Respiratory acidosis/ alkalosis

[CBG23]

So, I am reading up on acid-base disturbances, which have always given me a bit of trouble. I think I am understanding them a lot better now, but am still confused about how the different lung diseases in particular cause either resp. acidosis or alkalosis. Different resources say different things and the sources I've taken a look at don't really do a good job of explainingthe reason why a particular disease causes acidosis or alkalosis.

Take for example, restrictive and obstructive lung diseases. I can understand that with an obstructive lung disease you have trouble getting air out of the lungs, so less CO2 is removed --> respiratory acidosis.

But what about restrictive lung disease? Different books say different things - some say that they cause resp. acidosis, while others say they cause resp. alkalosis. Nobody seems to give a good explanation either way. I think I can reason out that restrictive lung disease, esp. interstitial lung disease, --> imparied diffusion of CO2 out of the lungs --> resp. acidosis).

What about pulmonary edema and pneumonia? Some sources say resp acidosis and some say resp alkalosis?

Finally, one of the major causes I've seen for resp. alkalosis is hypoxemia (due to stimulation of peripheral chemoreceptors). However, it seems that most pulmonary causes of hypercapnia would also cause hypoxemia. So why wouldn't all pulmonary causes of hypercapnia cause a respiratory alkalosis?

Finally, I've noticed that severe anemia is listed as a cause of respiratory alkalosis, but can't find the mechanism for this. Since anemia only decreases O2 content and doesn't affect the PaO2, I'm guessing it has nothing to do with peripheral chemoreceptor stimulation...

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[sineapse]

Take for example, restrictive and obstructive lung diseases. I can understand that with an obstructive lung disease you have trouble getting air out of the lungs, so less CO2 is removed --> respiratory acidosis.

But what about restrictive lung disease? Different books say different things - some say that they cause resp. acidosis, while others say they cause resp. alkalosis. Nobody seems to give a good explanation either way. I think I can reason out that restrictive lung disease, esp. interstitial lung disease, --> imparied diffusion of CO2 out of the lungs --> resp. acidosis).

What about pulmonary edema and pneumonia? Some sources say resp acidosis and some say resp alkalosis?

Finally, one of the major causes I've seen for resp. alkalosis is hypoxemia (due to stimulation of peripheral chemoreceptors). However, it seems that most pulmonary causes of hypercapnia would also cause hypoxemia. So why wouldn't all pulmonary causes of hypercapnia cause a respiratory alkalosis?

Finally, I've noticed that severe anemia is listed as a cause of respiratory alkalosis, but can't find the mechanism for this. Since anemia only decreases O2 content and doesn't affect the PaO2, I'm guessing it has nothing to do with peripheral chemoreceptor stimulation...

My two cents: Mebbe the true picture in anemia is actually a metabolic acidosis with compensatory hyperventilation due to tissue hypoxia and increased blood lactate.

Pulmonary oedema and pneumonia would activate J receptors increasing respiratory rate > resp. alkalosis

Remember a lot of these cases will be in sickies giving mixed pictures, such as your pneumonia giving you sepsis > lactate up > metabolic acidosis + the whole respiratory component

 

[cowme]

Neuromuscular diseases are usually included restrictive lung disease (like ALS), which cause hypoventilation, and respiratory acidosis. That would be my main choice (chronic respiratory acidosis, that is).

However, as with all respiratory diseases, dyspnea can lead to flares of hyperventilation, which could cause short term alkalosis as well, but if I had to pick one underlying choice for restrictive lung diseases, I would say acidosis.

 

[OveractiveBrain]

So, I am reading up on acid-base disturbances, which have always given me a bit of trouble. I think I am understanding them a lot better now, but am still confused about how the different lung diseases in particular cause either resp. acidosis or alkalosis. Different resources say different things and the sources I've taken a look at don't really do a good job of explainingthe reason why a particular disease causes acidosis or alkalosis.

Take for example, restrictive and obstructive lung diseases. I can understand that with an obstructive lung disease you have trouble getting air out of the lungs, so less CO2 is removed --> respiratory acidosis.

But what about restrictive lung disease? Different books say different things - some say that they cause resp. acidosis, while others say they cause resp. alkalosis. Nobody seems to give a good explanation either way. I think I can reason out that restrictive lung disease, esp. interstitial lung disease, --> imparied diffusion of CO2 out of the lungs --> resp. acidosis).

What about pulmonary edema and pneumonia? Some sources say resp acidosis and some say resp alkalosis?

Finally, one of the major causes I've seen for resp. alkalosis is hypoxemia (due to stimulation of peripheral chemoreceptors). However, it seems that most pulmonary causes of hypercapnia would also cause hypoxemia. So why wouldn't all pulmonary causes of hypercapnia cause a respiratory alkalosis?

Finally, I've noticed that severe anemia is listed as a cause of respiratory alkalosis, but can't find the mechanism for this. Since anemia only decreases O2 content and doesn't affect the PaO2, I'm guessing it has nothing to do with peripheral chemoreceptor stimulation...

As with everything physiology, lets take a step back and work towards some answers. This boils down to acid-base, but we can make it easier by focusing only on the respiratory component (what you're asking leaves out the hard metabolic stuff). So in case some one stumbles on this thread and wants to be able to follow along, lets start with the very beginning.

Normal pH is 7.4... Know I know there is a range, 7.35-7.45, but for a conceptual understanding, lets just say normal is 7.4. Anything below that is acidotic. Anything above that is alkalotic. Acidotic means more acid. Alkalotic means less acid.

Since we are focusing on respiratory pH changes, the only acid we have to concern ourselves with is CO2. the respiratory acid. CO2 isn't an acid! Oh, but it might as well be. It is the buffer gas that transports hydrogen ions through the blood. Simply said, more CO2 = more acid = acidosis; less CO2 = less acid = alkalosis.

So whenever you think of any respiratory condition, you have to think to yourself, "does this disease increase or decrease respiratory acid?" The simple answer is that when people breathe less, CO2 accumulates and when people breathe more, CO2 is blown off. CO2 is the respiratory acid, and can change minute to minute. It is the immediate control of the body's pH (relative to the slow acting renal changes involving bicarb).

So think about things that would have you breathe less. What would that do to the CO2? Increase it. Then to the pH? Decrease it, make it more acid. Ok, so what makes you breathe less? Opiates (respiratory depression), obesity (chest wall limits expansion), stroke, diaphragmatic rupture, diaphragmatic anything really, cervical trauma (impinging the nerves that drive respiration), pain/fracture, etc. Of course, some other things sneak in here. COPD (specifically emphysema) "breathes less" in that there is a reduced surface area for gas exchange and also air trapping.

What about things that would have you breathe more? What would that do to the CO2? Decrease it. Then to the pH? Increase it, make it more alkalotic. Ok, so what makes you breathe more? Tachypnea. When do you get tachypneic? When you exercise, during a panic attack, or during a pulmonary embolism. Usually, tachypnea is a compensatory mechanism for something else. Usually its hypoxemia. You get hypoxemic in anemia (low Hgb means no transport for whatever oxygen you breathe), you get hypoxemic in pneumonia (both the cytokines and the barrier of pus limit oxygenation), you get hypoxemic in alot of things. Such as Pulmonary Edema

But tachypnea may be a compensation of something else. The respiratory system is the means in which acid-base is controlled on a minute to minute basis. So what if there were a lactic acidosis from sepsis? The body is acidotic. What does the body do? Blows off CO2 to reduce the acid effect. Tachypnea may be in response to a metabolic acidosis, producing a respiratory alkalosis that is compensatory to the metabolic acidosis.

So its all about breathing more or breathing less

 

[OveractiveBrain]

Finally, one of the major causes I've seen for resp. alkalosis is hypoxemia (due to stimulation of peripheral chemoreceptors). However, it seems that most pulmonary causes of hypercapnia would also cause hypoxemia. So why wouldn't all pulmonary causes of hypercapnia cause a respiratory alkalosis?

This, on the other hand, is a very difficult question to answer. It comes down to the fact that oxygen is diffusion limited while CO2 is perfusion limited.

The best example of this is a pulmonary embolism. I;ve discussed this before, so won't rehash it again. Basically, pulmonary embolism leads to vasodilation and leaky capillaries by increasing K in the equation: [K(Pcap-Pint) - (pcap - pint)]. If you don't recognize the equation, skip it. Just get leaky capillaries.

With leaky capillaries, the diffusion barrier increases. Diffusion = Concentration Graident / diffusion barrier. So diffusion barrier up, diffusion down. That is, for diffusion limited gases (like oxygen). So hypoxemia may be present, leading to tachypnea. Still little oxygen gets in, but because CO2 is not limited by the diffusion (and perfusion is usually up in response), it is blown off.

Hopefully from the two posts you can feel that the answer for any one disease is going to be a challenging mix of physiology, anatomy, and pathophysiologic response. Don't be too concerned if you cant get all of them every time. The fact is, in real life, the patient is usually normal, and you will get an Arterial Blood Gas (some say Venous is just as good) to get help you get a feel for the patient. You won't be doing too much disease --> ABG, but rather they other way, ABG --> disease, where rationalizing it is much easier.

 

[jdh71]

So, I am reading up on acid-base disturbances, which have always given me a bit of trouble. I think I am understanding them a lot better now, but am still confused about how the different lung diseases in particular cause either resp. acidosis or alkalosis. Different resources say different things and the sources I've taken a look at don't really do a good job of explainingthe reason why a particular disease causes acidosis or alkalosis.

Take for example, restrictive and obstructive lung diseases. I can understand that with an obstructive lung disease you have trouble getting air out of the lungs, so less CO2 is removed --> respiratory acidosis.

But what about restrictive lung disease? Different books say different things - some say that they cause resp. acidosis, while others say they cause resp. alkalosis. Nobody seems to give a good explanation either way. I think I can reason out that restrictive lung disease, esp. interstitial lung disease, --> imparied diffusion of CO2 out of the lungs --> resp. acidosis).

What about pulmonary edema and pneumonia? Some sources say resp acidosis and some say resp alkalosis?

Finally, one of the major causes I've seen for resp. alkalosis is hypoxemia (due to stimulation of peripheral chemoreceptors). However, it seems that most pulmonary causes of hypercapnia would also cause hypoxemia. So why wouldn't all pulmonary causes of hypercapnia cause a respiratory alkalosis?

Finally, I've noticed that severe anemia is listed as a cause of respiratory alkalosis, but can't find the mechanism for this. Since anemia only decreases O2 content and doesn't affect the PaO2, I'm guessing it has nothing to do with peripheral chemoreceptor stimulation...

There simply isn't anything about restrictive lung disease, or pulmonary edema, or pneumonia or fribrosis that makes them an either/or disease for resp acidosis or resp alkalosis. There's been a lot said on this thread already, none of it "wrong", but I'm not convinced conceptually entirely helpful. You get resp alkalosis because you've had an increase in minute ventilation - full stop. If you're hypoxic, such as in decompensated/decompsating pneumonia or pulmonary fibrosis or pulmonary edema, you breath faster, and you get alkalotic. That's it. There is nothing about fibrosis or pneumonia or pulmonary edema in and of themselves (the fibrosis does not prevent the exchange of CO2 enough to matter) that will cause a resp acidosis unless resp falure has occurred and you are now not breathing.

 

[mdeast]

This, on the other hand, is a very difficult question to answer. It comes down to the fact that oxygen is diffusion limited while CO2 is perfusion limited.

The best example of this is a pulmonary embolism. I;ve discussed this before, so won't rehash it again. Basically, pulmonary embolism leads to vasodilation and leaky capillaries by increasing K in the equation: [K(Pcap-Pint) - (pcap - pint)]. If you don't recognize the equation, skip it. Just get leaky capillaries.

With leaky capillaries, the diffusion barrier increases. Diffusion = Concentration Graident / diffusion barrier. So diffusion barrier up, diffusion down. That is, for diffusion limited gases (like oxygen). So hypoxemia may be present, leading to tachypnea. Still little oxygen gets in, but because CO2 is not limited by the diffusion (and perfusion is usually up in response), it is blown off.

Hopefully from the two posts you can feel that the answer for any one disease is going to be a challenging mix of physiology, anatomy, and pathophysiologic response. Don't be too concerned if you cant get all of them every time. The fact is, in real life, the patient is usually normal, and you will get an Arterial Blood Gas (some say Venous is just as good) to get help you get a feel for the patient. You won't be doing too much disease --> ABG, but rather they other way, ABG --> disease, where rationalizing it is much easier.

BOTH oxygen and CO2 are almost always perfusion limited. Oxygen can sometimes be diffusion limited in extreme circumstances, but what you're saying is giving the OP some false info.

 

[OveractiveBrain]

BOTH oxygen and CO2 are almost always perfusion limited. Oxygen can sometimes be diffusion limited in extreme circumstances, but what you're saying is giving the OP some false info.

PE = Hypoxemia and Hypocapnia... not enough oxygen in, and too much CO2 out. O2 would be diffusion limited. CO2 would, well, not be.

 

[hemoglobincell]

Chronic bronchitis - terminal bronchioles are mucous-plugged = respiratory acidosis.
Pretty much everything else has a hyperventilation component and thus is respiratory alkalosis.
Also, to correct an earlier point, anemia does not cause hypoxemia (defined as a drop in PaO2), but instead causes hypoxia (inadequate tissue oxygenation). In anemia, respiratory alkalosis is compensatory to lactic acidosis.

 

[cameraGEEK]

Finally, one of the major causes I've seen for resp. alkalosis is hypoxemia (due to stimulation of peripheral chemoreceptors). However, it seems that most pulmonary causes of hypercapnia would also cause hypoxemia. So why wouldn't all pulmonary causes of hypercapnia cause a respiratory alkalosis?

I have also wondered about this ... I am confused as to when one could have hypercapnia without hypoxemia; or when one may have hypoxemia without hypercapnia?

Often it seems like we are meant to assume that when one is high, the blood levels of the other should be low, but this doesn't seem right - we can't assume that if CO2 is high, blood O2 is low? Is there an equation that relates blood levels of each?

I especially wonder because of the different effects each hypercapnia, hypocapnia, hypoxemia has on vasculature... if one were to have hypercapnia, but not hypoxemia, would there still be a need for blood vessel dilation? Perhaps there should be because you'd need to get rid of the CO2 metabolite, but not for the purpose of bringing more O2 to the tissue if it's not needed?

 

[CuriousGeorge2]

I have also wondered about this ... I am confused as to when one could have hypercapnia without hypoxemia; or when one may have hypoxemia without hypercapnia?

Often it seems like we are meant to assume that when one is high, the blood levels of the other should be low, but this doesn't seem right - we can't assume that if CO2 is high, blood O2 is low? Is there an equation that relates blood levels of each?

I especially wonder because of the different effects each hypercapnia, hypocapnia, hypoxemia has on vasculature... if one were to have hypercapnia, but not hypoxemia, would there still be a need for blood vessel dilation? Perhaps there should be because you'd need to get rid of the CO2 metabolite, but not for the purpose of bringing more O2 to the tissue if it's not needed?

Alveolar Gas Equation: PAO2= PiO2 - PACO2/R
In general, PACO2 is assumed to be equal to PaCO2. Also, unless there is a problem with diffusion or V/Q mismatch, PAO2~PaO2

 

[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.....

 

[Priapism4tooLong]

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.....

Are you asking why hco3 doesn't affect pH?

 

[Priapism4tooLong]

I'm pretty sure thats what you are asking. I don't have a master in chemistry or a doctorate in chemistry for that matter but i THINK, pH has something to do with the concentrations of hydrogen ions. Something like negative logarithm of hydrogen ion concentration.

 

[Dires]

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.....

Someone please correct me if I am wrong, but this is how I've come to understand it:

Your blood pH is normally slightly basic due to the presence if HCO3 reabsorption by the kidney. It is used as a buffer in your blood. During some circumstances where there is an increase in protons, they are buffered by the surplus HCO3 available. H2CO3 is a very weak acid so it is rare that a proton will break off (the free protons are what do damage). Although the viable pH range is 6.8 to 7.8 PTs aren't doing to got below 7 which makes sense... By the time they reach that low of a PH their bodies natural stories of HCO3 could be used up and thus a blood test may yield untraceable amounts of HCO3 in the blood. Thus body will up regulate reabsorption. When you think about it a fluctuation from 7.4 to 7.2 requires a lot of free protons to buffer out with the HCO3.

Edit: I stated it was rare for H2CO3 to lose its proton. That is unless carbonic anhydrase is in the building.

 

[Priapism4tooLong]

Someone please correct me if I am wrong, but this is how I've come to understand it:

Your blood pH is normally slightly basic due to the presence if HCO3 reabsorption by the kidney. It is used as a buffer in your blood. During some circumstances where there is an increase in protons, they are buffered by the surplus HCO3 available. H2CO3 is a very weak acid so it is rare that a proton will break off (the free protons are what do damage). Although the viable pH range is 6.8 to 7.8 PTs aren't doing to got below 7 which makes sense... By the time they reach that low of a PH their bodies natural stories of HCO3 could be used up and thus a blood test may yield untraceable amounts of HCO3 in the blood. Thus body will up regulate reabsorption. When you think about it a fluctuation from 7.4 to 7.2 requires a lot of free protons to buffer out with the HCO3.

Edit: I stated it was rare for H2CO3 to lose its proton. That is unless carbonic anhydrase is in the building.

you aren't wrong, but clincally its a lot more complicated than this. But H2CO3 is a weak acid because it will not totally disassociate all of its H+ however it will give up one of its H's easily (from what i remember). If you are acidic not only will you reabsorb HCO3 from kidneys but you will hyperventilate due to increase CO2 production.

 

[Priapism4tooLong]

Wait 6.8-7.8 is not a viable ph range, patient would be dead if they stayed at 6.8

 

[junaidyounis]

Are you asking why hco3 doesn't affect pH?

Yes you are right I was asking was hco3 loss with protons....one other explanation somewhere else was this..."BECAUSE THE STARTING CONCENTRATIOS OF H+ AN BICARBONATE IN ECF ARE VERY DIFFERENT - the [H+] in the normal state is 40 nanoequivalents (nEq/L) per liter, whereas the [HCO3-] is regulated to 24 milliequivalents (mEq/L). Note that mEq is 1000 times more than nEq. A change of pH from 7.4 to 7.2 requires a rise in H from 40 to 60 nEq/L (a 50% increase). The total amount of HCO3 also rises by the same amount (20 nEq/L), however because the amount of HCO3 in the ECF is much more large, this change is relatively insignificant. The actual change in [HCO3-] is on the order of a 0.001% increase"......I wanted to know that is this true what the explainer wrote or there is different view on this....thank you so much for your time

 

[Priapism4tooLong]

Yes you are right I was asking was hco3 loss with protons....one other explanation somewhere else was this..."BECAUSE THE STARTING CONCENTRATIOS OF H+ AN BICARBONATE IN ECF ARE VERY DIFFERENT - the [H+] in the normal state is 40 nanoequivalents (nEq/L) per liter, whereas the [HCO3-] is regulated to 24 milliequivalents (mEq/L). Note that mEq is 1000 times more than nEq. A change of pH from 7.4 to 7.2 requires a rise in H from 40 to 60 nEq/L (a 50% increase). The total amount of HCO3 also rises by the same amount (20 nEq/L), however because the amount of HCO3 in the ECF is much more large, this change is relatively insignificant. The actual change in [HCO3-] is on the order of a 0.001% increase"......I wanted to know that is this true what the explainer wrote or there is different view on this....thank you so much for your time

that is true, and it makes sense. .. but correct me if im wrong but when measuring pH it is a count of H+ not hco3. Im not sure i am understanding this. Someone please help me

 

[junaidyounis]

Yes you are right...that measuring ph we count H+ not concentration of bicarbonate.in simple PH simply means power of protons.nad I have gone tbrough all these things for months.even once spoke to anesthetist and after explaning he said acid base and electrolytes if studied well incdepth are one of challenging concepts in medicine....thank u again for your cooperation on this topic

 

[junaidyounis]

due to hypoventilation there in increase in paco2 in body and there iss NET INCREASE OF H+ resulting in respiratory acidosis. and seeing equation CO2 (g) + H20 (l) <=> H2CO3 (aq) <=> H+ (aq) + HCO3- (aq ) it shifts to right to increase co2. as we see both H+ and HCO3 are formed equally so how come there is net increase of just H+ as HCO3 are also formed along with H+.when ratio of formation is equal then how come net increase is H+. so how come acidosis accour. your help will be great coz im stuck

 

[DermViser]

due to hypoventilation there in increase in paco2 in body and there iss NET INCREASE OF H+ resulting in respiratory acidosis. and seeing equation CO2 (g) + H20 (l) <=> H2CO3 (aq) <=> H+ (aq) + HCO3- (aq ) it shifts to right to increase co2. as we see both H+ and HCO3 are formed equally so how come there is net increase of just H+ as HCO3 are also formed along with H+.when ratio of formation is equal then how come net increase is H+. so how come acidosis accour. your help will be great coz im stuck

Was it necessary to bump this up 7 months later after your last post in April?

 

[Instatewaiter]

Obviously