Mechanisms of Arrhythmogenesis


If a microelectrode is introduced into a single myocardial cell, an action potential (Figure 1) can between the inside and the outside of the cell (inside negative). The resting membrane potential of a normal Purkinje cell is approximately – 90 millivolts (mv) with respect to the outside of the cell. When the membrane potential is depolarized to a certain threshold level, an action potential occurs with a rapid upstroke (phase 0); a return toward zero from the initial overshoot or early rapid repolarization (phase 1); a plateau (phase 2); final rapid repolarization (phase 3); and resting membrane potential and diastolic depolarization (phase 4). The normal resting potential is maintained by the active (i.e., energy-requiring) exclusion of sodium and the accumulation of potassium inside the cell. Phase 0 or rapid depolarization is due chiefly to the opening of the sarcolemmal channels to sodium entrance in atrial and ventricular muscle and cells in the His-Purkinje system. Calcium is important in the maintenance of the action potential plateau of fast sodium channel-dependent cells and in the generation of the action potential upstroke in show calcium channel-dependent cells such as those of the sinus and AV nodes. Phase 3 is mediated chiefly by an outward potassium current and the membrane returns to its negative resting potential during electrical diastole.
Automaticity is a property of some cardiac tissue to undergo gradual phase 4 depolarization spontaneously until threshold potential is reached and the cell initiates an action potential that is propagated from one cell to another. Normal automaticity is present in sinus nodal tissue, some atrial and junctional tissue, the bundle branches and Purkinje fibers. The sinus node discharges more rapidly than the other cells and is the normal pacemaker of the heart.
Conduction is the propagation of a cardiac impulse and is most closely influenced by the amplitude and upstroke velocity of phase 0 of the action potential.
Refractoriness is a property of cardiac tissue during which a stimulus occurring soon after a previous action potential fails to elicit another normal action potential; it is most closely related to the duration of phase 3 of the cardiac action potential in most cardiac tissues.
Although the autonomic nervous system may affect atrial and ventricular tissue to a small extent the most prominent autonomic effects are observed on the sinus and the AV nodes. Sympathetic stimulation increases the rate of automaticity and increases conduction velocity, whereas parasympathetic (vagal) activation does the opposite. Baroreceptors in the carotid sinus, located at the bifurcation of the internal and external carotid arteries, activate the vagus nerve when blood pressure increases and reflexively decrease heart rate and AV nodal conduction velocity. The genesis of cardiac arrhythmias is divided into disorders of impulse formation, disorders of impulse conduction, and combinations of the two (Table 1). One cannot unequivocally determine the mechanism for most clinical arrhythmias, but each arrhythmia may be most consistent with or best explained by a particular electrophysiological mechanism. Disorders of impulse formation are defined as an inappropriate discharge rate of the normal pacemaker (the sinus node) or abnormal discharge from an ectopic pacemaker that usurps control of the atrial or ventricular rhythm. An appropriate discharge rate of a subsidiary pacemaker that takes control of the cardiac rhythm upon sinus slowing is termed an escape beat or rhythm, whereas an inappropriately rapid discharge rate of an ectopic pacemaker (abnormally increased automaticity) that usurps control of the cardiac rhythm from the normal sinus mechanism is termed a premature complex or when they occur in a series, an ectopic tachycardia.

Action potentials recorded from different tissues in the heart remounted with a His bundle recording and scalar ECG from a patient to illustrate the timing during a single cardiac cycle

Figure 1. Action potentials recorded from different tissues in the heart remounted with a His bundle recording and scalar ECG from a patient to illustrate the timing during a single cardiac cycle. SN = Sinus nodal potential; A = Atrial muscle potential; AVN = Atrioventricular nodal potential; PF = Purkinje fiber potential; V = Ventricular muscle potential; HB = His bundle recording; II = lead II. The A-H interval measured in the His bundle recording approximates AV nodal conduction time, and the H-V interval approximates His-Purkinje system conduction time.

Table 1. Genesis of Arrhythmias

Genesis of Arrhythmias

Dr. Afsaneh Jeddi

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