A patient with severe hyperkalemia (serum K+ 7.5 mEq/L) develops flaccid weakness despite the expected depolarization of muscle membranes. The reduced excitability is best explained by:

• A Persistent inactivation of voltage-gated sodium channels ✓
• B Hyperpolarization of the resting membrane potential away from threshold
• C Increased potassium conductance raising the action potential overshoot
• D Enhanced activity of the Na-K ATPase hyperpolarizing the membrane

Explanation

High extracellular K+ depolarizes the resting membrane potential toward zero. Sustained partial depolarization holds voltage-gated Na+ channels in the inactivated state, so few channels are available to open on further stimulation and excitability falls. This distinguishes depolarization block from hypokalemia, where the membrane hyperpolarizes and a larger stimulus is required. The pump cannot compensate acutely for this degree of channel inactivation.

Reference: Ganong's Review of Medical Physiology, 27th ed.

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