Nodal Tissue and Rhythmic Excitation of Heart

Nodal Tissue


The human heart has a special system for rhythmic self-excitation and repetitive contraction approximately 100,000 times each day, or 3 billion times in the average human lifetime. This impressive feat is performed by a system that:

  1. Generates rhythmical electrical impulses to initiate rhythmical contraction of the heart muscle, and
  2. Conducts these impulses rapidly through the heart.

When this system functions normally, the atria contract about one sixth of a second ahead of ventricular contraction, which allows filling of the ventricles before they pump the blood through the lungs and peripheral circulation.

Another special importance of the system is that it allows all portions of the ventricles to contract almost simultaneously, which is essential for the most effective pressure generation in the ventricular chambers.

Also Read, How a Nerve Impulse is Generated?

What is Nodal Tissue?

Nodal tissue is the specialized excitatory and conductive system of the heart that controls cardiac contractions. The following figure shows the sinus node (also called sinoatrial or S-A node) in which the normal rhythmical impulses are generated; the internodal pathways that conduct impulses from the sinus node to the atrioventricular (A-V) node; the A-V node in which impulses from the atria are delayed before passing into the ventricles; the A-V bundle, which conducts impulses from the atria into the ventricles; and the left and right bundle branches of Purkinje fibers, which conduct the cardiac impulses to all parts of the ventricles.

Sinus Node (Sinoatrial Node)

The sinus node (also called sinoatrial node) is a small, flattened, ellipsoid strip of specialized cardiac muscle about 3 millimeters wide, 15 millimeters long, and 1 millimeter thick. It is located in the superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava.

The fibers of this node have almost no contractile muscle filaments and are each only 3 to 5 micrometers in diameter, in contrast to a diameter of 10 to 15 micrometers for the surrounding atrial muscle fibers. However, the sinus nodal fibers connect directly with the atrial muscle fibers so that any action potential that begins in the sinus node spreads immediately into the atrial muscle wall.

Automatic Electrical Rhythmicity of Sinus Node Fibers

Some cardiac fibers have the capability of self-excitation, a process that can cause automatic rhythmical discharge and contraction. This capability is especially true of the fibers of the heart’s specialized conducting system, including the fibers of the sinus node.

For this reason, the sinus node ordinarily controls the rate of beat of the entire heart, as discussed in detail later on. First, let us describe this automatic rhythmicity.

Mechanism of SA Node Rhythmicity

Let us compare action potentials recorded from inside a sinus nodal fiber for three heartbeats and, by comparison, a single ventricular muscle fiber action potential.

Note that the “resting membrane potential” of the sinus nodal fiber between discharges has a negativity of about −55 to −60 millivolts, in comparison with −85 to −90 millivolts for the ventricular muscle fiber.

The cause of this lesser negativity is that the cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions, and positive charges of the entering sodium and calcium ions neutralize some of the intracellular negativity.

Cardiac muscle has three main types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are:

  1. Fast sodium channels
  2. L-type calcium channels (slow sodium-calcium channels), and
  3. Potassium channels

Opening of the fast sodium channels for a few 10,000ths of a second is responsible for the rapid upstroke spike of the action potential observed in ventricular muscle because of rapid influx of positive sodium ions to the interior of the fiber.

Then the “plateau” of the ventricular action potential is caused primarily by slower opening of the slow sodium-calcium channels, which lasts for about 0.3 second. Finally, opening of potassium channels allows diffusion of large amounts of positive potassium ions in the outward direction through the fiber membrane and returns the membrane potential to its resting level.

However, there is a difference in the function of these channels in the sinus nodal fiber because the ‘resting’ potential is much less negative—only −55 millivolts in the nodal fiber instead of the −90 millivolts in the ventricular muscle fiber.

At this level of −55 millivolts, the fast sodium channels mainly have already become ‘inactivated,’ which means that they have become blocked. The cause of this is that any time the membrane potential remains less negative than about −55 millivolts for more than a few milliseconds, the inactivation gates on the inside of the cell membrane that close the fast sodium channels become closed and remain so.

Therefore, only the slow sodium-calcium channels can open (i.e., can become ‘activated’) and thereby cause the action potential. As a result, the atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. Also, after the action potential does occur, return of the potential to its negative state occurs slowly as well, rather than the abrupt return that occurs for the ventricular fiber.

Self-Excitation of Nodal Tissues

Because of the high sodium ion concentration in the extracellular fluid outside the nodal fiber, as well as a moderate number of already open sodium channels, positive sodium ions from outside the fibers normally tend to leak to the inside.

Therefore, between heartbeats, influx of positively charged sodium ions causes a slow rise in the resting membrane potential in the positive direction. Thus, the ‘resting’ potential gradually rises and becomes less negative between each two heartbeats.

When the potential reaches a threshold voltage of about −40 millivolts, the L-type calcium channels become ‘activated’, thus causing the action potential. Therefore, basically, the inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.

Why does this leakiness to sodium and calcium ions not cause the sinus nodal fibers to remain depolarized all the time? Two events occur during the course of the action potential to prevent such a constant state of depolarization.

First, the L-type calcium channels become inactivated (i.e., they close) within about 100 to 150 milliseconds after opening, and second, at about the same time, greatly increased numbers of potassium channels open. Therefore, influx of positive calcium and sodium ions through the L-type calcium channels ceases, while at the same time large quantities of positive potassium ions diffuse out of the fiber.

Both of these effects reduce the intracellular potential back to its negative resting level and therefore terminate the action potential. Furthermore, the potassium channels remain open for another few tenths of a second, temporarily continuing movement of positive charges out of the cell, with resultant excess negativity inside the fiber; this process is called hyperpolarization.

The hyperpolarization state initially carries the ‘resting’ membrane potential down to about −55 to −60 millivolts at the termination of the action potential.

Why is this new state of hyperpolarization not maintained forever? The reason is that during the next few tenths of a second after the action potential is over, progressively more and more potassium channels close. The inward-leaking sodium and calcium ions once again overbalance the outward flux of potassium ions, which causes the ‘resting’ potential to drift upward once more, finally reaching the threshold level for discharge at a potential of about −40 millivolts.

Then the entire process begins again: self-excitation to cause the action potential, recovery from the action potential, hyperpolarization after the action potential is over, drift of the ‘resting’ potential to threshold, and finally re-excitation to elicit another cycle. This process continues throughout a person’s life.

Internodal and Interatrial Fibers transmit Cardiac Impulses through the Atria

The ends of the sinus nodal fibers connect directly with surrounding atrial muscle fibers. Therefore, action potentials originating in the sinus node travel outward into these atrial muscle fibers.

In this way, the action potential spreads through the entire atrial muscle mass and, eventually, to the A-V node. The velocity of conduction in most atrial muscle is about 0.3 m/sec, but conduction is more rapid, about 1 m/sec, in several small bands of atrial fibers.

One of these bands, called the anterior interatrial band, passes through the anterior walls of the atria to the left atrium. In addition, three other small bands curve through the anterior, lateral, and posterior atrial walls and terminate in the A-V node; these are called, respectively, the anterior, middle, and posterior internodal pathways.

The cause of more rapid velocity of conduction in these bands is the presence of specialized conduction fibers. These fibers are similar to even more rapidly conducting ‘Purkinje fibers’ of the ventricles, which are discussed as follows.

AV Node delays Impulse Conduction from Atria to Ventricles

The atrial conductive system is organized so that the cardiac impulse does not travel from the atria into the ventricles too rapidly; this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins.

It is primarily the A-V node and its adjacent conductive fibers that delay this transmission into the ventricles. The A-V node is located in the posterior wall of the right atrium immediately behind the tricuspid valve. Note that the impulse, after traveling through the internodal pathways, reaches the A-V node about 0.03 second after its origin in the sinus node.

Then, there is a delay of another 0.09 second in the A-V node itself before the impulse enters the penetrating portion of the A-V bundle, where it passes into the ventricles. A final delay of another 0.04 second occurs mainly in this penetrating A-V bundle, which is composed of multiple small fascicles passing through the fibrous tissue separating the atria from the ventricles.

Thus, the total delay in the A-V nodal and A-V bundle system is about 0.13 second. This delay, in addition to the initial conduction delay of 0.03 second from the sinus node to the A-V node, makes a total delay of 0.16 second before the excitatory signal finally reaches the contracting muscle of the ventricles.

The slow conduction in the transitional, nodal, and penetrating A-V bundle fibers is caused mainly by diminished numbers of gap junctions between successive cells in the conducting pathways, so there is great resistance to conduction of excitatory ions from one conducting fiber to the next. Therefore, it is easy to see why each succeeding cell is slow to be excited.

Rapid Transmission in Ventricular Purkinje System

Special Purkinje fibers lead from the A-V node through the A-V bundle into the ventricles. Except for the initial portion of these fibers where they penetrate the A-V fibrous barrier, they have functional characteristics that are quite the opposite of those of the A-V nodal fibers.

They are very large fibers, even larger than the normal ventricular muscle fibers, and they transmit action potentials at a velocity of 1.5 to 4.0 m/sec, a velocity about six times that in the usual ventricular muscle and 150 times that in some of the A-V nodal fibers. This velocity allows almost instantaneous transmission of the cardiac impulse throughout the entire remainder of the ventricular muscle.

The rapid transmission of action potentials by Purkinje fibers is believed to be caused by a very high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up the Purkinje fibers.

Therefore, ions are transmitted easily from one cell to the next, thus enhancing the velocity of transmission. The Purkinje fibers also have very few myofibrils, which means that they contract little or not at all during the course of impulse transmission.

One-Way Conduction Through the A-V Bundle

A special characteristic of the A-V bundle is the inability, except in abnormal states, of action potentials to travel backward from the ventricles to the atria. This characteristic prevents re-entry of cardiac impulses by this route from the ventricles to the atria, allowing only forward conduction from the atria to the ventricles.

Furthermore, it should be recalled that everywhere, except at the A-V bundle, the atrial muscle is separated from the ventricular muscle by a continuous fibrous barrier. This barrier normally acts as an insulator to prevent passage of the cardiac impulse between atrial and ventricular muscle through any other route besides forward conduction through the A-V bundle.

In rare instances, an abnormal muscle bridge does penetrate the fibrous barrier elsewhere besides at the A-V bundle. Under such conditions, the cardiac impulse can re-enter the atria from the ventricles and cause serious cardiac arrhythmias.

Distribution of the Purkinje Fibers in the Ventricles— The Left and Right Bundle Branches

After penetrating the fibrous tissue between the atrial and ventricular muscle, the distal portion of the A-V bundle passes downward in the ventricular septum for 5 to 15 millimeters toward the apex of the heart.

Then, the bundle divides into left and right bundle branches that lie beneath the endocardium on the two respective sides of the ventricular septum. Each branch spreads downward toward the apex of the ventricle, progressively dividing into smaller branches. These branches in turn course sidewise around each ventricular chamber and back toward the base of the heart.

The ends of the Purkinje fibers penetrate about one third of the way into the muscle mass and finally become continuous with the cardiac muscle fibers. The total elapsed time averages only 0.03 second from the time the cardiac impulse enters the bundle branches in the ventricular septum until it reaches the terminations of the Purkinje fibers.

Therefore, once the cardiac impulse enters the ventricular Purkinje conductive system, it spreads almost immediately to the entire ventricular muscle mass.

Control of Excitation and Conduction

In the discussion thus far of the genesis and transmission of the cardiac impulse through the heart, we have noted that the impulse normally arises in the sinus node. In some abnormal conditions, this is not the case. Other parts of the heart can also exhibit intrinsic rhythmical excitation in the same way that the sinus nodal fibers do; this capability is particularly true of the A-V nodal and Purkinje fibers.

The A-V nodal fibers, when not stimulated from some outside source, discharge at an intrinsic rhythmical rate of 40 to 60 times per minute, and the Purkinje fibers discharge at a rate somewhere between 15 and 40 times per minute. These rates are in contrast to the normal rate of the sinus node of 70 to 80 times per minute.

Why then does the sinus node rather than the A-V node or the Purkinje fibers control the heart’s rhythmicity? The answer derives from the fact that the discharge rate of the sinus node is considerably faster than the natural self-excitatory discharge rate of either the A-V node or the Purkinje fibers. Each time the sinus node discharges, its impulse is conducted into both the A-V node and the Purkinje fibers, also discharging their excitable membranes.

However, the sinus node discharges again before either the A-V node or the Purkinje fibers can reach their own thresholds for self-excitation. Therefore, the new impulse from the sinus node discharges both the A-V node and the Purkinje fibers before self-excitation can occur in either of these sites.

Thus, the sinus node controls the beat of the heart because its rate of rhythmical discharge is faster than that of any other part of the heart. Therefore, the sinus node is almost always the pacemaker of the normal heart.