Acidosis & Alkalosis - Causes and Compensations
Alkalosis and Acidosis: 4 simple acid-base disorders
Metabolic acid-base disorders present as imbalances between bicarbonate, the primary extracellular buffer, and fixed, aka, non-volatile, acids.
Respiratory acid-base disorders present as imbalances between bicarbonate and carbon dioxide, the volatile acid.
Distinguishing Features
Acid-base Disorders are distinguishable by their arterial blood profiles, compensatory respiratory and renal mechanisms, and common causes.
Acidemia
Metabolic acidosis
Metabolic acidosis is characterized by arterial Bicarbonate < 20 mEq/L due to 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 system compensates 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.
Normal anion gap causes include:
- Diarrhea
- Renal tubular acidosis
- Renal failure
- Hyperchloremia
- Addison disease
- Acetazolamide
- Spironolactone
- Saline infusion
- 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
Respiratory acidosis is characterized by Pco2 > 44 mmHg, due to 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.
Causes of respiratory acidosis: 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
Alkalemia is defined as a pH > 7.45
Respiratory alkalosis
Respiratory alkalosis is characterized by 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**
Hyperventilation "blows off" too much carbon dioxide and lowers its arterial partial pressure. Can be due to stimulation of the medullary respiratory center, hypoxemia (low blood oxygen), and physical or mental distress.
Metabolic alkalosis
Metabolic alkalosis is characterized by arterial Bicarbonate > 28 mEq/L, due to 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.
Metabolic alkalosis is most commonly caused by vomiting (HCL is lost from the body).
Other causes include loop and thiazide diuretics, which increase bicarbonate excretion in the urine, and hyperaldosteronism (excessive aldosterone secretion), which causes over-excretion of hydrogen ions.
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.
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