Cardiovascular Physiology Concepts
                                    Richard E. Klabunde, Ph.D.

Normal Impulse Conduction

• Sequence of Cardiac Electrical Activation
• Regulation of Conduction
• Conduction Defects and their Treatment

Sequence of Cardiac Electrical Activation

The action potentials generated by the SA node spread throughout the atria primarily by cell-to-cell conduction.   There is some functional evidence for the existence of specialized conducting pathways within the atria (termed internodal tracts), although this is controversial. The conduction velocity of action potentials in the atrial muscle is about 0.5 m/sec. As the wave of action potentials depolarizes the atrial muscle, the cardiomyocytes contract by a process termed excitation-contraction coupling.

Normally, the only pathway available for action potentials to enter the ventricles is through a specialized region of cells (atrioventricular node, or AV node) located in the inferior-posterior region of the interatrial septum. The AV node is a highly specialized conducting tissue (cardiac, not neural in origin) that slows the impulse conduction considerably (to about 0.05 m/sec) thereby allowing sufficient time for complete atrial depolarization and contraction (systole) prior to ventricular depolarization and contraction.

The impulses then enter the base of the ventricle at the Bundle of His and then follow the left and right bundle branches along the interventricular septum.  These specialized fibers conduct the impulses at a very rapid velocity (about 2 m/sec).  The bundle branches then divide into an extensive system of Purkinje fibers that conduct the impulses at high velocity (about 4 m/sec) throughout the ventricles. This results in depolarization of ventricular myocytes and ventricular contraction.

The conduction system within the heart is very important because it permits a rapid and organized depolarization of ventricular myocytes that is necessary for the efficient generation of pressure during systole. The time (in seconds) to activate the different regions of the heart are shown in the figure to the right. Atrial activation is complete within about 0.09 sec (90 msec) following SA nodal firing. After a delay at the AV node, the septum becomes activated (0.16 sec). All the ventricular mass is activated by about 0.23 sec.

Regulation of Conduction

The conduction of electrical impulses throughout the heart, and particularly in the specialized conduction system, is strongly influenced by autonomic nerve activity. Sympathetic activation increases conduction velocity in nodal and non-nodal tissues by increasing the slope of phase 0 of the action potentials. This leads to more rapid depolarization of adjacent cells. This positive dromotropic effect of sympathetic activation results from norepinephrine binding to beta-adrenoceptors, which increases intracellular cAMP. Therefore, drugs that block beta-adrenoceptors (beta-blockers) decrease conduction velocity and can produce AV block.

Parasympathetic (vagal) activation decreases conduction velocity (negative dromotropy) in nodal and non-nodal tissues by decreasing the slope of phase 0 of the action potentials. This leads to slower depolarization of adjacent cells. Acetylcholine, released by the vagus nerve, binds to cardiac muscarinic receptors, which decreases intracellular cAMP. Excessive vagal activation can produce AV block. Drugs such as digitalis, which increase vagal activity to the heart, are used to reduce AV nodal conduction in patients that have atrial flutter or fibrillation. These atrial arrhythmias lead to excessive ventricular rate (tachycardia) that can be suppressed by partially blocking impulses being conducted through the AV node.

Because conduction velocity depends on the rate of tissue depolarization, which is related to the slope of phase 0 of the action potential, conditions (or drugs) that alter phase 0 will affect conduction velocity.  For example, conduction can be altered by changes in membrane potential, which can occur during myocardial ischemia and hypoxia. Cellular hypoxia leads to membrane depolarization, inhibition of fast Na⁺ channels, a decrease in the slope of phase 0, and a decrease in action potential amplitude in non-nodal cardiac muscle. These membrane changes result in a decrease in speed by which action potentials are conducted within the heart. Antiarrhythmic drugs such as quinidine (a Class IA antiarrhythmic) that block sodium channels and cause a decrease in conduction velocity in non-nodal tissue.

Phase 0 action potentials at the AV node is not dependent on fast sodium channels, but instead are generated by the entry of calcium into the cell through slow-inward, L-type calcium channels. Blocking these channels with a calcium-channel blocker such as verapamil or diltiazem reduces the conduction velocity of impulses through the AV node and can produce AV block.

Conduction Defects

If the conduction system becomes damaged or dysfunctional, as can occur during ischemic conditions or myocardial infarction, electrical conduction becomes impaired. This can have a number of consequences. First, activation of the heart will be delayed, and in some cases, the sequence of activation will be altered. This can seriously impair ventricular pressure development. Second, damage to the conducting system can precipitate tachyarrhythmias by reentry mechanisms. Click here to learn more about altered impulse conduction.

RK Revised 04/06/07

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

© 1999-2008 Richard E. Klabunde, all rights reserved.