Electrical Activity of the Heart

If the heart of a frog is removed from the body and all neural innervations are severed, it will still continue to beat as long as the myocardial cells remain alive. The automatic nature of the heartbeat is referred to as automaticity. As a result of experiments with isolated myocardial cells and clinical experience with patients who have specific heart disorders, many regions within the heart have been shown to be capable of originating action potentials and functioning as pacemakers. In a normal heart, however, only one region demonstrates spontaneous electrical activity and by this means functions as a pacemaker. This pacemaker region is called the sinoatrial node, or SA node. The SA node is located in the right atrium, near the opening of the superior vena cava.

Pacemaker Potential

The cells of the SA node do not maintain a resting membrane potential in the manner of resting neurons or skeletal muscle cells. Instead, during the period of diastole, the SA node exhibits a slow spontaneous depolarization called the pacemaker potential. The membrane potential begins at about -60 mV and gradually depolarizes to -40 mV, which is the threshold for producing an action

Heart and Circulation potential in these cells. This spontaneous depolarization is produced by the diffusion of Ca2+ through openings in the membrane called slow calcium channels. At the threshold level of depolarization, other channels, called fast calcium channels, open, and Ca2+ rapidly diffuses into the cells. The opening of voltage-regulated Na+ gates, and the inward diffusion of Na+ that results, may also contribute to the upshoot phase of the action potential in pacemaker cells (fig. 13.17). Repolarization is produced by the opening of K+ gates and outward diffusion of K+, as in the other excitable tissues previously discussed. Once repolarization to -60 mV has been achieved, a new pacemaker potential begins, again culminating with a new action potential at the end of diastole.

Some other regions of the heart, including the area around the SA node and the atrioventricular bundle, can potentially produce pacemaker potentials. The rate of spontaneous depolarization of these cells, however, is slower than that of the SA node. Thus, the potential pacemaker cells are stimulated by action potentials from the SA node before they can stimulate themselves through their own pacemaker potentials. If action potentials from the SA node are prevented from reaching these areas (through blockage of conduction), they will generate pacemaker potentials at their own rate and serve as sites for the origin of action potentials; they will function as pacemakers. A pacemaker other than the SA node is called an ectopic pacemaker, or alternatively, an ectopic focus. From this discussion, it is clear that the rhythm set by such an ectopic pacemaker is usually slower than that normally set by the SA node.

Myocardial Action Potential

Once another myocardial cell has been stimulated by action potentials originating in the SA node, it produces its own action potentials. The majority of myocardial cells have resting membrane potentials of about -90 mV. When stimulated by action potentials from a pacemaker region, these cells become depolarized to threshold, at which point their voltage-regulated Na+ gates open. The upshoot phase of the action potential of nonpacemaker cells is due to the inward diffusion of Na+. Following the rapid reversal of the membrane polarity, the membrane potential quickly declines to about -15 mV. Unlike the action potential of other cells, however, this level of depolarization is maintained for 200 to 300 msec before repolarization (fig. 13.18). This plateau phase results from a slow inward diffusion of Ca2+, which balances a slow outward diffusion of cations. Rapid repolarization at the end of the plateau phase is achieved, as in other cells, by the opening of K+ channels and the rapid outward diffusion of K+ that results.

Conducting Tissues of the Heart

Action potentials that originate in the SA node spread to adjacent myocardial cells of the right and left atria through the gap junctions between these cells. Since the myocardium of the atria is separated from the myocardium of the ventricles by the fibrous skeleton of the heart, however, the impulse cannot be conducted directly from the atria to the ventricles. Specialized conducting tissue, composed of modified myocardial cells, is thus required. These specialized myocardial cells form the AV node, bundle of His, and Purkinje fibers.

■ Figure 13.17 Pacemaker potentials and action potentials in the SA node. The pacemaker potentials are spontaneous depolarizations. When they reach threshold, they trigger action potentials,

0 50 100 150 200 250 300 350 400 Milliseconds

■ Figure 13.18 An action potential in a myocardial cell from the ventricles. The plateau phase of the action potential is maintained by a slow inward diffusion of Ca2+ The cardiac action potential, as a result, is about 100 times longer in duration than the "spike potential" of an axon.

Once the impulse has spread through the atria, it passes to the atrioventricular node (AV node), which is located on the inferior portion of the interatrial septum (fig. 13.19). From here, the impulse continues through the atrioventricular bundle, or bundle of His (pronounced "hiss"), beginning at the top of the interventricular septum. This conducting tissue pierces the fibrous skeleton of the heart and continues to descend along the interventricular septum. The atrioventricular bundle divides into right and left bundle branches, which are continuous with the Purkinje fibers within the ventricular

386 Chapter Thirteen

■ Figure 13.19 The conduction system of the heart. The conduction system consists of specialized myocardial cells that rapidly conduct the impulses from the atria into the ventricles.

Action Contraction (measured

Action Contraction (measured


walls. Stimulation of the Purkinje fibers causes both ventricles to contract simultaneously and eject blood into the pulmonary and systemic circulation.

Conduction of the Impulse

Action potentials from the SA node spread very quickly—at a rate of 0.8 to 1.0 meter per second (m/sec)—across the myocar-dial cells of both atria. The conduction rate then slows considerably as the impulse passes into the AV node. Slow conduction of impulses (0.03 to 0.05 m/sec) through the AV node accounts for over half of the time delay between excitation of the atria and ventricles. After the impulses spread through the AV node, the conduction rate increases greatly in the atrioventricular bundle and reaches very high velocities (5 m/sec) in the Purkinje fibers. As a result of this rapid conduction of impulses, ventricular contraction begins 0.1 to 0.2 second after the contraction of the atria.

Excitation-Contraction Coupling in Heart Muscle

Depolarization of myocardial cells stimulates the opening of voltage-gated Ca2+ channels in the sarcolemma (plasma membrane of the myocardial cells). This allows Ca2+ to diffuse down its concentration gradient into the cell. The Ca2+ that enters the cytoplasm from the extracellular fluid serves as a stimulus for the opening of Ca2+ release channels in the sarcoplasmic reticulum, which stores Ca2+ (by active transport) during muscle relaxation. Since the Ca2+ release channels in the sarcoplasmic reticulum are opened by the increased Ca2+ concentration in the cytoplasm, this mechanism is called calcium-stimulated-calcium-release. The Ca2+ entering across the sarcolemma serves mainly as a stimulus, while the Ca2+ released from the sarcoplasmic reticulum contributes most to the rise in cytoplasmic Ca2+ concentration during depolarization of the myocardial cell.

■ Figure 13.20 Correlation of the myocardial action potential with myocardial contraction. The time course for the myocardial action potential (A) is compared with the duration of contraction (B). Notice that the long action potential results in a correspondingly long absolute refractory period and relative refractory period. These refractory periods last almost as long as the contraction, so that the myocardial cells cannot be stimulated a second time until they have completed their contraction from the first stimulus.

Once Ca2+ is in the cytoplasm, it binds to troponin and stimulates contraction (described in chapter 12). As a result, myocardial cells contract when they are depolarized (fig. 13.20). During repolarization, the cytoplasmic concentration of Ca2+ is lowered by active transport of Ca2+ out of the cell across the sarcolemma (using a Na+-Ca2+ exchanger), and by active transport of Ca2+ into the cisternae of the sarcoplasmic retic-ulum. This allows relaxation to occur during repolarization (fig. 13.20).

Unlike skeletal muscles, the heart cannot sustain a contraction. This is because the atria and ventricles behave as if each were composed of only one muscle cell; the entire myocardium of each is electrically stimulated as a single unit and contracts as a unit. This contraction, corresponding in time to the long action potential of myocardial cells and lasting almost 300 msec, is analogous to the twitch produced by a single skeletal muscle fiber (which lasts only 20 to 100 msec in comparison). The heart normally cannot be stimulated again until after it has relaxed from its previous contraction because myocardial cells have long refractory periods (fig. 13.20) that correspond to the long duration of their action potentials. Summation of contractions is thus prevented, and the myocardium must relax after each contraction. By this means, the rhythmic pumping action of the heart is ensured.

Fox: Human Physiology, 13. Heart and Circulation Text © The McGraw-Hill

Eighth Edition Companies, 2003

Heart and Circulation 387



P-Q segment

P-Q segment

QRS complex

Action potential of | myocardial cell in ventricles

Action potential of | myocardial cell in ventricles




contract contract

+1 T

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2 0-l

1 1

- ^









<b c 2


.a m s -90-1-

■ Figure 13.21 The electrocardiogram (ECG). The ECG indicates the conduction of electrical impulses through the heart (a) and measures and records both the intensity of this electrical activity (in millivolts) and the time intervals involved (b).

Abnormal patterns of electrical conduction in the heart can produce abnormalities of the cardiac cycle and seriously compromise the function of the heart. These arrhythmias may be treated with a variety of drugs that inhibit specific aspects of the cardiac action potentials and thereby inhibit the production or conduction of impulses along abnormal pathways. Drugs used to treat arrhythmias may (1) block the fast Na2+ channel (quinidine, procainamide, lidocaine); (2) block the slow Ca2+ channel (verapamil); or (3) block P-adrenergic receptors (propranolol, atenolol). By this means, the latter drugs block the ability of catecholamines to stimulate the heart.

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