Antiarrhythmic Drugs, Animation

(USMLE topics, cardiology) The 5 classes of agents according to Vaughan Williams classification, mechanism of action.
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ANTI-Arrhythmic agents are drugs used to SUPPRESS abnormal rhythms of the heart. They act to either:
- interfere with the dynamics of cardiac action potentials by blocking a certain ion channel,
or
- block the sympathetic effects of the autonomic nervous system on the heart, to slow down heart rate.
There are 5 classes of antiarrhythmic drugs:
- Class I: Sodium-channel blockers: these drugs bind to and block the fast sodium channels that are responsible for the DE-polarizing phase in contractile myocytes. The result is a SLOWER depolarization with a smaller amplitude. This REDUCED conduction velocity helps to SUPPRESS formation of re-entrant circuits, hence the use of these drugs for treating re-entrant tachycardias.
Class I agents are divided further into subclass IA, IB and IC. These subclasses differ in the STRENGTH of sodium channel blockage, and in their effect on the duration of action potentials and the effective refractory period, the ERP. While subclass IC has no effect on ERP, IA prolongs and IB shortens ERP, respectively. Changes in ERP may have different outcomes for different types of arrhythmias. A longer ERP generally reduces cardiac excitability, but prolonged repolarizations may increase the risk of torsades de pointes, a type of tachycardia caused by afterdepolarizations.
- Class II: Beta-blockers: these drugs bind to beta1-adrenergic receptors and block the sympathetic influences that act through these receptors. Sympathetic nerves release catecholamines which act to increase SA node firing rate and cardiac conductibility, especially at the AV node. Useful in treatment of tachycardias that originate upstream of the AV node, known as supraventricular tachycardias, or SVT.
- Class III: Potassium-channel blockers: these agents block the potassium channels responsible for the repolarizing phase. The result is a SLOWED repolarization, hence a PROLONGED duration of action potentials and refractory period. This reduces the heart’s excitability and suppresses re-entrant tachycardias. However, these drugs may also CAUSE arrhythmias because slow repolarizations are associated with LONGER QT intervals and INcreased risks of torsades de pointes.
- Class IV: Calcium-channel blockers: these drugs block calcium channels that are responsible for DE-polarization in SA and AV nodal cells. Blocking these channels results in a LOWER sinus rate and SLOWER conduction through the AV node. However, because calcium is also involved in cardiac myocyte contraction, these agents also reduce contractility of the heart and should not be used in case of systolic heart failures.
- Class V includes all drugs that act by other or unknown mechanisms.

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[@shivakrishnaraotavarekar4389]

Class 1A:Prolong the action potential duration by slowing phase 0 depolarization and delaying repolarization (phase 3).
Class 1B:Mild effect on phase 0 and shortened repolarization.
Class 1C :blocking rapid sodium channels, thereby slowing down the Phase 0
Class II : suppress adrenergically mediated ectopic activity.
Class III: prolongation of repolarization (phase3); AP is widened and ERP is increased.
Class IV : inhibit Ca2+ mediated slow channel inward current.

[@zacharymarsh9342]

This was seriously soooo helpful!!! Thank you for making this and sharing it!

[@tummy540]

you have literally saved me through CVS. Thank you so much ma'am ♥️

[@malakshammari5818]

Nice , brief and helpful
Keep up with this beautiful explanations!!

[@ashishsinghal6190]

truly awesome video and too much helpful . pls upload some videos like this

[@salsabilwayz8584]

Thank you so much Ma'am. I couldn't understand how conduction was slowed by class 1a aa drugs.

[@alptekinakturk4185]

nice summary, thank you

[@yohaneswilliam1995]

Simple, and much helpful, thanks.

[@afriyiebeatrice9263]

This was very well understood.great job

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So simple and so well explained, too. Thank you!

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You're very welcome!

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Wow ... I have my book Infront of me.... literally my next 40 pages in 4 minutes

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Thank you Dr

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Amazing job 👏🏻

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Please make video about Thymosins(types and their functions)..thanks

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thank you it's very helpful

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Really really helpful..thanks a lot

[@modjadjibeautymaake7728]

Loved this simplified explanation of anti-arrythmic drugs as well as the fact that it is short. Thank you so much!!!!

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i love the work guys♥

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Thank you ma'am ❤

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From Iraq , thanks ❤❤❤

[@medicalchannel-2113]

Thank you

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Thanks

[@agastyaagarwal4539]

Thank you soooo much🤩😇

[@seamuswarren]

I’m on a 1C.
Do anti-arrhythmic impact contractile tissue in other muscles?

[@adityavarma6380]

Thank u

[@petremitrov]

Excelent!

[@user-dr7fw8pr6m]

thank you perfect video can someone answer this :
slowing down the influx of sodium ions into cardiac muscle cells causing a decrease in the excitability of the cells it has a beta adrenergic blocker which can cause bradycardia and bronchospasm :
sotalol
propafenone
verapamil
mexitilene

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This is amaxing thank you , you helped me ALOT

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Thank you. .. saving video as usual

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Great

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Sup future doctors?

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Hey! Graduated ?

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[@salsabilwayz8584]

I have some queries :like how class 1a prolong ERP n class 1b shortens it. 2 when does class 1b act on sodium channel in open state or inactivated state.

[@zeelpatel8049]

1a prolong ERP via the effect on K+ channel blocking property.And 1b shortens via increasing diastole and extends time for recovery(Couduction=APD+DIASTOLE).1b block inactivted Na channels.
hope this will help.

[@FlavourlessQuark]

How can Ic drugs have no effect on ERP if they stay attached to channels the longest?

[@zeelpatel8049]

they act only on phase 0 Na channels.no other effect(ANS).

[@tejaswinijadhav3293]

What is widening the Ap ?
Please reply

[@eylul1512]

Action potential ☠️

[@educationworld7530]

👌

[@anasjahangir1936]

The bestest video available on this stupid topic!

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quick and dirty

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Ulcerative colitis please