Hyperkalemia Treatment Algorithm
For acute hyperkalemia, immediately administer IV calcium gluconate if potassium >6.5 mEq/L or any ECG changes are present, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive removal strategies based on renal function. 1, 2
Initial Assessment and Classification
Verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique or arterial sampling 1, 2. Pseudohyperkalemia is a critical pitfall that can lead to unnecessary aggressive 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, 2. However, ECG changes indicate urgent treatment regardless of the absolute potassium level 1. Look specifically for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes 1, 2. A critical caveat: ECG findings are highly variable and less sensitive than laboratory tests, so their absence does not exclude the need for immediate intervention 1, 3.
Acute Management Protocol
Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes)
Administer IV calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present 1, 2:
- Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 1, 2
- Calcium chloride (10%): 5-10 mL IV over 2-5 minutes 1, 2
Critical understanding: Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily for 30-60 minutes 1, 2. If no ECG improvement within 5-10 minutes, repeat the dose 1. Continuous cardiac monitoring is mandatory during and after administration 1.
Special consideration: In patients with malignant hyperthermia and hyperkalemia, calcium should only be used in extremis as it may contribute to calcium overload of the myoplasm 1.
Step 2: Intracellular Potassium Shift (Onset: 15-30 minutes, Duration: 4-6 hours)
Administer all three agents together for maximum effect 1:
- Insulin 10 units regular IV + 25-50g dextrose (50 mL of 50% dextrose or 25g in D50W) 1, 2, 3
- Nebulized albuterol 10-20 mg in 4 mL 1, 2
- Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
Critical pitfall: Always administer glucose with insulin to prevent hypoglycemia 1, 2. Patients with low baseline glucose, no diabetes history, female sex, and altered renal function are at higher risk 1. Monitor glucose levels closely 1.
Do not use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 1, 2. Its effects take 30-60 minutes to manifest and work through increased distal sodium delivery 1.
Insulin can be repeated every 4-6 hours as needed, carefully monitoring serum potassium and glucose levels 1. The standard dose is 10 units of regular insulin IV, though some protocols recommend 0.1 units/kg (approximately 5-7 units in adults) 1.
Step 3: Potassium Removal from Body
Choose based on renal function and clinical urgency 1, 2:
For Adequate Kidney Function:
- Loop diuretics: Furosemide 40-80 mg IV to increase renal potassium excretion 1, 2. Titrate to maintain euvolemia, not primarily for potassium management 1.
For All Patients (Subacute Treatment):
Avoid sodium polystyrene sulfonate (Kayexalate) for acute management due to delayed onset of action, limited efficacy data, and risk of intestinal necrosis and bowel perforation 1, 4. The FDA label explicitly states it should not be used as emergency treatment for life-threatening hyperkalemia 4. Concomitant administration with sorbitol is not recommended due to increased risk of intestinal necrosis 4.
For Severe Cases or Renal Failure:
- Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially in patients with renal failure, oliguria, or cases unresponsive to medical management 1, 2, 5, 3. This is the definitive treatment for removing potassium from the body 5, 3.
Medication Management During Acute Episode
Temporarily discontinue or reduce at K+ >6.5 mEq/L 1, 2:
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) 1, 2
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1
- NSAIDs 1
- Trimethoprim 1
- Heparin 1
- Beta-blockers 1
- Potassium supplements and salt substitutes 1
Critical principle: Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD, as these provide mortality benefit 1, 2. Instead, temporarily hold or reduce, then restart at lower dose once potassium <5.0-5.5 mEq/L with concurrent potassium binder therapy 1, 2.
Chronic Hyperkalemia Management
For Patients on RAAS Inhibitors with K+ 5.0-6.5 mEq/L:
Initiate an approved potassium-lowering agent (patiromer or SZC) and maintain RAAS inhibitor therapy unless an alternative treatable cause is identified 1, 2. This approach allows continuation of life-saving cardiovascular medications 1, 2.
For Patients on RAAS Inhibitors with K+ >6.5 mEq/L:
Discontinue or reduce RAAS inhibitor temporarily, initiate a potassium-lowering agent, and monitor closely 1, 2. Once potassium normalizes, restart RAAS inhibitor at lower dose with concurrent binder therapy 1.
Dietary Management:
Limit foods rich in bioavailable potassium, especially processed foods 1. Avoid salt substitutes containing potassium and herbal supplements that raise K+ (alfalfa, dandelion, horsetail, nettle) 1. However, evidence linking dietary potassium intake to serum levels is limited, and potassium-rich diets provide cardiovascular benefits including blood pressure reduction 1.
Monitoring Protocol
Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2. Reassess 7-10 days after dose changes 1, 2.
High-risk patients require more frequent monitoring 1, 2:
- Chronic kidney disease
- Heart failure
- Diabetes mellitus
- History of hyperkalemia
After acute treatment with insulin/glucose or beta-agonists, recheck potassium every 2-4 hours until stabilized, as these agents have short duration of effect (2-4 hours) and potassium can rebound 1.
Critical Pitfalls to Avoid
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1, 2
- Do not delay treatment while waiting for repeat lab confirmation if ECG changes are present 1
- Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 1, 2. Failure to initiate concurrent potassium removal strategies will result in recurrent hyperkalemia 1
- Never use sodium bicarbonate without metabolic acidosis 1, 2
- Never give insulin without glucose 1, 2
- Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease or CKD—use potassium binders instead 1, 2
Special Populations
Patients with CKD Stage 4-5:
Maintain target potassium 4.0-5.0 mEq/L to minimize mortality risk, though patients with advanced CKD tolerate higher levels (3.3-5.5 mEq/L) due to compensatory mechanisms 1. Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 1, 2.
Hemodialysis Patients:
Target predialysis potassium 4.0-5.5 mEq/L 1. Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels 1. Monitor for rebound hyperkalemia within 4-6 hours post-dialysis 1.