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Acid-Base Homeostasis

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

  • See Also
  1. Arterial Blood Gas
  2. ABG Interpretation
  3. A-a Gradient
  4. Anion Gap
  5. Respiratory Physiology
  • Physiology
  • Blood pH and Buffering Systems in General
  1. pH is a measure of Hydrogen Ion concentration
    1. pH=log (1/H)
      1. Where H is Hydrogen Ion concentration in gram moles per liter
    2. Neutral pH in water
      1. Hydrogen Ion is typically 10^-7 and is balanced by 10^-7 hydroxyl ion (OH)
    3. Body pH
      1. Normal arterial pH is 7.40 (Hydrogen Ion 40 nmole/L)
      2. Gastric Acid pH <3
      3. Pancreatic Secretion pH >8
  2. Blood pH is normally maintained between 7.35 and 7.45 via buffers
    1. Weak acids buffer pH in a narrow range near 7.40
      1. Weak base (WB-) bound to Hydrogen Ions (H+) dissociate when a strong acid (SA) is present
      2. H+WB- => H+SA + WB-
    2. Extracellular buffers
      1. Bicarbonate buffering system is the main extracellular buffer
      2. CO2 + H2O <=> H2CO3 <=> HCO3- + H+
    3. Intracellular buffers
      1. Intracellular Proteins, ammonia and phosphates
      2. Ammonia buffering system
        1. Ammonia (weak base) + Hydrogen Ion => Ammonium (NH3- + H+ => NH4)
        2. Glutamine is metabolized in renal tubule cells to Ammonium and bicarbonate
        3. Ammonium (NH4) is excreted in urine, while bicarbonate is reabsorbed in capillaries
      3. Phosphate buffering system
        1. Hydrogen phosphate + Hydrogen Ion => Dihydrogen Phosphate (HPO4 + H+ => H2PO4)
        2. Dihydrogen Phosphate (H2PO4) is excreted in urine
    4. Images: Acid Base Homeostasis
      1. acidBaseHomeostasis.png
  3. Low Electrolyte concentrations (Sodium, Potassium, chloride) decrease Hydrogen Ion concentration (Metabolic Alkalosis)
    1. Hyponatremia
      1. Increased Sodium reabsorption results in secretion of the hydrogen cation in exchange
      2. Bicarbonate absorption increases with Sodium reabsorption
      3. Aldosterone increases with Hyponatremia resulting in further Hydrogen Ion secretion
    2. Hypokalemia
      1. When Potassium is at normal level, it is excreted in exchange for Sodium
      2. When Potassium is reabsorbed in Hypokalemia, another cation is needed to exchange for Sodium
      3. In this case of Hypokalemia, Hydrogen Ion is secreted in exchange for Sodium absorption
    3. Hypochloremia
      1. Chloride is not available for reabsorption with Sodium from the renal tubule
      2. Another cation, in this case Hydrogen Ion, is secreted to balance negatively charged lumen
  • Physiology
  • Bicarbonate buffering system (CO2-HCO3-)
  1. Bicarbonate buffering system equation
    1. CO2 + H2O <=> H2CO3 <=> HCO3- + H+
    2. Presence of strong acid shifts equation left toward CO2 + H2O
    3. Presence of strong base shifts equation right toward HCO3- and H+ ion
  2. Buffering Equation 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-)
    3. Under normal conditions blood bicarbonate (HCO3-) to dissolved CO2 ratio is 20:1
  3. pH and Hydrogen Ion (H+) are proportional to HCO3-/pCO2
    1. H+ : HCO3-/ pCO2
    2. Henderson-Hasselbach equation
      1. pH = 6.1 + log10 (HCO3-/(pCO2*0.03))
      2. where dissolved CO2 in plasma is only 3% of pCO2
    3. Hydrogen Ion increases (and pH decreases)
      1. Increased pCO2 (Respiratory Acidosis) OR
      2. Decreased HCO3- (Metabolic Acidosis)
    4. Hydrogen Ion decreases (and pH increases)
      1. Decreased pCO2 (Respiratory Alkalosis) OR
      2. Increased HCO3- (Metabolic Alkalosis)
  4. Homeostasis is maintained via respiratory (pCO2) and renal (HCO3-) mechanisms
    1. Lung function maintains pCO2 near 40 mmHg
      1. CO2 is a weak acid, and is the only acid excreted by the lung (all other acids are renally excreted)
      2. Brainstem responds to increased CO2 and H+ ion levels to increase Respiratory Rate reflexively
      3. Low oxygen level (O2) stimulates carotid and aortic body receptors (CN 9/10) to increase Respiratory Rate
    2. Renal Function maintains bicarbonate (HCO3-) near 25 mEq/L
      1. Bicarbonate is filtered by glomerulus and reabsorbed in renal tubules combined with Hydrogen Ion
      2. Total extracellular bicarbonate is 350 mEq for a 70 kg male
      3. Renal tubules excrete Hydrogen Ion
      4. Urine tends to be acidic (due to excess acid production over base production daily)
  5. Bicarbonate gains or losses impacts acidosis
    1. Bicarbonate loss (e.g. Diarrhea) results in an increase in Hydrogen Ion (acidosis)
    2. Hydrogen Ion loss (e.g. Vomiting) results in bicarbonate gain (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. Acid Base Homeostasis
    1. acidBaseHomeostasis.png
  2. Nephron
    1. nephron.png
  • Resources
  1. Acid-Base Interpreter
    1. https://fpnimages.blob.core.windows.net/$web/images/acidBaseApp.html
  • References
  1. Goldberg (2014) Clinical Physiology, Medmaster, Miami, p. 27-31
  2. Marino (2014) ICU Book, p. 587-99
  3. Preston (2011) Acid-Base Fluids and Electrolytes, p. 3-30
  4. Rose (1989) Clinical Physiology of Acid-Base and Electrolyte Disorders, p. 261-85