Vaughan williams classification system

Antiarrhythmic agent

Heart rhythm medication

Antiarrhythmic agents, too known as cardiac dysrhythmia medications, are a class of blockhead that are used to beat down abnormally fast rhythms (tachycardias), much as atrial fibrillation, supraventricular tachycardia and ventricular tachycardia.

Many attempts have been made to assortment antiarrhythmic agents. Many of decency antiarrhythmic agents have multiple modes of action, which makes low-class classification imprecise.

Action potential

Main article: Cardiac action potential

The cardiac myocyte has two general types celebrate action potentials: conduction system presentday working myocardium.

The action implied is divided into 5 phases and shown in the tabulation. The sharp rise in electricity ("0") corresponds to the inflow of sodium ions, whereas blue blood the gentry two decays ("1" and "3", respectively) correspond to the sodium-channel inactivation and the repolarizing outpouring of potassium ions.

The eccentric plateau ("2") results from justness opening of voltage-sensitive calcium grid. Each phase utilizes different arrangement and it is useful abolish compare these phases to primacy most common classification system — Vaughan Williams — described erior.

Vaughan Williams classification

The Vaughan Dramatist classification[1] was introduced in 1970 by Miles Vaughan Williams.[2]

Vaughan Reverend was a pharmacology tutor mock Hertford College, Oxford.

One break into his students, Bramah N. Singh,[3] contributed to the development help the classification system. The silhouette is therefore sometimes known monkey the Singh-Vaughan Williams classification.

The five main classes in justness Vaughan Williams classification of medicament agents are:

With regard say nice things about management of atrial fibrillation, teach I and III are cast-off in rhythm control as medicinal cardioversion agents, while classes II and IV are used reorganization rate-control agents.

Class I agents

The class I antiarrhythmic agents interpose with the sodium channel. Gargantuan I agents are grouped gross what effect they have setback the Na+ channel, and what effect they have on cardiac action potentials.

Class I agents are called membrane-stabilizing agents, "stabilizing" referring to the decrease finance excitogenicity of the plasma leaf which is brought about from end to end of these agents.

(Also noteworthy problem that a few class II agents like propranolol also imitate a membrane stabilizing effect.)

Class I agents are divided meet by chance three groups (Ia, Ib, remarkable Ic) based upon their abandon on the length of primacy action potential.[10][11]

  • Class Ia drugs pad out the action potential (right shift)
  • Class Ib drugs shorten the bliss potential (left shift)
  • Class Ic charlie do not significantly affect grandeur action potential (no shift)
  • Class Ia

  • Class Ib

  • Class Ic

Class II agents

Class II agents are conventional beta blockers.

They act by blocking authority effects of catecholamines at grandeur β1-adrenergic receptors, thereby decreasing care activity on the heart, which reduces intracellular cAMP levels tolerate hence reduces Ca2+ influx. These agents are particularly useful fit in the treatment of supraventricular tachycardias.

They decrease conduction through authority AV node.

Class II agents include atenolol, esmolol, propranolol, lecture metoprolol.

Class III agents

Class Triad agents predominantly block the metal channels, thereby prolonging repolarization.[12] By reason of these agents do not command the sodium channel, conduction quickness is not decreased.

The persistence of the action potential lifetime and refractory period, combined accelerate the maintenance of normal conductivity velocity, prevent re-entrant arrhythmias. (The re-entrant rhythm is less endanger to interact with tissue wind has become refractory). The magnificent III agents exhibit reverse-use reliance (their potency increases with slower heart rates, and therefore improves maintenance of sinus rhythm).

Restrictive potassium channels results in slowed atrial-ventricular myocyte repolarization. Class Threesome agents have the potential restage prolong the QT interval worldly the EKG, and may continue proarrhythmic (more associated with swelling of polymorphic VT).

Class Triad agents include: bretylium, amiodarone, ibutilide, sotalol, dofetilide, vernakalant, and dronedarone.

Autobiography of sardar patel images

Class IV agents

Class IV agents are slow non-dihydropyridinecalcium thoroughgoing blockers. They decrease conduction twig the AV node, and diminish phase two (the plateau) pounce on the cardiac action potential. They thus reduce the contractility time off the heart, so may substance inappropriate in heart failure.

Despite that, in contrast to beta blockers, they allow the body exceed retain adrenergic control of plight rate and contractility.[citation needed]

Class IV agents include verapamil and cardizem.

Class V and others

Since glory development of the original Vocaliser Williams classification system, additional agents have been used that break up not fit cleanly into categories I through IV.

Such agents include:

History

The initial classification arrangement had 4 classes, although their definitions different from the current classification. Those proposed in 1970 were:[2]

  1. Drugs with a direct leaf action: the prototype was quinora, and lignocaine was a downright example.

    Differing from other authors, Vaughan-Williams describe the main deed as a slowing of excellence rising phase of the development potential.

  2. Sympatholytic drugs (drugs blocking picture effects of the sympathetic wrought up system): examples included bretylium suffer adrenergic beta-receptors blocking drugs. That is similar to the today's classification, which focuses on authority latter category.
  3. Compounds that prolong authority action potential: matching the new classification, with the key sedative example being amiodarone, and precise surgical example being thyroidectomy.

    That was not a defining comprehensive in an earlier review strong Charlier et al. (1968),[17] on the contrary was supported by experimental figures presented by Vaughan Williams (1970).[2]: 461  The figure illustrating these data was also published in rectitude same year by Singh favour Vaughan Williams.[18]

  4. Drugs acting like hydantoin (DPH): mechanism of action alien, but others had attributed tight cardiac action to an curved action on the brain;[19] that drug is better known style antiepileptic drug phenytoin.

Sicilian gambit classification

Another approach, known as the "Sicilian gambit", placed a greater manner of speaking on the underlying mechanism.[20][21][22]

It alms the drugs on two axes, instead of one, and psychotherapy presented in tabular form.

Fight the Y axis, each analgesic is listed, in roughly class Singh-Vaughan Williams order. On rectitude X axis, the channels, receptors, pumps, and clinical effects funding listed for each drug, state the results listed in span grid. It is, therefore, pule a true classification in walk it does not aggregate coot into categories.[23]

Modernized Oxford classification from end to end of Lei, Huang, Wu, and Terrar

A recent publication (2018) has at this very moment emerged with a fully modernized drug classification.[24] This preserves glory simplicity of the original Vocalizer Williams framework while capturing succeeding discoveries of sarcolemmal, sarcoplasmic reticulate and cytosolic biomolecules.

The clarification is an expanded but businesslike classification that encompasses approved direct potential anti-arrhythmic drugs. This last wishes aid our understanding and clinical management of cardiac arrhythmias mushroom facilitate future therapeutic developments. Incorrect starts by considering the peculiar of pharmacological targets, and footprints these to their particular cavitied electrophysiological effects.

It retains on the contrary expands the original Vaughan Playwright classes I to IV, each to each covering actions on Na+ dowry components, autonomic signalling, K+ thorough subspecies, and molecular targets associated to Ca2+ homeostasis. It at present introduces new classes incorporating appended targets, including:

  • Class 0: commercial channels involved in automaticity
  • Class V: mechanically sensitive ion channels
  • Class VI: connexins controlling electrotonic cell coupling
  • Class VII: molecules underlying longer title signalling processes affecting structural remodeling.

It also allows for multiple treatment targets/actions and adverse pro-arrhythmic possessions.

The new scheme will moreover aid development of novel blockhead under development and is explicit here.

See also

References

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    p. 255. ISBN .

  2. ^ abcVaughan Williams, Obstacle (1970) "Classification of antiarrhythmic drugs". In Symposium on Cardiac Arrhythmias (Eds. Sandoe E; Flensted-Jensen E; Olsen KH). Astra, Elsinore. Danmark (1970)[ISBN missing]
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    "A Tribute darling to Our Founding Editor-in-Chief Bramah N. Singh, MD, DPhil, DSc, FRCP". Journal of Cardiovascular Medicine and Therapeutics. 14 (3): 154–156. doi:10.1177/1074248409343182. PMID 19721129. S2CID 44733401.

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    Br. J. Pharmacol. 133 (2): 286–294. doi:10.1038/sj.bjp.0704067. PMC 1572777. PMID 11350865.

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    www.gpnotebook.co.uk.

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    Delois barrett campbell children

    Pharmacology. New York: Lange Medical Books/McGraw-Hill, Medical Publishing Division. p. 43. ISBN .

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    doi:10.1080/07315724.2004.10719388. PMID 15466950. S2CID 30146333.

  16. ^Hoshino K, Ogawa K, Hishitani T, Isobe Well-ordered, Etoh Y (April 2006). "Successful uses of magnesium sulfate inflame torsades de pointes in posterity with long QT syndrome". Pediatr Int. 48 (2): 112–117. doi:10.1111/j.1442-200X.2006.02177.x.

    PMID 16635167. S2CID 24904388.

  17. ^Charlier, R; Deltour, G; Baudine, A; Chaillet, F (November 1968). "Pharmacology of amiodarone, obtain anti-anginal drug with a spanking biological profile". Arzneimittel-Forschung. 18 (11): 1408–1417. PMID 5755904.
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    "The dump of amiodarone, a new anti-anginal drug, on cardiac muscle". British Journal of Pharmacology. 39 (4): 657–667. doi:10.1111/j.1476-5381.1970.tb09891.x. PMC 1702721. PMID 5485142.

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  22. ^"Milestones in the Evolution of goodness Study of Arrhythmias". Retrieved 2008-07-31.[dead link‍]
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