Renal/Urology · PANCE / PANRE

Hyperkalemia

Serum K >5.0 mEq/L; cardiac arrhythmia risk drives urgent intervention.

Also known as: hyperkalemia, high potassium

Overview

Serum potassium concentration >5.0-5.5 mEq/L (varies by lab). Severity: mild 5.5-6.0, moderate 6.1-6.9, severe ≥7.0 or any level with ECG changes. Acuity, EKG changes, and underlying cause determine urgency of intervention.

Epidemiology

Affects ~1-10% of hospitalized patients. Most common in patients with CKD, heart failure, diabetes, and those on RAAS inhibitors, MRAs, or potassium-sparing diuretics.

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Risk factors

CKD (decreased excretion)
Medications: ACEi (lisinopril, ramipril), ARB (losartan, valsartan), MRA (spironolactone, eplerenone, finerenone), potassium-sparing diuretic (amiloride, triamterene), trimethoprim, heparin, NSAIDs, beta-blockers, digoxin (overdose)
Type 4 RTA (hypoaldosteronism — diabetic nephropathy)
Adrenal insufficiency (Addison disease)
Massive cell breakdown: rhabdomyolysis, tumor lysis syndrome, hemolysis, severe burns
Acidosis (intracellular-extracellular shift)
Insulin deficiency / DKA
Excessive intake (salt substitutes, supplements, transfusion of old blood)

Pathophysiology

Potassium is the major intracellular cation; only 2% extracellular. Hyperkalemia results from impaired renal excretion (CKD, hypoaldosteronism), cellular shifts (acidosis, insulin deficiency, hyperosmolality, beta-blockade, succinylcholine, digoxin toxicity), increased intake/release (rhabdomyolysis, tumor lysis), or pseudohyperkalemia (hemolyzed sample, thrombocytosis, leukocytosis). Elevated extracellular K reduces the resting membrane potential, increasing excitability initially, then impairing repolarization and conduction, ultimately causing cardiac arrest.

Clinical presentation

Symptoms

Often asymptomatic until severe or rapidly developing
Muscle weakness, paralysis (severe; ascending similar to Guillain-Barré)
Paresthesias
Palpitations, lightheadedness
Cardiac arrest (life-threatening)

Signs / physical exam

Often unremarkable physical exam
Bradycardia, irregular rhythm
Hyporeflexia, flaccid paralysis in severe cases
Findings of underlying cause (volume status, signs of CKD, diabetic features)

Classic findings

ECG progression: peaked T waves → PR prolongation → loss of P waves → wide QRS → sine wave pattern → ventricular fibrillation/asystole.

Differential diagnosis

Pseudohyperkalemia — Hemolyzed sample, fist clenching with tourniquet, thrombocytosis, leukocytosis; repeat with non-hemolyzed sample or whole blood K
True hyperkalemia from CKD — Elevated creatinine, known CKD; cumulative effect with ACEi/ARB/MRA
Drug-induced — Recent ACEi/ARB/MRA/TMP-SMX initiation; review medication list
Rhabdomyolysis / tumor lysis — Elevated CK + hyperkalemia + hyperphosphatemia + hypocalcemia + AKI
Adrenal insufficiency — Hyperkalemia + hyponatremia + hypotension; ACTH stimulation test
Type 4 RTA — Hyperkalemia + non-gap metabolic acidosis in diabetic; mild hyperkalemia
DKA — Insulin deficiency shifts K out of cells; total body K is depleted despite hyperkalemia at presentation

Diagnostic workup

Diagnostic criteria

Confirmed serum K >5.0 mEq/L. ECG should be obtained urgently in any K >6.0 or any patient with cardiovascular symptoms or comorbidities.

Labs

BMP — confirm K elevation, assess creatinine and bicarbonate
Repeat sample if hemolysis suspected; whole blood K if pseudohyperkalemia suspected
CBC (high WBC or platelet count may cause pseudohyperkalemia)
ABG — assess for acidosis
CK if rhabdomyolysis suspected
Magnesium — concurrent low Mg makes K refractory to replacement; correct hypomagnesemia
Urine K and urine creatinine (TTKG historical, less used) to assess renal handling
Cortisol, aldosterone, renin if adrenal insufficiency or hypoaldosteronism suspected
Digoxin level if applicable

Imaging

Generally not indicated for hyperkalemia evaluation itself

Diagnostic algorithm

Treatment	Mechanism	Onset	Duration
Calcium gluconate 1-2 g IV	Stabilizes cardiac membrane (NOT lower K)	1-3 min	30-60 min
Insulin 10 U + D50 25 g IV	Shifts K intracellularly	15-30 min	2-6 h
Albuterol 10-20 mg neb	Beta-2 driven K shift	30 min	2-4 h
Sodium bicarbonate	Shifts K (less effective in CKD)	30-60 min	Hours
Furosemide IV	Renal K excretion	30 min-2 h	Hours
Patiromer / Na zirconium cyclosilicate	Binds K in GI tract	1-7 h	Sustained with daily dosing
Hemodialysis	Definitive K removal	Within minutes of initiation	Until next session

Stepwise treatment of acute hyperkalemia: stabilize → shift → remove.

Treatment

First-line

ECG immediately — guides urgency. ECG changes or K >6.5 → emergency treatment.
STABILIZE MEMBRANE (if ECG changes): IV calcium gluconate 1-2 g over 5-10 min (or calcium chloride 1 g via central line). Onset 1-3 min, duration 30-60 min. Repeat if no ECG improvement. CAUTION in digoxin toxicity — give slowly.
SHIFT K INTO CELLS:
Insulin 10 units IV + dextrose (D50 25 g) — onset 15-30 min, duration 2-6 h
Beta-2 agonist nebulized (albuterol 10-20 mg) — onset 30 min, additive with insulin
Sodium bicarbonate (if acidotic; less effective in CKD) — 50-100 mEq IV
REMOVE K FROM BODY:
Loop diuretic — furosemide, bumetanide — if kidney function and volume permit
Potassium binder — patiromer (oral, slower onset hours), sodium zirconium cyclosilicate (oral, onset 1 h)
Sodium polystyrene sulfonate (Kayexalate) — older agent; bowel necrosis risk especially with sorbitol; avoid in postoperative or ileus patients
Hemodialysis — definitive treatment for ESRD or severe refractory hyperkalemia
Stop contributing medications: ACEi/ARB/MRA, K-sparing diuretic, NSAID, TMP-SMX, supplements

Second-line / adjunct

Treat underlying cause (DKA — insulin; rhabdomyolysis — fluids; adrenal insufficiency — steroids)
Long-term prevention in CKD/HF: dietary K restriction, optimize diuretic, chronic potassium binder (patiromer, sodium zirconium cyclosilicate) to enable continued RAAS therapy
Repeat K every 2-4 h until stable
Cardiology consultation if persistent ECG changes or arrhythmia
Recheck K and ECG after each intervention

Complications

Cardiac arrhythmia: bradyarrhythmias, AV block, ventricular fibrillation, asystole
Sudden cardiac death
Muscle weakness/paralysis
Bowel necrosis from Kayexalate (especially with sorbitol)
Hypoglycemia from insulin treatment (monitor glucose hourly)
Discontinuation of beneficial RAAS therapy in heart failure / CKD without binders

PANCE pearls

Order of treatment in severe hyperkalemia: STABILIZE (calcium) → SHIFT (insulin/dextrose, beta-agonist, bicarbonate) → REMOVE (diuretic, binder, dialysis). 'C-BIG-K-Drop' mnemonic.
Calcium gluconate STABILIZES the cardiac membrane but does NOT lower potassium. Calcium chloride has 3× the elemental calcium of gluconate but causes tissue necrosis if extravasated.
Insulin + dextrose temporarily shifts K into cells but does not eliminate it; total body K unchanged.
Kayexalate (SPS) has limited efficacy and notable risk of intestinal necrosis. Patiromer and sodium zirconium cyclosilicate are preferred modern alternatives.
Pseudohyperkalemia clues: hemolyzed sample (mention by lab), discrepancy between serum and plasma K, severe thrombocytosis or leukocytosis. Always confirm before invasive treatment.
Patients with CKD or HF on ACEi/ARB benefit from chronic K binder therapy to maintain RAAS blockade — KDIGO 2024 endorsement.

Images

Hyperkalemia ECG progression — peaked T waves (early) → PR prolongation → QRS widening → sine wave (terminal)

References

KDIGO 2020 — KDIGO Controversies Conference on Potassium Management in Kidney Disease
AHA 2020 — AHA Adult Advanced Cardiac Life Support Guidelines (hyperkalemia in cardiac arrest)
Lindner et al. 2020 — Acute Hyperkalemia in the Emergency Department (J Emerg Med 2020)

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