R5 Metabolic Acidosis and Metabolic Alkalosis

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R5 Metabolic Acidosis and Metabolic Alkalosis
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2013-03-09 12:37:09
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Renal II
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Renal II
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  1. How do acid-base disorders occur?
    • 1. Renal/pulmonary function is abnormal
    • 2. Acid/base load exceeds excretory capacity
    • 3. Both
  2. CO2-Bicarbonate Buffer System
    -any buffer system can be used to analyze pH, by convention we use CO2-bicarb



    First step is catalyzed by carbonic anhydrase, second step occurs freely
  3. Normal Lab Values
    • -there can be significant variation in normal values
  4. -emia vs. -osis
    -emia = "state of the blood"

    Acidemia: decrease in blood pH below the normal range of 7.36-7.44

    Alkalemia: elevation in blood pH above the normal range of 7.36-7.44

    -osis = refers to a process

    • Metabolic acidosis
    • Metabolic alkalosis
    • Respiratory acidosis
    • Respiratory alkalosis
  5. Single vs Multiple Processes
    • Single Process
    • -"simple" acid-base disturbance
    • -there is compensation for the disturbance

    • Multiple Processes
    • -"mixed" acid-base disturbance
    • -compensation for a simple acid-base disturbance is not a separate process
  6. Rules of Compensation
    • 1. Compensation returns pH toward, but not TO, normal values
    • **exception: chronic respiratory alkalosis can have pH in the normal range (ie: high altitude)

    2. Compensatory response serve to maintain the ratio of PCO2/HCO3- or lung/kidney

    3. Compensation for respiratory disturbances has an acute component an a slower chronic component (kidney)

    4. Compensation for metabolic disorders is only through changes in ventilation

    5. Therefore respiratory disturbances are classified as "acute" vs "chronic" but metabolic disturbances are not
  7. Henderson-Hasselbach Equation


  8. H+ Ion Concentration Equation
  9. Compensation Time Courses
    • Chemical, Passive Buffering
    • -by the extracellular fluid
    • -secs-mins

    • Cellular Buffering
    • -within hours

    • Respiratory Compensation
    • -12 hours to achieve steady state

    • Renal Compensation
    • -1-3 days to reach steady state
    • -primarily due to induction of new enzymes necessary for renal acidification

  10. Acid-Base Disorders and Compensation
    • Metabolic Acidosis
    • -decrease PCO2 (increased ventilation)

    • Metabolic Alkalosis
    • -increase PCO2 (decrease ventilation)

    • Acute Respiratory Acidosis
    • -increase HCO3- (intracellular buffers)

    • Chronic Respiratory Acidosis
    • -increase HCO3- (increase NH4+ excretion)

    • Acute Respiratory Alkalosis
    • -decrease HCO3- (intracellular buffers)

    • Chronic Respiratory Alkalosis
    • -decrease HCO3- (decrease reabsorption of HCO3-, decrease NH4+ excretion)
  11. Approach to acid-base disturbances


    • 1. Determine pH from ABG
    • 2. Compare HCO3- concentration vs the arterial PCO2 to distinguish metabolic from respiratory
    • 3. Calculate expected compensation for the primary disorder
    • ** if the compensation is different than expected/calculated a mixed acid-base disorder exists
  12. Calculating appropriate compensation


    • Many different was to calculate expected compensation:
    • 1. Last two digits of pH = PCO2
    • 2. Winter's formula
    • PCO2 = (1.5 x HCO3-) + 8 ± 2

    • Nomogram:
  13. Acid Production/Excretion
    • 2 Classes of Daily Acid Production:
    • 1. Volatile Acids (14,000 mmol/day)
    • -gaseous CO2
    • -disposed of by the lungs

    • 2. Non-Volatile Acids (1 mEq/kg/day)
    • -AAs, NAs, phosphoproteins are metabolized to sulfuric, phosphoric and hydrochloric acid
    • -must be disposed of by the kidneys

    • Acid Excretion by the Kidney
    • 1. Free H+ excreted (<1%, down to pH of 5-5.5)
    • 2. Bound to base buffers (phosphate and sulfate) (30%)
    • 3. Ammonium- NH4+ (majority)

    • Sites of H+ Excretion:
    • 1. Proximal Tubule (Na+/H+ Antiporter)
    • 2. Distal Tubule (CCD H+ ATPase)
  14. Net Acid Excretion Equation
    NAE = titratable acids + NH4+ - urinary HCO3-

    **normal urine should have almost no free HCO3-
  15. Serum Anion Gap
    -distinguishes the causes of metabolic acidosis

    Na+ + UC = Cl- + HCO3- + UA

    UA-UC = Na+ - (Cl- + HCO3-)

    • Normal AG = 12
    • -largely comprised of albumin
  16. Increased Anion Gap
    • 1. Add HCl to plasma
    • -H+ ions titrated by HCO3-
    • -HCO3- in plasma decreases
    • -to remain electroneutral Cl- increases
    • -AG remains the same

    • 2. Add Organic Acid
    • -increases the UA
    • -AG increases

  17. Urine Anion Gap
    -useful in assessing normal AG metabolic acidosis

    Urine AG = (Na+ + K+) - Cl-

    • Normal kidney function (GI cause):
    • -range 0 to -50 (NEGATIVE)
    • -Major unmeasured cation is NH4+
    • -as kidney responds appropriately to acid load it increases NH4+ excretion
    • -NH4+ must be excreted with a Cl- ion
    • -Increased Cl- in urine --> negative UAG

    • Abnormal Kidney Function (dRTA):
    • -UAG is POSITIVE
    • -impaired distal H+ and NH4+ excretion

  18. Clinical Utility of serum/urine anion gap


    • ELEVATED Serum AG:
    • -Ketoacidosis
    • -Lactic Acidosis
    • -Ethylene Glycol
    • -Methanol
    • -Salicylates

    • NORMAL Serum AG
    • POSITIVE Urine AG
    • -dRTA

    • NORMAL Serum AG
    • NEGATIVE Urine AG
    • -Diarrhea
    • -Parenteral nutrition (AAs --> HCl)
    • -Ileal diversion
  19. Osmolar Gap
    -useful in elevated serum AG metabolic acidosis

    • Calculated Posm
    • Posm = 2Na+ + Glucose/18 + BUN/2.8

    Osmolar Gap = Measured Posm - Calculated Posm

    Normal Osmolar Gap = 10-15 mmol/L

    **If > 20-25 with elevated AG metabolic acidosis --> ethylene glycol or methanol OD
  20. Types of Metabolic Acidosis
    • 1. Increased Anion Gap
    • "MUDPILES"
    • -Methanol
    • -Uremia
    • -DKA-Propylene glycol
    • -Iron tablets
    • -Lactic Acidosis
    • -Ethylene glycol
    • -Siacylates

    • "KULT"
    • Ketoacidosis
    • Uremia
    • Lactic Acidosis
    • Toxins (methanol, ethylene glycol, salicylates, paraldehyde)

    • 2. Normal Anion Gap
    • -Renal tubular acidoses
    • -Diarrhea
    • -Parenteral nutrition
    • -GI fistulas/diversions
  21. Uremia
    • Early CKD (Stages 2-4)
    • -associated with normal AG acidosis
    • -tubular function impairment
    • -impaired NH4+ excretion

    • Late CKD (Stages 4-5)
    • -associated with increased AG acidosis
    • -due to low GFR --> retention of unmeasured anions (sulfates, phosphates, hippurates, urates)

    • Treatment of Uremic Acidosis:
    • 1. Oral Bicarb to keep serum bicarb > 20-22 mEq/L (in states of chronic acidosis H+ is buffered by bone --> osteopenia)
    • -Treatment may slow progression of kidney disease
    • -NaHCO3 pills or Shohl's solution (sodium/potassium citrate --> esp if patient is hypokalemic)

    2. Dialysis
  22. Ketoacidosis
    • 1. Diabetic
    • 2. Starvation/Alcohol related
  23. Diabetic Ketoacidosis
    • Pathophysiology:
    • -insulin deficiency leads to fatty acid oxidation
    • --> ketone production (ketonuria, ketoacidosis)

    • Clinical Presentation:
    • -appear very ill
    • -typically hyperglycemic
    • -glucosuric
    • -high AG metabolic acidosis
    • -Volume depleted (significant losses of free water through osmotic diuresis)
    • -Losses of Na, K, PO4

    • Treatment:
    • -insulin
    • -volume expansion
    • -K and PO4 (may be high on presentation but will fall with treatment)
  24. Starvation/Alcohol-Related Ketoacidosis
    • Pathophysiology:
    • -typical scenario of binge drinking follwed by low food intake
    • -ketoacid production with β-hydroxybuyrate over acetoacetate (due to NADH from EtOH metabolism)

    • Clinical Presentation:
    • -volume depletion
    • -metabolic acidosis
    • -can have other acid base disturbances (metabolic alkalosis from vomiting, respiratory alkalosis from liver disease)

    • Treatment:
    • -IV fluids and carbohydrates (dextrose and 0.9% saline)
  25. Lactic Acidosis
    • Type A:
    • -seen in states of sustained anaerobic metabolism and poor tissue perfusion
    • **any condition that compromises oxygen delivery will generate excess lactic acid
    • -often seen in ICU patients

    • Type B:
    • -NO TISSUE HYPOPERFUSION
    • -accumulate lactic acid in other ways
    • -DM, uremia, malignancies
    • -ingestion of toxins
    • -inborn errors of metabolism
    • -D-Lactic Acidosis

    • D-Lactic Acidosis
    • -vs L-Lactic acidosis
    • -occurs in JI bypass, short bowel syndromes
    • -due to metabolism of overgrown GP organisms in the gut
    • -carbs reach colon due to short bowel --> metabolized to D-lactic acid
    • -after carbo loading can develop CNS Syndrome (cerebellar, mental status changes)
    • -patients look intoxicated
  26. Treatment of Lactic Acidosis
    • Type A:
    • 1. Correct underlying condition --> restore tissue perfusion
    • 2. NaHCO3 therapy (controversial: ketoacids metabolized to bicarb --> excess CO2 that diffuses into the intracellular compartments --> intracellular acidosis --> can impair myocardial contractility)
    • 3. Keep pH > 7.1

    • Type B:
    • 1. Correct underlying condition
    • 2. Think of D-lactic acidosis in the appropriate circumstance (pts look intoxicated)
  27. Metabolic Acidosis due to Intoxications (high AG)
    • Ethylene Glycol
    • -antifreeze
    • -metabolized to a variety of smaller acids
    • -high osmolar gap
    • -sweet taste
    • -can cause renal failure (crystal formation)
    • -CNS/heart/renal toxicity

    • Methanol
    • -high osmolar gap
    • -CNS depression
    • -optic disc hyperemia/nerve damage --> blindness
    • -Tx with IV EtOH (competes for ADH) or fomeprizole
  28. Renal Tubular Acidoses
    -involve either decreased HCO3- reclamation or abnormal distal acidification

    • Causes:
    • 1. Reduced H+ ion secretion
    • 2. Decreased ammoniagenesis
    • 3. Both

    • Type I
    • Type II
    • Type IV
  29. Type I RTA
    • -"distal" RTA
    • -hypokalemic RTA
    • -decreased H+ ATPase activity
    • -cannot lower urine pH < 6.0
    • -often seen in: CNS disease, rarely in RA, SCA, hyperparathyroidism
  30. Type II RTA
    • -"proximal" RTA
    • -failure to fully reclaim HCO3-
    • -isolated or part of general PT disorder (Fanconi Syndrome)
    • -CAIs can create the same phenotype
  31. Type IV RTA
    99% of adult RTA

    • -"distal" RTA
    • -hyperkalemic
    • -decrease in negative lumen potential of the CCD
    • -interferes with H+ and K+ secretion

    • Common Causes:
    • -hyperaldosteronism
    • -ENaC Inhibition/dysfunction (amiloride)
    • -generalized dysfunction of distal nephron with interstitial diseas
  32. How to distinguish Type 1 and Type 2 RTA


    Raise serum HCO3- and track HCO3- excretion in the urine

    • Normal:
    • -able to reabsorb HCO3- and keep it out of the urine

    • Type I:
    • -won't see bicarb in the urine until you see changes in the serum bicarb

    • Type II:
    • -urine bicarb excretion rises rapidly (defect in PT reabsorb of bicarb)

    • Type I:
    • -urine pH is always high

    • Type II:
    • -urine pH will be low at low serum bicarb
    • -as serum bicarb increases urinary pH raises
  33. Metabolic Alkalosis
    • -generated by loss of acid or gain in bicarb
    • -maintained by impaired renal excretion of bicarbonate (ie: volume depletion)
    • -frequently associated with hypokalemia

    • Causes:
    • -diuretics (loops, thiazide)
    • -vomiting
    • -NG suction
    • -administration of bicarb (uncommon)
    • -hyperaldosteronism
    • -Bartter/Gitelman syndromes
  34. Vomiting and Metabolic Alkalosis
  35. Urine Chloride
    -more valuable in determining volume status than urine sodium in metabolic alkalosis

    -urine chloride will remain low until volume status is restored

    -Chloride responsiveness can also help distinguish volume depleted (responsive) and primary hyperaldosteronism (unresponsive)
  36. Respiratory Acidosis Causes
    • Hypoventilation

    • -CNS depression
    • -Neuromuscular disease
    • -Lung/Chest wall deformaties
    • -airway disease
  37. Respiratory Alkalosis
    • Hyperventilation

    • -CNS stimulation
    • -Hypoxia
    • -Pulmonary disease
  38. Mixed Disturbances
    • Suspect when:
    • 1. Lack of expected compensation
    • 2. Compensation too little/too much
    • 3. PCO2 and HCO3 are abnormal in opposite directions
    • 4. pH normal but PCO2 or HCO3 are abnormal
    • 5. pH should not return to normal just with compensation
  39. Mixed Disturbances: Common Scenarios
    1. Metabolic alkalosis and chronic respiratory acidosis (COPD and diuretics)

    2. Respiratory alkalosis and metabolic acidosis (sepsis and salicylates)

    3. Chronic respiratory acidosis and metabolic acidosis (COPD and shock)

    4. Anion gap acidosis and metabolic acidosis (DKA and vomiting)
  40. Delta/delta
    -Change in AG/change in HCO3

    -used in the setting of mixed metabolic acidosis and metabolic acidosis

    -if the alkalosis pre-dates the acidosis than the start HCO3- value will be higher

    -for the same increase in organic anions the HCO3 will not fall as far from the normal value

    D/d > 2 = preexisting metabolic alkalosis

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