Hersch, that's a great question. What the adjusted anion gap does is to provide an estimate of what the AG would be if the pt's low albumin could be corrected. In other words, if a pt has an alb of 2mg/dL & AG of 12, it superficially looks normal. However, if u could correct the low alb to 4, you'd find the AG incr. to 17. It's why I favor the term "adjusted anion gap" over "corrected anion gap", because the later implies the measured AG is wrong, which isn't the case.
An anion gap of 4 is generally abnormal, but you would want to check with the lab that ran the sample to see what its normal range is. The normal range of any lab test varies slightly depending upon the specific method the lab uses. If your anion gap is truly low, by far the most common explanation for this is low albumin, which is often from poor diet but can also be seen with a large variety of chronic diseases.
Amazing lecture Dr Strong, I'm studying for my final medical school exams and have struggled with acidosis since first year of medical school. You lecture series has addressed my confusion with this topic. Thank you
@ramseet chhabra, you're correct to question whether the AG of 7 is truly "normal", when I mentioned that labs commonly report a normal range of AG of 8-12 mEq/L. I suppose it's actually lower than normal, though we don't typically discuss "low anion gap metabolic acidosis" as a specific entity, since it's usually the consequence of a normal anion gap acidosis + a condition that leads to a lowering of the AG that's not directly related to acid-base status (e.g. hypoalbuminemia - at least in the conventional model of acid-base analysis). In this particular example, the normal gap metabolic acidosis is likely from either CKD or hypoaldosteronism. While severe and/or end-stage renal failure typically leads to an elevated AG acidosis (caused by accumulation of unmeaured anions such as sulfates and phosphates), mild or early renal failure can lead to a normal AG acidosis through an impairment in acid excretion.
@@lehu8529 Impossible to say from just the given "abrupt onset of dyspnea x 2 hours". It could be from fluid overload from CKD, though that's usually more gradual. Same with pneumonia. Other possibilities that can cause a more sudden onset of dyspnea than those diagnoses include pulmonary embolism, an arrhythmia, acute MI, or a panic attack.
Thank you Doctor Eric Strong . although i might need to watch a couple time but it is a lot clearer , Doctors around the world thank you . You use your valuable free time to do this.
Thank you so much for the video!! A question: on minute 2:56 , why the Anion gap formula isn't Anion gap=unmeasured Cations - unmeasured Anions? (It's shown the other way around)
Hi Dr Strong, Thank you SO much for your videos. They are incredibly well structured and I can't imagine how long they would have taken you to make. A quick question, in patients with electrolyte disturbances caused by pathophysiology independent on acid:base disturbances, does the anion gap become hard or even impossible to interpret?
I'm not aware of an obvious one other than to simply convert mmHg to kPa or vice versa for the PCO2. (1 kPa = 7.5mmHg, 1mmHg=0.133 kPa). Converting mmol/L to meq/L is a little tricky because it depends upon the chemical properties of the ion or molecule, but for sodium, bicarb, and chloride, 1meq/L=1mmol/L. If there is anyone else on here that has a lot of experience interpreting ABGs in a location that uses SI units, please feel free to leave a comment explaining what approach you use.
At 10:56, i dont get why it became 6. As far as my math is concern, 2.5 x (4-1.5) = 6.25. Is this rounded off? The .25 is not needed, just the whole number?
18:06 needs a 2nd look .Albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. . A normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis. Should we SUBTRACT then 2.5 x(4- mAlb) from the computed AG? Rather than ADD as presented. Please comment ASAP. Thanks
Dr. Strong.... In ex 3: how can you say that AG of 7 is normal? I know the pt never overcompensates but Cl ion is elevated in the vignette (although, I can't understand how as the pt has renal failure). Is there a different mechanism that is increasing Cl? Could you please explain AG = 7 is considered normal? Thanks :)
Awesome video! I think something that would also be helpful, in addition to walking through how to determine the type of acid-base disturbance in the examples, is to provide the diagnosis or cause of the acid-base disturbance (e.g. salicylate toxicity, DKA, or whatever it may be)
Thanks for stopping by and the feedback! Combining the analysis of the numbers with a discussion of etiologies felt a little long to put together into one video up front, so etiologies got separate videos (lessons 8-12), and I put both the analysis and differential diagnosis together in lessons 13 and 20.
It's possible that your anion gap is just low, but everything else (e.g. your other electrolytes, albumin, etc....) is fine, in which case I wouldn't necessarily worry about it, especially if you are feeling well and are generally healthy. But I would probably ask your doctor about it all the same.
AirCarty87, first I would confirm the high anion gap (AG) with another check, and also look at your lab's reference range (since some labs include potassium in the calculation, which would make a normal AG closer to 12-16). If it's confirmed high, and you are otherwise feeling ok, I wouldn't get too concerned. Since the AG is only an indirect measure, there is also no need to directly reverse it per se, but you should still check with your doctor to see if he/she has an explanation.
BUN refers only to the nitrogen in urea. Nitrogen accounts for a little less than half of the urea's molecular mass is (28 out of 60). In countries where urea (and not only the nitrogen in urea) is determined, a typical normal range for urea is 20 to 40 mg/dL, which is about twice the normal range for BUN (7 to 20 mg/dL).
DrMythology, good question that I probably should have either clarified in the narration or just have changed the numbers by one to prevent the appearance of a contradiction. In this case, the patient has mild hyperkalemia, and as potassium is an "unmeasured" cation, and excess of it leads to a lower than anticipated anion gap. (every 1meq/L that the K is above 4.0, the expected anion gap should be 1meq/L lower than "normal").
Hello, I´m confused. In the first 2 examples it is said that we check the PCO2 (Step 2) and if is deranged in the same direction as the bicarb, then the process is metabolic. However, in example 3 it is said that if PCO2 is deranged in opposite direction as pH, the process is respiratory. Then, what is the relation to look for? PCO2 with bicarb or PCO2 with pH? I remember lesson 3 saying it was with pH. Please clarify, Thank you
This is almost never enough of an effect to be clinically relevant, but in this particular case, it would shift the expected "normal" anion gap from 8-12 down to 7-11.
hello doctor, im very worry about my anion gap level which is 16.20 is that too high this has me very worried and I don't know what to do to reverse it. Thank you!!!
Really like the videos..One quick question as I was getting use to using the short cut for met. acidosis by comparing the first two digits of pH after decimal to PaCO2 I noticed that the difference is 4 when you are doing the first example in lecture 5. pH is 7.32 and PaCO2 is 28 vs Winters is 1. My question is really when do you consider this number to compensated vs uncompensated(2* abnormality)? I sure do hope you still read this, but completely understand if you don't have time as I can relate;)
That's a great question. People frequently cite Winters' formula as PCO2 = (1.5 x HCO3) + 8 +/- 2, with the +/-2 term allowing for some variability in how different people's physiology operates. (I might be wrong, but I think Winters' original paper also included the +/-2 term. However, no one ever talks about how close the two digits of pH after the decimal needs to be (i.e. what is the range of normal compensation responses). Unfortunately, because the 2 digit shortcut underestimates appropriate compensation sometimes, and overestimates appropriate compensation other times (depending upon the pH), it is very difficult to create a single yet accurate rule for deciding when the number is consistent with appropriate compensation. I just did a back of the envelope calculation for this, but it looks like as an extremely rough rule, for a moderately severe metabolic acidosis (i.e. HCO3 14-20 range), the 2 pH digits after the decimal should be within 4 of the HCO3 to consider compensation appropriate. But that rule falls apart when the HCO3 drops below 12-14. And all of this assumes that the +/-2 term in Winters' formula is actually a valid representation of the variation in compensation between people at extremes of pH, which I suspect is probably not true. (i.e. the normal variation in compensation to extreme metabolic acidosis is probably much wider than the equation allows for).
Isn't it possible to have a low anion gap metabolic acidosis? And wouldn't hyperkalemia, hypernatremia, hypermagnesemia, hypercalcemia, etc.(basically high levels of any positively charged electrolyte) cause a high anion gap and hypokalemia, hyponatremia, etc.(low levels of any positively charged electrolyte) cause a low or even negative anion gap?
what exactly happens when there is an increase in unmeasured cations and albumin? how it makes the sodium lower and the meaured anions lower respectievley?
Thanks for a message. I definitely had some volume issues during the first couple of years I was making these videos. They've been fixed for more recent videos.
Dr Eric, I live in Bogota where the concentration on HCO3- is around 17, the altitude is AMSL. Does the body compensate this lower concentration of anion increasing Cl- or other unmeassured anion? Why does the concentration of HCO3 decreases if the PaCO2 is about 66 here? shouldnt it be compensated with higher levels of HCO3? I don't even know why here the PaCO2 is that high if the lower pressure of O2 is compensated with hyperventilation..... these questions keep me awake at night!
Great lectures. But the current classification of RTA now Type 1 or Classical is refer to as Distal RTA, RTA Type 2 as Proximal RTA and Type 4 cause by mineralocorticoid deficiency still refer to as Type 4 RTA.
+George Schagar Thanks for pointing this out. I feel like the shift in preferred terminology has been kind of slow over the past decade, but you are probably right that most nephrologists now refer to these as distal and proximal (which makes much more sense).
Dear Dr. Eric, thank you very much for your videos as they make studying much easier. I have a question for example 4. You say metabolic acidosis because her pCO2 is low, but isn´t it a normal range (32-45mmHG)? Why additionally a respiratory acidosis, as pCO2 is still in normal range? I would be very grateful for an answer.
If the acidosis was caused by respiratory acidosis, pCO2 will be ABOVE the normal range. Hence the primary cause of the acidosis is metabolic. In a normal patient with metabolic acidosis, the pCO2 will be lower than normal (calculate appropriate pCO2 using Winter's formula). Hence 34 is considered high in this case and there is a presence of both metabolic and respiratory acidosis
Sir, Hydrogen ions are cations, so do they fall under the category of unmeasured cations ?, if so then in elevated gap metabolic acidosis when unmeasured anions are increased there should also be some increase of of unmeasured cations due to excess hydrogen ions ( considering the fact that some of these hydrogen ions are neutralised by bicarbonate ions). Plz clarify. Sutirtha
Sutirtha, you are right that H+ could be considered an unmeasured cation, but it is a matter of scale. A typical serum sodium concentration is 140 mEq/L. A typical serum H+ concentration is 0.00004 mEq/L. So the concentration of H+ is negligible when considering the anion gap. Although it may be unexpected that the H+ concentration is so low, it's easy to see from the definition of pH: pH = -log (H+ concentration). The reason it often seems unexpected is that most people assume that the H+ concentration is roughly the same as the HCO3- concentration; since H2CO3 dissociates into H+ and HCO3- is seems natural to expect roughly equal amounts of each. However, this is just one of countless reactions that involve the two ions. A much higher fraction of H+ gets excreted in the urine, and some gets buffered by proteins and bone, resulting in the highly unequal serum concentrations. Hope that helps.
Low albumin lowers the anion gap. We calculate anion gap using: Anion gap= [Na+]- ([HCO3-]+[Cl-]) I don't see how low albumin affects the our equation so that it lowers the anion gap...does it decrease [Na+] or increase [HCO3-] or [Cl-]? Thank you for your help!!
in the very beginning he said that anion gap is the difference between unmeasured anion and unmeasured cation.....that means AG=Unmeasured anion - Unmeasured cation..........since albumin is a protein with negative charge(anion) which is usually unmeasured whenever its value increases it increases the anion gap and whenever its value decreases it decreases the anion gap... :)
Sir how can hyperalbiminemia cause high anion gap!!??? Albumin is a negatively charged molecule.....so it should decrease the anion gap [as, Anion gap = {+ve charges} - {-ve charges}]. Similarly how can increased unmeasured cations (K+, Ca++, Mg++) cause low anion gap.....the anion gap should increase in these cases, isn't it??
Sir, plz help us regarding the treatment of the various types of acidosis and alkalosis. Also in metabolic alkslosis the books mention the causes are divided into saline responsive (urine chloride les than 20 meq) and saline resistant (urine chloride more than 20 meq). Would be glad if u kindly elaborate. Sutirtha
The individual etiologies of metabolic alkaloses are covered in video 10 in this ABG series. Regarding the saline responsive and saline resistant distinction, I've always found this specific terminology unnecessarily confusing. Saline responsive alkaloses are essentially those associated with volume depletion (e.g. contraction alkalosis from diarrhea, vomiting, excessive NG suction, diuretics). These etiologies are usually quickly apparent from history, and the alkalosis get better with administration of saline. Saline resistant alkaloses are those not associated with volume depletion (e.g. various forms of hyperaldosteronism, severe hypokalemia), which may not be apparent from history, and require additional testing. The alkalosis here do not get better with saline. Because the "saline responsive" alkaloses are almost always identifiable by history alone, measurement of urine chloride is almost never necessary (despite what most textbooks suggest).
These situations where you're simply increasing unmeasured anions, how does that increase anion gap, unless that is inextricably associated with a simultaneous drop in bicarbonate? E.g. the vague term, "renal failure..." what is failing? Filtration? Reabsorption? From the wording in the video, it seems that renal failure means the former, so then why wouldn't bicarb also not be filtered, and thus retained same as phosphate & sulfate? And if that's the case, there shouldn't be a measured increased AG. If all you're doing is adding unmeasured anions without also reducing bicarbonate, then how do you get an increased gap? In hyperphosphatemia, or an alkalosis-mediated increase in net negative charge on plasma proteins, again, unless there is also a simultaneous decrease in HCO3-, then how could the higher unmeasured anions cause an increased gap?
Hypoxemia beyond a certain degree is a very strong stimulus to increase ventilation. If a process causes hypoxemia without having a significant *direct* impact on CO2 exchange, the respiratory centers of the brain will increase ventilation, which will drive down CO2, leading to a respiratory alkalosis. This is seen in pulmonary edema from heart failure, pneumonia, and pulmonary embolisms (among other situations). It's discussed more in lesson 12 of this series ("Respiratory Alkalosis").
Hersch, that's a great question. What the adjusted anion gap does is to provide an estimate of what the AG would be if the pt's low albumin could be corrected. In other words, if a pt has an alb of 2mg/dL & AG of 12, it superficially looks normal. However, if u could correct the low alb to 4, you'd find the AG incr. to 17. It's why I favor the term "adjusted anion gap" over "corrected anion gap", because the later implies the measured AG is wrong, which isn't the case.
An anion gap of 4 is generally abnormal, but you would want to check with the lab that ran the sample to see what its normal range is. The normal range of any lab test varies slightly depending upon the specific method the lab uses. If your anion gap is truly low, by far the most common explanation for this is low albumin, which is often from poor diet but can also be seen with a large variety of chronic diseases.
Amazing lecture Dr Strong, I'm studying for my final medical school exams and have struggled with acidosis since first year of medical school. You lecture series has addressed my confusion with this topic. Thank you
@ramseet chhabra, you're correct to question whether the AG of 7 is truly "normal", when I mentioned that labs commonly report a normal range of AG of 8-12 mEq/L. I suppose it's actually lower than normal, though we don't typically discuss "low anion gap metabolic acidosis" as a specific entity, since it's usually the consequence of a normal anion gap acidosis + a condition that leads to a lowering of the AG that's not directly related to acid-base status (e.g. hypoalbuminemia - at least in the conventional model of acid-base analysis). In this particular example, the normal gap metabolic acidosis is likely from either CKD or hypoaldosteronism. While severe and/or end-stage renal failure typically leads to an elevated AG acidosis (caused by accumulation of unmeaured anions such as sulfates and phosphates), mild or early renal failure can lead to a normal AG acidosis through an impairment in acid excretion.
What's the origin of the respiratory alkalosis in example #3? Fluid overload from CKD?
@@lehu8529 Impossible to say from just the given "abrupt onset of dyspnea x 2 hours". It could be from fluid overload from CKD, though that's usually more gradual. Same with pneumonia. Other possibilities that can cause a more sudden onset of dyspnea than those diagnoses include pulmonary embolism, an arrhythmia, acute MI, or a panic attack.
TOO GOOD... EXCEPTIONAL... WHAT I COULD NOT LEARN IN MY 5 AND HALF YEARS , YOU TAUGHT ME IN 15MINS.... tHANK YOU SO MUCH...KEEP IT UP SIR...:)
Thank you Doctor Eric Strong . although i might need to watch a couple time but it is a lot clearer , Doctors around the world thank you . You use your valuable free time to do this.
Can’t thank you enough for such a brilliant lectures dr strong
this is the first time i ever understood anion gap ... thank you very much
Nashwa Maaly I'm right there with ya....Eric, you're much appreciated.
Great set of lectures, clear and informative.
The examples at the end are great! Thank you so much!
just ran across these videos... they all look very informative. Thank you
Thank you so much for the video!! A question: on minute 2:56 , why the Anion gap formula isn't Anion gap=unmeasured Cations - unmeasured Anions? (It's shown the other way around)
Hi Dr Strong,
Thank you SO much for your videos. They are incredibly well structured and I can't imagine how long they would have taken you to make. A quick question, in patients with electrolyte disturbances caused by pathophysiology independent on acid:base disturbances, does the anion gap become hard or even impossible to interpret?
I'm not aware of an obvious one other than to simply convert mmHg to kPa or vice versa for the PCO2. (1 kPa = 7.5mmHg, 1mmHg=0.133 kPa). Converting mmol/L to meq/L is a little tricky because it depends upon the chemical properties of the ion or molecule, but for sodium, bicarb, and chloride, 1meq/L=1mmol/L. If there is anyone else on here that has a lot of experience interpreting ABGs in a location that uses SI units, please feel free to leave a comment explaining what approach you use.
Thank you I made it through the RRT exams but your explanation is the best so far... Thank you
At 10:56, i dont get why it became 6. As far as my math is concern, 2.5 x (4-1.5) = 6.25. Is this rounded off? The .25 is not needed, just the whole number?
18:06 needs a 2nd look .Albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. . A normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis.
Should we SUBTRACT then 2.5 x(4- mAlb) from the computed AG? Rather than ADD as presented. Please comment ASAP. Thanks
Great video!! It helped me a lot! keep on doing videos like this one!! Greetings from México!
Dr. Strong.... In ex 3: how can you say that AG of 7 is normal? I know the pt never overcompensates but Cl ion is elevated in the vignette (although, I can't understand how as the pt has renal failure). Is there a different mechanism that is increasing Cl? Could you please explain AG = 7 is considered normal? Thanks :)
Awesome video! I think something that would also be helpful, in addition to walking through how to determine the type of acid-base disturbance in the examples, is to provide the diagnosis or cause of the acid-base disturbance (e.g. salicylate toxicity, DKA, or whatever it may be)
Thanks for stopping by and the feedback! Combining the analysis of the numbers with a discussion of etiologies felt a little long to put together into one video up front, so etiologies got separate videos (lessons 8-12), and I put both the analysis and differential diagnosis together in lessons 13 and 20.
Dear Dr Eric
In example 3: could it be a respiratory alkalosis with chronic compensation?
Very helpful video in understanding how to operate these concepts .Thank you.
Thank you Dr. Strong!
It's possible that your anion gap is just low, but everything else (e.g. your other electrolytes, albumin, etc....) is fine, in which case I wouldn't necessarily worry about it, especially if you are feeling well and are generally healthy. But I would probably ask your doctor about it all the same.
Thank you for ur Videos
Very informative
THANKS SO MUCH , IT IS SEEMED TO BE EASY TO UNDERSTAND ABG
5:07 why chloride isn't compensating by increasing its conc just like normal anion gap acidosis
AirCarty87, first I would confirm the high anion gap (AG) with another check, and also look at your lab's reference range (since some labs include potassium in the calculation, which would make a normal AG closer to 12-16). If it's confirmed high, and you are otherwise feeling ok, I wouldn't get too concerned. Since the AG is only an indirect measure, there is also no need to directly reverse it per se, but you should still check with your doctor to see if he/she has an explanation.
BUN refers only to the nitrogen in urea. Nitrogen accounts for a little less than half of the urea's molecular mass is (28 out of 60). In countries where urea (and not only the nitrogen in urea) is determined, a typical normal range for urea is 20 to 40 mg/dL, which is about twice the normal range for BUN (7 to 20 mg/dL).
DrMythology, good question that I probably should have either clarified in the narration or just have changed the numbers by one to prevent the appearance of a contradiction. In this case, the patient has mild hyperkalemia, and as potassium is an "unmeasured" cation, and excess of it leads to a lower than anticipated anion gap. (every 1meq/L that the K is above 4.0, the expected anion gap should be 1meq/L lower than "normal").
Hello, I´m confused. In the first 2 examples it is said that we check the PCO2 (Step 2) and if is deranged in the same direction as the bicarb, then the process is metabolic. However, in example 3 it is said that if PCO2 is deranged in opposite direction as pH, the process is respiratory. Then, what is the relation to look for? PCO2 with bicarb or PCO2 with pH? I remember lesson 3 saying it was with pH. Please clarify, Thank you
This is almost never enough of an effect to be clinically relevant, but in this particular case, it would shift the expected "normal" anion gap from 8-12 down to 7-11.
Strong explanations 💪 tnx a lot
Thank u 🙏 it was amazing explanation!
I am struggling to understand why in example 3, there is a further metabolic acidemia and not metabolic alkalosis considering the HCO3- of 14
Excellent explanation..thank you very much sir
Thank you Doc
Thank you Dr ,I watch this
This is awesome
Thank you so much for this
Really well done
hello doctor, im very worry about my anion gap level which is 16.20 is that too high this has me very worried and I don't know what to do to reverse it. Thank you!!!
Thank you so much from Nepal
Thank you Dr Strong
How come organic acids are anions? Thx!
love ur explanation. thanks a lot
Really like the videos..One quick question as I was getting use to using the short cut for met. acidosis by comparing the first two digits of pH after decimal to PaCO2 I noticed that the difference is 4 when you are doing the first example in lecture 5. pH is 7.32 and PaCO2 is 28 vs Winters is 1. My question is really when do you consider this number to compensated vs uncompensated(2* abnormality)? I sure do hope you still read this, but completely understand if you don't have time as I can relate;)
That's a great question. People frequently cite Winters' formula as PCO2 = (1.5 x HCO3) + 8 +/- 2, with the +/-2 term allowing for some variability in how different people's physiology operates. (I might be wrong, but I think Winters' original paper also included the +/-2 term. However, no one ever talks about how close the two digits of pH after the decimal needs to be (i.e. what is the range of normal compensation responses). Unfortunately, because the 2 digit shortcut underestimates appropriate compensation sometimes, and overestimates appropriate compensation other times (depending upon the pH), it is very difficult to create a single yet accurate rule for deciding when the number is consistent with appropriate compensation. I just did a back of the envelope calculation for this, but it looks like as an extremely rough rule, for a moderately severe metabolic acidosis (i.e. HCO3 14-20 range), the 2 pH digits after the decimal should be within 4 of the HCO3 to consider compensation appropriate. But that rule falls apart when the HCO3 drops below 12-14. And all of this assumes that the +/-2 term in Winters' formula is actually a valid representation of the variation in compensation between people at extremes of pH, which I suspect is probably not true. (i.e. the normal variation in compensation to extreme metabolic acidosis is probably much wider than the equation allows for).
last example adjusted should be 29 right ? 12+2.5 first then 4-2 is 2 then 14.5 multiply by 2
Hi. In your video, you mentioned that positive ions are anions. Aren't they cations? Please correct me if I'm wrong
sir why we are adjusting aniongap according to albumin how albumin play role in anion gap
Any good books that talk about this with illustrations?
Very helpful!
Isn't it possible to have a low anion gap metabolic acidosis? And wouldn't hyperkalemia, hypernatremia, hypermagnesemia, hypercalcemia, etc.(basically high levels of any positively charged electrolyte) cause a high anion gap and hypokalemia, hyponatremia, etc.(low levels of any positively charged electrolyte) cause a low or even negative anion gap?
what exactly happens when there is an increase in unmeasured cations and albumin? how it makes the sodium lower and the meaured anions lower respectievley?
@1:04 "An elevated anion gap indicates the presence of a non??? measured anion" I didn't catch what you said there. Non what?
non routinely measured anion
Great lecture! thank you
At 12:29 he should have said "the PaCO2 is deranged in the same direction as the pH"
Thanks. You are correct. Added an annotation to clarify.
I thought I was going crazy lol
Thanks for your uploads! I hope you can adjust your sound level to be a bit louder in your future videos.
Thanks for a message. I definitely had some volume issues during the first couple of years I was making these videos. They've been fixed for more recent videos.
I love this channel. Sorry for not noticing that this is an old video. New subscriber from Saudi Arabia :D
No problem! We are glad to have you!
Dr Eric, I live in Bogota where the concentration on HCO3- is around 17, the altitude is AMSL. Does the body compensate this lower concentration of anion increasing Cl- or other unmeassured anion? Why does the concentration of HCO3 decreases if the PaCO2 is about 66 here? shouldnt it be compensated with higher levels of HCO3? I don't even know why here the PaCO2 is that high if the lower pressure of O2 is compensated with hyperventilation..... these questions keep me awake at night!
hernan625 *the altitude is 2700 meters AMSL*
hernan625 Sorry, I misread the values, the PaCO2 is about 30 mmHg here, please ignore the last two questions
sir, tanku for your great work. sir wil u plz explain how normal
gapmetabolic acidosis and elevated gap metabolic acidosis present together
Great lectures. But the current classification of RTA now Type 1 or Classical is refer to as Distal RTA, RTA Type 2 as Proximal RTA and Type 4 cause by mineralocorticoid deficiency still refer to as Type 4 RTA.
+George Schagar Thanks for pointing this out. I feel like the shift in preferred terminology has been kind of slow over the past decade, but you are probably right that most nephrologists now refer to these as distal and proximal (which makes much more sense).
i got results from the doctor saying my anion gap was 4 which was abnormal, is it?
Dear Dr. Eric,
thank you very much for your videos as they make studying much easier. I have a question for example 4.
You say metabolic acidosis because her pCO2 is low, but isn´t it a normal range (32-45mmHG)?
Why additionally a respiratory acidosis, as pCO2 is still in normal range?
I would be very grateful for an answer.
If the acidosis was caused by respiratory acidosis, pCO2 will be ABOVE the normal range. Hence the primary cause of the acidosis is metabolic. In a normal patient with metabolic acidosis, the pCO2 will be lower than normal (calculate appropriate pCO2 using Winter's formula). Hence 34 is considered high in this case and there is a presence of both metabolic and respiratory acidosis
Sir,
Hydrogen ions are cations, so do they fall under the category
of unmeasured cations ?, if so then in elevated gap metabolic acidosis when unmeasured anions are increased there should also be some increase of of unmeasured cations due to excess hydrogen ions ( considering the fact that some of these hydrogen ions are neutralised by bicarbonate ions). Plz clarify. Sutirtha
Sutirtha, you are right that H+ could be considered an unmeasured cation, but it is a matter of scale. A typical serum sodium concentration is 140 mEq/L. A typical serum H+ concentration is 0.00004 mEq/L. So the concentration of H+ is negligible when considering the anion gap. Although it may be unexpected that the H+ concentration is so low, it's easy to see from the definition of pH: pH = -log (H+ concentration). The reason it often seems unexpected is that most people assume that the H+ concentration is roughly the same as the HCO3- concentration; since H2CO3 dissociates into H+ and HCO3- is seems natural to expect roughly equal amounts of each. However, this is just one of countless reactions that involve the two ions. A much higher fraction of H+ gets excreted in the urine, and some gets buffered by proteins and bone, resulting in the highly unequal serum concentrations. Hope that helps.
Low albumin lowers the anion gap. We calculate anion gap using: Anion gap= [Na+]- ([HCO3-]+[Cl-])
I don't see how low albumin affects the our equation so that it lowers the anion gap...does it decrease [Na+] or increase [HCO3-] or [Cl-]? Thank you for your help!!
in the very beginning he said that anion gap is the difference between unmeasured anion and unmeasured cation.....that means AG=Unmeasured anion - Unmeasured cation..........since albumin is a protein with negative charge(anion) which is usually unmeasured whenever its value increases it increases the anion gap and whenever its value decreases it decreases the anion gap... :)
Sir how can hyperalbiminemia cause high anion gap!!???
Albumin is a negatively charged molecule.....so it should decrease the anion gap [as, Anion gap = {+ve charges} - {-ve charges}].
Similarly how can increased unmeasured cations (K+, Ca++, Mg++) cause low anion gap.....the anion gap should increase in these cases, isn't it??
Sir, plz help us regarding the treatment of the various types of acidosis and alkalosis. Also in metabolic alkslosis the books mention the causes are divided into saline responsive (urine chloride les than 20 meq) and saline resistant (urine chloride more than 20 meq). Would be glad if u kindly elaborate. Sutirtha
The individual etiologies of metabolic alkaloses are covered in video 10 in this ABG series. Regarding the saline responsive and saline resistant distinction, I've always found this specific terminology unnecessarily confusing. Saline responsive alkaloses are essentially those associated with volume depletion (e.g. contraction alkalosis from diarrhea, vomiting, excessive NG suction, diuretics). These etiologies are usually quickly apparent from history, and the alkalosis get better with administration of saline.
Saline resistant alkaloses are those not associated with volume depletion (e.g. various forms of hyperaldosteronism, severe hypokalemia), which may not be apparent from history, and require additional testing. The alkalosis here do not get better with saline.
Because the "saline responsive" alkaloses are almost always identifiable by history alone, measurement of urine chloride is almost never necessary (despite what most textbooks suggest).
These situations where you're simply increasing unmeasured anions, how does that increase anion gap, unless that is inextricably associated with a simultaneous drop in bicarbonate? E.g. the vague term, "renal failure..." what is failing? Filtration? Reabsorption? From the wording in the video, it seems that renal failure means the former, so then why wouldn't bicarb also not be filtered, and thus retained same as phosphate & sulfate? And if that's the case, there shouldn't be a measured increased AG. If all you're doing is adding unmeasured anions without also reducing bicarbonate, then how do you get an increased gap?
In hyperphosphatemia, or an alkalosis-mediated increase in net negative charge on plasma proteins, again, unless there is also a simultaneous decrease in HCO3-, then how could the higher unmeasured anions cause an increased gap?
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Thanks a lot ,interesting.
Thank you sir
Its not played ...????after 2 lectures ...
example 3...how is it possible for someone to have dyspnea and low CO2????
Hypoxemia beyond a certain degree is a very strong stimulus to increase ventilation. If a process causes hypoxemia without having a significant *direct* impact on CO2 exchange, the respiratory centers of the brain will increase ventilation, which will drive down CO2, leading to a respiratory alkalosis. This is seen in pulmonary edema from heart failure, pneumonia, and pulmonary embolisms (among other situations). It's discussed more in lesson 12 of this series ("Respiratory Alkalosis").
Oh yes right! Thank you for your quick response.
its helpful tnx
Thanks
its helpful
Tq
05:55
more volume please
nice
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