Cardiac Muscle Action Potential

Time To Read

2–3 minutes

Date Last Modified

Recall/Review

Let’s compare cardiac muscle to skeletal muscle, like your bicep. Skeletal muscle, such as your bicep, is composed of cylinders of skeletal muscle. Each of these cylinders connects to the brain via a neuron. They connect at a place called a neuromuscular junction. One muscle fiber in your bicep contracts and can’t lift something. Then, the brain sends another action potential to depolarize more skeletal muscle fibers.

Skeletal muscle can contract again one to two milliseconds later. This is a reflection of relatively short refractory periods compared to cardiac muscle.  Refractory periods of skeletal muscle are based on the time it takes the sodium and potassium channels to recover.  This quick recovery of skeletal muscle allows for rapid contractions. It also enables an event called tetany. Tetany is a sustained, uncontrollable muscle contraction.  An example is the lockjaw or sustained muscle contraction of the masseter muscle.

It is now that you should go back and familiarize yourself with action potentials from the nervous system chapter.  I will use these terms like you know what they mean.  If you don’t know what they mean, now is your chance to stop this video. You should watch one on action potentials.


Comparison

Each skeletal muscle fiber needs a connection to the brain. However, cardiac muscle fiber does not require it. With cardiac muscle, we have pacemaker cells that spontaneously depolarize which is called automaticity. These pacemaker cells share their depolarization with the surrounding cardiomyocytes, rendering a connection to the brain unnecessary. I mean…yes…there are neurons to the brain, but we discuss them later and they only modify, not set, heart contractions. Cardiomyocytes share their action potentials with their neighboring cells through gap junctions. These channels connect the cytoplasm of adjacent cells and allow ions to flow across from one cell to the next. 

The refractory period of a cardiomyocyte is very long compared to a skeletal muscle.  Skeletal muscle can have action potentials in very quick succession with refractory periods one to two milliseconds. In cardiac muscle the refractory period can be 15 to 200 milliseconds. That’s a big difference. This difference is created by this plateau that cardiomyocytes have in their action potential.  It’s not like a normal action potential. The plateau extends the refractory period making one cardiomyocyte wait before contracting again.


Cardiomyocyte AP

This plateau keeps the cardiomyocyte positively charged or depolarized for a long period.  At first, you might think that it’s because potassium ions are not flowing out of the cell. They should be flowing out during repolarization.  False, they are. However, there are calcium cations flowing into the cell. The flow of calcium cations occurs with each of these cations having two extra protons. In comparison, potassium has one extra proton. This difference caused the plateau and keeps the cardiomyocyte more positive for a longer period of time.

The plateau prevents the cardiomyocyte from having another action potential right on top of the first.  Basically, the plateau makes a cardiac muscle fiber wait a little before it can contract again.  Drugs like digoxin can affect calcium channels, altering the plateau’s duration.  An overdose of digoxin produces one eternal plateau.  And death.  It causes death. People dying from dig overdose have one last action potential that never stops. 



List of terms