Metabolic alkalosis - NYSORA

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Metabolic alkalosis

Metabolic alkalosis

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

metabolic alkalosis, chloride-responsive, isotonic saline, potassium, magnesium, hypomagnesemia, diuretics, spironolactone, eplerenone, amiloride, triamterene, chloride-resistant, adrenal hyperplasia, adlosterone blockers, hyperaldosteronism, sodium, chronic kidney disease, peritoneal dialysis, hemodialysis, renal replacement therapy, bartter syndrome, non-steroidal anti-inflammatory drugs, gitelman syndrome, vomiting, proton pump inhibitors, h2 blockers, alkali, licorice

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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