ARRHYTHMIA

Dr. M. Ramadevi
ARRHYTHMIA
• Definition: An abnormality of the cardiac rhythm is called cardiac
arrhythmia.

Improper beating of the heart whether irregular , too fast or too

slow.
ARRHYTHMIA
• Rhythm- rhythm controlled by sinus node at a rate of 60-100
beats/min;
• each P wave followed by QRS and each QRS preceded by a P wave.
• Origin
• Rate
• Propagation
• Conduction velocity
Conduction speed of cardiac tissue

TISSUE CONDUCTION
RATE (m/s)
SA node 0.05

Atrial pathway 1

AV node 0.05

Bundle of His 0.05

Purkinje system 4

Ventricular muscle 1

4
Conducting system
BASIC ELECTROPHYSIOLOGY
•PHYSIOLOGICAL PROPERTIES OF MYOCARDIAL CELL
Automaticity: ability to initiate an impulse
Excitability: ability to respond to a stimulus
Conductivity: ability to transmit an impulse
Contractility: ability to respond with pumping action
• Depolarization and repolarization of a cardiac cell generates action
potential
• ECG is the composite representation of action potential of all
cardiac cell.
Heart Excitation Related to ECG
Pathology

• SA node
• Atrial cell
• AV junction
• Ventricular cell
• Abnormal pathways
Mechanism of production
• Tachyarrhythmia
• Increased automaticity
• Triggered activity
• Re entry
• Bradyarrhythmia
• Abnormally slow automaticity
• Abnormal conduction within the AV node or the distal AV conduction
system
ACCELERATED AUTOMATICITY
• It occurs due to increasing the rate of diastolic depolarization or
changing the threshold potential.

• changes are thought to produce sinus tachycardia, escape rhythms

and accelerated AV nodal (junctional) rhythms.
TRIGGERED ACTIVITY
• Myocardial damage - oscillations of the transmembrane potential at
the end of the action potential - 'after depolarizations', may reach
threshold potential and produce an arrhythmia.
• abnormal oscillations - exaggerated by pacing, catecholamines,
electrolyte disturbances, and some medications.
Re-entry (or circus movement)
• The mechanism of re-entry occurs when a 'ring' of cardiac tissue
surrounds an inexcitable core (e.g. in a region of scarred
myocardium).
• The majority of regular paroxysmal tachycardias are produced
by this mechanism
SA node problems
• SA node can fire to slow – bradyarrhythmia

• SA node can fire to fast – tachyarrhythmia

Sinus Bradycardia

• Sinus bradycardia : rate less than 60 beats per minute in day or less
than 50 during night
• Causes :
• Physiological – athletes, during sleep
• Pathological –
• Extrinsic causes
• Intrinsic causes ( SSS, ac.infarction)
• C/F: Asymptomatic
• Syncope, confusion, weakness.

Treatment : identify the cause and treat

Atropine- 0.6 mg IV- acute symptomatic
Temporary pacemaker- acute symptomatic and reversible cause
Permanent pacemaker- symptomatic and irreversible cause
Sinus tachycardia
• Resting heart rate is more than 100 bpm
• Causes :
• Non cardiac causes: fever ,pain ,infection, hypo volemia, exercises, anxiety/
emotion
- HF with compensatory tachycardia

C/F: Palpitations ,onset and termination is gradual

HR not more than 160bpm
• Treatment : Treat underlying cause
• Symptomatic: beta blockers, verapamil
Sinus tachycardia converted to NSR
Atrial tachyarrhythmias
• Atrial fibrillation
• Atrial flutter
• Atrial tachycardia
• Atrial ectopic beats
• All arise from atrial myocardium
• Common etiologies
Atrial cell problems
• Atrial cell fire occationally from focus --artial
premeture contractions

• Fire continuously with reentrant – atrial flutter

• Fire continuously from multiple foci – arial fibrillation
AV Junction problems
• Fire continuously due to reentrant looping circuits – paraxysmal
supraventricular tachycardia
AV Junction problems
• Block impulses from SA node –AV junctional blocks
ATRIAL FIBRILLATION
• Characterized by disorganised, rapid and irregular atrial activation
with loss of atrial contraction and with an irregular ventricular rate
(that is determined by AV nodal conduction)
Types of AF
• Paroxysmal AF : AF that terminates spontaneously or with
intervention within 7 days of onset.
• Persistent AF : Continuous AF that is sustained >7 days.
• Long-standing persistent AF: Continuous AF >12 months in duration.
• Permanent AF : When the patient and clinician make a joint decision
to stop further attempts to restore and/or maintain sinus rhythm.
 MECHANISM
• Focal activation – In which AF originates from an area of
focal activity.
• Multiple wavelet mechanism – In which multiple small
wandering wavelets are formed. The fibrillation is
maintained by re-entry circuits formed by some of the
wavelets.
The hallmark of AF is chaotic atrial impulses leading to
irregularly irregular ventricular contraction, usually with
incessant tachycardia
• Cardiac : • Non Cardiac :
-HTN, Hyperthyroidism
-CCF , CAD ,MI COPD,
Dilated cardiomyopathy Pheochromocytoma
Myocarditis /pericarditis Pulmonary embolism
WPW syndrome Alcohol abuse
Sick sinus syndrome
Caffiene and smoking
Cardiac tumors
Idiopathic
Cardiac surgery
Clinical features
• Palpitations
• If ventricular rhythm is rapid – reduced CO
- symptoms of pulmonary congestion
Dyspnea, PND, Orthopnea
- symptoms of inadequate perfusion
Dizziness, syncope, angina
- systemic embolism
stroke, Abdominal pain ,leg pain
 ECG
- Irregularly irregular rhythm.
- No P waves.
- Absence of an isoelectric baseline.
- Variable ventricular rate.
- Fibrillatory waves may be present and
can be either fine (amplitude < 0.5mm)
or coarse (amplitude >0.5mm).
- Fibrillatory waves may mimic P waves
leading to misdiagnosis.
Irregular narrow-complex tachycardia at ~135 bpm.

Coarse fibrillatory waves in V1.

Treatment
• Treat the underlying cause
• Acute management-
- ventricular rate control – drugs which block AV node
( class Ic, class III)
- cardioversion – DC shock, anti arrhythmic drugs IV
- anticoagulation
• If pt is unstable : ( shock, hypotension, pulmonary edema, AC.MI)
• Electrical DC cardioversion

200 J 360 J twice

• If patient is less unstable: high risk of thromboembolism for
cardioversion
- Digoxin
- beta blockers
- calcium channel blockers ( verapamil, diltiazem)
Target rate is – 60-80 beats at rest
90-115 beats at moderate exercise.
 If pt not responded with in 2-3 days

Do trans esophageal Echo

If NO thrombus if thrombus
Cardioversion anticoagulation for 4 wks
then cardioversion
followed by 4 wks anticoagulation
• Pharmocological cardioversion
• Amiodarone 300- 400 mg twice daily for 2- 4 weeks followed by 200 mg per
day
Long term control
• Rate control:
• AV nodal slowing drugs
• Warfarin
• Rhythm control:
• Anti arrhhythmic drugs
• Warfarin
Resistant : Radio frequency ablation of AV node with permanent pacemaker
insertion
ATRIAL FLUTTER
• Atrial rate is typically between 250-350 bpm
• Clinical features: same as A.Fibrillation
• ECG – regular saw tooth like waves ( F waves) between QRS
complexes.
 ECG

--Narrow complex tachycardia

- Regular atrial activity at ~300 bpm
- Flutter waves (“saw-tooth” pattern) best seen in
leads II, III, aVF

- Flutter waves in V1 may resemble P waves

-- Loss of the isoelectric baseline
Treatment
• DC cardioversion at 50 J - initial management of choice
• Procainamide 15mg /kg body wt. over 60 mts, maintainance 1-4
mg /min. for 6 hours cardioversion
• Verapamil
• Dogoxin and betablockers
• Amiodarone – 15 mg /min. for 10 min, 1 mg /min for 6 hrs – to
restore normal SR & prevent recurrence
• Radio frequency ablation
AV Conduction block
• It is a partial or complete interruption of impulses transmission from
Atrium to Ventricle .
• Block may be
- AV node
- Bundle of HIS
TYPES
1 . First degree heart block ( first degree AV block)
2. Second degree heart block (second degree AV block)
3. Third degree heart block (third degree AV block)
 FIRST DEGREE HEART BLOCK

• First-degree atrio-ventricular block (AV block), is a

disease of the electrical conduction system of the
heart in which the PR interval is lengthened beyond
0.20 seconds.

• Early atrial depolarization followed by conduction to

the ventricles with delay.
• It is not consider complete block ,it is just slow down of impulses that
come from SA node more than the normal .
Temporary causes
- Acute myocardial Infarction: specially Inferior MI .

- Medications : Beta Blockers , calcium channel blockers or Digoxin .

- Inflammation : myocarditis , Rheumatic fever or Lupus .

- Electrolyte disturbances – like hypokalemia & hypomagnesemia

- Infections : Toxoplasmosis .
Permanent causes
- Acute myocardial infarction : specially Anterior MI .

- Degeneration of Conduction system : advanced age or cardiac

calcification of mitral or aortic valve .

- Iatrogenic damage : arrhythmia Ablation at the site of AV Junction or

Valve surgery (Tricuspid valve replacement)
ECG
 Prolongation of PR interval more than 0.2 second or more than 5
small squares .
 Constant PR interval from beat to beat .
 Regular Rhythm .
 Normal Rate or slightly slow .
SECOND DEGREE AV BLOCK
• Second-degree atrio-ventricular (AV) block, or second-degree heart
block, is characterized by disturbance, delay, or interruption of atrial
impulse conduction through the AV node to the ventricles.
TYPES
• Mobitz Type I (Wenkebach phenomenon)

• Mobitz Type II
CAUSES
• Drugs (beta-blockers, calcium channel blockers,
amiodarone)
• Cardiomyopathy
• rheumatic fever, myocarditis
• varicella-zoster virus infection
• Rheumatic diseases
• Hypoxia
• Hyperkalemia
• Hypothyroidism
• inferior wall myocardial infarction
Mobitz Type I (Wenkebach phenomenon)

• Conduction through the AV Node – progressively delayed

conducti on until a drop beat is seen
- It is not considered a complete block
ECG
• PR Interval prolongs with each beat until a dropped beat is
seen
• The PR Interval is NOT constant
• After each dropped beat, the PR interval is normal and the
cycle starts again
Mobitz Type II

- This type of block occur below AV node at the level of Hiss Bundle.
- Considered incomplete but high risk to be complete.
- Some of electrical impulses are unable to reach ventricles
ECG
- Recurrent appearance of non-conducted P waves which is blocked and
not followed by QRS complex ( indicate to block of impulses to reach
ventricle ) .
- PR interval and PP interval are constant .
- QRS usually normal but sometimes become Wide
THIRD DEGREE HEART BLOCK
- Characterized by Atrio-ventricular dissociation .
- This blockage level is infra-nodal ( Bilateral Bundle Branches ) .
- Atrial and ventricular activities are unrelated due to complete block
of electrical impulses to reach the ventricle.
- Another pacemaker distal to the block takes
over in order to activate the ventricles or
ventricular standstill will occur.
CAUSES
• Congenital
• Idiopathic fibrosis
• Ischemic heart diseases
• Infiltrative – amyloidosis, sarcoidosis, malignancies
• Infections– Endocaditis, chagas disease, Lymes
disease
• Cardiac surgery
• Drug induced- Digoxin, amiodarone
• Connective tissue diseases
ECG
- Dissociation between P wave and QRS
- P wave may overlap on T wave or QRS complex .
- PR interval is not constant
- Rate usually less than 40 .
- QRS complex usually wide and sometimes normal .
Clinical manifestations
Usually first degree and sometimes second degree are asymptomatic .
The most common signs and symptoms :
- Sever Bradycardia .
- Hypotension .
- Syncope ( fainting ) .
- Chest pain .
- Dyspnea .
- Dizziness .
Treatment
• First degree and second degree Mobitz type I does not require
treatment.
• Acute Inferior wall MI with block- Inj. Atropine 0.6 mg IV , rpt dose if
necessory.
• Inj. Isoprenaline 1-5 mg in 500ml of 5 % Dextrose slow IV till
temporary pacemaker
• If it fails – Temporary pacemaker
• Permanent pacemaker – second degree mobitz type 2 block and
complete heart block.
WPW syndrome
•Wolff–Parkinson–White syndrome (WPW) a preexcitation syndrome is
caused by the presence of an abnormal accessory electrical
conduction pathway between the atria and the ventricles.
• This is often congenital
ACCESSORY PATHWAYS
• Bundle of Kent – Atria to ventricles
• Manheim fibres
• James bundle
 Cardiac activation
PHASE 1
• Atrial activation- normal
PHASE 2
• Ventricular pre-excitation
• sinus activation occurs through both normal , anomalous
pathway
• anomalous pathway lacks AV nodal conduction delay
• so sinus impulse conducted at a rapid rate
• this enables ventricles to be activated or pre exited- short PR
interval , delta wave
• Further activation through normal pathway
PHASE 3
• Narrow terminal QRS
ECG
• Short PR interval
• Slurred initial upstroke of QRS – delta wave
• Relatively normal , narrow terminal QRS –main QRS deflection
• Slight widening of QRS
• Secondary STT changes
 MANAGEMENT
• Anti- arrhythmic drugs – class I c,3
• Radio frequency ablation
• Surgical ablation