Management of Hyperkalemia

Immediate Assessment and Risk Stratification

Obtain an ECG immediately in every patient with hyperkalemia, regardless of the potassium level, because ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent need for treatment even when laboratory values are only mildly elevated. 1

Verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment 1
Classify severity: mild (5.0–5.9 mEq/L), moderate (6.0–6.4 mEq/L), or severe (≥6.5 mEq/L) 1
Any patient with potassium >6.0 mEq/L OR any ECG changes requires hospital admission for immediate treatment and continuous cardiac monitoring, as this represents a medical emergency with high risk of fatal arrhythmias 2

Emergency Management of Severe Hyperkalemia (≥6.5 mEq/L or ECG Changes)

Step 1: Cardiac Membrane Stabilization (Within 1–3 Minutes)

Administer IV calcium gluconate 10% (15–30 mL) over 2–5 minutes immediately—this is the only intervention that protects against fatal arrhythmias within minutes, though it does NOT lower potassium levels. 1

Alternatively, use calcium chloride 10% (5–10 mL) if central venous access is available, as it is more potent 1
Effects begin within 1–3 minutes but last only 30–60 minutes 1
Repeat the dose if ECG does not improve within 5–10 minutes 1
Never delay calcium administration while awaiting repeat potassium levels when ECG changes are present 1
Monitor continuously during and for 5–10 minutes after administration 1

Step 2: Shift Potassium Intracellularly (Administer All Three Simultaneously)

Give 10 units regular insulin IV push plus 25 g dextrose (50 mL of 50% dextrose) to lower potassium by 0.5–1.2 mEq/L within 30–60 minutes, lasting 4–6 hours. 1, 3

Always administer glucose with insulin—hypoglycemia can be fatal 1
Monitor blood glucose closely after administration, especially in patients with low baseline glucose, no diabetes, female sex, or impaired renal function 1
Effects can be repeated every 4–6 hours as needed, with potassium and glucose monitoring every 2–4 hours 1

Administer nebulized albuterol 10–20 mg in 4 mL over 10–15 minutes to provide an additional 0.5–1.0 mEq/L reduction within 30 minutes, lasting 2–4 hours. 1

The combined insulin-glucose plus albuterol regimen is more effective than either alone 1
Can be repeated every 2 hours if needed 1

Administer sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis is documented (pH <7.35 and bicarbonate <22 mEq/L)—it is ineffective without acidosis and wastes critical time. 1

Onset of action is slower (30–60 minutes) compared to insulin or albuterol 1
Do not use as monotherapy for hyperkalemia 1

Step 3: Remove Potassium from the Body (Definitive Treatment)

Hemodialysis is the most reliable and effective method for severe hyperkalemia and should be initiated urgently in the following situations: 1

Serum potassium >6.5 mEq/L unresponsive to medical therapy 1
Oliguria or anuria 1
End-stage renal disease 1
Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis) 1
Severe renal impairment (eGFR <15 mL/min) 1
Persistent ECG changes despite medical management 1
In hemodynamically unstable patients, continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis 1

For patients with adequate renal function (eGFR >30 mL/min) and urine output, administer IV furosemide 40–80 mg to increase renal potassium excretion. 1

Initiate sodium zirconium cyclosilicate (SZC/Lokelma) 10 g three times daily for 48 hours for rapid potassium removal (onset ~1 hour), then 5–15 g once daily for maintenance. 1, 4

SZC reduces serum potassium within 1 hour of a single 10-g dose 1
Each 5 g dose contains approximately 400 mg sodium; monitor for edema, particularly in heart failure or renal disease 4
Separate other oral medications by at least 2 hours before or after SZC 4

Patiromer (Veltassa) 8.4 g once daily is an alternative for subacute management (onset ~7 hours), titrated up to 25.2 g daily based on potassium levels. 1

Must be separated from other oral medications by at least 3 hours 1
Monitor magnesium levels, as patiromer causes hypomagnesemia 1

Avoid sodium polystyrene sulfonate (Kayexalate) due to risk of bowel necrosis, colonic ischemia, and lack of efficacy data for acute hyperkalemia. 1

Step 4: Medication Management During Acute Episode

Immediately hold the following medications when potassium >6.5 mEq/L: 1

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

After acute resolution, restart RAAS inhibitors at a lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy—do NOT permanently discontinue these life-saving medications. 1

Management of Moderate Hyperkalemia (6.0–6.4 mEq/L Without ECG Changes)

If no ECG changes are present, initiate intracellular shifting agents (insulin-glucose and albuterol) and potassium binders without calcium. 1, 2

Use the same insulin-glucose and albuterol regimens as for severe hyperkalemia 1
Start SZC 10 g three times daily for 48 hours or patiromer 8.4 g once daily 1
Add loop diuretics (furosemide 40–80 mg) if eGFR >30 mL/min 1
Temporarily reduce or hold RAAS inhibitors until potassium <5.0 mEq/L 1
Recheck potassium within 2–4 hours after initial interventions 2

Management of Mild Hyperkalemia (5.0–5.9 mEq/L)

For asymptomatic patients with normal ECG and potassium 5.0–5.5 mEq/L, do NOT initiate acute interventions such as calcium, insulin, or albuterol. 1

Medication Review and Adjustment

Review and eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
For patients on RAAS inhibitors with potassium 5.0–6.5 mEq/L, initiate a potassium binder (patiromer or SZC) while maintaining RAAS inhibitor therapy—do NOT discontinue these drugs as they provide mortality benefit 1
If on mineralocorticoid receptor antagonists (spironolactone), reduce dose by 50% when potassium >5.5 mEq/L (e.g., 25 mg → 12.5 mg daily) 2

Enhance Potassium Excretion

Add loop diuretics (furosemide 40–80 mg daily) if adequate renal function (eGFR >30 mL/min) 1
Consider thiazide diuretics as an alternative 1

Dietary Modifications

Limit potassium intake to <3 g/day (50–70 mmol/day) 2
Avoid high-potassium foods: bananas, oranges, melons, potatoes, tomato products, legumes, lentils, chocolate, yogurt 2
Eliminate salt substitutes containing potassium chloride 2
Note: Evidence linking dietary potassium to serum levels is limited, and potassium-rich diets provide cardiovascular benefits; dietary restriction should focus on reducing nonplant sources of potassium 5

Monitoring Protocol

Recheck potassium within 24–48 hours after initial interventions 2
Check potassium within 1 week after starting or escalating RAAS inhibitors 1
Reassess 7–10 days after initiating potassium binder therapy 1
Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 1

Special Populations

Patients with Chronic Kidney Disease

Maintain RAAS inhibitors aggressively using potassium binders in proteinuric CKD, as these drugs slow CKD progression and provide mortality benefit 1
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 in dialysis patients to minimize mortality risk 1

Patients on Hemodialysis

Start SZC 5 g once daily on non-dialysis days, adjusting weekly in 5 g increments based on predialysis potassium 1
Alternatively, use patiromer 8.4 g once daily with food, separated from other medications by ≥3 hours 1
Monitor for hypokalemia, as acute illness (decreased oral intake, diarrhea) can increase risk 4
Consider adjusting dialysate potassium concentration (typically 2.0–3.0 mEq/L) based on predialysis levels 1

Patients with Heart Failure on RAAS Inhibitors

Do NOT permanently discontinue RAAS inhibitors or mineralocorticoid receptor antagonists due to hyperkalemia—use dose reduction plus potassium binders to maintain mortality and morbidity benefits 2
For patients on spironolactone + ACE inhibitor/ARB with potassium >5.5 mEq/L, reduce spironolactone by 50% and recheck potassium in 2–3 days 2
Discontinue spironolactone only if potassium >6.0 mEq/L, ECG changes appear, or creatinine >2.5 mg/dL 2

Critical Pitfalls to Avoid

Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
Do NOT delay calcium administration while awaiting repeat potassium levels if ECG changes are present 1
Never administer insulin without glucose—hypoglycemia can be fatal 1
Do NOT use sodium bicarbonate without documented metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L)—it is ineffective and wastes time 1
Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1
Do NOT permanently discontinue RAAS inhibitors—use potassium binders to enable continuation of these life-saving medications 1
Avoid sodium polystyrene sulfonate (Kayexalate) due to risk of bowel necrosis and lack of efficacy 1
Do NOT ignore the 5.5 mEq/L threshold for dose reduction of mineralocorticoid receptor antagonists—waiting until 6.0 mEq/L increases arrhythmia risk 2

Monitoring After Treatment

Recheck potassium 1–2 hours after insulin/glucose or albuterol administration 1
Continue potassium checks every 2–4 hours during acute treatment until stable 1
Obtain repeat ECG to confirm resolution of cardiac changes 1
Monitor for rebound hyperkalemia 2–4 hours after temporary measures wear off 1
Check potassium within 1 week after starting or adjusting potassium binders 1
Monitor magnesium levels in patients on patiromer 1
Watch for edema in patients on SZC due to sodium content 4

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