HYPOKALEMIA

Serum K <3.5 mEq/L — GI losses, renal wasting, or transcellular shifts; always check and replace Mg first or K will not normalize

SYMPTOMS / ASSOCIATED SX

  • Mild (K 3.0–3.5): often asymptomatic; cramps, fatigue

  • Moderate (K 2.5–3.0): weakness, constipation, palpitations, polyuria (nephrogenic DI)

  • Severe (K <2.5): flaccid paralysis, ileus, respiratory failure, ventricular arrhythmias

  • ECG: T wave flattening/inversion, U waves (best in V2–V3), ST depression

  • Always check Mg — hypomagnesemia prevents K repletion; must replace Mg concurrently

DENIES

  • Vomiting/diarrhea/laxative use (GI losses)

  • Diuretic use (renal wasting)

  • Eating disorder/laxative abuse (bulimic hypokalemia)

  • Insulin administration (transcellular shift in DKA treatment)

SOCIAL HISTORY

  • Alcohol use; diuretic compliance; dietary K intake; laxative/enema use

MAIN ETIOLOGY

  • GI losses: vomiting (UNa <20 — renal K wasting from alkalosis + aldosterone); diarrhea; laxatives; NGT; high-output ostomy

  • Renal wasting: loop/thiazide diuretics (most common); hyperaldosteronism; RTA type I/II; hypomagnesemia; amphotericin B

  • Transcellular shift: insulin, beta-agonists, alkalosis (K decreases ~0.3 per 0.1 pH rise), hypothermia, hypokalemic periodic paralysis

MOST COMMON DDX

  • Urine K <20 mEq/day (appropriate conservation): GI losses, poor intake, remote diuretics

  • Urine K >20 mEq/day (renal wasting): active diuretics, hyperaldosteronism, Bartter/Gitelman, RTA, hypomagnesemia

  • Primary hyperaldosteronism: HTN + hypoK + metabolic alkalosis → aldosterone:renin ratio >30

  • Bartter/Gitelman: young, normotensive, metabolic alkalosis, elevated renin/aldosterone

  • Hypokalemic periodic paralysis: acute flaccid paralysis triggered by carbohydrates or insulin

DATA

  • BMP; serum Mg (MUST replace before K will normalize); ECG

  • Urine K/Cr spot ratio: >2.5 mEq/mmol Cr = renal wasting; <1.5 = extrarenal

  • Urine Cl (vomiting: UCl <10; diuretics: UCl >20)

  • Plasma aldosterone + renin (if HTN + hypoK + alkalosis); cortisol (Cushing's)

HOME MEDS

  • Loop/thiazide diuretics — reduce dose; switch to K-sparing if indicated

  • Amphotericin B — causes renal K and Mg wasting; switch to lipid formulation

  • K supplements — increase dose; NEVER mix KCl in D5W (insulin release worsens hypoK)

PLAN

  • Replete Mg FIRST if <2.0 mg/dL — K will not normalize until Mg is repleted

  • Oral K replacement (preferred for mild-moderate, tolerating PO):

    • KCl 40 mEq PO q2–4h; each 10 mEq KCl raises serum K ~0.1 mEq/L (rough guide)

    • Total body K deficit: ~100–200 mEq per 1 mEq/L decrease (highly variable)

  • IV K replacement (symptomatic, arrhythmia, unable to PO, K <2.5):

    • Peripheral IV: max 10 mEq/h (pain and phlebitis at higher rates)

    • Central IV: max 20 mEq/h with continuous telemetry

    • Cardiac arrest from hypoK: 2 mEq/min IV for first 15 min then reduce

    • Mix in NS or LR ONLY — NEVER in dextrose solutions

  • Dietary K: bananas, oranges, potatoes, beans; 40–80 mEq/day additional

  • K-sparing strategies if ongoing losses: amiloride 5–10 mg PO daily or spironolactone 25–50 mg PO daily

  • DISCHARGE:

    • Oral KCl 20–40 mEq PO daily if ongoing losses; BMP in 3–5 days

    • Evaluate for hyperaldosteronism if refractory or recurrent hypoK + HTN

RED FLAGS

  • K <2.5 + VT/VF → 40 mEq IV over 2h via central line with telemetry

  • Respiratory muscle weakness + K <2.0 → airway risk; ICU

  • Hypokalemia + digoxin → dramatically increases toxicity; target K >4.0 in digoxin patients

  • Hypokalemic periodic paralysis: avoid glucose solutions; oral KCl preferred; neurology consult

  • DKA: total body K depleted despite normal/high serum K; replace K aggressively when K <5.0 during insulin infusion

SENIOR IM RESIDENT PEARLS

  • Mg is the gatekeeper for K: hypoMg causes renal K wasting (ROMK channel requires Mg); K WILL NOT normalize until Mg is repleted — always check and replace Mg first

  • U waves on ECG: positive deflection after T wave, best in V2–V3; can be mistaken for prolonged QT — measure QU interval, not QT

  • Albuterol lowers K 0.5–1.0 mEq/L per treatment — check before and after high-dose nebulization

  • Common mistake: replacing K without Mg — K replacement will fail

  • Vomiting-induced hypoK: vomit itself is low in K (~10 mEq/L); hypoK results from renal K wasting in response to metabolic alkalosis + aldosterone-driven secretion

  • Common mistake: mixing KCl in D5W — glucose triggers insulin which shifts K intracellularly; always use NS or LR