Alkalosis and Acidosis

4 SIMPLE ACID-BASE DISORDERS

  • Metabolic acid-base disorder presents as an imbalance between bicarbonate, the primary extracellular buffer, and fixed, aka, non-volatile, acids.
  • Respiratory acid-base disorder presents as an imbalance between bicarbonate and carbon dioxide, the volatile acid.
  • Acid-base Disorders are distinguishable by their arterial blood profiles, compensatory respiratory and renal mechanisms, and common causes.

ACIDEMIA

pH < 7.35

Metabolic acidosis

  • Bicarbonate < 20 mEq/L
  • Caused by either a gain in hydrogen ions and/or a loss of bicarbonate, which lowers pH.
  • Consequently, the arterial blood profile shows reduced bicarbonate concentration and elevated hydrogen ion concentration.
  • In response to a drop in pH, the respiratory systemcompensates with hyperventilation:
    • Excess carbon dioxide is “blown off,” which lowers the partial pressure of carbon dioxide in the blood; the arterial blood profile reflects this.
  • Though slower to respond, renal bicarbonate conservation and acid excretion produce a more effective and longer-lasting pH elevation.

Anion Gap

Causes of metabolic acidosis into at least two categories: those associated with a normal anion gap (AG), and those associated with an elevated anion gap.

  • In a routine blood test, only some cations and anions are measured; the anions that are not measured constitute the “anion gap.”
    • Because the total concentration of anions must be equal to the total concentration of cations, we know that the anion gap, the unmeasured anions, must be equal to:
      The measured cations (usually sodium) minus the measured anions (usually bicarbonate and chloride).
    • A normal average anion gap value is 12 mEq/L (typical range = 8 – 16 mEq/L).
  • Thus, an increased anion gap indicates that bicarbonate, a measured anion, has been lost and replaced by the unmeasured ions
  • A normal anion gap indicates that chloride is the ion that replaced the lost bicarbonate, which makes sense given that it is the other measured anion in the anion gap equation.
  • Common causes of a normal anion gap include:
    • Diarrhea
    • Renal tubular acidosis
    • Renal failure
    • Hyperchloremia
    • Addison disease
    • Acetazolamide
    • Spironolactone
    • Saline infusion
  • Common causes of an increased anion gap include MUDPILES:
    • Methanol intoxication (methanol is also called “wood alcohol,” commonly found in antifreeze and industrial settings)
    • Uremia
    • Diabetic ketoacidosis
    • Paraldehyde (which is sometimes used to treat alcoholism and certain convulsive and mental disorders)
    • Iron overdose
    • Lactic acid
    • Ethylene glycol poisoning (ethylene glycol is a compound commonly found in antifreeze)
    • Salicylate ingestion (key ingredient in aspirin, poisoning is common in children)

Respiratory acidosis

  • Pco2 > 44 mmHg
  • Caused by a gain in carbon dioxide and bicarbonate.
  • The degree of change in pH depends on the duration of the disorder:
    • The pH is more reduced in acute acidosis than in chronic because, in chronic acidosis, sufficient time has elapsed for renal mechanisms to have some effect.
  • There is no respiratory compensation when the respiratory system is itself the source of the imbalance.
    • To raise pH, the nephrons conserve bicarbonate and excrete hydrogen ions; notice that this is similar to the renal response to metabolic acidosis.

Caused by:

  • Hypoventilation
    • Inhibition of the medullary respiratory center, which can be induced by sedatives or brainstem lesions
    • Neuromuscular defects that inhibit the anatomical structures responsible for ventilation
    • Gas exchange defects, such as COPD.

ALKALEMIA

pH > 7.45

Respiratory alkalosis

  • Pco2 < 36 mmHg
  • pH is increased in proportion to the duration of the disorder.
  • There is no respiratory compensation for respiratory-induced acid-base disturbances.
  • Nephrons excrete excess bicarbonate and reduce titratable acid and ammonium ion secretion to conserve hydrogen ions; this is similar to the renal response to metabolic alkalosis.

Caused by:

  • Hyperventilation, which “blows off” too much carbon dioxide and lowers its arterial partial pressure.
    • Stimulation of the medullary respiratory center, hypoxemia (low blood oxygen), and physical or mental distress.

Metabolic alkalosis

  • Bicarbonate > 28 mEq/L
  • Caused by a loss of hydrogen ions and/or a gain in bicarbonate, which raises pH.
  • Consequently, the arterial blood profile shows elevated bicarbonate concentration, and decreased hydrogen concentration.
  • In response to elevated pH, hypoventilation retains carbon dioxide, which increases its arterial partial pressure; this is reflected in the arterial blood profile.
  • The nephrons increase bicarbonate excretion, and, by reducing secretion of titratable acids and ammonium, conserve hydrogen ions; these actions lower pH.

Most commonly caused by

  • Vomiting (HCL is lost from the body)
  • Loop and thiazide diuretics, which increase bicarbonate excretion in the urine.
    • Vomiting and diuretics cause extracellular fluid volume contraction, which, as we’ve learned elsewhere, triggers hormonal responses that increase bicarbonate reabsorption and maintain the metabolic alkalosis.
  • Hyperaldosteronism (excessive aldosterone secretion) causes over-excretion of hydrogen ions.

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