Acute and Ongoing Management of Severe Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer IV calcium gluconate to stabilize the cardiac membrane, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis while holding RAAS inhibitors temporarily—once stabilized, restart RAAS inhibitors at lower doses with concurrent potassium binder therapy rather than permanently discontinuing these life-saving medications. 1, 2

Immediate Assessment (First 5 Minutes)

Verify True Hyperkalemia

Exclude pseudohyperkalemia from hemolysis, fist clenching during phlebotomy, or prolonged tourniquet time by repeating the sample with proper technique or obtaining arterial blood 1, 2
Symptoms are typically nonspecific (weakness, palpitations), making ECG and laboratory confirmation essential 2

Obtain 12-Lead ECG Immediately

ECG changes indicate urgent treatment regardless of the exact potassium value 1, 2
Look for peaked T waves (earliest sign, K⁺ >5.5 mEq/L), flattened P waves, prolonged PR interval, widened QRS complex, or sine-wave pattern 1, 2
Absent or atypical ECG changes do NOT exclude the need for immediate intervention—ECG findings are highly variable and less sensitive than laboratory tests 2, 3

Classify Severity

Mild: 5.0–5.9 mEq/L 1, 2
Moderate: 6.0–6.4 mEq/L 1, 2
Severe: ≥6.5 mEq/L 1, 2

Acute Management Algorithm (K⁺ ≥6.0 mEq/L or ECG Changes)

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

Administer calcium immediately if ECG changes are present:

Calcium gluconate 10%: 15–30 mL IV over 2–5 minutes (preferred for peripheral access) 1, 2, 3
Alternative: Calcium chloride 10%: 5–10 mL IV over 2–5 minutes (central line preferred due to tissue injury risk) 1, 2
Repeat dose in 5–10 minutes if no ECG improvement 1, 2
Duration: 30–60 minutes (temporary effect only) 1, 2
Critical caveat: Calcium does NOT lower potassium—it only stabilizes the cardiac membrane 1, 2, 3

Step 2: Intracellular Potassium Shift (Onset 15–60 Minutes)

Administer all three agents together for maximum effect:

Insulin + Glucose (Most Effective)

Insulin regular 10 units IV push + dextrose 50% (D50W) 50 mL (25 grams) 1, 2, 3
Expected potassium reduction: 0.5–1.2 mEq/L within 30–60 minutes 1, 2
Duration: 4–6 hours (rebound hyperkalemia common after) 1, 2
Never give insulin without glucose—hypoglycemia can be fatal 1, 2
Monitor glucose at 30 minutes, 1 hour, 2 hours, and 4 hours post-administration 1

Nebulized Albuterol (Adjunctive)

Albuterol 10–20 mg in 4 mL nebulized over 10 minutes 1, 2, 3
Expected potassium reduction: 0.5–1.0 mEq/L within 30–60 minutes 1, 2
Duration: 2–4 hours 1, 2
Combination with insulin is more effective than either alone 1, 2

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if pH <7.35 and bicarbonate <22 mEq/L 1, 2, 3
Onset: 30–60 minutes (slower than insulin/albuterol) 1, 2
Do NOT use without documented acidosis—it is ineffective and wastes time 1, 2

Step 3: Definitive Potassium Removal

Loop Diuretics (If Adequate Renal Function)

Furosemide 40–80 mg IV if eGFR >30 mL/min and adequate urine output 1, 2, 3
Promotes urinary potassium excretion through increased distal sodium delivery 1, 2
Titrate to maintain euvolemia, not primarily for potassium management 2

Hemodialysis (Most Reliable Method)

Indications for urgent dialysis: 1, 2, 3

Severe hyperkalemia (K⁺ >6.5 mEq/L) unresponsive to medical therapy
Oliguria or end-stage renal disease
Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)
Acute kidney injury with rising potassium despite treatment

Hemodialysis is the most effective and reliable method for potassium removal, especially in renal failure 1, 2, 4, 3

Medication Management During Acute Episode

Temporarily Hold These Medications (K⁺ >6.5 mEq/L):

RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) 1, 2
Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1, 2
NSAIDs (impair renal potassium excretion) 1, 2
Trimethoprim, heparin, beta-blockers 1, 2
Potassium supplements and salt substitutes 1, 2

Acute Phase Monitoring

Recheck potassium 1–2 hours after insulin/glucose or albuterol therapy 1, 2
Continue potassium checks every 2–4 hours during acute treatment until levels stabilize 1, 2
Repeat ECG if initial presentation included cardiac abnormalities 1, 2
Monitor glucose closely to prevent hypoglycemia from insulin therapy 1

Ongoing Management After Acute Resolution

Step 1: Initiate Potassium Binder Therapy (Once K⁺ <5.5 mEq/L)

Preferred agents (superior to sodium polystyrene sulfonate): 1, 2, 5

Sodium Zirconium Cyclosilicate (SZC/Lokelma) – Faster Onset

Initial dose: 10 g three times daily for 48 hours 1, 2, 5
Maintenance: 5–15 g once daily (titrate based on potassium levels) 1, 2, 5
Onset of action: ~1 hour (suitable for urgent scenarios) 1, 2, 5
Mean potassium reduction: 0.7 mEq/L at 48 hours with 10 g TID 5
92% of patients achieved normokalemia (3.5–5.0 mEq/L) within 48 hours 5
Effective in CKD, heart failure, diabetes, and patients on RAAS inhibitors 5

Patiromer (Veltassa) – Subacute Management

Initial dose: 8.4 g once daily with food 1, 2
Titrate up to 25.2 g daily based on potassium response 1, 2
Onset of action: ~7 hours 1, 2
Separate from other oral medications by at least 3 hours (reduces absorption of ciprofloxacin, levothyroxine, metformin) 1, 2
Monitor magnesium levels (can cause hypomagnesemia) 2

Avoid sodium polystyrene sulfonate (Kayexalate): Associated with bowel necrosis, colonic ischemia, and lack of efficacy data 1, 2, 6

Step 2: Restart RAAS Inhibitors at Lower Dose

Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular disease, heart failure, and proteinuric CKD: 1, 2, 6

Restart ACE inhibitor/ARB at 50% of previous dose once K⁺ <5.0 mEq/L 1, 2
Use concurrent potassium binder therapy to enable continuation of these life-saving medications 1, 2, 6
Target maintenance potassium: 4.0–5.0 mEq/L to minimize mortality risk 1, 2

Step 3: Optimize Diuretic Therapy

Continue or initiate loop diuretics (furosemide 40–80 mg daily) if adequate renal function 1, 2
Promotes ongoing urinary potassium excretion 1, 2

Step 4: Address Underlying Causes

Review and eliminate contributing medications (NSAIDs, trimethoprim, heparin) 1, 2
Correct metabolic acidosis if present 2, 6
Evaluate for acute kidney injury or worsening CKD 2

Chronic Management Monitoring Protocol

Initial Monitoring (After Starting Potassium Binder)

Check potassium and renal function within 1 week of starting or adjusting potassium binder dose 1, 2
Recheck 7–10 days after restarting or increasing RAAS inhibitor dose 1, 2

Ongoing Monitoring Frequency

Every 1–2 weeks during dose titration phase 2
At 3 months, then every 6 months thereafter 1, 2
More frequent monitoring for high-risk patients: CKD (eGFR <60), heart failure, diabetes, history of recurrent hyperkalemia 1, 2

Target Potassium Ranges

General population: 4.0–5.0 mEq/L 1, 2
Advanced CKD (stage 4–5): 3.3–5.5 mEq/L (broader range tolerated due to compensatory mechanisms) 2

Special Population Considerations

Diabetic Patients

Severe hyperglycemia (>1,000 mg/dL) creates hyperosmolar environment that drives potassium out of cells, producing extreme hyperkalemia (>7.0 mEq/L) even without marked acidosis 1
Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism) is common in diabetic nephropathy 1

CKD Patients

Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression 1, 2, 6
Patients with advanced CKD tolerate higher potassium levels (3.3–5.5 mEq/L acceptable for stage 4–5) 2

Hemodialysis Patients

Target predialysis potassium: 4.0–5.5 mEq/L 2
Start SZC 5 g once daily on non-dialysis days, titrate weekly in 5 g increments based on predialysis levels 2
Alternative: Patiromer 8.4 g once daily, titrate to 16.8–25.2 g daily 2
Monitor for rebound hyperkalemia 4–6 hours post-dialysis 2

Critical Pitfalls to Avoid

Never delay calcium administration while awaiting repeat potassium levels if ECG changes are present—ECG changes indicate urgent need regardless of exact value 1, 2, 3
Never give insulin without glucose—hypoglycemia can be fatal 1, 2
Never use sodium bicarbonate without documented metabolic acidosis (pH <7.35, HCO₃ <22 mEq/L)—it is ineffective as monotherapy and wastes time 1, 2, 3
Remember that calcium, insulin, and albuterol are temporizing measures only—they do NOT remove potassium from the body; rebound hyperkalemia occurs 2–4 hours after administration 1, 2, 3
Do NOT permanently discontinue RAAS inhibitors because of hyperkalemia—instead adjust dose and employ potassium binders to maintain these mortality-reducing medications 1, 2, 6
Avoid sodium polystyrene sulfonate (Kayexalate)—associated with bowel necrosis and lacks efficacy data; use newer binders (SZC or patiromer) instead 1, 2, 6
Monitor closely for hypokalemia when using potassium binders—hypokalemia may be even more dangerous than hyperkalemia, particularly in cardiac patients 1, 2

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