Management of Hyperkalemia
Immediate Assessment and Risk Stratification
Verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or improper phlebotomy technique before initiating aggressive treatment 1, 2. Obtain an ECG immediately, as cardiac manifestations (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of the absolute potassium level 2, 3. However, absent or atypical ECG changes do not exclude the necessity for immediate intervention—ECG findings are highly variable and less sensitive than laboratory values 2, 4.
Classify severity: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L) 2, 3. Potassium >6.5 mEq/L or any ECG changes constitute a medical emergency requiring immediate treatment 3, 5.
Acute Management Algorithm
Step 1: Cardiac Membrane Stabilization (Immediate - Within 1-3 Minutes)
Administer intravenous calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present 2, 3. Calcium chloride (10%): 5-10 mL IV over 2-5 minutes is preferred over calcium gluconate because it provides more rapid increase in ionized calcium concentration 3. Alternatively, use calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 2, 3.
Monitor ECG continuously during administration 3. If no ECG improvement within 5-10 minutes, repeat the dose 2, 3. Critical caveat: calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes for 30-60 minutes 2, 3, 5. Never administer calcium through the same IV line as sodium bicarbonate, as precipitation will occur 3.
Step 2: Shift Potassium Intracellularly (Onset 15-30 Minutes, Duration 4-6 Hours)
Administer all three agents together for maximum effect 2:
Insulin with glucose: 10 units regular insulin IV with 25g dextrose (50 mL of D50W) over 15-30 minutes 2, 3. Verify potassium is not below 3.3 mEq/L before administering insulin 2. Monitor glucose closely to prevent hypoglycemia, especially in patients with low baseline glucose, no diabetes, female sex, or altered renal function 2.
Nebulized albuterol: 10-20 mg in 4 mL over 15 minutes 2, 3. This provides adjunctive therapy with short duration of effect (2-4 hours) 2.
Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 2, 3. Do not use in patients without metabolic acidosis—it is ineffective and wastes time 2.
These are temporizing measures only—rebound hyperkalemia can occur within 2-4 hours 3. Insulin/glucose can be repeated every 4-6 hours as needed, carefully monitoring potassium and glucose levels 2.
Step 3: Eliminate Potassium from Body (Definitive Treatment)
Loop diuretics: Furosemide 40-80 mg IV increases renal potassium excretion if adequate kidney function exists (eGFR >30 mL/min) 2, 3. Titrate to maintain euvolemia, not primarily for potassium management 2.
Newer potassium binders (preferred over sodium polystyrene sulfonate):
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance 2. Onset of action ~1 hour, making it suitable for urgent scenarios 2.
- Patiromer (Veltassa): 8.4g once daily with food, titrated up to 25.2g daily based on potassium levels 2. Onset of action ~7 hours 2. Separate from other oral medications by at least 3 hours 2, 6.
Sodium polystyrene sulfonate (Kayexalate): 15-60g orally or 30-50g rectally every 6 hours 6. However, this agent has significant limitations including delayed onset of action, risk of intestinal necrosis and bowel perforation (especially with sorbitol), and should be avoided for acute management 2, 6. Concomitant administration of sorbitol is not recommended 6.
Hemodialysis: The most reliable and effective method for severe hyperkalemia, especially in patients with renal failure, oliguria, or cases refractory to medical management 2, 3, 5, 4. Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes 2.
Medication Management
Immediately review and temporarily hold or reduce contributing medications 2:
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists): Hold if K+ >6.5 mEq/L 1, 2
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1, 2
- NSAIDs and COX-2 inhibitors 1, 2, 7
- Trimethoprim-sulfamethoxazole 1, 2
- Heparin 1, 2
- Beta-blockers 1, 2, 7
- Potassium supplements and salt substitutes 1, 2
Critical principle: Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD, as these provide mortality benefit and slow disease progression 1, 2. Instead, temporarily reduce or hold when K+ >6.5 mEq/L, then restart at lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy 2.
Chronic Hyperkalemia Management
For patients on RAAS inhibitors with K+ 5.0-6.5 mEq/L: Initiate patiromer or sodium zirconium cyclosilicate while maintaining RAAS inhibitor therapy 1, 2. This approach allows continuation of life-saving cardiovascular medications 1, 2, 8.
For patients with K+ >6.5 mEq/L: Discontinue or reduce RAAS inhibitor temporarily, initiate potassium-lowering agent when levels >5.0 mEq/L, and monitor closely 1, 2.
Optimize diuretic therapy with loop or thiazide diuretics to increase urinary potassium excretion 2. Consider fludrocortisone cautiously only when other options are exhausted, as it carries risks of fluid retention, hypertension, and vascular injury 2.
Monitoring Protocol
Check potassium within 1 week of starting or escalating RAAS inhibitors 2. Reassess 7-10 days after initiating potassium binder therapy 2. During acute treatment, monitor potassium every 2-4 hours until stabilized 2.
Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 2. High-risk patients (CKD, diabetes, heart failure, elderly) require more frequent monitoring 1, 2.
When initiating potassium-lowering therapy, monitor closely not only for efficacy but also to protect against hypokalemia, which may be even more dangerous than hyperkalemia 9, 2.
Special Populations
Patients with advanced CKD (stage 4-5): Tolerate higher potassium levels due to compensatory mechanisms, with optimal range 3.3-5.5 mEq/L versus 3.5-5.0 mEq/L for stage 1-2 CKD 2. Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 2.
Hemodialysis patients: Target predialysis potassium 4.0-5.5 mEq/L 2. Consider sodium zirconium cyclosilicate 5g once daily on non-dialysis days, adjusted weekly in 5g increments 2. Monitor for rebound hyperkalemia 4-6 hours post-dialysis 2.
Dietary Considerations
Evidence linking dietary potassium intake to serum levels is limited, and a potassium-rich diet provides cardiovascular benefits including blood pressure reduction 2. Stringent dietary restrictions may not be necessary in patients receiving potassium binder therapy 2. However, eliminate high-potassium salt substitutes and herbal supplements (alfalfa, dandelion, horsetail, nettle) 1, 2.
Critical Pitfalls to Avoid
- Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 2
- Never use sodium bicarbonate without metabolic acidosis—it is ineffective 2
- Never give insulin without glucose—hypoglycemia can be life-threatening 2
- Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 2, 3
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
- Avoid triple combination of ACE inhibitor + ARB + MRA due to excessive hyperkalemia risk 2