40 y/o male with PMHx of metastatic colon cancer s/p chemo, resection with ostomy, cirrhosis due to liver mets, recent admission for hyponatremia and recurrent ascites who presents to the ED North side resus as a transfer from Bay Ridge for hypotension, requiring critical care. Patient did not have labs drawn at Bay ridge but EKG was done:
Low voltage, slight sinus tachycardia at a rate of 101.
Upon arrival on North side the patient had labs drawn:
After the ED team got the lab results, the nurse came over and stated the patient's cardiac monitor looks like QRS was widened, so they got the patient's EKG:
sinus tachycardia at 100bpm, widened QRS
And ordered the patient 2g Calcium Gluconate and Insulin Lispro 5u, which in our order set looks like this:
The nurse drew up the medications and brought it bedside, but before administering the medications, the patient's family looked concerned as the patient just became unresponsive.
Nurse checked for a pulse, the patient did not have a pulse, CPR started.
ROSC was achieved within 10 minutes, patient was intubated, placed on pressors for hypotension.
Patient's repeat labs revealed only slight hyperkalemia, but profoundly acidotic, did not have a repeat arrest while in the Emergency Department, but expired during his course.
Hyperkalemia is something that we see very often in the Emergency Department. We have an order set to help manage it, but there isn't an official hyperkalemia management algorithm.
Our order set is based off literature from the last 20+ years, but here is a review of hyperkalemia management and ongoing controversies
Hyperkalemia Treatment
Membrane Stabilization (Rafique 2021, Weisberg 2008)
For ECG changes or K⁺ > 6.5–7.0 mEq/L
IV calcium
Calcium gluconate (preferred)
Calcium chloride (more potent but vesicant)
10 mL of 10% solution IV over 2–5 minutes
Repeat every 5–10 minutes if ECG changes persist
Onset: <5 minutes; Duration: 30–60 minutes
Safe even in digoxin toxicity per updated literature (contraindication is outdated)
Intracellular Redistribution (Moussavi 2019, Keeney 2019, Ibarra 2024)
Insulin + Glucose - Shifts potassium into cells via Na⁺/K⁺ ATPase activation
5 units or 0.1u/kg of regular insulin + prolonged D10 infusion (250 mL over 2 hours) reduces rebound hypoglycemia
Onset: ~15-30 minutes; lowers K⁺ by 0.6-1.2 mEq/L
Beta-2 Agonist (Albuterol)
Nebulized 10–20 mg
Onset: ~30 minutes; lowers K⁺ by ~0.5 mEq/L
Additive to insulin; useful when IV access is delayed
Less effective in patients on beta-blockers
Elimination of Potassium
Hemodialysis - most rapid and definitive method indicated in:
Refractory hyperkalemia
Anuric or oliguric renal failure
Cardiac arrest due to hyperkalemia
Loop Diuretics
Furosemide if volume status and renal function permit
GI Binders:
Sodium polystyrene sulfonate (SPS / Kayexalate
Onset 2-6 hrs; low efficacy; risk of colonic necrosis, especially when combined with sorbitol
Patiromer & Sodium Zirconium Cyclosilicate (ZS-9)
Safer alternatives with better GI tolerability but not for emergent use due to slow onset
Controversies in Hyperkalemia Management
Reliability of ECG (Meyers 2017, Weisberg 2008)
ECG findings are neither sensitive nor specific
Many patients with severe hyperkalemia have normal ECGs
Others progress directly to VF/asystole with minimal ECG changes
Normal ECGs cannot rule out severe hyperkalemia
Sodium Polystyrene Sulfonate (SPS) Use (Sterns 2010, Parks 2019, Gupta 2021)
Poor efficacy in acute setting
Associated with intestinal necrosis, especially with sorbitol
Should be avoided in ED settings; consider alternatives
Insulin Dosing and Dextrose (Moussavi 2019, Keeney 2019, Ibarra 2024)
Previously thought that 10u regular insulin is required
5u or weight-based (0.1u/kg) is equally effective
Reduces risk of hypoglycemia, especially in ESRD, low body weight, or nondiabetics
D50 bolus alone may not match insulin duration
D10 infusion lowers risk of delayed hypoglycemia and is now preferred
Pseudo- and Spurious Hyperkalemia
Hemolysis, high WBC/platelet count, poor draw technique can falsely elevate K⁺
If patient has normal GFR and ECG, may not require treatment even if K⁺ > 5.5–6.0
Bicarbonate Use (Weisberg 2008, Rafique 2021, Long 2018, Gupta 2021)
Controversial benefit unless pH <7.2
It helps correct acidemia and facilitates K shifts into cells via H⁺/K⁺ exchange
May augment the effect of insulin and beta-agonists when used in acidemic patients, although it is rarely sufficient as monotherapy
Bicarbonate is specifically indicated in cases of TCA overdose requiring alkalinization, which may coincide with hyperkalemia
Minimal or no effect on serum potassium in patients with normal acid-base status
Bicarbonate infusion is slow-acting, taking hours to shift potassium compared to minutes with insulin or albuterol
Large-volume sodium bicarbonate infusions may lead to hypernatremia, volume overload, or metabolic alkalosis, particularly in patients with renal or heart failure
Alkalosis induced by bicarbonate can lower ionized calcium, potentially worsening arrhythmogenic risk in some settings
Sodium bicarbonate alone is not shown to reverse ECG changes caused by hyperkalemia and is not a substitute for calcium in membrane stabilization
Takeaways:
Give Calcium gluconate every 5-10 minutes until ECG changes resolve
Even if Potassium is not >6.0, patient may still have severe hyperkalemia
If there are ECG changes and suspected hyperkalemia, treat aggressively but a "normal" ECG alone cannot "rule out" hyperkalemia
Sodium Bicarbonate may only be effective in patients with acidosis to help augment other agents in reducing potassium levels, but otherwise not recommended