How to manage a patient with hyperkalemia and hypertension?

Management of Hyperkalemia with Hypertension

In patients with hyperkalemia and hypertension, maintain RAAS inhibitor therapy (ACE inhibitors, ARBs) using newer potassium binders (patiromer or sodium zirconium cyclosilicate) rather than discontinuing these life-saving medications, as discontinuation leads to worse cardiovascular and renal outcomes. 1

Initial Assessment

Verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment 1. Classify severity as 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 complexes—these findings mandate urgent treatment regardless of potassium level 1. However, absent ECG changes do not exclude the need for intervention 2.

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

Cardiac Membrane Stabilization

• Administer calcium gluconate 10% solution: 15-30 mL (1.5-3 grams) IV over 2-5 minutes to stabilize cardiac membranes 1
• Effects begin within 1-3 minutes but are temporary (30-60 minutes) and do not reduce total body potassium 3, 1
• Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 1
• Continuous cardiac monitoring is mandatory during and after administration 1

Intracellular Potassium Shift

• Administer 10 units of regular insulin IV with 50 mL of 50% glucose (25 grams) as first-line therapy 2

• Onset of action within 15-30 minutes, effects last 4-6 hours 1

• Monitor glucose closely to prevent hypoglycemia, especially in patients with low baseline glucose, no diabetes history, female sex, or altered renal function 1

• Add nebulized albuterol 20 mg in 4 mL as adjunctive therapy 1

• Effects last 2-4 hours and can be repeated as needed 1

• Sodium bicarbonate should ONLY be used if concurrent metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1

• Do not use in patients without acidosis—it is ineffective and potentially harmful 1

Potassium Removal

• Administer loop diuretics (furosemide 40-80 mg IV) if adequate kidney function exists to increase renal potassium excretion 1
• Hemodialysis is the most reliable and effective method for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1, 4

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

Medication Optimization

Do NOT discontinue RAAS inhibitors permanently as this leads to worse cardiovascular and renal outcomes 1. Instead, implement the following algorithm:

For K+ 5.0-6.5 mEq/L:

• Initiate approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) 1
• Maintain RAAS inhibitor therapy at current dose 1
• Eliminate contributing medications: NSAIDs, trimethoprim, heparin, potassium supplements, salt substitutes 1

For K+ >6.5 mEq/L:

• Temporarily reduce or hold RAAS inhibitor 1
• Initiate potassium-lowering agent 1
• Restart RAAS inhibitor at lower dose once K+ <5.5 mEq/L with concurrent potassium binder therapy 1

Potassium Binder Selection

Patiromer (Veltassa): 5

• Starting dose: 8.4 grams once daily
• Titrate up to 25.2 grams daily based on potassium levels
• Onset of action: ~7 hours
• Separate from other oral medications by at least 3 hours 5

Sodium zirconium cyclosilicate (SZC/Lokelma): 1

• Acute phase: 10 grams three times daily for 48 hours
• Maintenance: 5-15 grams once daily
• Onset of action: ~1 hour
• Preferred for more rapid potassium reduction 1

Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, limited efficacy, and risk of bowel necrosis 1

Diuretic Therapy

Optimize loop or thiazide diuretics (furosemide 40-80 mg daily) to promote urinary potassium excretion if adequate renal function present 1. Titrate to maintain euvolemia, not primarily for potassium management 1.

Fludrocortisone increases potassium excretion but carries significant risks of fluid retention, hypertension, and vascular injury—use cautiously 3

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors 1. Reassess 7-10 days after initiating potassium binder therapy 1.

High-risk patients require more frequent monitoring: those with chronic kidney disease, heart failure, diabetes, or history of hyperkalemia 1.

Dietary Considerations

Do not routinely restrict dietary potassium as evidence linking dietary intake to serum levels is limited, and potassium-rich diets provide cardiovascular benefits including blood pressure reduction 1. If dietary modification is necessary, focus on reducing non-plant sources of potassium rather than eliminating all potassium-rich foods 6.

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
• 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 permanently discontinue RAAS inhibitors in patients with heart failure or proteinuric kidney disease—use potassium binders instead 1

Team Approach

Optimal management involves cardiologists, nephrologists, primary care physicians, nurses, pharmacists, and dietitians working collaboratively 3, 1.