Why cant tetany of the heart occur
The longer myocardial action potential of myocardium helps prevent the sustained contraction called tetanus. To understand how a longer action potential prevents tetanus, relationship between action potentials, refractory periods, and contraction in skeletal and cardiac muscle cells. Refractory period is the time following an action potential during which a normal stimulus cannot trigger a second action potential.
In cardiac muscle, the long action potential red curve means the refractory period and the contraction end almost simultaneously. By the time a second action potential can take place, the myocardial cell has almost completely relaxed. Consequently, no summation occurs. See figure below. In contrast, the skeletal muscle action potential and refractory period are ending just as contraction begins.
For this reason, a second action potential fired immediately after the refractory period causes summation of the contractions. If a series of action potentials occurs in rapid succession, the sustained contraction known as tetanus results. You are commenting using your WordPress. In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. 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.
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. Despite this initial difference, the other components of their action potentials are virtually identical. In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization.
The rapid depolarization period typically lasts 3—5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. The relatively long plateau phase lasts approximately ms.
The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between and ms Figure 5. Figure 5. The extended refractory period allows the cell to fully contract before another electrical event can occur. The absolute refractory period for cardiac contractile muscle lasts approximately ms, and the relative refractory period lasts approximately 50 ms, for a total of ms.
This extended period is critical, since the heart muscle must contract to pump blood effectively and the contraction must follow the electrical events. Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life.
Calcium ions play two critical roles in the physiology of cardiac muscle. Their influx through slow calcium channels accounts for the prolonged plateau phase and absolute refractory period that enable cardiac muscle to function properly.
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.
This mechanism is virtually identical to that of skeletal muscle. 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. Since the SA node is the pacemaker, it reaches threshold faster than any other component of the conduction system. It will initiate the impulses spreading to the other conducting cells.
The SA node, without nervous or endocrine control, would initiate a heart impulse approximately 80— times per minute. 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. Without the SA node, the AV node would generate a heart rate of 40—60 beats per minute.
If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30—40 impulses per minute. 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. 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.
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. Figure 6. In a lead ECG, six electrodes are placed on the chest, and four electrodes are placed on the limbs.
By careful placement of surface electrodes on the body, it is possible to record the complex, compound electrical signal of the heart. This tracing of the electrical signal is the electrocardiogram ECG , also commonly abbreviated EKG K coming kardiology, from the German term for cardiology.
Careful analysis of the ECG reveals a detailed picture of both normal and abnormal heart function, and is an indispensable clinical diagnostic tool.
The standard electrocardiograph the instrument that generates an ECG uses 3, 5, or 12 leads. The greater the number of leads an electrocardiograph uses, the more information the ECG provides. A normal ECG tracing is presented in Figure 7. Each component, segment, and interval is labeled and corresponds to important electrical events, demonstrating the relationship between these events and contraction in the heart. The small P wave represents the depolarization of the atria. The atria begin contracting approximately 25 ms after the start of the P wave.
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. The ventricles begin to contract as the QRS reaches the peak of the R wave. Lastly, the T wave represents the repolarization of the ventricles. Figure 7. The major segments and intervals of an ECG tracing are indicated in the image below.
Segments are defined as the regions between two waves. Intervals include one segment plus one or more waves. 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. 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.
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. Figure 8 correlates events of heart contraction to the corresponding segments and intervals of an ECG.
Figure 8. This diagram correlates an ECG tracing with the electrical and mechanical events of a heart contraction.
Each segment of an ECG tracing corresponds to one event in the cardiac cycle. Occasionally, an area of the heart other than the SA node will initiate an impulse that will be followed by a premature contraction. 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.
An ectopic focus may be stimulated by localized ischemia; exposure to certain drugs, including caffeine, digitalis, or acetylcholine; elevated stimulation by both sympathetic or parasympathetic divisions of the autonomic nervous system; or a number of disease or pathological conditions.
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. 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 general, the size of the electrical variations, the duration of the events, and detailed vector analysis provide the most comprehensive picture of cardiac function.
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. T waves often appear flatter when insufficient oxygen is being delivered to the myocardium. 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.
As useful as analyzing these electrical recordings may be, there are limitations. 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. 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. Common abnormalities that may be detected by the ECGs are shown in Figure 9.
Figure 9. In the event that the electrical activity of the heart is severely disrupted, cessation of electrical activity or fibrillation may occur.
In fibrillation, the heart beats in a wild, uncontrolled manner, which prevents it from being able to pump effectively. Ventricular fibrillation see Figure 10b is a medical emergency that requires life support, because the ventricles are not effectively pumping blood.
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. A defibrillator effectively stops the heart so that the SA node can trigger a normal conduction cycle. 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.
These devices contain simple and direct verbal instructions that can be followed by nonmedical personnel in an attempt to save a life. Cardiac muscle is a unique tissue forming the wall of the heart. Like skeletal muscle fibres, cardiac muscle cells contain an orderly arrangement of myofibrils and have cross-striations, but significant differences exist in their structures and functions.
The most obvious structural difference is that cardiac muscle cells are branched and each cardiac cell contacts several others at specialized sites called intercalated discs. These cellular connections contain gap junctions that allow the movement of ions and small molecules and the rapid passage of action potentials from cell to cell, resulting in their simultaneous contraction.
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