How hyperkalemia is tested on Step 1

Expect an ECG description, a drug list, or a crush injury, and questions on the mechanism or which treatment acts first.

HyperkalemiaShift out of cellsAcidosis, low insulin, lysis↓ Renal excretionLow GFR, low aldosteronePseudoHemolyzed sample
Three buckets. Excess intake alone rarely causes hyperkalemia when the kidneys work.

Causes in detail

Most potassium (about 98%) is inside cells, so small shifts change the serum level a lot.

MechanismExamplesWhy
Insulin deficiencyDKA, hyperglycemic statesInsulin normally drives K⁺ into cells via Na⁺/K⁺-ATPase
β-adrenergic blockadeNonselective β blockersβ2 stimulation normally moves K⁺ into cells
Digoxin toxicityOverdoseInhibits Na⁺/K⁺-ATPase
Cell lysisRhabdomyolysis, tumor lysis, hemolysis, burnsRelease of intracellular K⁺
SuccinylcholineBurns, crush injury, denervationUpregulated acetylcholine receptors release K⁺
Low aldosterone effectACE inhibitors, ARBs, spironolactone, adrenal insufficiency, type 4 RTALess K⁺ secretion by principal cells
ENaC blockadeAmiloride, triamterene, trimethoprimLess lumen-negative potential to drive K⁺ secretion

Hyperosmolality (hyperglycemia, mannitol) drags K⁺ out of cells with water (solvent drag).

ECG progression

The ECG does not track potassium precisely, but the sequence is classic.

Rising K⁺EarlyTall, peaked T wavesModeratePR prolongation, flattened or lost P wavesSevereQRS widening, bradycardiaPre-arrestSine-wave pattern → VF or asystole
ECG sequence. Any ECG change is an indication for immediate IV calcium.

Treatment: C-BIG-K-D

Treatments differ in what they do: stabilize, shift, or remove.

StabilizeIV calciumShiftInsulin + glucose,albuterolRemoveBinders, loopdiureticDialysisIf refractory orrenal failure
Stabilize → shift → remove. Calcium does not lower potassium; it buys time.
TreatmentMechanismOnset
Calcium gluconate or chlorideRaises threshold potential, stabilizing myocardiumMinutes
Insulin with glucoseActivates Na⁺/K⁺-ATPase → K⁺ into cells15–30 minutes
Albuterol (β2 agonist)Activates Na⁺/K⁺-ATPase → K⁺ into cells15–30 minutes
Sodium bicarbonateShifts K⁺ in when metabolic acidosis is presentVariable
Binders (patiromer, sodium zirconium cyclosilicate, sodium polystyrene sulfonate)Bind K⁺ in the gutHours
Loop diureticsIncrease renal K⁺ excretionHours
HemodialysisRemoves K⁺ directlyImmediate once started

In digoxin toxicity, digoxin immune Fab treats both the toxicity and the hyperkalemia.

Worked example

Link the cause to the mechanism and the first step.

functions Worked example — crush injury

A man is freed after 6 hours trapped under debris. Potassium is 7.4 mEq/L, CK is 48,000 U/L, and the ECG shows peaked T waves and a QRS of 150 ms. What is the cause, and what is given first?

  1. Crushed muscle releases intracellular potassium and myoglobin (rhabdomyolysis).
  2. QRS widening indicates a high risk of imminent arrhythmia.
  3. First give IV calcium to stabilize the myocardium; it acts in minutes.
  4. Then shift potassium (insulin with glucose, albuterol), give fluids for rhabdomyolysis, and arrange dialysis if needed.

Answer. Hyperkalemia from rhabdomyolysis. IV calcium first, then insulin with glucose and albuterol, then removal.