What is the management of hyperkalemia?

Management of Hyperkalemia

For acute hyperkalemia with ECG changes or potassium ≥6.5 mEq/L, immediately administer IV calcium gluconate 15-30 mL of 10% solution over 2-5 minutes to stabilize cardiac membranes, followed simultaneously by insulin 10 units with 25g dextrose IV and nebulized albuterol 10-20 mg to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis. 1

Severity Classification and Initial Assessment

• Classify hyperkalemia severity: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L) 1
• Obtain an ECG immediately to assess for peaked T waves, flattened P waves, prolonged PR interval, or widened QRS—these findings mandate urgent treatment regardless of the exact potassium level 1, 2
• Verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment 1, 2

Critical caveat: ECG changes can be highly variable and less sensitive than laboratory values, but their presence indicates immediate life-threatening risk. Conversely, absent ECG changes do not exclude the need for urgent intervention if potassium is severely elevated. 1, 3

Acute Management Algorithm (K+ ≥6.5 mEq/L or ECG Changes)

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

• Administer IV calcium gluconate 10% solution: 15-30 mL (1.5-3 grams) over 2-5 minutes with continuous cardiac monitoring 1, 2
• If no ECG improvement within 5-10 minutes, repeat the dose of 15-30 mL IV over 2-5 minutes 1
• Duration of effect is only 30-60 minutes—calcium does NOT lower potassium, it only temporarily stabilizes cardiac membranes 1, 2

Critical pitfall: Never delay calcium administration while waiting for repeat lab confirmation if ECG changes are present. Never administer calcium through the same IV line as sodium bicarbonate as precipitation will occur. 1

Step 2: Shift Potassium Intracellularly (Onset: 15-30 minutes, Duration: 4-6 hours)

• Insulin 10 units regular IV with 25g dextrose (50 mL of 50% glucose) is the first-line agent for shifting potassium 4, 1, 3
• Nebulized albuterol 10-20 mg in 4 mL as adjunctive therapy, with effects lasting 2-4 hours 1
• Repeat insulin/glucose every 4-6 hours as needed if hyperkalemia persists, with careful monitoring of serum potassium and glucose every 2-4 hours 4

Critical pitfall: Never give insulin without glucose—hypoglycemia can be life-threatening. Patients with low baseline glucose, no diabetes, female sex, and altered renal function are at highest risk. Verify potassium is not below 3.3 mEq/L before administering insulin. 4, 1

Step 3: Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

• Administer sodium bicarbonate 50 mEq IV over 5 minutes ONLY if pH <7.35 and bicarbonate <22 mEq/L 4, 1
• Effects take 30-60 minutes to manifest and are mediated through increased distal sodium delivery and correction of acidosis 4, 1

Critical pitfall: Do not use sodium bicarbonate in patients without metabolic acidosis—it is ineffective and wastes time. 1

Step 4: Remove Potassium from the Body

• Loop diuretics (furosemide 40-80 mg IV) increase renal potassium excretion if adequate kidney function exists 1, 2
• Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially in patients with renal failure, oliguria, or cases unresponsive to medical management 4, 1, 5, 6

Important distinction: Calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. Failure to initiate definitive removal strategies will result in recurrent life-threatening hyperkalemia. 1

Chronic Hyperkalemia Management (K+ 5.0-6.5 mEq/L)

Medication Review and Adjustment

• Identify and eliminate contributing medications: NSAIDs, trimethoprim, heparin, potassium-sparing diuretics (spironolactone, amiloride, triamterene), beta-blockers, potassium supplements, and salt substitutes 1, 2
• For K+ 5.0-6.5 mEq/L: maintain RAAS inhibitor therapy and initiate approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) 1, 2
• For K+ >6.5 mEq/L: temporarily reduce or hold RAAS inhibitor until potassium <5.0 mEq/L, then restart at lower dose with concurrent potassium binder therapy 1

Critical principle: Do not permanently discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) in patients with cardiovascular disease or proteinuric CKD—these drugs provide mortality benefit and slow disease progression. Use potassium binders to enable continuation of life-saving medications. 1, 2, 7

Potassium Binder Therapy (Preferred Agents)

Sodium zirconium cyclosilicate (SZC/Lokelma):

• Starting dose: 10g three times daily for 48 hours, then 5-15g once daily for maintenance 1
• Onset of action: approximately 1 hour, making it suitable for more urgent outpatient scenarios 1
• Mechanism: exchanges hydrogen and sodium for potassium with highly selective binding 1

Patiromer (Veltassa):

• Starting dose: 8.4g once daily with food, titrated up to 25.2g daily based on potassium levels 1, 2
• Onset of action: approximately 7 hours 1
• Mechanism: exchanges calcium for potassium in the colon 1
• Separate from other oral medications by at least 3 hours 1
• Monitor magnesium levels as patiromer causes hypomagnesemia 1

Sodium polystyrene sulfonate (Kayexalate):

• Avoid this agent due to delayed onset, limited efficacy, and significant risk of bowel necrosis and fatal gastrointestinal injury 1, 2, 8
• FDA limitation: should not be used as emergency treatment for life-threatening hyperkalemia due to delayed onset of action 8

Diuretic Optimization

• Loop or thiazide diuretics (furosemide 40-80 mg daily) promote urinary potassium excretion by stimulating flow to renal collecting ducts 1, 2
• Titrate to maintain euvolemia, not primarily for potassium management 1

Fludrocortisone consideration: increases potassium excretion but carries significant risks of fluid retention, hypertension, and vascular injury—use cautiously and only when other options are exhausted. 1, 2

Monitoring Protocol

• Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2
• Reassess 7-10 days after initiating potassium binder therapy 1, 2
• High-risk patients require more frequent monitoring: those with chronic kidney disease, heart failure, diabetes, or history of hyperkalemia 1, 2
• For patients on potassium binders, monitor closely for hypokalemia, which may be even more dangerous than hyperkalemia 1

Special Population: Chronic Kidney Disease

• Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 1, 7
• Optimal potassium range is broader in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 CKD versus 3.5-5.0 mEq/L for stage 1-2 CKD 1
• Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk in hemodialysis patients 1

Special Population: Hemodialysis Patients

• First-line agent: sodium zirconium cyclosilicate 5g once daily on non-dialysis days, adjusted weekly in 5g increments based on predialysis potassium 1
• Second-line agent: patiromer 8.4g once daily with food, titrated up to 16.8g or 25.2g daily based on response 1
• Monitor for potassium rebound 4-6 hours post-dialysis as intracellular potassium redistributes to extracellular space 1
• Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels and interdialytic trends 1

Dietary Considerations

• Evidence linking dietary potassium intake to serum levels is limited, and a potassium-rich diet provides cardiovascular benefits including blood pressure reduction 1
• Newer potassium binders may allow for less restrictive dietary potassium restrictions, enabling patients to benefit from potassium-rich foods 1, 7
• Focus on reducing nonplant sources of potassium rather than blanket dietary restriction 7
• Avoid "low-salt" substitutes which have high potassium content 1

Team Approach

• Optimal chronic hyperkalemia management involves a multidisciplinary team: cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians 4, 1, 2
• Regular monitoring of serum potassium levels is crucial, especially when starting new medications 4
• Maintaining adequate hydration supports renal potassium excretion 4

Common Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 1
• Remember that calcium, insulin, and beta-agonists do not remove potassium from the body—they only temporize 1
• Ensure glucose is administered with insulin to prevent hypoglycemia 1
• Do not use sodium bicarbonate in patients without metabolic acidosis—it is only indicated when acidosis is present 1
• Avoid the triple combination of ACE inhibitor + ARB + MRA due to excessive hyperkalemia risk 1