Figure 1418

(a) Membrane potential recording from a ventricular muscle cell. (b) Simultaneously measured permeabilities P to potassium, sodium, and calcium during the action potential of (a).

channels because there is a delay in their opening (Figure 14-18b). The flow of positive calcium ions into the cell just balances the flow of positive potassium charge out of the cell and keeps the membrane depolarized at the plateau value.

Ultimately, repolarization does occur when the permeabilities of calcium and potassium return to their original state.

The action potentials of atrial cells, except those of the SA node, are similar in shape to those just described for ventricular cells, although the duration of their plateau phase is shorter.

In contrast, there are extremely important differences between action potentials of the vast majority of

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Circulation CHAPTER FOURTEEN

Circulation CHAPTER FOURTEEN

Nodal Cell Action Potential

FIGURE 14-19

Comparison of action potentials in (a) a ventricular muscle cell (from Figure 14-18) and (b) a sinoatrial (SA)-nodal cell. The most important difference is the presence of the pacemaker potential in the SA node.

FIGURE 14-19

Comparison of action potentials in (a) a ventricular muscle cell (from Figure 14-18) and (b) a sinoatrial (SA)-nodal cell. The most important difference is the presence of the pacemaker potential in the SA node.

the atrial and ventricular myocardial cells, as just described, and those in the conducting system. Figure 14-19b illustrates the action potentials of a myocardial cell from the SA node. Note that the resting potential of the SA-node cell is not steady but instead manifests a slow depolarization. This gradual depolarization is known as a pacemaker potential; it brings the membrane potential to threshold, at which point an action potential occurs. Following the peak of the action potential, the membrane repolarizes, and the gradual depolarization begins again.

Thus, the pacemaker potential provides the SA node with automaticity, the capacity for spontaneous, rhythmical self-excitation. The slope of the pacemaker potential—that is, how quickly the membrane potential changes per unit time—determines how quickly threshold is reached and the next action potential elicited. The inherent rate of the SA node—the rate exhibited in the total absence of any neural or hormonal input to the node—is approximately 100 depolarizations per minute.

What is responsible for the pacemaker potential? There are multiple ion-permeability changes that contribute to this gradual depolarization. The most important one, however, is movement of sodium ions into the cells through a special set of voltage-gated plasmamembrane channels that are opened by the re-polarizing phase of the preceding action potential. (Recall that the more common voltage-gated sodium channels of nerve, skeletal muscle, and nonconducting-system cardiac muscle are opened by depolarization occurring in the on-going action potential).

Several other portions of the conducting system are capable of generating pacemaker potentials, but the inherent rate of these other areas is slower than that of the SA node, and so they normally are "captured" by the SA node and do not manifest their own rhythm. However, they can do so under certain circumstances and are then termed ectopic pacemakers, an example of which is given in the next paragraph.

Recall that excitation travels from the SA node to both ventricles only through the AV node; therefore, drug- or disease-induced malfunction of the AV node may reduce or completely eliminate the transmission of action potentials from the atria to the ventricles. If this occurs, autorhythmic cells in the bundle of His, no longer driven by the SA node, begin to initiate excitation at their own inherent rate and become the pacemaker for the ventricles. Their rate is quite slow, generally 25 to 40 beats/min, and it is completely out of synchrony with the atrial contractions, which continue at the normal, higher rate of the SA node. Under such conditions, the atria are ineffective as pumps since they are often contracting against closed AV valves. Fortunately, atrial pumping, as we shall see, is relatively unimportant for cardiac function except during strenuous exercise.

The current treatment for all severe AV conduction disorders, as well as for many other abnormal rhythms is permanent surgical implantation of an electrical device, a pacemaker, that stimulates the ventricular cells at a normal rate.

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