Arrhythmias 101

The Basics
SA Node and AV node cells are
slow conductors activated by
calcium, thus blocked by calcium
channel blockers such as
verapamil

Atrium, Bundle of His, and

ventricle cells are fast conducting
and activated by sodium, thus
blocked by sodium channel
blockers (class 1 anti-arrhythmics)
such as quinidine, lidocaine and
propafenone.
 4 Mechanisms of
Arrhythmia
reentry (most common)
automaticity
parasystole
triggered activity
 Reentry Requires
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those
pathways.
3. Slow conduction in the unblocked pathway.
Large reentry circuits, like a-flutter, involve the
atrium.
Reentry in WPW involves atrium, AV node,
ventricle and accessory pathways.
 Automaticity
Heart cells other than those of the SA
node depolarize faster than SA node
cells, and take control as the cardiac
pacemaker.
Factors that enhance automaticity
include:
SANS, PANS, CO2, O2, H+, stretch,
hypokalemia and hypocalcaemia.
Examples: Ectopic atrial tachycardia or
multifocal tachycardia in patients with
chronic lung disease OR ventricular
ectopy after MI
 Parasystole
is a benign type of automaticity
problem that affects only a small
region of atrial or ventricular cells.
3% of PVCs
 Triggered activity
is like a domino effect where the arrhythmia
is due to the preceding beat.
Delayed after-depolarizations arise during
the resting phase of the last beat and may be
the cause of digitalis-induced arrhythmias.
Early after-depolarizations arise during the
plateau phase or the repolarization phase of
the last beat and may be the cause of
torsades de pointes (ex. Quinidine induced)
 Diagnosis
What tools to use and when to
use it
 Exercise testing
Symptoms only appear or worsen with
exercise.
Also used to evaluate medication
effectiveness (esp. flecanide &
propafenone)
You can assess SA node function with exercise
testing.
Mobitz 1 (Wenkebach) is blockage at the AV
node, so catecholamines from exercise actually
help!
Mobitz 2 is blockage at bundle of His, so it
worsens as catecholamines from exercise increase
AV node conduction, thus prognosis is worse.
*PVCs occur in 10% without and 60% of
patients with CAD. *PVCs DO NOT predict
severity of CAD (neither for nor against)!
Bradyarrhythmias
 Sick Sinus Syndrome

Conduction problem with no junctional

escape during sinus pause
Diagnose with ECG or Holter. If
inconclusive, need electrophysiologic
testing.
If asymptomatic, leave alone. If
symptomatic, needs pacemaker.
 First Degree AV Block

Delay at the AV node results in

prolonged PR interval
PR interval>0.2 sec.
Leave it alone
Second Degree AV Block
Type 1 (Wenckebach)

Increasing delay at AV node until a p wave is

not conducted.
Often comes post inferior MI with AV node
ischemia
Gradual prolongation of the PR interval before
a skipped QRS. QRS are normal!
No pacing as long as no bradycardia.
Second Degree AV Block
Type 2

Diseased bundle of HIS with BBB.

Sudden loss of a QRS wave because p
wave was not transmitted beyond AV
node. QRS are abnormal!
May be precursor to complete heart
block and needs pacing.
Third Degree AV Block

Complete heart block where atria and

ventricles beat independently AND atria
beat faster than ventricles.
Must treat with pacemaker.
LBBB
Left Bundle Branch Block

Left ventricle gets a delayed impulse

QRS is widened (at least 3 boxes)
V5 and V6 have RR (rabbit ears)
Be careful not to miss any hiding q
waves!
Pacemaker if syncope occurs
Right Bundle Branch
Block
Right Bundle Branch Block

Right ventricle gets a delayed impulse

QRS is widened (at least 3 boxes)
V1 and V2 have rSR
Pacemaker if syncope occurs.
 Bifascicular Block

RBBB plus LABB OR RBBB plus LPBB

QRS is widened (at least 3 boxes)
V5 and V6 have RR (rabbit ears)
V1 and V2 have rSR
Pacemaker if syncope occurs
 Tachyarrhythmias
The speed demons(HR >100)
 Tachyarrhythmias
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter
Ventricular tachycardia
Monomorphic
Polymorphic (Torsades de pointe)
Ventricular fibrillation
Supraventricular Tachycardia
 SVT
Reentrant arrhythmia at AV node that is
spontaneous in onset
May have neck fullness, hypotension
and/or polyuria due to ANP
Narrow QRS with tachycardia
First line is vagal maneuvers
Second line is adenosine or verapamil
For chronic SVT, class 1A or 1C or
amiodarone or sotalol work well
Ablation will cure it too, but we usually
do this only in young patients
Multifocal Atrial Tachycardia
 MAT
Automatic atrial rhythm from
various different foci
Seen in hypoxia, COPD, atrial
stretch and local metabolic
imbalance.
Three or more types of p waves
and a rate > 100
Digoxin worsens it, so treat with
oxygen and slow channel blocker
like verapamil or diltiazem.
Wolf Parkinson White
 WPW
Ventricles receive partial signal normally
and partially through accessory pathway
Symptomatic tachycardia, short PR
interval (<0.12), a delta wave and
prolonged QRS (>0.12)
Electrophysiologic testing helps to
identify the reentry pathway and
location of the accessory pathway
 WPW
Because WPW has both normal conduction
through the AV node and accessory pathway
conduction that bypasses the AV node, a-fib
can happen via the accessory pathway
Inhibition of the AV node will end up in
worsening the a-fib because none of the
signals are slowed down by the AV node
before hitting the ventricle.
* Do not use any meds that will slow AV node
conduction, ie digoxin, beta-blockers,
adenosine or calcium channel blockers.
* The best choice is procainamide as it slows the
accessory pathway. *If patient becomes
hypotensive, cardiovert immediately!
Atrial Flutter
 Atrial Flutter
Atrial activity of 240-320 with sawtooth
pattern. Usually a 2:1 conduction
pattern; if it is 3:1 or higher, there is AV
node damage
Treatment is to slow AV node
conduction with amiodarone,
propafenone or sotalol
DC cardiovert if <48 hours or unstable
You can also ablate the reentry pathway
within the atrium between the tricuspid
and the IVC.
Atrial Fibrillation
 A-Fib
Can be due to HTN, cardiomyopathy,
valvular heart desease, sick sinus,
WPW, thyrotoxicosis or ETOH
Therapy is either rate control via
slowing AV node conduction with
stroke prophylaxis or rhythm control
 Rate control
Beta-blockers
Continuation after CABG may prevent a-fib
Good for hyperthyroid or post-MI patients with
a-fib
Carvedilol decreases mortality in patients with
CHF
Esmolol is good for acute management
Digoxin actually increases vagal tone,
thus indirectly slowing AV node
conduction. But it is used essentially only
in patients with LV dysfunction because its
inotropic.
 Rate control
Calcium Channel Blockers
Nondihydropyridines (verapamil or
dilitiazem) block AV node conduction but
also have negative inotropy, so dont use in
CHF.
Dihydropyridines (nifedipine, amlodipine,
felodipine) have no effect on AV node
conduction
Adenosine is too short acting to be of
any use in a-fib
Last choice is AV node ablation and
permanent pacing
 Rhythm control
Rhythm control does not decrease
thromboembolic risk and may be
proarrhythmic
Class 1A (quinidine, procainamide, disopyramide)
slows conduction through HIS can cause torsades
de pointes during conversion. They also enhance
AV node conduction, so they should be used only
after rate is controlled
Class 1B (lidocaine, meilitine, tocainide) are
useless for a-fib
Class 1C (propafenone, and flecainide) slow
conduction through HIS are good first choice.
Amiodarone is good if patient is post-MI
or has systolic dysfunction.
Ventricular Tachycardia
Ventricular Tachycardia

Impulse is initiated from the ventricle

itself
Wide QRS, Rate is 140-250
If unstable DC cardiovert
If not, IV Amiodarone and/or DCCV
Consider procainamide
Nonsustained ventricular tachycardia needs no
treatment
 Torsades de Pointes

Twisting of the points is usually caused by

medication (quinidine, disopyramide, sotalol,
TCA), hypokalemia or bradycardia especially
after MI
Has prolonged QT interval
Acute: Remove offending medication. Shorten
the QT interval with magnesium, lidocaine,
isoproterenol, or temporary overdrive pacing
Chronic: may need pacemaker/ICD,
amiodarone, beta-blockers
 Ventricular Fibrillation

Most common in acute MI, also drug

overdose, anesthesia, hypothermia &
electric shock can precipitate
Absence of ventricular complexes
Usually terminal event
Use Amiodarone if refractory to DCCV.
Treatment
Classification of Anti-
arrhythmics
Where did you say you
worked?
 When in doubt
Amiodarone

A m io d a r o n e
IV

S V T V T A t r ia l F ib o r f lu t t e r
 Amiodarone.
Modes of action.
Mainly class III action on the
outgoing K+ channels.
Class Ib action on the Na+
channels.
Non competitive alpha antagonism
(class III)
 Klasifikasi Obat Anti-
aritmia
Dikelompokkan menurut efek
elektrofisiologik dan mekanisme kerjanya
Kelas I secara langsung mengubah arus
kation pada membran, khususnya ion K +
dan Na+
Kelas II obat yang terutama mempunyai
efek tak langsung terhadap parameter
elektrofisiologi, melalui kesanggupannya
dalam menghambat reseptor beta
 Kelas III belum jelas mekanisme
kerjanya, tetapi mempunyai
kemampuan untuk memperlambat
repolarisasi membran
(memperpanjang refractoriness)
Kelas IV mempunyai efek depresi
yang relatif selektif terhadap kanal Ca +
+
 Anti-aritmia Kelas IA
Menghambat arus masuk ion Na+, menekan
depolarisasi fase 0, dan memperlambat
kecepatan konduksi serabut purkinje.
Indikasi pemberian antiaritmia golongan ini
adalah: fibrilasi atrium, atrium flutter,
paroksismal SVT, takikardi ventrikuler
Contoh: kuinidine, prokainamide,
disopiramide
 Anti-aritmia Kelas IB
Jauh lebih kurang efektif dibanding
dengan Kelas IA efek obat kelas IB
terhadap refractoriness dan
kesigapan atrium sangat kecil
Indikasi Takikardi ventrikular,
aritmia yang diinduksi digitalis
Contoh Obat: Lidokain, Fenitoin,
Tokainid, Meksiletin
 Anti-aritmia Kelas IC
Memiliki afinitas yang tinggi terhadap kanal
Na+
Anti-aritmia yang paling poten dalam
memperlambat konduksi dan menekan arus
masuk Na+ ke dalam sel dan kompleks
prematur ventrikel spontan
Memperpanjang periode refrakter
Indikasi fibrilasi atrium dan paroksismal
SVT
Contoh Flekainid, enkainid,
 Anti-aritmia Kelas II
Semua -blocker meningkatkan
masa refrakter pada nodus AV
Indikasi premature beats,
paroksismal SVT, fibrilasi dan
flutter atrium, takikardi ventrikel
 Anti-aritmia Kelas III
Memperpanjang lama potensial aksi dan masa
refrakter efektif serabut purkinje dan otot
ventrikel
Memperpanjang masa refrakter tanpa
mempengaruhi penjalaran impuls
Indikasi takikardi ventrikel, atrial fibrilasi
dan flutter
Contoh Amiodaron
 Anti-aritmia Kelas IV
Penghambat kanal Ca++
Penekanan potensial aksi Ca++ dependent dan
perlambatan konduksi di nodus AV
Efek dari verapamil dan diltiazem menurunkan
kecepatan konduksi melalui nodus AV dan
memperpanjang masa refrakter fungsional nodus
AV
Verapamil dengan dosis 5-10 mg IV selama 2-3
menit
Indikasi SVT paroksismal, flutter dan fibrilasi
atrium
Who gets a pacemaker?
Pasien-pasien dengan bradikardia yang
mengalami penurunan kesadaran atau
keterbatasan dalam beraktivitas fisik.
Pasien dengan AV blok derajat 2 atau 3
yang simtomatik
AV blok derajat 3 kongenital dengan QRS
lebar
AV blok setelah operasi jantung
3rd degree AV block with wide QRS or BBB.
AV blok dengan QRS lebar atau Bundle
Branch Block