There are broadly two types of cardiac tissue.
The first type is ordinary myocardial (atrial and ventricular) muscle, responsible for the pumping action of the heart.
The second type is specialised conducting tissue that initiates the cardiac electrical impulse and determines the order in which the muscle cells contract. The important property of being able to form impulses spontaneously is called automaticity and is a feature of certain parts of the conducting tissue, e.g. the sinoatrial (SA) and atrioventricular (AV) nodes. The SA node has the highest frequency of spontaneous discharge, 70 times per minute, and thus controls the contraction rate of the heart, making the cells more distal in the system fire more rapidly than they would do spontaneously, i.e. it is the pacemaker. If the SA node fails to function, the next fastest part takes over. This is often the AV node (45 discharges per min) or a site in the His-Purkinje system (25 discharges per min).
Altered rate of automatic discharge or abnormality of the mechanism by which an impulse is generated from a centre in the nodes or conducting tissue, is one cause of cardiac arrhythmia, e.g. atrial fibrillation, flutter or tachycardia.
Nearly all cells in the body exhibit a difference in electrical voltage between their interior and exterior, the membrane potential. Some cells, including the conducting and contracting cells of the heart, are excitable; an appropriate stimulus alters the properties of the cell membrane, ions flow across it and elicit an action potential. This spreads to adjacent cells, i.e. it is conducted as an electrical impulse and, when it reaches a muscle cell, causes it to contract; this is excitation-contraction coupling.
In the resting state the interior of the cell (conducting and contracting types) is electrically negative with respect to the exterior due to the disposition of ions (mainly sodium, potassium and calcium) across its membrane, i.e. it is polarised. The ionic changes of the action potential first result in a rapid redistribution of ions such that the potential alters to positive within the cell (depolarisation); subsequent and slower flows of ions then restore the resting potential (repolarisation). These ionic movements may be separated into phases which are briefly described here and in Figure 25.1, for they help to explain the actions of antiarrhythmic drugs.1
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