Flashcards in Antiarrhythmics Deck (40):
Class IA drugs?
Quinidine, disopyramide, procainamide
Class IB drugs?
Lidocaine, mexiletine, tocainimide
Class IC drugs?
Class II drugs?
Metoprolol, propranolol, esmolol, atenolol, timolol
Class III drugs?
Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
Class IV drugs?
Verapamil > diltiazem
Which drugs are state dependent (selectively depress tissue that is frequently depolarized such as tachycardia?
Class I drugs
What do all class I drugs have in common?
Decrease slope of phase 0, decreasing conduction of AP and thus rate of contraction
MOA of class IA?
Increase AP duration, delays phase 3 repolarization (increases ERP and prolonged QTi)
MOA of class IB?
Preferentially affects ischemic or depolarized tissue, phase 3 (ERP) is shortened as well as the entire AP
MOA of class IC?
NO effect on AP
AEs of HA, tinnitus, vertigo and psychosis?
Quinidine - cinchonism
Drug induced lupus?
Best for post-MI?
Class IB drugs
Contraindicated post-MI as it may cause arryhthmias?
Class IC drugs
May exacerbate heart failure?
Class IC drugs (watch out in pts with low ejection fraction)
MOA of class II drugs?
Decreases SA and AV node activity by decreasing cAMP, decreasing Ca current, decreasing contractility and HR. Suppress abnormal pacemakers by decreasing slope of phase 4. Increases PR interval by affecting AV node particularly.
1st line for persistent a-fib in presence of structural heart damage?
AEs of B-blockers?
Impotence, exacerbation of asthma, bradycardia, AV block, CHF, sedation/sleep alterations, may mask signs of hypoglycemia
Tx for B-blocker OD?
MOA of class III drugs?
Block K efflux, increases AP duration and ERP (prolonged QTi)
AEs of sotalol?
Torsades, excessive B-block
AEs of ibutilide?
AEs of amiodarone?
Pulmonary fibrosis, hepatotoxicity, thyroid toxicity, corneal deposits, blue/gray skin deposits resulting in photodermatitis, ataxia, CV effects
Why can amiodarone block Na, K, and C and have alpha and B-blocking effects?
It alters the lipid membrane
MOA of class IV drugs?
Block Ca channels in SA and AV nodes, slowing phase 4 depolarization, decreasing conduction velocity, prolonging PR interval and ERP
MOA of adenosine?
Increase K efflux out of SA and AV nodal cells, hyperpolarizing the cell and decreasing HR
Use for adenosine?
DOA for adenosine?
VERY short (15 secs)
AEs of adenosine?
Flushing, hypotension, chest pain, dyspnea
What blocks the effects of adenosine?
Theophylline and caffeine
MOA of K?
Increases threshold for cardiac APs, decreasing excitation and thus HR
Use for K?
Suppresses ectopic pacemakers, esp those assoc with digoxin toxicity
Use for Mg?
Torsades, digoxin toxicity
MOA of digoxin?
Inhibits Na/K ATPase, which inhibits the Na/Ca exchanger causing increased contractility; stimulates vagus nerve causing decreased HR
Use for digoxin?
AEs of digoxin?
N/V/D, blurry yellow vision, ECG changes (increased PRi, decreased QTi, ST-scooping, T-wave inversion), cardiac arrythmias, hyperkalemia
What exacerbates digoxin AEs?
2) Renal failure
Digoxin toxicity tx?
Tx the hypokalemia, anti-dig Fab, lidocaine, Mg