SUPRAVENTRICULAR

ARRHYTHMIAS

ELAINE EUSTACE PEREIRA

1001A76020

TYPES
Atrial Fibrillation
Atrial Flutter
Atrioventricular
Nodal
Tachycardia (AVNRT)
Atrioventricular
Re-Entry
(AVRT)

Re-Entry
Tachycardia

ATRIAL FIBRILLATION
CAUSES
Cardiac

Non-Cardiac

Hypertensive heart
disease

Thyrotoxicosis

Ischemia

Infection

Rheumatic heart
disease

Significant electrolyte
abnormalities

Cardiomyopathy

Alcohol & Drugs

Sick sinus rhythm

Catecholamine excess

 Classification of AF according to
American Heart Association (AHA)
1. Paroxysmal

2. Persistent

Episodes of AF that last > 7 days

May require either pharmacologic or
electrical intervention to terminate

3. Permanent

AF that has persisted for >1 year,

either because cardioversion has
failed or has not been attempted

Episodes of AF that terminate

spontaneously within 7 days
(most episodes last < 24 hours)

under

 PATHOPHYSIOLOGY
Caused by interaction between ectopic
atrial triggers within the pulmonary veins
& alterations to electrical & structural
properties of the atrial myocardium
Disorganized atrial depolarization without
effective atrial contraction
ECG FINDINGS
Increased rate (300-400 bpm)
Irregularly irregular rhythm
Absent P waves
Irregular QRS complexes

MANAGEMENT

1. Hemodynamically unstable:
.Hypotension, heart failure symptoms, chest pain,
syncope
.DC Cardioversion
.Initiate anti-coagulation therapy (LMWH) prior to the
procedure & post procedure due to risk of thrombus
formation in left atrium despite restoring sinus
rhythm
2. Hemodynamically stable:
.Beta blocker (Metoprolol) / calcium channel blocker
(Diltiazem) - first line agents for rate control in AF
.Flecainide used for patients without any structural
heart disease
.Amiodarone used for patients with history of
structural heart disease or coronary disease

 Radiofrequency Catheter Ablation Therapy

Aim is to either isolate triggers within the

pulmonary veins or to alter the atrial substrate
with atrial ablation
Paroxysmal AF is usually caused by triggered
and ectopic activity in pulmonary veins.
Therefore,
ablation
around
the
veins
terminates the arrhythmia
In persistent AF, triggering foci and re-entry
circuits may coexist in the atrial tissue,
requiring more extensive mapping and ablation
to terminate the AF. Hence, this yields a lower
success rate when compared to ablation used
to treat paroxysmal AF

Risk of
Thromboembolism in AF

ATRIAL FLUTTER
A right atrial arrhythmia where the atria
contract at a rate of approximately 300
beats per min BUT the ventricular rate is
approximately 150 beats per min when
there is 2:1 AV node block
Typical ECG shows P waves that are
upright in V1 & negative in the inferior
leads (II, III & aVF) creating a saw tooth
pattern

Management

Beta blocker or calcium channel blocker

slows down the ventricular rate by blocking
the AV node
Anti-arrhythmic drug (Amiodarone) prevents
recurrent episodes of atrial flutter
Anti-coagulant
(LMWH)

to
prevent
thromboembolic complications which may
lead to ischemic stroke
Radiofrequency ablation for restoration of
sinus rhythm, eliminates the need for longterm anti-coagulation and anti-arrhythmic
medications

ATRIOVENTRICULAR NODAL REENTRY TACHYCARDIA (AVNRT)

Responsible for approximately 60% of
narrow complex tachycardias
Occurs in people who have two atrial
conduction paths into their AV node
A perpetual circuit is formed involving
these pathways with passive excitation of
the atria & ventricles

 ECG FINDINGS
Appearance
of
a
narrow
complex
tachycardia with a retrograde inverted P
wave, either hidden in the QRS complex or
visible shortly afterwards

MANAGEMENT

Vagal maneuvers
Valsalva maneuver safest, simple to perform
Carotid sinus massage only in the absence
of a history of carotid disease, used with
caution in the elderly
Application of ice pack to the face effective
for children
These maneuvers slow or block AV nodal
conduction & terminate the AVNRT
Performed before initiating drug treatment

 Pharmacological Therapy
A bolus of IV Adenosine (1st dose - 6 mg
infused rapidly, followed by rapid normal
saline flush & then 2nd dose - 12 mg)
Beta blocker or calcium channel blocker
to be continued long term in order to
reduce the risk of recurrence of the
arrhythmia

ATRIOVENTRICULAR RE-ENTRY
TACHYCARDIA (AVRT)
AVRT is maintained by a circuit involving the
native conduction system & an accessory
pathway between the atria & ventricles
Accessory pathways are anomalous strands
of conducting myocardial tissue that bridge
the annulus of the AV valve and they are
capable of rapid conduction
Seen in Wolff-Parkinson-White Syndrome

 ECG FINDINGS
Slurring and slow rise of the initial
upstroke of the QRS complex (delta wave)
Shortened PR interval
Widened QRS complex

 MANAGEMENT
Termination
of
AVRT
by
blocking
conduction through the AV node with: Vagal maneuvers
IV Adenosine
IV Diltiazem
IV Amiodarone
Electrical
cardioversion

hemodynamically unstable patients

for

 Radiofrequency ablation of the accessory

pathway
Maintenance of sinus rhythm in patients
with recurrent, symptomatic episodes may
be achieved with one of the following
drugs: Beta blocker
Calcium channel blocker
Class IC anti-arrhythmic (Flecainide)
Class III anti-arrhythmic (Amiodarone)

REFERENCES
Medscape
Davidsons Principles
Medicine (21st Edition)

&

Practice

of

http://www.cdc.gov/dhdsp/data_statistics/f
act_sheets/fs_atrial_fibrillation.htm

THANK YOU
!