Cardiac Arrhythmias

Amelia Arindanie
SA node
60 – 100 x/min

AV node
40-50x/min

Berkas His

Serabut Purkinje

Ventrikel
30 x/min
 Definition
• Normal sinus rhythm (60-90bpm), SA node pacemaker
• Arrhythmia; any abnormality of impulse formation,
regularity or site of origin of cardiac impulse or disturbance
of conduction that alters the normal sequence of activity of
atria and ventricles.
• Arrhythmias can be caused by coronary ischemia,
electrolyte disturbances, overstimulation of the sympathetic
nervous system, and other conditions or drugs that perturb
cardiac transmembrane potentials.
 Classification
1. Characteristics:
a. flutter – very rapid but regular contractions
b. tachycardia – increased rate
c. bradycardia – decreased rate
d. fibrillation – disorganized contractile activity

2. Sites involved:
a. ventricular
b. atrial
c. sinus
d. AV node
e. Supraventricular (atrial myocardium or AV node)
 Arrhythmia

Disorders of Disorders of
impulse impulse
formation conduction

Triggered
Automaticity Reentry
activity

Altered
Abnormal
normal DAD EAD
automaticity
automaticity
Tachyarrhythmia
 Tachyarrhythmia
Narrow complex tachycardia
• Regular
Sinus Tachycardia
 AVNRT
 AVRT
 Atrial Tachycardia
 Atrial Flutter
 Junctional Tachycardia
• Irregular
 Sinus Tachycardia with premature beat
 Atrial Fibrillation
 Multifocal atrial tachycardia
 Atrial Flutter
 Tachyarrhythmia
1. SINUS TACHYCARDIA / ST
response to a sympathetic stimulus (hypoxia,
vasopressors, inotropes, pain, dehydration,
hyperthyroidism, etc
No spesific treatment
Treat based on causes
 SVT
• AVRT – AVNRT (HR 160-250/min)
• Haemodynamics instability  electrical
cardioversion : 50 J
• Stabil :
 vagal maneuvers ; make sure no bruit, right and
left side  IV Adenosine, 6-12-12 mg, infus at
brachial vein,
 IV antiarrhythmic drugs should be administered for arrhythmia
termination in hemodynamically stable patients.

The advantage of adenosine relative to IV calcium-channel or beta blockers

relates to its rapid onset and short half-life.
 Atrial Flutter
• Electrical signals come from the atria, often causing the
ventricles to contract faster and increase the heart rate.
• The ECG pattern develops a signature “sawtooth” pattern.
• Hemodynamics compromised  electrical cardioversion :
50 J
• IV ibutilide, sotalol, procainamide, and flecainide. If on
TPM : burst atrial pacing (overdrive suppression)
 Atrial Fibrillation
• Electrical signals come from atria and very fast (350-600/min)
• The ECG shows normal but irregular QRS complexes and no P
waves
• Increase in:
Acute illness and surgery
septic shock  up to half
CAD
Valvular heart disease
Electrolyte disturbances
Hyperthyroidism
 MULTIFOCAL ATRIAL
TACHYCARDIA
 Rapid irregular atrial rhythm arising from multiple ectopic
focal within the atria
 irregular atrial tachycardia, ± 3 p wave morphologies
& PR intervals in the same lead
 Causes: hypoxia (pulmonary disease), theophylline,
metabolic derangements, and end-stage
cardiomyopathy
 treatment: underlying & AV nodal blockers
 Monomorphic Ventricular
Tachycardia with pulse
• A condition in which an electrical signal is sent from the
ventricles at a very fast but often regular rate
• Hemodynamic instability :
Decreased level of consciousnes, hypotention, syok,
ischemic angina, heart failure
Electrical cardioversion 100-200J
• Stable :
EF <40% Amiodarone 150 mg IV bolus over 10
minutes 360 mg (1 mg/min) over 6 hours
540 mg (0.5 mg/min) over the remaining 18
hours. max dose is 2.2 g over 24 hours
Lidocaine 0.5 to 0.75 mg/kgdrip 1-4 mg/min
 Polymorphic Ventricular
Tachycardia
• It may present with syncope attack and occasionally
ventricular fibrillation
• Caused by congenital, electrolyte disorder, drugs
(procainamide, disopyramide,sotalol,
phenothiazines, quinidine, some antibiotics,
antihistamines, tricyclic antidepressants
• Treatment: underlying cause
Mg SO4 1-2 g IV push over 30S 60 min
 Ventricular Fibrillation
• A condition in which many electrical signal are sent
from ventricles at a very fast and erratic rate, and
as a result the ventricles are unable to fill with
blood and pump
• The ECG show shapeless, rapid osscillations and
there is no hint of organized complex
• Clinically VF means “Cardiac Arrest” , it is life
threatening because there is no pulse and requires
prompt defibrillation to restore the normal rhythm
and function of th hearrt
 WOLFF-PARKINSON-WHITE
SYNDROME
• Wide QRS complexs due to abnormal ventricular
depolariation via accessory pathway (Kent)
• QRS complex change in shape and morphology
• Treatment : Procainamide , ibutilide, and flecainide
Adenosine should be used with caution
 Catheter ablation
 Premature Ventricular
Contraction
• A condition in which an electrical signal originates in
the ventricles and causes the venticles to contract
before receiving the electrical signal from the atria
• ECG show wide and bizarre QRS complex
• Early “R on T” vetricular premature beats may
induce VF
• PVCs are not uncommon and often do not cause
symptoms
• Treated only if symptomatic with beta-blockers
Bradyarrhythmia
 Bradyarrhythmia
• Physiological variant due to strong vagal tone or
atheletic training.
• Common cause:
Intrinsic; acute
ischemia and
Extrinsic; hypothermia, infarction of the
hypothyroidism, raised sinus node,
intracranial pressure, drug chronic
therapy. degenerative
changes such as
fibrosis of the
atriu and sinus
node
 Sick Sinus Syndrome
• Syndrome encompassing a number of sinus nodal abnormality:
1. Persistent spontaneous sinus bradycardia not caused by drugs
and inappropriate for the physiological circumstance
2. Sinus arrest or exit block
3. Combinations of SA and AV conduction disturbances
4. Alternation of paroxysmal of rapid regular or irregular atrial
tachyarrhythmias and periods of slow atrial and ventricular rate
• Chronic symptomatic sick sinus syndrome requiress permanent
pacing, with additional antiarrhythmic drugs or ablation therapy
 Atrioventricular Block
First degree AV Block
• ECG shows prolonged PR interval
• Seldom of clinical significance, and unlikely to
progress
 Second Degree AV Block
Mobitz type I
• Wenchebach Phenomenon
• Gradually increasing P-R intervals
• Patients with Wenckebach AV block are usuallyy
monitoress.
 Second Degree AV Block
Mobitz type II
• The P waves is sporadically not conducted. Occurs
when a dropped QRS complex is not Preceded by
progressive PR interval prolongation
• Pacing is usually indicated in Mobitz II block
 Third Degree AV Block
TAVB
• Common in elderly age groups due to idiopathic
bundle branch fibrosis; other cause include CAD,
congenital
• ECG shows bradcardia, p wave continue, unrelated
to junctional or ventricular escape rhythm
• Treatment is permanent pacing.
while waiting pacing :
drip dopamin 2-10 micro
drip epinfrin 2-10 micro
AV Block
Pacemaker
 Bundle Branch Block
Right Bundle Branch Block
• Commonly seen and usually benign
• Caused by CAD, chronic Corpulmonale, congenital
• ECG : QRS complex is seen to be widened , wide S
wave in I, aVL, V5 and V6, rSR’ pattern or notched R
wave in V1
 Left Bundle Branch Block
• Activation of left vetricle is delayed and contract
later than right venticle
• LBBB may mask signs of myocardial infarction
• Caused by CAD, dilated cardiomyopathy, Long
standing HT, aortic stenosis
• ECG: wide QRS complex and changes in ST-T
segment in I, V5-V6, deep S wave in V1-V2
Thank You