Metabolic alkalosis: Difference between revisions
| Line 54: | Line 54: | ||
===Normal or high urine chloride (> 10mEQ/dL)=== | ===Normal or high urine chloride (> 10mEQ/dL)=== | ||
* With hypertension | * With hypertension | ||
** Cushing's syndrome, | ** [[Cushing's syndrome]], | ||
** Primary aldosteronism (Conn's syndrome), | ** Primary aldosteronism ([[Conn's syndrome]]), | ||
** Renal artery stenosis | ** [[Renal artery stenosis]] | ||
* Patients with renal failure who are given too much of supplemental alkali have similar presentation. | * Patients with renal failure who are given too much of supplemental alkali have similar presentation. | ||
Revision as of 21:46, 2 September 2012
| 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.
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.
Differential diagnosis of metabolic alkalosis
- Urine chloride is used to narrow down the differential diagnosis of metabolic alkalosis.
Low urine chloride (<10mEq/dl)
- In conditions of volume depletions like:
- Vomiting,
- Nasogastric tube suction
- Over diuresis.
- Other condition with similar presentation without volume depletion is hypercapnia
Normal or high urine chloride (> 10mEQ/dL)
- With hypertension
- Cushing's syndrome,
- Primary aldosteronism (Conn's syndrome),
- Renal artery stenosis
- Patients with renal failure who are given too much of supplemental alkali have similar presentation.