How should hyperkalemia be treated based on the serum potassium level and electrocardiogram changes?

Hyperkalemia Treatment Algorithm

Hyperkalemia treatment must be stratified by ECG changes and serum potassium level, with immediate intravenous calcium administration for any ECG abnormalities, followed by simultaneous therapies to shift potassium intracellularly (insulin/glucose plus albuterol) and definitive removal strategies based on renal function. 1, 2

Immediate Assessment

Obtain an ECG immediately—ECG changes indicate severe cardiotoxicity requiring urgent treatment regardless of the exact potassium value. 1, 2 Do not delay treatment while waiting for repeat laboratory confirmation if ECG changes are present. 3

ECG Progression in Hyperkalemia

The ECG follows a predictable sequence as potassium rises: 4, 1

• Peaked/tented T waves (earliest finding, typically K+ >5.5 mmol/L) 1, 2
• Flattened or absent P waves, prolonged PR interval (moderate hyperkalemia) 1
• Widened QRS complex, deepened S waves (K+ >6.5 mmol/L) 1
• Sine-wave pattern, idioventricular rhythms, ventricular fibrillation, or asystole (severe hyperkalemia, K+ >7-8 mmol/L) 1

Critical caveat: ECG changes are highly variable and not as sensitive as laboratory testing—the absence of ECG changes does not rule out dangerous hyperkalemia, particularly in patients with chronic kidney disease, diabetes, or heart failure who may tolerate higher levels without ECG manifestations. 1, 2, 3

Verify True Hyperkalemia

Rule out pseudohyperkalemia from hemolysis, repeated fist clenching, poor phlebotomy technique, or slow specimen processing when ECG findings don't match laboratory values. 1, 2, 3

Treatment Algorithm Based on Severity

SEVERE HYPERKALEMIA (K+ ≥6.5 mEq/L OR Any ECG Changes)

Administer ALL therapies simultaneously for maximum effect—do not wait for one to work before starting the next. 1, 3

Step 1: Cardiac Membrane Stabilization (IMMEDIATE)

Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes OR calcium chloride 10%: 5-10 mL IV over 2-5 minutes 1, 2, 3

• Onset: 1-3 minutes; Duration: 30-60 minutes 1, 3
• Monitor ECG continuously during and for 5-10 minutes after administration 1, 3
• If no ECG improvement within 5-10 minutes, repeat the dose 1, 3
• Critical: Calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes 1, 3
• Never administer calcium through the same IV line as sodium bicarbonate (precipitation will occur) 3
• Use calcium cautiously in patients with elevated phosphate levels (risk of calcium-phosphate precipitation) 3

Step 2: Shift Potassium Intracellularly (SIMULTANEOUS)

Give all three agents together for additive effect: 1, 2, 3

Insulin + Glucose:

• 10 units regular insulin IV + 25g glucose (50 mL D50) over 15-30 minutes 1, 2, 3
• Onset: 15-30 minutes; Duration: 4-6 hours 3
• Monitor blood glucose closely to prevent hypoglycemia 2, 3
• Can be repeated every 4-6 hours if hyperkalemia persists 3

Nebulized Albuterol:

• 10-20 mg nebulized over 15 minutes 1, 2, 3
• Onset: 15-30 minutes; Duration: 2-4 hours 3
• Provides additive benefit when combined with insulin/glucose 1, 2

Sodium Bicarbonate (ONLY if metabolic acidosis present):

• 50 mEq IV over 5 minutes 1, 2, 3
• ONLY use if pH <7.35 and bicarbonate <22 mEq/L 1, 3
• Onset: 30-60 minutes 3
• Poor efficacy when used alone; ineffective without concurrent acidosis 1, 3

Step 3: Remove Potassium from Body (DEFINITIVE)

Loop Diuretics (if adequate renal function):

• Furosemide 40-80 mg IV 1, 3
• Titrate to maintain euvolemia, not primarily for potassium management 3

Hemodialysis (most effective method):

• Reserved for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 3, 5
• Most reliable and effective method for potassium removal 3
• Monitor for rebound hyperkalemia within 4-6 hours post-dialysis 3

Newer Potassium Binders (for ongoing management):

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily 3
  • Onset: ~1 hour 3
• Patiromer (Veltassa): 8.4g once daily, titrated up to 25.2g daily 3
  • Onset: ~7 hours 3
  • Separate from other oral medications by at least 3 hours 3

Avoid sodium polystyrene sulfonate (Kayexalate): Significant limitations including delayed onset, risk of bowel necrosis, and intestinal ischemia. 3, 5

Step 4: Medication Review

Temporarily discontinue or reduce: 3

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) if K+ >6.5 mEq/L 3
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 3
• NSAIDs 3
• Trimethoprim 3
• Heparin 3
• Beta-blockers 3
• Potassium supplements and salt substitutes 3

MODERATE HYPERKALEMIA (K+ 6.0-6.4 mEq/L, No ECG Changes)

Shift potassium intracellularly and initiate potassium removal: 3

• Insulin + glucose: 10 units regular insulin IV + 25g glucose 3
• Nebulized albuterol: 10-20 mg 3
• Loop diuretics if adequate renal function 3
• Initiate potassium binder (patiromer or SZC) 3
• Reduce RAAS inhibitor dose by 50% (e.g., spironolactone 25mg to 12.5mg) 3
• Check potassium within 1-2 hours after initial interventions 2

MILD HYPERKALEMIA (K+ 5.0-5.9 mEq/L, No ECG Changes)

Do NOT initiate acute interventions (calcium, insulin, albuterol) for mild hyperkalemia without ECG changes or symptoms. 3

Management approach: 3

• Review and eliminate contributing medications (NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes) 3
• Consider loop diuretics (furosemide 40-80 mg daily) if adequate renal function 3
• For patients on RAAS inhibitors with K+ 5.0-6.5 mEq/L: Initiate potassium binder (patiromer or SZC) and MAINTAIN RAAS inhibitor therapy 3
• Check potassium within 1 week 3

Special Population: Chronic Kidney Disease

Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression and provide mortality benefit. 3 Do not permanently discontinue RAAS inhibitors due to hyperkalemia. 3

Optimal potassium range in advanced CKD: 3

• Stage 4-5 CKD: 3.3-5.5 mEq/L 3
• Stage 1-2 CKD: 3.5-5.0 mEq/L 3

For CKD patients with K+ >6.5 mEq/L: 3

• Temporarily hold or reduce RAAS inhibitor 3
• Initiate potassium binder 3
• Restart RAAS inhibitor at lower dose once K+ <5.0 mEq/L 3

Monitoring Protocol

Continuous cardiac monitoring is essential throughout treatment. 1, 2

Recheck potassium: 2, 3

• Within 1-2 hours after initial interventions for severe/moderate hyperkalemia 2
• Every 2-4 hours after insulin administration 3
• Within 1 week of starting or escalating RAAS inhibitors 3
• 7-10 days after initiating potassium binder therapy 3

Monitor blood glucose closely after insulin administration to prevent hypoglycemia. 2, 3

Monitor magnesium levels in patients on patiromer (risk of hypomagnesemia). 3

Critical Pitfalls to Avoid

Never delay calcium administration when ECG changes are present—it works within 1-3 minutes to prevent cardiac arrest. 1, 2

Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 3

Never use sodium bicarbonate in patients without metabolic acidosis—it is only indicated when pH <7.35 and bicarbonate <22 mEq/L. 1, 3

Never give insulin without glucose—hypoglycemia can be life-threatening. 3

Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize. 3 Definitive removal strategies (diuretics, binders, dialysis) must be initiated simultaneously.

Never permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD—use potassium binders to enable continuation of these life-saving medications. 3