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Antiarrhytmic drugs

The substances belonging to the different classes of chemical compounds and belonging to various pharmacological groups can have the normalizing impact on the broken rhythm of warm reductions.

So, in the arrhythmias connected with emotional pressure at patients without serious heart diseases drugs can render antiarrhytmic effect calming (sedative, tranquilizing). A number of the means influencing an efferent and afferent innervation has antiarrhytmic activity (holinoblokator and cholinomimetics (see Atropine, Carbacholinum.), adrenoblockers and adrenomimetik (see - Adrenoblockers, Isadrinum), local anesthetics (see Lidocaine, Trimecainum, Pyromecainum), some antiepileptic drugs (see Difenin), the drugs containing potassium salts (see Potassium chloride, the Asparkam, Pananginum), antagonists of calcium ions (see Verapamil, Nifedipine), etc.

At the same time there is a number of drugs which main pharmacological property is the normalizing influence on a heart rhythm at different types of arrhythmias. These means and also a number of Ab - adrenoblockers, antagonists of calcium ions, lidocaine and other local anesthetics, anticonvulsant drug combine dipheninum in connection with their significant antiarrhytmic activity in Kgruppu of antiarrhytmic drugs.

There are various classifications of antiarrhytmic drugs.

Now Vogen-Williams's classification (E.M. Vaughan-Williams) subdividing antiaritmik into 4 groups is most widespread:

U I group - membrane stabilizing means (hinidinopodobny);
U II group - A b - adrenoblockers;
U III group - the drugs which are slowing down repolarization (the main representative Amiodaronum; here Ornidum, or a bretylium rank a sympatholytic);
U IV group - blockers of calcium channels (antagonists of calcium ions).

The first group includes a number of the drugs differing on some features of action. Conditionally it is subdivided into 3 subgroups:

Subgroup of IA - quinidine, novokainamid, Disopyramidum;
Subgroup of IB - local anesthetics (lidocaine, Trimecainum, Pyromecainum) and also meksiletin and dipheninum;
Subgroup of IC - Ajmalinum, Ethmosinum, etatsizin, allapinin.

Some antiarrhytmic drugs have to a degree properties of various subgroups.

The choice of antiarrhytmic means for optimum use at any given form of arrhythmia demands knowledge not only the nature of arrhythmia, but also the mechanism of effect of drug, the sum of its pharmacological properties.

In the mechanism of effect of all antiarrhytmic drugs the leading role is played by influence on cellular membranes, on transport of ions through them (Na+, K+, Sa2+) and also the impact on electrophysiologic processes interconnected with it in a myocardium, on depolarization of electric membrane potential of cardiomyocytes.

Various groups of antiarrhytmic means and separate drugs differ by some types of influence on these processes. So, drugs of subgroup of IA and IC generally suppress transport of ions of sodium through "fast" natrium channels of a cellular membrane. Drugs of subgroup of IB increase permeability of membranes for potassium ions. Quinidine along with oppression of transport of ions of sodium reduces receipt in cardiomyocytes of calcium ions. The same combined impact is made by new antiarrhytmic drug a bonnekor.

Drugs I of group reduce the maximum speed of depolarization, raise an excitation threshold, slow down conductivity on a ventriculonector and Purkinye fibers, slow down recovery of reactivity of membranes of cardiomyocytes.

Group drugs II (Ab - adrenoblockers) reduce influence on heart of adrenergic impulses which can in certain conditions matter in pathogenesis of arrhythmias. In the mechanism of antiarrhytmic effect of these drugs a part is played by suppression under their impact of activation of adenylatecyclase of cellular membranes and reduction of formation of the cyclic AMF promoting transfer of effects of catecholamines. Drugs of this group reduce transmembrane transfer of ions of sodium, increase transfer of potassium ions, reduce excitability of myofibrils and Purkinye fibers, reduce the speed of carrying out excitement. The majority of A b - adrenoblockers slow down a sinoatrial rate, sinuatrial and atrioventricular conductivity, have negative inotropic effect.

On the influence the main representative of drugs III of group - Amiodaronum which increases action potential duration is unique, slows down carrying out an impulse on all sites of the carrying-out system of heart, urezhat a sinoatrial rate, causes lengthening of an interval of Q - T. It has no significant effect on sokratitelny ability of a myocardium. Amiodaronum has a wide range of antiarrhytmic action and at the same time is active anti-anginal drug.

Ornidum (bretylium) ranked as the III group has generally sympatholytic effect (see Ornidum), limiting thus influence of catecholamines on a myocardium; at the same time it increases, like Amiodaronum, action potential duration.

Group drugs III influence transmembrane transfer of ions a little.

Group drugs IV (verapamil, nifedipine, etc.) inhibit slow transmembrane current of calcium ions in myocardium cells that promotes decrease in automatism of the ectopic centers and influences a repeated entrance of excitement.

Features of the mechanism of effect of drugs of various groups are important for specification of indications and contraindications when prescribing any given antiarrhythmic drug.

When choosing drug it is necessary to consider not only its specific antiarrhytmic features, but also the general pharmacological properties (influence on other functions and the systems of an organism) and also possible side effects.

It is necessary to consider that antiarrhytmic drugs in connection with their action on the carrying-out system of heart can in certain conditions have pro-arrhythmic (aritmogenny) effect.
Ajmalinum
Allapininum
Amiodaronum
Bonnecor
Disopyramidum
Mexiletine hydrochloride
Neo-Gilurythmal
Novocainamidum
Ornidum
The prolonged dosage forms of quinidine ()
Propafenone
Pulsnorma
Chinidinum
Aethacizinum
Aetmozinum
Diseases

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