Potassium disorders
98% of K is intracellular. Insulin and β2 agonists shift K in; acidosis and succinylcholine shift K out.
Homeostasis
Ingested K is absorbed in the intestine, then taken up and sequestered by liver and muscle via insulin and β2 receptors → ↑Na-K-ATPase (). 98% of K is intracellular, mostly muscle.
- Urinary K excretion follows Na delivery to the distal nephron (macula densa) → K excretion; ↓Na delivery → K retention.
- A rise in serum K triggers aldosterone → principal-cell K secretion → urinary K excretion.
Hyperkalemia
Symptoms: muscle cramps, ascending weakness, paralysis, conduction delay (CHB, BBB, sinus arrest), arrhythmia (VT/VF, asystole, idioventricular) (). Acute changes are the dangerous ones — STAT ECG. Treat if ECG changes, K >6, rapid rise, or symptoms. Elimination is the actual treatment; everything else is a . Address reversible factors (volume, low-K diet, meds).
- it is not a hemolyzed sample, platelets >500k, WBC >120 (the lab only flags RBC hemolysis, not WBC lysis), or a K-containing infusion. Get a blood-gas K if the ECG and the number disagree.
- ECG march: peaked T waves → ↓QT → ↑PR ± AV block, flat P → wide QRS ± BBB → sine wave → PEA / asystole / VF. The ECG does not correlate tightly with the [K+] ().
- Sine waves can be misread as VT. Do not give amiodarone for suspected hyperK — it is deadly.
Etiologies — ABCDD
- Acidosis, ↓ aldosterone; β-blocker, blood; cell lysis / turnover; drugs, DM, decreased GFR.
- Redistribution (usually transient unless excretion is also impaired): cell lysis (hemolysis, rhabdo, TLS), acidosis, ↓insulin, hyperosmolarity, meds (digoxin, β-blockers, minoxidil), hyperkalemic periodic paralysis, post-hypothermia.
- ↓ renal K excretion (persistent hyperK): ↓ aldo production/action — ACE inhibitors/ARBs, NSAIDs, K-sparing diuretics, calcineurin inhibitors, pentamidine, TMP, type IV RTA. Impaired distal Na delivery — hypovolemia, CHF, cirrhosis. AKI/CKD, especially oliguric, usually GFR <15.
- Other: ureterojejunostomy (urine K reabsorbed).
- 1
Stabilize membranes
Calcium gluconate 2–3 g via a peripheral line, or CaCl2 1–2 g via a central line; repeat q5 min PRN. Onset 1–3 min, lasts 30–60 min. First-line if any ECG change. Does not lower K. Avoid if on digoxin.
- 2
Shift K inside
Insulin 5 U IV + D50 25 g if glucose <250 (onset 10–30 min, lasts 4–6 h, ↓K 0.5–1.5 mEq/L). Albuterol 10–20 mg nebulized (15–30 min, lasts 15–90 min; avoid in active ACS or significant tachyarrhythmia). Bicarb 1–2 amps IV or a drip if acidemic (5–10 min, lasts 1–2 h).
- 3
Remove K from the body
Furosemide ≥40 mg IV (or ~40 × Cr if K >6); give with NS if they need volume to diurese; add a thiazide if volume-overloaded. Lokelma 10 g TID > patiromer 8.4 g daily (slower); avoid if SBO / constipation / ileus; space 2 h from other meds. Hemodialysis lowers K immediately (session ~3 h); expect rebound from shifts. iHD clears K faster than CRRT.
Kayexalate use has declined in favor of Lokelma given weak efficacy and GI complications ().
| Strategy | Treatment | Onset | Duration | Notes |
|---|---|---|---|---|
| Stabilize | Calcium gluconate 2–3 g peripheral, or CaCl2 1–2 g central; q5 min PRN | 1–3 min | 30–60 min | First-line if any ECG Δ. Stabilizes membranes. Avoid if on digoxin. |
| Shift | NaHCO3 1–2 amps IV or drip | 5–10 min | 1–2 h | Drives K in. Especially if acidemic. |
| Shift | Insulin 5 U IV + D50 25 g (if glucose <250) | 10–30 min | 4–6 h | ↓K 0.5–1.5 mEq/L. Watch late hypoglycemia. |
| Shift | Albuterol 10–20 mg nebulized | 15–30 min | 15–90 min | Avoid in active ACS or significant tachyarrhythmia. |
| Remove | Furosemide ≥40 mg IV (~40 × Cr if K >6); ± NS; ± thiazide if overloaded | 30 min | Variable | Urinary K excretion. |
| Remove | Lokelma 10 g TID > patiromer 8.4 g daily | 1 h; 7 h | 24 h | Exchanges K for Ca or Na in the gut. Avoid if ileus. Space 2 h from meds. |
| Remove | Hemodialysis | Immediate | ~3 h | Removes K; rebound from intracellular shifts. Prefer iHD over CVVH if they can tolerate it. |
Hypokalemia
Usually symptomatic at K <3: cramps, ileus, ascending weakness (can hit respiratory muscle), rhabdomyolysis, paralysis, worse hepatic encephalopathy in cirrhosis (). ECG: flat T waves, ST depression, U waves, ↑QT, atrial or ventricular ectopy → VT/VF (especially if K <2.5, susceptible patients, or on digoxin).
| Bucket | Think |
|---|---|
| Lab artifact | Pseudo-hypokalemia: WBC >100 absorb K if the sample sits out. Check a blood-gas K. |
| Inadequate intake | Unlikely as the sole cause; usually stacked on another etiology. |
| Redistribution | ↑pH, ↑insulin, refeeding, ↑β-adrenergic activity (albuterol, epinephrine), ↑ blood-cell production (post G-CSF), hypothermia, toxins (cesium, barium, chloroquine), antipsychotics, hypokalemic or thyrotoxic periodic paralysis. |
| Extrarenal losses | Diarrhea (chronic, VIPoma, villous adenoma, laxatives), vomiting / NGT. |
| Renal losses, no HTN | ↑ urine flow (primary polydipsia, excess IVF), ↓Mg, meds (amphotericin B, ifosfamide, cisplatin, gentamicin). Acidemia: DKA, type II (proximal) and some type I (distal) RTA. Alkalemia: diuretics, UGI losses (secondary hyperaldo), Bartter (~loop), Gitelman (~thiazide). Other: ↑ urine anions (β-hydroxybutyrate in DKA, bicarb from UGI losses, toluene + penicillin metabolites). |
| Renal losses, with HTN | Primary hyperaldo: ↑aldo, ↓renin (adrenal adenoma). Secondary: ↑aldo, ↑renin (RAS, renin-secreting tumor). Other: ↑ glucocorticoid or ↑ENaC activity (Cushing, Liddle, black licorice). |
- 10 mEq raises K by ~0.1 mmol/L — a rough rule. Caution if ↑Cr or if the low K is from transcellular shift (periodic paralysis).
- Oral KCl preferred (ER tablet or IR powder): safer, fast, and many of these patients are chloride-depleted. Dose to the deficit.
- IV KCl if they cannot take PO: max 10 mEq/h on the floor, 20 mEq/h in the ICU on telemetry / central line.
- Always replete Mg; otherwise K wasting continues via ROMK ().
- Avoid dextrose-containing solutions — they can acutely worsen hypokalemia (dextrose → ↑insulin → K shifts in).