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ANTIARRHYTHMIC RX

Use Mechanism of Action Toxicities Notes


Class I: Na Reentry arrhythmia
Suppress AbNL autoM
Moderate
Na @ O&I: 0,1,2,3 (C @4)
K (SE)
Antimuscarinic
NL & Depolarized tissue=discriminate
Anti-M: worsen
supravent arrhythmia,
HR, conduction delay
@AV
K: APD=QT=EAD
ERPAV
Contractility
Prolong QTtorsades
des pointes
discrimuniD in
NL=new reentry

Class IA Quinidine

Prototype; not used anymore

GI N/D (30% pt)
Local anesthetic action
Reversible
thrombocytopenia
HA, dizzy, tinnitus

0 slope (widen QRS)
APD (prolong QT)
Procainamide

Weakest anti-MDOC Lupus-like Rxn in slow
acetylators
N-acetyl metabolite
prolongs t
1/2

Give procainamide in
progressively increasing dose
Disopyramide Strongest anti-M activity


Class IB Prevent PVC
MI
Arrhythmia

Lidocaine
Mexilitine
Short acting
ERP (inactivation of Na) w/o APD
Recovery rate of Na channels (3)
Thr of Na excitation=autoM of fast
AP=PVC (His-Pur)
Vc NOT affected (QRS )
Target depol tissue (affect NL)

CNS: convulsion,
tremors, nystagmus

IV only (high 1
st
pass)
Hepatic intrinsic clearance
Class IC Reentry


Flecainide
Propafenone
Long acting
More potent Na than IA
Vc (widen QRS)uniD to biD
Mild K-ORAPD=QT (less than IA)
NL & Depol (indiscrim)
UniD in NLreentry
arrhythmia (since IC
prolong ERP, risk of
reentry is much higher
than IA)

EKG with widest QRS
Class II: Tachycardia
PVC
Atrial arrhythmia
DAD
Rate control
Reentrylife saving
post MI

Propranolol
Esmolol
4 slope=autoM
(cAMPHCNslope)
AV cond via L-Ca influx (IC Ca
overload)=prolong PR
of APD & ERP only if SANS
SANS
contractility
reentry by shortening ERP (SANS)
Affect NL & AbNL
AV block
contractility if dose
too high which will
result in death
direct effect on APD
unless SANS is active
Since SANS is always active
which shortens APD & ERP,
will prevent the
shortening & thus reentry
Use in lose doses post MI
EADs are worsened by
Class III: K Reentry

Kdelay repolAPD=ERP
Bradycardia
MOST potent K


Amidodarone
(mother of all
antiarrhythmic Rx)
- Reentry
K (APD),Na (QRS), Ca (Ca
overload), (SANS)
ERP=QT, PR, QRS on EKG
risk of EAD, ie. Torsades de Pointes
(, Ca)
Reentry via ERP, QRS, SANS
Lipophilic, t
1/2
=20d
Accum in tissue
Reversible corneal
microdeposits (20%)
Irrev periph
neuropathy & pulm
fibrosis (10%)
thyroid fxnT4 to T3
conversion
Start with low dose

Sotalol

with Class III activity of APD
QT & Ventricular & Atrial ERP

Bretylium
Class IV: Ca Control ventricular
rate in case of
supraventricular
arrhythmia (SVA)
AV cond=PR contractility
VasoD due to altered Ca
currenttransient
reflex tachycardia
Caution in Wolff-Parkinson-
White syndrome (aka
Accessory Pathway
Arrhythmia)
Not classified
Cardiac
glycoside
Digoxin
- SVT (SV tachy)
vagal tone: hyperpol, ERP, AV cond
Suppress atrial pacemakers
AV block
Arrhythmia, esp w/K
Antimuscarinic Atropine
- Sinus brady
AV cond
sinus rate

Adenosine
- Quickly reduce
ventricular rate
(ie. Afib)
- Paroxysmal SVT
Adenosine Receptor agonist (t
1/2
<10s)
kACh in SA, AV, AtriaHyperpol (esp
AV)opens K channels, AP, autoM
cAMP effects=blunt Adr effect

IV only
Short term Tx
All pt experience chest
discomfort & dyspnea
EKG: HR, PR
Denervated hearts are
supersensitive
Action by adenosine R
antagonists (caffeine,
theophylline)
Action potentiated by
adenosine uptake
(dipyridamole)
Others Magnesium sulfate
- SVA assoc Mg dfcn
- Rx induced TdP
- Digtalis induced
arrhythmia

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