Ia (Intermediate
Na channel
blocker) / ↓↓ / ↓↓ / ↓ / Intermediate association and dissociation with receptor. ↑ QRS and ↑↑QT. Good for atrial and ventricular tachyarrhythmias.
Disopyramide / ↓ / For HOCM, vagal AFib, vasovagal (antivagal properties from Ach effect). Negative inotrope.
Procainamide / For refractory VT (nonischemic), though 1st line is BB+amio. Also for WPW c AFib (because AV node doesn’t have Na channels. It preferentially affects Na and K channels of accessory pathways, His and Purkinje, while not affecting or shortening AV node refractoriness). Hypotension (α) – load slowly. Lupus like rxn. Metabolite is NAPA, cleared by kidney, and is a Class III and can prolong QT.
Quinidine / +++ drug interactions (Coumadin, dig), agranulocytosis. Used in Brugada syndrome. Ciachonism – tinnitus + diarrhea.
Ib
(Fast Na channel blocker) / ↓ / Fast drug association and dissociation with receptor. No increase QRS or QT at normal HR. Works on injured cells (ie ischemia), such as ischemia induced VTach. Not helpful in atrial tachycardias. Check QRS periodically (need treadmill test to increase HR to check QRS).
Lidocaine / For refractory VT (ischemic). CNS toxicity. Cleared by liver.
Mexilitine / Like a PO lidocaine.
Ic
(Slow Na channel blocker) / ↓↓↓ / ↓ / ↓
(P) / Slow drug association and dissociation with receptor, and therefore has the most use-dependence. ↑↑ QRS, mild ↑QT, which worsens at faster HR. Useful in AFib, but contraindicated in CAD, structural heart dz, LVH (worse outcomes, CAST trial). R/o CAD. Also, Ic’s can convert AFib to slow Aflutter (HR 300>200), but AV node may conduct 200 and thus increase HR. Need AV nodal block too. “Pill in the pocket” strategy.
Flecainide
Propafenone / Metabolite has no BB effect, but 7% of people lack P450 to metabolize.
Encainide
II (Beta blocker) / ↓↓↓
Metoprolol, atenolol, timolol, propranolol, etc
III (K channel blocker) / ↓↓↓ / ↑QT. Amiodarone and dofetilide are the only 2 that can be used in heart failure.
Amiodarone / ↓ / ↓ / Last line 2/2 toxicities. Least proarrythmic.
Dofetilide / AFib. +++ drug interactions (hctz, trimaterene, verapamil, azoles; warfarin ok). Must admit to load. Start highest dose based on QTc and Cr. If QT ↑by 15%, decrease by half. Tikosyn.com
Ibutilide / Short acting, for cardioversion. 1mg/10min. 50% success. Check QT and tele x 4h.
Sotalol / ↓ / For AFib or VT. Start 80 bid. No inpatient load if normal Cr. OK in CAD but contraind in LV dysfunction (unless ICD).
IV (Ca channel blocker) / (non-dihydropyridines)
Verapamil / ↓↓↓ / More negative inotrope than Dilt.
Diltiazem / ↓↓
V
Digoxin
Adenosine
Na channels:
Openclosed (resting)
Inactive
Amiodarone:
-used too much; best drug for AFib but last line 2/2 toxicities
-generally no torsades
-loading – no set way. Full load is 10g. Need a lot because its so lipophilic. Can keep bolusing if needed, ACLS 300mg.
- oral – 400 bid or tid then taper to 400 qd then 200 qd
- IV – 1g load: 150mg load then 1mg/min x 6h then 0.5mg/min x 18h
-Toxicities
- Eye – scotoma, corneal deposits, optic neuritis
- CNS – peripheral neuropathy
- Skin – turn blue; photosensitivity
- Liver – hepatitis
- Thyroid –
- Type I Graves (stop amiodarone, and can’t ablate because thyroid is saturated) (get endocrine)
- Type II hyperT initially, then chronic hypoT (ok to continue amio)
- Lung – acute ARDS, pulmonary fibrosis
Normal heart: Flecainide/Propafenone>Sotalol>Tikosyn>Ablation…………..Amiodarone
CAD: Sotalol>Tikosyn>Ablation
LV dysfunction: Tikosyn…..AV node ablation+biV or amiodarone
Periop: Amiodarone, then stop.
Keys to antiarrhythmics:
Na channel blockers inhibit depolarization, thus prolong your QRS. They also exhibit “use-dependence” (class Ic>Ia>Ib), which means the drugs are more potent at faster heart rates. This is why the Ic drugs (flecainide, etc) are great for AFib.
K channel blockers inhibit repolarization, thus prolong your QT. They also exhibit “reverse use-dependence”, which means the drugs are more potent at slower heart rates. Thus, if someone on these drugs has a very prolonged QT, one way to treat them is stop the drug and speed up their heart rate (temporary pacemaker) to prevent torsades.