ACID/BASE. A. What is her acid-base disorder, what is her anion gap, and what is the likely cause?

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1 These fluid and electrolyte problems are modified from those in a previous textbook for this sequence, Renal Pathophysiology edited by James A. Shayman M.D., Professor of Internal Medicine, University of Michigan, J.B. Lippincott, 1995, with the kind permission of the author. They provide an excellent review of major fluid and electrolyte issues in a case-oriented format. Case 1 ACID/BASE A 45-year-old woman had persistent diarrhea for 2 days. On examination, she was tachypneic, with a respiratory rate of 22 breaths/minute. Her blood gases and other laboratory values were as follows: arterial ph, 7.20; pco 2, 19 mm Hg; HCO 3 -, 7 meq/l; Na +, 140 meq/l; K +, 4.7 meq/l; Cl -, 122 meq/l. A. What is her acid-base disorder, what is her anion gap, and what is the likely cause? B. What is the cause of her tachypnea? C. How should she be treated? A. Diarrhea causes significant HCO 3 - losses from the gastrointestinal tract, equivalent to the addition of HCl. The anion gap is 140 meq/l (122 meq/l + 7 meq/l) = 11 meq/l, which is normal. Therefore, this patient has a hyperchloremic metabolic acidosis. B. The tachypnea reflects respiratory compensation of a metabolic acidosis and is responsible for the decreased pco 2. There are several ways to assess whether the the respiratory compensation is appropriate. One is to use an acid-base nomogram. Another useful tool based on nomogram data is that predicted compensation is a decrease in pco 2 of 1.2 x (delta HCO 3 - ) = 20.4 which is essentially equal to that observed in this patient. Thus, the decrease in pco 2 is the appropriate respiratory compensation for a metabolic acidosis and she has only a single disorder. C. Administer sodium bicarbonate.

2 Case 2 A patient in the intensive care unit with encephalitis had the following blood gas profile: ph, 7.50; pco 2, 20 mm Hg; HCO 3 -, 14 meq/l. What is the acid-base disorder? How should this patient be treated? The ph is increased, and the pco 2 is decreased. This is a respiratory alkalosis secondary to central nervous system respiratory center stimulation. The condition must be relatively chronic, because there has been substantial renal compensation. The disorder itself should not be treated. In fact, the low pco 2 may serve to partially counteract the cerebral edema. As this case demonstrates, it is important not to assume that any patient with a decreased HCO 3 - has a metabolic acidosis.

3 Case 3 A 25-year-old patient with epilepsy suffered a grand mal seizure. Immediately after the seizure, the following laboratory values were obtained: arterial ph, 7.14; pco 2, 45 mm Hg; HCO 3 -, 14 meq/l; Na +, 140 meq/l; Cl -, 98 meq/l. What kind of acidosis is present? What is the anion gap, and why is it increased? This is a case of increased anion gap metabolic acidosis secondary to lactic acid production from skeletal muscles during tonic-clonic seizure activity. The anion gap is 140 meq/l (98 meq/l + 17 meq/l) = 25 meq/l. There is also a respiratory acidosis due to depressed ventilation during the seizure.

4 Case 4 A patient has an arterial blood ph of 7.4 and a pco 2 of 20 mm Hg. A. What is the HCO - 3 concentration? B. What, if any, acid-base disorder(s) is/are present? Assume ph = 7.4 is normal. A. [HCO 3 - ] = 24 x pco 2 /[H + ] = 24 x 20/40 = 12 meq/l. B. Because ph is normal, because both the pco 2 and the [HCO 3 - ] are abnormally low, and because normal compensatory processes do not completely correct the ph for an acid-base disorder, these data depict a patient with a combined metabolic acidosis and respiratory alkalosis.

5 Case 5 A previously well patient is brought to the emergency room in sever respiratory distress. Physical examination and chest X-ray films suggest acute pulmonary edema. Laboratory test values are as follows: arterial ph 7.02 pco 2 60 mm Hg - HCO 3 15 meq/l po 2 40 mm Hg Cl - 95 meq/l Na meq/l A. What acid-base disorder(s) is/are present? B. Why is the HCO - 3 decreased? A. The blood is academic; therefore, at least one type of acidosis is present. The pco 2 is high, and the [HCO 3 - ] is low, both of which would increase [H + ]. Neither of these changes could be compensatory. Therefore, this patient has combined metabolic and respiratory acidoses. B. Although there is not enough clinical information presented to explain the cause of the metabolic acidosis, it is a high anion gap acidosis. The most likely explanation is lactic acidosis caused by anoxia and poor tissue perfusion in a patient with severe congestive heart failure and pulmonary edema.

6 Case 6 A 24-year-old man with insulin dependent diabetes mellitus develops symptoms of a viral infection. He is febrile, anorexic, and nauseated, and he has vomited several times in the 48-hour period before admission to the hospital. Because he was not eating, he took no long-lasting insulin the day previous to or the day of admission to the hospital. On admission, his laboratory test values are as follows: arterial ph 7.36 pco 2 35 mm Hg - HCO 3 20 meq/l Cl - 90 meq/l Na meq/l K mm Hg A. Is/are there any significant acid-base disorder(s) present? If so, which one(s)? B. How should this patient be treated? A. This patient has severe ketoacidosis and a concurrent metabolic alkalosis caused by vomiting and volume contraction. The highly elevated anion gap (30 meq/l) shows that substantial amounts of an unmeasured anion (i.e., ketones) are present. The fact that the anion gap is significantly greater than the change from normal in [HCO 3 - ] provides the major clue that two disorders are present. If untreated, this patient will become severely acidemic (i.e., blood ph will decrease) as well as acidotic within a few hours. B. Because the patient is severely acidotic despite relatively normal blood ph and [HCO 3 - ], he should be aggressively treated like any patient with diabetic ketoacidosis with volume replacement, intravenous insulin, potassium supplementation, and careful monitoring of blood sugar and anion gap.

7 Case 7 A 21-year-old Andean Indian woman had no known medical problems. She was accepted into the first-year medical school class at a prestigious American university. Before leaving home, she underwent a complete history and physical, including blood tests. Everything was normal except for a serum HCO 3 - of 15 meq/l (normal, meq/l). When she arrived in America, the intern who reviewed her medical records was concerned that she might have a metabolic acidosis. On examination, there were no abnormalities noted, and on repeat blood testing, the serum HCO 3 - was 24 meq/l. The intern was puzzled, but the student had the explanation and escaped without further testing. Case Discussion This case illustrates several important concepts in the diagnostic approach to a patient with a potential acid-base disorder. Contrary to the expectation of the intern, the Andean student did not have metabolic acidosis, but instead had a chronic respiratory alkalosis. The mass action equation H + = 24 x pco 2 /HCO 3 - illustrates that the H + is dependent on both pco 2 and HCO 3 -. Therefore, it is impossible to reliably make the diagnosis of an acid-base disorder when only one of those critical laboratory values is known. In other words, a low HCO 3 - does not necessarily mean that the H + is increased. If the pco 2 is also decreased, so that the ratio of pco 2 to HCO 3 - is low, the H + will also be low. This is exactly what happened in the case of the Andean student. For people living at extreme elevations, hypoxia caused by low ambient atmospheric oxygen levels causes a chronic increase in ventilation and decrease in pco 2. As noted previously, renal mechanisms compensate for the low pco 2 by decreasing renal ammonium excretion and bicarbonate reabsorption, thereby decreasing the [HCO 3 - ]. This normal compensatory change was the only abnormality found in the medical student s initial laboratory evaluation. Had a complete (and unnecessary) evaluation been conducted, including an arterial blood gas, the decreased pco 2 and decreased H + would have been detected. The lack of any metabolic abnormality was proven when the student descended to an elevation with normal atmospheric oxygen levels. Without the need for increased ventilation, the pco 2 rapidly rose to normal levels, and somewhat more slowly, the HCO 3 - level also rose to normal levels, as documented by the second set of laboratory values.

8 Case 8 A 38-year-old male electrician with chronic glomerulonephritis had been followed by a medical house officer in the clinic at the university hospital for the past 3 years. Because the house officer is leaving the university, she asks an incoming intern to take over the care of this patient. On the first day of his internship, he is paged to the emergency room to see the patient. The patient complains of increasing shortness of breath and a productive cough. The patient has a temperature of 39ºC and rales in his lower left posterior lung field, and he was tachypneic, with a respiratory rate of 22 breaths /minute. The emergency department resident says that the arterial blood gasses show that the patient is mildly hypoxic, but there is no significant acid-base disorder because the ph was normal. The new intern is somewhat perplexed by this diagnosis and asks to see the laboratory test values, which are as follows: blood urea nitrogen, 85 mg/dl; creatinine, 7.2 mg/dl, HCO 3 -,12 mm; ph, 7.4; pco 2, 20 mm Hg. Having just completed his renal rotation as a fourth-year medical student, the new intern knows exactly what is happening Case Discussion This case illustrates the principle that when two counteracting acid-base disorders are present, the ph of the blood can be high, low, or normal. Because compensatory processes do not return the ph to normal, an equation or nomogram is not needed to diagnose a combined or mixed acid-base disorder in this case. The two counteracting disorders are metabolic acidosis and respiratory alkalosis. The metabolic acidosis is the result of chronic renal failure, and the respiratory alkalosis occurred because of the patient s pneumonia, which was confirmed by chest X-ray films. If this diagnosis seems confusing, individually consider the laboratory abnormalities: decreased HCO 3 - concentration and decreased pco 2. If the decreased HCO 3 - concentration was the only primary change (i.e., if only a metabolic acidosis was present), the expected compensatory decrease in pco 2 as for Case I would be approximately 1.2 mm Hg for every 1-mM fall in [HCO 3 - ]= 1.2 mm Hg x (24 mm Hg 14 mm Hg) = 12 mm Hg, or a decrease from 40 mm Hg to 28 mm Hg. Because this patient s actual pco 2 level is considerably less than 28 mm Hg, it follows that there is some other primary stimulus for the decreased pco 2. Another relationship that can is derived from the acid-base nomogram is that if the decrease in pco 2 was the only primary change (i.e. if only a metabolic acidosis was present), the expected compensatory decrease in HCO 3 - concentration would be 2 mm for every 10-mm Hg fall in pco 2 if the respiratory alkalosis was acute, or 5 meq/l for every 10-mm Hg fall in pco 2 if the respiratory alkalosis was chronic. Therefore, the expected fall in HCO 3 - concentration would be 2 mm = 4 mm in acute respiratory alkalosis. Because the fall in HCO 3 - concentration is actually much greater than predicted, even if the respiratory alkalosis was chronic, which almost certainly it was not, this indicates that some other primary cause explained the decrease in HCO 3 - concentration.