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05.06.2015, admin  
Category: Gh Hormone

Recall that cardiac muscle shares a few characteristics with both skeletal muscle and smooth muscle, but it has some unique properties of its own. There are two major types of cardiac muscle cells: myocardial contractile cells and myocardial conducting cells. Compared to the giant cylinders of skeletal muscle, cardiac muscle cells, or cardiomyocytes, are considerably shorter with much smaller diameters.
Cardiac muscle undergoes aerobic respiration patterns, primarily metabolizing lipids and carbohydrates.
Damaged cardiac muscle cells have extremely limited abilities to repair themselves or to replace dead cells via mitosis.
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. 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. 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 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. 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 Purkinje fibers are additional myocardial conductive fibers that spread the impulse to the myocardial contractile cells in the ventricles.
Action potentials are considerably different between cardiac conductive cells and cardiac contractive cells. Contractile cells demonstrate a much more stable resting phase than conductive cells at approximately ?80 mV for cells in the atria and ?90 mV for cells in the ventricles. The absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, and the relative refractory period lasts approximately 50 ms, for a total of 250 ms. The pattern of prepotential or spontaneous depolarization, followed by rapid depolarization and repolarization just described, are seen in the SA node and a few other conductive cells in the heart. By careful placement of surface electrodes on the body, it is possible to record the complex, compound electrical signal of the heart.
ECG Abnormalities Occassionally, an area of the heart other than the SA node will initiate an impulse that will be followed by a premature contraction. While interpretation of an ECG is possible and extremely valuable after some training, a full understanding of the complexities and intricacies generally requires several years of experience.
In the event that the electrical activity of the heart is severely disrupted, cessation of electrical activity or fibrillation may occur. When arrhythmias become a chronic problem, the heart maintains a junctional rhythm, which originates in the AV node. Fatty acids and glucose from the circulation are broken down within the mitochondria to release energy in the form of ATP. The heart is regulated by both neural and endocrine control, yet it is capable of initiating its own action potential followed by muscular contraction. It prevents additional impulses from spreading through the heart prematurely, thereby allowing the muscle sufficient time to contract and pump blood effectively. How does the delay of the impulse at the atrioventricular node contribute to cardiac function? It ensures sufficient time for the atrial muscle to contract and pump blood into the ventricles prior to the impulse being conducted into the lower chambers. Gap junctions within the intercalated disks allow impulses to spread from one cardiac muscle cell to another, allowing sodium, potassium, and calcium ions to flow between adjacent cells, propagating the action potential, and ensuring coordinated contractions. Without a true resting potential, there is a slow influx of sodium ions through slow channels that produces a prepotential that gradually reaches threshold. Here we have covered the spasticity condition which is the altering of skeletal muscle performance in muscle tone involving hypertonia.
A torn calf muscle is similar to an Achilles tendon tear or rupture, but occurs higher up in the back of the leg. This is the most severe calf strain with a complete tearing or rupture of muscle fibres in the lower leg.
As with most soft tissue injuries the initial treatment is RICE - Rest, Ice, Compression and Elevation.
Your calf muscle is a large powerful group of muscles that can produce sufficient force to run, jump and hop. Anti-inflammatory medication (if tolerated) and natural substances eg arnica may help reduce your pain and swelling. Keep your foot elevated above your heart (where possible) to allow for gravity to help drain your calf and lower leg swelling.
It is important to lengthen and orientate your healing scar tissue via massage, muscle stretches and neurodynamic mobilisations. Calf strength and power should be gradually progressed from non-weight bear to partial and then full weight bear and resistance loaded exercises. Most calf injuries occur during high speed activities, which place enormous forces on your body (contractile and non-contractile).
Your PhysioWorks physiotherapist will discuss your goals, time frames and training schedules with you to optimise you for a complete return to sport.
For more specific advice about your calf injury, please contact your PhysioWorks physiotherapist. Not the least of these exceptional properties is its ability to initiate an electrical potential at a fixed rate that spreads rapidly from cell to cell to trigger the contractile mechanism.
The myocardial contractile cells constitute the bulk (99 percent) of the cells in the atria and ventricles. Cardiac muscle also demonstrates striations, the alternating pattern of dark A bands and light I bands attributed to the precise arrangement of the myofilaments and fibrils that are organized in sarcomeres along the length of the cell ([link]a). 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 ([link]b). 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. 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. The SA node has the highest inherent rate of depolarization and is known as the pacemaker of the heart.
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 (see [link]).
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 septum prevents the impulse from spreading directly to the ventricles without passing through the AV node.
They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart.
In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. Despite this initial difference, the other components of their action potentials are virtually identical. This extended period is critical, since the heart muscle must contract to pump blood effectively and the contraction must follow the electrical events.
Their influx through slow calcium channels accounts for the prolonged plateau phase and absolute refractory period that enable cardiac muscle to function properly.
Since the SA node is the pacemaker, it reaches threshold faster than any other component of the conduction system. This tracing of the electrical signal is the electrocardiogram (ECG), also commonly abbreviated EKG (K coming kardiology, from the German term for cardiology). Each component, segment, and interval is labeled and corresponds to important electrical events, demonstrating the relationship between these events and contraction in the heart. Such an area, which may actually be a component of the conduction system or some other contractile cells, is known as an ectopic focus or ectopic pacemaker.


In general, the size of the electrical variations, the duration of the events, and detailed vector analysis provide the most comprehensive picture of cardiac function. In fibrillation, the heart beats in a wild, uncontrolled manner, which prevents it from being able to pump effectively.
A first-degree or partial block indicates a delay in conduction between the SA and AV nodes. In order to speed up the heart rate and restore full sinus rhythm, a cardiologist can implant an artificial pacemaker, which delivers electrical impulses to the heart muscle to ensure that the heart continues to contract and pump blood effectively.
Oxygen from the lungs is brought to the heart, and every other organ, attached to the hemoglobin molecules within the erythrocytes.
Both fatty acid droplets and glycogen are stored within the sarcoplasm and provide additional nutrient supply. The conductive cells within the heart establish the heart rate and transmit it through the myocardium.
Spasticity occurs in disorders of the central nervous system impacting the upper motor neuron in the form of a lesion, such as spastic diplegia, but it can also present in various types of multiple sclerosis, which are autoimmune conditions. Your physiotherapist will guide you on an eccentric calf strengthening program when your injury healing allows.
Contractile cells conduct impulses and are responsible for contractions that pump blood through the body.
Cardiac muscle cells undergo twitch-type contractions with long refractory periods followed by brief relaxation periods. However, newly formed or repaired cells are rarely as functional as the original cells, and cardiac function is reduced. As more cells are joined together, the fastest cell continues to assume control of the rate.
It initiates the sinus rhythm, or normal electrical pattern followed by contraction of the heart.
The contractile cells then begin contraction from the superior to the inferior portions of the atria, efficiently pumping blood into the ventricles.
There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle (see [link], step 3). The left bundle branch supplies the left ventricle, and the right bundle branch the right ventricle.
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 [link], step 5).
Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential.
This phenomenon accounts for the long refractory periods required for the cardiac muscle cells to pump blood effectively before they are capable of firing for a second time.
In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization.
Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life. Calcium ions also combine with the regulatory protein troponin in the troponin-tropomyosin complex; this complex removes the inhibition that prevents the heads of the myosin molecules from forming cross bridges with the active sites on actin that provide the power stroke of contraction. Careful analysis of the ECG reveals a detailed picture of both normal and abnormal heart function, and is an indispensable clinical diagnostic tool.
For example, an amplified P wave may indicate enlargement of the atria, an enlarged Q wave may indicate a MI, and an enlarged suppressed or inverted Q wave often indicates enlarged ventricles.
Additionally, it will not reveal the effectiveness of the pumping, which requires further testing, such as an ultrasound test called an echocardiogram or nuclear medicine imaging.
Atrial fibrillation (see [link]b) is a serious condition, but as long as the ventricles continue to pump blood, the patient’s life may not be in immediate danger. These artificial pacemakers are programmable by the cardiologists and can either provide stimulation temporarily upon demand or on a continuous basis.
The myocardial conducting cells (1 percent of the cells) form the conduction system of the heart.
T (transverse) tubules penetrate from the surface plasma membrane, the sarcolemma, to the interior of the cell, allowing the electrical impulse to reach the interior. 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 ([link]c). In the event of a heart attack or MI, dead cells are often replaced by patches of scar tissue. 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 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. This delay in transmission is partially attributable to the small diameter of the cells of the node, which slow the impulse. Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right.
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. Conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of ?60 mV up to about –40 mV. These cardiac myocytes normally do not initiate their own electrical potential, although they are capable of doing so, but rather wait for an impulse to reach them. This rapid influx of positively charged ions raises the membrane potential to approximately +30 mV, at which point the sodium channels close. The SA node, without nervous or endocrine control, would initiate a heart impulse approximately 80–100 times per minute. The standard electrocardiograph (the instrument that generates an ECG) uses 3, 5, or 12 leads. The large QRS complex represents the depolarization of the ventricles, which requires a much stronger electrical signal because of the larger size of the ventricular cardiac muscle. For example, the PR segment begins at the end of the P wave and ends at the beginning of the QRS complex. Occasional occurances are generally transitory and nonlife threatening, but if the condition becomes chronic, it may lead to either an arrhythmia, a deviation from the normal pattern of impulse conduction and contraction, or to fibrillation, an uncoordinated beating of the heart. T waves often appear flatter when insufficient oxygen is being delivered to the myocardium. It is also possible for there to be pulseless electrical activity, which will show up on an ECG tracing, although there is no corresponding pumping action.
Ventricular fibrillation (see [link]d) is a medical emergency that requires life support, because the ventricles are not effectively pumping blood.
A second-degree or incomplete block occurs when some impulses from the SA node reach the AV node and continue, while others do not. Normally, these two mechanisms, circulating oxygen and oxygen attached to myoglobin, can supply sufficient oxygen to the heart, even during peak performance. The normal path of transmission for the conductive cells is the sinoatrial (SA) node, internodal pathways, atrioventricular (AV) node, atrioventricular (AV) bundle of His, bundle branches, and Purkinje fibers. Even though cardiac muscle has autorhythmicity, heart rate is modulated by the endocrine and nervous systems.
Except for Purkinje cells, they are generally much smaller than the contractile cells and have few of the myofibrils or filaments needed for contraction. The T tubules are only found at the Z discs, whereas in skeletal muscle, they are found at the junction of the A and I bands. The refractory period is very long to prevent the possibility of tetany, a condition in which muscle remains involuntarily contracted. Autopsies performed on individuals who had successfully received heart transplants show some proliferation of original cells. 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 ([link]). In addition, there is a specialized pathway called Bachmann’s bundle or the interatrial band that conducts the impulse directly from the right atrium to the left atrium.


Portions of the right bundle branch are found in the moderator band and supply the right papillary muscles.
This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The resulting movement of sodium ions creates spontaneous depolarization (or prepotential depolarization). Approximately 20 percent of the calcium required for contraction is supplied by the influx of Ca2+ during the plateau phase. Although each component of the conduction system is capable of generating its own impulse, the rate progressively slows as you proceed from the SA node to the Purkinje fibers.
The greater the number of leads an electrocardiograph uses, the more information the ECG provides. The PR interval starts at the beginning of the P wave and ends with the beginning of the QRS complex. An elevation of the ST segment above baseline is often seen in patients with an acute MI, and may appear depressed below the baseline when hypoxia is occurring.
In a hospital setting, it is often described as “code blue.” If untreated for as little as a few minutes, ventricular fibrillation may lead to brain death.
In this instance, the ECG would reveal some P waves not followed by a QRS complex, while others would appear normal. The action potential for the conductive cells consists of a prepotential phase with a slow influx of Na+ followed by a rapid influx of Ca2+ and outflux of K+.
Their function is similar in many respects to neurons, although they are specialized muscle cells. The importance of strongly binding these cells together is necessitated by the forces exerted by contraction. In the heart, tetany is not compatible with life, since it would prevent the heart from pumping blood. 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. 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. These factors mean that it takes the impulse approximately 100 ms to pass through the node.
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. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately 225 ms. At this point, calcium ion channels open and Ca2+ enters the cell, further depolarizing it at a more rapid rate until it reaches a value of approximately +5 mV.
Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly.
The term “lead” may be used to refer to the cable from the electrode to the electrical recorder, but it typically describes the voltage difference between two of the electrodes.
The PR interval is more clinically relevant, as it measures the duration from the beginning of atrial depolarization (the P wave) to the initiation of the QRS complex. The most common treatment is defibrillation, which uses special paddles to apply a charge to the heart from an external electrical source in an attempt to establish a normal sinus rhythm ([link]). Bundle branch blocks occur within either the left or right atrioventricular bundle branches. In the third-degree or complete block, there is no correlation between atrial activity (the P wave) and ventricular activity (the QRS complex). Contractile cells have an action potential with an extended plateau phase that results in an extended refractory period to allow complete contraction for the heart to pump blood effectively.
Myocardial conduction cells initiate and propagate the action potential (the electrical impulse) that travels throughout the heart and triggers the contractions that propel the blood. In addition, the sarcoplasmic reticulum stores few calcium ions, so most of the calcium ions must come from outside the cells.
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.
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.
This is believed to allow tension to develop on the chordae tendineae prior to right ventricular contraction.
At this point, the calcium ion channels close and K+ channels open, allowing outflux of K+ and resulting in repolarization. This is due in large part to the opening of the slow Ca2+ channels, allowing Ca2+ to enter the cell while few K+ channels are open, allowing K+ to exit the cell. If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30–40 impulses per minute.
The 12-lead electrocardiograph uses 10 electrodes placed in standard locations on the patient’s skin ([link]). Since the Q wave may be difficult to view in some tracings, the measurement is often extended to the R that is more easily visible. A defibrillator effectively stops the heart so that the SA node can trigger a normal conduction cycle. Hemiblocks are partial and occur within one or more fascicles of the atrioventricular bundle branch.
Even in the event of a total SA block, the AV node will assume the role of pacemaker and continue initiating contractions at 40–60 contractions per minute, which is adequate to maintain consciousness. Recognizable points on the ECG include the P wave that corresponds to atrial depolarization, the QRS complex that corresponds to ventricular depolarization, and the T wave that corresponds to ventricular repolarization.
Perhaps soon this mystery will be solved, and new advances in treatment will be commonplace. With extreme stimulation by the SA node, the AV node can transmit impulses maximally at 220 per minute. When the membrane potential reaches approximately ?60 mV, the K+ channels close and Na+ channels open, and the prepotential phase begins again. The bundle branches would have an inherent rate of 20–30 impulses per minute, and the Purkinje fibers would fire at 15–20 impulses per minute. In continuous ambulatory electrocardiographs, the patient wears a small, portable, battery-operated device known as a Holter monitor, or simply a Holter, that continuously monitors heart electrical activity, typically for a period of 24 hours during the patient’s normal routine. Should there be a delay in passage of the impulse from the SA node to the AV node, it would be visible in the PR interval. Because of their effectiveness in reestablishing a normal sinus rhythm, external automated defibrillators (EADs) are being placed in areas frequented by large numbers of people, such as schools, restaurants, and airports. Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers (see [link], step 4). Once the membrane potential reaches approximately zero, the Ca2+ channels close and K+ channels open, allowing K+ to exit the cell. While a few exceptionally trained aerobic athletes demonstrate resting heart rates in the range of 30–40 beats per minute (the lowest recorded figure is 28 beats per minute for Miguel Indurain, a cyclist), for most individuals, rates lower than 50 beats per minute would indicate a condition called bradycardia. These devices contain simple and direct verbal instructions that can be followed by nonmedical personnel in an attempt to save a life.
Typically, cardiomyocytes have a single, central nucleus, but two or more nuclei may be found in some cells. Damaged hearts or those stimulated by drugs can contract at higher rates, but at these rates, the heart can no longer effectively pump blood. Depending upon the specific individual, as rates fall much below this level, the heart would be unable to maintain adequate flow of blood to vital tissues, initially resulting in decreasing loss of function across the systems, unconsciousness, and ultimately death.
At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats.



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