The conduction system is responsible for the characteristic of autorythmicity of the myocardium. This page will include the anatomy and physiology of this specialized system. First let's examine the anatomy of the conduction system.
The heart's conduction system consists of the sinoatrial node, the atrioventricular node, internodal fasiculus, and the atrioventricular bundle, which divides into right and left branches. These two branches teminate into the purkinje fibers, otherwise called the subendocardial plexus. These fibers will become contiuous with the ventricular myocardial fibers. The above structures mentioned are all specially differentiated cardiac muscle fibers, separated from the normal myocardium by delicate envelopes of connective tissue. See diagram.
The sinoatrial node is located in the superior lateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava. This structure is usually five to eight millimeters in length, and occupies the whole thickness of the wall in the right atrium. The fibers of the sinoatrial node connect directly with the atrial fibers, so the action potential beginnning in the node speads immediately into the atria. See diagram.
The atrioventricular node is located in the interatrial septum, resting with its inferior surface on the fibrous atrioventricular ring. This is in the proximity of the attachment for the septal cusp of the tricuspid valve. The atrioventricular node is oval in shape and a little smaller than the sinoatrial node. Within the septum, the node extends forward from the opening of the coronary sinus, and continues anteriorly into the atrioventricular bundle. The atrioventricular bundle will then pass through the fibrous ring connecting the node to the ventricles. See diagram.
Connecting the sinoatial node to the atrioventricular node are internodal fasciculi. These fasciculi are thought to help transmit the impulse from the sinoatrial node to the atrioventricular node. However, impulses generated in the sinoatrial node spead to the atrioventricular node uniformily through the atrial myocardium. It is still somewhat unclear of the functioning of these fasciculi. See diagram.
The atrioventricular bundle or fasciculus is responsible for the activation of the ventricles. The thickness of this bundle is that of a wooden matchstick. This bundle is located in the posterior septal wall of the right atrium immediately behind the tricuspid valve and adjacent to the opening of the coronary sinus. The bundle passes through the fibrous ring in a hole located at the margin of the right trigone (this trigone is located between the aortic valve and the tricuspid valve). This is the only connection between the myocardium of the atria and the ventricles. On the ventricular side of the ring, the bundle runs downward and forward, running along the posterior margin of the membranous part of the interventricular septum. It then branches into a right and a left crus or bundle branch. These two branches straddle the uppper border of the muscular part of the interventricular septum. Each branch heads toward the apex of the ventricles under the endocardium of the septum. See diagram.
The right branch of the atrioventricular bundle crosses from the septum to the ventricular wall along the moderator band (or septomarginal bundle). The left branch, on the other hand, breaks up inpo branches and reaches the ventricular wall along several trabeculae carneae. These branches spread out as the subendocardial purkinje fibers over the ventricular wall and over the papillary muscles. Because of this arrangement, the impulses dispatched from the atrioventricular node first activate ventricular muscle in the region of the apex, assuring a "milking" action of the ventricles toward the openings of the aorta and the pulmonary trunk. See diagram.
The heart contains two specialized types of cardiac muscle cells. The majority, around 99 percent, of the cardiac muscle cells are contractile cells and are responsible for the mechanical work of pumping the heart. The second type of cardiac muscle cells are the autorhythmic cells. The function of these cells is to initiate and conduct action potentials that are responsible for the contraction of the working cells.
The cardiac muscle displays a pacemaker activity as opposed to a nerve or skeletal muscle cell which displays a membrane that remains at a constant resting potential unless stimulated. Pacemaker activity is defined as the membranes of cardiac muscle cells slowly depolarizing between action potentials until threshold is reached, at which time the membranes fire or has an action potential. These action potentials, generated by the autorhythmic cardiac muscle cells, will then spread throughout the heart triggering rhythmic beating without any nervous stimulation.
The specialized autorhythmic cells of cardiac muscle comprising the conduction system serve two main functions:1.) to generate rhythmical impulses to cause rhythmical contraction of the heart muscle and 2.) conducting these impulses rapidly throughout the heart. When this system works properly, the atria contract about one sixth of a second ahead of ventricular contraction. This will allow extra filling of the ventricles before they pump the blood through the lungs and peripheral circulation. Another important function of this system is it allows all portions of the ventricles to contract alomost simultaneously, which is essential for effective pressure generation in the ventricular chambers. In order to assure the rythmical beating of the heart the rates at which these autorhythmical cells are capable of generating action potentials differ due to differences in their rates of slow depolarization to threshold. Please refer to the table below.
| PURKINJE FIBERS |
As you can see from the above table, the sinoatrial node is capable of depolarizing the greatest extent. For this reason, the sinus node usually controls the rate of beat of the entire heart.
The potential of the sinoatrial node fibers between discharges has a negativity o fonly -55 to -60 millivolts in comparison with a ventricular muscle fiber which depolarizes at -85 to -90 millivolts. The cause of this reduced negativity is that the cell membranes of the sinus fibers are naturally leaky to sodium ions.
Before going any further a quick review of the role that membrane ion channels play in the depolarization and repolarization of cardiac muscle will be provided. There are three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are as follows:
- fast sodium channels
- slow calcium-sodium channels
- potassium channels
Opening of the fast sodium channels is responsible for the rapid spikelike onset of the action potential observed in ventricular muscle because of the rapid influx of positive sodium ions to the interior of the fiber. Next you have a plateau of the ventricular action potential caused primarily by a slower opening of the slow calcium-sodium channels. Lastly, increased opening of the potassium channels and diffusion of large amounts of positive potassium ions out of the fiber return the membrane potential to its resting level.
There is a difference in the function of the above mentioned channels in the sinoatrial node fibers. The reason for this is the much lesser negativity of teh "resting" potential, -55 millivolts. At this level of negativity, the fast sodium channels have basicly become "inactivated", meaning they have become blocked. The reason for this is any time the membrane potential remains less negative than around -60 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 calcium- sodium channels can open or become "activated", and cause the action potential. As a result, the action potential is slower to develop than that of the ventricular muscle, and it also recovers with a slow decrement of the potential rather than the abrupt recovery that occurs for the ventricular fiber.
The ends of the sinoatrial node fibers fuse with the surrounding atrial muscle fibers, and action potentials originating in the sinus node travel outward into these fibers. Therefore, the action potential travels through the entire atrial muscle mass and, eventually, reaching the atrioventricular node. The velocity of conduction in most of the atrial muscle is around .3 milliseconds. However, the velocity of conduction will be faster in several other pathways in the right atrial muscle. One of these, the anterior interatrial band, passes through the anterior walls of the atria to the left atrium and conducts the cardiac impulse at a velocity of around one millisecond. Three other similar pathways exist. These pathways curve through the atrial walls and terminate in the atrioventricular bundle (refer to anatomy of conduction system). These pathways also conduct the impulse at a faster rate.
The impulse initiating in the sinoatrial node travels through the internodal pathways and reaches the atrioventricularbundle. Here the impulse is delayed a total of around .16 seconds. The cause of this slow conduction through the atrioventricular bundle is partly due to the small fiber size as compared to normal atrial muscle fibers. However, two other factors will contribute more to the delay. First, all of these fibers have resting membrane potentials that are much less negative than the normal resting potential of other cardiac muscle. Secondly, few gap junctions connect these muscle cells in the pathway, so there is a large resistance to the conduction of excitatory ions from one cell to the next. Thus, with both low voltage to drive the ions and great resistance to the movement of the ions, you can see why each succeeding cell is slow to be excited.
The fibers located in the purkinje system are very large, even larger than ventricular muscle fibers, and transmit action potentials at a velocity of 1.5 to 4.0 milliseconds. This velocity translates to 6 times that in normal cardiac muscle. This high rate of transmission of action potentials could be caused by a high level of permeability of the gap junctions at the intercalated discs between the successive cardiac cells that make up these purkinje fibers.
Once the impulse reaches the purkinje fibers, it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves. The velocity of transmission is now only around 0.3 tp 0.5 milliseconds, equating to one sixth that in the purkinje sysem.
The cardiac muscle wraps around the heart in a double spiral. Fibrous septa exist between the spiraling layers. The cardiac impulse, therefore, does not travel directly outward toward the surface of the heart but instead angulates toward the surface along the directions of the spirals.
For effective pumping of the ventricles to exist the purkinje sysem must send the action potential to almost all portions of the ventricles within in a short amount of time. This will allow both ventricles to begin contracting at around the same time.
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