Hyperkalemia Workup and Management
Initial Assessment and Classification
Immediately obtain an ECG and verify the potassium level is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment. 1
Severity Classification
- Mild hyperkalemia: 5.0-5.9 mEq/L 1
- Moderate hyperkalemia: 6.0-6.4 mEq/L 1, 2
- Severe hyperkalemia: ≥6.5 mEq/L 1, 2
ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of the absolute potassium level. 1 However, absent or atypical ECG changes do not exclude the necessity for immediate intervention. 3
Initial Laboratory Workup
- Complete metabolic panel (electrolytes, BUN, creatinine, glucose) 1
- Complete blood count 1
- Urinalysis 1
- Venous blood gas if metabolic acidosis suspected 1
- Magnesium level 1
Acute Hyperkalemia Management
Step 1: Cardiac Membrane Stabilization (if K+ ≥6.5 mEq/L OR any ECG changes)
Administer IV calcium immediately—this is the first priority to prevent fatal arrhythmias. 1, 2
- 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 1, 2
- Duration: 30-60 minutes (temporary only) 1, 2
- Repeat dose: If no ECG improvement within 5-10 minutes, give second dose 1
- Critical caveat: Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily 1, 2
Continuous cardiac monitoring is mandatory during and after calcium administration. 1
Step 2: Shift Potassium Intracellularly
Administer all three agents together for maximum effect: 1
Insulin + Glucose (First-line)
- Insulin: 10 units regular insulin IV 1
- Glucose: 25g dextrose (50 mL of 50% dextrose) IV 1
- Onset: 15-30 minutes 1, 2
- Duration: 4-6 hours 1, 2
- Can be repeated every 4-6 hours as needed 1
- Monitor glucose closely to prevent hypoglycemia 1
Beta-2 Agonist
- Albuterol: 10-20 mg nebulized in 4 mL over 10 minutes 1, 3
- Onset: 15-30 minutes 1
- Duration: 2-4 hours 1
- Can be repeated as needed 1
Sodium Bicarbonate (ONLY if metabolic acidosis present)
- Indication: pH <7.35, bicarbonate <22 mEq/L 1
- Dose: 50 mEq IV over 5 minutes 1
- Onset: 30-60 minutes 1
- Do NOT use without metabolic acidosis—it is ineffective and wastes time 1, 2
Step 3: Remove Potassium from the Body
Loop Diuretics (if adequate renal function)
Hemodialysis (most effective method)
- Indications: 1, 2
- Severe hyperkalemia unresponsive to medical management
- Oliguria or end-stage renal disease
- Acute kidney injury with rising potassium
- Most reliable method for potassium removal 1, 4
Potassium Binders (for subacute/chronic management)
- Sodium zirconium cyclosilicate (SZC/Lokelma): 1
- Acute: 10g three times daily for 48 hours
- Maintenance: 5-15g once daily
- Onset: ~1 hour
- Patiromer (Veltassa): 1
- Starting dose: 8.4g once daily with food
- Titrate up to 25.2g daily based on response
- Onset: ~7 hours
- Separate from other oral medications by 3 hours
- Avoid sodium polystyrene sulfonate (Kayexalate): Delayed onset, limited efficacy, risk of bowel necrosis 1, 2
Chronic Hyperkalemia Management
Medication Review and Adjustment
Do NOT permanently discontinue RAAS inhibitors—these provide mortality benefit in cardiovascular and renal disease. 1, 2
Algorithm for RAAS Inhibitor Management:
- K+ 5.0-6.5 mEq/L: 1, 2
- Initiate potassium binder (patiromer or SZC)
- Maintain RAAS inhibitor therapy
- Monitor closely
- K+ >6.5 mEq/L: 1, 2
- Temporarily discontinue or reduce RAAS inhibitor
- Initiate potassium binder
- Restart RAAS inhibitor at lower dose once K+ <5.0 mEq/L
Medications to Review/Discontinue:
- NSAIDs 1, 2
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1
- Trimethoprim 1
- Heparin 1
- Beta-blockers 1
- Potassium supplements 1
- Salt substitutes (high potassium content) 1, 2
Dietary Modifications
Evidence linking dietary potassium intake to serum levels is limited, and potassium-rich diets provide cardiovascular benefits. 1 Focus on:
- Reducing nonplant sources of potassium 5
- Avoiding processed foods high in bioavailable potassium 1
- Eliminating salt substitutes 1, 2
Monitoring Protocol
- After starting/escalating RAAS inhibitors: Check K+ within 7-10 days 1, 2
- After initiating potassium binder: Check K+ within 1 week 1
- High-risk patients (CKD, heart failure, diabetes): More frequent monitoring 1, 2
- Ongoing: Every 1-2 weeks until stable, then at 3 months, then every 6 months 1
Special Populations
Chronic Kidney Disease
- Stage 4-5 CKD: Optimal K+ range 3.3-5.5 mEq/L (broader than normal) 1
- Target K+ 4.0-5.0 mEq/L minimizes mortality risk 1
- Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression 1, 2
Heart Failure
- Both hypokalemia and hyperkalemia increase mortality 1
- Target K+ 4.0-5.0 mEq/L strictly 1
- Use potassium binders to enable continuation of RAAS inhibitors 1, 2
Dialysis Patients
- Target predialysis K+ 4.0-5.5 mEq/L 1
- Monitor for rebound hyperkalemia 4-6 hours post-dialysis 1
- Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) 1
Critical Pitfalls to Avoid
- Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
- Do NOT use sodium bicarbonate without metabolic acidosis—it is only indicated when acidosis is present 1, 2
- Do NOT forget to administer glucose with insulin—hypoglycemia can be life-threatening 1
- Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 1, 2
- Do NOT delay treatment while waiting for repeat lab confirmation if ECG changes are present 1
- Do NOT permanently discontinue RAAS inhibitors—use potassium binders instead 1, 2
- Do NOT ignore magnesium levels—hypomagnesemia can affect potassium homeostasis 1
Team Approach
Optimal chronic hyperkalemia management involves a multidisciplinary team: cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians. 1