Hyperkalemia

Why examiners ask this

Hyperkalemia bridges pharmacology, renal physiology and resuscitation. It arrives as a potassium of 5.9 on the morning of a dialysis patient's fistula revision, as peaked T waves after succinylcholine in a patient with a burn, or as the arrest at the end of a massive transfusion. It tests judgment on whether to proceed, application of knowledge on the mechanism of each drug, and organization when the rhythm goes wide.

The 60-second answer

Decision points and the "why"

• Proceed or postpone — for an elective case I postpone at a potassium above 5.5 mmol/L and treat; for a dialysis patient I ask when the last dialysis was and whether the potassium is at their baseline. An emergency proceeds with treatment started, an arterial line, and no succinylcholine. The number that changes my mind is the ECG: a chronic 5.8 with a normal ECG is a different patient from an acute 5.8 with peaked T waves.
• Calcium first — it antagonizes the depolarizing effect on the myocyte membrane and works in 1–3 minutes; it buys the time for everything else. Calcium chloride 1 g gives three times the elemental calcium of 1 g of gluconate, and the effect lasts only 30–60 minutes, so I repeat it if the ECG changes persist.¹ I give it even with digoxin on board when the alternative is arrest.
• Insulin and dextrose — potassium starts to fall within 15 minutes, drops 0.65–1.0 mmol/L at a peak of 30–60 minutes, and the effect lasts only about 2 hours before it rebounds;¹ the hypoglycemia comes late and I check glucose hourly. I give the dextrose with the insulin unless the glucose is already above 250 mg/dL.
• Hyperventilation and bicarbonate — a 0.1 rise in pH lowers potassium by roughly 0.5 mmol/L; hyperventilation is the fastest tool I have under anesthesia. Bicarbonate works only when there is acidosis to correct, and the sodium load matters in renal failure.
• Removal — furosemide 40–80 mg if there is urine, dialysis if there is not; sodium zirconium cyclosilicate works within about an hour and is now recommended for severe hyperkalemia, while the old resin is no longer routine.¹
• Succinylcholine — it raises potassium by 0.5–1 mmol/L in everyone; it is contraindicated after the acute phase of major burns, multiple trauma, extensive denervation and upper motor neuron injury, with the risk peaking at 7–10 days, because extrajunctional receptors release far more.² I treat it as safe only in the first 24 hours. I use rocuronium with sugammadex available instead.

The complication they will inject

The ECG goes from peaked T waves to a sine wave and the pulse disappears. This is a hyperkalemic arrest and I run ACLS with the specific treatment attached: chest compressions and epinephrine as standard, calcium chloride 1 g repeated every 5 minutes, insulin 10 units with dextrose, bicarbonate 50–100 mEq and hyperventilation; AHA 2025 grades these as of uncertain benefit in arrest and advises against inhaled beta-agonists.³ I say that the arrest will not resolve until the potassium falls, so I continue compressions longer than I would for another cause and I call for emergent dialysis. I look for the source: the succinylcholine I just gave, old packed cells through the rapid infuser, a rhabdomyolysis from a tourniquet or a crush, or malignant hyperthermia if the end-tidal CO2 has been climbing. In the ward version, a dialysis patient who missed a session needs an urgent operation: I treat, place an arterial line, avoid succinylcholine, and dialyze first if time allows.

Pitfalls that cost points

• Giving insulin and glucose first and calcium later, or forgetting calcium altogether.
• Listing the shifting drugs without saying that none of them remove potassium.
• Saying "I would cancel" for a dialysis patient at 5.6 with a normal ECG and a baseline of 5.5.
• Avoiding lactated Ringer's because it "contains potassium" and then giving large volumes of saline, whose acidosis raises the potassium more.
• Forgetting the rebound after insulin and the hypoglycemia at hour two.

Rapid-why

Q: Why does calcium work when it does not change the potassium? A: It restores the gap between resting membrane potential and threshold, so the myocyte can depolarize normally; the potassium is unchanged but the membrane is stabilized.

Q: Why is the ECG more important than the level? A: The rate of rise determines the effect; chronic renal patients tolerate 6.0 with a normal ECG while an acute rise to 6.0 produces a wide QRS.

Q: Why does succinylcholine release so much potassium after a burn? A: Receptors spread from the junction to the whole muscle membrane, so depolarization opens channels across the entire fiber, and the efflux is enough to arrest the heart.

Q: Why does old blood raise the potassium? A: Stored red cells leak potassium about 1 mEq/L per day, toward a plateau near 60 mEq/L, and irradiation speeds the leak;⁴ under a rapid infuser that reaches the heart before it dilutes.

Numbers to know

Links

• succinylcholine, Chronic kidney disease and the dialysis patient, Malignant hyperthermia, ACLS adapted to the operating room, Massive hemorrhage and transfusion
• Atlas: Monitor atlas: perioperative cardiac events
• AHA Guidelines for CPR and ECC (2025, Part 10: special circumstances); UK Kidney Association hyperkalaemia guideline (2023)