Learning objectives

• Describe the pathophysiology of metabolic alkalosis
• Diagnose metabolic alkalosis
• Manage metabolic alkalosis

Background

• Metabolic alkalosis is defined as an increase in serum pH to >7.45
• Mostly due to a primary increase in serum bicarbonate (HCO3-)
• Associated with a secondary increase in CO2 arterial pressure (PaCO2)
• Usually accompanied by hypokalemia and hypochloremia
• Common aced-base disorder in critically ill patients

Pathophysiology

• Intracellular shift of hydrogen ions
  • E.g. hypokalemia
  • Decrease in serum hydrogen ions results in a relative increase in bicarbonate
• Renal loss of hydrogen ions
  • Pathologies that increase the levels of mineralocorticoids or the effect of aldosterone lead to hypernatremia, hypokalemia, and hydrogen loss
  • Loop and thiazide diuretics can induce secondary hyperaldosteronism
  • Genetic defects leading to decreased expression of ion transporters in the loop of Henle (Bartter disease, Gitelman disease)
• Retention/addition of bicarbonate
  • Overdose of exogenous sodium bicarbonate
  • Compensatory mechanism for hypercarbia: hypoventilation and CO2 retention result in renal compensation over time by retaining bicarbonate (post-hypercapnia syndrome)
• Contraction alkalosis
  • Occurs when a large volume of sodium-rich, bicarbonate low fluid is lost 
  • Diuretic use, cystic fibrosis, congenital chloride diarrhea
  • Net concentration of bicarbonate increases
• Evaluation of etiology: Urinary chloride
  • Chloride responsive (urine chloride <10 mEq/L): Gastrointestinal hydrogen loss, congenital chloride diarrhea syndrome, contraction alkalosis, diuretic therapy, post-hypercapnia syndrome, cystic fibrosis, exogenous alkalotic agent use, villous adenoma, high volume ileostomy output
  • Chloride resistant (urine chloride >20 mEq/L): Retention of bicarbonate, intracellular shift of hydrogen, hyperaldosteronism, Bartter syndrome, Gitelman syndrome, Cushing’s syndrome, exogenous mineralocorticoids, congenital adrenal hyperplasia, licorice, Liddle syndrome
• Adverse effects
  • Decreased myocardial contractility
  • Arrhythmias
  • Decreased cerebral blood flow
  • Delirium
  • Increased neuromuscular excitability
  • Impaired peripheral oxygen unloading
  • Compensatory increase in arterial pCO2
  • Net effect resulting in hypoxia

Diagnosis

• Elevated serum HCO3- and pCO2
• Determine respiratory compensation
  • PaCO2 (mmHg) = 40 + 0.6 × (HCO3-  –  24 mmol/l)

Management

Suggested reading

• Brinkman JE, Sharma S. Physiology, Metabolic Alkalosis. [Updated 2022 Jul 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482291/
• Tinawi M. Pathophysiology, Evaluation, and Management of Metabolic Alkalosis. Cureus. 2021;13(1):e12841. Published 2021 Jan 21.

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