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Anti-arrhythmics

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Class
Class
I
antia
rrhyt
hmic
drugs

Class
IA
antiar
rhyth
mics
Dru Main mechanism of Exa
g
action
mple
gro
s
up
Fast

sodi
um
cha
nnel
bloc
kers


Class
IB
antiar
rhyth
mics


Inhibit
conducti
on
velocity
(negativ
e dromo
tropy),
particul
arly in
depolari

zed
tissue
(e.g.,
during t
achycar
dia):
Statedepende
nt: the
faster
the heart

rate, the
greater
the
effect
→↓
the slop
e of 
phase
0 depola
rization
Membra
ne
stabilize
rs

Separate
d into 3
subgrou
ps based
Use
Adverse Effects
Paroxysmal

supraventricular
tachycardia(PSVT):
AVNRTand AVRT(r

eentry

Especially antidrom

ic AVRT and WPW
(procainamide)
Atrial
fibrillation(AFib)
and atrial flutter 
Ventricular

tachycardia (VT) 
QT
prolongation→ tors
ade de pointes
Thrombocytopenia
Quinidine
Quinism(cinchonis
m): loss of visual
acuity, hearing
loss, tinnitus, headac
he, psychosis
Procainamide
Drug fever
Drug-induced
lupus
erythematosus(reve
rsible)
Disopyramide: antic
holinergiceffects
Moderate
blockade
of Na+ 
channels
(intermedi
ate

association
/dissociati
on)

Prolong a
ction
potential (
AP) durati
on(right
shift)
→ prolong
effective
refractory
period (ER
P)
Minimal
blocking
of the
K+ channel
Quin

idine
Proc
aina
mide
Diso

pyra
mide
Ajm

aline
Weak 
blockade
of Na+ 
channels
(fast
association
/dissociati
on)
Shorten
AP duratio
n(left
shift) →
slow ERP
Lido
 VT (especially post CNS: dizziness,
caine MI)
nausea, seizures
Mexi
 AV block III, VES
letin
e


Class
Class
IC
antiar
rhyth
mics
Dru Main mechanism of Exa
g
action
mple
gro
s
up
upon 
their
effects
on the
Na+ cha
nnel and
the AP

duration

Use
Adverse Effects
Strongest
effect
on ischemi
c myocard
ium
Strong 
blockade
of Na+
channels 
(slow
association
/dissociati
on) →
QRS
prolongati
on
No to
minimal
effect on
AP duratio
n (no shift)
→ ERP un
affected
 Inhibit β-adrenergic
Class II  Beta
antiarrhyth bloc activation of
mic drugs ker adenylate cyclase
→ ↓ cAMP → ↓ 
Ca2+
 Decrease slope of 
phase 4
in pacemaker cells,
leading to a slower 
conduction velocity

Flec
ainid

e
Prop
afen
one
PSVT
 Proarrhythmia: cont
AFib(cardioversion): raindicated postStructural heartdiseas MI!
e must be ruled out
prior to use!
Atrial flutter
Meto

prolo
l 
Esm

olol
Prop
ranol
ol 
Aten

olol
Tim
olol
AFib (frequency
control)
Atrial flutter
PSVT
Premature
ventricular
contractions
VT
Atrial premature
beats [1]





AV
block, bradycardia
Sedation, CNSdepre
ssion
Erectile dysfunction
Exacerbation
of asthma, COPD,
and psoriasis
If given
with cocaine toxicity
and pheochromocyto
ma→ exacerbation
due to
unopposed α1 agonis
Class
Dru Main mechanism of Exa
g
action
mple
gro
s
up


 Inhibit potassium 
Class III  Pota
antiarrhyth ssiu delayed rectifier
currents
mic drugs m
cha Prolongs AP

nnel duration (Reverse
bloc use-dependence)
ker and effective

refractory
period (ERP)

 No effect on
conduction velocity


Use
Adverse Effects
Carv
edilo
l
Sotal
ol
Ami

odar
one
Dron

edar
one
Sotal
ol 
Bret
yliu
m
Ibuti
lide
Dofe
tilide
m (except labetalol a
nd carvedilol )
AFib(cardioversion
and long-termrhythm
control)
Atrial flutter

VT (not bretylium);
see also advanced
cardiac life support
Sotalol: supraventric
ular
arrhythmias and vent

ricular arrhythmias






 Inhibit slow calcium

Class IV  Calc
antiarrhyth ium channels
mic drugs cha Decrease slope
nnel of phase 0 and 4 →
bloc slower conduction
ker velocity

 Prolong repolarizat
ion of AV node
 Decreasing
conduction velocity
leads to
increased refractor
Vera

pami
l 
Dilti

azem

Nife
dipin
e
AFib (frequency
control)
Atrial flutter
PSVT
Multifocal atrial
tachycardia








QT
prolongation → tors
ades de pointes
Amiodarone
Lowest risk
of ventricular
arrhythmiacompared
to other drugs in its
class
Reversible corneade
posits
Photosensitivityof
the skin
Pulmonary fibrosis
Liver dysfunction
Peripheral
neuropathy
Thyroiddysfunction
Sotalol: beta
blocker adverse
effects
Verapamil
AV
block, bradycardia
Obstipation
Nifedipine
Headache, flush, pitt
ing edema
Reflex tachycardia
Diltiazem
Both verapamiland n
ifedipineadverse
Class
Dru Main mechanism of Exa
g
action
mple
gro
s
up
Use
Adverse Effects
effects, but less
prominent
y period and PR
interval
 See section on

Class V  Vari
antiarrhyth able “Other
mic drugs mec antiarrhythmic
hani drugs” below for 
sms details.


Ade
nosi
ne
Digo
xin
Mag
nesiu
m
sulfa
te
See section on
“Other
antiarrhythmic
drugs” below for
details.

All antiarrhythmic drugs are also potentially proarrhythmic! Intravenous administration
should be done with ECG monitoring!
References:
[2][3][4][5][6][7][8][9]
Other antiarrhythmic drugs
Adenosine (drug)













Mechanism of action: transient AV node block
Potassium channel activation → ↑ potassium efflux → hyperpolarization → ↓
calcium influx → decrease in intracellular cAMP → acute termination
of supraventricular tachycardia
Indications:
Drug of choice for narrow QRS tachycardias, such as paroxysmal supraventricular
tachycardias: AVNRT and orthodromic AVRT (except pre-excited tachycardias)
Diagnostic value: exposing underlying AFib in supraventricular tachyarrhythmias
Adverse Effects:
Chest pain, flushing, hypotension, bronchospasm
Sense of impending doom
Asystole (rare)
Contraindications
Pre-excitation syndrome: antidromic AVRT including Wolf-Parkinson-White syndrome
AV block
Asthma
Digoxin



Mechanism of action: Inhibition of Na+/K+-ATPases → higher
intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers →higher
intracellular Ca2+ concentration → increased contractility, decreased heart rate
Indications: tachyarrhythmias (e.g., AFib)
See cardiac glycosides for details.
Magnesium sulfate











Mechanism of action: decreases calcium influx → prevents early afterdepolarizations
Indications:
Torsades de pointes
Eclampsia
Constipation
Tocolysis
Adverse effects:
Drowsiness
Flush
Loss of reflexes
Respiratory depression
I -channel blocker
f






Ivabradine
Mechanism of action: Lowers heart rate by blocking the If channel in the pacemaker
cells of the SA node
Indications: Drug of last resort for symptomatic relief of stable coronary heart
disease and congestive heart failure (NYHA II-IV) in sinus rhythm
Adverse effects:
Visual changes
Bradycardia