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Resting and Action Potential of the Heart Resting cell potential is a potential difference between the intracellular (−85 millivolts) and extra cellular (positive) spaces. The action potential of cardiac muscle about 105 millivolts, which means that the intracellular potential rises from (very negative-85mv) between beats to a slightly (positive about +20mv) during each beat. In the course of this process, the resting potential of (−85 mV) reverses for a brief period up to +20mV. This total tension or potential difference of 105 mV is defined as the action potential, and it is the signal for the myocardium to contract, (depolarization)of cell membrane remains for about 0.2 second exhibiting a plateau followed at the end of plateau by rapid repolarization .The presence of this plateau in the action potential causes ventricular contraction to last for longer time than the skeletal muscle. Cardiac muscle action potential caused by opening of two types of channels: 1- Fast sodium channels. 2- Slow calcium channels also called calcium-sodium channels. The slow Ca – Na channels are slower to open and even more important remain open for several tenth of seconds. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fibers, this maintains a prolonged period of depolarization, causing the plateau in the action potential. Further more the calcium ions that inter during this plateau phase activate the muscle contractile process. Immediately after the onset of the action potential, the permeability of the cardiac muscle membrane for potassium ions decreases about fivefold. This decreased potassium permeability may result from the excess calcium influx through the calcium channels. The decreased potassium permeability greatly decreases the outflux of positively charged potassium ions during the action potential plateau and thereby prevents early return of the action potential voltage to its resting level. When the (slow Ca – Na channels ) do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential . The Conduction System Removed heart from the body can continue to beat spontaneously outside the body for a prolonged period without the need for an external nerve supply. The heart possesses an autonomous source of impulses, the sinoatrial node (SA) that lies in the right atrium at the level of its junction with the superior vena cava. This so-called pacemaker for the entire heart. Its depolarization normally generates the current that leads to depolarization of all other cardiac muscle cells, and so its discharge rate determines the heartbeats, (number of times the heart contracts), a frequency of about 60−70 beats per minute. The action potential initiated in the SA node spreads throughout the myocardium, passing from cell to cell by way of gap junctions, and transmitted throughout the right atrium and from the right atrium to the left atrium does not depend on fibers of the conducting system. The spread is rapid enough that the two atria are depolarized and contract at essentially the same time. The spread of the action potential to the ventricles is more complicated and involves the rest of the conducting system (Fig5A and 5B). The link between atrial depolarization and ventricular depolarization is a Cardiovascular System Lecture No; 3 Dr. Abdul-Majeed Alsaffar 13 portion of the conducting system called the atrioventricular (AV) node, which is located at the base of the right atrium. The action potential spreading through the right atrium causes depolarization of the AV node. This node manifests a particularly important characteristic: For several reasons related to the electrical properties of the AV-node cells, the propagation of action potentials through the AV node are relatively slows (requiring approximately 0.1s). This delay allows atrial contraction to be complete before ventricular excitation occurs. After leaving the AV node, the impulse enters the wall—the interventricular septum—between the two ventricles via the conducting system fibers termed the bundle of His (or atrioventricular bundle) after its discoverer (pronounced Hiss). It should emphasize that the AV node and the bundle of His constitute the only electrical link between the atria and the ventricles. There are no others because a layer of no conducting connective tissue, pierced by the bundle of His, completely separates each atrium from its ventricle. Within the interventricular septum the bundle of His divides into right and left bundle branches, which eventually leave the septum to enter the walls of both ventricles. These fibers in turn make contact with Purkinje fibers, large conducting cells that rapidly distribute the impulse throughout much of the ventricles. Finally, the Purkinje fibers make contact with non-conducting system ventricular myocardial cells, via which the impulse spreads through the rest of the ventricles. The rapid conduction along the Purkinje fibers and the diffuse distribution of these fibers cause depolarization of all right and left ventricular cells more or less simultaneously, and ensure a single coordinated contraction. Actually, depolarization and contraction begin slightly earlier in the bottom (apex) of the ventricles and spread upward. The result is a more efficient contraction, like squeezing a tube of toothpaste from the bottom up. The cardiac frequency, impulse velocity, and force of contraction are influence by the autonomic nervous system (sympathetic and parasympathetic). Thus, cardiac activity adjusted to the body's need increased cardiac volume during heavy physical labor. Cardiovascular System Lecture No; 3 Dr. Abdul-Majeed Alsaffar 14 Fig 5A the conducting system of the heart. Fig 5 B The Sequence of cardiac excitation. The blue above color denotes areas that are depolarized. Impulse spread from right atrium to left atrium is via the atrial muscle cells where the atria contact each other in their shared wall. References 1. Textbook of Medical Physiology 11th, Edition .by Guyton A.C. 2. Human Physiology The Basis of Medicine 2nd, Edition. by Gillian Pocock and Christopher D.R. 3. Human Physiology: The Mechanism of Body Function 10th Edition. by Vander, et al Cardiovascular System Lecture No; 3 Dr. Abdul-Majeed Alsaffar 15