Drug Class MOA Route Indications Contraindications Side Effects Notes

Class Ia Class I: Na+ o blocking Na+ PO SVTs: Afib, hypotension, Diarrhea, lupus,
Quinidine Channel Blocker delays the 0 phase Aflutter prolonged QT Cinchonism,
of the cardiac Torsades de Pointes
action potential
Class Ib= Class I: Na+ o Slowed conduction IV Ventricular Stokes-Adam, CNS effects
Lidocaine Channel Blocker velocity arrhythmias Wolff-Parkinson-
o Decreased (post AMI) White
automaticity
Class Ic= Class I: Na+ o Potential decrease PO SVTs MI, prolonged QT Worsens life-
Propafenone Channel Blocker in inotropy threatening
arrhythmias
o Can increase the
threshold voltage
for the action
potential (must
reach more
positive voltage to
trigger 0 phase)
Amiodarone Class III= K+ blocking K+ channels PO SVTs: Afib, iodine sensitivity, Pulmonary fibrosis, Amiodarone
Channel Blocker prolongs the action Aflutter; thyroid or thyroid dysfunction, has a
potential by increasing Ventricular pulmonary disease, peripheral particularly
arrhythmias; prolonged QT neuropathy, liver
the length of the long half-life
adjuvant toxicity, ocular
refractory period therapy with deposits, Torsades de (t1/2>53
--results in longer QT ICDs Pointes days)=
intervals (this is "pharmacologi
hallmark of this class. c mortgage"
Know this.)
Amiodarone is
generally less
proarrhythmic
than Class I
drugs and is
widely
prescribed as
 an
antiarrhythmic
Sotalol is
another Class
III drug
Propanolol Class II = -blockers o block sympathetic PO, IV SVTs: sinus severe bradycardia sympatholytic: Note that
activation of the tach and (CHF) bradycardia, Propanolol
SA node others hypotension would also be
o result is decreased contraindicate
automaticity and d in a patient
increased delay at with asthma
AV node (long PR due to its
interval) nonspecifc -
antagonism.
Metoprolol or
atenolol are
good options
for 1-
selective
antagonists.
Verapamil Class IV= Ca++ o blocking calcium PO, IV SVTs: control Severe hypotension, o Note that
blockers channels delays ventricular hypotension, decreased dihidropyridin
SA and AV node rate Wolff-Parkinson- inotropy e Ca++ channel
White
depolarization blockers
o results in slower (nifedipine)
sinus rhythm and are not used as
increased delay at antiarrhythmic
AV node (long PR s
interval) o Recognize
Diltiazem as
another
commonly
 used Ca++
blocker

Adenosine Misc o acts on GPCR in IV SVTs: can be Severe AV block, Minor

AV node= causes used to Dx hypotension,
K+ channel based SVT source bronchospasm
hyperpolarization
o hyperpolarization
means it is harder
to fire action
potential= sinus
bradycardia
o also causes AV
nodal conduction
delays (long PR
interval)
o Can inhibit reentry
arrhythmias by
decreasing the
refractory period
(essentially
decreases the
"sweetspot" time
window for the
loop to occur)