[Applause] [Music] hello this is the fourth lecture of this course on interpreting abgs and I'm Eric strong from the palala veterans hospital and Stanford University today I will be discussing the phenomenon of compensation and the diagnosis of mixed acid-based disorders the learning objectives are as follows first to understand the basic mechanisms of physiologic compensation as they relate to interpreting abgs second to be familiar with the specific compensation formulas and their Alternatives finally to be able to use an assessment of compensation to identify the presence of a second acid-based disorder the topic of compensation was first introduced in lecture two but to remind you the body attempts to compensate for acidbase disorders in such a way as to mitigate derangements of arterial pH a primary metabolic disorder will result in respiratory compensation a primary respiratory disorder will result in metabolic compensation compensation does not return the pH all the way to normal and patients never overco compensate let's take a quick look at the very basic mechanisms of compensation for the four General types of acid based disorders in a metabolic acidosis the serum bicarb is abnormally low and thus so is the pH the body's response to this that is its respiratory compensation is to increase minute ventilation increasing minute ventilation lowers pco2 and thus tries to increase pH back closer to normal in a metabolic alkalosis the bicarb is high and thus so is the pH the body responds by decreasing ventilation which increases pco2 and drives pH back down somewhat in a respiratory acidosis pco2 is too high and the pH is too low the body's metabolic response is to absorb more bicarb in the proximal tubal of the kidney and to increase excretion of hydrogen ions in the distal tubule this increases serum bicarb and helps to increase pH finally in a respiratory alkalosis pco2 is too low and the pH too high the kidneys then reabsorb less bicarb and excrete less hydrogen ions before I move on to talk about how we can use the phenomenon of compensation to help diagnose mixed acidbase disorders there are two other aspects of compensation that I need to quickly mention first the speed with which compensation develops after the onset of an asset-based disturbance is very important as we'll see shortly how fast do these processes occur the respiratory compensation for a primary metabolic disorder is measurable within minutes but may take up to 24 hours to be maximally stimulated depending upon the circumstances the metabolic compensation for a primary respiratory disorder takes a bit longer I've seen estimates of anywhere from 12 hours to 5 days I think no one really knows for sure because as with much of acidbase analysis this time delay is largely estimated from observations in healthy volunteers and may not strictly apply to critically ill patients the second additional aspect of compensation I need to mention is that the body's compensatory mechanisms for a metabolic alkalosis is relatively poor compared to that of the three other major classes of acidbase disorders as I recently mentioned the body compensates for metabolic alkalosis by decreasing ventilation and thus increasing pco2 if you remember the alol gas equation shown here you might see that by increasing pco2 P big ao2 will necessarily decrease that is the partial pressure of oxygen in the alveolar space will be low which will result result in a lower arterial partial pressure of oxygen in other words hypoventilation will necessarily lead to some degree of hypoxia in patients with normal gas exchange at Baseline hypoxia is a strong stimulus to breathe more this hypoxia induced desire to increase one's ventilation significantly blunts the relative hypoventilation driven by metabolic alkalosis so now how can we use compensation to identify mixed acid based disorders by predicting the normal compensatory response to primary acidbase disorders mixed disorders can be identified specifically if a given patient is not compensating as predicted a second or even third acid-based abnormality must be present for example imagine you have identified the presence of a primary metabolic acidosis in a patient in whom the serum bicarb is 10 mil equivalents per liter from an equation I'll show shortly you would predict that the pco2 should be approximately equal to 23 mm of mercury due to respiratory compensation however what if the patient actually has a pco2 measured at 35 millim of mercury what's the possible explanation a second primary acidbase disorder must be present in this particular case since the pco2 is higher than predicted it is consistent with the concurrent presence of a primary respiratory acidosis in order to predict what the expected compensation should be generations of previous researchers have empirically derived a set of formulas with a different one for each primary disorder in fact to make things even more complicated there's actually more than one formula in common usage for each disorder the following chart represents the formulas which in my experience appear to be the most commonly used in the United States for a metabolic acidosis the compensation formula is as follows pco2 should be approximately equal to 1.5 * the bicarb Plus 8 this is known as Winter's formula named after Robert winter a pediatrician from Columbia University who helped derive it in the 1960s for a metabolic alkalosis pco2 should be approximately equal to 40 + 0.7 times the difference between measured bicarb and 24 for respiratory acidosis and alkalosis it depends upon whether the pathologic processes are acute or chronic remember it takes anywhere from 12 hours to 5 days for a respiratory process to become chronic as it pertains to acidbase balance for an acute respiratory acidosis the bicarb should be approximately equal to 24 plus the difference between measured pco2 and 40 / 10 10 for chronic respiratory acidosis the bicarb should be 24 + 4 * the difference between pco2 and 40 over 10 for an acute respiratory alkalosis B carb should be 24 minus 2 * the difference between 40 and the PC2 over 10 and finally for a chronic respiratory alkalosis bicarb should be 24 minus 5 times the difference between 40 and the pco2 over 10 how much variation is allowed for by the approximately equal sign here for example it's very common for people to cite Winter's formula as pco2 = 1.5 * b car + 8 plus or minus 2 owing to substantial variation in compensation between different individuals and between different specific acidoses or alkalosis the confidence intervals for these equations should likely be much wider one authoritative Source cites a plus or minus of five mm of mercury for pco2 when estimating respiratory compensation for metabolic disorders and plus or minus 3 Mill equivalents per liter of bicarb when estimating metabolic compensation for respiratory disorders this wider range of error appropriately reflects the degree of uncertainty we have when diagnosing complicated acidbase disturbances as I mentioned before there are some alternative approaches to calculating compensation I won't go over all all of them but here is one alternative to calculating compensation for respiratory disorders for an acute respiratory acidosis bicarb should increase 1 mil equivalent per liter for each 10 millim of mercury the pco2 is above 40 for a chronic respiratory acidosis bicarb should increase four for each 10 the pco2 is above 40 for an acute respiratory alkalosis bicarb should decrease to for each 10 the pco2 is below 4 and finally for a chronic respiratory alkalosis bicarb should decrease five for each 10 the PC2 is below 40 the astute viewer May recognize that these shortcuts are actually mathematically equivalent to the equations presented on the last slide but most people find it easier to remember these relationships when it's presented in this manner there is actually an extremely easy alternative to calculating compensation for metabolic disturbances in a metabolic disorder with appropriate compensation the pco2 in millim of mercury is approximately the same as the first two digits of the pH after the decimal point to see what I I mean exactly by that here is a quick example in this ABG the pH is 7.27 the pco2 is 25 and the bicarb is 11 now take the first two digits of the pH after the decimal which in this case is 27 and compare it to the pco2 they are approximately equal to one another therefore there is appropriate physiologic compensation for this metabolic acidosis I've been teaching acid-based disorders to how staff and students for some time and I initially hated this particular shortcut because it seemed that a trick so simple couldn't possibly be as accurate as necessary however I have since conceded that I was wrong on this here's a graph where measured serum bicarb in a metabolic acidosis is on the x-axis and the predicted pco2 as a result of compensation is on the Y AIS the blue line here represents the p2s uh that are predicted by the shortcut for example in a metabolic acidosis with a bicarb is 16 we expect the pco2 to be about 31 how does this formula compare to predictions from the empirically and scientifically derived Winters formul I'd say it's pretty darn close uh especially once you dealing with B carb levels under 20 mole equivalent per liter how does the shortcut compare to the formal compensation equation for metabolic alkalosis here is the shortcuts predictions of pco2 over a range of serum bicarbs from 24 to 40 and here is the formal equation this is definitely approximation that is close enough to use at the bedside so now let's go through three quick examples to see how an assessment of compensation Works in practice here is example one where the pH is 7.50 the pco2 is 48 and the bicarb is 34 steps one and two of acidbase analysis remain the same checking the ph and then the pco2 and then step three will be evaluating compensation so first the pH of 7.5 Z is higher than normal so therefore this patient has an alkalemia and at least one alkalosis next look at the pco2 of 48 this is higher than the normal pco2 of 40 since the ph and pco2 are deranged in the same direction the problem here is metabolic in origin and thus a metabolic alkalosis now for step three we will take a look at the compensation formula for metabolic alkalosis which states that the predicted pco2 should be approximately equal to 40 + 0.7 * the difference between measured by carb and 24 is that true in this case yes therefore we'd say that this patient has appropriate respiratory compensation using the shortcut method 50 from the pH is approximately equal to 48 from the pco2 and we reach the same conclusion let's move to example number two the pH is 7.12 pco2 is 32 and bicarb is 10 step one check the pH pH is low so there is an acidemia step two check the pco2 the pco2 is also low so the process is metabolic and thus a metabolic acidosis step three evaluate compensation for this we will use wind formula so does the pco2 approximately equal 1.5 * the bicarb Plus 8 32 is not close enough to 23 therefore a second disorder is present since pco2 is higher than predicted uh this second process must be a respiratory acidosis using a shortcut method 12 from the pH is not approximately equal to 32 from the pco2 and again we reached the same conclusion that uh respiratory compensation is not appropriate example number three in this case we have a brief clinical vignette a 24y old man is found unresponsive on the floor soiled with vomit he was last seen 4 hours prior and appeared well at that time his ABG is as follows pH 7.34 pco2 65 bicarb 34 step one pH is low so there is an acidemia step two the pco2 is high so there is a respiratory acidosis step three evaluate compensation from the vignette it seems highly likely that the pathologic process in question is acute in onset therefore we will use our shortcut for an acute respiratory acid osis is the bicarb increased by 1 mil equivalent per liter for each 10 mm of mercury the pco2 is above 40 since the measured 65 is 25 above the normal 40 and 25 is 2 and A2 * 10 we would expect the bicarb to be 2.5 mil equivalents per liter above normal you should generally use 24 as a quote normal bicarb for acidbase problems therefore the expected by carb from this respiratory acidosis would be approximately 26 and a half this is significantly different from the measure bicarb of 34 thus a second disorder is present the bicarb is higher than predicted so the second disorder is a metabolic alkalosis you might have expected this conclusion from the fact that despite a moderately elevated pco2 of 65 on the ABG the pH of 7 .34 is remarkably close to normal and as I've said before compensation never returns your pH to normal so that's a little bit about the phenomenon of compensation in acid-based disorders and how to use compensation to identify the presence of an additional acidosis or alkalosis in the next lecture I will talk about the an Gap [Music]