Porth's Essentials of Pathophysiology, 4e

387

Control of Cardiovascular Function

C h a p t e r 1 7

Bundle of His

AV node

SA node

Left posterior fascicle

Left anterior fascicle

A

Purkinje fibers

B

FIGURE 17-11. Conduction system of the heart and action potentials. (A) Action potential of sinoatrial (SA) and atrioventricular (AV) nodes. (B) Atrial muscle action potential. (C) Action potential of ventricular muscle and Purkinje fibers.

Right bundle

C

branch Left bundle branch

Action Potentials An action potential represents the sequential change in electrical potential that occurs across a cell membrane when excitation occurs (see Chapter 1, “Understanding Membrane Potentials”). Action potentials can be divided into three parts: the resting or unexcited state during which the membrane is polarized (positive on the outside and negative on the inside of the membrane), depolariza- tion or change in the direction of polarity (positive on the inside and negative on the outside), and repolariza- tion or reestablishment of polarity of the resting mem- brane potential. The sodium (Na + ), potassium (K + ), and calcium (Ca ++ ) ions are the major electrical charge carri- ers in cardiac muscle cells. Disorders of the ion channels along with disruption in the flow of these current-carry- ing ions are increasingly being linked to the generation of cardiac arrhythmias and conduction disorders. The action potential of cardiac muscle is divided into five phases: phase 0 —the upstroke or rapid depo- larization; phase 1 —early repolarization; phase 2 —the plateau; phase 3 —rapid repolarization; and phase 4 — the resting membrane potential (Fig. 17-12A). Cardiac muscle has three types of membrane ion channels that contribute to the voltage changes that occur during these phases of the action potential. They are the (1) fast sodium (Na + ) channels, (2) slow calcium (Ca ++ ) chan- nels, and (3) potassium (K + ) channels. During phase 0 in atrial and ventricular muscle and in the Purkinje conduction system, opening of the fast Na + channels for a few ten-thousandths of a second is responsible for the spikelike onset of the action poten- tial. The point at which the Na + gates open is called the depolarization threshold. When the cell has reached this threshold, a rapid influx of Na + to the interior of the cell membrane causes the membrane potential to shift from a resting membrane potential of approximately −90 mV to +20 mV. Phase 1 occurs at the peak of the action potential and signifies inactivation of the fast Na + channels with an

delays impulse transmission. A further delay occurs as the impulse travels through the transitional fibers and into the AV bundle, also known as the bundle of His. This delay provides a mechanical advantage whereby the atria can complete their ejection of blood before ventricular contraction begins. Under normal circum- stances, the AV node provides the only connection between the atrial and ventricular conduction systems. The atria and ventricles would beat independently of each other if the transmission of impulses through the AV node were blocked. The Purkinje system , which supplies the ventricles, has large specialized fibers that allow for rapid conduc- tion and almost instantaneous excitation of both the right and left ventricles. This rapid rate of conduction is necessary for the swift and efficient ejection of blood from the heart. Fibers of the Purkinje system originate in the AV node and then travel downward in the AV bundle into the ventricular septum, where they divide to form the right and left bundle branches that lie beneath the endocardium on the two respective sides of the ventricu- lar septum. The main trunk of the left bundle branch extends for approximately 1 to 2 cm before fanning out as it enters the septal area and divides further into two segments: the left posterior and anterior fascicles. The AV nodal fibers, when not stimulated, discharge at an intrinsic rate of 45 to 50 times a minute, and the Purkinje fibers discharge at 15 to 40 times per minute. Although the AV node and Purkinje system have the abil- ity to control the rhythm of the heart, they do not nor- mally do so because the discharge rate of the SA node is considerably faster. Each time the SA node discharges, its impulses are conducted into the AV nodal and Purkinje fibers, causing them to fire. Should the SA node fail to discharge, the AV node can assume the pacemaker func- tion of the heart, and the Purkinje system can assume the pacemaker function of the ventricles should the AV junc- tion fail to conduct impulses from the atria to the ven- tricles. Under these circumstances, the heart rate reflects the intrinsic firing rate of the prevailing structures.