Okay. Antiarrhythmics drugs seem complicated in the beginning but hopefully they would get better by studying some diagrams and drawing them. Lippincott pharm book has many good pictures. I'm not sure about pharm recall.
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It is my personal opinion that it will be the to memorize those drugs by categories. What I mean is that all of class IA drugs have a same mechanism, IB drugs same and IC drugs same. So, as long as we know which drugs belong to which category, we can easily know what each does.
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With Sanjai's recommendation, (thanks to Sanjai!) I listened to Doctors in Training. These audio files are too big to send out via email but they are all over the places in internet. I got the 2010 audio version.
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DIT said some good mneumics to start. I think I sent out about this menumonics while ago but here it is! I also like the FIRST AID mneumonics on pg.280 because their mneumonics contain more similar words/rhyms to actual names of the drugs while DIT's mneumonics only uses first letters of each drug. Sometimes, remembering the mneumonics is more difficult than remembering the actual contents. lol.
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No // Bad boy // Keeps // Clean

NO
[Na+] channel blockers. Class I
BAD BOY
B-blockers. Class II
KEEPS
[K+] channel blockers. Class III.
CLEAN
[Ca+2] channel blockers. Class IV.
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Police Department Questions // The Little Man // For Pushing Ecstasy.

Police Department Questions
Procainamide, Disopyramide, Quinidine. Class IA (*Not commonly used)
The LIttle Man
Tocainide, Lidocaine, Mexiletine. Class IB (*Most commonly used)
For Pushing Ecstasy
Flecainide, Encainide, Propafenone. Class IC.
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In continuation from Sanjai's awesome IA drugs mneumonics...here is class IB drugs that I noted from the Kaplan lecture.
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Class IB ;
It blocks
1) Fast [Na+] channels
2) Inactivated [Na+] channels (M gate opened and h gate closed), therefore, preventing it from going back to the resting state (M gate closed and h gate opened). This mechanism is specific to hypoxic and ischemic heart as it keeps those cells in the hypoxic tissues to enter refractory --> Slowing the conduction.
3) Slow [Na+] window current --> decreased action potential duration. **I didn't know this before that slow [Na+] channel opens during plateau phase to keep integrity of the membrane while K+ and Ca2+ are passing out/in. --> ultimately, this would allow shorten action potential so that there is more time for diastole/filling

Lidocaine.
Usage;
1. The same drug that you would use for anesthetics. Used for Post-MI, Open-heart surgery and Digoxin toxicity (or digitalis-induced arrhythmias).
2. Digoxin toxicity was very emphasized in both of Kaplan and DIT. (but i still struggle to get the big concept..) What I understood is that digoxin or positive inotropy can cause tachyrhythmia when it is given too much. As an antidote (FIRST AID p.279), you would give Lidocaine.

Side-effects;

1. First pass metabolism digests this drug so only used via IV --> cannot send patients home with this drug --> if necessary, use Mexiletine or Tocainide (oral) instead.

2. CNS toxicity or seizure. However it has the least cardiotoxicity among conventional anti-arrhythmics.

Mexiletine and Tocainide
Same as Lidocaine, however they are available as oral formulations.
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