosis -- usually compensated

Aspirin at toxic dose - 1) respiratory depression-- resp acidosis; and 2) severe uncoupling of Oxidative phosphorylayion --- metabolic acidosis

In this case respiration is not suppressed RR is 30/min
Pco2 will decrease so left with B n C

Toxic dose likely to cause Met acidosis so I ll go with B


nice explanation but this patient took toxic dose(50 tabs is toxic dose,10 tabs can be consudered high dose)
this pxt should therfore have respiratory depression--->respiratory acidosion,high co2,low ph.
at presention,HCO3 should still be normal in acute state,it takes the kidney 3-5days to compensate.
something is wrong somewhere with the question/answer
Answer right this is from official usmle.org
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Old 09-23-2012
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First: Resp Alkalosis: Direct stimulation ASA in respiratory centers...then Second: Metabolic Acidosis (Accumulation of Lactid Acid)...The starting problem is Resp Alkalosis so most of the time you will find the case in Alkalosis or in a Mixed Resp Alkalosis and Met Acidosis, the second case will have a slight alkalotic pH also, close to normal but alkalotic anyways; because the body never overcompensate or even compensate, the starting problem is reflected in the pH.

Acid-base abnormalities
— A variety of acid-base disturbances can occur with salicylate intoxication. Salicylates stimulate the respiratory center directly, resulting in an early fall in the PCO2 and respiratory alkalosis . An anion-gap metabolic acidosis then follows, due primarily to the accumulation of organic acids, including lactic acid and ketoacids . (See "Approach to the adult with metabolic acidosis").

The net effect of these changes is that most adults have either a respiratory alkalosis or a mixed respiratory alkalosis-metabolic acidosis; pure metabolic acidosis is unusual in adults , but it may be seen in children who are brought to medical care soon after ingestion. Acute respiratory acidosis is rare in the early stages of aspirin toxicity, but it may be seen in later stages of profound poisoning. Respiratory acidosis that occurs early in the course of aspirin poisoning should suggest coingestion with a respiratory depressant. Approximately one-third of adults who self-poison ingest one or more other medications, many of which are respiratory depressants
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Old 09-23-2012
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Quote:
at presention,HCO3 should still be normal in acute state,it takes the kidney 3-5days to compensate.
something is wrong somewhere with the question/answer
No it should Not...
because aspirin is an acid, which instantly after getting to blood couples with HCO3 and lower it...
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