‣
Signature ✍️
- Laboratory 🐮 : primary metabolic alkalosis (↑ [bicarbonate]) → compensatory respiratory acidosis (↑ pCO2)
- Clinical 🐮 : generally asymptomatic, but if patient has chronic severe respiratory acidosis (e.g. OHS, COPD), new primary metabolic alkalosis can precipitate CO2 narcosis by virtue of interval compensation for the primary metabolic disorder (e.g. ”post-diuretic somnolence”)
‣
Principles ❗
Pathophysiology: Generation 🚰
- Exogenous
- Milk alkali syndrome (e.g. calcium carbonate)
- Endogenous
- Gastric Parietal Cell (i.e. HCl Secretion)
- Vomiting
- NG suction
- α-intercalated Cell (i.e. ↑ RAAS) ⊕ ↑ Na delivery to collecting duct
- e.g. dehydration-related contraction alkalosis ⊕ diuretic
Pathophysiology: Propagation 🚱
- Hypokalemia: efflux of intracellular potassium into the extracellular space is balanced by influx of extracellular sodium & protons into cells (i.e. facilitates extracellular alkalosis)
- Hypochloremia: results in ↓ activity of Pendrin, which is an enzyme of the collecting duct that secretes bicarbonate in exchange for chloride
Treatment - 3 Pillars 🍌
- Pillar #1: address generation of metabolic alkalosis (e.g. remove exogenous alkali, antiemetics for vomiting, resuscitation of dehydration)
- Pillar #2: address propagation of metabolic alkalosis (i.e. replete potassium, replete chloride)
- Pillar #3: consider augmenting correction of alkalosis with acetazolamide if actively diuresing (i.e. block the reabsorption of bicarbonate in the proximal tubule), & consider prophylactic mineralocorticoid receptor antagonist while diuresing (e.g. spironolactone)
‣
DDx 🏳️🌈
‣
- ↓ Urine Chloride (<10 mEq/L)
- Contraction alkalosis
- Vomiting & NG suction
- ↑ Urine Chloride (>40 mEq/L)
- Diuretics
- Bartter syndrome (”loop mimicker”)
- Gitelman syndrome (”thiazide mimicker”)
‣
- BP normal ⊕ Normokalemia
- Milk alkali syndrome
- BP normal ⊕ Hypokalemia
- Hypokalemia
- BP ↑ ⊕/⊖ Hypokalemia (“Mineralocorticoid Excess”)
- Hyperaldosteronism DDx
- Hypercortisolism DDx*
- Licorice addiction
⚪ Note: since ectopic ACTH production generally leads to the highest cortisol levels, the presence of frank hypokalemia may suggest ectopic ACTH-related hypercortisolism. In this instance, the cortisol concentration is so high that cortisol’s breakdown enzyme (11β-hydroxysteroid dehydrogenase type 2) is completely saturated, & resultant leftover cortisol binds to the mineralocorticoid receptor, simulating aldosterone’s effect
‣
References 📚
- Marino’s ICU Book (Pendrin Graphic)
