Delta Ratio in Acid-Base Disorders

This is Eric Strong again, and this is the sixth lecture in this course on understanding ABGs. The topic today is the delta ratio and its use in diagnosing complex acid-based derangements. The learning objective are as follows. First, to understand the relationship between the production of pathologic acids and the serum bicarbonate concentration. Next, to be able to calculate the delta ratio and the delta gap, and to be familiar with their limitations. Last to be able to use the delta ratio to identify the presence of multiple metabolic disorders and triple acid-base disorders. Before I go further, I want to point out that with each layer of complexity in ABG interpretation, the certainty with which we can make diagnoses becomes less. Although I have presented a fairly protocolized approach to acid-base analysis so far, and will continue to do so in this lecture, I caution against being overly dogmatic when diagnosing mixed metabolic disorders. I personally allow diagnosis of a triple acid-base disorder to alter management on a particular patient only when the triple disorder is quantitatively dramatic and when its existence is consistent with a clinical scenario at hand. To understand the delta ratio, one must first realize something about how the body maintains electrical neutrality during an elevated gap acidosis. and how the body buffers the presence of pathologic acids. Here we have a simple balance scale, which will represent the balance between negative and positive charge in the extracellular space. The basket on the left is filled with anions, and the basket on the right is filled with cations. Now suppose that some amount of pathologic acid is formed, for example lactic acid or keto acids. The acid dissociates into a hydrogen ion and its anionic form, the newly formed anions which contribute to the anion gap we learned about in lecture 5 are added to the extracellular space's burden of negative charge. This appears to disrupt the balance of the charges and would be a problem except that some bicarbonate ion is removed from the scale by buffering the hydrogen cations released from dissociation of the acid. Thus, the balance is maintained. I hope the cartoon helps to illustrate that at first glance during an elevated gap metabolic acidosis, there should be a 1 to 1 ratio between the increase in anion gap and the decrease in bicarbonate. In other words, in order to generate a pathologic unmeasured anion from a newly formed molecule of acid, that acid's donatable hydrogen must also be buffered by a bicarbonate ion. The delta ratio is a calculation that compares the increase in the anion gap to the decrease in bicarb. Specifically, the delta ratio equals the difference between the measured anion gap and the normal anion gap, divided by the difference between the normal bicarb and the measured bicarb. The measured anion gap should actually be adjusted for low albumin as discussed in the last lecture. Also, normal values for the anion gap and for the bicarb should be based on the specific lab testing the patient's samples. For purposes of this lecture, I will continue to use a normal anion gap of 12mEq. per liter and a normal bicarb of 24 vLq per liter. Although contrary to what was just suggested a minute ago by the cartoon, the delta ratio is not always 1. That previous suggestion was based on the assumption that all pathologic acids are buffered by extracellular bicarbonate, while in reality, some fraction of these acids are actually buffered by bone and intracellular buffers. This results in a delta ratio slightly greater than 1 in certain situations. The expected delta ratio during an elevated gap metabolic acidosis depends upon the etiology of the elevated gap. For example, during a lactic acidosis, studies have demonstrated a typical delta ratio to be 1.6. with a range of about 1.0 to 2.0. More specifically, at the earliest onset of the lactic acidosis, the ratio starts at 1.0 and then increases over the first several hours of illness. With ketoacidosis, the expected delta ratio truly is 1.0, with a range of 0.8 to 1.2. The exception to this is if GFR is acutely decreased from concurrent volume depletion, which reduces the range of GFR. at which the body can eliminate the keto acids, which would otherwise reduce the change in the anion gap. The expected ratio in kidney disease is quite variable, depending on the extent of tubular damage relative to the decrease in GFR. Finally, in methanol and ethylene glycol ingestion, there are no reports in the literature to suggest what the expected ratio should be, but it is probably between 1.0 and 2.0. Let's take a look at how the delta ratio shifts in different mixed metabolic disorders. I'll first start with a combined elevated gap metabolic acidosis and a metabolic alkalosis. As this is a demonstration, I will work with the simplifying but incorrect assumption that only extracellular bicarbonate buffers newly produced pathologic acid. Here is a rough breakdown of the cations and anions of a person with normal acid-base status. In this case, as you can see, the sodium is 140, the bicarb is 24, and the chloride is 104. This makes the anion gap 12. If this person develops an elevated gap metabolic acidosis, we see that the pathologic acids adds to the unmeasured anions, and to make room for this, the bicarb is necessarily reduced. In this particular example, the bicarb is reduced down to 12, which will mean that the anion gap is increased up to 24. So the delta anion gap will be measured minus normal, which is 24 minus 12, which is 12. the delta bicarb will be the normal bicarb of 24 minus the measured bicarb of 12, which will also be 12. Thus, we can see that the delta anion gap equals the delta bicarbonate, giving us a ratio of 1. If this same person were to then also develop a concurrent metabolic alkalosis, how would this impact the electrolytes? The anion gap will be the same at 24, so in order to make room for the additional 6 mEq per liter of bicarb, the chloride is now reduced by that same amount. Thus the delta anion gap is still 12, but the delta bicarb is now 6. The delta ratio, which is the delta anion gap divided by the delta bicarb, will be 12 divided by 6, or 2. This ratio is higher than expected if an elevated gap acidosis were the only metabolic process. For a different example, let's look at the combination of an elevated gap acidosis and a normal gap acidosis. The first bit's the same, starting at a normal acid-base status with an anion gap of 12 and a bicarb of 24. We give the person an elevated gap metabolic acidosis, increasing the anion gap to 24 and lowering the bicarb to 12. Now when we add a concurrent normal gap metabolic acidosis, the unmeasured anions stay the same, but the bicarb is reduced with an increase in chloride of equal magnitude. Here the anion gap is again 24, but now with a bicarb of 6. This gives a delta anion gap of 12 and a delta bicarb of 18. To calculate the delta ratio, we just take the former divided by the latter, or 12 divided by 18, which is approximately 0.7. This ratio is thus lower than expected if an elevated gap acidosis were the sole process. This chart will summarize how to use the delta ratio to determine what pathologic metabolic disorders are present. If the measured delta ratio is lower than the expected range for the specific etiology of the elevated gap acidosis, then the pathologic disorders present include both the elevated gap metabolic acidosis and a normal gap metabolic acidosis. If the measured delta ratio falls within the expected range, then the patient likely has an elevated gap metabolic acidosis only with no other metabolic disorders. Though this does not mean the patient couldn't have a concurrent respiratory disorder, the delta ratio only reflects metabolic disorders. If the measured delta ratio is higher than the expected range, the patient likely has both an elevated gap metabolic acidosis and a metabolic alkalosis. I'm going to talk just for a minute or two about a closely related concept frequently called the delta gap, which is a commonly used alternative to the delta ratio. The delta gap is the difference between the measured and normal anion gap minus the difference between the normal and measured bicarb. The common utilization of the delta gap assumes a one-to-one tradeoff between accumulation of unmeasured anions and utilization of bicarb. With this assumption, if there is an isolated elevated gap metabolic acidosis and no other metabolic disorders, the delta gap should be equal to zero with a range from negative six to positive six milliequivalents per liter. As I pointed out before, this assumption is probably only valid in the presence of ketoacidosis for reasons that are unfortunately beyond the scope of this lecture. Most clinicians who use the delta gap use a slightly altered form which may look more familiar to you. Let's substitute the delta bicarb with 24 minus measured bicarb, and then distribute the minus sign and remove those parentheses. We'll shift the 24 to the other side of the equal sign. If we know that the delta gap should be equal to 0 plus or minus 6, then the left side of the equation simplifies to 24 plus or minus 6. Then switch the two sides and we are left with this. In other words, if the only metabolic process present is an elevated gap acidosis, the delta anion gap plus the measured bicarb should equal 24 plus or minus 6. Within the context of calculating the delta gap, this range of 18 to 30 is commonly thought of as being quote the normal range for serum bicarb. If the delta anion gap added to the measured bicarb is within the quote acidemic range for bicarb that is, if it's less than 18, it suggests the concurrent presence of both an elevated gap and a normal gap metabolic acidosis. If the delta gap is within the quote alcholemic range for bicarb that is greater than 30, it suggests the concurrent presence of both an elevated gap metabolic acidosis and a metabolic alkalosis. There are a number of potential problems with using the delta gap to diagnose acid-based disorders. First, the quote normal range of 18 to 30 that is assumed here is actually much greater than the true normal range for bicarb, which is generally closer to 22 to 26, depending upon your lab. More importantly, it does not account for intracellular and bone buffering of non-volatile acids, which leads to a tendency to over-diagnose a concurrent metabolic alkalosis and to under-diagnose a concurrent normal gap acidosis. This is a greater problem in the presence of lactic acidosis than of ketoacidosis. Overall, I find the delta gap to be less accurate than the delta ratio. When one considers that the diagnosis of mixed metabolic disorders is already relatively prone to error due to the assumed simplifications of an underlying physiology that can actually be quite complex, adding in the additional uncertainty of the delta gap calculation seems as likely to give you the wrong answer as the right. Therefore, if you are trying to diagnose a mixed metabolic disorder, I'd recommend sticking with the delta ratio. So let's go through three examples to see how the delta ratio works in practice. Example 1. A 75-year-old woman from a skilled nursing facility presents with fever and profuse diarrhea for two days. Her vital signs are temperature 38.5, heart rate 130, and blood pressure 78 over 30. And here is her ABG and basic serum chemistries. As always, the first step in interpreting this ABG is to check the pH. It's low, so there is an acidemia present. Step 2 is to check the PCO2. As it's deranged in the same direction as the pH, the process is metabolic, and thus a metabolic acidosis. Step 3, evaluate compensation. We'll use Winter's formula. and ask if the pCO2 is approximately equal to 1.5 times the bicarb plus 8. It is, so compensation is appropriate, which tells us that there is not likely to be a respiratory disorder present. Step 4, calculate the anion gap. Remember, this is the sodium minus the sum of chloride and bicarb. So let's plug in 128, 94, and 14. The anion gap is 20. which is elevated, so the metabolic acidosis identified in step 2 is an elevated gap metabolic acidosis. Now from this lecture, we'll add step 5, which instructs us if the anion gap is elevated, to calculate the delta ratio. To remind you once more, the delta ratio is the delta anion gap divided by the delta bicarb. The measured anion gap of 20 is 8 more than normal, and the bicarb of 14 is 10 less than normal. Therefore, the delta ratio is 0.8. At this point, we need to start to consider what the etiology is of the patient's acid-base disturbance. specifically the etiology of the elevated gap acidosis. We'll talk much more about differential diagnosis in future lectures, but given her history and vital signs, it seems highly likely she has a lactic acidosis. The expected delta ratio for lactic acidosis is between 1.0 and 2.0. Since this ratio of 0.8 is less than 1.0, there is an additional normal gap metabolic acidosis. That is, the bicarb is too low to simply be a consequence of buffering the lactic acid. Thus, the patient's final diagnosis is a combined elevated gap metabolic acidosis and a normal gap metabolic acidosis. Example 2. A 34-year-old type 1 diabetic man comes to the emergency room with fever, nausea, vomiting, and abdominal pain for one day. Step 1. The low pH tells us he has an asthma attack. acidemia, and step 2 tells us again that it is a metabolic acidosis. For step 3, we'll use Winter's formula again. Does 27 approximately equal 1.5 times 12 plus 8? It does, and therefore compensation is appropriate. Step 4, calculate the anion gap. We'll take 140 and subtract 98 and 12 from it. The anion gap is 30, so there is an elevated anion gap metabolic acidosis. Finally, step 5, since the anion gap is elevated, we'll calculate the delta ratio. The measured anion gap of 30 is 18 more than normal And the measured bi- bicarb of 12 is 12 less than normal. Therefore, the delta ratio is 1.5. Unlike the last example, which was likely involving a lactic acidosis, the clinical vignette here strongly suggests ketoacidosis. This means that the range in which the delta ratio is expected to fall is different. Instead of being between 1.0 and 2.0, as it was for lactic acidosis, for ketoacidosis it should fall between 0.8 and 1.2. Thus, this patient's delta ratio is higher than expected, which would be consistent with a concurrent metabolic alkalosis. Final diagnosis, an elevated gap metabolic acidosis and a metabolic alkalosis. In this particular case, the elevated gap acidosis is probably from ketoacidosis as already mentioned, while the metabolic alkalosis is from a combination of vomiting up hydrochloric acid along with some contraction alkalosis from dehydration. Our last example. This one is a little more involved. A 48-year-old alcoholic man is found unconscious in his apartment, soiled with vomit. He was last seen leaving a party six hours prior. Checking the PIN. pH we obviously have in acidemia. With Step 2, since the PCO2 is elevated, the first process we identify here is actually a respiratory acidosis. Step 3, evaluate compensation. The the respiratory acidosis is likely acute in nature, so we need to ask if the bicarb is increased by 1 mEq per liter for every 10 mmHg, the PCO2 is above 40. If that were true, we would expect a measured bicarb around 26 or 27. Is the measured 22 close enough to 26 to say it's appropriate compensation? I'm going to say no here, but it's a borderline call to which one could possibly say yes. Interestingly, it actually doesn't matter whether you say compensation is is appropriate, as in this case you will actually reach the same conclusion in the end. But for now, I will say that the bicarb is too low, and thus there is a metabolic acidosis present. To calculate the anion gap, we take 136, minus 98, and 22, which gives us 16. Since we are given the albumin, which is remarkably low, we need to adjust the anion gap to compensate for this. Remembering from last lecture, the adjusted anion gap equals the measured anion gap plus 2.5 times 4 minus the measured albumin. For this patient, the adjusted anion gap works out to be about 22. Therefore, the metabolic rate is about 22. Acidic metabolic acidosis identified in step 3 is an elevated gap acidosis. Finally, step 5, calculate the delta ratio. The adjusted anion gap of 22 is 10 higher than normal, and the measured biochemical bicarb of 22 is 2 less than normal. This gives us a delta ratio of 5, which will be higher than expected, irrespective of the etiology of the elevated gap. Therefore, this patient also has a metabolic alkalosis. So in summary, the patient's acid-base disturbances include a respiratory acidosis, an elevated gap metabolic acidosis, and a metabolic alkalosis. This is one of those dreaded triple acid-base disorders. What could be going on to cause this patient's situation? Well, I haven't provided much information, but I would speculate the patient has an alcoholic ketoacidosis from his alcoholism and then got acutely and severely intoxicated, which resulted in central respiratory depression, along with developing a metabolic alkalosis from vomiting. A lactic acidosis is also possible, perhaps from aspiration-induced sepsis. That concludes this lecture on the delta ratio. In the next lecture, I will discuss how to identify mixed acid-base disorders when the overall pH is normal.

First, to understand the relationship between the production of pathologic acids and the serum bicarbonate concentration. Next, to be able to calculate the delta ratio and the delta gap, and to be familiar with their limitations. Last to be able to use the delta ratio to identify the presence of multiple metabolic disorders and triple acid-base disorders.

Before I go further, I want to point out that with each layer of complexity in ABG interpretation, the certainty with which we can make diagnoses becomes less. Although I have presented a fairly protocolized approach to acid-base analysis so far, and will continue to do so in this lecture, I caution against being overly dogmatic when diagnosing mixed metabolic disorders. I personally allow diagnosis of a triple acid-base disorder to alter management on a particular patient only when the triple disorder is quantitatively dramatic and when its existence is consistent with a clinical scenario at hand. To understand the delta ratio, one must first realize something about how the body maintains electrical neutrality during an elevated gap acidosis.

and how the body buffers the presence of pathologic acids. Here we have a simple balance scale, which will represent the balance between negative and positive charge in the extracellular space. The basket on the left is filled with anions, and the basket on the right is filled with cations. Now suppose that some amount of pathologic acid is formed, for example lactic acid or keto acids. The acid dissociates into a hydrogen ion and its anionic form, the newly formed anions which contribute to the anion gap we learned about in lecture 5 are added to the extracellular space's burden of negative charge.

This appears to disrupt the balance of the charges and would be a problem except that some bicarbonate ion is removed from the scale by buffering the hydrogen cations released from dissociation of the acid. Thus, the balance is maintained. I hope the cartoon helps to illustrate that at first glance during an elevated gap metabolic acidosis, there should be a 1 to 1 ratio between the increase in anion gap and the decrease in bicarbonate. In other words, in order to generate a pathologic unmeasured anion from a newly formed molecule of acid, that acid's donatable hydrogen must also be buffered by a bicarbonate ion. The delta ratio is a calculation that compares the increase in the anion gap to the decrease in bicarb.

Specifically, the delta ratio equals the difference between the measured anion gap and the normal anion gap, divided by the difference between the normal bicarb and the measured bicarb. The measured anion gap should actually be adjusted for low albumin as discussed in the last lecture. Also, normal values for the anion gap and for the bicarb should be based on the specific lab testing the patient's samples. For purposes of this lecture, I will continue to use a normal anion gap of 12mEq.

per liter and a normal bicarb of 24 vLq per liter. Although contrary to what was just suggested a minute ago by the cartoon, the delta ratio is not always 1. That previous suggestion was based on the assumption that all pathologic acids are buffered by extracellular bicarbonate, while in reality, some fraction of these acids are actually buffered by bone and intracellular buffers. This results in a delta ratio slightly greater than 1 in certain situations. The expected delta ratio during an elevated gap metabolic acidosis depends upon the etiology of the elevated gap.

For example, during a lactic acidosis, studies have demonstrated a typical delta ratio to be 1.6. with a range of about 1.0 to 2.0. More specifically, at the earliest onset of the lactic acidosis, the ratio starts at 1.0 and then increases over the first several hours of illness.

With ketoacidosis, the expected delta ratio truly is 1.0, with a range of 0.8 to 1.2. The exception to this is if GFR is acutely decreased from concurrent volume depletion, which reduces the range of GFR. at which the body can eliminate the keto acids, which would otherwise reduce the change in the anion gap. The expected ratio in kidney disease is quite variable, depending on the extent of tubular damage relative to the decrease in GFR. Finally, in methanol and ethylene glycol ingestion, there are no reports in the literature to suggest what the expected ratio should be, but it is probably between 1.0 and 2.0.

Let's take a look at how the delta ratio shifts in different mixed metabolic disorders. I'll first start with a combined elevated gap metabolic acidosis and a metabolic alkalosis. As this is a demonstration, I will work with the simplifying but incorrect assumption that only extracellular bicarbonate buffers newly produced pathologic acid. Here is a rough breakdown of the cations and anions of a person with normal acid-base status. In this case, as you can see, the sodium is 140, the bicarb is 24, and the chloride is 104. This makes the anion gap 12. If this person develops an elevated gap metabolic acidosis, we see that the pathologic acids adds to the unmeasured anions, and to make room for this, the bicarb is necessarily reduced.

In this particular example, the bicarb is reduced down to 12, which will mean that the anion gap is increased up to 24. So the delta anion gap will be measured minus normal, which is 24 minus 12, which is 12. the delta bicarb will be the normal bicarb of 24 minus the measured bicarb of 12, which will also be 12. Thus, we can see that the delta anion gap equals the delta bicarbonate, giving us a ratio of 1. If this same person were to then also develop a concurrent metabolic alkalosis, how would this impact the electrolytes? The anion gap will be the same at 24, so in order to make room for the additional 6 mEq per liter of bicarb, the chloride is now reduced by that same amount. Thus the delta anion gap is still 12, but the delta bicarb is now 6. The delta ratio, which is the delta anion gap divided by the delta bicarb, will be 12 divided by 6, or 2. This ratio is higher than expected if an elevated gap acidosis were the only metabolic process.

For a different example, let's look at the combination of an elevated gap acidosis and a normal gap acidosis. The first bit's the same, starting at a normal acid-base status with an anion gap of 12 and a bicarb of 24. We give the person an elevated gap metabolic acidosis, increasing the anion gap to 24 and lowering the bicarb to 12. Now when we add a concurrent normal gap metabolic acidosis, the unmeasured anions stay the same, but the bicarb is reduced with an increase in chloride of equal magnitude. Here the anion gap is again 24, but now with a bicarb of 6. This gives a delta anion gap of 12 and a delta bicarb of 18. To calculate the delta ratio, we just take the former divided by the latter, or 12 divided by 18, which is approximately 0.7. This ratio is thus lower than expected if an elevated gap acidosis were the sole process. This chart will summarize how to use the delta ratio to determine what pathologic metabolic disorders are present.

If the measured delta ratio is lower than the expected range for the specific etiology of the elevated gap acidosis, then the pathologic disorders present include both the elevated gap metabolic acidosis and a normal gap metabolic acidosis. If the measured delta ratio falls within the expected range, then the patient likely has an elevated gap metabolic acidosis only with no other metabolic disorders. Though this does not mean the patient couldn't have a concurrent respiratory disorder, the delta ratio only reflects metabolic disorders. If the measured delta ratio is higher than the expected range, the patient likely has both an elevated gap metabolic acidosis and a metabolic alkalosis. I'm going to talk just for a minute or two about a closely related concept frequently called the delta gap, which is a commonly used alternative to the delta ratio.

The delta gap is the difference between the measured and normal anion gap minus the difference between the normal and measured bicarb. The common utilization of the delta gap assumes a one-to-one tradeoff between accumulation of unmeasured anions and utilization of bicarb. With this assumption, if there is an isolated elevated gap metabolic acidosis and no other metabolic disorders, the delta gap should be equal to zero with a range from negative six to positive six milliequivalents per liter.

As I pointed out before, this assumption is probably only valid in the presence of ketoacidosis for reasons that are unfortunately beyond the scope of this lecture. Most clinicians who use the delta gap use a slightly altered form which may look more familiar to you. Let's substitute the delta bicarb with 24 minus measured bicarb, and then distribute the minus sign and remove those parentheses. We'll shift the 24 to the other side of the equal sign.

If we know that the delta gap should be equal to 0 plus or minus 6, then the left side of the equation simplifies to 24 plus or minus 6. Then switch the two sides and we are left with this. In other words, if the only metabolic process present is an elevated gap acidosis, the delta anion gap plus the measured bicarb should equal 24 plus or minus 6. Within the context of calculating the delta gap, this range of 18 to 30 is commonly thought of as being quote the normal range for serum bicarb. If the delta anion gap added to the measured bicarb is within the quote acidemic range for bicarb that is, if it's less than 18, it suggests the concurrent presence of both an elevated gap and a normal gap metabolic acidosis.

If the delta gap is within the quote alcholemic range for bicarb that is greater than 30, it suggests the concurrent presence of both an elevated gap metabolic acidosis and a metabolic alkalosis. There are a number of potential problems with using the delta gap to diagnose acid-based disorders. First, the quote normal range of 18 to 30 that is assumed here is actually much greater than the true normal range for bicarb, which is generally closer to 22 to 26, depending upon your lab. More importantly, it does not account for intracellular and bone buffering of non-volatile acids, which leads to a tendency to over-diagnose a concurrent metabolic alkalosis and to under-diagnose a concurrent normal gap acidosis. This is a greater problem in the presence of lactic acidosis than of ketoacidosis.

Overall, I find the delta gap to be less accurate than the delta ratio. When one considers that the diagnosis of mixed metabolic disorders is already relatively prone to error due to the assumed simplifications of an underlying physiology that can actually be quite complex, adding in the additional uncertainty of the delta gap calculation seems as likely to give you the wrong answer as the right. Therefore, if you are trying to diagnose a mixed metabolic disorder, I'd recommend sticking with the delta ratio.

So let's go through three examples to see how the delta ratio works in practice. Example 1. A 75-year-old woman from a skilled nursing facility presents with fever and profuse diarrhea for two days. Her vital signs are temperature 38.5, heart rate 130, and blood pressure 78 over 30. And here is her ABG and basic serum chemistries.

As always, the first step in interpreting this ABG is to check the pH. It's low, so there is an acidemia present. Step 2 is to check the PCO2. As it's deranged in the same direction as the pH, the process is metabolic, and thus a metabolic acidosis.

Step 3, evaluate compensation. We'll use Winter's formula. and ask if the pCO2 is approximately equal to 1.5 times the bicarb plus 8. It is, so compensation is appropriate, which tells us that there is not likely to be a respiratory disorder present. Step 4, calculate the anion gap.

Remember, this is the sodium minus the sum of chloride and bicarb. So let's plug in 128, 94, and 14. The anion gap is 20. which is elevated, so the metabolic acidosis identified in step 2 is an elevated gap metabolic acidosis. Now from this lecture, we'll add step 5, which instructs us if the anion gap is elevated, to calculate the delta ratio. To remind you once more, the delta ratio is the delta anion gap divided by the delta bicarb. The measured anion gap of 20 is 8 more than normal, and the bicarb of 14 is 10 less than normal.

Therefore, the delta ratio is 0.8. At this point, we need to start to consider what the etiology is of the patient's acid-base disturbance. specifically the etiology of the elevated gap acidosis. We'll talk much more about differential diagnosis in future lectures, but given her history and vital signs, it seems highly likely she has a lactic acidosis.

The expected delta ratio for lactic acidosis is between 1.0 and 2.0. Since this ratio of 0.8 is less than 1.0, there is an additional normal gap metabolic acidosis. That is, the bicarb is too low to simply be a consequence of buffering the lactic acid. Thus, the patient's final diagnosis is a combined elevated gap metabolic acidosis and a normal gap metabolic acidosis.

Example 2. A 34-year-old type 1 diabetic man comes to the emergency room with fever, nausea, vomiting, and abdominal pain for one day. Step 1. The low pH tells us he has an asthma attack. acidemia, and step 2 tells us again that it is a metabolic acidosis. For step 3, we'll use Winter's formula again.

Does 27 approximately equal 1.5 times 12 plus 8? It does, and therefore compensation is appropriate. Step 4, calculate the anion gap. We'll take 140 and subtract 98 and 12 from it.

The anion gap is 30, so there is an elevated anion gap metabolic acidosis. Finally, step 5, since the anion gap is elevated, we'll calculate the delta ratio. The measured anion gap of 30 is 18 more than normal And the measured bi- bicarb of 12 is 12 less than normal. Therefore, the delta ratio is 1.5. Unlike the last example, which was likely involving a lactic acidosis, the clinical vignette here strongly suggests ketoacidosis.

This means that the range in which the delta ratio is expected to fall is different. Instead of being between 1.0 and 2.0, as it was for lactic acidosis, for ketoacidosis it should fall between 0.8 and 1.2. Thus, this patient's delta ratio is higher than expected, which would be consistent with a concurrent metabolic alkalosis. Final diagnosis, an elevated gap metabolic acidosis and a metabolic alkalosis. In this particular case, the elevated gap acidosis is probably from ketoacidosis as already mentioned, while the metabolic alkalosis is from a combination of vomiting up hydrochloric acid along with some contraction alkalosis from dehydration.

Our last example. This one is a little more involved. A 48-year-old alcoholic man is found unconscious in his apartment, soiled with vomit. He was last seen leaving a party six hours prior. Checking the PIN.

pH we obviously have in acidemia. With Step 2, since the PCO2 is elevated, the first process we identify here is actually a respiratory acidosis. Step 3, evaluate compensation. The the respiratory acidosis is likely acute in nature, so we need to ask if the bicarb is increased by 1 mEq per liter for every 10 mmHg, the PCO2 is above 40. If that were true, we would expect a measured bicarb around 26 or 27. Is the measured 22 close enough to 26 to say it's appropriate compensation?

I'm going to say no here, but it's a borderline call to which one could possibly say yes. Interestingly, it actually doesn't matter whether you say compensation is is appropriate, as in this case you will actually reach the same conclusion in the end. But for now, I will say that the bicarb is too low, and thus there is a metabolic acidosis present.

To calculate the anion gap, we take 136, minus 98, and 22, which gives us 16. Since we are given the albumin, which is remarkably low, we need to adjust the anion gap to compensate for this. Remembering from last lecture, the adjusted anion gap equals the measured anion gap plus 2.5 times 4 minus the measured albumin. For this patient, the adjusted anion gap works out to be about 22. Therefore, the metabolic rate is about 22. Acidic metabolic acidosis identified in step 3 is an elevated gap acidosis. Finally, step 5, calculate the delta ratio. The adjusted anion gap of 22 is 10 higher than normal, and the measured biochemical bicarb of 22 is 2 less than normal.

This gives us a delta ratio of 5, which will be higher than expected, irrespective of the etiology of the elevated gap. Therefore, this patient also has a metabolic alkalosis. So in summary, the patient's acid-base disturbances include a respiratory acidosis, an elevated gap metabolic acidosis, and a metabolic alkalosis.

This is one of those dreaded triple acid-base disorders. What could be going on to cause this patient's situation? Well, I haven't provided much information, but I would speculate the patient has an alcoholic ketoacidosis from his alcoholism and then got acutely and severely intoxicated, which resulted in central respiratory depression, along with developing a metabolic alkalosis from vomiting.

A lactic acidosis is also possible, perhaps from aspiration-induced sepsis. That concludes this lecture on the delta ratio. In the next lecture, I will discuss how to identify mixed acid-base disorders when the overall pH is normal.

Transcript for:Delta Ratio in Acid-Base Disorders

Transcript for:
Delta Ratio in Acid-Base Disorders