Metabolic alkalosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]
Synonyms and keywords:
Overview
The normal physiological pH of blood is 7.35 to 7.45. An increase above this range is known to be Alkalosis. Metabolic Alkalosis is defined as a disease state where blood pH is more than 7.45 due to secondary metabolic processes.
Historical Perspective
Alkalosis is defined as elevation of physiologic blood pH above 7.45. Metabolic alkalosis is caused by metabolic imbalance causing alkalosis by trapping Bicarbonate ions or loss of hydrogen in body. The discovery of electrochemistry of gas and electricity was first explored in 17th and 18th centuries . Later in late 1880s definition of acid was first developed and modified by numerous scientists from 1880s to 1950s until the epidemic era of Polio. Stewart combined all the ideas from pre-1950 and proposed a way of studying acid-base balance in clinical settings.
Classification
Metabolic Alkalosis can be classified according to pathophysiology, etiology and chloride responsiveness or urinary chloride concentration.
Pathophysiology
The primary pH buffers in maintaining chemical equilibrium of physiological Blood pH are alkaline Bicarbonate ions(HCO3) and acidic carbon dioxide(CO2). When there is increase amount of Bicarbonate(HCO3) in body or decrease amount of carbon dioxide or loss of hydrogen ions it causes alkalosis. Metabolic alkalosis occurs due to trapping of Bicarbonate ions (HCO3) or loss of hydrogen ions in body due to some metabolic causes for example- gastrointestinal loss of hydrogen ions, intracellular shifting of hydrogen ions, renal hydrogen loss, increased bicarbonate ions in extracellular compartment, diuretic induced alkalosis or contraction alkalosis. Patient with normal renal physiology will compensate this increase amount of bicarbonate through excretion. But impaired renal function secondary to chloride depletion, hypokalemia, hyperaldosteronism, reduced glomerular function rate, reduced effective arterial blood volume (EABV)) in heart failure or cirrhosis will lead to metabolic alkalosis. When the physiologic blood pH is above 7.45, it triggers respiratory center to cause hypoventilation, thus decreased PCO2 leading to compensatory respiratory acidosis. The PCO2 increases about 0.5 to 0.7 mmHg to every 1.0 mM increase in plasma bicarbonate concentration. In severe Metabolic alkalosis PCO2 can reach 60 mmHg. The mortality rate with metabolic alkalosis is 45% with arterial blood pH 7.55 to 80% with arterial blood pH of 7.65. Treatment is usually supportive based on cause of the disease.
Causes
Causes of Metabolic Alkalosis are Vomiting, Diarrhea, Diuretics, Cystic Fibrosis, Primary Hyperaldosteronism, Secondary hyperaldosteronism, laxative use, CKD, elactrolyte and nutritional imbalances, Milk-alkali syndrome, Blood transfusion, Genetic diseases for instances Bartter, Liddle, Gitelman syndrome etc. Among them, life threatening causes are loss of gastric acid, excessive use of loop and thiazide diuretics.
Differentiating Metabolic alkalosis from other Diseases
Metabolic alkalosis might be consequence of several conditions such as exogenous HCO3− loads, medications and poisoning, gastrointestinal, renal, endocrine, and systemic diseases.
Epidemiology and Demographics
Metabolic Alkalosis has the highest incidence and prevalence rate among the other acid base disorder in hospitalized patient. Limited data are found on its predilection to race, age, gender, region.
Risk Factors
Common risk factors in the development of Metabolic Alkalosis include Vomiting, Milk-alkali syndrome, Severe hypokalemia, Primary hyperaldosterinism, Cushing syndrome, Diuretics use and genetic disease for instances- Bartter and gitelman Disease.
Screening
There is insufficient evidence to recommend routine screening for Metabolic alkalosis.
Natural History, Complications and Prognosis
Common complications of Metabolic alkalosis include hypokalemia, hypomagnesaemia, hypophosphatemia, coronary arterial blood flow reduction, arrhythmia, anaerobic glycolysis, reduced ventilation leading to low arterial oxygen saturation, increased CO2, decreased blood flow to cerebral arteries leading to altered mental status, lethargy, tetany, delirium, seizure.
Diagnosis
Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies