Immediate Treatment for Hyperkalemia

For patients presenting with hyperkalemia, immediate treatment depends on severity and ECG changes: administer IV calcium first for cardiac protection if ECG changes are present or potassium ≥6.5 mEq/L, followed immediately by insulin/glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis. 1

Severity Classification and Initial Assessment

Mild hyperkalemia: 5.0-5.9 mEq/L 2, 1
Moderate hyperkalemia: 6.0-6.4 mEq/L 2, 1
Severe hyperkalemia: ≥6.5 mEq/L, which is life-threatening 2, 1
ECG changes indicate urgent treatment regardless of potassium level, including peaked T waves, flattened P waves, prolonged PR interval, and widened QRS 2, 1
Exclude pseudo-hyperkalemia from hemolysis or improper blood sampling by repeating measurement with appropriate technique or arterial sampling 2

Step 1: Cardiac Membrane Stabilization (Immediate - Within 1-3 Minutes)

Administer IV calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present 2, 1

Calcium Administration Protocol

Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 2, 1
Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes (more rapid effect, preferred for central access) 2, 1
Onset of action: 1-3 minutes 2, 1
Duration: 30-60 minutes (temporary effect only) 2, 1
Mechanism: Stabilizes cardiac membranes but does NOT lower serum potassium 2, 1

Critical Monitoring During Calcium Administration

Continuous cardiac monitoring is mandatory during and for 5-10 minutes after calcium administration 2
If no ECG improvement within 5-10 minutes, repeat the calcium dose 2, 1
Monitor heart rate and stop if symptomatic bradycardia occurs 2

Important Caveats for Calcium

Never delay calcium administration while waiting for repeat potassium levels if ECG changes are present 2
Do not administer calcium through the same IV line as sodium bicarbonate (precipitation will occur) 2
Use calcium cautiously in patients with elevated phosphate levels due to calcium-phosphate precipitation risk 2
In malignant hyperthermia with hyperkalemia, calcium should only be used in extremis as it may contribute to myoplasmic calcium overload 2

Step 2: Shift Potassium into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)

Administer all three agents together for maximum effect 2, 1

Insulin with Glucose (First-Line)

Standard dose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 2, 1
Alternative dose: Some protocols recommend 0.1 units/kg (approximately 5-7 units in adults) 2
Onset: 15-30 minutes 2, 1
Duration: 4-6 hours 2, 1
Mechanism: Stimulates Na+/K+-ATPase pump, driving potassium into cells 1

Critical Safety Considerations for Insulin

Verify potassium is not below 3.3 mEq/L before administering insulin 2
Always administer glucose with insulin to prevent hypoglycemia 2, 1
Monitor glucose levels every 2-4 hours after administration 2
Patients at higher risk for hypoglycemia: low baseline glucose, no diabetes history, female sex, altered renal function 2
Insulin can be repeated every 4-6 hours if hyperkalemia persists, with careful monitoring of glucose and potassium 2

Nebulized Beta-2 Agonists (Adjunctive Therapy)

Albuterol: 10-20 mg nebulized over 15 minutes 2, 1
Alternative: Salbutamol 20 mg in 4 mL nebulized 2
Onset: 15-30 minutes 2, 1
Duration: 2-4 hours (short-lived effect) 2, 1
Mechanism: Stimulates Na+/K+-ATPase pump via beta-2 receptor activation 2, 1
Expected effect: Reduces serum potassium by approximately 0.5-1.0 mEq/L 2

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

Indication: Use ONLY in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 2, 1
Dose: 50 mEq IV over 5 minutes 2, 1
Onset: 30-60 minutes (slower than insulin/glucose) 2, 1
Mechanism: Promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release 2
Critical caveat: Do NOT use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 2, 1

Step 3: Eliminate Potassium from Body (Definitive Treatment)

Loop Diuretics (If Adequate Renal Function)

Furosemide: 40-80 mg IV 2, 1
Mechanism: Increases renal potassium excretion by stimulating flow to renal collecting ducts 2
Effective only in patients with adequate kidney function 2, 1
Titrate to maintain euvolemia, not primarily for potassium management 2

Hemodialysis (Most Effective Method)

Hemodialysis is the most reliable and effective method for severe hyperkalemia, especially in patients with renal failure 2, 1
Indications: Severe hyperkalemia unresponsive to medical management, oliguria, or end-stage renal disease 2, 1
Potassium levels can rebound within 4-6 hours post-dialysis as intracellular potassium redistributes 2
Monitor patients with severe initial hyperkalemia (>6.5 mEq/L) more frequently (every 2-4 hours initially) due to rebound risk 2

Potassium Binders (Subacute to Chronic Management)

Newer FDA-Approved Agents (Preferred)

Sodium zirconium cyclosilicate (SZC/Lokelma):
- Dose: 10g three times daily for 48 hours, then 5-15g once daily for maintenance 2
- Onset: ~1 hour (rapid, suitable for urgent scenarios) 2
- Mechanism: Exchanges hydrogen and sodium for potassium 2
- Advantage: Reduces serum potassium within 1 hour of a single 10g dose 2
Patiromer (Veltassa):
- Dose: Starting at 8.4g once daily with food, titrated up to 25.2g daily based on potassium levels 2, 3
- Onset: ~7 hours 2
- Mechanism: Binds potassium in exchange for calcium in the colon, increasing fecal excretion 2
- Administration: Separate from other oral medications by at least 3 hours 2
- Limitation: Not for emergency treatment due to delayed onset 3

Older Agent (Avoid for Acute Management)

Sodium polystyrene sulfonate (Kayexalate): 15-50g orally or rectally with sorbitol 1
Significant limitations: Delayed onset, limited efficacy, risk of bowel necrosis and intestinal ischemia 2
Should be avoided for acute management 2

Critical Monitoring and Follow-Up

Acute Phase Monitoring

Check potassium levels every 2-4 hours during acute treatment until stabilized 2, 1
Recheck potassium within 1-2 hours after insulin/glucose or beta-agonist therapy (effects last only 2-4 hours) 2
Continuous cardiac monitoring for patients with ECG changes 2, 1

Post-Acute Monitoring

Rebound hyperkalemia can occur after 2 hours as temporary measures wear off 1
Initiate potassium-lowering agents as early as possible to prevent rebound 1
Monitor closely to avoid overcorrection and hypokalemia, which may be even more dangerous than hyperkalemia 4, 2

Medication Management During Acute Episode

Medications to Temporarily Discontinue or Reduce

RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists): Discontinue or reduce temporarily at K+ ≥6.5 mEq/L 4, 2
Potassium-sparing diuretics: Spironolactone, amiloride, triamterene 2
NSAIDs and COX-2 inhibitors: Cause sodium retention and worsen renal function 2
Other contributing medications: Trimethoprim, heparin, beta-blockers 2
Potassium supplements and salt substitutes: Eliminate entirely 2

Medications to Maintain When Possible

Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD, as these provide mortality benefit 4, 2
Restart RAAS inhibitors at lower dose once potassium <5.0-5.5 mEq/L with concurrent potassium binder therapy 2

Common 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, 1
Never use sodium bicarbonate without metabolic acidosis—it is only indicated when acidosis is present 2, 1
Always administer glucose with insulin to prevent hypoglycemia 2, 1
Do not delay treatment while waiting for repeat lab confirmation if ECG changes are present 2
Failure to initiate concurrent potassium-lowering therapies will result in recurrent life-threatening arrhythmias within 30-60 minutes after calcium wears off 2

Special Population Considerations

Patients on RAAS Inhibitors with Chronic Hyperkalemia

For potassium 5.0-6.5 mEq/L: Initiate approved potassium-lowering agent (patiromer or SZC) and maintain RAAS inhibitor therapy unless alternative treatable etiology identified 4, 2
For potassium >6.5 mEq/L: Discontinue or reduce RAAS inhibitor temporarily, initiate potassium-lowering agent when levels >5.0 mEq/L, monitor closely 4, 2
Reassess potassium 7-10 days after starting or increasing RAAS inhibitor doses 2

Patients with Chronic Kidney Disease

Patients with advanced CKD tolerate higher potassium levels due to compensatory mechanisms 2
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 2
Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 2

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