Arterial pH >7.45 defines alkalosis. Metabolic alkalosis is indicated by an increase in plasma bicarbonate (HCO3) level.
It is the consequence of disorders that cause either a loss of hydrogen ions from the body or an increase in plasma HCO3. The severity of alkalosis depends on the severity of underlying disorder and may be more severe if both metabolic and respiratory alkalosis are present.
The main mechanisms involved can be either one or a combination of following:
Loss of hydrogen ions from the body
Hydrogen ions can be lost from the body either through the gastrointestinal tract or through the kidneys. In the body, hydrogen ions may shift from the extracellular fluid into the cells. If loss of hydrogen ions exceeds its production by the diet and metabolism, the serum bicarbonate level increases, leading to metabolic alkalosis. Loss of hydrogen ions through the stomach and kidneys is accompanied by the production of HCO3.
Administration of HCO3 or addition of HCO3-generating substances
Intake of bicarbonate or substances such as citrate, acetate, or lactate that increase bicarbonate production in excess of hydrogen ion production in the body will lead to metabolic alkalosis. This is usually compensated by the kidneys with normal function by renal excretion of bicarbonate.
Severe circulating volume contraction.
This leads to loss of extracellular fluid and relative increase in bicarbonate concentration.
Metabolic alkalosis generally requires an initiation factor that starts the process and a maintenance factor that continues the imbalance by preventing renal excretion of excess HCO3. Sometimes, the same factor may be responsible for both initiation and maintenance.
- Primary hyperaldosteronism
- Secondary hyperaldosteronism
- Renal artery stenosis
- Cushing's syndrome
- Liquorice ingestion
- Tobacco chewing
- Apparent mineralocorticoid excess
- Liddle's syndrome
- Bartter's syndrome
- Gitelman's syndrome
- Profound potassium depletion
- Hypercalcaemia of non-hyperparathyroid aetiology
- Post-starvation refeeding syndrome
- Transfusion of blood products (sodium citrate)
- Villous adenoma
- Chloride diarrhoea
- Cystic fibrosis
Dinkar Kaw, MD
Professor of Medicine
Division of Nephrology
Department of Medicine
University of Toledo College of Medicine
DK declares that he has no competing interests.
Dr Dinkar Kaw would like to gratefully acknowledge Dr Joseph I. Shapiro, a previous co-contributor to this monograph. JIS declares that he has no competing interests.
Chris Abbiss, BSc
School of Exercise
Biomedical and Health Science
Edith Cowan University
CA declares that he has no competing interests.
Mark Cowan, MD, FCCP
Assistant Professor of Medicine
Division of Pulmonary and Critical Care Medicine
The University of Maryland
Chief of Pulmonary and Critical Care Medicine
Baltimore VA Medical Center
MC declares that he has no competing interests.
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