[Pathophysiology of cardiac arrhythmias involving autonomic transmitters]

In general cardiac arrhythmias of different types and origins may be attributed to only a few basic electrophysiological effects. These are: changes in impulse formation, in impulse conduction, and/or in refractoriness. Autonomic transmitters are able to exert these effects on the heart and may therefore also induce or support cardiac arrhythmias. The stimulation of sympathetic nerves to the heart (transmitter noradrenaline) enhances via adrenergic beta-receptors the formation of impulses in nomotopic and heterotopic pacemakers by increasing the slope of their slow diastolic depolarizations. In principle identical effects are exerted by noradrenaline on abnormal ectopic pacemakers. Moreover, so-called triggered activity resulting from early or delayed after-depolarizations may be induced by sympathetic activation. In the normal atrial or ventricular myocardium as well as in the specialized ventricular conducting system the sympathetic transmitters are without direct influence on the conduction velocity. However, in the AV node, conduction velocity is markedly increased by noradrenaline. In the depolarized myocardium noradrenaline favours the generation of slowly propagated responses and may thus help to induce arrhythmias due to reentry. The refractory period is shortened by noradrenaline in the working myocardium and in the specialized conducting system. The described effects of noradrenaline are attributed to an increase of the slow inward current (Isi) carried by Ca2+ and Na+ ions. Moreover, a shift of the activation kinetics of the pacemaker current (If) to more positive potentials is discussed. Under the influence of beta receptor blockers, certain effects of noradrenaline may be unmasked which are mediated by adrenergic alpha receptors.(ABSTRACT TRUNCATED AT 250 WORDS)