Integrate knowledge of sodium, potassium, and membrane potentials to choose the best explanation for why a rapid rise in extracellular potassium concentration (hyperkalemia) can lead to cardiac conduction abnormalities.

Hyperkalemia increases osmotic water loss across the myocardium that mechanically stretches conduction fibers, and this mechanical distortion is the primary cause of observed arrhythmias rather than any change in membrane potential.

Higher extracellular K+ leads to immediate hyperpolarization of cardiac cells which speeds up sodium channel recovery and therefore always causes benign increases in heart rate without conduction disturbances.

Increased extracellular K+ preferentially binds to calcium-binding sites in troponin, making contraction more efficient and protecting against arrhythmia, so any observed conduction disturbances must originate from other electrolyte abnormalities.

Elevated extracellular K+ reduces the gradient across the membrane, depolarizes resting membrane potential, inactivates sodium channels, and impairs action potential initiation and conduction in cardiac myocytes, producing arrhythmias.