Acidosis-alkalosis question

[Phloston]

Let's say we've got someone who's been vomiting, and he's given himself metabolic alkalosis. So to compensate, he begins hypoventilating to increase his pCO2.

My question is:

Is it metabolic alkalosis with respiratory compensation as long as his pCO2 is increased beyond the normal range (implying efforts to lower the pH), or is it respiratory compensation only if his pH returns to the normal range of 7.35-7.45?

In other words, must compensation be marked by the successful return to normal pH, or is it just the body's effort to return the pH to normal by modifying a second parameter?

Thanks,

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[ijn]

I don't think it's compensation if you get back to subnormal ranges. To me that suggests respiratory alkalosis plus metabolic acidosis - i.e. salicylate toxicity. The body doesn't compensate perfectly (w/ the exception of respiratory alkalosis due to altitude.) I agree with your latter statement with slight alteration - compensation is the body's effort to return a pH that is closer to normal.

 

[Myxedema]

No, it doesn't have to return to the normal value. Calculate the expected change in pCO2 (roughly 0.7 x change of HCO3- from the baseline) and decide if there's appropriate compensation or not.

 

[Phloston]

I'm not quite following you. Could you please elaborate?

 

[Myxedema]

Let's assume we have a vomiting patient with these lab values:

pH: 7.48
HCO3- : 28 mEq/L
pCO2: 43 mm Hg

HCO3- is 28 - 24 = 4 mEq/L above the optimal baseline. So, the increase in pCO2 should be: 0.7 x 4 : 2,8 mm Hg, from the baseline of 40 mm Hg. Since pCO2 is 43 mm Hg, we can say that there's an appropriate respiratory compensation for that patient.

 

[Phloston]

Let's assume we have a vomiting patient with these lab values:

pH: 7.48
HCO3- : 28 mEq/L
pCO2: 43 mm Hg

HCO3- is 28 - 24 = 4 mEq/L above the optimal baseline. So, the increase in pCO2 should be: 0.7 x 4 : 2,8 mm Hg, from the baseline of 40 mm Hg. Since pCO2 is 43 mm Hg, we can say that there's an appropriate respiratory compensation for that patient.

My impression was that as long as pH was outside of the normal range, there's decompensation. It's the same way with hypovolaemic shock, for instance. We may get "compensatory" peripheral vasoconstriction, but if CO still falls and insufficient perfusion of vital organs occurs, it's decompensated, not compensated.

The point I'm making is that it's not the mere occurrence of a secondary compensatory mechanism that defines compensation as much as it is a successful return to the primary parameters.

I just don't want to screw this up on an easy question on the real USMLE. Even if the patient is trying to compensate, if the pH is not normal, then I would still think compensation has not occurred.

 

[Myxedema]

On the contrary, compensation mechanisms rarely bring pH to normal levels. So, even if there's appropriate compensation response, still there would be acidosis/alkalosis.

 

[Phloston]

On the contrary, compensation mechanisms rarely bring pH to normal levels. So, even if there's appropriate compensation response, still there would be acidosis/alkalosis.

Sleep apnoea carries one of the most notable successful compensatory mechanisms. The repeated respiratory acidosis renders these patients with increased serum bicarbonate levels, enabling long-term compensation within the normal pH range.

 

[Myxedema]

Sleep apnoea carries one of the most notable successful compensatory mechanisms. The repeated respiratory acidosis renders these patients with increased serum bicarbonate levels, enabling long-term compensation within the normal pH range.

Ok, but I disagree with the last part: http://tinyurl.com/c2smypf

Compensatory responses are not strong enough to keep the pH constant (they do not correct the acid-base derangement); they only to limit the change in pH that results from a primary change in PCO2 or HCO3.

 

[Phloston]

The short paragraph on the top of p. 534 is exactly what I needed to see. Thanks so much again for a helpful post.

However, I have seen that sleep apnoea is compensated for. This is because the respiratory acidosis is only intermittent. Perhaps it depends on the severity (e.g. severe Pickwickian syndrome).

 

[tk0102]

The short paragraph on the top of p. 534 is exactly what I needed to see. Thanks so much again for a helpful post.

However, I have seen that sleep apnoea is compensated for. This is because the respiratory acidosis is only intermittent. Perhaps it depends on the severity (e.g. severe Pickwickian syndrome).

1) Persistent--not intermittent--hypercapnia would result in metabolic compensation. And only some OSA patients are persistently hypercapnic, for not entirely clear reasons.

2) Certainly Pickwickian Syndrome could result in persistent hypercapnia (because of restrictive lung mechanics), but Pickwickian Syndrome is not a marker of severity of OSA--they're two different, albeit interrelated, pathological entities.

Myxedema is totally spot-on re: expected compensation.

 

[junaidyounis]

Hello friends...I wanted to ask that in in hyperventilation when paco2 decreases and this equation shifts to left.i read in literature that H+ and HCO3 combine to form carbonic acid and carbonic acid dissociates into co2 nad h2o as compensation.. due to hyperventilation and fall in paco2 ph level rises leading to alkalosis. My question is when H+ and Hco3 both combine to form carbonic acid and further then why they write just protons are lost and ph rises and causes alkalosis....why dosent loss of hco3 affect ph ..in my mind it was both are lost so ph shoudnt changee..please help me I can elaborate more if my question is not clear.....