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84 Cards in this Set

  • Front
  • Back
Class I
sodium channel blockers
Class IA: action
moderate phase 0 depression and slowed conduction

prolong repolarization
Class IA: drugs
quinidine, procainamide, and disopyramide
Class IB: action
minimal phase 0 depression and slow conduction, shorten repolarization
Class IB: drugs
lidocaine, mexiletine, tocainide
Class IC: action
marked phase 0 depression and slow conduction

little effect on repolarization
Class IC: drugs
flecainide, propafenone, moricizine
Class II
beta-adrenergic blockers
Class II drugs
metoprolol and esmolol
Class III
K+ blockers

(prolong repolarization)
Class III drugs
amiodarone, sotalol, ibutilide, and dofetilide
Class IV
Calcium channel blockers
Class IV drugs
verapamil and diltiazem
Class I: Na+ channel blockers

general aspects
act of FAST reponse cells:

reduce membrane responsiveness

depress conduction velocity

reduces Phase 4 diastolic depolarization

Prolong effective refractory period
Class I Na+ channel blockers are USE DEPENDENT
implies that the more the cells are in the open or inactivated state, the more impact of class I drugs...the faster the heart is beating, the more this will work...
Drugs of Class IA
quinidine, procainamide, and disopyramide
Direct effects of Class IA drugs
decrease phase 4 depolarization

decrease conduction velocity

increase end refractory period
Indirect effects of Class IA drugs
blocks K+ channels

after depolarizations
Uses of Class IA drugs
atrial flutter or fibrillation

NOT a 1st line therapy

only for structurally normal hearts (proarrhthmia risk)
Class IA: quinidine
some alpha-adrenergic blockade effect

severe GI effects (anticholingergic)

inhibits p450 system

increase in mortality...dont use much anymore
Class IB drugs
lidocaine and mexilitene
Class IB direct effects
decrease of phase 4 depolarization

increase block of sodium channels (decrease conduction velocity) at high HR or in depolarized cells

decreases action potential duration and effective refractory period

dissociates rapidly at resting Em


(minimal phase 0 depression and slowing of conduction...shortens repolarization)
Class IC drugs
flecainide and propafenone
Direct effects of Class IC
decrease in phase 4 depolarization

decrease in conduction velocity

dissociates from Na channel slowly
First line drugs for treatment of atrial fibrillaion if NO STRUCTURAL heart disease
Class IC: flecainide and propafenone
Side effects of Class IC
significant structural heart disease (hypertrophy) with the myocardium itself

highly proarrhythmic drugs
Class II drugs
beta blockers!!!

beta adrenergic blockers

effect on diastolic depolarization
Drugs of Class II
propranolol and esmolol
Action of Class II drugs
bind to beta-adrenergic receptors on cardiac cell membranes to competitively inhibit norepinephrine binding

NO EFFECT in absence of catecholamines

Class III
K+ channel blockers
Class III drugs



Class III


K+ channel blockade
also has Na+ channel blocking properties

NOT first line...has a lot of organ toxicities

Effect on AP: increases AP duration and increases effective refractory period
Class III

K+ channel blockade

has beta-adrenergic blocking properties


excreted in the kidneys
Class III drugs

K+ channel blockade

has fast acting IV form
Class III drugs

K+ channel blockade


Has fast acting IV form
Reverse use dependence
class III drugs

when you slow down the heart, you extend down the repolarization and have more opportunity to work...can extend the action potential further
Amiodarone stuff
potentially affects every organ system, except the joints

remind patients frequently about the lungs (and the sun)

surveillance monitoring: TSH, LFTs, CXR every 3-6 months; annual optic nerve exam
Class IV
Calcium channel blockers
Class IV drugs
diltiazem and verapamil
Action of Class IV drugs
acts primarily on slow response cells (SA and AV node), which are dependent on Ca++ influx for phase 0 of the action potential

depresses conduction velocity
Class IV: Calcium channel blockers

Major electrophysiologic effects
Impact on slow response cells:

depress phase 4 depolarization
depress conduction velocity
depress Vmax
Major side effects for Calcium channel blockers
*negative chronotropic effect (decreases automaticity of SA node)

*negative inotropid effect (decreases Ca++ influx during plateau phase of ventricular action potential)

*hypotension (decreases Ca++ influx into vascular smooth muscle cells)

can cause peripheral edema and constipation
only acts on atrium

has very rapid onset/metabolism

quick action

if youa re AV node dependent, you can give this

hyperpolarizes SN and AVN cells by causing outward flow of potassium...shortens refractory period and also causes bradycardia

has a very direct effect on potassium channels...significantly slows conduction...basically causes heart block
Mechanisms of atrial fibrillation
*multiple reentrant wavelets
*focally triggered AF
*SVT-induced AF
*multiple unstable reentrant circuits
*single stable reentrant circuits
Slows AV node conduction
adenosine (acute, iv only)

Digoxin (acute and long term)

Calcium channel blockers
Diltiazem and verapamil (both acute and long term)

Beta blockers
esmolol (acute and iv only)
propranolol (acute and long term)
metoprolol (acute and long term)

AADs: amiodarone and sotalol
Sinus node function...suppressing drugs
Beta blockers

Calcium channel blockers

Class Ia, Ic, and III AADs

sympatholytic antihypertensive drugs

lithium, cimetidine, amitriptyline, phenytoin, digoxin
Class I basic mechanism:
Sodium channel blockade
What does class I do??
reduces phase 0 slope and peak of action potential
Drugs for Phase IA??
quinidine, procainamide, and disopyramide
What does Class IA do??
has a moderate reduction in phase 0 slope

increases APD

increases effective refractory period
What does IB do??
this is a weak one

has a small reduction in phase 0 slope

reduces APD

decreases ERP
drugs of class IB??
lidocaine and mexilitine
What does class IC do???

pronounced reduction in phase 0 slope

no effect on APD or ERP
What do phase II drugs do??
beta blockade!!!

block sympathetic activity to reduce the rate and conduction
What do Class III drugs do??
these are potassium channel blockades

these delay repolarization (phase 3) and thereby increase action potential duration and effective refracotry period
Drugs of Class III
sotalol, dofetilide, and amiodarone
What are class IV drugs??
calcium channel blockers
What do class IV drugs do??
block L-type calcium channels

most effective at SA and AV nodes

reduce the rate and conduction
Which drug will NOT prolong repolarization??

Because class IC drugs are strong Na channel blockers and will not change the ERP at all
(only class 1a prolongs conduction and repolarization)
you can decrease automaticity with...
beta blockers
beta blockers...
prolong depolarization

class II
Some of these drugs are proarrhythmics...
Usually torsade from EAD's

K+ blockers!!!!

incessant monomorphic VT: type 1C

almost never: amiodarone
Which drugs are superior to other antiarrhythmic drugs in the treatment of sustained VT??

The best treatment in the prevention of SCD in a patient with a low EF and sustained VT or cardiac arrest is:
empiric ICD
Role for antiarrhythmic drug therapy for VT
acute treatment strategy

chronic treatment has been relegated to secondary role (after ICD) in cardiac disease...WITH THE EXCEPTION OF BETA BLOCKERS

If the EF is preserved Sotalol and Amiodarone may still be used but rarely

Ablation rapidly supplanting the limited role of antiarrythmics in the treatment of VT
What about beta blockers?
Class II

lots of them, IV and po

hepatic metabolism and renal excretion

short to long half lives

mild efficacy for arrhythmia suppression BUT IMPROVE SURVIVAL!!!!

causes fatigue, bradycardia, and impotence

Class Ib

rapid first pass metabolism
(IV/IM only)

hepatic metabolism

short half life (3 hours)

modest efficacy

acute treatment for VT
IV lidocaine and amiodarone are used

IV and PO

liver metabolism

very long half life (1-3 months)


liver, lung, thyroid, neurotoxicity, ocular issues (cornea and retina), photosensitivity

Amiodarone - very heterogenous
potent K+ channel blocker

modest Na channel blocker

modest Ca channel blocker

modest alpha and beta adrenergic receptor blocker
Uses of amiodarone
used for all arrhythmias (V tach)
Common drug interactions with Amiodarone
can double or triple INR values in patients on warfarin

can increase levels of sodium channel blockers

can increase digoxin levels

(know this one)
Class III drug

IV or po form (no first pass metabolism)

RENAL excretion

medium half life (10-20hrs)

reasonable efficacy

fatigue, bradycardia

Which antiarrhythmics are safe in renal disease?
amiodarone, quinidine, mexilitine, and propafenone
Which antiarrythmics do NOT prolong refractory periods?!?

IC (Flecainide, Propafenone)
IB (lidocaine/mexilitine)
Which two antiarrythmics have major drug interactions?
amiodarone and quinidine
Take home point 1
antiarrhythmics (with the exception of Flecainide and Propafenon (ICs) and Lidocaine and Mexilitine (IBs) can SIGNIFICANTLY PROLONG THE REPOLARIZATION and therefore can result in Torsade de Pointe as a form of Proarrhythmia
Take home point 2

the only antiarrhythmic that has ever been shown to improve mortality in the postinfarct patient
Take home point 3

preferable to any antiarrhythmic in the treatment of high risk arrhythmia patients (low EF <40% or with sustained VT)
Drug class of Digoxin
most common member from this class is called digitalis glycosides

this is considered both an antiarrhythmic agent and an inotropic agent
Pharmacodynamics of Digoxin
therpeutic levels cause a vagotonic effect that is useful in slowing AV conduction in patients with atrial fibrilliation

toxic levels increase automaticity of all areas of the heart except the SA node

increase Ca++ flux into sarcomere
Pharmacokinetics of Digoxin
bioavailability 60-95% (best with capsule)

can be given slowly IV

redistribution over about 8 hours

clearance 80% renal

half life: 30-40 hours (normal GFR)

markedly high Vd (about 6-7 L/kg)
Toxicity of Dogoxin
contraindicated in patients with VF, hypertrophic cardiomyopathy (IHSS), AV block, WPW syndrome, sinus node disease, hypoxia

common ADRs: nausea, vomiting, visual changes, agitation or nightmares, increased automaticity, AV block