can someone explain antiarrythmics?

[bulldog]

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any good explanations out there? i'm looking through FA, qbank etc. and all the Class I-IV sound the same in terms of the clinical use. i know the different mechanisms, but when u use what is still hazy.

i.e. what's difference between atrial fib, "acute atrial and ventricular arrythmias", svt, and ventricular tachy?

 

[LovingItAll]

any good explanations out there? i'm looking through FA, qbank etc. and all the Class I-IV sound the same in terms of the clinical use. i know the different mechanisms, but when u use what is still hazy.

i.e. what's difference between atrial fib, "acute atrial and ventricular arrythmias", svt, and ventricular tachy?

What books do you have? Plenty of people have explained this well in those books. I thought both Lippicott's Pharm and Lange Pharm Review did good jobs. As for the different types of arrythmias, I can recommend a couple of good pathophys books.

 

[Sinnman]

No. It's too complicated and changes too frequently.

If I were you I would know the following for step 1:

The mechanism of each drug/class.
Adenosine is the DOC for SVT, followed by verapamil.
Atropine is DOC for most bradycardia (except 2nd type II and 3rd degree block).
Lidocaine is used for ventricular dysrhythmia (VT, VF and PVCs)
Amiodarone is pretty much good for anything (know SEs)
Magnesium is probably DOC for Torsades.
For A. fib., anticoagulate if >48 hrs. Use ditiazem or B-beta blocker for RVR.

That's all I can think of off the top of my head. If you really know the mechanisms and the phys, you could probably answer any other questions. I had nothing more complicated than that on my test. The problem is that recommendations change frequently. I think that NBME knows this and therefore only hits "classical" uses (see above) or test knowledge of mechanisms and SEs.

Good luck!

 

[mellow yellow]

I'll try my best to summarize the important uses. I agree that antiarrhythmics can be somewhat confusing and really the only way to know where they're clinically useful is to take a rotation in cards. So here goes..


Class Ia: quinidine, procainamide, disopyramide. Not used in cards really. Major class side effect = torsades due to QT prolongation.
Class Ib: lidocaine, mexiletine, phenytoin.
Lido is useful in the setting of acute ventricular arrhythmias (VT, VF); do not use as prophylaxis for ventricular arrhythmias as they are associated with increased mortality in this setting.
Class Ic: flecainide, propafenone. Useful for SVT prophylaxis. Also used to treat Atrial fibrillation in persons without structural heart disease/MI.

Class II: beta blockers like metoprolol, etc... Work by decreasing heart's response to catacholamines and thus slow down heart rate. Useful for SVT prophylaxis, and useful in acute and chronic Afib rate control.

Class III: amiodarone, sotalol.
Amiodarone actually displays the affects of all four classes! Know all of the clinically important side effects including pulmonary fibrosis, hyper/hypothyroidism, transaminitis, blue skin syndrome (photosensitivity), corneal pigment deposition, and torsades. Can be used in setting of ventricular arrhythmias, and for rhythm control of Afib chronically. Sotalol can also be used to treat afib in pts without CHF.

Class IV: adenosine, calcium channel blockers.
Adenosine is the DOC for acute conversion of SVT (AVNRT).
CCBs (verapamil, diltiazem) useful for rate control of Afib, especially in acute setting. Can also be used for rate control in acute setting of Aflutter.


Digoxin: not really an antiarrhythmic but has antiarrhythmic properties. Useful for rate control of Afib, especially in patients with impaired systolic function.

I hope this is useful... It's about all I can come up with at the moment...

 

[bulldog]

thanks. btw, can u guys point out how to detect svt vs vt? i.e. what are some buzzwords associated w/ svt that u'd see?

 

[idq1i]

thanks. btw, can u guys point out how to detect svt vs vt? i.e. what are some buzzwords associated w/ svt that u'd see?

svt is narrow. vt is wide

 

[hyperbaric]

thanks. btw, can u guys point out how to detect svt vs vt? i.e. what are some buzzwords associated w/ svt that u'd see?

svt originates from the AV junction (=AV node+bundle of His) (i.e. supra-ventricular), QRS 0.6-0.10 sec (narrow)

vt originates from the ventricles, QRS >=0.10 sec (wide)

 

[mellow yellow]

svt is narrow. vt is wide

actually, it's not always wide... the differential diagnosis of a wide complex tachycardia that is >140 includes VT and SVT with aberrancy. For the purposes of step 1 or 2, if you see wide complex tachycardia think VT. The only way to truly differentiate between the two requires an EP study.

 

[Idiopathic]

actually, it's not always wide... the differential diagnosis of a wide complex tachycardia that is >140 includes VT and SVT with aberrancy. For the purposes of step 1 or 2, if you see wide complex tachycardia think VT. The only way to truly differentiate between the two requires an EP study.

For step 1 purposes, you will not see VT with aberrancy. You will likely not see SVT either, but if you did, remember that vagal maneuvers are the initial treatment of choice, beta-blockers (esmolol) and CCB's (cardizem) can also be considered...you may not see adenosine as a choice.

Also, remember that SVT will look just like sinus tachycardia, only at a rate of >150 (i.e. you should see p waves). V-tach will be wide, for board purposes.

Also, as above, remember that maneuvers (i.e. vagal for SVT, shock for v-fib, do nothing for stable AV block) are your first treatments, while the drugs mentioned here are usually acceptable pharmacologic treatments.

I would know things like:
1) What for atrial arrythmias vs. ventricular arrythmias? I wouldnt worry about specific conditions.
2) When not to use a specific drug (i.e. WPW)
3) S/E of drugs, notably digoxin, amiodarone...all class III drugs generally do mora harm than good. Amiodarone can cause hypo or hyperthyroid, so remember that link.