What are the steps for managing hyperkalemia?

Hyperkalemia Management

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 cardiac membranes, followed by insulin 10 units with 50 mL of 50% dextrose IV and nebulized albuterol 20 mg to shift potassium intracellularly. 1, 2

Classification and Initial Assessment

Before initiating treatment, verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique or arterial sampling. 2, 3

Severity classification:

• Mild: 5.0-5.9 mEq/L 2, 3
• Moderate: 6.0-6.4 mEq/L 2, 3
• Severe: ≥6.5 mEq/L 2, 3

Obtain an ECG immediately to look for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes—these findings indicate urgent treatment regardless of potassium level. 2 However, do not rely solely on ECG findings as they are highly variable and less sensitive than laboratory tests; absent or atypical ECG changes do not exclude the necessity for immediate intervention. 2, 4

Acute Management Algorithm

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

Administer IV calcium immediately if:

• Potassium >6.5 mEq/L 2, 5
• Any ECG changes present 2, 4

Dosing options:

• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 6, 2
• Calcium chloride (10%): 5-10 mL IV over 2-5 minutes 2

The effects begin within 1-3 minutes but are temporary (30-60 minutes) and do not reduce serum potassium—this only temporizes while other treatments take effect. 2 Critical caveat: In patients with malignant hyperthermia and hyperkalemia, calcium should only be used in extremis as it may contribute to calcium overload of the myoplasm. 2

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

First-line combination therapy:

• Insulin 10 units IV with 50 mL of 50% dextrose (or 25 grams glucose) 1, 2
• PLUS nebulized albuterol 20 mg in 4 mL 1, 2

This combination provides additive effects. 1, 4 Insulin and beta-agonists redistribute potassium to the intracellular space but do not reduce total body potassium. 1 Beta-agonists have a short duration of effect (2-4 hours), and glucose must be administered with insulin to prevent hypoglycemia. 1, 2

Important monitoring: Verify that potassium levels are not below 3.3 mEq/L before administering insulin. 2 Patients with low baseline glucose, no history of diabetes mellitus, female sex, and altered renal function are at higher risk of hypoglycemia. 2 Monitor glucose and potassium levels every 2-4 hours after initial administration. 2

Repeat dosing: If hyperkalemia persists or recurs after 4-6 hours, the dose of insulin with glucose can be repeated. 2, 4

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

Administer sodium bicarbonate IV only if:

• Metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2

Do not use sodium bicarbonate in patients without metabolic acidosis—it is only indicated when acidosis is present. 2 Sodium bicarbonate promotes potassium excretion through increased distal sodium delivery and counters the release of potassium into the blood caused by metabolic acidosis. 6, 2 Effects take 30-60 minutes to manifest. 2

Step 4: Potassium Removal from Body

Diuretics (for patients with adequate kidney function and hypervolemia):

• Furosemide 40-80 mg IV increases renal potassium excretion 2, 4
• Loop or thiazide diuretics promote urinary potassium excretion by stimulating flow to renal collecting ducts 6, 2

Hemodialysis (most effective method for potassium removal):

• Indicated for severe cases unresponsive to medical management 1, 6
• Required in patients with oliguria or end-stage renal disease 1, 2
• Most reliable method to remove potassium from the body 2, 5

Chronic Management

Medication Review and Optimization

Review and adjust medications that may contribute to hyperkalemia: ACE inhibitors, ARBs, mineralocorticoid antagonists (MRAs), NSAIDs, and beta-blockers. 2 However, maximum RAAS inhibitor therapy should be considered when indicated, as tolerated. 1 Hyperkalemia should be treated if it develops, and reinitiation of RAAS inhibitors (if discontinued) should be considered after resolution of acute hyperkalemia. 1

RAAS inhibitor management algorithm:

• Potassium >5.0 mEq/L: Initiate an approved potassium-lowering agent and maintain RAAS inhibitor therapy unless an alternative treatable cause is identified 2
• Potassium >6.5 mEq/L: Discontinue or reduce RAAS inhibitors temporarily, initiate a potassium-lowering agent, and monitor potassium levels closely 2

Potassium Binders

Newer FDA-approved agents (preferred for long-term management):

• Patiromer 6, 2, 3
• Sodium zirconium cyclosilicate 6, 2, 3

These newer potassium binders may facilitate optimization of RAAS inhibitor therapy in patients with heart failure. 1, 3 Avoid chronic use of sodium polystyrene sulfonate (SPS) alone or in combination with sorbitol due to possible severe gastrointestinal side effects including intestinal necrosis. 3, 7 Additionally, sodium polystyrene sulfonate should not be used as emergency treatment for life-threatening hyperkalemia because of its delayed onset of action. 7

Alternative agents:

• Fludrocortisone increases potassium excretion but carries risks of fluid retention, hypertension, and vascular injury 6, 2

Dietary Modifications

Provide orientation on low potassium diets and monitor patients' adherence. 8 Maintaining adequate hydration supports renal potassium excretion. 6

Monitoring Protocol

After acute episode resolution:

• Reassess potassium within 1 week of starting or escalating RAAS inhibitors 1, 2
• Check potassium 7-10 days after starting or increasing RAAS inhibitor doses 2

High-risk patients requiring more frequent monitoring:

• Chronic kidney disease 2
• Heart failure 2
• Diabetes mellitus 2
• History of hyperkalemia 2

Special Populations

Patients with cardiovascular disease on RAAS inhibitors: Require careful monitoring of potassium levels, with assessment 7-10 days after starting or increasing doses. 2

Patients with diabetic nephropathy: May develop hyperkalemia from hyporeninemic hypoaldosteronism syndrome. 9

Patients requiring thromboprophylaxis: Maintain thromboprophylaxis in patients with mild or moderate hyperkalemia, and consider temporary suspension only in cases of severe hyperkalemia. 3 The use of newer potassium binders (patiromer or sodium zirconium cyclosilicate) may allow safe continuation of thromboprophylaxis in patients with hyperkalemia. 3

Key Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Remember that calcium, insulin, and beta-agonists do not remove potassium from the body—they only temporize 2
• Ensure glucose is administered with insulin to prevent hypoglycemia 2
• Do not use sodium bicarbonate in patients without metabolic acidosis 2
• Identify and remove other potential risk factors for hyperkalemia whenever possible 1

Team Approach

Optimal management involves cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians working collaboratively. 6, 2