If you administer an antidysrhythmic drug that is a complete sodium channel blocker, which outcome would you expect?

If you administer an antidysrhythmic drug that is a complete sodium channel blocker, which outcome would you expect?

• A. It would prevent the development of phase 0, thereby inhibiting depolarization.
• B. It would cause excessive muscular contraction, because sodium is the principle cation in myofibril contraction.
• C. It would prevent the efflux (outflow) of calcium from within the cell.
• D. It would impede the sodium-potassium pump from replacing the ions to their original locations.

Answer: (A)

Blocking fast sodium channels stops the rapid depolarization phase. Phase 0 of the cardiac action potential is driven by a swift inward Na+ current through these channels. If they’re blocked completely, there’s almost no Na+ influx to drive the upstroke, so the slope of phase 0 is lost and depolarization is inhibited. That’s why the expected outcome is prevention of phase 0 and, consequently, slowed or blocked conduction through the myocardium. The other options don’t fit because calcium handling and the Na+/K+ pump aren’t directly governed by Na+ channel blockade, and contraction is driven by calcium dynamics rather than sodium influx.

Blocking fast sodium channels stops the rapid depolarization phase. Phase 0 of the cardiac action potential is driven by a swift inward Na+ current through these channels. If they’re blocked completely, there’s almost no Na+ influx to drive the upstroke, so the slope of phase 0 is lost and depolarization is inhibited. That’s why the expected outcome is prevention of phase 0 and, consequently, slowed or blocked conduction through the myocardium.

The other options don’t fit because calcium handling and the Na+/K+ pump aren’t directly governed by Na+ channel blockade, and contraction is driven by calcium dynamics rather than sodium influx.