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. The condition typically cannot last long if the kidneys are functioning properly. Signs and symptoms
Mild cases of metabolic alkalosis often cause no symptoms. Typical manifestations of moderate to severe metabolic alkalosis include abnormal sensations, neuromuscular irritability, tetany, abnormal heart rhythms (usually due to accompanying electrolyte abnormalities such as low levels of potassium in the blood), coma, seizures, and temporary waxing and waning confusion. Causes
The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels. Chloride-responsive (Urine chloride < 25 mEq/L)
Loss of hydrogen ions – Most often occurs via two mechanisms, either vomiting or via the kidney. Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. In the hospital setting this can commonly occur from nasogastric suction tubes. Severe vomiting also causes loss of potassium (hypokalemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis. Congenital chloride diarrhea – rare for being a diarrhea that causes alkalosis instead of acidosis. Contraction alkalosis – This results from a loss of water in the extracellular space, such as from dehydration.
CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. Respiratory compensation, though, is incomplete. The decrease in [H+] suppresses the peripheral chemoreceptors, which are sensitive to pH. But, because respiration slows, there is an increase in pCO2 which would cause an offset of the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO2 in the cerebral spinal fluid. So, because of the central chemoreceptors, respiration rate would be increased. Renal compensation for metabolic alkalosis, less effective than respiratory compensation, consists of increased excretion of HCO3− (bicarbonate), as the filtered load of HCO3− exceeds the ability of the renal tubule to reabsorb it. To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used: 

pCO2 = 0.7 [HCO3] + 20 mmHg ± 5
pCO2 = 0.7 [HCO3] + 21 mmHg

Treatment
To effectively treat metabolic alkalosis, the underlying cause(s) must be corrected. A trial of intravenous chloride-rich fluid is warranted if there is a high index of suspicion for chloride-responsive metabolic alkalosis caused by loss of gastrointestinal fluid (e.g., due to vomiting). Terminology
Alkalosis refers to a process by which the pH is increased. Alkalemia refers to a pH which is higher than normal, specifically in the blood. See also
Hypokalemia
Metabolic acidosis
Respiratory acidosis
Respiratory alkalosis

References


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