Acid-base fluids and electrolytes made ridiculously simple

Answer: They will all increase the measured osmolality if added to the ex- tracellular fluid. 19. Which of the following will increase the calculated serum osmolality when added to the extracellular fluid? Urea Glucose Sodium Ethanol Methanol Isopropanol Ethylene glycol Mannitol Sorbitol Answer: Only urea, glucose and sodium are included in the formula for calculated osmolality. Therefore, only urea, glucose and sodium will add to the calculated osmolality if added to extracellular fluid. 20. Which of the following will increase the osmolal gap when added to the ex- tracellular fluid? Urea Glucose Sodium Ethanol Methanol Isopropanol Ethylene glycol Mannitol Sorbitol Answer: OSM GAP = OSM(,,,,) - OSM(ca,c) Urea, glucose, and sodium are all included in the formula for calculated osmolality. They will add to both the calculated osmolality and the mea- sured osmolality and therefore will not change the osmolal gap if added to the extracellular fluid. The other compounds will increase the measured osmolality but not the calculated osmolality and will therefore increase the osmolal gap. 21. At approximately what level of GFR would a patient have problems ex- creting the daily dietary potassium load? At this point, the patient will be- gin to develop positive potassium balance, leading to hyperkalemia. Answer: The upper limit of potassium excretion is roughly proportional to the GFR. If the GFR is 100% of normal, the maximum amount of potas- sium which could be excreted in one day is roughly 10 mEq per kg body weight. This is about 70 X 10 = 700 mEq in a 70 kg person. If the GFR is reduced to 50% of normal the maximum amount of potassium that can

be excreted in one day falls to approximately 50% X 700 = 350 mEq. This is a rough approximation of maximum potassium excretion because compensatory renal potassium secretory mechanisms will increase potas- sium excretion, and stool potassium losses also increase as the body de- fends itself against hyperkalemia. If the GFR is further reduced to 20% of normal, the maximal potassium excretion would fall to the range of about 140 mEq1day (20% of 700 mEq1day). The average diet has about 1 mEq of potassium per kg body weight, which amounts to about 70 mEqIday in a 70 kg person. For a diet con- taining 70 mEqIday, the GFR would need to be reduced to approximately 701700 = 10% of normal before hyperkalemia develops. In fact, the GFR is usually below this level when hyperkalemia develops based upon usual dietary intake. Hyperkalernia may develop at less profound levels of re- nal failure if the potassium intake is increased or if there is a hidden potas- sium load. For example, a person with a diet high in potassium would develop hyperkalemia with less impairment of the GFR. A patient with a GFR 15% of normal would develop hyperkalemia if dietary potassium is over the range of 15% X 700 = 105 mEq1day. As mentioned above: this is only a rough approximation of maximum potassium excretion. The clinical point is that ifa patient has mild to moderate renal fail- ure and hyperkalemia, the hyperkulemia should not be simply ascribed to renal failure alone. A vigorous search for other causes of hyper- kulemia is needed. 22. How much potassium is there in the ECFV of a 70 kg man? Answer: The very delicate nature of the transcellular distribution of potassium is illustrated by the following calculation: TBW = .6X 70kg=42L ECFV = 113 X 42 L = 14 L Potassium concentration in ECFV 4.0 mEqL Total potassium in ECFV: 4.0 mEqL X 14 L = 56 mEq The calculated amount of potassium in the entire ECFV (56 mEq) is less than that contained in three routine supplemental 20 mEq doses of KC1 or the potassium in four glasses of orange juice! Even a small increase in the amount of extracellular potassium could cause a large increase in the ECF potassium concentration. Adding 56 mEq to the ECFV would result in an increase of potassium concentration from 4.0 mEqL to 8.0 mEqL! Thankfully, we do not double our potassium concentration after four glasses of orange juice because homeostatic mechanisms maintain the striking difference between intracellular and extracellular potassium con- centrations and, therefore, the ECFV potassium concentration. 23. How much potassium is there in the ECFV of a 40 kg woman? Answer: TBW = .5 X 40 kg = 20 L ECFV = 113 X 20 L = 6.7 L

FIGURE 9-1. Three Step Approach to Acid-Base Disorders Step 1: Identify the most apparent disorder. Disorder PH Pcoz HCO3- Metabolic acidosis Decreased Decreased (secondary) Decreased (primary) Metabolic alkalosis Increased Increased (secondary) Increased (primary) Respiratory acidosis Decreased Increased (primary) Increased (secondary) Respiratory alkalosis Increased Decreased (primary) Decreased (secondary) Step 2: Apply the formulas to determine if compensation is appropriate. If not, a second disorder co-exists. Metabolic acidosis: PCOZ = 1.5 X [HC03-] + 8 Metabolic alkalosis: PCOZ = 40 + .7 X ( [ H C O S - ( ~ ~ ~ ~ ~ ~ ) ] - [HCO3-(normal)] ) Respiratory acidosis: Acute: [HCO3-] increases by 1 mEqn for every 10 mm Hg increase in PCOZ Chronic: [HC03-] increases by 3.5 mEqL for every 10 mm Hg increase in PC02 Respiratory alkalosis: Acute: [HCOs-] decreases by 2 mEqn for every 10 mm Hg decrease in PCOZ Chronic: [HC03-] decreases by 5 mEqL for every 10 mm Hg decrease in PC02 Step 3: Calculate the anion gap. AG = [Na+] - ([Cl-] + [HCOs-I) The normal AG is 9-16 mEq/L. If AG > 20 mEqn, high AG acidosis is probably present. If AG > 30 mEq/L, high AG acidosis is almost certainly present. For lactic acidosis, the ratio of the increase in the anion gap to the decrease in the HCO3- averages approximately 1.5. In ketoacidosis, the ratio of the increase in the anion gap to the decrease in the HC03- averages approximately 1 .O. In respiratory disorders, the PCO~ is abnormal and we want to see if there is also a coexisting metabolic disorder. We ask: What should the [HC03-] be after compensation? If the [HC03-] differs significantly from that predicted by the formula for compensation, then a coexisting metabolic disorder is present. Apply the formula for the disorder you have identified to see if the compensation is correct. If the compensation is not what is predicted by the formula, then an additional disorder is present. Step 3: Calculate the anion gap. The normal value of the anion gap used in this book is 9-16 mEq/L, although many hospitals may prefer to use the smaller range 10-14. If the calculated anion gap is normal, you are finished. The presence of an increased anion gap is a powerful clue to the diagnosis of metabolic acidosis. If the anion gap is increased above 20 mEq/L, then an an- ion gap metabolic acidosis is probably present. If the anion gap is increased above 30 mEq/L, then an anion gap metabolic acidosis is almost certainly pre- sent, regardless of the pH and [HC03-1.

If a high anion gap acidosis due to lactic acidosis or ketoacidosis is pre- sent, then it may be helpful to compare the change in the anion gap to the change in the bicarbonate concentration. By doing this, one may identify an additional "hidden" metabolic disorder, either a metabolic alkalosis or a nor- mal anion gap metabolic acidosis. Step 1: Identify One Disorder. Look at the pH, PCOZ and [HC03-] to identify the most apparent acid-base disorder. In general: If the pH is low (<7.35), either a metabolic acidosis or a respiratory acido- sis is present; if the [HC03-] is low: metabolic acidosis; if the PCOZ is high: respiratory acidosis. If the pH is high (>7.45), either a metabolic alkalosis or a respiratory al- kalosis is present; if the [HC03-] is high: metabolic alkalosis; if the PCOZ is low: respiratory alkalosis. If the pH is normal, but either the [HC03-] or the PCOZ, (or both) is abnor- mal, then pick the most abnormal of the [HC03-] or PCOZ. For example: pH 7.40, PCOZ 60 mm Hg, HC03 36 mEq/L. Both the PCOZ and the [HC03-] are abnormal. Because the pH is normal in this case, you could start by diag- nosing either a metabolic alkalosis ([HC03-] 36 mEqL ) or a respiratory acidosis (PCOZ 60 mm Hg). This method will allow you to start either way. Step 2: Apply the Formulas to See If Compensation Is Correct. Apply the formulas for expected compensation to determine if a second disorder is present. This section deals with what the formulas for expected compensation to simple disorders mean and how to use them. Once you iden- tify a disorder, the general question is: Is the compensation close to that pre- dicted by the formula for expected compensation? Once you have made a diagnosis of one disorder, then apply the formula for that specific disorder to see if the compensation is, appropriate. For metabolic disorders ask: What should the PCO~ be after compensation? For respiratory disorders ask: What should the [HC03-] be after compensation? The formulas give approxima- tions for the expected compensation for acid-base disorders. If the compensa- tion is not consistent with the given formula, then a second disorder is present. Remember to use the values of both the PCOZ and the [HC03-] from the arterial blood gas (ABG) for purposes of determining if compensation is appropriate (Step 2). Also, remember to use serum values to calculate the anion gap (Step 3). In this book, the serum bicarbonate and the calculated bicarbonate from the ABG are almost always equal, but this is not always the case in clinical practice.

to this is obtained by using the formula for expected respiratory compensation for a metabolic alkalosis. That is: the PCOZ should be equal to PC02 = 40 + 0.7 X ([HC03- (measured)] - [HC03- (normal)]) where [HC03-(measured)] is the patient's measured bicarbonate and [HC03-(,o,- ,,1)] is the normal bicarbonate concentration, roughly 24-26 mEq/L. What if the measured PCOZ differs from this value? A significant devia- tion means that there is also a respiratory disorder present, because the PCOZ is not behaving as we would expect. If the measured PCOZ is higher than predicted by the formula, then a coexisting respiratory acidosis is present. If the mea- sured PCOZ is lower than predicted, then a coexisting respiratory alkalosis is present. This formula is an approximation, and there is an especially wide pa- tient to patient variation in the respiratory response to metabolic alkalosis. Therefore, for metabolic alkalosis, we should allow the PCOZ to be 2 5 mm Hg off from that predicted by the formula. A more significant deviation in either direction from the value predicted by the expected compensation formula, however, indicates that in addition to a metabolic alkalosis, there is also a res- piratory disorder present. The maximum value PC02 can reach in compensating for a metabolic al- kalosis is about 55 mm Hg. A PCOZ of more than 55 mm Hg generally implies that a respiratory acidosis is also present, regardless of the [HC03-1. Respiratory Disorders A respiratory acidosis is a process that causes a primary increase in the PCOZ. A respiratory alkalosis is a process that causes a primary decrease in the PCOZ. Respiratory disorders are divided into acute and chronic. Acute means minutes to an hour or so and chronic means more than 24-48 hours. The rea- son for this seemingly arbitrary distinction is that the full renal compensation for respiratory disorders takes at least 24-48 hours. That is, when a metabolic acidosis develops, the increase in minute ventilation comprising the respiratory compensation occurs rapidly and the Pc02 falls right away. In a respiratory dis- order, however, the kidneys take at least 24-48 hours to fully adjust the [HC03-] to its new compensatory value. A short way of saying this is that the lungs adjust the PCOZ much faster than the kidneys can adjust the [HC03-1 ! For example, in the case of a respiratory acidosis, the primary de- rangement is an increase in PCOZ. The renal compensation for a respiratory acidosis leads to a secondary increase in [HC03-1. Although the renal com- pensation tending to increase the [HC03-] begins right away, it takes at least 24-48 hours for the kidney to increase the [HC03-] to its new steady state value. Therefore, the formulas for predicted compensation for respira- tory disorders depend upon whether the disorder is acute (minutes to an hour or so) or chronic (24-48 or more hours, at which time the renal com- pensation has fully taken place).

For an acute respiratory acidosis, the serum HC03- concentration rises about 1 mEqL for every 10 mm Hg increase in PCOZ. For a chronic respiratory acidosis (after 24-48 hours), the serum HC03- bicarbonate concentration rises about 3.5 mEqL for every 10 mm Hg increase of Pc02. For respiratory alkalosis the PCO~ falls, and therefore the compensation is for the serum HCO3- concentration to decrease as well. How much? For acute respiratory alkalosis (minutes to an hour or so), the serum HC03- concentration will fall about 2 mEqL for every 10 mm Hg drop in P C O ~ For chronic respiratory al- kalosis (more than 24-48 hours), the serum HC03-concentration will fall by about 5 mEq/L for every 10 mm Hg fall in PCOZ. In summary, for respiratory disorders: Respiratory acidosis: Acute: [HC03-] increases by 1 mEqL for every 10 mm Hg increase in Pco~. Chronic: [HC03-] increases by 3.5 mEqn for every 10 mm Hg increase in Pco~. Respiratory akalosis: Acute: [HC03-] decreases by 2 mEq/L for every 10 mm Hg decrease in Pco~. Chronic: [HC03-] decreases by 5 mEq/L for every 10 mm Hg decrease in Pco~. Example 1: A patient's PC02 increases from 40 mm Hg to 60 mm Hg during a chronic respiratory acidosis. For a chronic respiratory acidosis, the serum [HC03-1 rises about 3.5 mEqL for every 10 mm Hg increase of Pco~. The compensatory change in serum [HC03-] would be an increase of 2 X 3.5 = 7 mEqL. The multiplication factor 2 is used because the increase in PCO~ is 20 ( = 2 X 10 increase in Pco~). Example 2: A patient has a PCOZ of 40 and a [HC03-] of 24 mEqL. An acute respiratory alkalosis develops and the PCOZ falls to 20 mm Hg. What should the [HCO3-] be after compensation? Answer: The [HC03-] should decrease by 2 X 2 = 4 mEqL. The multipli- cation factor 2 is used because a decrease in PCO~ of 20 mm Hg = 2 X 10 decrease in PC02. The [HC03-] should be 24 - 4 = 20 mEq/L after compen- sation for the acute respiratory alkalosis. Example 3: A patient has a Pcoz of 40 and a [HC03-] of 24 mEqn. An acute respiratory acidosis develops and the PCO~ rises to 70 mm Hg. What should the [HC03-] be after compensation? Answer The [HC03-] should increase by 3 X 1 = 3 mEq/L. The multipli- cation factor 3 is used because an increase in PCOZ of 30 mm Hg = 3 X 10 increase in PCOZ. The [HC03-] should be 24 + 3 = 27 mEqn after compen- sation for the acute respiratory acidosis.

one could logically expect that if the AG increases because of a high anion gap acidosis, the HCO3- concentration would decrease by an equal amount. For example, if a lactic acidosis or diabetic ketoacidosis increases the anion gap by 15 IT&@ , the HC03- concentration might be expected to fall by an equal amount, 15 mEqn. A one-to-one relationship between the increase in the anion gap and the decrease in bicarbonate is often not the case, however. One reason is that hy- drogen ion is buffered intracellularly and by bone as well as by the HCO3- in extracellular fluid. Simply put: HC03- does not have to buffer all the hy- drogen ion by itself, but "gets help" from other buffer systems. Therefore, the [HC03-] may decrease by an amount less than the increase in the anion gap. For lactic acidosis, the ratio of the increase in the AG to the decrease in the [HC03-] is not usually 1 .O, but on the average may actually be closer to 1.5 because of this extra buffering of hydrogen ion outside the ECF. That is, for lactic acidosis, approximately: Change in AGlChange in [HC03-] = 1.5 or, rearranging: Change in [HC03-] = Change in AGl1.5 Using this very rough formulation, we might expect that if a lactic acidosis in- creases the AG by 15 mEqL, then the [HC03-] would fall by about: Change inAGl1.5 = 1511.5 = 10 mEq/L, not 15 rnEqL. For ketoacidosis, the ratio of the increase in the AG to the decrease in the [HC03-] is closer to 1 .O, perhaps because some ketoanions, which constitute the increase in the AG, may be lost in the urine. Therefore, for ketoacidosis, approximately: Change in [HC03-] = Change in AG It should be carefully restated that this is a very rough way to estimate the ex- pected fall in [HC03-] for a given increase in AG when there is a lactic aci- dosis or a ketoacidosis. For uremic acidosis and the other causes of high anion gap metabolic acidosis, the relationship between the increase in the AG and the decrease in the bicarbonate is unpredictable. How can we use this information in the setting of lactic acidosis or ketoacidosis? A measured [HC03-] much higher than predicted by the in- crease in anion gap is a clue that a "hidden" metabolic alkalosis may also be present. A measured [HC03-] much less than predicted by the increase in an- ion gap is a clue that a "hidden" normal anion gap metabolic acidosis may also be present. When I diagnose a high anion gap acidosis due to a lactic acidosis or a ketoacidosis, I compare the predicted fall in bicarbonate (based upon what you

would expect from the increase in anion gap) to the actual fall in bicarbonate, then use the following guidelines: A measured [HC03-] much higher than predicted by the increase in anion gap is a clue that a "hidden" metabolic alkalosis may also be present. A measured [HC03-] much less than predicted by the increase in anion gap is a clue that a "hidden" normal anion gap metabolic acidosis may also be present. Example 1: A patient begins with a serum [HC03-] of 24 and an AG of 12. She develops a lactic acidosis. The AG increases from 12 to 22. Approxi- mately, what would you expect the [HC03-] to be? Answer: The 10 mEq/L of H+ is buffered not only by extracellular HC03-, but also by intracellular buffers and by bone. The [HC03-] would be expected to decreases by about: Change in AGl1.5 = 1011.5 = 6.7 mEq/L. The ex- pected [HC03-] is therefore: 24 - 6.7 = 17.3 mEq/L. The increase of 10 mEq/L in the AG is accompanied by an opposing de- crease in the[HC03-] of 6.7 mEq/L. I realize that the decimal places may look strange with regard to the HC03- concentration, especially because this is only an approximate method anyway. I am going to leave the decimals in, however, so you can follow the calculations'as we go. I know that it really doesn't make much sense to talk about a [HC03-] of 17.3 mEq/L. Example 2: A patient begins with a serum [HC03-] of 24 mEqL and an an- ion gap of 12 mEq/L. A ketoacidosis develops, and the anion gap increases from 12 to 22 mEq/L. What should the resulting [HC03-] be? Answer: The AG has increased by 10 mEq/L. Therefore, the [HC03-] should decrease by about 10 mEqL (remember that the Change in AGIChange in [HCO3-] averages about 1.0 in ketoacidosis). Therefore, the bicarbonate would be expected to fall from 24 mEq /L to 14 mEq/L (24 - 10 = 14 mEq/L). The increase in AG should be associated with an opposing change in the [HC03-1. Example 3: A patient starts with AG 12, serum [HC03-] 24. ABG: pH 7.40, [HC03-] 24 and PCO~ 40. A lactic acidosis develops, and the AG rises from 12 to 32 mEq/L. The [HC03-] does not fall: It stays at 24 mEq/L. The pH remains I 7.40 and the PCO~ is 40. What has happened? Answer Beginning with the 3-step approach: Step 1: Everything looks normal. No acid-base disorder so far. Step 2: The PCO~ is normal and appropriate for the normal [HCO-] of 24. Therefore, no respiratory disorder is present. Step 3: The AG has increased by 20 mEq/L. By considering the change in the anion gap, 20 mEq/L, the predicted [HC03-] would fall by about: Change in AG11.5 = 2011.5 = 13.3 mEq/L. The expected [HC03-] would be 24 - 13.3 = 10.7 mEq/L. But we can see that

be roughly 24 - 10 = 14 rnEq/L. But the [HC03-] is 4 mEq/L, which is 10 mEqn less than predicted by the AG metabolic acidosis alone. Something is "pushing the [HC03-] down." What is it? Answer: It is a second metabolic acidosis. This second "hidden" acidosis is of the nonnal anion gap type. This patient has two independent metabolic aci- doses: a high anion gap acidosis and a normal anion gap metabolic acidosis. Example 6: A patient presents to the emergency room in septic shock with the following: an anion gap that has increased from 12 to 30 (change in AG is 18) and a serum [HC03-] that has decreased from 26 to 4 (change in [HC03-] is 22). ABG: The PCO~ has fallen from 40 to 15, the [HC03-] has fallen to 4, and the pH has fallen from 7.40 to 7.05. What is your diagnosis? Answer: Step 1: The pH has fallen and the [HC03-] has fallen: metabolic acidosis. Step 2: What should the PCO2 be? PC02 = (1.5 X 4) + 8 = 14. The measured PCO~ matches the predicted Pco~. Therefore, there is no respiratory dis- order present. Step 3: A high anion gap acidosis in the setting of septic shock is most likely a lactic acidosis. The change in the AG is 18. We would expect the [HCO3-] to fall by about 1811.5 = 12 mEq/L. This would lead to a [HC03-] of 26 - 12 = 14 mEq/L. But the [HC03-] has fallen to 4. The [HC03-] is much less than predicted by a high anion gap acido- sis alone. Something is pushing down the-[HC03-] by an additional 10 rnEq/L. The decrease in [HC03-] is explained by a coexisting nor- mal anion gap metabolic acidosis. These examples have pointed out how using the anion gap can identify additional "hidden" metabolic disorders in cases of lactic acidosis and keto- acidosis. In actuality, using the change in the anion gap to predict the change in bicarbonate is only an approximate method. Nevertheless, a significant de- viation from this approximation suggests that an additional metabolic disorder may be present. That is: If the measured bicarbonate concentration is significantly higher than predicted by the increase in the AG, a "hidden" metabolic alkalosis may be present. If the measured bicarbonate concentration is significantly less than pre- dicted by the increase in the AG, then a "hidden" normal anion gap meta- bolic acidosis may be present. Exercises: Putting the Three Steps Together For the sake of the following exercises assume that all the patients have the same baseline lab values: pH 7.40, PCO~ 40, [HC03-] 24, AG 12. All the

changes and calculations for solving the cases should be based upon these baseline values. Case 1 A patient presents with: pH 7.15, calculated [HC03-] 6 mEq/L, PCOZ 18 mm Hg, sodium 135 mEq/L, chloride 114 mEq/L,, potassium 4.5 mEqL, serum [HC03-] 6 mEq/L. Step 1 : This patient has a very severe metabolic acidosis. Step 2: For a metabolic acidosis, what should the PCOZ be? We want to know whether this is a simple metabolic acidosis or if there is also a respira- tory disorder present. The question we ask is: What should the PCOZ be after compensation? We answer this question with the formula for ex- pected respiratory compensation for metabolic acidosis: The patient's PCOZ of 18 is close to the 17 we would expect for the appropriate respiratory compensation for a simple metabolic acidosis. Therefore, we con- clude that there is no respiratory disorder present. Step 3: The anion gap is AG = 135 - (6 + 114) = 15 mEq/L (normal). We are finished. There are no further steps if the AG does not suggest a high AG acidosis. Answer: Simple normal anion gap metabolic acidosis. The differential diag- nosis is listed in Fig. 7-1. Case 2 A patient presents with: pH 7.08, [HC03-] 10, PCOZ 35, anion gap 14 mEq/L. Step 1: The [HC03-] is 10, and the pH is 7.08. There is a severe metabolic acidosis. Step 2: What should the PCOZ be? The PCO~ should be: The PCOZ of 35 mm Hg is much higher than we would expect! Therefore, there is something pushing the PCO2 up. It is a coexisting respiratory acidosis. There is a respiratory acidosis present as well as a metabolic acidosis. Step 3: The anion gap is 14 (normal). We are finished. Answer: Normal anion gap metabolic acidosis plus respiratory acidosis. The patient's Pcoz is 35. This is much higher than predicted by the for- mula. Therefore, the patient has a respiratory acidosis which might represent "tiring out" of the patient's respiration and impairment of his ability to com- pensate for the metabolic acidosis. It could also be a clue to a coincident pul- monary process. The rising PCO2 is a dangerous sign in metabolic acidosis, because further increase in the PCO2 could lead to a precipitous fall in pH.

There are two distinct acid-base disorders present, each with its own set of potential causes. The patient has a metabolic alkalosis secondary to one or more of the causes listed in Fig. 8-1 plus a respiratory alkalosis. The causes for each disorder should be considered separately. Case 5 A previously well patient presents with 30 minutes of respiratory distress and pH 7.26, Pc02 60, [HC03-] 26, AG 14. Step 1 : The PCO~ is up. The pH is down. Respiratory acidosis. The history says acute. Step 2: For respiratory disorders we ask: What should the [HC03-] be? Re- member that the calculations for metabolic compensation are in terms of changes of 10 in Pcoz. The PCOZ is up by 20 which is 2 X 10. For an acute respiratory acidosis, the [HC03-] should change by 1 mEqL for every 10 mm Hg increase in the PCOZ. Therefore, the [HC03-] should change by 2 X 1 mEqL = 2 mEqL. Using 24 as normal, the [HC03-] should become: 24 + 2 = 26. Therefore, the compensation is appropriate, and there is no metabolic disorder. Step 3: The AG is normal. We are finished. Answer Acute respiratory acidosis. Case 6 Anxious. Can't seem to get enough air for last 4 days. pH 7.42, PCO~ 30, [HC03-] 19, AG 16. Step 1: PCOZ down. pH up. Respiratory alkalosis. The history indicates chronic respiratory alkalosis. Step 2: What should the [HC03-] be? Remember that the calculations for meta- bolic compensation are in terms of changes of 10 in PCOZ. The PCO~ is down by 10 which is 1 X 10. For a chronic respiratory alkalosis, the [HC03-] should be down by 5 for every 10 mrn Hg decrease in Pco~. For this chronic respiratory alkalosis, the [HC03-] should be down by 1 X 5. The [HC03-] should be 24 - 5 = 24 - 5 = 19. Therefore, the com- pensation is appropriate, and there is no metabolic disorder. Step 3: The AG is normal. We are finished. Answer: Chronic respiratory alkalosis. It is of interest that chronic respiratory alkalosis is the only simple disorder in which compensation can bring the pH back into the normal range (7.42 in this case). Case 7 Short of breath. Two weeks. pH 7.38, PCO~ 70, [HC03-] 40, AG 16. Step 1: PCOZ up. Respiratory acidosis. By history: chronic. Step 2: What should the [HC03-] be? The PCOZ is up by 30 which is 3 X 10. For this chronic respiratory acidosis, the [HCOs-] should increase by

3 X 3.5 = 10.5. Using 24 as normal, the [HC03-] should become: 24 + 10.5 = 35.5. In short: For this chronic respiratory acidosis the [HC03-] should be 24 + (3 X 3.5) = 35.5. The patient's [HC03-] is higher than it should be. Therefore, there is a modest metabolic alka- losis present as well. The high [HC03-] is not just compensation for the respiratory acidosis but is caused by a separate acid-base disorder: metabolic alkalosis. Step 3: The AG is normal Answer: Chronic respiratory acidosis plus metabolic alkalosis. There are two distinct acid-base disorders present in this patient. Both dis- orders are pathologic - one is not compensation for the other, even though the pH may be close to normal. In other words, this patient has two processes going on at the same time that tend to offset each other: A metabolic alkalosis that is secondary to one of the causes listed in Fig. 8-1 plus a respiratory aci- dosis. Causesfor each of the two disorders should be considered separately. I Case 8 Try approaching case 7 the other way, starting with metabolic alkalosis. Step 1 : The [HC03-] is high: metabolic alkalosis. Step 2: For a metabolic alkalosis, what should the PCOZ be? It should be 40 + .7 X (40 - 24) = 5 1. The PCOZ is much higher than this. Some- thing is pushing it up: a respiratory acidosis. (Also, remember that for compensation for a metabolic alkalosis the Pcoz should not be higher than 55 mm Hg: It is higher than 55 mm Hg, indicating that a respira- tory acidosis is present.) Step 3: The AG is normal. Answer: Metabolic alkalosis plus respiratory acidosis. The pH is often close to normal when offsetting disorders are present. Each disorder is pushing the pH in the opposite direction. If given the choice of a metabolic or a respiratory disorder of equal sever- ity being present at the same time, I will generally start my analysis of the data 1 from the standpoint of the metabolic disorder first, because it will avoid the question of acute versus chronic and which formula to apply. The 3-step method will work either way, however, whether you begin with the metabolic disorder or the respiratory disorder. I just find that beginning with the meta- bolic disorder is sometimes less cumbersome. Case 9 A patient presents with: pH 7.68, PCO2 35, [HC03-] 40, AG 18. Step 1 : The pH is up and the [HC03-] is up: metabolic alkalosis. Step 2: What should the PCOZ be? Apply the formula for metabolic alkalosis: Pcoz = 40 + .7 X ( [HC03- (,&)] - [HC03- (norm*)]) = 40 + .7 X (40 - 24) = 40 + 11.2 = 51.2. The patient's PCOZ of 35 mrn Hg is

Case 12 Apatient presents with: pH 7.65, PCOZ 30, [HC03-] 32, AG 30. The patient has a temperature of 102 degrees and a blood pressure 80150. He is diaphoretic. The urinalysis shows numerous white blood cells and many bacteria. Aurine dipstick test for ketones is negative. Step 1: pH is up. [HCO3-] is up (metabolic alkalosis), and PCOZ is down (res- piratory alkalosis). Let's start with the metabolic alkalosis though it would work out either way. Step 2: For metabolic alkalosis what should the PCOZ be? PCOZ = 40 + .7 X (32 - 24) = 45.6. The patient's PCOZ of 30 is much lower than 45.6. Therefore, respiratory alkalosis is also present. Step 3: The anion gap is 30! Therefore, a high anion gap acidosis is present. We are up to three disorders. Captain, I don't think our engines can stand the heat! The most likely cause of high anion gap acidosis in this patient is lactic acidosis. The change in the anion gap is 30 - 12 = 18. We compare this to the change in [HCOs-1. The expected decrease in [HC03-] is roughly: Change in AG11.5 = 1811.5 = 12. The [HC03-] did not decrease, but is up by 8 mEqlL. It should be down by roughly 12 mEqL. Therefore, the [HC03-] is about 20 mEqL higher than we would expect. This means that there is a severe meta- bolic alkalosis acting to push the [HC03-] up by roughly 20 mEqL in addi- tion to a very severe high anion gap acidosis acting to push the [HC03-] down by roughly 12 mEqL. The metabolic alkalosis and the metabolic acidosis tend to cancel each other, but they are both quite severe. Answer: Metabolic alkalosis (severe), AG metabolic acidosis (severe), and respiratory alkalosis (moderate to severe). Note that the [HC03-] of 32 mEqL does not look too bad at first glance. Calculating the AG and then comparing the increase in the AG to the decrease in [HC03-] was helpful in this case. Case 13 A patient presents with diabetic ketoacidosis: pH 6.95, PCOZ 28, [HC03-] 6, AG 32. Step 1: The metabolic acidosis is so severe that this patient is in danger of cardiovascular collapse. Step 2: What should the PCO~ be? PCOZ = (1.5 X 6) + 8 = 17. The pa- tient's PCO2 is much higher than expected for this metabolic acido- sis. The higher than expected PCOZ indicates a respiratory acidosis, possibly secondary to respiratory muscle fatigue. Some might call this "inadequate compensation" instead of respiratory acidosis be- cause the value of the PCOZ is low, not high. They would be par- tially correct, but let's just stick to our original terminology so as not to gum things up. This is a severe metabolic acidosis in which the patient's respiratory compensation is beginning to "tire out."

Remember that patients cannot keep their P C O ~ in the 10-20 range indefinitely without eventually tiring out. Therefore, this patient has a metabolic acidosis and a respiratory acidosis secondary to respiratory muscle fatigue. Step 3: The anion gap is 32. Therefore an anion gap acidosis is present. The increase in the anion gap is 20 mEq/L, supporting the diagnosis of AG acidosis. The predicted fall in the [HC03-] is roughly 20 mEq/L. The fall in the [HC03-] is 18, which is very close to 20. Therefore, the [HC03-] is close to what it should be for a ketoacidosis alone, and there is no "hidden" metabolic disorder. Answer: AG acidosis secondary to diabetic ketoacidosis; respiratory acidosis due to respiratory muscle fatigue. Case 14 A patient with recurrent episodes of small bowel obstruction presents with severe abdominal pain and vomiting: pH 7.33, PCO~ 35, [HC03-] 18, AG 33. Urine dipstick negative for ketones. The blood pressure is 82154 and the heart rate 116. Step 1: [HC03-] down, pH down. Metabolic acidosis. Most likely a lactic acidosis. Looks pretty mild at first glance. Step 2: What should the PCO~ be? (1.5 X 18) + 8 = 35. No respiratory disorder. Step 3: The anion gap of 33 indicates that an anion gap acidosis is present. The increase in anion gap is 21. The decrease in the [HC03-] should be somewhere around 2111.5 = 14 for a lactic acidosis, but is only 6. Therefore, there is probably a "hidden" metabolic alkalo- sis acting to "push" the bicarbonate to a higher level. Answer: Severe (18 mEq/L) anion gap metabolic acidosis plus metabolic alkalosis. Case 15 A 21-year-old diabetic patient presents with vomiting and pH 7.75, PCO~ 24, [HC03-] 32, AG 30. The urine is strongly positive for ketones and serum ketones are strongly positive. Step 1: The pH is way up. [HC03-] is up. PCO~ is down. Both of these are pushing the pH up. This is an example of a synergistic disorder in which the pH gets pushed the same way by both the PCO~ and the [HC03-1. This patient has life-threatening alkalemia. You could start with either the PCO~ or the [HC03-] in this case. I prefer to start with the metabolic alkalosis. Step 2: What should the PCO~ be? 40 + .7 X (32-24) = 45.6 mm Hg. The pa- tient's PCO~ of 24 mm Hg is much lower than predicted. Severe respi- ratory alkalosis is present in addition to the metabolic alkalosis.