ACUTE AND CHRONIC METABOLIC ALKALOSIS (BASE BICARBONATE EXCESS)
Metabolic alkalosis is a clinical disturbance characterized by a high pH (decreased H+ concentration) and a high plasma bicar-bonate concentration. It can be produced by a gain of bicarbon-ate or a loss of H+ (Khanna & Kurtzman, 2001).
Probably the most common cause of metabolic alkalosis is vomiting or gastric suction with loss of hydrogen and chloride ions. The disorder also occurs in pyloric stenosis, in which only gastric fluid is lost. Gastric fluid has an acid pH (usually 1–3); therefore, loss of this highly acidic fluid increases the alkalinity of body fluids. Other situations predisposing to metabolic alkalosis include those associated with loss of potassium, such as diuretic therapy that promotes excretion of potassium (eg, thiazides, furo-semide), and excessive adrenocorticoid hormones (as in hyper-aldosteronism and Cushing’s syndrome).
Hypokalemia produces alkalosis in two ways: (1) the kidneys conserve potassium, and thus H+ excretion increases; and (2) cel-lular potassium moves out of the cells into the ECF in an attempt to maintain near-normal serum levels (as potassium ions leave the cells, hydrogen ions must enter to maintain electroneutrality). Excessive alkali ingestion from antacids containing bicarbonate or from using sodium bicarbonate during cardiopulmonary re-suscitation can also cause metabolic alkalosis.
Chronic metabolic alkalosis can occur with long-term diuretic therapy (thiazides or furosemide), villous adenoma, external drain-age of gastric fluids, significant potassium depletion, cystic fibro-sis, and the chronic ingestion of milk and calcium carbonate.
Alkalosis is primarily manifested by symptoms related to de-creased calcium ionization, such as tingling of the fingers and toes, dizziness, and hypertonic muscles. The ionized fraction of serum calcium decreases in alkalosis as more calcium combines with serum proteins. Because it is the ionized fraction of calcium that influences neuromuscular activity, symptoms of hypocal-cemia are often the predominant symptoms of alkalosis. Respira-tions are depressed as a compensatory action by the lungs. Atrial tachycardia may occur. As the pH increases above 7.6 and hypo-kalemia develops, ventricular disturbances may occur. Decreased motility and paralytic ileus may also occur.
Symptoms of chronic metabolic alkalosis are the same as for acute metabolic alkalosis, and as potassium decreases, frequent pre-mature ventricular contractions or U waves are seen on the ECG.
Evaluation of arterial blood gases reveals a pH greater than 7.45 and a serum bicarbonate concentration greater than 26 mEq/L. The PaCO2 increases as the lungs attempt to compensate for the excess bicarbonate by retaining CO2. This hypoventilation is more pronounced in semiconscious, unconscious, or debilitated patients than in alert patients. The former may develop marked hypoxemia as a result of hypoventilation. Hypokalemia may accompany metabolic alkalosis.
Urinary chloride levels may help to identify the cause of meta-bolic alkalosis if the patient’s history provides inadequate infor-mation. Metabolic alkalosis is the setting in which urine chloride concentration may be a more accurate estimate of volume than is the urine sodium concentration. Urine chloride concentrationshelp to differentiate between vomiting or diuretic ingestion or one of the causes of mineralocorticoid excess. Hypovolemia and hypochloremia in patients with vomiting or cystic fibrosis, those receiving nutritional repletion, or those taking diuretics produce urine chloride concentrations less than 25 mEq/L. Signs of hypo-volemia are not present and the urine chloride concentration ex-ceeds 40 mEq/L in patients with mineralocorticoid excess or alkali loading; these patients usually have expanded fluid volume. The urine chloride concentration should be less than 15 mEq/L when decreased chloride levels and hypovolemia occur.
Treatment of metabolic alkalosis is aimed at reversing the under-lying disorder (Khanna & Kurtzman, 2001).
Sufficient chloride must be supplied for the kidney to absorb sodium with chloride (allowing the excretion of excess bicarbon-ate). Treatment also includes restoring normal fluid volume by administering sodium chloride fluids (because continued volume depletion serves to maintain the alkalosis). In patients with hy-pokalemia, potassium is administered as KCl to replace both K+ and Cl− losses. Histamine-2 receptor antagonists, such as cimeti-dine (Tagamet), reduce the production of gastric HCl, thereby decreasing the metabolic alkalosis associated with gastric suction. Carbonic anhydrase inhibitors are useful in treating metabolic al-kalosis in patients who cannot tolerate rapid volume expansion (eg, patients with heart failure). Because of volume depletion from GI loss, the patient’s fluid intake and output must be monitored carefully. Management of chronic metabolic alkalosis is aimed at correcting the underlying acid–base disorder.
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