The normal electrical conduction in the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to (and stimulate) the myocardium (Cardiac muscle). 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.
In order to maximize efficiency of contraction and cardiac output, the conduction system of the heart has:
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 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. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and 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 (the absolute refractory period), 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 .
Signals arising in the SA node stimulate the atria to contract and travel to the AV node. After a delay, the stimulus is conducted through the bundle of His to the Purkinje fibers and the endocardium at the apex of the heart, then finally to the ventricular epicardium.
Microscopically, the wave of depolarization propagates to adjacent cells via gap junctions located on the intercalated disk. The heart is a 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.
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 Bachman'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.
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. And 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 two bundle branches taper out to produce numerous Purkinje fibers, which stimulate individual groups of myocardial cells to contract.
The last event of the cycle is the repolarization of the ventricles.
An impulse (action potential) that originates from the SA node at a rate of 60 - 100 beats/minute (bpm) is known as normal sinus rhythm. If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known as sinus bradycardia. If SA nodal impulse occur at a rate exceeding 100 bpm, 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 (the AV node is not able to initialize its own impulses) and 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.
The content of this section is licensed under the GNU Free Documentation License (local copy). It uses material from the Wikipedia article "Electrical conduction system of the heart" modified June 23, 2008 with previous authors listed in its history.