Alkalosis, Metabolic

KEY FEATURES

• High serum HCO₃^– with alkalemia (high pH)

• Evaluate effective circulating volume by physical examination

• Urinary chloride concentration differentiates saline-responsive alkalosis from saline-unresponsive alkalosis

• Etiology can be classified into chloride responsive or chloride unresponsive (Table 23–15)

• Chloride responsive (UCl– < 20 mEq/L)

  • Involves the loss of chloride and extracellular volume

  • In vomiting and nasogastric suction, loss of acid (HCl) generates the alkalosis and volume contraction from Cl^– loss maintains the alkalosis

  • Distally acting diuretics that cause chloride loss, eg, loop and thiazide diuretics, are a common cause of metabolic alkalosis; U_Cl^– levels can be unreliable when diuretics have been used since they increase U_Cl^– excretion

• Chloride unresponsive (U_Cl^– > 20 mEq/L)

  • Excess mineralocorticoid disorders typically associated with hypertension, hypokalemia, metabolic alkalosis, and mild hypernatremia

CLINICAL FINDINGS

• No characteristic symptoms or signs

• However, hypopnea can be present in severe cases

• Hypertension may be present in mineralocorticoid-excess disorders

• Alkalemia decreases oxygen delivery by shifting the oxygen disassociation curve of hemoglobin

• Concomitant hypokalemia may cause weakness and hyporeflexia

• pH > 7.48 is associated with increased risk for mortality

DIAGNOSIS

• The arterial blood pH and bicarbonate are elevated

• With respiratory compensation, arterial PCO₂ is increased

• The compensatory increase in PCO₂ rarely exceeds 55 mm Hg; higher PCO₂ values imply a superimposed primary respiratory acidosis

• Serum potassium and chloride are decreased

• The urinary chloride can differentiate between a chloride-response (< 20 mEq/L) and unresponsive (> 20 mEq/L) cause

TREATMENT

• Mild alkalosis is generally well tolerated

• Severe or symptomatic alkalosis (pH > 7.60) requires urgent treatment

• Chloride-responsive

  • Involves volume expansion with chloride salts, generally in the form of intravenous normal saline, until a euvolemic state has been achieved

  • Volume expansion reduces proximal tubular bicarbonate reabsorption and increases distal tubular delivery of chloride, where it is exchanged for bicarbonate by the luminal ...