Arrhythmias 101

Fundamentals and what you

should know for the big, bad
BOARDS!
 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
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

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.
 Reentry Mechanism

Premature Beat Impulse

Cardiac
Repolarizing Tissue Conduction
(long refractory period) Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The fast conducting pathway is blocked because of its
long refractory period so the beat can only go down the
slow conducting pathway

 Reentry Mechanism

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast

pathway
 Reentry Mechanism

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation re-enters the pathway and continues in a
circular movement. This creates the re-entry circuit

 Reentry Circuits

AV Nodal Reentry
SVT
Ventricular Re-entry
Atrial Reentry ventricular tachycardia
atrial tachycardia SANode
atrial fibrillation
atrial flutter

Atrio-Ventricular
Reentry
WPW
SVT

 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

 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
 Event Monitors
Holter monitoring: Document
symptomatic and asymptomatic
arrhythmias over 24-48 hours. Can also
evaluate treatment effectiveness in a-
fib, pacemaker effectiveness and
identify silent MIs.
Trans-telephonic event recording:
patient either wears monitor for several
days or attaches it during symptomatic
events and an ECG is recorded and
transmitted for evaluation via
telephone. Only 20% are positive,
but
 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
 Signal Averaged ECG
Used only in people post MI to evaluate
risk for v-fib or v-tach.
Damage around the infarct is variable,
so this measures late potentials (low-
signal, delayed action potentials) as
they pass through damaged areas.
Positive predictive value is 25%-50%
but negative predictive value is 90%-
95%, thus if test is negative, patient is
at low risk.

 Electrophysiologic
Testing
Catheters are placed in RA, AV node,
Bundle of HIS, right ventricle, and
coronary sinus (to monitor LA and LV).
Used to evaluate cardiogenic syncope of
unknown origin, symptomatic SVT,
symptomatic WPW, and sustained v-tach.
*Ablative therapy is beneficial in AV node
reentry, WPW, atrial tachycardia, a-flutter,
and some v-tach. Complication is 1%

Bradyarrhythmias
The slow pokes (HR<60)
 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
 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.

 Cardioversion for A-Fib
Cardiovert if symptomatic
Patients with a-fib for more than 2
days should be receive 3 weeks of
anticoagulation before electrical
cardioversion.
Give coumadin for 4 weeks after
cardioversion

 Anticoagulation Rules
for A-Fib
Everybody who has rheumatic heart
disease should be anticoagulated
If <65 yo and with h/o DM, HTN, CHF,
CVA, prosthetic valves, thyrotoxicosis,
LV dysfunction or LA enlargement, then
give coumadin
If no risk factors, do nothing.
65-75 yo with any of above risk factors,
give coumadin; if no additional risk factors,
give coumadin or aspirin
>75 yo give coumadin but keep INR 2-
2.5 due to increased risk of bleed

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
Here comes the fun part!
 Classification of Anti-
Class Action
arrhythmics Examples Side Effects
1A Fast sodium channel blocker varies Q uinidine, Class: nausea, vomiting
depolarization and action potential procainamide, Q uinidine: hemolytic
duration disopyramide anemia, thrombocytopenia,
tinnitus
Procainamide: lupus
1B Lidocaine, Lidocaine: dizziness,
M exiletine confusion, seizures, coma
M exiletine: tremor, ataxia,
rash

1C Flecainide, Flecainide: pro-arrhythmia,

Propafenone nausea, dizzyness
2 beta-blockers

 Where did you say you
worked?

Location of Activity Anti-arrhythmic

AV Node Adenosine, Calcium channel blockers, B-
blockers, Digoxin
AV Node, Accessory Pathway, Bundle of Propafenone, Amiodarone, Sotolol
HIS, ventricle
Atrial, Ventricular, Accessory Pathway, Q uinidine, Procainamide, Lidocaine,
Bundle of HIS Disopyramide, Flecanide, Ibutilide,
Bretylium, Dofetilide

When in doubt
Amiodarone

Amiodarone
IV

SVT VT Atrial Fib or flutter

 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)

Magnesium indications.
1. Torsades de point from any reason.
2. Arrhythmias in a patient with known
hypomagnesaemia.
3. Consider its use in acute ischaemia
to prevent early ventricular
arrhythmias.
4. Digoxin induced arrhythmias.

Who gets a pacemaker?
Syncope, presyncope or exercise
intolerance that can be attributed to
bradycardia
Symptomatic 2nd or 3rd degree AV block
Congenital 3rd degree AV block with wide
QRS
Advanced AV block after cardiac surgery
Recurrent type 2 2nd degree AV block after
MI
3rd degree AV block with wide QRS or BBB.

QUESTIONS