Although the PCO2 of 32 is lower than 40 (which would initially argue against a resp. acidosis), it is not nearly as low as predicted by the compensation equation. (Winter's formula predicts that the PCO2 in a metabolic acidosis will be approx. equal to (1.5 x HCO3) + 8, which in this case is 23.) In other words, if the resp. system was working normally, it would be doing some extreme hyperventilation in an attempt to counteract the extremely low pH from the metabolic acidosis.
Thank you very much for these lectures. Acid-base-physiology has always haunted me as one of my weaker points. Your videos however, have really helped to clarify the concepts!
Hello Dr. Strong, I would like to note an exception to the statement you made regarding "compensation does not return the pH to normal". "Chronic respiratory alkalosis when prolonged is an exception to this rule and often returns the pH to a normal value. " (Harrison's 19th edition, ch. 66).
The converse of this is slightly incongruous, in that there can be "partial metabolic compensation" for a respiratory disorder if the respiratory process has not been going on for long enough for the kidneys to have completely adjusted their handling of H+ and HCO3- for the degree of respiratory-induced acid-base imbalance. Hope this helps!
In this case, the degree of hyperventilation is not extreme, but actually more modest. It's not uncommon for people to refer to this situation as "partial compensation", but I think that terminology is misleading since it under-emphasizes that there must be a primary respiratory disorder present in order for the respiratory compensation to not be complete. Sometimes, a resp. disorder that's labeled as "partial compensation" can actually be more acutely important than the metabolic process.
Your answer will probably be: because it is more complicated then you think. Right? My way of thinking about this problem is probably to superficial and needs adjusting. Many thanks by the way for your effort to help the medical community.
@strong Medicine, Sir firstly I love your lectures, I want to thank you for providing them for students and physicians around the world; secondly I have a question regarding example number 3 , if the disorder was acute and respiratory , how come it has an elevated HCO3 ? wouldn't it be to soon as metabolic compensation takes a minimum of 24 h ? or is it a product of the second metabolic disorder (metabolic alkalosis)? :)
Hi Dr Strong, Firstly thank you for your amazing lectures. I found the series on ABG interpretation incredibly useful as it managed to be both thorough and easy to follow at the same time. Definitely the best resource on this topic I've found. I just had a question regarding compensation- you said the body never overcompensates, which I take to mean under normal physiological circumstances. But what about after we intervene? Specifically, a patient with acute on chronic type 2 respiratory failure (eg. infective exacerbation of COPD) who we then put on bipap. Say if we successfully ventilate them but 'overtreat' and return the CO2 to normal levels, could they then have a metabolic alkalosis because their bicarb (which is normally elevated at baseline) hasn't decreased as metabolic compensation takes longer to occur? Thank you!
+Yin Yuan That's a good question, and people have different terms they use to describe this. For example, some refer to this as a "post-hypercapnic metabolic alkalosis". It's best to not think of it as "overcompensation" as much as normal compensation which has persisted beyond the duration of the original primary acid-base disturbance. Perhaps it's semantics, but it seems like a more logical way to frame the physiology.
Dr strong in example #2 ( pH=7.12, PaCO2=32, HCO3=10) When we use winter's formula to calculate expected PaCO2 , it comes out to be equal to 23 , but when we use role of last two digits it equal 12? isn't the rule of last two digits the shortcut of winter's , why they produce different values in that case ?
Hi Dr Strong, Thank you again so much for these mind-blowingly great videos. In patients with acute on chronic disorders (let's say acute on chronic hypercapnia secondary to an infective exacerbation of COPD), would you use the acute or chronic formula for calculating if compensation was adequate?
Hi. How can we identify primary disorders if pH is normal? For example, pH is normal, pC02 is low, bicarbonate is low. Is it compensated respiratory alkalosis or compensated metabolic acidosis? Thank you!
Hello Dr Strong! Thank you very much for helping us in medical studies! I really appreciate it! The third exp of The fourth lesson of ABG interpretation is confusing me because i can not understand why The 2nd disorder is a metabolic alkalosis. I read all The answers that you gave to The other students but i still cant understand it. Is there any rules to follow to avoid my or our confusion? Thank so much in advance and have a Nice weekend!
Thanks for another excellent video! One question, how do we decide if to use the acute vs the chronic formula for respiratory disorders? Is it only based on the clinical scenario given (as was demonstrated here)
Hi Dr Eric. When evaluating compensation for metabolic disorders by looking at the last two digits of the pH and PaCO2 (shortcut method), how close do you think is 'close enough'? In the examples that you give in this video and when the problem has appropriate compensation, the last 2 digits of the pH and PaCO2 don't seem to differ by more than 2 numbers. But in later videos, even when they differ by up to 4 numbers (so eg: pH of 7.50 and PaCO2 of 54), this is still 'appropriate' compensation if calculated by the Winter's Formula.
thanks for this informative lecture which help us a lot to understand concepts of acid base disorders.can you explain the last example that either it is acute or chronic respiratory acidosis.still confuse by compensation concepts.
The bicarb should actually be around 50 Paco2 increased by 25 so bicarb should be 24+25=50 If it was chronic then patient should be responsive with baseline around 55-60 Hence not chronic
When the cause of metabolic alkalosis is extra renal for example vomiting (given normal kidney function) will we have a renal compensation apart from the not so robust respiratory one ? Thanks for amazing videos!
THANK YOU VERY MUCH YOU ARE GREAT YOU EXPLAIN IT IN SUCH A GREAT WAY THANK YOU THANK THANK YOU BUT I HAVE A QUESTION: i don not really absorb that when you say the actual is greater than the expected so the secendary disorder is .... ??? what is base for that ?? i mean if it is lower what does it mean and if it is upper or greater than predected what does it mean ?>?? please answer me ????
IMHO, it is not an approximation that is close enough to use at the bed side. The graph 11:35 is incorrect. For example, pH 7.123, PCO2 21 mmHg, HCO3- 6.7 mEq/L The shortcut gives you 12 as opposed to 18 drawn in the graph. For another example, pH 7.464, PCO2 48.3 mmHg, HCO3- 33.9 mEq/L Although 44.73, derived from Winter's formula, is close to 46, derived from the shortcut, this difference is enough to neglect the comorbid respiratory acidosis that is actually present. According to my experience of trying this shortcut formula, the accuracy of this shortcut formula is as low as flipping coins(, although I've tried this only a few times). The expected PCO2 should be calculated based on HCO3-, rather than pH.
When calculating expected compensation, is it better to use baseline values (if available) instead of fixed presumed normal values? An example where this would make a difference in calculation is hypercapnia at baseline in COPD. What do you think?
great lecture sir bt is hw to distinguish between acute and chronic process as patient coming to er are mstly acute on chronic wat formulas to apply then
Same thing I'm wondering. How do we decide if to use the acute vs the chronic formula for respiratory disorders? Some sources online have an equation which uses the change in PH, but Dr. Strong judged based on the clinical setting
Hello Dr Strong or anyone reading this comment kindly help me out I’ve got a question In example number 2 Actual reduction of PCO2 from base line (32) is higher than that of calculated compensation (23) Therefore am I right ? The secondary base disorder that needs to be present is RESPIRATORY ALKALOSIS and not respiratory acidosis. Kindly help me out ( I am highly confused with it ) Thanks in advance
I am confused with example 3. the secondary disorder is METABOLIC ALKALOSIS, Why is it alkalemia if your pH is below 7.35...it should be metabolic ACEDEMIA right?
In example 3, there are 2 processes present: One is a respiratory acidosis, which in general is a pathophysiologic process that tends to drive the pH towards acidemia. The second is a metabolic alkalosis, which in general is a pathophysiologic process that tends to drive the pH towards alkalemia. So the 2 processes are pushing the pH in different directions. In this case, the respiratory acidosis just happens to be more prominent, so the pH ends up being a little acidemic. (A nuanced but important point is that the more "prominent" acid-base disorder is not always the one most clinically relevant or dangerous)
In example 3, I thought if pH and PaCO2 are in same direction, it means respiratory? If they were "deranged" it would be metabolic? What am I not understanding?
If pH and PaCO2 are deranged in *opposite* directions, it means that at least one respiratory disorder is present. For example, in a respiratory acidosis (e.g. COPD exacerbation), the pH will be lower than 7.35 while the PaCO2 will be much higher than 40.
What I do not get is that you say there is a resp acidosis. Why isn't the PCo2 in this case not more than 40 mm HG? I would say there is metabolic acidose with a partial respidatory compensation. You can perhaps argue that teh PCO2 is lowered beacause of the hyperventilation that has occur to get more acid out of the system. Wich thinking fault am i making here?
Hello, in the last example why is the secondary disorder metabolic alkalosis instead of metabolic acidosis? Would someone please care to explain as I can't seem to make sense of it
coolgirlrom Here the actual increase of HCO3 from baseline (34) is HIGHER than that of the calculated compensation ( which is 26.5). Therefore the seconds disorder present is metabolic alkalosis 😊
ABGs are like ECGs - they cannot be reliably interpreted in isolation. They require some amount of clinical history to know if acid-base derangement are likely acute or chronic, since we use different compensation formulas for those two possibilities. If the clinical history for example 3 was a 60 year old smoker presenting to the clinic with progressively worsening dyspnea and cough for 6 months, then yes, the ABG would be most consistent with a chronic respiratory acidosis with normal compensation. But in this case, the fact that it's a young (presumably healthy) person with an acute illness means a chronic process is unlikely, and we must interpret the ABG with that in mind.
@@StrongMed wow im really surprised you replied this fast ... woah thanks a lot for your concern and early reply really it is much appreciated dr Strong .... my point is after calculating whether this is acute or chronic using the delta ph over delta co2 or by the other method evry 10 co2 change equals 0.04 channge in ph in chronic and 0.08in acute i found out ,,, surprisingly ... it is chronic ... so does this mean that these formulas are wrong and the clinical situation is the only determinant of chronicity of resp disorders ? finally thanks again dr strong for your kind reply and im really loving this abg series analysis as an intensivist they are enourmesly helpful thanks a lot
I have to disagree with this appropriate compensation would mean a normalized pH. example one pH is not compensated. It would be uncompensated metabolic alkalosis.
This is a common misconception. Appropriate physiologic compensation of a single acid-base disorder does not bring one's pH back into the normal range unless the acid-base disorder is relatively mild. That's why compensation equations and related rules of thumb were empirically measured.
It's based on your clinical impression. This is one of the things that makes it impossible to analyze an ABG in isolation from a history or clinical vignette.
by the last example why not say that is primary metabolic alkalemia with uncomplete respiratory compensation due to respiratory acidosis?? pls answer anyone :(
In this case, it would be confusing to describe this as a metabolic alkalosis with incomplete respiratory compensation since the pH is not only lower than respiratory compensation (i.e. the patient is "overcompensating", which doesn't happen), but is even lower than normal. Thus the respiratory acidosis is having a quantitatively larger effect on the pH. Sometimes in ABG analysis the word "primary" gets used in an imprecise way to mean "the first acid-base disorder which our algorithm happens to identify", and typically is also the acid-base disorder which has the greatest quantitative impact on the pH. But the disorder that is first identified is not necessarily the first that happens chronologically, nor the necessarily the most clinically relevant.
After more than a decade!!! This channel is a miracle!! Thank you som much!! Just the shortcut is awesome by itself!
Thank you Erik your a true gentleman for allowing these learning resources to be shares around the world. The introductory music is fantastic too ☺
By far the most informative, coherent video I've seen about ABG compensation. Thank you!
one of the best lectures on acid-base I have come across on youtube
Although the PCO2 of 32 is lower than 40 (which would initially argue against a resp. acidosis), it is not nearly as low as predicted by the compensation equation. (Winter's formula predicts that the PCO2 in a metabolic acidosis will be approx. equal to (1.5 x HCO3) + 8, which in this case is 23.) In other words, if the resp. system was working normally, it would be doing some extreme hyperventilation in an attempt to counteract the extremely low pH from the metabolic acidosis.
Thank you Dr Strong,I listen to this second time.
REAL MVP. Literally crushed my cardio pulm unit in medical school because of you. The best
Difficult concept explained simply and clearly . Thank you .
Thank you very much for these lectures. Acid-base-physiology has always haunted me as one of my weaker points. Your videos however, have really helped to clarify the concepts!
Your teaching style is so awesome 👍
Hello Dr. Strong, I would like to note an exception to the statement you made regarding "compensation does not return the pH to normal".
"Chronic respiratory alkalosis when prolonged is an exception to this rule and
often returns the pH to a normal value. " (Harrison's 19th edition, ch. 66).
Thank you for your awesome lecture.
You saved my day❤❤❤
The converse of this is slightly incongruous, in that there can be "partial metabolic compensation" for a respiratory disorder if the respiratory process has not been going on for long enough for the kidneys to have completely adjusted their handling of H+ and HCO3- for the degree of respiratory-induced acid-base imbalance.
Hope this helps!
Thanks so much for these series of lectures!
the shortcut method is really helpful.
In this case, the degree of hyperventilation is not extreme, but actually more modest. It's not uncommon for people to refer to this situation as "partial compensation", but I think that terminology is misleading since it under-emphasizes that there must be a primary respiratory disorder present in order for the respiratory compensation to not be complete. Sometimes, a resp. disorder that's labeled as "partial compensation" can actually be more acutely important than the metabolic process.
Well-explained! Thank you Dr Strong! 💪
Great lecture , this one is the best :)
Thank you very much Eric. This video was awesome...
(also the other videos)
Your answer will probably be: because it is more complicated then you think. Right?
My way of thinking about this problem is probably to superficial and needs adjusting.
Many thanks by the way for your effort to help the medical community.
@strong Medicine, Sir firstly I love your lectures, I want to thank you for providing them for students and physicians around the world; secondly I have a question regarding example number 3 , if the disorder was acute and respiratory , how come it has an elevated HCO3 ? wouldn't it be to soon as metabolic compensation takes a minimum of 24 h ? or is it a product of the second metabolic disorder (metabolic alkalosis)? :)
Hi Dr Strong,
Firstly thank you for your amazing lectures. I found the series on ABG interpretation incredibly useful as it managed to be both thorough and easy to follow at the same time. Definitely the best resource on this topic I've found.
I just had a question regarding compensation- you said the body never overcompensates, which I take to mean under normal physiological circumstances. But what about after we intervene? Specifically, a patient with acute on chronic type 2 respiratory failure (eg. infective exacerbation of COPD) who we then put on bipap. Say if we successfully ventilate them but 'overtreat' and return the CO2 to normal levels, could they then have a metabolic alkalosis because their bicarb (which is normally elevated at baseline) hasn't decreased as metabolic compensation takes longer to occur?
Thank you!
+Yin Yuan That's a good question, and people have different terms they use to describe this. For example, some refer to this as a "post-hypercapnic metabolic alkalosis". It's best to not think of it as "overcompensation" as much as normal compensation which has persisted beyond the duration of the original primary acid-base disturbance. Perhaps it's semantics, but it seems like a more logical way to frame the physiology.
Thank you!
Really good videos!
AMAZING!
Great video sir
Dr strong in example #2 ( pH=7.12, PaCO2=32, HCO3=10)
When we use winter's formula to calculate expected PaCO2 , it comes out to be equal to 23 , but when we use role of last two digits it equal 12?
isn't the rule of last two digits the shortcut of winter's , why they produce different values in that case ?
Hi Dr Strong,
Thank you again so much for these mind-blowingly great videos. In patients with acute on chronic disorders (let's say acute on chronic hypercapnia secondary to an infective exacerbation of COPD), would you use the acute or chronic formula for calculating if compensation was adequate?
This is very useful. thanxs
This really hurt the cerebrum - but really really good - thank you
Hi. How can we identify primary disorders if pH is normal? For example, pH is normal, pC02 is low, bicarbonate is low. Is it compensated respiratory alkalosis or compensated metabolic acidosis? Thank you!
You're in luck! That's the topic of the 7th video in the series: ua-cam.com/video/NFmulAR6Bwg/v-deo.html
@@StrongMed thank you very much!
Hello Dr Strong!
Thank you very much for helping us in medical studies! I really appreciate it!
The third exp of The fourth lesson of ABG interpretation is confusing me because i can not understand why The 2nd disorder is a metabolic alkalosis. I read all The answers that you gave to The other students but i still cant understand it. Is there any rules to follow to avoid my or our confusion?
Thank so much in advance and have a Nice weekend!
Thanks for another excellent video! One question, how do we decide if to use the acute vs the chronic formula for respiratory disorders? Is it only based on the clinical scenario given (as was demonstrated here)
Hi Dr Eric. When evaluating compensation for metabolic disorders by looking at the last two digits of the pH and PaCO2 (shortcut method), how close do you think is 'close enough'? In the examples that you give in this video and when the problem has appropriate compensation, the last 2 digits of the pH and PaCO2 don't seem to differ by more than 2 numbers. But in later videos, even when they differ by up to 4 numbers (so eg: pH of 7.50 and PaCO2 of 54), this is still 'appropriate' compensation if calculated by the Winter's Formula.
I hate (love) those shortcuts. Thank you so much Sir. May Allah bless you.
thanks for this informative lecture which help us a lot to understand concepts of acid base disorders.can you explain the last example that either it is acute or chronic respiratory acidosis.still confuse by compensation concepts.
Excellant .
Hello Doc ,Shouldn't the 3rd example answer be chronic respiratory acidosis ??? So metabolic compensation by retaining HCO3
I agree with you. I didn't see any second disorder in that example. That is purely a chronic compensation for resiratory acidosis.
The bicarb should actually be around 50
Paco2 increased by 25 so bicarb should be 24+25=50
If it was chronic then patient should be responsive with baseline around 55-60
Hence not chronic
When the cause of metabolic alkalosis is extra renal for example vomiting (given normal kidney function) will we have a renal compensation apart from the not so robust respiratory one ?
Thanks for amazing videos!
THANK YOU VERY MUCH YOU ARE GREAT YOU EXPLAIN IT IN SUCH A GREAT WAY THANK YOU THANK THANK YOU
BUT I HAVE A QUESTION:
i don not really absorb that when you say the actual is greater than the expected so the secendary disorder is .... ???
what is base for that ??
i mean if it is lower what does it mean
and if it is upper or greater than predected what does it mean ?>??
please answer me ????
at what time do we consider acute or chronic? Is over 24 hrs with the condition chronic? thanks
I come back to this video every time I revise acid base. Best one on the youtube! Kudos!
Again this is just gold haha!
thanks Dr Strong
Thanks!
Thank you!
IMHO, it is not an approximation that is close enough to use at the bed side.
The graph 11:35 is incorrect.
For example,
pH 7.123, PCO2
21 mmHg, HCO3- 6.7 mEq/L
The shortcut gives you 12 as opposed to 18 drawn in the graph.
For another example,
pH 7.464, PCO2
48.3 mmHg, HCO3- 33.9 mEq/L
Although 44.73, derived from Winter's formula, is close to 46, derived from the shortcut, this difference is enough to neglect the comorbid respiratory acidosis that is actually present.
According to my experience of trying this shortcut formula, the accuracy of this shortcut formula is as low as flipping coins(, although I've tried this only a few times).
The expected PCO2 should be calculated based on HCO3-, rather than pH.
When calculating expected compensation, is it better to use baseline values (if available) instead of fixed presumed normal values? An example where this would make a difference in calculation is hypercapnia at baseline in COPD. What do you think?
great lecture sir bt is hw to distinguish between acute and chronic process as patient coming to er are mstly acute on chronic wat formulas to apply then
Same thing I'm wondering. How do we decide if to use the acute vs the chronic formula for respiratory disorders? Some sources online have an equation which uses the change in PH, but Dr. Strong judged based on the clinical setting
absolutely incredible
Thank you so much ...
Thank youuu so much!
Thank you!!
is it right to say that in last example chronic resp acidosis with compensation of met alkalosis?
exactly
For example 2, 12 is nowhere near 23. Is that a situation where the shortcut method is not useful?
Thanks 🌼
Thank u so much...
Is the last example a chronic respiratory acidosis situation?
exactly by calculations its not acute at all
Hello Dr Strong or anyone reading this comment kindly help me out
I’ve got a question
In example number 2
Actual reduction of PCO2 from base line (32) is higher than that of calculated compensation (23)
Therefore am I right ? The secondary base disorder that needs to be present is RESPIRATORY ALKALOSIS and not respiratory acidosis.
Kindly help me out ( I am highly confused with it )
Thanks in advance
Thank you
Super !!!!
Appropriate respiratory compensation(+/-3), metabolic compensation (+/-5)???
I am confused with example 3. the secondary disorder is METABOLIC ALKALOSIS, Why is it alkalemia if your pH is below 7.35...it should be metabolic ACEDEMIA right?
In example 3, there are 2 processes present: One is a respiratory acidosis, which in general is a pathophysiologic process that tends to drive the pH towards acidemia. The second is a metabolic alkalosis, which in general is a pathophysiologic process that tends to drive the pH towards alkalemia. So the 2 processes are pushing the pH in different directions. In this case, the respiratory acidosis just happens to be more prominent, so the pH ends up being a little acidemic.
(A nuanced but important point is that the more "prominent" acid-base disorder is not always the one most clinically relevant or dangerous)
In example 3, I thought if pH and PaCO2 are in same direction, it means respiratory? If they were "deranged" it would be metabolic? What am I not understanding?
If pH and PaCO2 are deranged in *opposite* directions, it means that at least one respiratory disorder is present. For example, in a respiratory acidosis (e.g. COPD exacerbation), the pH will be lower than 7.35 while the PaCO2 will be much higher than 40.
What I do not get is that you say there is a resp acidosis. Why isn't the PCo2 in this case not more than 40 mm HG? I would say there is metabolic acidose with a partial respidatory compensation. You can perhaps argue that teh PCO2 is lowered beacause of the hyperventilation that has occur to get more acid out of the system. Wich thinking fault am i making here?
Hello, in the last example why is the secondary disorder metabolic alkalosis instead of metabolic acidosis? Would someone please care to explain as I can't seem to make sense of it
coolgirlrom Here the actual increase of HCO3 from baseline (34) is HIGHER than that of the calculated compensation ( which is 26.5). Therefore the seconds disorder present is metabolic alkalosis 😊
@@dr.shabrishgowda1309 but if consider it to be chronic resp acidosis, then everything fits in.
There are mistakes in Examples 1,2
about the pco2
Can you be more specific? I rechecked them and don't see any errors.
Strong Medicine if pco2 above 40 means Acidosis
12:52
Exactly
I resolved as respiratory alkalosis too
can someone tell me why example number 3 is not chronic resp acidosis wih normal compensation ... other than the acute vomiting part cuz i dont buy it
ABGs are like ECGs - they cannot be reliably interpreted in isolation. They require some amount of clinical history to know if acid-base derangement are likely acute or chronic, since we use different compensation formulas for those two possibilities. If the clinical history for example 3 was a 60 year old smoker presenting to the clinic with progressively worsening dyspnea and cough for 6 months, then yes, the ABG would be most consistent with a chronic respiratory acidosis with normal compensation. But in this case, the fact that it's a young (presumably healthy) person with an acute illness means a chronic process is unlikely, and we must interpret the ABG with that in mind.
@@StrongMed wow im really surprised you replied this fast ... woah thanks a lot for your concern and early reply really it is much appreciated dr Strong ....
my point is after calculating whether this is acute or chronic using the delta ph over delta co2 or by the other method evry 10 co2 change equals 0.04 channge in ph in chronic and 0.08in acute i found out ,,, surprisingly ... it is chronic ... so does this mean that these formulas are wrong and the clinical situation is the only determinant of chronicity of resp disorders ?
finally thanks again dr strong for your kind reply and im really loving this abg series analysis as an intensivist they are enourmesly helpful
thanks a lot
"To make things even more complicated" , why would you do that on purpose?
I dont know HOW to say thank you THANKSSSSS
Thanks
GOD BLESS U
Tq
I have to disagree with this appropriate compensation would mean a normalized pH. example one pH is not compensated. It would be uncompensated metabolic alkalosis.
This is a common misconception. Appropriate physiologic compensation of a single acid-base disorder does not bring one's pH back into the normal range unless the acid-base disorder is relatively mild. That's why compensation equations and related rules of thumb were empirically measured.
Hello Doc. How can you know if the pathology is acute or chronic? Thank you
It's based on your clinical impression. This is one of the things that makes it impossible to analyze an ABG in isolation from a history or clinical vignette.
@@StrongMed Thank you for answering doc. You're doing God's work for these videos. Have a nice day.
I have a question , how do you know if the pathologic process is acute or chronic ?!
It's an educated guess based on the patient's history. There's no way to tell just from the lab tests alone.
@@StrongMed Thank you for your answer
I find myself looking at the bicarb for determining metabolic alkelosis this that less accurate
by the last example why not say that is primary metabolic alkalemia with uncomplete respiratory compensation due to respiratory acidosis?? pls answer anyone :(
In this case, it would be confusing to describe this as a metabolic alkalosis with incomplete respiratory compensation since the pH is not only lower than respiratory compensation (i.e. the patient is "overcompensating", which doesn't happen), but is even lower than normal. Thus the respiratory acidosis is having a quantitatively larger effect on the pH.
Sometimes in ABG analysis the word "primary" gets used in an imprecise way to mean "the first acid-base disorder which our algorithm happens to identify", and typically is also the acid-base disorder which has the greatest quantitative impact on the pH. But the disorder that is first identified is not necessarily the first that happens chronologically, nor the necessarily the most clinically relevant.
NICE
My entire life i didn't understand anything so welll
😍😍😍
Wooowwwwww
Sorry, i was talking about example 2
Ok cool but how the HELLLLL can we know if its too high or too low. you never mentioned that point. immediate Dislike
If what is too high or too low?