Normal Impulse Conduction

Sequence of Cardiac Electrical Activation

The action potentials generated by the SA node spread throughout the atria primarily by cell-to-cell conduction at a velocity of about 0.5 m/sec. There is some functional evidence for the existence of specialized conducting pathways within the atria (termed internodal tracts), although this is controversial. 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 rapid depolarization of ventricular myocytes throughout both ventricles.

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 influenced by autonomic nerve activity. This autonomic control is most apparent at the AV node. Sympathetic activation increases conduction velocity in the AV node by increasing the rate of depolarization (increasing slope of phase 0) of the action potentials. This leads to more rapid depolarization of adjacent cells, which leads to a more rapid conduction of action potentials (positive dromotropy). Sympathetic activation of the AV node reduces the normal delay of conduction through the AV node, thereby reducing the time between atrial and ventricular contraction. The increase in AV nodal conduction velocity can be seen as a decrease in the P-R interval of the electrocardiogram.

Sympathetic nerves exert their actions on the AV node by releasing the neurotransmitter norepinephrine that binds to beta-adrenoceptors, leading to an increase in 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) at the AV node by decreasing the slope of phase 0 of the nodal action potentials. This leads to slower depolarization of adjacent cells, and reduced velocity of conduction. 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 sometimes 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.

Phase 0 of action potentials at the AV node is not dependent on fast sodium channels as in non-nodal tissue, but instead is 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.

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. In non-nodal cardiac tissue, 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. These membrane changes result in a decrease in speed by which action potentials are conducted within the heart. 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.