Aspirin Toxicity

[aspiringmd1015]

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Hey guys, little confused on my aspirin concepts. We all know its an uncoupler of Oxidative Phospho, but was wondering how this can increase your respiration causing resp alkalosis?

 

[Jabbed]

Hey guys, little confused on my aspirin concepts. We all know its an uncoupler of Oxidative Phospho, but was wondering how this can increase your respiration causing resp alkalosis?

Aspirin toxicity has two main physiologic effects:

1. The respiratory effects of salicylism are due to stimulation of the respiratory center in the medulla mediated by aspirin's effects on prostaglandins. This respiratory stimulation induces hyperventilation and respiratory alkalosis.

2. ASA's uncoupling effects on the ETC induce hyperthermia and metabolic acidosis.

Initial presentation is respiratory alkalosis followed by fever and metabolic acidosis develops later. Incidentally, can you see why aspirin toxicity is such an easy diagnosis to miss? Hyperthermia, metabolic acidosis, and tachypnea in an older patient looks identical to sepsis.

 

[FalconSlice]

Aspirin toxicity has two main physiologic effects:

1. The respiratory effects of salicylism are due to stimulation of the respiratory center in the medulla mediated by aspirin's effects on prostaglandins. This respiratory stimulation induces hyperventilation and respiratory alkalosis.

2. ASA's uncoupling effects on the ETC induce hyperthermia and metabolic acidosis.

Initial presentation is respiratory alkalosis followed by fever and metabolic acidosis develops later. Incidentally, can you see why aspirin toxicity is such an easy diagnosis to miss? Hyperthermia, metabolic acidosis, and tachypnea in an older patient looks identical to sepsis.

Also to mention that aspirin (aka ASA- acetylsalicylic ACID) is obviously an acid. Taking acid gives you AG-met acidosis. Another layer for you.

 

[Jabbed]

Also to mention that aspirin (aka ASA- acetylsalicylic ACID) is obviously an acid. Taking acid gives you AG-met acidosis. Another layer for you.

Technically yes, but the exogenous acetylsalicylic acid is actually quantitatively less important than the lactic acid that it induces the production of.

 

[FalconSlice]

Technically yes, but the exogenous acetylsalicylic acid is actually quantitatively less important than the lactic acid that it induces the production of.

Not arguing with you, just adding on. As I said "Another layer." It also helps to generally think of any addition of acid to cause ag-acidosis

 

[Jabbed]

Not arguing with you, just adding on. As I said "Another layer." It also helps to generally think of any addition of acid to cause ag-acidosis

Not arguing with you either, just clarifying 🙂

 

[aspiringmd1015]

how does the hyperthermia induce metabolic acidosis?

 

[dfib slim]

how does the hyperthermia induce metabolic acidosis?

It doesn't. Both hyperthermia and metabolic acidosis are manifestations of the oxphos uncoupling. Uncoupled oxphos-->less ATP generated-->increased anaerobic respiration-->increased lactic acid-->metabolic acidosis.

 

[aspiringmd1015]

Aspirin toxicity has two main physiologic effects:

1. The respiratory effects of salicylism are due to stimulation of the respiratory center in the medulla mediated by aspirin's effects on prostaglandins. This respiratory stimulation induces hyperventilation and respiratory alkalosis.

2. ASA's uncoupling effects on the ETC induce hyperthermia and metabolic acidosis.

Initial presentation is respiratory alkalosis followed by fever and metabolic acidosis develops later. Incidentally, can you see why aspirin toxicity is such an easy diagnosis to miss? Hyperthermia, metabolic acidosis, and tachypnea in an older patient looks identical to sepsis.

so from what ive read, the hyperventilation and resp alk are due to the increased 02 consumption with increasing the rate of the ETC, which will trigger hyperventilation and thus resp alk.
so is it a direct effect? this is what becker pharm states.

 

[cs24]

Warning- free 150 spoiler alert below

Question on the aspirin physio question (#48). How much time should pass before we assume the predominant respiratory alkalosis gives way to a predominately metabolic acidosis? The question had a lady 3 hr post aspirin OD and the answer was low pCO2, low pH, and low bicarb.

I picked low pCO2, high pH, and high bicarb because I remembered goljan saying it was initially alkalosis followed by acidosis, and it had only been three hours so I went with the high pH. However, now I am wondering if the key is that the bicarb would be low regardless due to addition of acid (the only answer with low pCO2 and low bicarb also had low pH). Anyone with more insight on this? Am I missing something obvious?

 

[Jabbed]

Warning- free 150 spoiler alert below

Question on the aspirin physio question (#48). How much time should pass before we assume the predominant respiratory alkalosis gives way to a predominately metabolic acidosis? The question had a lady 3 hr post aspirin OD and the answer was low pCO2, low pH, and low bicarb.

I picked low pCO2, high pH, and high bicarb because I remembered goljan saying it was initially alkalosis followed by acidosis, and it had only been three hours so I went with the high pH. However, now I am wondering if the key is that the bicarb would be low regardless due to addition of acid (the only answer with low pCO2 and low bicarb also had low pH). Anyone with more insight on this? Am I missing something obvious?

The answer choice that you picked would describe A) a mixed respiratory alkalosis AND metabolic alkalosis or B) a compensated

Here's a timeline:
1. Uncompensated respiratory alkalosis: high pH, low pCO2, normal bicarb
2. Uncompensated respiratory alkalosis AND compensated metabolic acidosis: ~normal to low pH, low pCO2, low bicarb
3. Decompensated metabolic acidosis: low pH, high pCO2, low bicarb

It's important to note that due to the acute nature of salicyclism you will not be able to compensate for the respiratory alkalosis. Also be aware that your pH can actually be reasonably close to 7.4 due to the opposing acidosis/alkalosis (a pH of exactly 7.4 is actually suggestive of mixed acid/base disorder).

 

[pd1112]

Warning- free 150 spoiler alert below

Question on the aspirin physio question (#48). How much time should pass before we assume the predominant respiratory alkalosis gives way to a predominately metabolic acidosis? The question had a lady 3 hr post aspirin OD and the answer was low pCO2, low pH, and low bicarb.

I picked low pCO2, high pH, and high bicarb because I remembered goljan saying it was initially alkalosis followed by acidosis, and it had only been three hours so I went with the high pH. However, now I am wondering if the key is that the bicarb would be low regardless due to addition of acid (the only answer with low pCO2 and low bicarb also had low pH). Anyone with more insight on this? Am I missing something obvious?

I haven't seen the question, but I'm assuming the choices could be ruled out based on knowing the possible most common A-B disturbances in aspirin toxicity, not by having to guess the time course. If there is one that is solely resp. alk. as @Jabbed described, then forget what I said.

Probably not step 1 level, but FWIW, MC presentation in adults is mixed resp-alk + met-ac, 2nd MC simple resp-alk. Adults could present with resp-ac if taken in addition to respiratory depressants, which occurs fairly often in intentional OD. In kids, simple met-ac & mixed resp-ac + met-ac are more common because they lose respiratory drive faster than adults.

 

[cs24]

The answer choice that you picked would describe A) a mixed respiratory alkalosis AND metabolic alkalosis or B) a compensated

Here's a timeline:
1. Uncompensated respiratory alkalosis: high pH, low pCO2, normal bicarb
2. Uncompensated respiratory alkalosis AND compensated metabolic acidosis: ~normal to low pH, low pCO2, low bicarb
3. Decompensated metabolic acidosis: low pH, high pCO2, low bicarb

It's important to note that due to the acute nature of salicyclism you will not be able to compensate for the respiratory alkalosis. Also be aware that your pH can actually be reasonably close to 7.4 due to the opposing acidosis/alkalosis (a pH of exactly 7.4 is actually suggestive of mixed acid/base disorder).

I haven't seen the question, but I'm assuming the choices could be ruled out based on knowing the possible most common A-B disturbances in aspirin toxicity, not by having to guess the time course. If there is one that is solely resp. alk. as @Jabbed described, then forget what I said.

Probably not step 1 level, but FWIW, MC presentation in adults is mixed resp-alk + met-ac, 2nd MC simple resp-alk. Adults could present with resp-ac if taken in addition to respiratory depressants, which occurs fairly often in intentional OD. In kids, simple met-ac & mixed resp-ac + met-ac are more common because they lose respiratory drive faster than adults.

Thanks, very helpful. I see where my gap in understanding of acid base is now. When Goljan said mixed disorders were more for step two than step one I promptly neglected them in my study, but I'll be sure to learn this one at least.