Further, these routes are known as the slow or fast pathways, which are considered to be functionally and anatomically distinct. The slow pathway typically crosses the isthmus between the coronary sinus and the tricuspid annulus; it has a longer conduction time, but a shorter effective refractory period. The fast pathway is commonly a superior route, emanating from the interatrial septum, and has a faster conduction rate but, in turn, a longer effective refractory period.
Though the primary function of the atrioventricular node may seem simple, that is to relay conduction between the atria and ventricles, its structure is very complex [1]. As a means to describe these complexities, mathematical arrays and finite element analysis models have been constructed to elucidate the underlying structure-function relationship of the node [19]. In general, the atrioventricular node is located in the so-called floor of the right atrium, over the muscular part of the interventricular septum, inferior to the membranous septum: i.
Following atrioventricular nodal excitation, the slow pathway conducts impulses to the His bundle, indicated by a longer interval between atrial and His activation. Currently, there is interest in the ability to place pacing leads to preferentially activate the bundle of His; in such approaches, ultrasound or other imaging modalities are used to map the electrical characteristic His potentials to position the pacing leads [20].
After leaving the bundle of His, the normal wave of cardiac depolarization spreads first to both the left and right bundle branches; these pathways rapidly and simultaneously carry depolarization to the apical regions of both the left and right ventricles see Figure 1. Finally, the signal broadly travels through the remainder of the Purkinje fibers and ventricular myocardial depolarization spreads. In certain pathological conditions, direct accessory connections from the atrioventricular node and the penetrating portion of the bundle of His to the ventricular myocardium have been described [21].
Yet, the function and prevalence of these connections, termed Mahaim fibers, is poorly understood. A rare bundle of Kent, an additional aberrant pathway when present, exists between the atria and ventricles and is associated with the clinical manifestation of ventricular tachycardias also known as Wolff-Parkinson-White syndrome. Therapeutically, this accessory pathway is electrically identified and then commonly ablated as a curative procedure. The left bundle branch splits into fascicles as it travels down the left side of the ventricular septum just below the endocardium.
Its fascicles extend for a distance of 5 to 15 mm, fanning out over the left ventricle. These membrane changes result in a decrease in speed by which action potentials are conducted within the heart. This can have a number of consequences. First, activation of the heart will be delayed, and in some cases, the sequence of activation will be altered. This can seriously impair ventricular pressure development. Second, damage to the conducting system can precipitate tachyarrhythmias by reentry mechanisms.
Click here to learn more about altered impulse conduction. Antiarrhythmic drugs such as quinidine a Class IA antiarrhythmic that block fast sodium channels cause a decrease in conduction velocity in non-nodal tissue.
Cardiovascular Physiology Concepts Richard E. Klabunde, PhD. Klabunde, all rights reserved Web Design by Jimp Studio. The SA node impulses also travel to the AV node, which stimulates ventricular contraction.
The SA node generates its own action potentials, but may be influenced by the autonomic nervous system. Without autonomic nervous stimulation, the SA node will set the heart rate itself, acting as the primary pacemaker for the heart.
The SA node fires to set a heart rate in a range of 60— beats per minute bpm , a normal range that varies from person to person. The AV node is a bundle of conducting tissue not formally classified as nerve tissue located at the junction between the atria and ventricles of the heart. The AV node receives action potentials from the SA node, and transmits them through the bundle of His, left and right bundle branches, and Purkinje fibers, which cause depolarization of ventricular muscle cells leading to ventricular contraction.
The AV node slightly slows the neural impulse from the SA node, which causes a delay between depolarization of the atria and the ventricles. The normal firing rate in the AV node is lower than that of the SA node because it slows the rate of neural impulses. Without autonomic nervous stimulation, it sets the rate of ventricular contraction at 40—60 bpm. Certain types of autonomic nervous stimulation alter the rate of firing in the AV node.
Sympathetic nervous stimulation still increases heart rate, while parasympathetic nervous stimulation decreases heart rate by acting on the AV node. The Cardiac Conduction System : The system of nerves that work together to set the heart rate and stimulate muscle cell depolarization within the heart.
It can also detect enlargement of the heart, decreased blood flow, or the presence of current or past heart attacks. ECGs are the primary clinical tool to measure electrical and mechanical performance of the heart. The ECG works by detecting and amplifying tiny electrical changes on the skin that occur during heart muscle depolarization. The output for the ECG forms a graph that shows several different waves, each corresponding to a different electrical and mechanical event within the heart.
Changes in these waves are used to identify problems with the different phases of heart activity. The first wave on an ECG is the P wave, indicating atrial depolarization in which the atria contract atrial systole. Increased or decreased P waves can indicate problems with the potassium ion concentration in the body that will alter nerve activity.
A missing P wave indicates atrial fibrillation, a cardiac arrhythmia in which the heart beats irregularly, preventing efficient ventricular diastole. This is generally not fatal on its own. The QRS complex refers to the combination of the Q, R, and S waves, and indicates ventricular depolarization and contraction ventricular systole. The QRS complex represents action potentials moving from the AV node, through the bundle of His and left and right branches and Purkinje fibers into the ventricular muscle tissue.
Abnormalities in the QRS complex may indicate cardiac hypertrophy or myocardial infarctions. The T Wave indicates ventricular repolarization, in which the ventricles relax following depolarization and contraction. The ST segment refers to the gap flat or slightly upcurved line between the S wave and the T wave, and represents the time between ventricular depolarization and repolarization.
An elevated ST segment is the classic indicator for myocardial infarctions, though missing or downward sloping sloping ST segments may indicate myocardial ischemia. Following the T wave is the U wave, which represents repolarization of the Purkinje fibers.
It is not always visible on an ECG because it is a very small wave in comparison to the others. During ventricular fibrillation, the heart beats extremely fast and irregularly and can no longer pump blood, acting as a mass of quivering, disorganized muscle movements.
Ventricular fibrillation will cause sudden cardiac death within minutes unless electrical resuscitation with an AED is performed immediately. It generally occurs with myocardial infarcations and heart failure, and is thought to be caused by action potentials that re-enter the AV nodes from the muscle tissue and induce rapid, irregular, weak contractions of the heart that fail to pump blood.
The closing of the heart valves produces a sound. Heart sounds are a useful indicator for evaluating the health of the valves and the heart as a whole. There is a very slight split between the closure of the mitral and tricuspid valves, but it is not long enough to create multiple sounds.
As septal depolarization moves from left to right, the depolarization vector is directed towards the - electrode of lead II RA , and therefore a negative-going deflection Q-wave is produced. Cardiac axis The cardiac axis refers to the mean direction of the wave of ventricular depolarization in the frontal plane, measured from a zero reference point.
In the example to the right, notice that there are tall R waves in leads I and II, and that in lead III, the R and the S waves are of equal size and opposite direction. Let us now calculate the direction of depolarization of the ventricular muscle.
We have to arrive at a vector such that the projections of this vector onto the three lead axes is consistent with the height of the QRS complexes in the three leads. It is rather defined to be the time from the beginning of the P-wave to the beginning of the QRS complex. Thus the PR interval is measured from the beginning of the P-wave to the beginning of the R-wave only if the first deflection in the QRS complex happens to be an R-wave i.
It is rather defined as the time from the beginning of the QRS complex to the end of the T-wave. It is generated by electrical activity more specifically depolarization or activation of the muscle.
Purkinje fibre cells are NOT nerve cells. Rather, they are specialized cardiac muscle cells.
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