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| Cardiac conduction system | |
|---|---|
 Components of the heart's conduction system | |
 Basic representation of cardiac electrical conduction | |
| Details | |
| Identifiers | |
| Latin | systema conducens cordis |
| MeSH | D006329 |
| TA98 | A12.1.06.002 |
| TA2 | 3952 |
| FMA | 9476 |
| Anatomical terminology | |
Thecardiac conduction system (CCS, also called theelectrical conduction system of the heart)[1] transmits thesignals generated by thesinoatrial node – theheart'spacemaker, to cause theheart muscle tocontract, and pump blood through the body'scirculatory system. Thepacemaking signal travels through theright atrium to theatrioventricular node, along thebundle of His, and through thebundle branches toPurkinje fibers in thewalls of the ventricles. The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles.[2]
The conduction system consists of specializedheart muscle cells, situated within themyocardium.[3] There is askeleton of fibrous tissue that surrounds the conduction system which can be seen on anECG. Dysfunction of the conduction system can causeirregular heart rhythms including rhythms that aretoo fast ortoo slow.
Electrical signals arising in theSA node (located in the rightatrium) stimulate the atria to contract. Then the signals travel to theatrioventricular node (AV node), which is located in theinteratrial septum. After a short delay that gives the ventricles time to fill with blood, the electrical signal diverges and is conducted through the left and rightbundle branches ofHis to the respectivePurkinje fibers for each side of the heart, as well as to theendocardium at the apex of the heart, then finally to the ventricular epicardium; causing the ventricles to contract.[2] These signals are generated rhythmically, which results in the coordinated rhythmic contraction and relaxation of the heart.
On the microscopic level, the wave ofdepolarization propagates to adjacent cells viagap junctions located on theintercalated disc. The heart is afunctional syncytium as opposed to a skeletal musclesyncytium. In a functional syncytium, electrical impulses propagate freely between cells in every direction, so that the myocardium functions as a single contractile unit. This property allows rapid, synchronous depolarization of the myocardium. While advantageous under normal circumstances, this property can be detrimental, as it has potential to allow the propagation of incorrect electrical signals. These gap junctions can close to isolate damaged or dying tissue, as in amyocardial infarction (heart attack).
Embryologic evidence of generation of the cardiac conduction system illuminates the respective roles of this specialized set of cells. Innervation of the heart begins with a brain only centeredparasympatheticcholinergic first order. It is then followed by rapid growth of a second ordersympatheticadrenergic system arising from the formation of thethoracicspinal ganglia. The third order of electrical influence of the heart is derived from thevagus nerve as the other peripheral organs form.[4]
Cardiac muscle has some similarities to neurons and skeletal muscle, as well as important unique properties. Like a neuron, a given myocardial cell has a negativemembrane potential when at rest. Stimulation above a threshold value induces the opening ofvoltage-gated ion channels and a flood ofcations into the cell. The positively charged ions entering the cell cause thedepolarization characteristic of an action potential. Like skeletal muscle, depolarization causes the opening ofvoltage-gated calcium channels and release of Ca2+ from thet-tubules. This influx of calcium causescalcium-induced calcium release from thesarcoplasmic reticulum, and free Ca2+ causesmuscle contraction. After a delay,potassium channels reopen, and the resulting flow of K+ out of the cell causesrepolarization to the resting state.[5][6]
There are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most importantly the spontaneous depolarizations necessary for the SA node's pacemaker activity.
In order to maximize efficiency of contractions andcardiac output, the conduction system of the heart has:
Anelectrocardiogram is a recording of the electrical activity of the heart.
Under normal conditions, electrical activity is spontaneously generated by theSA node, the cardiac pacemaker. This electrical impulse is propagated throughout the rightatrium, and throughBachmann's bundle to the leftatrium, stimulating themyocardium of the atria to contract. The conduction of the electrical impulses throughout the atria is seen on theECG as theP wave.[5][7]
As the electrical activity is spreading throughout the atria, it travels via specialized pathways, known asinternodal tracts, from the SA node to theAV node.[8]
The AV node functions as a critical delay in the conduction system. Without this delay, theatria andventricles would contract at the same time, and blood wouldn't flow effectively from the atria to the ventricles. The delay in the AV node forms much of thePR segment on the ECG, and part of atrial repolarization can be represented by the PR segment.
The distal portion of the AV node is known as thebundle of His.[9] The bundle of His splits into two branches in the interventricular septum: the left bundle branch and the right bundle branch. The left bundle branch activates theleft ventricle, while the right bundle branch activates theright ventricle.
The left bundle branch is short, splitting into the left anterior fascicle and the left posterior fascicle. The left posterior fascicle is relatively short and broad, with dual blood supply, making it particularly resistant to ischemic damage. The left posterior fascicle transmits impulses to the papillary muscles, leading tomitral valve closure. As the left posterior fascicle is shorter and broader than the right, impulses reach the papillary muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-tensioning of the chordae tendinae, increasing the resistance to flow through the mitral valve during left ventricular contraction.[5] This mechanism works in the same manner as pre-tensioning of car seatbelts.
The two bundle branches taper out to produce numerousPurkinje fibers, which stimulate individual groups of myocardial cells to contract.[5]
The spread of electrical activity through the ventricular myocardium produces theQRS complex on the ECG.
Atrial repolarization occurs and is masked during theQRS complex by ventricular depolarization on the ECG.
The last event of the cycle is the repolarization of theventricles. It is the restoring of the resting state. In the ECG, repolarization includes the J point, ST segment, and T and U waves.[10]The transthoracically measured PQRS portion of an electrocardiogram is chiefly influenced by thesympathetic nervous system. The T (and occasionally U) waves are chiefly influenced by theparasympathetic nervous system guided by integratedbrainstem control from thevagus nerve and the thoracicspinal accessory ganglia.
An impulse (action potential) that originates from the SA node at a relative rate of 60–100 bpm is known as a normalsinus rhythm. If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known assinus bradycardia. If SA nodal impulses occur at a rate exceeding 100 bpm, the consequent rapid heart rate issinus tachycardia. These conditions are not necessarily bad symptoms, however. Trained athletes, for example, usually show heart rates slower than 60 bpm when not exercising. If the SA node fails to initialize, the AV junction can take over as the main pacemaker of the heart. The AV junction consists of the AV node, the bundle of His, and the surrounding area; it has a regular rate of 40 to 60 bpm. These "junctional" rhythms are characterized by a missing or inverted P wave. If both the SA node and the AV junction fail to initialize the electrical impulse, the ventricles can fire the electrical impulses themselves at a rate of 20 to 40 bpm and will have a QRS complex of greater than 120 ms. This is necessary for the heart to be in good function.
Anarrhythmia is an abnormal rhythm or speed of rhythm of the heartbeat. A slowheart rate of 60 or less beats per minute is defined asbradycardia. A fast heart rate of more than 100 beats per minute is defined astachycardia.An arrhythmia is defined as one that is notphysiological such as the lowered heart rate that a trained athlete may naturally have developed; the resting heart rates may be less than 60 bpm.
When an arrhythmia cannot be treated bymedication (or other standardcardioversion measures), anartificial pacemaker may beimplanted to control the conduction system.
