How should hyperkalemia be managed, including assessment, membrane stabilization, intracellular potassium shift, potassium removal, and correction of underlying causes?

Hyperkalemia Treatment

For acute hyperkalemia with ECG changes or potassium ≥6.5 mEq/L, immediately administer IV calcium gluconate 10% (15-30 mL over 2-5 minutes) to stabilize the cardiac membrane, followed simultaneously by insulin 10 units IV with 25 grams dextrose and nebulized albuterol 10-20 mg to shift potassium intracellularly, then initiate definitive potassium removal with hemodialysis for severe cases or loop diuretics if renal function permits. 1, 2

Severity Classification and Initial Assessment

Classify hyperkalemia severity immediately:

• Mild: 5.0-5.5 mEq/L 1, 2
• Moderate: 5.5-6.0 mEq/L (some sources 6.0-6.4 mEq/L) 1, 2
• Severe: ≥6.0 mEq/L (or ≥6.5 mEq/L) 1, 2, 3

Obtain a 12-lead ECG immediately regardless of potassium level, looking for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes—these findings mandate urgent treatment even if potassium is only mildly elevated. 4, 1, 2 ECG changes are highly variable and less sensitive than laboratory values, but their presence indicates immediate cardiac risk. 4, 1

Rule out pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment. 4, 1, 5 Plasma potassium is typically 0.1-0.4 mEq/L lower than serum levels due to platelet potassium release during coagulation. 4

Acute Hyperkalemia Management Algorithm

Step 1: Cardiac Membrane Stabilization (Onset 1-3 minutes)

Administer IV calcium gluconate 10%: 15-30 mL over 2-5 minutes (or calcium chloride 10%: 5-10 mL if central access available) for any ECG changes or potassium ≥6.5 mEq/L. 4, 1, 2, 3 This protects against fatal arrhythmias but does NOT lower potassium levels. 4, 1, 2

• Effect duration: 30-60 minutes only 4, 1, 2
• Repeat dose: If no ECG improvement within 5-10 minutes, give another 15-30 mL 4, 1
• Critical caveat: Never delay calcium while awaiting repeat potassium levels if ECG changes are present 1
• Special population: In malignant hyperthermia, use calcium only in extremis due to myoplasmic calcium overload risk 1

Step 2: Intracellular Potassium Shift (Onset 15-30 minutes)

Administer all three agents simultaneously for maximum effect:

Insulin-Glucose Therapy (First-line):

• Dose: 10 units regular insulin IV push + 25 grams dextrose (50 mL D50W) 4, 1, 2, 3, 6
• Effect: Lowers potassium 0.5-1.2 mEq/L within 30-60 minutes 4, 1
• Duration: 4-6 hours 4, 1
• Monitoring: Check glucose every 30-60 minutes to prevent hypoglycemia 1
• Repeat dosing: Can repeat every 4-6 hours as needed, monitoring glucose and potassium every 2-4 hours 1
• High-risk patients: Those with low baseline glucose, no diabetes, female sex, or altered renal function are at higher hypoglycemia risk 1

Nebulized Beta-Agonist (Adjunctive):

• Dose: Albuterol 10-20 mg in 4 mL nebulized over 10-15 minutes 4, 1, 2, 3, 6
• Effect: Lowers potassium 0.5-1.0 mEq/L within 30 minutes 1
• Duration: 2-4 hours 4, 1
• Repeat: Can repeat every 2 hours if needed 1
• Additive benefit: Provides additional 0.5-1.0 mEq/L reduction beyond insulin-glucose alone 1

Sodium Bicarbonate (ONLY with metabolic acidosis):

• Indication: Use ONLY when pH <7.35 and bicarbonate <22 mEq/L 4, 1, 2
• Dose: 50 mEq IV over 5 minutes 4, 1, 6
• Onset: 30-60 minutes 1
• Mechanism: Promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release 4, 1
• Critical pitfall: Ineffective without documented acidosis—do not waste time 1, 7

Step 3: Definitive Potassium Removal

Hemodialysis (Most Reliable Method):

Absolute indications for urgent hemodialysis: 4, 1, 8

• Potassium >6.5 mEq/L unresponsive to medical therapy
• Oliguria or anuria
• End-stage renal disease
• Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)
• Severe renal impairment (eGFR <15 mL/min)
• Persistent ECG changes despite medical management

Hemodialysis removes potassium most effectively and reliably. 4, 1, 3, 7 In hemodynamically unstable patients, continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts. 1

Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes. 1

Loop Diuretics (If Adequate Renal Function):

• Dose: Furosemide 40-80 mg IV 4, 1, 2
• Requirement: eGFR >30 mL/min and adequate urine output 1
• Mechanism: Increases renal potassium excretion by stimulating flow to collecting ducts 4, 1
• Limitation: Effective only in non-oliguric patients with preserved kidney function 1

Potassium Binders (Sub-acute/Chronic Management):

Binder	Regimen	Onset	Key Points
Sodium zirconium cyclosilicate (SZC/Lokelma)	10 g TID × 48h, then 5-15 g daily	~1 hour	Suitable for urgent scenarios; reduces K+ within 1 hour [4,1,8]
Patiromer (Veltassa)	8.4 g daily with food, titrate to 25.2 g	~7 hours	Separate from other meds by ≥3 hours; for chronic control [4,1,8]
Sodium polystyrene sulfonate (Kayexalate)	AVOID	Variable	Risk of bowel necrosis, colonic ischemia; limited efficacy [4,1,7,8]

Medication Management During Acute Episode

Hold immediately when potassium >6.5 mEq/L: 1, 2

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
• NSAIDs
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
• Trimethoprim-containing agents
• Heparin
• Beta-blockers
• Potassium supplements and salt substitutes

After acute resolution (potassium <5.0 mEq/L):

• Restart RAAS inhibitors at lower dose—these provide mortality benefit in cardiovascular and renal disease 1, 8
• Initiate potassium binder (SZC or patiromer) to enable continuation of life-saving RAAS therapy 1, 8

Chronic Hyperkalemia Management

For patients on RAAS inhibitors with potassium 5.0-6.5 mEq/L:

• Initiate approved potassium-lowering agent (patiromer or SZC) while maintaining RAAS inhibitor therapy 4, 1, 8
• Do NOT permanently discontinue RAAS inhibitors—use binders to maintain these medications 1, 8

For patients with potassium >6.5 mEq/L:

• Temporarily discontinue or reduce RAAS inhibitor 4, 1
• Initiate potassium-lowering agent when levels >5.0 mEq/L 4, 1
• Restart RAAS inhibitor at lower dose once potassium <5.0 mEq/L with concurrent binder 1

Dietary modification:

• Limit high-potassium foods (bananas, oranges, potatoes, tomatoes, legumes, yogurt, chocolate) 2, 8
• Avoid salt substitutes containing potassium 4, 1, 2
• Evidence linking dietary potassium to serum levels is limited; focus on reducing non-plant sources 4, 8

Optimize diuretic therapy:

• Loop or thiazide diuretics promote urinary potassium excretion 4, 1, 2
• Titrate to maintain euvolemia, not primarily for potassium management 1

Monitoring Protocol

Acute phase:

• Recheck potassium 1-2 hours after insulin/glucose or beta-agonist therapy 1, 2
• Continue checks every 2-4 hours until stable 1, 2
• Obtain repeat ECG to confirm resolution of cardiac changes 1

Post-acute phase:

• Check potassium within 1 week after starting or escalating RAAS inhibitors 4, 1, 2
• Reassess 7-10 days after initiating potassium binder 4, 1, 2
• Individualize frequency based on eGFR, heart failure, diabetes, or hyperkalemia history 4, 1

High-risk patients requiring more frequent monitoring: 4, 1

• Chronic kidney disease (especially stage 4-5)
• Heart failure
• Diabetes mellitus
• History of recurrent hyperkalemia
• On multiple potassium-affecting medications

Critical Pitfalls to Avoid

Never delay calcium administration while awaiting repeat potassium levels when ECG changes are present—ECG abnormalities indicate urgent need regardless of exact potassium value. 1

Never give insulin without glucose—hypoglycemia can be fatal. 1

Recognize that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 4, 1, 2

Do not use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time. 1, 7

Do not permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications. 1, 8

Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 4, 1

Avoid sodium polystyrene sulfonate (Kayexalate)—significant risk of bowel necrosis and limited efficacy data. 4, 1, 7, 8

Special Populations

CKD patients (stage 4-5):

• Tolerate higher potassium levels (3.3-5.5 mEq/L) due to compensatory mechanisms 4, 1
• Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression 4, 1, 8
• Target potassium 4.0-5.0 mEq/L to minimize mortality risk 1

Dialysis patients:

• Hemodialysis is definitive treatment for severe hyperkalemia 4, 1, 3
• Target predialysis potassium 4.0-5.5 mEq/L 1
• Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on trends 1
• Potassium binders (particularly SZC) can reduce predialysis levels from >6.0 to <5.5 mEq/L 1

Heart failure patients:

• Both hypokalemia and hyperkalemia increase mortality—target 4.0-5.0 mEq/L 4, 1
• Maintain RAAS inhibitors and aldosterone antagonists using potassium binders 1, 8
• SGLT2 inhibitors may reduce hyperkalemia risk 1