Metabolic alkalosis

As described earlier, any process in which plasma bicarbonate is increased is referred to as metabolic alkalosis. This is usually the result of increased loss of acid from the stomach or kidney, potassium depletion accompanying diuretic therapy, excessive alkali intake, or severe adrenal gland hyperactivity.

Symptoms: There are no specific signs or symptoms, but if the alkalosis is severe, there may be apathy, confusion, stupor, and tetany as evidenced by a positive Chvostek's sign.

Treatment: Therapy for the primary disorder is essential. Saline solution should be administered intravenously and  in patients with hypokalemia due to diuretic therapy, potassium solution is to be administered. Only rarely will it be necessary to administer acidifying agents IV.

Patient care: Arterial blood gas values, serum potassium level, and fluid balance are monitored. The patient is assessed for anorexia, nausea and vomiting, tremors, muscle hypertonicity, muscle cramps, tetany, Chvostek's sign, seizures, mental confusion progressing to stupor and coma, cardiac dysrhythmia due to hypokalemia, and compensatory hypoventilation with resulting hypoxia. Prescribed oxygen, oral or IV fluids, sodium chloride or ammonium chloride, and potassium chloride if hypokalemia is a factor, along with therapy prescribed to correct the cause, are administered. Seizure precautions are observed; a safe environment and reorientation as needed are provided for the patient with altered thought processes. The patient's response to therapy is evaluated, and the patient is taught about the dangers of excess sodium bicarbonate intake if that is a factor. The ulcer patient is taught to recognise signs of metabolic alkalosis, including anorexia, weakness, lethargy, and a distaste for milk. If potassium-wasting diuretics or potassium chloride supplements are prescribed, the patient's understanding of the regimen's purpose, dosage, and possible adverse effects is ascertained.