Hyperkalemia Treatment
Hyperkalemia management is stratified by serum potassium level and the presence of ECG changes, with immediate cardiac membrane stabilization using IV calcium for any ECG abnormalities, followed by intracellular potassium shift using insulin-glucose and albuterol, and definitive removal via diuretics, potassium binders, or hemodialysis depending on severity and renal function. 1
Classification and Risk Stratification
Hyperkalemia severity determines treatment urgency 1, 2:
- Mild: 5.0–5.5 mEq/L
- Moderate: 5.5–6.0 mEq/L
- Severe: ≥6.0 mEq/L or any ECG changes regardless of potassium level 1, 2
ECG changes indicate urgent treatment need regardless of the exact potassium value 1. Characteristic findings include peaked T waves (>5.5 mEq/L), flattened P waves and prolonged PR interval (6.0–6.4 mEq/L), widened QRS (>6.5 mEq/L), and sine-wave pattern or ventricular arrhythmias (≥7–8 mEq/L) 1. However, ECG findings are highly variable and less sensitive than laboratory tests—do not rely solely on ECG 1.
Acute Hyperkalemia Management
Step 1: Cardiac Membrane Stabilization (Immediate)
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 (more potent; use via central line if available) 1, 2
Onset: 1–3 minutes; Duration: 30–60 minutes 1. Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily 1. Repeat the dose if no ECG improvement within 5–10 minutes 1, 2. Never delay calcium administration while awaiting repeat potassium levels if ECG changes are present 1.
Caution: In patients with elevated phosphate levels, use calcium cautiously due to calcium-phosphate precipitation risk 1. Never administer calcium through the same IV line as sodium bicarbonate (precipitation occurs) 1.
Step 2: Intracellular Potassium Shift (Administer Simultaneously)
Give all three agents together for maximum effect 1, 2:
Insulin-Glucose
- 10 units regular insulin IV + 25 g dextrose (50 mL D50W) 1, 2
- Onset: 15–30 minutes; Peak: 30–60 minutes; Duration: 4–6 hours 1
- Lowers potassium by 0.5–1.2 mEq/L 1, 2
- Always give glucose with insulin to prevent life-threatening hypoglycemia 1, 2
- Can be repeated every 4–6 hours if hyperkalemia persists, with careful glucose and potassium monitoring 1
Nebulized Albuterol
- 10–20 mg albuterol in 4 mL nebulized over 10–15 minutes 1, 2
- Onset: ~30 minutes; Duration: 2–4 hours 1
- Lowers potassium by 0.5–1.0 mEq/L 1, 2
- Can be repeated every 2 hours if needed 1
Sodium Bicarbonate (ONLY with Metabolic Acidosis)
- 50 mEq IV over 5 minutes ONLY if pH <7.35 and bicarbonate <22 mEq/L 1, 2
- Onset: 30–60 minutes 1
- Do NOT use without documented metabolic 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 for patients with eGFR >30 mL/min and adequate urine output 1, 2
- Increases renal potassium excretion by stimulating flow to renal collecting ducts 1
Hemodialysis (Most Effective Method)
Indications for urgent dialysis 1, 2:
- Serum potassium >6.5 mEq/L unresponsive to medical therapy
- Oliguria or anuria
- End-stage renal disease
- Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)
- Severe renal impairment (eGFR <15 mL/min)
- Persistent ECG changes despite medical management
Hemodialysis is the most reliable and effective method for severe hyperkalemia, especially in renal failure 1, 2.
Potassium Binders (Sub-Acute Management)
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5–15 g once daily for maintenance; onset ~1 hour 3, 1
- Patiromer (Veltassa): 8.4 g once daily, titrated up to 25.2 g daily; onset ~7 hours 3, 1
- Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, limited efficacy, and risk of bowel necrosis 1
Chronic Hyperkalemia Management
Medication Review and Adjustment
Hold or reduce contributing medications when potassium >6.5 mEq/L 1, 2:
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
- NSAIDs
- Potassium-sparing diuretics
- Trimethoprim, heparin, beta-blockers
- Potassium supplements and salt substitutes
For potassium 5.0–6.5 mEq/L on RAAS inhibitors: Initiate a potassium-lowering agent (patiromer or SZC) and maintain RAAS inhibitor therapy unless an alternative treatable cause is identified 1, 2. Do not permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease 1, 2.
For potassium >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitors, initiate a potassium-lowering agent, and restart RAAS inhibitors at a lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy 1, 2.
Dietary Modifications
Restrict potassium intake to <3 g/day (50–70 mmol/day) 1, 2. Avoid high-potassium foods: bananas, oranges, potatoes, tomatoes, salt substitutes, legumes, chocolate, yogurt, and certain herbal supplements (alfalfa, dandelion, horsetail, nettle) 1.
Evidence linking dietary potassium to serum levels is limited, and a potassium-rich diet has cardiovascular benefits in otherwise healthy individuals 1. However, in patients with hyperkalemia and CKD, dietary restriction is essential 1.
Monitoring Protocol
Check potassium within 1 week of 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.
After acute treatment: Recheck potassium within 1–2 hours after insulin/glucose or albuterol administration, then every 2–4 hours during the acute phase until stable 1, 2. Rebound hyperkalemia can occur 2–4 hours after temporary measures wear off 1, 2.
Special Populations
Chronic Kidney Disease (CKD)
Patients with stage 4–5 CKD tolerate higher potassium levels (3.3–5.5 mEq/L) due to compensatory mechanisms, but maintaining 4.0–5.0 mEq/L minimizes mortality risk 1. Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 1.
Heart Failure
Both hyperkalemia and hypokalemia increase mortality risk in heart failure patients 1. Target potassium 4.0–5.0 mEq/L 1. Consider aldosterone antagonists for mortality benefit while using potassium binders to prevent hyperkalemia 1.
Critical Pitfalls to Avoid
- Do NOT delay calcium administration while awaiting repeat potassium values if ECG changes are present 1, 2
- Never give insulin without glucose—hypoglycemia can be fatal 1, 2
- Do NOT use sodium bicarbonate without documented metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
- Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1, 2
- Do NOT permanently discontinue RAAS inhibitors due to hyperkalemia—use dose reduction plus potassium binders instead 1, 2
- Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
- Avoid sodium polystyrene sulfonate (Kayexalate) due to bowel necrosis risk and limited efficacy 1
Team Approach
Optimal management involves a multidisciplinary team: cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians 1. Educational initiatives on newer potassium binders are needed to improve chronic hyperkalemia management 1.