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Chapter: Modern Pharmacology with Clinical Applications: Pharmacological Management of Chronic Heart Failure

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Cardiac Electrophysiology: Automaticity

Automaticity can be defined as the ability of a cell to al-ter its resting membrane potential toward the excitation threshold without the influence of an external stimulus.

Automaticity

Automaticity can be defined as the ability of a cell to al-ter its resting membrane potential toward the excitation threshold without the influence of an external stimulus. The characteristic feature of cells with automaticity is a slow decrease in the membrane potential during dias-tole (phase 4) such that the membrane potential reaches threshold (Figure 16.2). During phase 4 in these pacemaker cells, the background potassium leak cur-rent decreases and an inward depolarizing current (If) is activated. 


In combination, this results in slow depolar-ization of the myocyte. If the membrane potential de-polarizes above the threshold for the opening of ICa , an action potential is generated.

Myocytes within the sinoatrial node possess the most rapid intrinsic rate of automaticity; therefore, the sinoatrial node serves as the normal pacemaker of the heart. Specialized cells within the atria, atrioventricular (A-V) node, and His-Purkinje system are capable of spontaneous depolarization, albeit at a slower rate. The more rapid rate of depolarization of the sinoatrial nodal cells normally suppresses all of the other cells with the potential for automaticity. The other cells will become pacemakers when their own intrinsic rate of depolariza-tion becomes greater than that of the sinoatrial node or when the pacemaker cells within the sinoatrial node are depressed. When impulses fail to conduct across the A-V node to excite the ventricular myocardium (heart block), spontaneous depolarization within the His-Purkinje system may become the dominant pacemaker maintaining cardiac rhythm and cardiac output.

The rate of pacemaker discharge within these spe-cialized myocytes is influenced by the activity of both divisions of the autonomic nervous system. Increased sympathetic nerve activity to the heart, the release of catecholamines from the adrenal medulla, or the exoge-nous administration of adrenomimetic amines will cause an increase in the rate of pacemaker activity through stimulation of β-adrenoceptors on the pace-maker cells (Figure 16.3).


The parasympathetic nervous system, through the vagus nerve, inhibits the spontaneous rate of depolar-ization of pacemaker cells. The release of acetylcholine from cholinergic vagal fibers increases potassium con-ductance (gK+ ) in pacemaker cells, and this enhanced outward movement of K+ results in a more negative potential, or hyperpolarization, of the sinoatrial cells. Thus, during vagal stimulation, the threshold potential of the sinoatrial node pacemaker cells is achieved more slowly and the heart rate is slowed.


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