Grade-Wise Management of Hyperkalemia
For hyperkalemia management, treatment intensity escalates based on three severity grades: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), and severe (≥6.5 mEq/L), with ECG changes mandating immediate aggressive therapy regardless of the absolute potassium level. 1, 2
Initial Assessment
Before initiating treatment, verify that hyperkalemia is not pseudohyperkalemia from hemolysis, repeated fist clenching, or inadequate phlebotomy technique by repeating the measurement with appropriate technique or arterial sampling 2, 3. Obtain an ECG immediately to check for peaked T waves (appearing at K+ >5.5 mEq/L), flattened P waves and prolonged PR interval (at 6.0-6.4 mEq/L), widened QRS complex (at >6.5 mEq/L), or sine-wave pattern/ventricular arrhythmias (at ≥7-8 mEq/L) 1, 3.
Mild Hyperkalemia (5.0-5.9 mEq/L)
Management Strategy
Do not initiate acute interventions such as calcium, insulin, or albuterol for mild hyperkalemia without ECG changes or symptoms. 2 Focus on identifying and eliminating reversible causes while preventing progression 2.
Medication Review and Adjustment
- Review and eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, and salt substitutes 2, 3
- For patients on RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) with cardiovascular disease or proteinuric CKD, do not discontinue these life-saving medications—instead initiate a potassium binder 1, 2
- Continue mineralocorticoid receptor antagonists if potassium ≤5.5 mEq/L; if potassium >5.5 mEq/L, reduce the MRA dose by 50% (e.g., spironolactone 25 mg to 12.5 mg or every other day) 3
Active Treatment
- Optimize diuretic therapy with loop diuretics (furosemide 40-80 mg daily) to increase urinary potassium excretion if eGFR >30 mL/min 2, 3
- Initiate potassium binders if RAAS inhibitors are required:
Monitoring
Check potassium within 1 week of starting or escalating RAAS inhibitors, and reassess 7-10 days after initiating potassium binder therapy 2, 3. Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 2.
Moderate Hyperkalemia (6.0-6.4 mEq/L)
Management Strategy
For moderate hyperkalemia without ECG changes, initiate intracellular shift therapies and potassium binders, reserving calcium for cases with electrocardiographic changes. 2
Step 1: Intracellular Potassium Shift (if no ECG changes)
Administer all three agents together for maximum effect 1:
- Insulin-glucose: 10 units regular insulin IV + 25 g dextrose (50 mL D50W) over 15-30 minutes; reduces K+ by 0.5-1.2 mEq/L within 30-60 minutes, lasts 4-6 hours 1, 2
- Nebulized albuterol: 10-20 mg in 4 mL over 10-15 minutes; reduces K+ by 0.5-1.0 mEq/L within 30 minutes, lasts 2-4 hours, can repeat every 2 hours 1, 2
- Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L); onset 30-60 minutes 1, 2
Critical caveat: Always administer glucose with insulin to prevent life-threatening hypoglycemia 1, 2. Monitor blood glucose closely, especially in patients with low baseline glucose, no diabetes history, female sex, or impaired renal function 3.
Step 2: Potassium Elimination
- Loop diuretics: Furosemide 40-80 mg IV if eGFR >30 mL/min and non-oliguric 2, 3
- Potassium binders: Initiate patiromer or SZC as described above for chronic management 2, 3
Medication Management
- Temporarily hold or reduce RAAS inhibitors until potassium <5.0 mEq/L 2, 3
- Hold NSAIDs, potassium-sparing diuretics, trimethoprim, heparin, beta-blockers, potassium supplements, and salt substitutes 2, 3
Monitoring
Re-measure serum potassium 1-2 hours after insulin/glucose or beta-agonist therapy, then every 2-4 hours until stable 1, 2.
Severe Hyperkalemia (≥6.5 mEq/L or Any ECG Changes)
Management Strategy
Severe hyperkalemia with ECG changes is a medical emergency requiring immediate three-step treatment: cardiac membrane stabilization, intracellular potassium shift, and definitive potassium removal. 1, 2, 4
Step 1: Cardiac Membrane Stabilization (IMMEDIATE)
Administer IV calcium first—this is the only immediate protection against fatal arrhythmias. 1, 2
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 1, 2
- Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred if central access available, more potent) 1, 2
- Onset: 1-3 minutes; duration: 30-60 minutes 1, 2
- Repeat dose if no ECG improvement within 5-10 minutes 1, 3
- Continuous cardiac monitoring is mandatory during and 5-10 minutes after administration 1, 2
Critical caveats:
- Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily 1, 2
- Never delay calcium administration while awaiting repeat potassium levels if ECG changes are present 1, 2
- Do not mix calcium with sodium bicarbonate in the same IV line (causes precipitation) 1
- Use calcium cautiously if elevated phosphate (risk of calcium-phosphate precipitation) 1, 3
Step 2: Intracellular Potassium Shift (SIMULTANEOUS with calcium)
Administer all three agents together for maximum effect 1, 2:
- Insulin-glucose: 10 units regular insulin IV + 25 g dextrose (50 mL D50W) over 15-30 minutes 1, 2
- Nebulized albuterol: 10-20 mg in 4 mL over 10-15 minutes 1, 2
- Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if pH <7.35 and bicarbonate <22 mEq/L 1, 2
The combined insulin-glucose plus nebulized beta-agonist regimen is more effective than either modality alone. 1, 5
Step 3: Definitive Potassium Removal
Choose based on renal function and clinical context 1, 2:
Hemodialysis (Most Effective and Reliable)
Hemodialysis is the gold-standard for rapid potassium removal. 1, 2, 4 Absolute indications include:
- Serum potassium >6.5 mEq/L unresponsive to medical therapy 1, 2
- Oliguria or anuria 1, 2
- End-stage renal disease 1, 2
- Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis) 1, 2
- eGFR <15 mL/min 1
- Persistent ECG changes despite medical management 1
In hemodynamically unstable patients (hypotensive, requiring vasopressors), continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts and reduce intradialytic hypotension risk 1.
Loop Diuretics
Furosemide 40-80 mg IV if eGFR >30 mL/min and adequate urine output 1, 2, 3.
Potassium Binders (Sub-acute Management)
- Sodium zirconium cyclosilicate (SZC): 10 g three times daily for 48 hours, then 5-15 g once daily; onset ~1 hour (suitable for urgent scenarios) 1, 2
- Patiromer: 8.4 g once daily with food; onset ~7 hours (for sub-acute/chronic control) 1, 2
- Sodium polystyrene sulfonate (Kayexalate): AVOID due to risk of bowel necrosis, colonic ischemia, and lack of efficacy data 1, 2, 3
Medication Management During Acute Episode
Temporarily hold when potassium >6.5 mEq/L: 1, 2
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
- NSAIDs
- Potassium-sparing diuretics
- Trimethoprim
- Heparin
- Beta-blockers
- Potassium supplements and salt substitutes
After Acute Resolution: Preventing Recurrence
- Restart RAAS inhibitors at a lower dose once potassium <5.0 mEq/L 1, 2
- Initiate patiromer or SZC to enable continuation of life-saving RAAS therapy 1, 2
- These medications provide mortality benefit in cardiovascular and renal disease 1, 2
Monitoring Protocol
- Re-measure serum potassium 1-2 hours after insulin/glucose or beta-agonist therapy 1
- Continue potassium checks every 2-4 hours until stable 1
- Obtain repeat ECG to confirm resolution of cardiac changes 1
- Check potassium within 1 week after initiating or escalating RAAS inhibitors 2
- Reassess 7-10 days after starting potassium binder 2
Critical Pitfalls to Avoid
- Never delay calcium administration while awaiting repeat potassium levels if ECG changes are present—ECG changes indicate urgent need regardless of exact potassium value 1, 2
- Never give insulin without glucose—hypoglycemia can be fatal 1, 2
- Never use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time 1, 2
- Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1, 2
- Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—use potassium binders to maintain these life-saving medications 1, 2
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 3
- Failure to initiate concurrent potassium-lowering therapies will result in recurrent life-threatening arrhythmias within 30-60 minutes after calcium's effect wears off 1
Special Populations
Chronic Kidney Disease
- Patients with advanced CKD (stage 4-5) tolerate higher potassium levels due to compensatory mechanisms 2, 3
- Optimal potassium range: 3.3-5.5 mEq/L for stage 4-5 CKD versus 3.5-5.0 mEq/L for stage 1-2 CKD 2
- Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk 2
- Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 2, 3
Pediatric Dosing
- Calcium gluconate: 100-200 mg/kg via slow IV infusion with ECG monitoring 1, 3
- Calcium chloride: 20 mg/kg (0.2 mL/kg of 10% solution) 1
- Dextrose: 200 mg/kg as D10W (not D50W in children) 1