Updated: 3/8/2023

Acid-Base Disorders

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  • The kidneys play an important role in regulating the body's acid-base status via
    • HCO3 reabsorption
      • this is the major extracellular buffer and is thus why it is important to conserve HCO3
        • ~99.9% of filtered HCO3 is reabsorbed
          • the proximal convoluted tubule is the site where most of the filtered HCO3 is reabsorbed
      • Na+H+ exchanger secretes H+ into the tubular lumen and combines with filtered HCO3to form H2CO3
        • H2CO3 is converted into CO2 and H2O with the aid of brush border carbonic anhydrase
          • CO2 and H2O enters the proximal tubular cell to be converted into H2CO3 via intracellular carbonic anhydrase
            • H2CO3 becomed HCO3 and H+
              • H+ gets secreted by the Na+-H+ exchanger to reabsorb more HCO3
                • there is no net secretion of H+ since it is being recycled
                • angiotensin II stimulates the Na+-H+ exchanger which subsequently increases HCO3 reabsorption
                  • this explains contraction alkalosis
              • HCO3 gets transported into the blood via
                • Na+-HCO3 cotransport
                • Cl-HCO3 exchanger
        • excess of HCO3 exceeds HCO3 reabsorption capacity and results in HCO3excretion
        • arterial CO2 and renal compensation
          • not completely understood
          • respiratory acidosis
            • increased CO2 exposed to renal cells generates more H+ to be secreted by the Na+-H+ exchanger 
              • this increases HCO3reabsorption
          • respiratory alkalosis
            • decreased CO2 exposed to renal cells decrease H+ secretion by the the Na+-H+ exchanger
              • this decreases HCO3 reabsorption
    • H+ excretion
      • H+ excretion is accompanied by new HCO3 synthesis and reabsorption
      • there are two mechanisms involved
        • excretion of titratable acid (e.g., urinary buffers such as inorganic phosphate)
          • this is accomplished by H+ATPase (which can be stimulated by aldosterone) and H+-K+ ATPase on α-intercalated cells of the late distal convoluted tubule and collecting ducts
            • H+ binds to HPO4-2 to form H2PO4 (the titratable acid)
              • every titratable acid that excreted results in the synthesis of HCO3
        • excretion of NH4+
          • proximal convoluted tubule
            • NH4+ is secreted via the Na+-H+ exchanger
              • glutamine is metabolized into glutamate and NH4+ by the enzyme glutaminase in the proximal convoluted tubular cells
              • NH3 is lipid soluble and diffuses from the tubular cell into the lumen because it is lipid soluble
                • Na+-Hexchanger secretes H+ which will bind to NH3 to form NH4+
                  • this is diffusion trapping
          • collecting duct
            • H+-ATPase and H+-K+ ATPase on α-intercalated cells secrete H+ to bind with NH3 and form NH4+
              • this is diffusion trapping
 Acid-Base Disorders
  • Acidosis results in acidemia due to an increased serum H+ (decreased pH)
  • Alkalosis results in alkalemia due to a decreased serum H+ (increased pH)
  • These acid base disorders may be due to primary disturbances in HCO3 (metabolic) or arterial CO2 (PCO2) (respiratory)
    • the Hendersen-Hasselbalch equation shows that changes in HCO3 or PCO2 changes pH
      • pH = pKa + log ([HCO3-]/(0.03 * PCO2)
  • Metabolic acidosis
    • due to a decrease in HCO3
      • either because of increased H+ or loss of HCO3
  • Metabolic alkalosis
    • due to an increase in HCO3
  • Respiratory acidosis 
    • due to an increase in CO2
      • secondary to hypoventilation (which retains CO2)
  • Respiratory alkalosis 
    • due to a decrease in CO2
      • secondary to hyperventilation
  • Winter's formula
    • determines expected respiratory compensation in response to metabolic acidosis 
    • PCO2 = 1.5 (HCO3-) + 8 +/- 2
      • if actual PCO2 is greater than expected PCO2 → also has a primary respiratory acidosis
      • if actual PCO2 is less than expected PCO2 also has a primary respiratory alkalosis
Acid-Base Disorders
Acid-Base Disorder pH PCO2 [HCO3-] Compensatory Response
Metabolic acidosis
  • ↓ (primary disturbance)
  • Hyperventilation
Metabolic alkalosis 
  • ↑ (primary disturbance)
  • Hypoventilation
Respiratory acidosis
  • ↑ (primary disturbance)
  • ↑ renal HCO3- reabsorption
Respiratory alkalosis
  • ↓ (primary disturbance)
  • ↓ renal HCO3- reabsorption

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(M1.RL.15.11) A 52-year-old man with a history of type I diabetes mellitus presents to the emergency room with increasing fatigue. Two days ago, he ran out of insulin and has not had time to obtain a new prescription. He denies fevers or chills. His temperature is 37.2 degrees Celsius, blood pressure 84/56 mmHg, heart rate 100/min, respiratory rate 20/min, and SpO2 97% on room air. His physical exam is otherwise within normal limits. An arterial blood gas analysis shows the following:

pH 7.25, PCO2 29, PO2 95, HCO3- 15.

Which of the following acid-base disorders is present?

QID: 104285

Metabolic acidosis with appropriate respiratory compensation



Respiratory acidosis with appropriate metabolic compensation



Mixed metabolic and respiratory acidosis



Metabolic alkalosis with appropriate respiratory compensation



Respiratory alkalosis with appropriate metabolic compensation



M 2 D

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