A 42-year-old man from Mumbai presents to the emergency department with acute onset weakness and tingling in his legs progressing to his arms over 2 hours. He reports recent gastroenteritis 3 weeks ago. On examination, he has ascending paralysis with areflexia and intact sensation. Nerve conduction studies show demyelination with conduction blocks. CSF analysis reveals elevated protein with normal cell count. During mechanical ventilation, continuous cardiac monitoring shows peaked T waves and prolonged QT interval on ECG. Serum potassium is 6.8 mEq/L. Which ion channel dysfunction best explains the cardiac dysrhythmia observed in this patient?

Explanation

## Clinical Context: Guillain-Barré Syndrome with Hyperkalemia This patient presents with classic Guillain-Barré syndrome (GBS)—acute demyelinating polyradiculoneuropathy. The complication here is **severe hyperkalemia** (K+ = 6.8 mEq/L), which is a known risk in GBS due to muscle breakdown and rhabdomyolysis. ## Mechanism of Hyperkalemia-Induced Cardiac Changes **Key Point:** Hyperkalemia causes peaked T waves and prolonged QT by altering the **repolarization phase** of the cardiac action potential. ### Normal Repolarization During phase 3 of the cardiac action potential, **K+ efflux** through voltage-gated K+ channels (primarily IK) restores the negative membrane potential. This outward K+ current is the dominant repolarizing force. ### Effect of Hyperkalemia 1. Elevated extracellular K+ reduces the K+ concentration gradient (inside-to-outside) 2. By the Nernst equation, the K+ equilibrium potential becomes **less negative** (moves from −90 mV toward 0 mV) 3. The driving force for K+ efflux **decreases** 4. Repolarization slows → **prolonged QT interval** 5. Early repolarization (phase 1–2) becomes exaggerated → **peaked T waves** **High-Yield:** The peaked T wave is the **earliest ECG sign of hyperkalemia** and reflects altered phase 2–3 repolarization kinetics. ## Why This Is Not the Other Options | Phase | Ion Channel | Effect of Hyperkalemia | ECG Finding | |-------|-------------|----------------------|-------------| | **Phase 0 (Depolarization)** | Na+ influx ↓ | Slowed QRS, prolonged PR | NOT peaked T | | **Phase 2 (Plateau)** | Ca2+ influx | Shortened plateau | NOT peaked T | | **Phase 3 (Repolarization)** | K+ efflux ↓ | **Slowed repolarization** | **Peaked T + prolonged QT** | | **Na+/K+ ATPase block** | Loss of gradient | Depolarization, arrhythmia | NOT selective peaked T | **Clinical Pearl:** Peaked T waves appear at K+ ~5.5–6.5 mEq/L; at K+ >7, you see loss of P wave, widened QRS, and sine-wave pattern—signs of imminent cardiac arrest. ## Management Tie-In **Key Point:** Acute hyperkalemia treatment targets: 1. **Shift K+ intracellularly:** insulin + glucose, β~2~-agonists (albuterol), sodium bicarbonate 2. **Remove K+ from body:** diuretics, cation exchange resins, dialysis 3. **Stabilize myocardium:** calcium gluconate (does NOT lower K+, but antagonizes membrane effects) [cite:Guyton & Hall Ch 5]