The action potential recorded in a ventricular muscle fiber, shown in Figure 1, averages about 105 millivolts, which means that the intracellular potential rises from a very negative value, about −85 millivolts, between beats to a slightly positive value, about +20 millivolts, during each beat. After the initial spike, the membrane remains depolarized for about 0.2 second, exhibiting a plateau, followed at the end of the plateau by abrupt repolarization. The presence of this plateau in the action potential causes ventricular contraction to last as much as 15 times as long in cardiac muscle as in skeletal muscle.

Fig1. Rhythmical action potentials (in millivolts) from a Purkinje  fiber and from a ventricular muscle fiber, recorded by means of  microelectrodes. 

What Causes the Long Action Potential and the Plateau? Why is the action potential of cardiac muscle so long and why does it have a plateau, when the action potential of skeletal muscle does not have a plateau? The basic biophysical answers to these questions were presented in Chapter 5, but they merit summarizing here as well.

At least two major differences between the membrane properties of cardiac and skeletal muscle account for the prolonged action potential and the plateau in cardiac muscle. First, the action potential of skeletal muscle is caused almost entirely by the sudden opening of large numbers of fast sodium channels that allow tremendous numbers of sodium ions to enter the skeletal muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. At the end of this closure, repolarization occurs, and the action potential is over within another thousandth of a second or so.

In cardiac muscle, the action potential is caused by opening of two types of channels: (1) the same voltage activated fast sodium channels as those in skeletal muscle and (2) another entirely different population of Ltype calcium channels (slow calcium channels), which are also called calciumsodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions f lows through these channels to the interior of the cardiac muscle fiber, and this activity maintains a prolonged period of depolarization, causing the plateau in the action potential. Further, the calcium ions that enter during this plateau phase activate the muscle contractile process, whereas the calcium ions that cause skeletal muscle con traction are derived from the intracellular sarcoplasmic reticulum.

The second major functional difference between cardiac muscle and skeletal muscle that helps account for both the prolonged action potential and its plateau is this: Immediately after the onset of the action potential, the permeability of the cardiac muscle membrane for potassium ions decreases about fivefold, an effect that does not occur in skeletal muscle. This decreased potassium permeability may result from the excess calcium influx through the calcium channels just noted. Regardless of the cause, the decreased potassium permeability greatly decreases the outflux of positively charged potassium ions during the action potential plateau and thereby pre vents early return of the action potential voltage to its resting level. When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.

Summary of Phases of Cardiac Muscle Action Potential. Figure 2 summarizes the phases of the action potential in cardiac muscle and the ion flows that occur during each phase.

Fig2.  Phases of action potential of cardiac ventricular muscle  cell and associated ionic currents for sodium (iNa+), calcium (iCa++),  and potassium (iK+).

Phase 0 (depolarization), fast sodium channels open. When the cardiac cell is stimulated and depolarizes, the membrane potential becomes more positive. Voltage gated sodium channels (fast sodium channels) open and permit sodium to rapidly flow into the cell and depolarize it. The membrane potential reaches about +20 millivolts before the sodium channels close.

Phase 1 (initial repolarization), fast sodium channels close. The sodium channels close, the cell begins to repolarize, and potassium ions leave the cell through open potassium channels.

Phase 2 (plateau), calcium channels open and fast potassium channels close. A brief initial repolarization occurs and the action potential then plateaus as a result of (1) increased calcium ion permeability and (2) decreased potassium ion permeability. The voltage-gated calcium ion channels open slowly during phases 1 and 0, and calcium enters the cell. Potassium channels then close, and the combination of decreased potassium ion efflux and increased calcium ion influx causes the action potential to plateau.

Phase 3 (rapid repolarization), calcium channels close and slow potassium channels open. The closure of calcium ion channels and increased potassium ion permeability, permitting potassium ions to rapidly exit the cell, ends the plateau and returns the cell membrane potential to its resting level.

Phase 4 (resting membrane potential) averages about −90 millivolts.

Velocity of Signal Conduction in Cardiac Muscle. The velocity of conduction of the excitatory action potential signal along both atrial and ventricular muscle fibers is about 0.3 to 0.5 m/sec, or about 1/250 the velocity in very large nerve fibers and about 1/10 the velocity in skeletal muscle fibers. The velocity of conduction in the specialized heart conductive system—in the Purkinje fibers—is as great as 4 m/sec in most parts of the system, which allows reasonably rapid conduction of the excitatory signal to the different parts of the heart, as explained in Chapter 10.

Refractory Period of Cardiac Muscle. Cardiac muscle, like all excitable tissue, is refractory to restimulation during the action potential. Therefore, the refractory period of the heart is the interval of time, during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle. The normal refractory period of the ventricle is 0.25 to 0.30 second, which is about the duration of the prolonged plateau action potential. There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult to excite than normal but nevertheless can be excited by a very strong excitatory signal, as demonstrated by the early “premature” contraction in the second example of Figure 3. The refractory period of atrial muscle is much shorter than that for the ventricles (about 0.15 second for the atria compared with 0.25 to 0.30 second for the ventricles).

Fig3. Force of ventricular heart muscle contraction, showing  also the duration of the refractory period and relative refractory  period, plus the effect of premature contraction. Note that premature  contractions do not cause wave summation, as occurs in skeletal  muscle. 

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