Management of Hyperkalemia

Immediate Assessment and Risk Stratification

First, verify that hyperkalemia is real—not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique—by repeating the measurement with proper technique or arterial sampling. 1, 2

Classify severity based on potassium level and ECG findings: 1, 3, 2

Mild: 5.0–5.9 mEq/L
Moderate: 6.0–6.4 mEq/L
Severe: ≥6.5 mEq/L

Obtain an ECG immediately in all patients with potassium >5.5 mEq/L. 1 ECG changes progress predictably: peaked T waves (K+ >5.5 mEq/L) → flattened P waves and prolonged PR interval (K+ 6.0–6.4 mEq/L) → widened QRS and deepened S waves (K+ >6.5 mEq/L) → sine-wave pattern, ventricular fibrillation, or asystole (K+ ≥7–8 mEq/L). 1, 3 However, ECG changes are highly variable and less sensitive than laboratory values—their absence does not rule out dangerous hyperkalemia. 1, 3

Emergency Cardiac Stabilization (K+ ≥6.5 mEq/L or Any ECG Changes)

Administer intravenous calcium immediately—do not delay while awaiting repeat potassium levels if ECG changes are present. 1, 3, 2

Calcium Administration

Calcium gluconate 10%: 15–30 mL IV over 2–5 minutes (preferred for peripheral access) 1, 3, 2
Calcium chloride 10%: 5–10 mL (500–1000 mg) IV over 2–5 minutes (use central line if available) 1, 3

Onset: 1–3 minutes. Duration: 30–60 minutes. 1, 3 Calcium does not lower serum potassium—it only stabilizes the cardiac membrane temporarily. 1, 3, 2

Monitor ECG continuously during and for 5–10 minutes after administration. 3 If no ECG improvement within 5–10 minutes, repeat the same dose. 1, 3

Critical pitfall: Never administer calcium through the same IV line as sodium bicarbonate—precipitation will occur. 3 Use calcium cautiously in patients with elevated phosphate (risk of calcium-phosphate precipitation). 3

Intracellular Potassium Shifting

Administer all three agents together for maximum effect: 3

1. Insulin + Glucose (First-Line)

Insulin: 10 units regular insulin IV 1, 3, 2
Glucose: 25 g dextrose (50 mL of D50) IV over 15–30 minutes 1, 3, 2

Onset: 15–30 minutes. Duration: 4–6 hours. 1, 3 Always give glucose with insulin to prevent life-threatening hypoglycemia. 1, 3, 2 Monitor glucose every 2–4 hours after administration. 1 Patients with low baseline glucose, no diabetes, female sex, and altered renal function are at higher risk of hypoglycemia. 1

2. Nebulized Albuterol (Adjunctive)

Albuterol: 10–20 mg in 4 mL nebulized over 10–15 minutes 1, 3, 2

Onset: 15–30 minutes. Duration: 2–4 hours. 1, 3 Augments insulin/glucose effect by an additional 0.5–1.0 mEq/L reduction. 3 The combined insulin-glucose plus beta-agonist regimen is more effective than either alone. 3

3. Sodium Bicarbonate (Only with Metabolic Acidosis)

Sodium bicarbonate: 50 mEq IV over 5 minutes 1, 3, 2

Use ONLY if metabolic acidosis is documented (pH <7.35, bicarbonate <22 mEq/L). 1, 3, 2 Sodium bicarbonate is ineffective as monotherapy without acidosis and wastes time. 1, 3 Onset: 30–60 minutes (slower than insulin or beta-agonists). 1, 3

Potassium Removal from the Body

Calcium, insulin, and beta-agonists are temporizing measures only—they do not remove potassium from the body. 1, 3, 2 Definitive treatment requires potassium elimination.

Loop Diuretics (If Adequate Renal Function)

Furosemide: 40–80 mg IV 1, 3, 2

Effective only when eGFR >30 mL/min and urine output is adequate. 3 Titrate to maintain euvolemia, not primarily for potassium management. 3

Hemodialysis (Most Effective Method)

Hemodialysis is the most reliable and effective method for severe hyperkalemia. 1, 3, 4

Indications: 1, 3

K+ >6.5 mEq/L unresponsive to medical therapy
Oliguria or end-stage renal disease
Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)

Monitor for rebound hyperkalemia within 4–6 hours post-dialysis as intracellular potassium redistributes to the extracellular space. 3 Patients with severe initial hyperkalemia (>6.5 mEq/L) require more frequent monitoring (every 2–4 hours initially). 3

Potassium Binders (Sub-Acute/Chronic Management)

Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, limited efficacy, and risk of bowel necrosis/intestinal ischemia. 1, 3, 5 Use newer potassium binders instead:

Sodium Zirconium Cyclosilicate (SZC/Lokelma)

Acute phase: 10 g three times daily for 48 hours 1, 3
Maintenance: 5–15 g once daily 1, 3
Onset: ~1 hour (suitable for urgent scenarios) 1, 3

Patiromer (Veltassa)

Starting dose: 8.4 g once daily with food 1, 3
Titration: Up to 25.2 g daily based on potassium response 1, 3
Onset: ~7 hours (reserved for sub-acute/chronic management) 1, 3
Administration: Separate from other oral medications by at least 3 hours to avoid reduced absorption 3
Monitoring: Check magnesium levels regularly (patiromer causes hypomagnesemia) 3

Medication Management During Acute Episode

Temporarily hold or reduce the following medications when K+ >6.5 mEq/L: 1, 3, 2

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

After acute resolution, restart RAAS inhibitors at a lower dose once K+ <5.0 mEq/L, using a concurrent potassium binder to maintain safety. 1, 3 Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD—these medications provide mortality benefit and slow disease progression. 1, 3

Long-Term Prevention and Chronic Management

For Patients on RAAS Inhibitors

Maintain RAAS inhibitor therapy using potassium binders rather than discontinuing these life-saving medications. 1, 3

K+ 5.0–6.5 mEq/L: Initiate patiromer or SZC while maintaining RAAS inhibitor therapy 1, 3
K+ >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium binder, then restart RAAS inhibitor at lower dose once K+ <5.0 mEq/L 1, 3

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors. 1, 3, 2 Reassess 7–10 days after dose changes. 1, 3 High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia) require more frequent monitoring. 1, 3, 2

Dietary Considerations

Evidence linking dietary potassium intake to serum levels is limited, and potassium-rich diets provide cardiovascular benefits including blood pressure reduction. 1, 3 Stringent dietary restrictions may not be necessary in patients receiving potassium binder therapy. 1, 3 Focus on reducing nonplant sources of potassium rather than blanket restrictions. 6

Special Populations

CKD patients: Optimal potassium range is broader (3.3–5.5 mEq/L for stage 4–5 CKD vs. 3.5–5.0 mEq/L for stage 1–2 CKD). 1, 3 Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression. 1, 3

Hemodialysis patients: Target predialysis potassium of 4.0–5.5 mEq/L to minimize mortality risk. 3 Consider SZC 5 g once daily on non-dialysis days, adjusted weekly in 5 g increments. 3

Critical Pitfalls to Avoid

Do not delay calcium administration while awaiting repeat potassium values if ECG changes are present. 1, 3, 2
Never administer insulin without glucose—hypoglycemia can be fatal. 1, 3, 2
Do not use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time. 1, 3, 2
Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1, 3, 2
Remember that calcium, insulin, and beta-agonists do not remove potassium from the body—they only temporize. 1, 3, 2
Do not permanently discontinue RAAS inhibitors due to hyperkalemia—use potassium binders to enable continuation of these life-saving medications. 1, 3

How should I manage a patient with hyperkalaemia, including emergency cardiac stabilization, intracellular potassium shifting, potassium removal, and long‑term prevention?

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