Electrical conduction system of the heart: Wikis


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Electrical conduction system of the heart
Electrical conduction system of the heart.svg
Isolated conduction system of the heart
RLS 12blauLeg.png
Heart; conduction system
Latin systema conducente cordis
Principle of ECG formation. Note that the red lines represent the depolarization wave, not bloodflow.

The normal electrical conduction in the heart allows the impulse that is generated by the sinoatrial node (SA node) to be propagated to (and stimulate) the myocardium. The myocardium contracts after stimulation. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped throughout the body.


Electrochemical mechanism

The neurons that innervate cardiac muscle hold some similarities to those of skeletal muscle as well as other important differences. These neurons are uniquely subject to influence by the sympathetic part of the autonomic nervous system. Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels and a flood of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. After depolarization, there's a brief repolarization that takes place with the eflux of potassium through fast acting potassium channels. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels - meanwhile potassium channels have closed - and there's a release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, slow acting Potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state.

Note that 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.

Conduction pathway

Signals arising in the SA node (and propagating to the left atrium via Bachmann's bundle) stimulate the atria to contract. In parallel, action potentials travel to the AV node via internodal pathways. After a delay, the stimulus is conducted through the bundle of His to the bundle branches and then to the purkinje fibers and the endocardium at the apex of the heart, then finally to the ventricular myocardium.

Microscopically, the wave of depolarization propagates to adjacent cells via gap junctions located on the intercalated disk. The heart is a functional syncytium (not to be confused with a true "syncytium" in which all the cells are fused together, sharing the same plasma membrane as in skeletal muscle). 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 normally advantageous, this property can be detrimental as it potentially allows the propagation of incorrect electrical signals. These gap junctions can close to isolate damaged or dying tissue, as in a myocardial infarction.

Depolarization and the ECG

The ECG complex. P=P wave, PR=PR interval, QRS=QRS complex, QT=QT interval, ST=ST segment, T=T wave

SA node: P wave

Under normal conditions, electrical activity is spontaneously generated by the SA node, the physiological pacemaker. This electrical impulse is propagated throughout the right atrium, and through Bachmann's bundle to the left atrium, stimulating the myocardium of the atria to contract. The conduction of the electrical impulse throughout the atria is seen on the ECG as the P wave.

As the electrical activity is spreading throughout the atria, it travels via specialized pathways, known as internodal tracts, from the SA node to the AV node.

AV node/Bundles: PR interval


The AV node functions as a critical delay in the conduction system. Without this delay, the atria and ventricles 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 the PR segment on the ECG. Part of atrial repolarization can be represented by PR segment.

The distal portion of the AV node is known as the bundle of His. 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 the left ventricle, while the right bundle branch activates the right 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 to mitral 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.

Purkinje fibers/ventricular myocardium: QRS complex

The two bundle branches taper out to produce numerous purkinje fibers, which stimulate individual groups of myocardial cells to contract.

The spread of electrical activity (depolarization) through the ventricular myocardium produces the QRS complex on the ECG.

Ventricular repolarization: T wave

The last event of the cycle is the repolarization of the ventricles. The transthoracically measured PQRS portion of an electrocardiogram is chiefly influenced by the sympathetic nervous system. The T (and occasionally U) waves are chiefly influenced by the parasympathetic nervous system guided by integrated brainstem control from the vagus nerve and the thoracic spinal accessory ganglia.


An impulse (action potential) that originates from the SA node at a rate of 60 - 100bpm is known as normal sinus rhythm. If SA nodal impulses occur at a rate less than 60bpm, the heart rhythm is known as sinus bradycardia. If SA nodal impulses occur at a rate exceeding 100bpm, the consequent rapid heart rate is sinus tachycardia. These conditions are not necessarily bad symptoms, however. Trained athletes, for example, usually show heart rates slower than 60bpm 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 "surrounds" the AV node and has a regular rate of 40 to 60bpm. 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 40bpm and will have a QRS complex of greater than 120ms.

Embryologic evidence

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 centered parasympathetic cholinergic first order. It is then followed by rapid growth of a second order sympathetic adrenergic system arising from the formation of the Thoracic Spinal Ganglia. The third order of electrical influence of the heart is derived from the Vagus Nerve as the other peripheral organs form.[1]

See also


  1. ^ "Innervation of the heart". Human Embryology: Organogenesis: Functional development of the heart. http://www.embryology.ch/anglais/pcardio/funktion02.html. 

External links


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