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Metabolic Acidosis

Metabolic Acidosis

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Metabolic Acidosis

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  1. Metabolic Acidosis Residents’ Conference 11/1/01 Romulo E. Colindres, MD

  2. Primary Acid-Base Disorders Disorder pH HCO3- pCO2 Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis

  3. Compensatory Responses toPrimary Acid-Base Disorders

  4. SERUM ANION GAP [Na + K] + Unmeasured Cations = [Cl + HCO3] + Unmeasured Anions [Na + K] - [Cl + HCO3] = Unmeasured Anions (UC) - Unmeasured Cations (UC) . CAN OMIT K. [Na] - [Cl + HCO3) = UA-UC; Normal Value: 10+/- 2mEq/L. Increase in anion gap usually indicates an increase in unmeasured anions: albumin, PO4, SO4, anions of organic acids.

  5. Anion Gap Proteins 16 K 5 Ca 5 Mg 2 Na+ 140 HCO3- 24 Cl- 104 Organic Acids 5 AG 12 Na+ 140 HCO3- 24 Cl- 104 PO4 SO4 3 Cations Anions AG = Na+ - (Cl+HCO3)

  6. Excessive Acid Production Endogenous Exogenous Bicarbonate Wasting Diarrhea Renal (Type 2 RTA) Decreased Excretion of Acid (Impaired NH4+ excretion) Renal Failure Impaired Distal Acidification (RTA 1) Hypoaldosteronism (RTA 4) Combination of Above CAUSES OF METABOLIC ACIDOSIS

  7. METABOLIC ACIDOSIS: INDICIS OF SEVERITY • pH <7.2 • [HCO3] < 10mEq/L • Massive continuous production of acid • Poor respiratory compensation ( pCO2 fall less than 1.25 mm Hg for each mEq/L fall in HCO3 concentration)

  8. Acid Production • Carbohydrates/Fats  15,000 mmol/d CO2 (Volatile acid) CO2 + H20  H2CO3  H+ + HCO3- Lungs • Proteins  50-100 mEq/d H2SO4 (Fixed Acid) • H+ + HCO3- H2CO3 • H+ + Intracellular Base-  HBase • H+ excretion in the kidney Limits rise in [H+]

  9. RENAL EXCRETION OF ACID • The kidneys must excrete 50 to 100 mEq of acid to regenerate the bicarbonate used to buffer the fixed acid generated from metabolism each day • The daily acid load cannot be excreted unless all of the filtered HCO3 is reabsorbed • Excretion of an acid urine is a necessary but not sufficient condition to excrete the daily acid load: free H+ concentration in the urine is very low (<0.05mEq/L) in a maximally acid urine • Acid excretion comes from H+ secretion and binding to NH4+ and phosphate

  10. Proximal Tubule: Bicarbonate Reabsorption Tubular lumen Peritubular capillary Na+ 3Na+ HCO3-+ H+ H+ ATPase 2K+ H2O H2CO3 HCO3- OH- + CO2 HCO3- CA CA Na+ Na+ CO2 + H2O

  11. Proximal Tubule: Titratable Acid Tubular lumen Peritubular capillary Na+ 3Na+ H+ HPO42- + H+ ATPase 2K+ H2O HCO3- OH- + CO2 HCO3- H2PO4- CA Na+ Na+

  12. Ammonia Synthesis and Transport Na + NH + NH + 4 4 2Cl- Tubular lumen Peritubular Na + capillary NH NH 3Na + 3 3 NH + + ATPase NH + 4 4 2K + H+ Glutamate- ATPase Glutaminase Glutamine NH + 4

  13. Renal Acid-Base Regulation • 4000 mEq HCO3- filtered in proximal tubule must be reabsorbed - no net acid excretion • Minimal urine pH is 4.5 only 40-80 mol per day can be excreted as free H+; Excretion of the daily acid load as free H+ would require 2000 liters of urine output/day • H+ is excreted in the form of urinary buffers, H2PO4- and NH4+

  14. METABOLIC ACIDOSIS WITH INCREASED ANION GAP NaHCO3 + Lactic acid--->Na Lactate + CO3H2----> [Na] - [Cl +HCO3 + Lactate] • Usually caused by increased production of endogenous or exogenous organic acid • Salt (anion) may be quickly metabolized or excreted yielding a hyperchloremic acidosis

  15.  Gap Metabolic Acidosis Due to Presence of Ketoacids Na+ 140 Pr, OA, P,S 12 Anion Gap = 25 pH = 7.25 HCO3 = 10 pCO2 = 25 AG = 25 Ketoacid 13 HCO3 10 Cl- 105

  16. Differential Diagnosis of AG Metabolic Acidosis Methanol poisoning Uremia (advanced, SO4, PO4) Diabetic ketoacidosis -Other ketoses EtOH Starvation Paraldehyde (rare) Ischemia-Lactate Ethylene glycol Salicylate toxicity

  17. DIFFERENTIAL DX OF  ANION & OSMOLAR GAP ACIDOSES

  18. KETOACIDOSIS EVOLVES FROM HIGH AG  NL. AG ACIDOSIS GFR INSULIN

  19. HYPERCHLOREMIC METABOLIC ACIDOSIS HCL + NaHCO3---> NaCl and H2CO3---> CO2 +H2O Therefore: anion gap unchanged since [Na] - (increased [Cl] + decreased [HCO3]). • Loss of HCO3 in stool • Loss of HCO3 in urine (RTA 2) • Decreased excretion of NH4 (RTA 1 and 4 and renal failure) • Increased production of acid but prompt excretion of anion (treatment of DKA, toluene)

  20. Normal Anion Gap Metabolic Acidosis in a Patient with Diarrhea Na+ 140 AG 12 pH = 7.32 HCO3- = 15 pCO2 = 30 AG = 12 HCO3 15 Cl- 113

  21. URINE ANION GAP:AN INDIRECT MEASUREMENT OF NH4+ EXCRETION IN HYPERCHLOREMIC METABOLIC ACIDOSIS Urine Anion Gap: [Na] + [K] - [Cl] Since: [Na] + [K] + Unmeasured (U) Cations = [Cl] + Unmeasured (U) Anions Therefore, [Na] + [K] - [Cl]= U Anions- U Cations U Anions = Sulfates, Phosphates, etc. U Cation = Mainly NH4+ Normal Value: 0 Hyperchloremic Metabolic Acidosis: -20 to -50 = Appropriately Increased NH4+ Excretion

  22. Practical Approach (Hyperchloremic metabolic acidosis) Urine Anion Gap NegativePositive Type 2 RTA Diarrhea DKA/Toluene HCl (Hyperalimentation) Urine pH and Plasma K Urine pH < 5.5, K Urine pH > 5.5, K nl/lowUrine pH > 5.5, K  Type 4 RTA Type 1 (secretory defect Type 1 (voltage) Early CRF or back-leak)

  23. METABOLIC ACIDOSIS:BICARBONATE THERAPY • Avoid if metabolic acidosis is transient and moderate and renal function is adequate, particularly with increased anion gap acidosis, since anions of organic acids can regenerate HCO3 • Only a small inmediate increase (2-3 mEq/L) in plasma [HCO3] is necessary to get patient out of danger if there is normal respiratory compensation

  24. Relationship Between pH and [HCO3-] 25 20 Small changes in [HCO3-] cause large changes in pH [HCO3-] meq/L 15 10 5 7.10 7.20 7.30 7.40 pH

  25. Therapy in Patients with Severe Acidosis • Initial goal is to raise the pH to ~7.20 • decreased risk of arrhythmias • improved cardiac contractility and responsiveness to catecholamines • Further correction is generally not necessary acutely • may cause volume overload • may reduce O2 delivery to the tissues • may result in hypercarbia

  26. METABOLIC ACIDOSIS:BICARBONATE THERAPY • Rapid I.V. administration of HCO3 is important only in patients with severe metabolic acidosis • Serial Measurements of [HCO3] • Give oral HCO3 if possible • Assume volume of distribution of HCO3 to be 50% of lean body weight

  27. METABOLIC ACIDOSIS: BICARBONATE THERAPY • Chronic renal failure: HCO3, not citrate to avoid Aluminum absorption. Give a large dose for several days to achieve a [HCO3] of approx.20mEq/L. Maintenance dose of about 40 mEq/day • Chronic RTA 1: 1-2 mEq/Kg/day of Na-K citrate after increasing [HCO3] to desired level • RTA 2: 10-15 mEq/Kg/day • RTA 4: Correct hyperkalemia

  28. Normal [H+] 40 nanoequivalents per liter  One-millionth the concentration of sodium, potassium and chloride

  29. Modified Henderson-Hasselbach Equation pCO2 [H+] = 24 [HCO3-]

  30. Bicarb-CO2 System in Response to H+ Load ECF 24 mEq/L HCO3- ECF 22 mEq/L HCO3- 30 mEq H+ 30 mmol CO2 = 2 mmol/L CO2 Dissolved CO2 1.2 mmol/L + 2 mmol/L = 3.2 mmol/L  pCO2 107 mmHg . 107 = 116 nEq/L  pH = 6.94 No change in VE [H+] = 24 . 22 37 = 39 nEq/L  pH = 7.396  VE [H+] = 24 22

  31. Change in Tubular Fluid pH Distal Ureteral Proximal Tubule, % convolution, urine % 0 100 0 20 40 60 80 100 0.2 0.2 D pH D 0 pH 0 0.4 0.4 0.8 0.8 1.2 1.2 1.6 2.0 2.4 Gottschalk CW, Lassiter WE, Mylle M, Am J Physiol , 198:581, 1960.

  32. Decreased Efficacy of Respiratory Compensation with Worsening Acidosis Condition HCO3- pCO2 H+ pH Normal 24 40 40 7.40 Moderately 15 30 50 7.30 Severe Life Threatening 5 20 100 7.00