Clinical manifestations and evaluation of metabolic alkalosis
- Michael Emmett, MD
Michael Emmett, MD
- Editor-in-Chief — Nephrology
- Section Editor — Fluid and Electrolytes
- Chief of Internal Medicine
- Baylor University Medical Center
- Harold Szerlip, MD, FACP, FCCP, FASN, FNKF
Harold Szerlip, MD, FACP, FCCP, FASN, FNKF
- Director, Nephrology Division, Baylor University Medical Center, Dallas
- Program Director, Nephrology Training Program, Baylor University Medical Center
- Clinical Professor of Medicine, Texas A&M College of Medicine
- Adjunct Professor of Medicine, Texas College of Osteopathic Medicine
Metabolic alkalosis, which is usually accompanied by hypokalemia, is defined as a disorder that causes elevations in the serum bicarbonate concentration and arterial pH. In a patient with an uncomplicated (simple) metabolic alkalosis, both parameters are above normal. However, this may not be present in patients with mixed acid-base disorders. (See "Simple and mixed acid-base disorders".)
The pathogenesis of metabolic alkalosis requires, sequentially, both the development or generation of alkalosis (related to the source of the additional bicarbonate) and the maintenance of the metabolic alkalosis (related to why the disorder persists and is not corrected by renal excretion of the excess bicarbonate). These issues are discussed in detail in other topics (see "Pathogenesis of metabolic alkalosis" and "Causes of metabolic alkalosis") but are briefly reviewed here:
●An elevation in the serum bicarbonate concentration is due to excessive hydrogen ion loss in the urine or gastrointestinal tract; hydrogen ion movement into cells; administration of sodium or potassium bicarbonate or the sodium or potassium salt of an organic anion, such as citrate or lactate, that is metabolized and thereby generates bicarbonate; and/or volume contraction around a relatively constant amount of extracellular bicarbonate (called a contraction alkalosis). This is called the "generation phase" of metabolic alkalosis.
●An inability to excrete the excess bicarbonate in the urine is due to intravascular volume contraction, reduced effective arterial blood volume (including heart failure and cirrhosis), chloride depletion, hypokalemia, renal impairment, or combinations of these factors. This is called the "maintenance phase" of metabolic alkalosis [1-3].
Patients with metabolic alkalosis usually develop respiratory compensation characterized by hypoventilation and an elevation in arterial PCO2. This lowers the arterial pH toward normal. However, the beneficial pH effect of hypoventilation is blunted because the elevation in arterial PCO2 increases renal acid excretion, producing a further rise in serum bicarbonate . These issues are discussed in detail elsewhere. (See "Simple and mixed acid-base disorders", section on 'Metabolic alkalosis' and "Simple and mixed acid-base disorders", section on 'Compensatory respiratory and renal responses'.)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- CLINICAL FEATURES
- Physical examination
- Arterial blood gases
- The cause is usually apparent from the history
- When the cause is not apparent from the history
- Diagnostic approach in unexplained metabolic alkalosis
- - Disorders associated with a low urine chloride concentration (less than 10 to 20 mEq/L)
- Vomiting or nasogastric suction
- Diuretic-induced alkalosis
- Other causes of metabolic alkalosis associated with low urine chloride concentration
- - Settings in which the urine chloride is not low (greater than 25 mEq/L)
- - Utility of urine chemistries in metabolic alkalosis
- - Hypokalemia
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