Metabolic alkalosis
| Metabolic alkalosis | |
| ICD-10 | E87.3 |
|---|---|
| ICD-9 | 276.3 |
| DiseasesDB | 402 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Metabolic alkalosis is an elevation of the pH in the bloodstream which results from decreased hydrogen ion concentration leading to increased bicarbonate and carbon dioxide concentrations, or alternatively a direct result of increased bicarbonate concentrations.
Pathophysiology
Loss of hydrogen ions
GI loss
- Vomiting (excretion of hydrogen ions and the retention of bicarbonate)
- Nasogastric tube suction
Renal
- Over-diuresis
- Hyperaldosteronism causing retention of sodium followed with compensatory excretion of hydrogen
- Administration of non-resorbable anions such as, penicillin, carbenicillin, which complexs with positively-charged hydrogen ions in the renal tubules.
Increase in the serum bicarbonate
- Ingestion of sodium bicarbonate, baking soda, citrate, lactate, or acetate.
Shift of hydrogen ions into intracellular space
- Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells, and in order to maintain electrical neutrality, hydrogen shifts into the cells, leaving behind bicarbonate.
Contraction alkalosis
- This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use. Since water is lost while bicarbonate is retained, the concentration of bicarbonate increases.
Compensation for Metabolic Alkalosis
- The body attempts to compensate for the increase in pH by retaining carbon dioxide (CO2) through hypoventilation (respiratory compensation). CO2 combines with elements in the bloodstream to form carbonic acid, thus decreasing pH.
- The pCO2 rises 0.5 - 1 for every 1 unit increase in serum HCO3 from a baseline of 24.
- The maximum pCO2 in compensation is 55-60.
- Renal compensation for metabolic alkalosis consists of increased excretion of HCO3- (bicarbonate), because the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it.
Epidemiology and Demographics
It is the most common acid-base disorder seen in hospital in the United States.
Causes
- Urine chloride is used to narrow down the differential diagnosis of metabolic alkalosis.
Low urine chloride (<10mEq/dl)
- Patients with low urine chloride and metabolic alkalosis respond well to treatment with volume repletion with saline, thus these conditions are often referred as saline-responsive metabolic alkalosis. Some conditions of volume depletions are:
- Vomiting,
- Nasogastric tube suction
- Over diuresis
- Other condition with similar presentation but without volume depletion is hypercapnia
Normal urine chloride (> 10mEQ/dL)
- With hypertension
- Cushing's syndrome,
- Primary aldosteronism (Conn's syndrome),
- Renal artery stenosis
- Renal failure + excess supplemented alkali
- Without hypertension
- Hypomagnesemia
- Hypokalemia,
- Bartter's syndrome (defect of sodium chloride resorption),
- Licorice ingestion (increases cortisol)