Hyperkalemia: Treatment Guidelines and ECG Changes
ECG Changes in Hyperkalemia
ECG changes indicate urgent treatment regardless of the absolute potassium level. 1
The characteristic ECG findings progress with increasing severity of hyperkalemia 1:
- Peaked T waves - typically the earliest finding, appearing tall, narrow, and symmetric 1
- Flattened or absent P waves - indicating atrial paralysis 1
- Prolonged PR interval - reflecting impaired atrial conduction 1
- Widened QRS complex - a dangerous sign indicating ventricular conduction delay 1
Critical caveat: ECG findings are highly variable and less sensitive than laboratory tests—do not rely solely on ECG to rule out severe hyperkalemia. 1 Some patients with life-threatening hyperkalemia may have minimal or no ECG changes, while others develop severe abnormalities at lower potassium levels. 1
Classification of Hyperkalemia Severity
The European Society of Cardiology classifies hyperkalemia as 1:
- Mild: 5.0-5.9 mEq/L
- Moderate: 6.0-6.4 mEq/L
- Severe: ≥6.5 mEq/L
However, treatment decisions should prioritize ECG changes and clinical context over arbitrary thresholds alone. 1 A patient with potassium 5.8 mEq/L and peaked T waves requires more aggressive treatment than an asymptomatic patient with potassium 6.2 mEq/L and normal ECG. 1
Acute Hyperkalemia Management Algorithm
Step 1: Cardiac Membrane Stabilization (if ECG changes present)
Administer IV calcium immediately for any patient with ECG changes or potassium >6.5 mEq/L. 1
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1
- OR Calcium chloride 10%: 5-10 mL IV over 2-5 minutes 1
Onset: 1-3 minutes | Duration: 30-60 minutes 1
Critical understanding: Calcium does NOT lower potassium—it only temporarily stabilizes cardiac membranes. 1 If no ECG improvement within 5-10 minutes, repeat the dose. 1 Continuous cardiac monitoring is mandatory during and after administration. 1
Special consideration: In malignant hyperthermia with hyperkalemia, calcium should only be used in extremis as it may contribute to calcium overload of the myoplasm. 1
Step 2: Shift Potassium Intracellularly
Administer all three agents together for maximum effect: 1
Insulin + Glucose 1:
- Regular insulin 10 units IV (some protocols use 0.1 units/kg, approximately 5-7 units in adults) 1
- PLUS 25g dextrose (50 mL of D50W) if glucose >250 mg/dL, give insulin alone 1
- Onset: 15-30 minutes | Duration: 4-6 hours 1
- Can be repeated every 4-6 hours if hyperkalemia persists 1
- Monitor glucose every 2-4 hours to prevent hypoglycemia 1
Nebulized Albuterol 1:
Sodium Bicarbonate (ONLY if metabolic acidosis present) 1:
- 50 mEq IV over 5 minutes 1
- Use ONLY when pH <7.35 and bicarbonate <22 mEq/L 1
- Onset: 30-60 minutes 1
- Do not use without documented acidosis—it is ineffective and wastes time 1
Critical pitfall: Never give insulin without glucose—hypoglycemia can be life-threatening. 1 Patients at higher risk include those with low baseline glucose, no diabetes history, female sex, and altered renal function. 1
Step 3: Remove Potassium from the Body
Choose based on renal function and clinical urgency: 1
Loop Diuretics (if adequate kidney function) 1:
- Furosemide 40-80 mg IV 1
- Increases renal potassium excretion by stimulating flow to collecting ducts 1
- Should be titrated to maintain euvolemia, not primarily for potassium management 1
Potassium Binders 1:
Sodium zirconium cyclosilicate (SZC/Lokelma):
Patiromer (Veltassa):
Hemodialysis 1:
- Most effective and reliable method for severe hyperkalemia 1
- Reserved for: severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1
- Potassium can rebound 2-4 hours post-dialysis as intracellular potassium redistributes 1
Avoid sodium polystyrene sulfonate (Kayexalate): Significant limitations including delayed onset, risk of bowel necrosis, and lack of efficacy data. 1
Medication Management During Acute Episode
Temporarily discontinue or reduce at K+ >6.5 mEq/L: 1
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) 1
- NSAIDs 1
- Potassium-sparing diuretics 1
- Trimethoprim 1
- Heparin 1
- Beta-blockers 1
- Potassium supplements and salt substitutes 1
Critical principle: Do not permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease. 1 Once potassium <5.5 mEq/L, restart at lower dose with concurrent potassium binder therapy. 1
Chronic/Recurrent Hyperkalemia Management
For patients on RAAS inhibitors with K+ 5.0-6.5 mEq/L: 1
- Initiate approved potassium-lowering agent (patiromer or SZC) 1
- Maintain RAAS inhibitor therapy unless alternative treatable cause identified 1
- This approach allows continuation of life-saving cardiovascular medications 1
For patients on RAAS inhibitors with K+ >6.5 mEq/L: 1
- Discontinue or reduce RAAS inhibitor temporarily 1
- Initiate potassium-lowering agent when levels >5.0 mEq/L 1
- Restart RAAS inhibitor at lower dose once potassium controlled 1
Monitoring Protocol
Check potassium within 1 week of starting or escalating RAAS inhibitors 1, especially in high-risk patients with:
After acute treatment: 1
- Recheck potassium every 2-4 hours initially until stabilized 1
- After insulin/glucose or beta-agonist therapy, recheck within 1-2 hours (effects wear off in 2-6 hours) 1
- After initiating potassium binder, reassess at 7-10 days 1
Individualize monitoring frequency based on: 1
- eGFR and CKD stage 1
- Presence of heart failure or diabetes 1
- History of recurrent hyperkalemia 1
- Concurrent medications affecting potassium 1
Common Pitfalls to Avoid
- Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 1
- Never use sodium bicarbonate without metabolic acidosis—it is ineffective 1
- Never give insulin without glucose 1
- Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
- Failure to discontinue or reduce RAAS inhibitors when K+ exceeds 6.0 mEq/L can lead to refractory hyperkalemia 1
Special Population: Patients with CKD
Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression. 1