Metabolic Alkalosis

DEFINITION Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range ( 7.35-7.45 ). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.
ETIOLOGY Chloride depletion -gastric losses: vomiting, mechanical drainage, bulimia -chloruretic diuretics: bumetanide, chlorothiazide, metolazone,etc. -diarrheal states: villous adenoma, congenital chloridorrhea posthypercapneic state -dietary chloride deprivation with base loading: chloride-deficient infant formulas -gastrocystoplasty -cystic fibrosis (high sweat chloride)

 Potassium depletion/mineralocorticoid excess -primary aldosteronism: adenoma, idiopathic, hyperplasia, renin responsive, glucocorticoid-suppressible, carcinoma -apparent mineralocorticoid excess primary deoxycorticosterone excess: 11b- and 17ahydroxylase deficiencies drugs: licorice (glycyrrhizic acid) as a confection or flavoring, carbenoxolone Liddle syndrome -secondary aldosteronism adrenal corticosteroid excess: primary, secondary, exogenous severe hypertension: malignant, accelerated, renovascular hemangiopericytoma, nephroblastoma, renal cell carcinoma -Bartter and Gitelman syndromes and their variants laxative abuse, clay ingestion

Hypercalcemic states -hypercalcemia of malignancy -acute or chronic milk-alkali syndrome Other -carbenicillin, ampicillin, penicillin -bicarbonate ingestion: massive or with renal insufficiency -recovery from starvation -hypoalbuminemia

PATOPHYSIOLOGY Metabolic alkalosis may be generated by one of the following mechanisms: Loss of hydrogen ions Shift of hydrogen ions into the intracellular space Alkali administration Contraction alkalosis

Hydrogen ions may be lost through the kidneys or the GI tract. Vomiting or nasogastric (NG) suction generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl). Whenever a hydrogen ion is excreted, a bicarbonate ion is gained in the extracellular space. Renal losses of hydrogen ions occur whenever the distal delivery of sodium increases in the presence of excess aldosterone, which stimulates the electrogenic epithelial sodium channel (ENaC) in the collecting duct. As this channel reabsorbs sodium ions, the tubular lumen becomes 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 the extracellular potassium concentration decreases, potassium ions move out of the cells. To maintain neutrality, hydrogen ions move into the intracellular space.

Administration of sodium bicarbonate in amounts that exceed the capacity of the kidneys to excrete this excess bicarbonate may cause metabolic alkalosis. This capacity is reduced when a reduction in filtered bicarbonate occurs, as observed in renal failure, or when enhanced tubular reabsorption of bicarbonate occurs, as observed in volume depletion (see Maintenance of metabolic alkalosis). Loss of bicarbonate-poor, chloride-rich extracellular fluid, as observed with thiazide diuretic or loop diuretic therapy or chloride diarrhea, leads to contraction of extracellular fluid volume. Because the original bicarbonate mass is now dissolved in a smaller volume of fluid, an increase in bicarbonate concentration occurs. This increase in bicarbonate causes, at most, a 2- to 4-mEq/L rise in bicarbonate concentration.

CLINICAL MANIFESTATION
The symptoms of metabolic alkalosis per se are difficult to separate from those of chloride, volume, or potassium depletion. Apathy, confusion, cardiac arrhythmias, and neuromuscular irritability (related in part, perhaps, to a low ionized plasma calcium) are common when alkalosis is severe

DIAGNOSTIC TEST BGA: - pH > 7,45 - HCO3 > 26 mEq/L -PaCO2 > 45 mmHg HCO3 serum > 26 mEq/L Electrolyte serum: potassium&chlorida EcG: dysritmia

CORRECTION The management of metabolic alkalosis depends primarily on the underlying etiology and on the patients volume status. In the case of vomiting, administer antiemetics, if possible. If continuous gastric suction is necessary, gastric acid secretion can be reduced with H2-blockers or more efficiently with proton-pump inhibitors. In patients who are on thiazide or loop diuretics, the dose can be reduced or the drug can be stopped if appropriate. Alternatively, potassium-sparing diuretics or acetazolamide can be added. Diuretics may be used to treat severe metabolic alkalosis in edematous states (eg, from congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), or right heart failure).

IV HCl may be indicated in severe metabolic alkalosis (pH >7.55) or when NaCl or KCl cannot be administered because of volume overload or advanced renal failure. HCl is available in preparations of 0.1 and 0.2 M, which contain 100 mmol H+/L and 200 mmol H+/L, respectively.

Potassium supplements may be used to correct metabolic alkalosis, which is often associated with hypokalemia.
Fluid replacement, used in chloride-responsive alkalosis with volume depletion.