What is the recommended management, including calcium gluconate and a glucose‑insulin‑dextrose (GIK) drip, for a patient with hyperkalaemia (serum potassium ≥6.0 mmol/L) and cardiac toxicity?

GIK Drip for Hyperkalemia with Cardiac Toxicity

For a patient with severe hyperkalemia (≥6.0 mmol/L) and cardiac toxicity, immediately administer IV calcium gluconate 15-30 mL (10%) over 2-5 minutes to stabilize the cardiac membrane, followed by a glucose-insulin-dextrose (GIK) drip consisting of 10 units regular insulin with 25 grams dextrose (50 mL D50W) to shift potassium intracellularly within 30-60 minutes. 1, 2, 3

Immediate Emergency Management (First 5 Minutes)

Step 1: Cardiac Membrane Stabilization

• Administer IV calcium gluconate (10%) 15-30 mL over 2-5 minutes as the absolute first intervention if any ECG changes are present (peaked T waves, widened QRS, prolonged PR interval, flattened P waves). 1, 4, 3
• Calcium chloride (10%) 5-10 mL IV over 2-5 minutes is an alternative, particularly if central access is available. 1, 3
• Onset of action: 1-3 minutes, but duration is only 30-60 minutes. 5, 1
• Critical caveat: Calcium does NOT lower potassium—it only temporarily protects the heart from arrhythmias. 5, 1, 2
• If no ECG improvement within 5-10 minutes, repeat the calcium dose immediately. 1, 3
• Continuous cardiac monitoring is mandatory throughout treatment. 1, 4

Step 2: Intracellular Potassium Shift with GIK Drip

• Administer 10 units regular insulin IV push with 25 grams dextrose (50 mL D50W) simultaneously. 1, 2, 3, 6
• Expected potassium reduction: 0.5-1.2 mEq/L within 30-60 minutes. 1, 6
• Glucose must always accompany insulin to prevent life-threatening hypoglycemia. 5, 1, 6
• Monitor blood glucose every 1-2 hours during and after insulin administration. 1, 6
• Recheck potassium within 1-2 hours after insulin/glucose administration. 1, 6

Step 3: Adjunctive Beta-Agonist Therapy

• Administer nebulized albuterol 10-20 mg in 4 mL over 10 minutes to augment the insulin effect. 5, 1, 3, 7
• Expected additional potassium reduction: 0.5-1.0 mEq/L within 30-60 minutes. 1, 6
• The combination of insulin-glucose plus nebulized beta-agonist is more effective than either alone. 1, 7
• Duration of effect is short (2-4 hours), so rebound hyperkalemia is common. 5, 1

Concurrent Sodium Bicarbonate (Only If Metabolic Acidosis Present)

• Sodium bicarbonate 50 mEq IV over 5 minutes should ONLY be used if concurrent metabolic acidosis is documented (pH <7.35, bicarbonate <22 mEq/L). 5, 1, 8
• Bicarbonate is ineffective as monotherapy for hyperkalemia without acidosis. 5, 1, 3
• Onset of action is slower (30-60 minutes) compared to insulin or beta-agonists. 5, 1
• Never administer calcium through the same IV line as bicarbonate—precipitation will occur. 1

Definitive Potassium Removal (Next 1-6 Hours)

Loop Diuretics (If Adequate Renal Function)

• Furosemide 40-80 mg IV increases renal potassium excretion in non-oliguric patients with preserved kidney function. 5, 1, 4
• Effective only if eGFR >30 mL/min and adequate urine output. 5, 1

Hemodialysis (Most Effective Method)

• Hemodialysis is the most reliable and effective method for severe hyperkalemia, particularly in patients with oliguria, end-stage renal disease, or refractory hyperkalemia despite medical management. 5, 1, 2, 3
• Indications: K+ >6.5 mEq/L unresponsive to medical therapy, oliguria, ESRD, or ongoing potassium release (tumor lysis syndrome, rhabdomyolysis). 5, 1, 4
• Monitor for rebound hyperkalemia 4-6 hours post-dialysis as intracellular potassium redistributes. 1

Potassium Binders (Subacute Management)

• Sodium zirconium cyclosilicate (SZC/Lokelma) 10 g three times daily for 48 hours reduces potassium within 1 hour and is effective for both acute and chronic management. 1, 3
• Patiromer (Veltassa) 8.4 g once daily has a slower onset (~7 hours) and is reserved for subacute or chronic management. 5, 1
• Sodium polystyrene sulfonate (Kayexalate) should be avoided due to delayed onset, limited efficacy, and risk of bowel necrosis. 1, 3, 6

Monitoring Protocol

Immediate Phase (0-6 Hours)

• Continuous cardiac telemetry for all patients with K+ >6.0 mEq/L or ECG changes. 1, 4, 2
• Recheck potassium within 1-2 hours after insulin/glucose administration. 1, 6
• Monitor blood glucose every 1-2 hours to detect hypoglycemia. 1, 6
• Obtain ECG to document resolution of peaked T waves, widened QRS, or prolonged PR interval. 1, 4
• Continue monitoring potassium every 2-4 hours during the acute treatment phase until stabilized. 1, 6

Post-Acute Phase (6-24 Hours)

• Monitor for rebound hyperkalemia, especially after temporary measures (insulin, albuterol) wear off. 1, 6
• Reassess potassium 4-6 hours after initial treatment, as effects of insulin and beta-agonists are transient. 5, 1

Medication Management During Acute Episode

Immediately Discontinue or Hold:

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) if K+ >6.5 mEq/L. 5, 1, 4
• NSAIDs, potassium-sparing diuretics (spironolactone, amiloride, triamterene). 5, 1, 8
• Trimethoprim, heparin, beta-blockers. 5, 1
• Potassium supplements and salt substitutes. 5, 1, 8

After Acute Resolution:

• Restart RAAS inhibitors at a lower dose once K+ <5.0 mEq/L with concurrent potassium binder therapy, as these medications provide mortality benefit in cardiovascular and renal disease. 1, 4
• Initiate patiromer or SZC to enable continuation of life-saving RAAS inhibitor therapy. 5, 1

Critical Pitfalls to Avoid

• Never delay calcium administration while waiting for repeat potassium levels if ECG changes are present—ECG changes indicate urgent need regardless of the exact potassium value. 1, 2, 3
• Never give insulin without glucose—hypoglycemia can be life-threatening. 5, 1, 6
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 5, 1, 2
• Do not use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time. 5, 1, 8
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1
• Failure to initiate concurrent potassium-removal therapies will result in recurrent life-threatening arrhythmias within 30-60 minutes. 1, 2

Special Considerations

Diabetic Ketoacidosis (DKA)

• Patients with DKA typically have total body potassium deficits of 3-5 mEq/kg despite initially normal or elevated serum levels. 9
• Add 20-30 mEq/L potassium to IV fluids once K+ falls below 5.5 mEq/L with adequate urine output. 9, 6
• If K+ <3.3 mEq/L, delay insulin therapy until potassium is restored to prevent life-threatening arrhythmias. 9

Chronic Kidney Disease

• Patients with advanced CKD tolerate higher potassium levels (3.3-5.5 mEq/L for stage 4-5 CKD) due to compensatory mechanisms. 1
• Hemodialysis is often required for definitive management in ESRD patients. 5, 1, 2

Rebound Hyperkalemia

• Potassium levels can rebound 2-4 hours after temporary measures wear off, especially in ongoing potassium release states (tumor lysis syndrome, rhabdomyolysis). 1, 6
• Monitor every 2-4 hours initially in patients with severe initial hyperkalemia (>6.5 mEq/L). 1