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)

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 ...