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Metabolic Alkalosis

SOURCE

Source: Devlin JW, Matzke GR. Acid–base disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146062232. Accessed March 3, 2017.

DEFINITION

  • Acid–base disorder characterized by increased pH with an increased serum bicarbonate (HCO3−) concentration.

ETIOLOGY

  • Clinical situations resulting in loss of H+ or gain of HCO3− and impairment of renal HCO3− excretion (Table 1)

TABLE 1.Causes of Metabolic Alkalosis Differentiated on the Basis of Their Responsiveness to Sodium Chloride
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TABLE 1. Causes of Metabolic Alkalosis Differentiated on the Basis of Their Responsiveness to Sodium Chloride
Sodium chloride–responsive (urinary chloride concentration <10 mEq/L [<10 mmol/L])

Gastrointestinal disorders.

 Vomiting.

 Gastric drainage.

 Villous adenoma of colon.

 Chloride diarrhea.
Diuretic therapy
Correction of chronic hypercapnia
Cystic fibrosis
Excessive bicarbonate therapy of organic acidosis
Mild/moderate potassium deficiency
Sodium chloride–resistant (urinary chloride concentration >20 mEq/L [>20 mmol/L])

Excess mineralocorticoid activity.

 Hyperaldosteronism.

 Cushing syndrome.

 Bartter syndrome.

 Gitelman syndrome.
Excessive black licorice intake
Profound potassium depletion
Magnesium deficiency
Liddle syndrome
Estrogen therapy
Unclassified
Alkali administration
Milk-alkali syndrome
Massive blood or plasma protein fraction transfusion
Nonparathyroid hypercalcemia
Carbohydrate refeeding after starvation
Large doses of penicillin

Reprinted with permission from DiPiro JT, Talbert RL, Yee GC, et al. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017.

PATHOPHYSIOLOGY

  • Initiated by increased pH and HCO3− that can result from:

    • Loss of H+ via gastrointestinal (GI) tract (eg, nasogastric suctioning, vomiting) or kidneys (eg, diuretics, Cushing syndrome)

    • Gain of bicarbonate (eg, administration of bicarbonate, acetate, lactate, or citrate)

  • Maintained by abnormal renal function that prevents kidneys from excreting excess bicarbonate.

  • Primary compensation: respiratory response to metabolic alkalosis is increased in PaCO2 by hypoventilation.

RISK FACTORS

  • Hospitalized patients with acid–base disturbances due to many factors, including (but not limited to):

    • Vomiting.

    • Nasogastric suctioning.

    • Secretory diarrhea.

    • Use of diuretics.

    • Administration of bicarbonate or infusion of organic anions metabolized to bicarbonate.

CLINICAL PRESENTATION

SIGNS AND SYMPTOMS

  • Mild to moderate alkalosis: symptoms may be related to underlying disorder.

    • Muscle weakness with hypokalemia.

    • Postural dizziness with volume depletion.

  • Severe alkalemia (pH >7.60) can be associated with cardiac arrhythmias and neuromuscular irritability.

DIAGNOSIS

MEANS OF CONFIRMATION AND DIAGNOSIS

  • Blood gases, serum electrolytes, medical history, and clinical condition are the primary tools for determining the cause of acid–base disorders and for designing therapy.

LABORATORY TESTS

  • Arterial blood gases (ABG) measured to determine oxygenation and acid–base status.

  • Metabolic panel.

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