The cardiac action potential differs from skeletal muscle action potentials in three ways: some cardiac muscle cells are self-excitable, all cardiac muscle cells are electrically connected by gap junctions and so contract together as a unit and the cardiac action potential has a much longer absolute refractory period--the period of time following a contraction during which the muscle cannot contract again. About 1% of cardiac fibers are auto-rhythmic, meaning they have the special ability to depolarize spontaneously and control the pace of the heart. These auto-rhythmic cells initiate the cardiac action potential. The cardiac action potential spans 5 phases, numbered 0-4.
Phase 0 of the cardiac action potential is the rapid depolarization phase. The auto-rhythmic cells of the heart have an unstable resting potential that continuously depolarizes, constantly drifting toward threshold levels. These spontaneously changing membrane potentials--called pacemaker potentials--trigger the contractions of the heart. During the rapid depolarization phase sodium ion channels on the membranes of the cells open up, and the influx of positive sodium ions helps to depolarize the cell further.
Phase 1 begins as the sodium ion channels begin to inactivate. Sodium influx slows, meanwhile the cell continues to lose potassium and chloride ions.
Phase 2 is the plateau phase of the cardiac action potential. When the threshold of approximately -40 mV is achieved, calcium ion channels open up. Calcium ions rush into the cell and begin the rising phase of the action potential, reversing the membrane potential.
Phase 3 is the rapid re-polarization of the cardiac action potential. Potassium channels open, potassium ions flow from the cell and the cell re-polarizes.
At phase 4 the cell has returned to resting membrane potential. However it will soon be stimulated to begin spontaneous depolarization again.