Management of Hyperkalemia and Hypokalemia
The treatment of hyperkalemia requires a stepwise approach based on severity, with immediate measures for cardiac stabilization followed by potassium shifting and elimination, while hypokalemia treatment involves appropriate potassium replacement based on severity and underlying cause. 1, 2
Classification of Potassium Disorders
Hyperkalemia
- Mild hyperkalemia: 5.0-5.9 mEq/L 1
- Moderate hyperkalemia: 6.0-6.4 mEq/L 1
- Severe hyperkalemia: ≥6.5 mEq/L (life-threatening) 1
- ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of potassium level 1
Hypokalemia
- Mild hypokalemia: 3.0-3.5 mEq/L 3
- Moderate hypokalemia: 2.5-3.0 mEq/L 3
- Severe hypokalemia: <2.5 mEq/L 3
Management of Hyperkalemia
Step 1: Cardiac Membrane Stabilization (Immediate Effect)
- Administer intravenous calcium for cardiac protection: 1
- Effects begin within minutes but are temporary (30-60 minutes) 1
- Does not lower serum potassium but protects against arrhythmias 1
Step 2: Shift Potassium into Cells (Effect within 15-30 minutes)
- Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2
- Nebulized beta-2 agonists: 10-20 mg albuterol over 15 minutes 1, 4
- Effect begins within 15-30 minutes and lasts 4-6 hours 1
- Sodium bicarbonate: 50 mEq IV over 5 minutes (most effective in patients with concurrent metabolic acidosis) 1, 2
Step 3: Eliminate Potassium from Body (Longer-term Effect)
- Loop diuretics: furosemide 40-80 mg IV (effective only in patients with adequate renal function) 1, 5
- Potassium binders: 1, 5
- Hemodialysis: most effective method for severe hyperkalemia, especially in patients with renal failure 1, 6
Special Considerations for Hyperkalemia
- Temporary measures (insulin/glucose, albuterol) provide only transient effects (1-4 hours), and rebound hyperkalemia can occur 1
- Monitor potassium levels closely during treatment to avoid overcorrection 1
- Review and adjust medications that may contribute to hyperkalemia (ACE inhibitors, ARBs, MRAs, NSAIDs, beta-blockers) 1, 5
- For patients on RAAS inhibitors with K+ >5.0 mEq/L, initiate potassium-lowering agent while maintaining RAAS inhibitor therapy if possible 7, 5
- For severe hyperkalemia (>6.5 mEq/L) in patients on RAAS inhibitors, discontinue or reduce RAAS inhibitor and initiate potassium-lowering agent 7, 5
Management of Hypokalemia
Assessment and Treatment Approach
- Determine severity based on serum potassium level and symptoms 3, 8
- Evaluate for underlying causes: diuretic use, gastrointestinal losses, poor intake, transcellular shifts 8
- Consider digitalis toxicity risk when correcting hypokalemia in digitalized patients 3
Potassium Replacement
- Oral replacement preferred for mild to moderate hypokalemia without urgent indications 3, 8
- Intravenous replacement for severe hypokalemia or when oral route not feasible 3, 8
Monitoring and Follow-up
- Monitor serum potassium during replacement therapy 3
- For patients on diuretics, consider lower diuretic doses or potassium-sparing diuretics 3
- In digitalized patients, too rapid correction of hypokalemia can precipitate digitalis toxicity 3
Common Pitfalls to Avoid
For Hyperkalemia
- Delaying treatment when K+ >5.0 mEq/L in high-risk patients 5
- Discontinuing beneficial RAAS inhibitor therapy prematurely rather than managing hyperkalemia 7, 5
- Relying solely on temporary measures without addressing potassium elimination 1
- Overlooking rebound hyperkalemia after temporary treatments 1
For Hypokalemia
- Administering potassium too rapidly, which can cause cardiac arrhythmias 3
- Failing to identify and address the underlying cause 3, 8
- Overlooking the risk of digitalis toxicity when correcting hypokalemia in digitalized patients 3
- Using controlled-release potassium preparations in patients at risk for GI ulceration 3