Acid-Base Homeostasis


Acid-Base Homeostasis, Acid-Base Equilibrium, Blood pH, Hydrogen Ion

  • Physiology
  • Bicarbonate buffering system (CO2-HCO3-)
  1. Blood pH is normally maintained between 7.35 and 7.45 via buffers
    1. Extracellular buffers
      1. Bicarbonate buffering system is the main extracellular buffer
    2. Intracellular buffers
      1. Intracellular proteins and phosphates
  2. Bicarbonate buffering system equation
    1. CO2 + H2O <=> H2CO3 <=> HCO3- + H+
  3. Describes a balance between bicarbonate (HCO3-) and carbon dioxide (CO2)
    1. Water (H2O) combines with carbon dioxide (CO2) to form carbonic acid (H2CO3) catalyzed by carbonic anhydrase
    2. Carbonic acid (H2CO3) may freely dissociate with Hydrogen Ion (H+) to form bicarbonate (HCO3-)
  4. Hydrogen Ion (H+) is proportional to pCO2 / HCO3-
    1. H+ : pCO2 / HCO3-
    2. Hydrogen Ion increases with increased pCO2 (Respiratory Acidosis) or decreased HCO3- (Metabolic Acidosis)
    3. Hydrogen Ion decreases with decreased pCO2 (Respiratory Alkalosis) or increased HCO3- (Metabolic Alkalosis)
  5. Homeostasis is maintained via respiratory (pCO2) and renal (HCO3-) mechanisms
    1. Lung function maintains pCO2 near 40 mmHg
    2. Renal Function maintains HCO3- near 25 mEq/L (total of 350 mEq extracellular bicarbonate for a 70 kg male)
  6. Bicarbonate gains or losses impacts acidosis
    1. Bicarbonate loss (e.g. Diarrhea) results in an increase in Hydrogen Ion (acidosis)
    2. Bicarbonate gain (e.g. Sodium Bicarbonate) results in a decrease in Hydrogen Ion (alkalosis)
  • Physiology
  • Acid generation via metabolism
  1. Carbohydrate and fat metabolism generates large amounts of CO2
    1. CO2 is quickly eliminated via respiration
  2. Protein is metabolized into nonvolatile acid (fixed acid)
    1. Fixed Acid generated cannot be excreted as CO2
    2. Fixed Acid is buffered with bicarbonate to form carbonic acid
    3. Hydrogen Ion is renally excreted, maintaining bicarbonate for further buffering
  • Physiology
  • Renal maintenance of bicarbonate
  1. Bicarbonate is freely filtered by the glomerulus and reabsorbed by proximal tubule
    1. Glomerulus loses ~3600 meq bicarbonate daily (given 100 ml/min GFR) that must be reclaimed
    2. Nearly all bicarbonate is reabsorbed by the proximal tubule
      1. Bicarbonate levels above 26 mEq/L cannot be completely reabsorbed by proximal tubule
    3. Bicarbonate reabsorption (Metabolic Alkalosis) is increased with specific triggers
      1. Volume depletion (known as contraction alkalosis)
      2. Angiotensin II increased levels
      3. pCO2 increased levels (compensates for Respiratory Acidosis)
      4. Hypokalemia
    4. Renal Tubular Acidosis Type II results from defective proximal tubule reabsorption
      1. Causes Metabolic Acidosis through bicarbonate loss
  2. Hydrogen Ion renal excretion
    1. Primary mechanism for excreting fixed acid (see protein metabolism above)
    2. Proton Pump (ATP fueled)
      1. Pumps one Hydrogen Ion into collecting tubule
      2. Releases one bicarbonate to pass freely back into capillaries in the renal interstitium
      3. Renal Tubular Acidosis Type I (distal) results from defective Hydrogen Ion pump
    3. Glutamine Hydrolysis (proximal tubule)
      1. Renal key mechanism to compensate for acidosis (more than Hydrogen Ion excretion)
      2. Results in two outputs
        1. Ammonium (NH4+) which is excreted into urine
        2. Bicarbonate (HCO3-) which is absorbed by capillaries
  • Physiology
  • Images
  1. Nephron
    1. nephron.png
  • References
  1. Marino (2014) ICU Book, p. 587-99
  2. Preston (2011) Acid-Base Fluids and Electrolytes, p. 3-30
  3. Rose (1989) Clinical Physiology of Acid-Base and Electrolyte Disorders, p. 261-85