Before We Start
Hyperkalemia — when potassium goes too high, the heart pays the price
Potassium is the primary intracellular cation — about 98% of the body's potassium is inside cells. The heart's electrical system is exquisitely sensitive to the ratio of potassium inside versus outside cardiac cells. When that ratio is disrupted by elevated serum potassium, the heart's electrical conduction becomes unstable — and cardiac arrest can follow.
Normal potassium: 3.5–5.0 mEq/L. Hyperkalemia is above 5.0 mEq/L. Severe, life-threatening hyperkalemia begins above 6.5 mEq/L. The MURDER mnemonic gives you the causes, symptoms, ECG changes, and treatments — everything you need to recognize and respond to this electrolyte emergency.
💡 Why Potassium Changes the ECG
Cardiac cells depolarize (fire) when potassium flows out and sodium flows in. The resting membrane potential of cardiac cells depends on the intracellular-to-extracellular potassium ratio. When extracellular potassium rises, this ratio shrinks — the resting membrane potential becomes less negative. The cell is now closer to its firing threshold, making it hyperexcitable and prone to dangerous arrhythmias. Think of it like a hair-trigger: even a small stimulus fires the gun.
The Mnemonic
MURDER — causes, signs, ECG changes, and treatment of hyperkalemia
M — Medications
The drugs that raise potassium — know them before prescribing combinations
Several medication classes significantly raise serum potassium. The danger increases exponentially when multiple potassium-raising drugs are combined in the same patient:
Potassium-raising drugs:
• ACE inhibitors (lisinopril, enalapril) — block aldosterone → potassium retained
• ARBs (losartan, valsartan) — same mechanism as ACE inhibitors
• Potassium-sparing diuretics (spironolactone, triamterene) — block aldosterone at kidney
• NSAIDs — reduce renal potassium excretion
• Heparin — suppresses aldosterone production
• Digoxin toxicity — inhibits Na/K ATPase, shifting potassium out of cells
• Succinylcholine (paralytic used in intubation) — causes potassium efflux from cells; can cause fatal hyperkalemia in burn patients, crush injuries, and denervation injuries
• Trimethoprim (component of Bactrim) — acts like a potassium-sparing diuretic in the kidney
The dangerous combination: ACE inhibitor + potassium-sparing diuretic + renal failure = severe hyperkalemia waiting to happen. This combination in an elderly patient with declining kidney function is a common and preventable cause of hyperkalemia hospitalization.
💊 "Spironolactone + lisinopril = double potassium retention." Both commonly prescribed for heart failure. Both retain potassium. Together they require consistent monitoring — potassium should be checked within 1 week of starting or dose-adjusting either drug, then regularly thereafter.
U — Urine output (decreased) / renal failure
The kidneys are the primary route of potassium excretion — when they fail, potassium climbs
The kidneys excrete approximately 90% of the body's potassium. In healthy kidneys, even if potassium intake is high, the excess is excreted in urine. When kidney function declines — acute kidney injury (AKI) or chronic kidney disease (CKD) — potassium clearance drops and serum potassium rises.
The relationship between eGFR and hyperkalemia risk:
• eGFR above 60: low hyperkalemia risk from kidney disease alone
• eGFR 30–60: moderate risk — potassium monitoring every 3–6 months
• eGFR below 30: high risk — potassium monitoring monthly or more often
• Dialysis patients: cannot excrete potassium at all between sessions — dietary restriction and dialysis scheduling are critical
Oliguria as an early warning: Urine output below 400mL/day (oliguria) is the threshold below which the kidneys cannot maintain potassium balance. A hospitalized patient with declining urine output needs potassium monitoring regardless of whether they have known kidney disease.
💊 "Dialysis patients eat with their lives." A patient on hemodialysis has virtually no ability to excrete potassium between sessions. High-potassium foods — bananas, oranges, potatoes, tomatoes, dried fruits, salt substitutes — can cause life-threatening hyperkalemia between dialysis sessions. Dietary counseling is not optional for dialysis patients; it is a matter of survival.
R — Redistribution
Potassium shifts from inside cells to the bloodstream
Even without excess potassium intake or kidney failure, potassium can rise rapidly in the blood when it shifts from the intracellular compartment (where 98% lives) to the extracellular space. This redistribution can cause sudden, severe hyperkalemia.
Causes of potassium redistribution:
• Acidosis — when blood pH drops, hydrogen ions enter cells and potassium exits to maintain electrical neutrality. For every 0.1 drop in pH, potassium rises approximately 0.5 mEq/L.
• Tissue destruction (rhabdomyolysis, crush injury, burns, tumor lysis syndrome) — damaged cells release their intracellular potassium into the bloodstream
• Insulin deficiency (DKA) — insulin normally drives potassium into cells. Without insulin, potassium stays extracellular.
• Succinylcholine administration — causes muscle fasciculations that release potassium from cells
• Massive hemolysis — red blood cells releasing potassium
The DKA example: A patient in DKA may have a normal or even high serum potassium despite total body potassium depletion — because acidosis and insulin deficiency have shifted potassium out of cells. When insulin is given to treat the DKA, potassium rushes back into cells — serum potassium can drop rapidly. This is why potassium must be repleted before or alongside insulin in DKA treatment.
D — Diet (excessive potassium intake)
High-potassium foods and salt substitutes in vulnerable patients
Dietary potassium is rarely the sole cause of dangerous hyperkalemia in patients with normal kidney function — healthy kidneys excrete excess potassium efficiently. But in patients with kidney disease, those on potassium-retaining medications, or dialysis patients, dietary potassium can push already-elevated levels into dangerous territory.
High-potassium foods patients may not realize are problematic:
• Bananas, oranges, avocados, kiwi
• Potatoes, sweet potatoes (especially with skin)
• Tomatoes, tomato sauce, tomato juice
• Dried fruits (raisins, prunes, apricots)
• Nuts and seeds
• Dark leafy greens (when consumed in large quantities)
• Salt substitutes — potassium chloride used instead of sodium chloride. A patient on an ACE inhibitor who switches to salt substitute for their "heart-healthy" diet can develop severe hyperkalemia.
The patient education gap: Many patients on ACE inhibitors or spironolactone are not informed about high-potassium foods and salt substitutes. This education is a nursing responsibility at every medication teaching encounter.
💊 "Salt substitute + ACE inhibitor = hyperkalemia emergency." A patient reduces sodium as instructed, switches to potassium chloride salt substitute for all cooking, and is on lisinopril. Within weeks, potassium reaches 6.8 mEq/L. This is preventable with patient education at the time of prescription.
E — ECG changes
The cardiac changes of hyperkalemia — from peaked T waves to sine wave
ECG changes in hyperkalemia follow a predictable progression as potassium rises. Each level of elevation produces characteristic findings:
Mild hyperkalemia (5.5–6.5 mEq/L):
• Tall, peaked, narrow T waves — the earliest and most sensitive ECG sign. T waves become tall, narrow, tent-shaped, and symmetric. Compare to normal T waves which are rounded and asymmetric.
Moderate hyperkalemia (6.5–7.0 mEq/L):
• Prolonged PR interval
• Widening QRS complex — the conduction system slows
• Flattened or absent P waves — atrial conduction fails
Severe hyperkalemia (above 7.0–8.0 mEq/L):
• Sine wave pattern — QRS and T wave merge into a smooth, undulating sine wave. This is a pre-terminal rhythm.
• Ventricular fibrillation
• Asystole
Clinical action when ECG changes appear: Peaked T waves alone → accelerate treatment but less urgency. Wide QRS or sine wave → cardiac emergency, call for help immediately, calcium gluconate IV now.
💊 "Peaked T waves first, wide QRS next, sine wave last — act before the last one." A telemetry nurse who spots new peaked T waves in a patient on spironolactone and lisinopril should immediately check the potassium level and notify the provider. Waiting for symptoms or more dramatic ECG changes means losing the therapeutic window.
R — Restore normal potassium (Treatment)
Five treatments in order — from stabilize to eliminate
Treatment of hyperkalemia follows a logical sequence based on urgency:
1. Calcium gluconate (or calcium chloride) — cardiac membrane stabilization
Given first when ECG changes are present (especially wide QRS). Does NOT lower potassium. Raises the threshold for cardiac cell firing — stabilizes the membrane and buys time for the other treatments to work. Effect: within 1–3 minutes, lasts 30–60 minutes. Dose: calcium gluconate 1g IV over 2–3 minutes.
2. Insulin + Dextrose — shift potassium into cells
Regular insulin 10 units IV drives potassium into cells within 15–30 minutes. Dextrose (D50W 25g IV) given simultaneously to prevent hypoglycemia — the insulin will lower glucose even as it lowers potassium. Lowers potassium by 0.5–1.0 mEq/L. Temporary effect — potassium will shift back out in 4–6 hours.
3. Sodium bicarbonate — correct acidosis to shift K+ into cells
Effective in patients with metabolic acidosis. Raising the pH drives potassium back into cells. Less effective in non-acidotic hyperkalemia.
4. Sodium polystyrene sulfonate (Kayexalate) or patiromer (Veltassa) — eliminate potassium through the gut
Ion exchange resins that bind potassium in the GI tract and excrete it in stool. Actual potassium removal from the body. Effect takes hours. Kayexalate causes constipation and can cause colonic necrosis — patiromer is safer with fewer GI complications.
5. Dialysis — the definitive treatment for severe or refractory hyperkalemia
Removes potassium directly from the blood. Necessary in renal failure patients or when other treatments fail.
💊 "C-BIG-K Drop" is a common memory tool for hyperkalemia treatment order: Calcium (stabilize), Bicarbonate (shift), Insulin+Glucose (shift), Kayexalate/patiromer (eliminate), Dialysis (remove). Each C-BIG-K step addresses potassium in a different way — stabilize first, then shift, then remove.
🏥 Clinical Scenario — Hyperkalemia Identified and Treated
Mr. Okonkwo, 66 years old, CKD Stage 4 (eGFR 22), on lisinopril 10mg and spironolactone 25mg daily for heart failure. Admitted for increasing fatigue and weakness. Morning labs: potassium 7.1 mEq/L. You are reviewing the telemetry strip when you see the results.
ECG
Telemetry assessment: Peaked, narrow T waves present in multiple leads. PR interval prolonged at 0.24 seconds. QRS 0.11 seconds — mildly widened. No P waves visible in some leads. ECG changes consistent with severe hyperkalemia. Call provider STAT.
Ca2+
Calcium gluconate 1g IV ordered and given over 3 minutes — cardiac membrane stabilization. Monitor for bradycardia during administration (give slowly). Effect expected within 2 minutes. ECG reviewed — T waves slightly less peaked. QRS width unchanged. Buys time for next steps.
Insulin
Regular insulin 10 units IV + D50W 25g IV given simultaneously. Blood glucose checked before and every 30 minutes after. Glucose pre: 142. At 30 minutes: potassium 6.4 mEq/L (down from 7.1), glucose 108. Shifted approximately 0.7 mEq/L — temporary but buys several hours.
Remove
Patiromer 8.4g PO ordered — binds potassium in the GI tract for elimination in stool. Effect in 7+ hours. Lisinopril and spironolactone held — both potassium-retaining drugs contributing to the problem. Nephrology consulted — emergent dialysis standing by if potassium does not respond. Potassium at 6 hours: 5.8 mEq/L. At 12 hours: 5.2 mEq/L. Patient stabilized.
⚠️ The Trap — Treating Hyperkalemia with Calcium Alone
A patient with a potassium of 7.0 mEq/L and peaked T waves receives calcium gluconate. The ECG improves — T waves are less peaked, the QRS narrows. The nurse and provider are reassured and the patient is monitored without further intervention.
What was missed: Calcium gluconate does NOT lower potassium. It stabilizes the cardiac membrane — it raises the threshold at which cardiac cells fire, making the heart more resistant to arrhythmia temporarily. The potassium is still 7.0 mEq/L and still dangerous.
The consequence: Calcium's effect lasts 30–60 minutes. When it wears off, the potassium is still dangerously elevated and cardiac membrane instability returns. The patient may go into ventricular fibrillation when the calcium effect dissipates.
The rule: Calcium stabilizes — it is always followed by treatments that actually lower potassium: insulin/dextrose to shift it, kayexalate/patiromer or dialysis to remove it. Calcium is the emergency bridge, not the treatment.