What are Class I antiarrhythmics?
sodium channel blockers
What are Class II antiarrhythmics?
beta blockers
What are Class III antiarrhythmics?
potassium channel blockers
What are Class IV antiarrhythmics?
calcium channel blockers
What are two other antiarrhythmics?
Adenosine and Magnesium.
What are the Class IA antiarrythmics?
Quinidine, Procainamide, Disopyramide
What is the mechanism of action of Class IA antiarrhythmics?
Slows conduction velocity in atria and his/purkinje fibers. Increases AP duration, increases effection refractory period. Increases QT interval.
What are the clinical uses for Class IA anti-arryhthmics?
Useful for atrial and ventricular arryhthmias, especially reentrant and ectopic SVT and VT; depresses automaticity of ectopic foci
What are the important toxicities of Class IA antiarrythmics? What is one important toxicity associated iwth each one.
Torsades (long QT), thrombocytopenia.
Quinidine: Cinchonism (headache, tinnitus)
Procainamide: Reversible SLE-like syndrome
Disopyramide: heart failure
What are the Class IB antiarrythmics?
Lidocaine, Mexilitine
What is the mechanism of action of Class IB antiarrythmics?
Decreases AP duration; increases conduction velocity of AV node/his-purk. Preferentially affect ischemic or
depolarized Purkinje and ventricular tissue.
Phenytoin can also fall into the IB category.
What is the clinical uses of Class IB antiarrhythmics?
Acute ventricular arrhythmias (especially postMI), digitalis-induced arrhythmias. IB is Best
post-MI.
What are toxicities associated with Class IB antiarrhythmics?
CNS stimulation/depression, cardiovascular
depression.
What are the Class IC antiarrhythmics?
Flecainide, Propafenone.
What is the mechanism of action of Class IC antiarrythmics?
Significantly prolongs ERP in AV node and
accessory bypass tracts. No effect on ERP in
Purkinje and ventricular tissue.
Minimal effect on AP duration.
What is the clinical uses of Class IC antiarrhythmics?
SVTs, including atrial fibrillation. Only as a last
resort in refractory VT.
What are toxicities associated with Class IC antiarrhythmics?
Proarrhythmic, especially post-MI
(contraindicated). IC is Contraindicated in
structural and ischemic heart disease.
How do Class II antiarrhythmics work?
Beta blockers. Decreased beta receptor activation, decreased cAMP, decreased Ca2+ current. Thereby decrease SA and AV nodal activity.
How do Class II antiarrhythmics affect the slope of phase 4 in pacemaker cells?
Decrease the slope; it takes longer to reach threshold. Suppress abnormal pacemakers.
Why does the PR interval increase with Class II antiarrhythmics?
The AV node is particularly sensitive.
Which Class 2 antiarryh is shortest acting?
esmolol
What are the clinical uses for class II antiarrhythmics?
SVT, ventricular rate control for atrial fibrillation and atrial flutter.
What is the toxicity associated with Class 2s?
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
Which beta blocker can cause dyslipidemia?
Metoprolol
Which beta blocker can exacerbate vasospasm in Prinzmetal’s angina?
propanolol
Which happens if you give beta blockers alone for pheo or cocaine toxicity?
There will be unopposed alpha agonism, will result in hypertension (soemtimes emergency)
How to treat beta blocker overdose?
Saline, atropine, glucagon
Which drugs are class III antiarrhythmics?
Amiodarone, Ibutilide, Dofetilide, Sotalol.
What is the mechanism of Class III antiarrhythmics?
Increase AP duration, ERP, and QT interval; prolongs phase 3.
What are the clinical uses for Class III antiarrhythmics?
Atrial fibrillation, atrial flutter; ventricular
tachycardia (amiodarone, sotalol).
What are the toxicities associated with sotalol?
Sotalol—torsades de pointes, excessive β
blockade.
What are the toxicities associated with ibutilide?
torsades
What are the toxicities associated with amiodarone?
Amiodarone—pulmonary fibrosis,
hepatotoxicity, hypothyroidism/
hyperthyroidism (amiodarone is 40% iodine by
weight), acts as hapten (corneal deposits, blue/
gray skin deposits resulting in photodermatitis),
neurologic effects, constipation, cardiovascular
effects (bradycardia, heart block, HF).
What are the tests you must order before starting amiodarone?
PFTs, LFTs, TFTs
Is amiodarone lipophilic?
yes
What are the Class IV antiarrhthymics?
Verapamil, diltiazem
What is the mechanism of Class IV antiarrhthymics?
decreases conduction velocity, prolongs ERP, prolongs PR interval.
What is the clinical use of Class IV antiarrhthymics?
Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.
What is the toxicity associated with Class IV antiarrhthymics?
Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression).
How does adenosine work?
K+ out of cells hyperpolarizing the cell and decreasing I
Ca. Drug of choice in diagnosing/abolishing
supraventricular tachycardia. Very short acting (~ 15 sec).
What drugs blunt the effects of adenosine?
Effects blunted by theophylline and
caffeine (both are adenosine receptor antagonists).
What are the adverse effects of adenosine?
Adverse effects include flushing, hypotension,
chest pain, sense of impending doom, bronchospasm.
When is Mg2+ used as an antiarrhythmic?
With torsades de pointes and digoxin toxicity.
