Metabolic alkalosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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. 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.

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.

Genetics

• [Disease name] is transmitted in [mode of genetic transmission] pattern.
• Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
• The development of [disease name] is the result of multiple genetic mutations.

Gross Pathology

• On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

• On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].