Mitochondria are plentiful, providing energy for the contractions of the heart. Typically, cardiomyocytes have a single, central nucleus, but two or more nuclei may be found in some cells. Cardiac muscle cells branch freely. A junction between two adjoining cells is marked by a critical structure called an intercalated disc , which helps support the synchronized contraction of the muscle. The sarcolemmas from adjacent cells bind together at the intercalated discs.
They consist of desmosomes, specialized linking proteoglycans, tight junctions, and large numbers of gap junctions that allow the passage of ions between the cells and help to synchronize the contraction.
Intercellular connective tissue also helps to bind the cells together. The importance of strongly binding these cells together is necessitated by the forces exerted by contraction.
Figure 1. Cardiac muscle undergoes aerobic respiration patterns, primarily metabolizing lipids and carbohydrates. Myoglobin, lipids, and glycogen are all stored within the cytoplasm. Cardiac muscle cells undergo twitch-type contractions with long refractory periods followed by brief relaxation periods. The relaxation is essential so the heart can fill with blood for the next cycle.
The refractory period is very long to prevent the possibility of tetany, a condition in which muscle remains involuntarily contracted. In the heart, tetany is not compatible with life, since it would prevent the heart from pumping blood. Damaged cardiac muscle cells have extremely limited abilities to repair themselves or to replace dead cells via mitosis. Recent evidence indicates that at least some stem cells remain within the heart that continue to divide and at least potentially replace these dead cells.
However, newly formed or repaired cells are rarely as functional as the original cells, and cardiac function is reduced. In the event of a heart attack or MI, dead cells are often replaced by patches of scar tissue. Autopsies performed on individuals who had successfully received heart transplants show some proliferation of original cells. If researchers can unlock the mechanism that generates new cells and restore full mitotic capabilities to heart muscle, the prognosis for heart attack survivors will be greatly enhanced.
To date, myocardial cells produced within the patient in situ by cardiac stem cells seem to be nonfunctional, although those grown in Petri dishes in vitro do beat. Perhaps soon this mystery will be solved, and new advances in treatment will be commonplace. If embryonic heart cells are separated into a Petri dish and kept alive, each is capable of generating its own electrical impulse followed by contraction.
When two independently beating embryonic cardiac muscle cells are placed together, the cell with the higher inherent rate sets the pace, and the impulse spreads from the faster to the slower cell to trigger a contraction. As more cells are joined together, the fastest cell continues to assume control of the rate.
A fully developed adult heart maintains the capability of generating its own electrical impulse, triggered by the fastest cells, as part of the cardiac conduction system. The components of the cardiac conduction system include the sinoatrial node, the atrioventricular node, the atrioventricular bundle, the atrioventricular bundle branches, and the Purkinje cells. Figure 2. Specialized conducting components of the heart include the sinoatrial node, the internodal pathways, the atrioventricular node, the atrioventricular bundle, the right and left bundle branches, and the Purkinje fibers.
Normal cardiac rhythm is established by the sinoatrial SA node , a specialized clump of myocardial conducting cells located in the superior and posterior walls of the right atrium in close proximity to the orifice of the superior vena cava. The SA node has the highest inherent rate of depolarization and is known as the pacemaker of the heart. It initiates the sinus rhythm , or normal electrical pattern followed by contraction of the heart.
This impulse spreads from its initiation in the SA node throughout the atria through specialized internodal pathways , to the atrial myocardial contractile cells and the atrioventricular node. The internodal pathways consist of three bands anterior, middle, and posterior that lead directly from the SA node to the next node in the conduction system, the atrioventricular node. The impulse takes approximately 50 ms milliseconds to travel between these two nodes.
The relative importance of this pathway has been debated since the impulse would reach the atrioventricular node simply following the cell-by-cell pathway through the contractile cells of the myocardium in the atria. Regardless of the pathway, as the impulse reaches the atrioventricular septum, the connective tissue of the cardiac skeleton prevents the impulse from spreading into the myocardial cells in the ventricles except at the atrioventricular node.
Figure 3 illustrates the initiation of the impulse in the SA node that then spreads the impulse throughout the atria to the atrioventricular node. Figure 3. The electrical event, the wave of depolarization, is the trigger for muscular contraction. The wave of depolarization begins in the right atrium, and the impulse spreads across the superior portions of both atria and then down through the contractile cells.
The contractile cells then begin contraction from the superior to the inferior portions of the atria, efficiently pumping blood into the ventricles. The atrioventricular AV node is a second clump of specialized myocardial conductive cells, located in the inferior portion of the right atrium within the atrioventricular septum.
The septum prevents the impulse from spreading directly to the ventricles without passing through the AV node. There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle see image above, step 3. This delay in transmission is partially attributable to the small diameter of the cells of the node, which slow the impulse. Also, conduction between nodal cells is less efficient than between conducting cells.
These factors mean that it takes the impulse approximately ms to pass through the node. This pause is critical to heart function, as it allows the atrial cardiomyocytes to complete their contraction that pumps blood into the ventricles before the impulse is transmitted to the cells of the ventricle itself.
With extreme stimulation by the SA node, the AV node can transmit impulses maximally at per minute. This establishes the typical maximum heart rate in a healthy young individual.
Damaged hearts or those stimulated by drugs can contract at higher rates, but at these rates, the heart can no longer effectively pump blood. Arising from the AV node, the atrioventricular bundle , or bundle of His , proceeds through the interventricular septum before dividing into two atrioventricular bundle branches , commonly called the left and right bundle branches.
The left bundle branch has two fascicles. The left bundle branch supplies the left ventricle, and the right bundle branch the right ventricle.
Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right. Portions of the right bundle branch are found in the moderator band and supply the right papillary muscles. Because of this connection, each papillary muscle receives the impulse at approximately the same time, so they begin to contract simultaneously just prior to the remainder of the myocardial contractile cells of the ventricles.
This is believed to allow tension to develop on the chordae tendineae prior to right ventricular contraction. There is no corresponding moderator band on the left. Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers see image above, step 4. This passage takes approximately 25 ms. The Purkinje fibers are additional myocardial conductive fibers that spread the impulse to the myocardial contractile cells in the ventricles. They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart.
The Purkinje fibers have a fast inherent conduction rate, and the electrical impulse reaches all of the ventricular muscle cells in about 75 ms see image above, step 5. Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom. This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately ms.
Action potentials are considerably different between cardiac conductive cells and cardiac contractive cells. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential. The resulting movement of sodium ions creates spontaneous depolarization or prepotential depolarization. This phenomenon explains the autorhythmicity properties of cardiac muscle Figure 4.
Figure 4. The prepotential is due to a slow influx of sodium ions until the threshold is reached followed by a rapid depolarization and repolarization. The prepotential accounts for the membrane reaching threshold and initiates the spontaneous depolarization and contraction of the cell. Your heart rate can increase beyond beats per minute to meet your body's increased needs during physical exertion.
Similarly, during periods of rest or sleep, when the body needs less oxygen, the heart rate decreases. Some athletes actually may have normal heart rates well below 60 because their hearts are very efficient and don't need to beat as fast. Changes in your heart rate, therefore, are a normal part of your heart's effort to meet the needs of your body.
The sympathetic and parasympathetic nervous systems are opposing forces that affect your heart rate. Both systems are made up of very tiny nerves that travel from the brain or spinal cord to your heart. The sympathetic nervous system is triggered during stress or a need for increased cardiac output and sends signals to your heart to increase its rate. The parasympathetic system is active during periods of rest and sends signals to your heart to decrease its rate. During stress or a need for increased cardiac output, the adrenal glands release a hormone called norepinephrine into the bloodstream at the same time that the sympathetic nervous system is also triggered to increase your heart rate.
This hormone causes the heart to beat faster, and unlike the sympathetic nervous system that sends an instantaneous and short-lived signal, norepinephrine released into the bloodstream increases the heart rate for several minutes or more. Author: Healthwise Staff. Medical Review: Rakesh K. This information does not replace the advice of a doctor. Healthwise, Incorporated, disclaims any warranty or liability for your use of this information.
Your use of this information means that you agree to the Terms of Use. Learn how we develop our content. To learn more about Healthwise, visit Healthwise. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated. Updated visitor guidelines. You are here Home » Electrical System of the Heart. Top of the page. Topic Overview What controls the timing of your heartbeat?
Your heart's electrical system controls the timing of your heartbeat by regulating your: Heart rate, which is the number of times your heart beats per minute.
Heart rhythm, which is the synchronized pumping action of your four heart chambers. Your heart's electrical system should maintain: A steady heart rate of 60 to beats per minute at rest. T he calories are burnt significant amount while your body is involved in physical exercise: various muscles, heart, and the respiratory system are all engaged at once.
Luigi Galvani gave the first scientific evidence that current can stimulate the muscle. During the 19th and 20th centuries, researchers analyzed and documented the accurate electrical properties that generate muscle movement. In the s, these investigations were shared during conferences with the Western sports establishments. However, results were contrary, perhaps because the mechanisms in which EMS worked were poorly understood. Recent medical physiology study pinpointed the mechanisms by which electrical muscle stimulation produces the adaptation of cells of muscles, blood vessels, and nerves.
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