Acidosis + alkalosis

Definition

• • Acidosis is said to occur when arterial pH falls below 7.35

  • Alkalosis occurs at a pH over 7.45

  • Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8

Base Excess

• • Calculated figure which provides an estimate of the metabolic component of the acid-base balance

  • Defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35 if the pCO2 were adjusted to normal

    • Base excess > +3 = metabolic alkalosis

    • Base excess < -3 = metabolic acidosis

  • A high base excess, thus metabolic alkalosis, usually involves an excess of bicarbonate

    • Compensation for primary respiratory acidosis

    • Excessive loss of HCl in gastric juice by vomiting

    • Renal overproduction of bicarbonate, in either contraction alkalosis or Cushing's disease

  • A base deficit (a below-normal base excess), thus metabolic acidosis, usually involves either excretion of bicarbonate or neutralization of bicarbonate by excess organic acids

    • Compensation for primary respiratory alkalosis

    • Diabetic ketoacidosis, in which high levels of acidic ketone bodies are produced

    • Lactic acidosis, due to anaerobic metabolism during heavy exercise or hypoxia

    • Chronic renal failure, preventing excretion of acid and resorption and production of bicarbonate

    • Diarrhea, in which large amounts of bicarbonate are excreted

    • Ingestion of poisons such as methanol, ethylene glycol, or excessive aspirin

  • The serum anion gap is useful for determining whether a base deficit is caused by addition of acid or loss of bicarbonate.

    • Base deficit with elevated anion gap indicates addition of acid (e.g., ketoacidosis).

    • Base deficit with normal anion gap indicates loss of bicarbonate (e.g., diarrhea)

      • The anion gap is maintained because bicarbonate is exchanged for chloride during excretion

Anion Gap

• • Calculated by subtracting the serum concentrations of chloride and bicarbonate (anions) from the concentrations of sodium and potassium (cations):

    • • = [Na⁺] + [K⁺] − [Cl⁻] − [HCO₃⁻]

  • Normal anion gap is <11 mEq/L

Compensatory mechanisms

• bicarbonate buffering system

  • Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.

• Respiratory compensation

• Renal compensation

Causes of metabolic acidosis

• • Increased anion gap

  • lactic acidosis

  • ketoacidosis

    • chronic renal failure (accumulation of sulfates, phosphates, urea)

    • intoxication:

      • organic acids (salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH)

      • sulfates, metformin (Glucophage)

    • massive rhabdomyolysis

  • Normal anion gap

    • longstanding diarrhea (bicarbonate loss)

  • pancreatic fistula

    • uretero-sigmoidostomy

    • Renal tubular acidosis (RTA)

    • intoxication:

    • ammonium chloride

      • acetazolamide (Diamox)

    • bile acid sequestrants

    • isopropyl alcohol

      • renal failure (occasionally)

    • Glue sniffing

    • toluene

Causes of metabolic alkalosis

• • Chloride-responsive (<10 mEq/L in urine)

    • Loss of hydrogen ions

      • Vomiting results in the loss of hydrochloric acid.

      • Severe vomitting also causes loss of potassium (hypokalaemia) and sodium (hyponatraemia)

        • The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions

          • Spares sodium/potassium pumps to prevent further loss of potassium

          • Leads to metabolic alkalosis.

    • Congenital chloride diarrhea

      • Rare for being a diarrhea that causes alkalosis instead of acidosis.

  • Contraction alkalosis

    • • Results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use

    • Diuretic therapy

      • Loop diuretics and thiazides can both initially cause increase in chloride, but once stores are depleted, urine excretion will be below < 25 mEq/L

      • The loss of fluid from sodium excretion causes a contraction alkalosis.

    • Posthypercapnia

      • Hypercapnia causes respiratory acidosis

      • Renal compensation with excess bicarbonate occurs to lessen the affect of the acidosis

      • Once carbon dioxide levels return to base line, the higher bicarbonate levels reveal themselves putting the patient into metabolic alkalosis

  • Chloride-resistant (>20 mEq/L in urine)

    • Retention of bicarbonate

    • Shift of hydrogen ions into intracellular space

      • Seen in hypokalemia

      • Due to a low extracellular potassium concentration, potassium shifts out of the cells

      • In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.

    • Alkalotic agents

      • Alkalotic agents, such as bicarbonate (administrated in cases of peptic ulcer or hyperacidity) or antacids, administered in excess can lead to an alkalosis.

    • Hyperaldosteronism

      • Renal loss of hydrogen ions occurs when excess aldosterone (Conn's syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney

      • This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule

      • Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis

      • Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine.[3]

    • Licorice

    • Bartter syndrome

      • A syndrome analogous to taking loop diuretics characterized with normotensive patients

  • Liddle syndrome

    • • A syndrome from defect sodium channel deletion characterized by hypertension and hypoaldosteronism.

    • 11β-hydroxylase deficiency and 17 alpha-hydroxylase deficiency

      • Both characterized by hypertension