Aritmia Cordis

Yudistira Panji Santosa

Important aspects in understanding arrhythmias

1. The mechanism :
- problems of impulse formation(automaticity)
- problems of impulse conduction (block or
reentry)
2. The site of origin : - supraventricular
- ventricular

The parts of Supraventricular and Ventricular Areas

Atrio-ventricular
node (AV node)
Sino-atrial
node (SA
node)

His
bundle

Left bundle
branch

Right bundle
branch

Purkinje

(SAN
)

RA

V
V

(AVN
)

HB
SAN

RA

AVN

LA

(HB)

LA

BB

(BB)

MECHANISM ABNORMAL IMPULS

FORMATION

1. Depressed
automaticity
2. Enhanced
automaticity
3. Triggered
automaticity

Depressed automaticity

Intrinsic
rate

Enhanced automaticity

Atrial or junctional or ventricular

rate exceed sinus rate
(tachycardia)

Triggered activity
A

RE-ENTRY
AVRT
AVNRT
- typical
- atypical

Ventricular asystole

Sinus tachycardia

Sinus tachycardia

normal physiologic response to exercise

or emotional stress or may be
pharmacologically induced by such drugs
as epinephrine, ephedrine, or atropine.
Exposure to alcohol, caffeine, or nicotine.
Persistence of sinus tachycardia usually
signals an underlying disorder (such as
heart failure, pulmonary embolism,
hypovolemia, or hypermetabolic states)

Premature Atrial Impulses

Atrial extrasystoles or premature atrial
contractions (PACs)

Found in normal individuals; myocardial ischemia,

rheumatic heart disease, myopericarditis, congestive
heart failure, and a variety of systemic abnormalities
including acid-base/electrolyte disturbances and
pulmonary diseases.
Caffeine, tobacco, or alcohol use as well as
emotional stress may initiate or exacerbate
premature atrial contractions.
Asymptomatic patients with no underlying heart
disease require no treatment other than removal of
the underlying or precipitating factors.
If patients are symptomatic, beta-adrenergic
blocking agents may provide relief.

supraventricular tachycardia (SVT)

Supraventricular
Tachyarrhythmias

All tachyarrhythmias that originate above

the bifurcation of the bundle of His
The atrial rate must be 100 or more beats
per minute for a diagnosis, but the
ventricular
rate may be less when AV conduction is
incomplete.
classified as paroxysmal (lasting seconds
to hours), persistent (lasting days to
weeks), or chronic (lasting weeks to
years).

ANTIARRHYTHMIC DRUGS

ANTIARRHYTHMIC DRUGS

VENTRICULAR
TACHYCARDIA

Ventricular tachycardia

Ventricular tachycardia and the diagnostic significance of

ventricular extrasystole

R on
T

VT is triggered by R on T ventricular
premature beat

ATRIAL FLUTTER

broad, atrial deflectionsF or flutter

waveswhich have a sawtooth
configuration in leads II, III, and aVF.
two types of atrial flutter: type I, or
classic, and type II
Type I flutter can be entrained and
interrupted with atrial pacing
techniques.It has an atrial rate of 280 to
320 per minute
Type II flutter has an atrial rate faster
than 340 per minute and cannot be
terminated by pacing

usual atrioventricular conduction ratio is 2:1 or

4:1
Most commonly it is associated with some form
of chronic heart disease, such as valvular
disease, congenital heart disease, or
cardiomyopathy
Treatment of choice in hemodynamically
compromising atrial flutter is low energy (10 to
50 W/s) electrical cardioversion
treatment is directed first to controlling the
ventricular rate with digoxin, verapamil, or
diltiazem and then adding a class IA
antiarrhythmic agent

ATRIAL FIBRILLATION

disorganized atrial deflections and an

irregular AV conduction sequence
resulting in a grossly irregular pattern of
the QRS complexes.
Atrial fibrillatory waves are best seen in
standard lead V1 and are usually evident
in II, III, and aVF.
Atrial fibrillation occurring in the absence
of structural heart disease is called lone
atrial fibrillation

Atrial fibrillation with controlled ventricular response.

Significant mitral or aortic valve disease,

hypertension, coronary artery disease,
cardiomyopathy, atrial septal defect, and
myopericarditis are all disease processes
frequently associated with atrial
fibrillation.
Pulmonary emboli and thyrotoxicosis are
well-known causes of atrial fibrillation.
Consumption of coffee, tobacco, or
alcohol and extreme stress or fatigue also
predispose to atrial fibrillation.

In the absence of underlying heart

disease, rest, sedation, and treatment
with digitalis is the treatment of choice
for short paroxysms.
Chronic therapy is based on the need to
control the ventricular rate during
recurrences and may be accomplished
with digitalis, beta blockers, or calcium
channel blockers, as described for atrial
flutter.

First Episode of Atrial Fibrillation

Paroxysmal Atrial Fibrillation
Persistent Atrial Fibrillation
Chronic Atrial Fibrillation

Anticoagulant in AF

anticoagulation is to limit the morbidity

and mortality from systemic and
pulmonary embolization
The decision the balance between the
relative risk of an embolic event versus
the risk of a major bleeding complication
secondary to anticoagulant therapy
International Normalized Ratio (INR) of
2.0 to 3.0.

VENTRICULAR
ARRHYTHMIAS

The QRST
complex in
ventricular
arrhythmia

The
apprearance
of the QRST
complex in
ventricular
extrasystole

appearance
of
extrasystol
e

Junctional
interferenc
e

1X

2X

Complete compensatory pause

Fusion beat

Intraventricular
interference

Ventricular Fibrillation

Coarse ventricular fibrillation

Fine ventricular fibrillation (coarse asystole)

BRADYARRHYTHMIAS

Sinus Bradycardia
Sick Sinus Syndrome
First-Degree Atrioventricular Block
Second-Degree Atrioventricular Block
Complete Atrioventricular Block

First-degree AV block. The PR interval is prolonged to 0.31

second

Second-degree AV block type I

Second-degree AV block type II.

Third-degree AV block occuring at level of AV node.

Diagnostic criteria
for bundle branch blocks

Complete left bundle branch

block

QRS duration 120 msec

Broad, notched R waves in lateral
precordial leads (V5 and V6) and usully
leads I and aVl
Small or absent initial r waves in right
precordial leads (V1 and V2) followed by
deep S waves
Absent septal q waves in left-sided leads

Diagnostic criteria
for bundle branch blocks
Complete right bundle branch block
QRS duration 120 msec
Broad, notched R waves (rsr, rsR, or
rSR) pattern in right precordial leads (V1
and V2)

Diagnostic criteria
for unifascicular blocks
Left anterior fascicular block
Frontal plane mean QRS axis: -45 to -90
degrees with rS patterns in lead II, III and
aVf and a qR pattern in lead aVl
QRS duration less than 120 msec
Left posterior fascicular block
Frontal plane mean QRS axis: 120
degrees
rS pattern in leads I and aVl with qR
patterns in inferior leads
QRS duration of less than 120 msec

s ritme, complete RBBB, LAD,

anterior fasicular hemiblock (Bifasicular block

Pocket Guide To Basic Dysrhythmias 3rd Ed . Robert J Huszar

Thank You