What is the acute management of hyperkalemia?

Acute Management of Hyperkalemia

For acute hyperkalemia, immediately administer IV calcium gluconate (15–30 mL of 10% solution over 2–5 minutes) if potassium ≥6.5 mEq/L or any ECG changes are present, then simultaneously give insulin 10 units IV with 25g dextrose plus nebulized albuterol 10–20 mg to shift potassium intracellularly, and finally initiate definitive potassium removal with loop diuretics (furosemide 40–80 mg IV) if renal function is adequate or hemodialysis if severe/refractory. 1, 2

Severity Classification and Initial Assessment

Classify hyperkalemia severity to guide treatment intensity:

• Mild: 5.0–5.9 mEq/L 1, 2, 3
• Moderate: 6.0–6.4 mEq/L 1, 2, 3
• Severe: ≥6.5 mEq/L (life-threatening emergency) 1, 2, 3

ECG changes mandate urgent treatment regardless of potassium level and include peaked T waves, flattened P waves, prolonged PR interval, widened QRS complex, or arrhythmias. 1, 2, 3 ECG findings can be highly variable and less sensitive than laboratory values, so never delay treatment while awaiting repeat potassium levels when ECG changes are present. 1

Exclude pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment by repeating the measurement with appropriate technique or arterial sampling. 1

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

Administer IV calcium first to protect against fatal arrhythmias in patients with severe hyperkalemia (≥6.5 mEq/L) or any ECG changes: 1, 2, 3

• Calcium gluconate 10%: 15–30 mL IV over 2–5 minutes (preferred for peripheral access) 1, 2, 3
• Calcium chloride 10%: 5–10 mL (500–1000 mg) IV over 2–5 minutes (preferred when central access available; provides more rapid increase in ionized calcium) 1, 2, 3

Critical points about calcium administration:

• Onset within 1–3 minutes, but effect lasts only 30–60 minutes 1, 2, 3
• Calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes 1, 2, 3
• Repeat the dose (15–30 mL calcium gluconate) if no ECG improvement within 5–10 minutes 1
• Continuous cardiac monitoring is mandatory during and for 5–10 minutes after administration 1
• Never administer calcium through the same IV line as sodium bicarbonate (precipitation will occur) 1
• Use cautiously in patients with elevated phosphate levels (risk of calcium-phosphate precipitation) 1
• In patients with malignant hyperthermia and hyperkalemia, calcium should only be used in extremis due to risk of myoplasmic calcium overload 1

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

Administer all three agents simultaneously for maximum effect: 1

Insulin-Glucose (Most Effective Shifting Agent)

• Standard dose: 10 units regular insulin IV push plus 25g dextrose (50 mL D50W) 1, 2, 3
• Onset: 15–30 minutes; peak effect: 30–60 minutes; duration: 4–6 hours 1, 2, 3
• Reduces serum potassium by 0.5–1.2 mEq/L 1
• Never give insulin without glucose—hypoglycemia can be fatal 1
• Monitor blood glucose closely after administration; patients with low baseline glucose, no diabetes, female sex, or impaired renal function are at higher risk of hypoglycemia 1
• Verify potassium is not below 3.3 mEq/L before administering insulin 1
• In severe hyperkalemia, insulin can be repeated every 4–6 hours as needed, carefully monitoring serum potassium and glucose levels 1

Nebulized Beta-2 Agonist (Adjunctive Therapy)

• Albuterol: 10–20 mg in 4 mL nebulized over 10–15 minutes 1, 2, 3
• Onset: ~30 minutes; duration: 2–4 hours 1, 2
• Reduces serum potassium by 0.5–1.0 mEq/L 1
• Can be repeated every 2 hours if needed 1
• Combined insulin-glucose plus nebulized beta-agonist is more effective than either alone 1

Sodium Bicarbonate (ONLY with Metabolic Acidosis)

• 50 mEq IV over 5 minutes 1, 2, 3
• Use ONLY when metabolic acidosis is documented (pH <7.35 and bicarbonate <22 mEq/L) 1, 2
• Onset: 30–60 minutes (slower than insulin or beta-agonists) 1, 2
• Promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release 1
• Do NOT use without documented acidosis—it is ineffective and wastes time 1

Common pitfall: Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. Rebound hyperkalemia is common after effects wane (2–6 hours). 1

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

Loop Diuretics (Renal Function Dependent)

• Furosemide 40–80 mg IV to increase urinary potassium excretion 1, 2, 3
• Effective only when eGFR >30 mL/min and adequate urine output 1
• Titrate to maintain euvolemia, not primarily for potassium management 1

Hemodialysis (Most Reliable and Effective Method)

Hemodialysis is the gold standard for severe hyperkalemia. Absolute indications include: 1, 2, 3

• 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

In hemodynamically unstable patients (hypotensive, requiring vasopressors), continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts and reduce risk of intradialytic hypotension. 1

Monitor for rebound hyperkalemia: Potassium levels can rebound within 4–6 hours post-dialysis as intracellular potassium redistributes to extracellular space. Check potassium every 2–4 hours initially in patients with severe initial hyperkalemia (>6.5 mEq/L) or ongoing potassium release. 1

Potassium Binders (Sub-Acute/Chronic Management)

Newer potassium binders are preferred over sodium polystyrene sulfonate: 1, 3

Agent	Dosing	Onset	Key Points
Sodium zirconium cyclosilicate (SZC/Lokelma) [1,4]	10g three times daily for 48h, then 5–15g once daily	~1 hour	Suitable for urgent outpatient scenarios; reduces potassium within 1 hour of single 10g dose
Patiromer (Veltassa) [1]	8.4g once daily with food, titrated up to 25.2g daily	~7 hours	Must be separated from other oral meds by ≥3 hours; monitor magnesium levels
Sodium polystyrene sulfonate (Kayexalate) [1,5]	AVOID	Variable	Risk of bowel necrosis, colonic ischemia, intestinal perforation; limited efficacy data

FDA warning on sodium polystyrene sulfonate: Cases of intestinal necrosis (potentially fatal) and serious GI adverse events (bleeding, ischemic colitis, perforation) have been reported, especially with concomitant sorbitol use. Avoid in patients with abnormal bowel function, post-surgical ileus, constipation risk, or inflammatory bowel disease. 5

Medication Management During Acute Episode

Immediately hold or reduce these medications when potassium >6.5 mEq/L: 1

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
• NSAIDs
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
• 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, using concurrent potassium binder (patiromer or SZC) to enable continuation of these life-saving medications. 1 Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease. 1

Monitoring Protocol

Acute Phase

• Re-measure serum potassium 1–2 hours after insulin/glucose or beta-agonist therapy 1
• Continue potassium checks every 2–4 hours until stable 1
• Obtain repeat ECG to confirm resolution of cardiac changes 1

Post-Acute Phase

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

Critical Pitfalls to Avoid

1. Do NOT delay calcium administration while awaiting repeat potassium levels when ECG changes are present—ECG changes indicate urgent need regardless of exact potassium value 1
2. Never give insulin without glucose—hypoglycemia can be fatal 1
3. Do NOT use sodium bicarbonate without documented metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L)—it is ineffective without acidosis 1
4. Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
5. Remember that calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize; failure to initiate definitive removal will result in recurrent life-threatening arrhythmias within 30–60 minutes 1
6. Avoid sodium polystyrene sulfonate (Kayexalate) for acute management due to delayed onset, limited efficacy, and risk of bowel necrosis 1, 5