American Society of Nephrology Board Review Course September, 1998

Introduction to Metabolic Acidosis

Robert G. Narins, M.D. Professor of Medicine, Chief, Division of Nephrology, Henry Ford Hospital, Detroit, MI. Director of Education, American Society of Nephrology.

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Respiratory Acid-Base Disorders

Thomas Dubose, Jr., M.D. Professor of Medicine and Integrative Biology. Director, Division of Renal Disease and Hypertension, Department of Medicine, University of Texas at Houston

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When we treat metabolic alkalosis, we generally think of two categories: The first is comprised by those patients with a low urine chloride. I have used a cut-off of 20 mEq/L, but in actual fact, most people with metabolic alkalosis and low urine chloride will have chlorides in the urine of less than 10 mEq/L. They will always be quite low. These patients will respond to sodium chloride administration. But you must also replace their potassium deficits. When the urine chloride is high, then you must treat in a cause-specific manner: Surgery for adenoma, angioplasty for renal artery stenosis if possible, or specific drug therapy, such as amiloride, in Liddle syndrome, as I have already mentioned, and spironolactone in some of the other disorders when patients are not surgical candidates. In the case of Bartter's syndrome, patients respond at least for a while to nonsteroid anti- inflammatory drugs

 Case 1: Post-surgical patient with nasogastric suction I would like to complete the metabolic alkalosis discussion by illustrating a case. This is a real-life case, I promise you. You are requested as a nephrologist consultant to evaluate a 45year old, obese woman in a surgical ICU who has an acid-base disturbance which has puzzled the surgeons. The mind boggles, actually. They are adamant that the patient is not volume depleted. It turns out they were right. In fact, they have a wedge pressure, and the pulmonary/capillary wedge pressure is 15. The patient is on NG suction and is receiving Ringer's lactate as IV fluid. This is a very common problem that you can see in the surgical ICU. Here are her laboratory data: The sodium is 140 mEq/L, the K is 3.8 mEq/L. I rarely see hypokalemia in the surgical ICU. I don't know about you. They are very cognizant of potassium and they give it. The chloride is 88 mEq/L.

So here is a patient with a chloride that is out of proportion to the sodium concentration. Remember that sodium changes in serum for one reason and one reason only. That reason is for hydration, for purposes of hydration. The sodium goes down with overhydration and up in dehydration. But the chloride can change for two reasons. The first is for purposes of hydration, which means, if you are following me, that if it changes for hydration, it will change in exact proportion to the change in sodium. But there is another reason that chloride can change. Chloride can change for purposes of acidbase balance. When chloride changes for purposes of acid-base balance, sodium can't. So there will be a disproportionate change in chloride. Here is a disproportionate reduction in chloride compared to the sodium. And as you see, the bicarbonate is quite high. The pH is up. The PCO2 is 48. You might look at the PCO2 here as it compares to this particular bicarbonate concentration. The anion gap is 12. One of the things that I neglected to tell you is that the anion gap does ride up a bit in any alkalemia, and it rides up because there is an increase in anionic protein. There is a charge effect of pH, if you will, and also because phosphofructokinase is stimulated by alkalemia. But the anion gap, again, when elevated significantly, is your friend and will not let you down. To indicate that there is a high anion gap acidosis, as was illustrated earlier by Dr. Narins, you should expect, however, a few mEq/L increase in any alkalemia. Here are the urine electrolytes. As is often the case, you don't have a chloride. There is a sodium and a potassium. They look pretty robust. The urine pH is alkaline.

Case 1: Questions
First question is: What is the acid-base disturbance? Is it simple or mixed? What limits the hypercapnic response to the metabolic alkalosis? So let's go back. I talked a bit about calculating what the hypercapnic response should be. This is too low, as you noticed. It is too low for this very high serum bicarbonate level. We would expect the PCO2 to be around 55, and it isn't; but the patient is on a ventilator. So she is being over-ventilated for that condition. That limits her hypercapnic response. So it is a mixed disorder.
What urine electrolyte is missing and needs to be ordered? I think the obvious answer for that is chloride. The urine chloride should be ordered. And what will you do the patient and how do you explain it to the surgeon? It may be easier to provide therapy for the patient than to explain what you are doing to the surgeon. The point is, that the patient is chloride deficient. This is an example of chloride depletion metabolic alkalosis, and the patient needs chloride. So that is the therapy -- isotonic sodium chloride. But this is a question that I would like you to consider because I didn't cover it when we talked about therapy. That is: How would you modify your approach if the patient is in heart failure? The answer to that is you might not give sodium chloride if the patient is in heart failure. I would hope you wouldn't. There are two things that you can do, and we are going to talk about that when we show the next case. The first is you can give acetazolamide. I personally think that is the simplest thing to do. It promptly results in excretion of bicarbonate. The only thing you have to worry about is the potassium and the phosphate, which might also come out. But it is a simple approach. Another approach is to give hypotonic hydrochloric acid, 0.1 N. That is a little more complicated, a little more difficult, and it can, of course, cause some problems that you are aware of with the red cells, etc. So that is that case.

Metabolic alkalosis in a patient with heart failure:The second case

is that of a 64-year old woman with severe congestive heart failure. Now we already know that. She is two days post- cholecystectomy; she is receiving NG suction, ventilatory support, and IV Ringer's lactate containing this amount of KCl. So it is sort of similar there . Case 2: Laboratory findings But her laboratory findings are a little different. She has a bicarbonate of 39 mEq/L; again a low serum chloride, even in proportion to this reduction in sodium, so it is a disproportionate decrease in chloride; about a 20 percent reduction, if you will, in chloride and about a 5 percent reduction in sodium. The BUN is 24 mg/dL; creatinine, 1.8. There is alkalemia; The PCO2, I don't see a value listed. It should have been on there, but I left it off. I apologize for that. But the PCO2 was appropriate. I take it back. In this case, it was a little bit low. Her wedge pressure is 20. So it is quite high. Here are her urine electrolytes. You have a low urinary chloride, which indicates that this patient has a chloride-responsive metabolic alkalosis, which should be no surprise.

 Here is the point. This patient has a history of heart failure and already has an elevated wedge pressure. So what is the most appropriate therapy? (A) Infusion of hydrochloric acid, (B) giving 5 percent dextrose -- that doesn't make much sense. (C) Isotonic saline -- that is what the books say, but this is a problem patient. (D) Giving Lasix -- well, that's not going to help. That will just make things worse. Whatever dose you chose, I think this is the appropriate answer: (E) Give acetazolamide, 250 to 500 mg IV, one or two times should do the trick. Now an acceptable answer is infusion of 0.1 N hydrochloric acid, if you do it slowly, and if you can trust your pharmacy to mix it up right. You give it centrally only, and so it is acceptable. But I think the safest first step is to give acetazolamide.