Fig. 24.1 The action potential of a cardiac cell that is capable of spontaneous depolarisation (SA or AV nodal, or His-Purkinje) indicating phases 0-4; the figure illustrates the gradual increase in transmembrane potential (mV) during phase 4; cells that are not capable of spontaneous depolarisation do not exhibit increase in voltage during this phase (see text).The modes of action of antiarrhythmic drugs of classes 1,11,111 and IV are indicated in relation to these phases
1 Grace A A, Canun A J 2000 Cardiovascular Research 45: 43-51.
Phase 2 is a period when there is a delay in repolarisation caused mainly by a slow movement of calcium ions from the exterior into the cell through channels that are selectively permeable to these ions ('long-opening' or L-channels).
Phase 3 is a second period of rapid repolarisation during which potassium ions move out of the cell.
Phase 4 begins with the fully repolarised state; for cells that discharge automatically, potassium ions then progressively move back into and sodium and calcium ions move out of the cell. The result is that the interior becomes gradually less negative until a (threshold) potential is reached which allows rapid depolarisation (phase 0) to occur, and the cycle is repeated. Automaticity is also influenced by prevailing sympathetic tone. Cells that do not discharge spontaneously rely on the arrival of an action potential from another cell to initiate depolarisation.
In phases 1 and 2 the cell is in an absolutely refractory state and is incapable of responding further to any stimulus but during phase 3, the relative refractory period, the cell will depolarise again if a stimulus is sufficiently strong. The orderly transmission of an electrical impulse (action potential) throughout the conducting system may be retarded in an area of disease, e.g. localised ischaemia or previous myocardial infarction. Thus an impulse travelling down a normal Purkinje fibre may spread to an adjacent fibre that has transiently failed to transmit, and pass up it in reverse direction. If this retrograde impulse should in turn re-excite the cells that provided the original impulse, a re-entrant excitation becomes established and may cause an arrhythmia, e.g. paroxysmal supraventricular tachycardia.
Most cardiac arrhythmias are probably due either to:
• impaired conduction in part of the system leading to the formation of re-entry circuits (> 90% of tachycardias) or
• altered rate of spontaneous discharge in conducting tissue. Some ectopic pacemakers appear to depend on adrenergic drive.
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