Metabolic Acidosis

ACID-BASE DISTURBANCES, Hospital A/P, Adults, Hospital A/P, Peds

Definition and Pathogenesis of Metabolic Acidosis

Definition — Metabolic acidosis is defined as an increase in the concentration of hydrogen ions in the body and reduction the HCO3 concentration. Look at the simplified pH equation above. The pH represents the concentration of hydrogen ions.  If bicarb increases, pH increases. If bicarb reduces, pH reduces. If paCO2 increases, PH decreases, and vice versa.

“Acidemia (as opposed to acidosis) is defined as a low arterial pH (<7.35), which can result from a metabolic acidosis, respiratory acidosis, or both. Not all patients with metabolic acidosis have a low arterial pH; the pH and hydrogen ion concentration also depend upon the coexistence of other acid-base disorders. Thus, the pH in a patient with metabolic acidosis may be low, high, or normal.”

Pathogenesis — Metabolic acidosis can be produced by three major mechanisms.

  1. Increased acid generation
  2. Reduced renal acid excretion
  3. Loss of bicarbonate

“In addition to classifying metabolic acidosis by the primary pathogenic mechanism, the serum anion gap can be used to categorize the metabolic acidoses into two groups: high anion gap metabolic acidosis and normal anion gap metabolic acidoses.

The normal anion gap metabolic acidoses must, by definition, manifest hyperchloremia (relative to the sodium concentration). Thus, the two groups can also be called high anion gap metabolic acidosis and hyperchloremic metabolic acidosis.

  1. Increased acid generation from DKA, Lactic Acidosis, and ingestions or infusions like methanol, ethylene glycol, diethylene glycol, or propylene glycol; aspirin poisoning, chronic acetaminophen ingestion, especially in malnourished women; D-lactic acid (generated from carbohydrates by GI bacteria); Toluene, etc.
  2. Reduced renal acid excretion: 1) Reduced acid excretion that occurs in conjunction with a reduction in glomerular filtration rate (i.e., the acidosis of renal failure); 2) Distal (type 1) RTA and type 4 RTA, in which tubular dysfunction is the primary problem and glomerular filtration is initially preserved.
  3. Loss of bicarbonate from the GI tract and kidneys. E.g. in severe diarrhea (the GI tract doesn’t reabsorb bicarb like it should. Remember that the pancreas produces a lot of bicarb that is secreted into the GI tract); When urine is exposed to GI mucosa (which occurs after ureteral implantation into the sigmoid colon or the creation of replacement urinary bladder using a short loop of ileum); Proximal (type 2) renal tubular acidosis (RTA), in which proximal bicarbonate reabsorption is impaired.”

 

What are the causes of metabolic acidosis?

Causes of Anion-Gap vs. Non-Anion Gap Metabolic Acidosis.

 

Nonvolatile acids

“A nonvolatile acid (also known as a fixed acid or metabolic acid) is an acid produced in the body from sources other than carbon dioxide, and is not excreted by the lungs. They are produced from e.g. an incomplete metabolism of carbohydrates, fats, and proteins. All acids produced in the body are nonvolatile except carbonic acid, which is the sole volatile acid. Common nonvolatile acids in humans are lactic acid, phosphoric acid, sulfuric acid, acetoacetic acid, and beta-hydroxybutyric acid. Humans produce about 1 – 1.5 mmoles of H+ per kilogram per day.[1] The nonvolatile acids are excreted by the kidneys. Lactic acid is usually completely metabolized by the body, and is thus not excreted from the body.” Source: https://en.wikipedia.org/wiki/Nonvolatile_acid

 

References / Resources

Read:
http://www.uptodate.com/contents/approach-to-the-adult-with-metabolic-acidosis

https://www.uptodate.com/contents/simple-and-mixed-acid-base-disorders

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