Action Potentials (AP) in Cardiac Muscle- What made cardiac AP longer

Action Potentials (AP) in Cardiac Muscle

The Cardiac Muscle action potential averages about 105 mv.

It rises from about -85 mv (between beats) to about +20 mv (during each beat).

After the initial spike, the membrane remains depolarized for about 0.2 second (plateau phase).

Plateau is followed by abrupt repolarization The presence of plateau in AP causes 15 times longer  ventricular contraction than in skeletal muscle
.

What made cardiac AP longer

Skeletal muscle AP is caused by sudden opening of fast Na channels (open for a few thousandths of a second).

In cardiac muscle AP is caused by opening of two types of channels:

(1) fast Na channels (same as those in skeletal muscle)

(2) slow Ca channels (also called Ca-Na channels).

Ca channels are slower to open, remain open for tenths of a second, Large numbers of Ca/Na flow inside causing plateau.

Ca entering during plateau activates contraction (in skeletal muscle activated by Ca from sarcoplasmic reticulum (SR)).

The second major difference between cardiac & skeletal muscle is the immediate decrease in “K” ions permeability after onset of AP.

“K” permeability decreases about fivefold (does not occur in skeletal muscle), preventing early return of the AP voltage.

When slow Ca-Na channels close (0.2 to 0.3 second) & Ca – Na ions influx ceases, membrane permeability of K ions increases rapidly.

This rapid loss of K immediately returns the membrane potential to its resting level (repolarization) & ending the AP.

The presence of plateau in AP causes 15 times longer  ventricular contraction than in skeletal muscle