Metabolic Alkalosis

Metabolic alkalosis is typically classified as chloride-sensitive and chloride-insensitive, indicating the treatment approach itself. Metabolic alkalosis results from either gain of bicarbonate or loss of acid. The relationship of metabolic alkalosis to chloride balance defines both pathophysiologic features of the disease and its therapy. Bicarbonate and chloride represent the major serum anions whose concentration may be readily altered, and their homeostasis is therefore closely intertwined.

Conditions that produce chloride loss, such as vomiting (which also produces acid loss), diarrhea, diuretic therapy, and chloride-wasting diseases (e.g., cystic fibrosis and chloride-wasting enteropathy) all tend to reduce both serum chloride concentration and extracellular volume. The reduction in extracellular volume produces increased mineralocorticoid activity, which enhances sodium reabsorption and potassium and hydrogen ion secretion in the distal tubule, which, in turn, enhance bicarbonate generation. The resulting increase in serum bicarbonate concentration eventually exceeds the tubule's maximum ability to reabsorb filtered bicarbonate. The resulting alkaline urine, because its anionic content is mostly bicarbonate, is largely free of chloride (<10 meq/L), though when diuretics have been administered, the urine chloride may be normal. The result is hypokalemic, hypochloremic alkalosis that responds to normal (chloride-responsive alkalosis).

Other diseases that cause metabolic alkalosis are usually associated with normovolemia or hypervolemia and often hypertension. These diseases usually cause excess mineralocorticoid activity, resulting in the same pathophysiologic cascade described above. However, the excess mineralocorticoid activity is not associated with hypovolemia, so the urine chloride is generally normal or elevated (>10 meq/L) and the alkalosis cannot be reversed with normal saline. Diseases producing "chloride-unresponsive alkalosis" and hypertension include renal artery stenosis, renin-secreting tumors, adrenal hyperplasia, hyperaldosteronism, Cushing syndrome, Liddle syndrome, and exogenous mineralocorticoids (e.g., licorice, Florinef). Chloride-unresponsive alkalosis caused by Bartter syndrome and Gitelman syndrome is usually associated with normotension.

The compensation for metabolic alkalosis involves reduction in alveolar ventilation, but the exact relationship between P co2 and hydrogen ion concentration is not well established. Most studies to date have been conducted either in dialysis patients or patients with conditions that predispose to alveolar hyperventilation (e.g., sepsis, pneumonia). As a guideline, Pco2 in patients with significant metabolic alkalosis should rise 0.7 mmHg for each milliequivalent increase in [HCO 3-]. The Pco2 also rarely rises above 55 mmHg in compensation for metabolic alkalosis.

The physiologic effects of alkalemia are substantial. Neurologic abnormalities—especially tetany, neuromuscular instability, and seizures—are common. Reduction in hydrogen ion concentration results in reductions in ionized calcium, potassium, magnesium, and phosphate levels. Constriction of arterioles occurs, resulting in reduced coronary and cerebral blood flow. Finally, refractory dysrhythmias may develop.15 Alkalemia may be of particular concern in patients with chronic obstructive pulmonary disease (COPD) because of the shift of the oxygen-hemoglobin to the left, making O 2 less available to the tissues. Many such patients are taking diuretics, which lead to a contraction alkalosis. Also, the alkalotic environment tends to depress ventilatory drive further.

Therapy of alkalemia, as with all acid-base disorders, emphasizes treatment of the underlying cause and careful supportive care. Acetazolamide produces significant bicarbonaturia and is effective in the treatment of metabolic alkalosis, but its use requires very careful monitoring of potassium, magnesium, and phosphate concentrations. If alkalemia is severe ([HCO3-] > 45 mmol/L) and associated with serious signs or symptoms not responsive to supportive care, the use of intravenous hydrochloric acid should be considered. A 0.1 normal solution (100 mmol/L), infused at no more than 0.2 mmol/kg/h through a central venous catheter is used; higher concentrations may produce degradation of catheter material.18 The dose is calculated as shown in Eq,, (Z), with the result in millimoles of bicarbonate.

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