Acid-Base

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Contents

Introduction

  1. The hydrogen ion concentration in extracellular fluid is determined by the balance between the partial pressure of CO2 and the concentration of HCO3
    1. maintaining a constant pCO2 and HCO3 concentration maintains a constant extracellular pH
    2. normal values: pH = 7.36-7.44; pCO2 = 36-44 mm Hg; HCO3 = 22 to 26 mEq/L
  2. When a primary acid-base disturbance alters one component of the pCO2/HCO3 ratio, the compensatory response alters the other component in the same direction to keep the ratio constant

Compensation

  1. Respiratory compensation#
    1. mediated by hydrogen ion chemoreceptors located in the carotid body at the carotid bifurcation and in the lower brainstem
  2. Metabolic compensation#
    1. the kidneys provide the compensation for respiratory acid-base disorders by adjusting HCO3 reabsorption in the proximal tubules
    2. compensatory response in the kidneys is not immediate but begins to appear in 6 to 12 hours and slowly increases to a steady state over several days

Rules of acid-base interpretation

    1. Primary metabolic disorders
      1. A primary metabolic acid-base disorder is present if the pH is abnormal and the pH and the pCO2 change in the same direction
      2. A superimposed respiratory acid-base disorder is present if the measured pCO2 is normal, the measured pCO2 is higher than expected or the measured pCO2 is lower than expected
    2. Primary respiratory disorders
      1. A primary respiratory acid-base disorder is present if the pCO2 is abnormal and the pCO2 and pH change in opposite direction
    3. Mixed disorders
      1. A mixed (acidosis and alkalosis) acid-base disorder is present if the pCO2 is abnormal and the pH is unchanged or normal, or if the pH is abnormal and the pCO2 is unchanged or normal
  1. Anion gap – parameter used to evaluate patients with a metabolic acidosis to determine whether the problem is an accumulation of hydrogen ions or a loss of HCO3
    1. anions and cations must be balanced
    2. in addition to Na, other unmeasured cations (UC) are potassium, calcium and magnesium (~11 mEq/L)
      1. potassium and calcium make up the bulk of unmeasured cations
    3. in addition to HCO3 and Cl, other unmeasured anions (UA) are proteins, organic acids, phosphates, and sulfates (~23 mEq/L)
      1. plasma proteins are the major source of unmeasured anions
    4. thus: Na + UC = (Cl + HCO3) + UA or Na – (Cl + HCO3) = UA - UC
    5. the charge difference between the two groups is roughly 12 mEq/L in favor of the anions, this is due mainly to plasma proteins thus a drop in plasma protein as in hypoalbuminemia will cause a drop in the anion gap
    6. a metabolic acidosis with a high anion gap is most likely caused by organic acid accumulation (e.g. lactic acids, ethylene glycol or ketoacidosis)
      1. usually must by > 30 mEq/L to be diagnostic
    7. a metabolic acidosis with a normal anion gap is caused by the loss of bicarbonate ion from the extracellular fluid (e.g. diarrhea) but the HCO3 loss is counterbalanced by a gain of Cl ions to maintain electrical charge neurtrality
    8. Mixed metabolic disturbances
      1. Mixed metabolic disturbances (e.g. ketoacidosis + diarrhea) can be identified using the relationship between the increase in AG and the decrease in serum HCO3 expressed as the AG excess/HCO3 deficit ratio (gap-gap)
        1. AG excess/HCO3 deficit = (AG-12)/24-HCO3)
        2. When hydrogen ions accumulate in the blood, the decrease in serum HCO3 is equivalent to the increase in AG and the AG excess/HCO3 deficit is 1
        3. When hyperchloremic acidosis is present, the ratio approaches 0
        4. When a mixed acidosis (high AG + normal AG) is present, the AG excess/HCO3 deficit ratio indicates the relative contribution of each type to the acidosis (e.g. 0.5 is an equal contribution of high AG and normal AG)
      2. diabetic ketoacidosis
        1. diabetic keotacidosis is expected to present as a high AG metabolic acidosis; after therapy with fluid and insulin, the high AG acidosis changes to a normal AG acidosis due mostly to the Cl load in the IV fluids
      3. when alkali is added in the presence of a high AG acidosis, the decrease in HCO3 is less than the decrease in AG and the AG excess/HCO3 deficit ratio is greater than 1 (often seen in the ICU due to gastric suctioning and diuretics)
    9. metabolic alkalosis
      1. Cl responsive – usually caused by volume and Cl depletion from NG loss, diuretics
      2. Cl resistant – can be caused by steroids due to mineralocorticoid excess, also seen in Mg depletion

Board Pearls

  1. Aspirin (Acetylsalicylic Acid) overdose leads to a metabolic acidosis and respiratory alkalosis.
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