Acid-Base Physiology & cases

Objectives

Examine an arterial blood gas (ABG) and electrolyte panel and recognize the presence of the acid-base disorder and describe pathophysiology

  • pH is maintained tightly between 7.35-7.45
  • Acid-base balance is maintained by normal pulmonary and renal excretion of CO2 and H+ (respectively)
  • Lungs can provide rapid elimination of CO2 and kidneys provide a slower response through elimination of acid (byproduct of protein metabolism)
  • ABG measures: pCO2, pH, and HCO3
  • Acidosis: process that tends to lower the pH (increase pCO2 and/or decrease HCO3)
  • Alkalosis: process that tends to raise the pH (decrease pCO2 and/or increase HCO3)
  • Acidemia: low pH
  • Alkalemia: high pH
11.PNG
  • Kidneys get rid of acid/reabsorb filtered bicarbonate through PCT and CD
    • PCT senses acidosis and increase HCO3 reabsorption and ammonium secretion (to trap H in urine) — CA in brush border will convert H2CO3 into H2O + CO2
      • Carbonic Anhydrase Inhibitors will cause sodium bicarb loss from PCT
    • CD secrete acid through the α-intercalated cells driven by aldosterone
    • Secreted acids appear in urine as NH4+
  • Types of renal tubular acidosis:
    • Proximal (Type II): loss of filtered bicarbonate
    • Distal (Type I): Failure of α-intercalated cell, leading to favoured K+ excretion by the principal cells. This will cause hypokalemia
    • Distal (Type IV): Problem with aldosterone, leading to failure of principal and α-intercalated cells. This will cause hyperkalemia
  • Expected Responses
    • Metabolic Acid-Base problems:
      • Acidosis: Acid gain or bicarb loss should result in 1:1 reduction in pCO2 (compensatory respiratory alkalosis) - can breath as fast as needed
      • Alkalosis: Increase in bicarbonate should result in almost 1:1 increase in pCO2 - can reduce breathing, but only to a certain point before hypoxic
    • Respiratory Acid-Base problems:
      • Acidosis:
        • Acute response: cells try to buffer to a small extend, about 1:10 increase in HCO3
        • Chronic response: slightly more pronounced due to renal system kicking in (about 4 times stronger, but still not close to equivalent
      • Alkalosis:
        • Acute response: cells try to shift buffers back to ICF, about 2:10 decrease in HCO3
        • Chronic response: renal acid secretion declines, bicarbonate loss increase (about 2 times stronger)

Provide a differential diagnosis for the acid-base abnormality from ABG

  • General process:
    • Look at ABG, examine pH
    • if pH <7.35, metabolic acidosis (low bicarb), or resp acidosis (high pCO2)
    • If pH >7.45, metabolic alkalosis (high bicarb), or resp alkalosis (low pCO2)
    • Once the primary disorder identified, is the expected compensation adequte? acute/chronic? is there a mixed disorder?
    • Compare the calculated anion gap to the expected, given serum albumin
    • If metabolic acidosis, determine if AGMA or NAGMA
    • If AGMA (MUDMILES!), consider osmolal gap, toxic ingestions, lactate, ketoacids, salicyclates, uremia
    • if NAGMA, consider bicarb loss (GI and PCT), vs failure to excrete H+ (CD)
    • If alkalosis, is ECF expanded or contracted?
  • Metabolic Acidosis
    • Pronounced anion gap:
      • MUDMILES:
        • Methanol
        • Uremia (accumulation of phosphates and sulfates)
        • Diabetic ketoacidosis
        • Metformin
        • Iron poisoning
        • Lactic acidosis
        • Ethylene glycol (antifreeze), or alcoholic ketoacidosis
        • Salicylate poisoning or Starvation ketoacidosis
      • Very fatal very quickly. Must treat source!!
      • Calculate osmolal gap. If wider than expected, suspect toxic alcohols
    • Normal anion gap, and bicarb is low (NAGMA):
      • Can be a loss of bicarb (PCT didn't reabsorb, or GI loss through diarrhea), or failure to secrete H+ by CD
      • To diagnose, must take a history
      • HARDUP:
        • Hyperalimentation
        • Acetazolamide
        • Renal tubular acidosis/insufficiency (RTA)*
        • Diarrhea* & Diuretics
        • Ureteroenterostomy
        • Pancreatic fissures
      • Examine urin net charge and pH
        • If urine Na + K «< Cl, then there is lots of NH4 and the distal nephron is working. Same if urine pH < 5.5
        • If urine Na + K ~= Cl, then there is not much NH4, and the distal nephron may be broken
        • Pitfall: If there is lots of other anions (e.g. sulfates, hippurate, bicarb, ketoacids), then Cl can be lower, and look like there is not enough H in urine

Describe the appropriate management for the acid-base abnormality

  • Acidosis:
    • Treat the underlying cause!!
      • Alcohol poisoning: emergency dialysis, fermepizole
      • Salicylates: hemodialysis
      • DM ketoacidosis: insulin
    • Provide buffer of Sodium Bicarb
      • if patient can't breathe out the excess CO2, this is not a good choice
      • If patient is overloaded in the ECF, the added sodium will make it worse
      • However, if pH < 7.1, or HCO3 <10-12 mmol/L, then any fall in HCO3 or rise in pCO2 will cause a rapid drop in pH, so should give bicarb!
  • Alkalosis:
    • Usually is the body responding to aldosterone
      • Primary (rarer): Coon's syndrome, adrenal hyperplasia, reninoma, or exogenous/endogenous compounds with MC actions
        • hypokalemia, increased pH are usually associated with hypertension due to aldosterone
      • Secondary (more common): Stimulation of the RAAS due to diretics, vomiting, Bartter's and Gitelman's
        • Associated with volume contraction
    • Look at urine lytes, Cl < 10 suggest a secondary cause unless patient on diuretics. Urine K or TTKG (Trans-tubular potassium gradient) high would confirm aldosterone action
    • Re-expand ECF with NaCl (secondary cause)
    • Ongoing hypokalemia tricks the kidneys into thinking there is acidosis, so must replace K
    • Block aldosterone if primary cause
    • (ACEi can be used in renal arterial stenosis alkalosis, avoid otherwise)

Calculate the anion-gap and osmolal gap

  • Anion Gap:
    • Difference between Na+ and Cl- and HCO3-
      • Normally should be 12 (negatively charged proteins are not measured)
    • For every 10g/L of albumin lower than 40, the expected AG should be lowered by 3
  • Osmolal Gap:
    • 2Na + urea + glucose (salty, sweet bunny)

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