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Bicarbonate Therapy in Severe Metabolic Acidosis Neil A. Kurtzman, MD Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock,

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Presentation on theme: "Bicarbonate Therapy in Severe Metabolic Acidosis Neil A. Kurtzman, MD Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock,"— Presentation transcript:

1 Bicarbonate Therapy in Severe Metabolic Acidosis Neil A. Kurtzman, MD Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas 79430

2 Metabolic acidosis: A primary fall in the bicarbonate concentration Metabolic acidosis: A primary fall in the bicarbonate concentration Due to either a gain of acid or a loss of base (usually HCO 3 ) Due to either a gain of acid or a loss of base (usually HCO 3 ) Acidemia refers solely to a fall in pH Acidemia refers solely to a fall in pH

3 Exogenous (eg, NH 4 Cl) Exogenous (eg, NH 4 Cl) Endogenous Endogenous Abnormal lipid metabolism DKA Abnormal lipid metabolism DKA Abnormal CHO metabolism Lactic acidosis Abnormal CHO metabolism Lactic acidosis Normal protein metabolism Uremic acidosis Normal protein metabolism Uremic acidosis Gain of Acid

4 Kraut and Kurtz did an online (Clin Exp Neprol 10: , 2006) survey of how intensivists and nephrologists gave HCO 3 to patients with metabolic acidosis Kraut and Kurtz did an online (Clin Exp Neprol 10: , 2006) survey of how intensivists and nephrologists gave HCO 3 to patients with metabolic acidosis Forty percent of the intensivists would not give bicarbonate unless the pH was less than 7.0 Forty percent of the intensivists would not give bicarbonate unless the pH was less than 7.0 Only 6% of nephrologists wait until pH gets this low (p < 0.01) Only 6% of nephrologists wait until pH gets this low (p < 0.01)

5 More than 80% of nephrologists consider the pCO 2 in making their decision to treat More than 80% of nephrologists consider the pCO 2 in making their decision to treat Only 59% of intensivists do (p<0.02) Only 59% of intensivists do (p<0.02) In patients with lactic acidosis, 86% of nephrologists treat with bicarbonate In patients with lactic acidosis, 86% of nephrologists treat with bicarbonate Two-thirds of intensivists give bicarbonate (p< 0.05) Two-thirds of intensivists give bicarbonate (p< 0.05)

6 60% of nephrologists treat DKA with bicarbonate 60% of nephrologists treat DKA with bicarbonate 28% of intensivists give bicarbonate to patients with DKA (p<0.01) 28% of intensivists give bicarbonate to patients with DKA (p<0.01) Both would administer bicarbonate by constant infusion, targeting an arterial pH of 7.2 Both would administer bicarbonate by constant infusion, targeting an arterial pH of 7.2 Seventy-five percent of nephrologists calculate the amount of bicarbonate required, while only one-third of intensivists do so Seventy-five percent of nephrologists calculate the amount of bicarbonate required, while only one-third of intensivists do so

7 Metabolic acidosis results from a loss of bicarbonate (eg diarrhea) Metabolic acidosis results from a loss of bicarbonate (eg diarrhea) Or from its titration to an anionic base that often can be converted back to bicarbonate (eg DKA or lactic acidosis) Or from its titration to an anionic base that often can be converted back to bicarbonate (eg DKA or lactic acidosis) This non-bicarbonate base anion is commonly termed potential bicarbonate This non-bicarbonate base anion is commonly termed potential bicarbonate

8 Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base which, given time, can be converted back to bicarbonate Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base which, given time, can be converted back to bicarbonate

9 1. What are the deleterious effects of acidemia and when are they manifest? 2. When is acidemia severe enough to warrant therapy? In considering acute bicarbonate replacement four questions should be considered

10 3. How much bicarbonate should be given and how is that amount calculated? 4. What are the deleterious effects of bicarbonate therapy?

11 Decreased myocardial contractility Decreased myocardial contractility Fall in cardiac output Fall in cardiac output Fall in BP Fall in BP Pulmonary venoconstriction Pulmonary venoconstriction Deleterious effects of acidemia

12 Decreased binding of norepinephrine to its receptors Decreased binding of norepinephrine to its receptors Acidemia may adversely affect cell functions such as enzymatic reactions, ATP generation, fatty acid biosynthesis, and bone formation/resorption Acidemia may adversely affect cell functions such as enzymatic reactions, ATP generation, fatty acid biosynthesis, and bone formation/resorption Deleterious effects of acidemia

13 Drugs which are salts of weak acids are more active during acidemia Drugs which are salts of weak acids are more active during acidemia More receptor binding More receptor binding More entry to cells More entry to cells Best example is ASA Best example is ASA Deleterious effects of acidemia

14 tolbutamide tolbutamide methotrexate methotrexate phenobarbital phenobarbital phenytoin phenytoin

15 Optimal extracelluar pH 7.4 Optimal extracelluar pH 7.4 Optimal intracellular pH 7.1 Optimal intracellular pH 7.1 Deviations from normal pH will obviously decrease the efficiency of all reactions Deviations from normal pH will obviously decrease the efficiency of all reactions

16 Acidemia protects the central nervous system against seizures, it sensitizes the myocardium to arrhythmias Acidemia protects the central nervous system against seizures, it sensitizes the myocardium to arrhythmias Extracellular pH is a surrogate for intracellular pH Extracellular pH is a surrogate for intracellular pH

17 Most authorities in acid-base physiology would give bicarbonate to a patient with an arterial pH < 7.1 Most authorities in acid-base physiology would give bicarbonate to a patient with an arterial pH < 7.1 Not a hard and fast rule Not a hard and fast rule More on this later More on this later When is acidemia severe enough to warrant therapy?

18 The volume of distribution of bicarbonate is approximately that of total body water The volume of distribution of bicarbonate is approximately that of total body water In patients with metabolic acidosis it is said to vary from 50% to greater than 100%, depending on the severity of the acidemia In patients with metabolic acidosis it is said to vary from 50% to greater than 100%, depending on the severity of the acidemia How much bicarbonate should be given and how is that amount calculated ?

19 Any calculated amount is approximate Any calculated amount is approximate Fernandez et al have derived a formula for calculating the bicarbonate space (KI 36: , 1989) Fernandez et al have derived a formula for calculating the bicarbonate space (KI 36: , 1989) ( / pHCO3) (body weight) ( / pHCO3) (body weight) How much bicarbonate should be given and how is that amount calculated?

20 At a pCO 2 of 13 mm Hg and HCO 3 of 4 mEq/l, the arterial pH is 7.1 At a pCO 2 of 13 mm Hg and HCO 3 of 4 mEq/l, the arterial pH is 7.1 Raise the HCO 3 to only to 8 mEq/L the blood pH will increase to 7.4 Raise the HCO 3 to only to 8 mEq/L the blood pH will increase to 7.4 This assumes the pCO 2 doesnt change This assumes the pCO 2 doesnt change How much bicarbonate should be given and how is that amount calculated?

21 If the bicarbonate concentration rises only 1 mEq/L the pH would be above 7.2 If the bicarbonate concentration rises only 1 mEq/L the pH would be above 7.2 Arterial pCO 2 typically however does not remain the same after bicarbonate infusion Arterial pCO 2 typically however does not remain the same after bicarbonate infusion In severely acidotic patients it rises 6.7 ± 1.8 mm Hg when an infusion of sodium bicarbonate is given (1.5 mmol/kg over 5min) In severely acidotic patients it rises 6.7 ± 1.8 mm Hg when an infusion of sodium bicarbonate is given (1.5 mmol/kg over 5min) How much bicarbonate should be given and how is that amount calculated?

22 Bicarbonate therapy is associated with an increase in mortality Bicarbonate therapy is associated with an increase in mortality True in humans and experimental animals under a variety of acidemic conditions True in humans and experimental animals under a variety of acidemic conditions Fall in blood pressure and cardiac output Fall in blood pressure and cardiac output What are the deleterious effects of bicarbonate therapy?

23 Shifts in ionized calcium Shifts in ionized calcium In strong acid acidosis potassium also shifts out of the cell In strong acid acidosis potassium also shifts out of the cell Sensitizes the heart to abnormal electrical activity and subsequent arrhythmias Sensitizes the heart to abnormal electrical activity and subsequent arrhythmias What are the deleterious effects of bicarbonate therapy?

24 Paradoxical intracellular acidosis – CO 2 shifts into cells Paradoxical intracellular acidosis – CO 2 shifts into cells Both volume expansion and hypernatremia can occur Both volume expansion and hypernatremia can occur Fulminate congestive heart failure with flash pulmonary edema may result Fulminate congestive heart failure with flash pulmonary edema may result What are the deleterious effects of bicarbonate therapy?

25 In vitro studies show that intracellular alkalinization hastens cell death following anoxia In vitro studies show that intracellular alkalinization hastens cell death following anoxia Stimulates superoxide formation, increases pro- inflammatory cytokine release, and enhances apoptosis Stimulates superoxide formation, increases pro- inflammatory cytokine release, and enhances apoptosis Relationship to human disorders unknown Relationship to human disorders unknown What are the deleterious effects of bicarbonate therapy?

26 Rebound alkalemia – especially with low arterial pCO 2 Rebound alkalemia – especially with low arterial pCO 2 Blood lactate and ketone bodies increase Blood lactate and ketone bodies increase This potential bicarbonate will be converted back to actual bicarbonate unless it lost in the urine This potential bicarbonate will be converted back to actual bicarbonate unless it lost in the urine What are the deleterious effects of bicarbonate therapy?

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28 Acetoacetate and beta-hydroxybutyrate are lost in the urine before the patient arrives at the hospital Acetoacetate and beta-hydroxybutyrate are lost in the urine before the patient arrives at the hospital The patient is truly bicarbonate deficient The patient is truly bicarbonate deficient More urinary loss of ketone bodies occurs following fluid administration and volume repletion More urinary loss of ketone bodies occurs following fluid administration and volume repletion DKA

29 Hyperchloremic metabolic acidosis the day after insulin therapy Hyperchloremic metabolic acidosis the day after insulin therapy Almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired Almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired Bicarbonate therapy markedly increases blood acetoacetate and beta-hydroxybutyrate levels Bicarbonate therapy markedly increases blood acetoacetate and beta-hydroxybutyrate levels DKA

30 Bicarbonate therapy delays the removal of ketone bodies from the blood Bicarbonate therapy delays the removal of ketone bodies from the blood Bicarbonate therapy markedly increases blood acetoacetate and beta-hydroxybutyrate levels Bicarbonate therapy markedly increases blood acetoacetate and beta-hydroxybutyrate levels DKA

31 Mortality greater than 80% Mortality greater than 80% Outcome depends on the treatment of its cause Outcome depends on the treatment of its cause Cardiogenic or hemorrhagic shock Cardiogenic or hemorrhagic shock Exogenous toxins such as cyanide or metformin Exogenous toxins such as cyanide or metformin Lactic Acidosis

32 CASE #1: A 20 year-old man with a five-year history of type 1 diabetes mellitus was admitted for the ninth time in diabetic ketoacidosis. He was poorly responsive and had Kussmaul respirations. Before any therapy he had a plasma Na of 140 mEq/L, K 4 mEq/L, Cl 109 mEq/L, CO 2 3 mEq/L, and his creatinine was 1 mg/dL. The arterial pH was 6.95, pCO 2 14 mm Hg, and the calculated HCO3 was 3 mEq/L.

33 Urine and blood ketones were strongly positive. He was treated with insulin and appropriate fluid and electrolyte replacement. He was not given bicarbonate. The next day he was fully oriented. His plasma Na was 142, K 4, Cl 114 and his CO 2 was 18 mEq/L. The remainder of his clinical course was unremarkable. Urine and blood ketones were strongly positive. He was treated with insulin and appropriate fluid and electrolyte replacement. He was not given bicarbonate. The next day he was fully oriented. His plasma Na was 142, K 4, Cl 114 and his CO 2 was 18 mEq/L. The remainder of his clinical course was unremarkable.

34 CASE #2: An 80 year old man was admitted with severe congestive heart failure. He was hypotensive and oliguric. He had both pulmonary and peripheral edema. His baseline creatinine was known to be 1.6 mg/dL. On arrival at the emergency room his plasma Na was 135 mEq/L, K 4 mEq/L, Cl 97 mEq/L, CO 2 7 mEq/L, and his creatinine was 2.5 mg/dl. His arterial pH was 7.1, pCO 2 20 mm Hg, and the calculated HCO 3 was 6 mEq/l. The blood lactate level was 20 mmol/L.

35 The patient was intubated and placed on a respirator keeping his pCO 2 at 20 mmHg. CVVHD was begun with a bath containing 14 mEq/L of bicarbonate. He was given an infusion of 300 mEq of bicarbonate over two hours; with a total body water of 43 liters, one would aim for a HCO 3 of 14 mEq/L: (7 mEq/L X 43 L = 301 mEq). At the end of that time his pH was 7.2 and the HCO 3 was 13 mEq/L. Five days later he was transferred out of the intensive care unit, his lactic acidosis resolved. The patient was intubated and placed on a respirator keeping his pCO 2 at 20 mmHg. CVVHD was begun with a bath containing 14 mEq/L of bicarbonate. He was given an infusion of 300 mEq of bicarbonate over two hours; with a total body water of 43 liters, one would aim for a HCO 3 of 14 mEq/L: (7 mEq/L X 43 L = 301 mEq). At the end of that time his pH was 7.2 and the HCO 3 was 13 mEq/L. Five days later he was transferred out of the intensive care unit, his lactic acidosis resolved.

36 Case #1 got no bicarbonate even though his pH was < 7.0 Case #1 got no bicarbonate even though his pH was < 7.0 Case #2 received bicarbonate though he had a higher pH Case #2 received bicarbonate though he had a higher pH Bicarbonate therapy must be individualized Bicarbonate therapy must be individualized

37 Desired HCO 3 – observed HCO 3 Desired HCO 3 – observed HCO 3 Use total body water Use total body water Assume pCO 2 will not change Assume pCO 2 will not change Give that amount which will raise the pH to 7.2 Give that amount which will raise the pH to 7.2

38 Reevaluate in two hours Reevaluate in two hours Make new plan based on the new data Make new plan based on the new data Correct the underlying cause(s) Correct the underlying cause(s)

39 Sandra Sabatini and Neil A. Kurtzman: Bicarbonate Therapy in Severe Metabolic Acidosis, JASN in press. Sandra Sabatini and Neil A. Kurtzman: Bicarbonate Therapy in Severe Metabolic Acidosis, JASN in press.


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