Metabolic alkalosis

Associated with increased bicarbonate level.

Occurs as a consequence of a loss of H+ from the body or a gain in HCO3-.

Manifests as alkalemia (pH >7.40).

Leads to alveolar hypoventilation, as a compensatory mechanism, with a rise in arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that would otherwise occur.

Arterial PaCO2 increases by 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration if the change is not within this range, then a mixed acid-base disturbance occurs.

Elevated bicarbonate concentration is observed when serum electrolyte measurements are measured.

An elevated serum bicarbonate concentration may be observed as a compensatory response to primary respiratory acidosis, however, a bicarbonate concentration greater than 35 mEq/L is almost always caused by metabolic alkalosis.

MA diagnosed by measuring serum electrolytes and arterial blood gases.

The serum anion gap may also help to differentiate between primary metabolic alkalosis and metabolic compensation for respiratory acidosis. (See Workup.)

Management depends on the underlying etiology and on the patient’s volume status.

The organ systems involved in metabolic alkalosis are mainly the kidneys and GI tract, and involves the generation of metabolic alkalosis and the maintenance of metabolic alkalosis, which usually overlap.

Metabolic alkalosis may be generated by loss of hydrogen ions, shift of hydrogen ions into the intracellular space, alkali administration and contraction alkalosis.

Hydrogen ions may be lost through the kidneys or the GI tract.

Vomiting or nasogastric suction generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid.

With the excretion of a hydrogen ion, a bicarbonate ion is gained in the extracellular space.

Renal losses of hydrogen ions occur whenever the distal sodium increases in the presence of excess aldosterone, which stimulates the electrogenic epithelial sodium channel (ENaC) in the collecting duct to reabsorb sodium ions causing the tubular lumen to become more negative, leading to the secretion of hydrogen ions and potassium ions into the lumen.

Shift of hydrogen ions into the intracellular space mainly develops with hypokalemia as potassium ions move out of the cells, to maintain neutrality, hydrogen ions move into the intracellular space.

Excess administration of sodium bicarbonate in amounts that exceed the capacity of the kidneys to excrete this excess bicarbonate, may cause metabolic alkalosis.

Decreased renal capacity to excrete sodium bicarbonate occurs in renal failure and volume depletion, when there is reduction of filtered bicarbonate

With thiazide diuretics or loop diuretics, or in the presence of chloride diarrhea the contraction of extra cellular fluid volume results in the loss of bicarbonate poor fluids, resulting in increased serum bicarbonate level.

Impaired renal perfusion from volume depletion or decreased effective volume such as occurs with edema heart failure or cirrhosis, increases the region angiotensin aldosterone system, increasing renal sodium ion reabsorption with enhanced hydrogen ion secretion.

When a hydrogen ion is secreted into the tubular lumen, a bicarbonate ion is gained into the systemic circulation.

Chloride depletion through the GI tract losses of gastric secretions, or through the kidneys with loop diuretics or thiazides enhances bicarbonate reabsorption.

Macula densa cells in the ascending limb and early distal tubule have an Na+/K+/2Cl- cotransporter in the apical membrane is regulated by chloride ions.

In the presence of chloride depeltion fewer chloride ions reach this transporter and the macula densa cells signal the juxtaglomerular apparatus to secrete renin, which increases aldosterone secretion via angiotensin II.

With alkalosis, the kidneys secrete the excess bicarbonate via the apical chloride/bicarbonate exchanger in the B-type intercalated cells of the collecting duct.

Many causes of metabolic alkalosis are also associated with hypokalemia.

Hypokalemia maintains metabolic alkalosis by shifting hydrogen ions intracellularly resulting in intracellular acidosis that enhances bicarbonate reabsorption in the collecting duct.

Hypokalemia stimulates the apical H+/K+ ATPase in the collecting duct increasing potassium ion reabsorption and corresponding hydrogen ion secretion.

Hypokalemia stimulates renal ammonia production with generation of bicarbonate.

Hypokalemia impairs chloride ion reabsorption enhancing hydrogen ion secretion, and reduces the glomerular filtration rate impairing renal excretion of the excess bicarbonate.

Most common causes are the use of diuretics and the external loss of gastric secretions.

Metabolic alkalosis causes divided into chloride-responsive alkalosis with urine chloride < 20 mEq/L, and chloride-resistant alkalosis with urine chloride >20 mEq/L, and other causes, include alkali-loading alkalosis.

The principal causes of chloride-responsive metabolic alkalosis are the loss of gastric secretions, intake of nonabsorbable antacids, and the use of thiazide or loop diuretics.

The loss of hydrochloric acid from stomach secretions through vomiting or nasogastric suction, causes a net gain of bicarbonate into the systemic circulation.

Ingestion of nonabsorbable antacids may generate metabolic alkalosis by buffering hydrogen ions in the stomach.

Renal artery stenosis stimulates the renin-angiotensin-aldosterone system, leading to hypertension and hypokalemic metabolic alkalosis.

Chloride-resistant alkalosis with hypotension or normotension may be a manifestation of Bartter syndrome.

Hypomagnesemia may lead to metabolic alkalosis.

The kidneys are able to excrete any excess alkali load, exogenous or endogenous. but in renal failure or in any condition that maintains the alkalosis, the kidneys have impaired ability to excrete excess bicarbonate.

The intravenous administration of penicillin or semisynthetic penicillins may cause hypokalemic metabolic alkalosis.

Metabolic alkalosis has been reported in patients with hypoproteinemia, as a decrease in plasma albumin of 1 g/dL is associated with an increase in plasma bicarbonate of 3.4 mEq/L.

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