Hyperkalemia and Atrioventricular Block: Mechanism and Management
Mechanism
Elevated extracellular K⁺ reduces the resting membrane potential gradient, inactivating voltage-gated Na⁺ channels in cardiac myocytes. This slows phase 0 depolarization, decreasing conduction velocity (dV/dt max) through the AV node and His-Purkinje system, manifesting as PR prolongation → higher-degree AV block → sine-wave pattern → asystole.
ECG Progression
- Peaked T waves (earliest, K⁺ >5.5 mEq/L).
- PR prolongation (1st-degree AV block).
- QRS widening (intraventricular conduction delay).
- Loss of P waves (sinus node suppression).
- Sine-wave pattern (fusion of wide QRS and T).
- VF/asystole.
Emergency Treatment
| Agent | Mechanism | Onset | Duration |
|---|---|---|---|
| Calcium gluconate 1 g IV | Stabilizes membrane (antagonizes K⁺ effect) | Minutes | 30–60 min |
| Insulin 10 U + D50 25 g IV | Drives K⁺ into cells | 15–30 min | 4–6 hrs |
| Albuterol 10–20 mg neb | β₂-agonist → K⁺ shift intracellular | 30 min | 2–4 hrs |
| Sodium bicarbonate | Alkalinization → intracellular K⁺ shift | 15–30 min | Variable |
| Loop diuretic (furosemide) | Enhances renal K⁺ excretion | 30–60 min | Hours |
| K⁺ binders (patiromer, SZC) | GI K⁺ binding | Hours | Days |
| Dialysis | Direct removal | Immediate | Session-dependent |