Dr.Syed Irfan

Def: An arrhythmia is defined as an abnormality of the cardiac rhythm or heartbeat pattern. The heartbeat may be too slow ie < 60 beats /min (bradycardia), too fast >100 beats /min (tachycardia), have extra beats (extra systole), skip a beat (missed beat), or irregular beats (dysarrhythmia).

Cardiac arrhythmias are caused by abnormality in the normal activation sequence of the myocardium. It may vary in severity and may be benign or even life threatening.

Tachycardia causes palpitation but is not necessarily an arrhythmia. Increased heart rate is a normal response to physical exercise and emotional stress.

Sinus tachycardia is caused by the action of the sympathetic nervous system on the sinus node. Increased sympathetic nervous system activity is caused by caffeine, amphetamine and hyperthyroidism.

Normally SA node is the pacemaker as it depolarizes spontaneously at a more rapid rate than any other area of the heart (approx 70 beats /min)

The AV node has an intrinsic rate of about 50-60 beats /min, the HIS-Purkinje system rate is about 30-40 beats /min. The latter rate is too slow to permit normal physiological activity and calls for implantation of electronic pacemaker.

Automaticity of a cardiac muscle refers to firing of an impulse on it’s own. Though all cells in the heart has the ability to initiate an action potential, only cells found in the conduction system (SA node, AV node, bundle of HIS and Purkinje fibers) of the heart are designed to routinely trigger heart beats. SA node is the single specialized location in the atrium which has the higher automaticity than the rest of the heart and is therefore responsible for initiating heart beat and setting the heart rate.

Any part of the heart that initiates an impulse is called an ectopic focus and by definition is a pathological phenomenon. Ectopic focus can produce sustained abnormal rhythm and decrease the pumping efficiency of the heart as signals reach the various parts of the heart muscle with different timing to usual and can be responsible for poor coordinated contraction.

There are 3 main mechanisms Increased automaticity

due to increase in normal automaticity in pacemaker fibers or development of abnormal automaticity due to spontaneous depolarization of ectopic fibers occur in various pathophysiological states. Increased automaticity is seen in

i) Increased endogenous or exogenous catecholemines

ii) Electrolyte disturbances eg hypokalemia iii) Hypoxia or ischemiaiv) Mechanical effects eg exercisev) Drugs eg digitalis

Re-entry is the common cause of sustained paroxysmal

tachyarrhythmia. a) Global re-entry between the atria and ventricles

may involve accessory conduction pathways (bypass tracts) such as bundle of Kent. Accessory pathways transmit impulses between the atria and the ventricles by multiple pathways. This type of reentry results into supreventricular tachyarrhythmia eg Wolff-Parkinson-White syndrome.

b) AV nodal re-entry tachycardia occur within AV nodal tissue. There may different conduction velocities and refractory periods in these multiple pathways within the AV node and a common cause of paroxysmal supraventricular tachycardia with impulses traveling from atria to ventricles and then from the ventricles back to the atria through the AV node.

Triggered activity is cause by secondary depolarization arising from an incompletely depolarized cell membrane in isolated Purkinje fibers.

Common causes of cardiac arrhythmias are

1. Congenital heart disease2. Coronary heart disease3. Systemic hypertension4. Long term nicotine exposure5. Idiosyncratic reaction to some food

and beverages eg caffeine, alcohol and various drugs.

Arrhythmias originating in the atria 1. Atrial fibrillation 2. Atrial flutter 3. Paroxysmal Supraventricular

tachycardia 4. Wolff-Parkinson-White syndrome 5. Premature atrial contraction 6. Sick sinus syndrome 7. Sinus arrhythmias 8. Sinus tachycardia 9. Multifocal atrial tachycardia

Cardiac arrhythmias originating in the ventricles

1. Premature ventricular contraction 2. Ventricular fibrillation 3. Ventricular tachycardia

Diagnosis ECG show fast heart beat, slow heart

beat or a long pause in the heart beat (asystole)

Complications i. Heart failure ii. Stroke Treatment include i. Permanent pacingii. Anticoagulant like warfarin reduce

the number of strokes and embolic events.

Extrasystole or atrial premature beats are beats arising from the atrium and occurring before the expected sinus beats. The premature beats can be irregular or occur at random.

Morphology of the P wave differs from sinus beats and varies depending upon the origin of the impulse in the atria. When beat arise high in the atria, P waves are upright in leads II, III and aVF, but when originating in the lower atria P waves are inverted in these leads. The P wave may conduct with normal or prolonged PR interval with narrow or aberrant QRS complex or may block and not be followed by any QRS complex.

Causes:i. Excess alcohol, cigarettes, fatigue, fever, anxiety

and infectious diseasesii. CCF, MIiii. Chronic pulmonary disease, hypoxia

S/si. Palpitation ii. Awareness of skipped beats or

fluttering

Treatment: No specific treatment is required

Complication May present at the onset of atrial

fibrillation

Atrial tachycardia can be caused by i. Increased atrial automaticityii. Sinuatrial diseaseiii. Digoxin toxicityIn atrial tachycardia (AT) heart’s

impulses come from somewhere in the atria other than the SA node, the normal pacemaker of the heart. The SA node is often suppressed and another site in the atrium regulates the heart’s rhythm and rate.

S/S i. Palpitation which can be skipping,

fluttering and pounding in the chestii. Fatigueiii. Chest pressure or painiv. Shortness of breadthv. Syncope or near-syncopevi. Dizziness or lightheadednessTreatment i. Betablockersii. Antiarrhythmic drugs eg amiodarone

Atrial Flutter is the most significant atrial tachyarrhythmia after atrial fibrillation. Atrial flutter is defined by stable, uniform atrial activation and is characterized by a macro (large) re-entry circuit within the right atrium, usually encircling the tricuspid annulus.

Atrial flutter commonly includes some form of A-V block which is usually 2:1, 3:1, or 4:1 with corresponding heart rate of 150, 100 and 75 (atrial beat ordinarily is 300 beats/min).

It is caused by multiple re-entrant or primarily generated (ectopic) atrial waveforms bombarding the AV node.

S/Si. Palpitation ii. Fatigueiii. Mild dyspneaiv. Pre-syncope v. Less common symptoms include angina, severe

dyspnea or syncope.Causesi. Longstanding hypertension ii. Valvular heart diseaseiii. LVF iv. CADv. Pericarditis vi. Pulmonary embolismvii. Hyperthyroidism viii. Diabetesix. Digital toxicity

Investigations i. ECG show saw-toothed flutter waves best seen in leads II,

III, aVF and V1 P wave rate 300 / min 2:1, 3:1,or 4:1 block ii. Haltor Monitoring or 24 hrs ECG help to identify

arrhythmias in patients with non-specific symptoms.Treatmenti. Control of ventricular rate by a. cardiac glycosides eg digoxin b. beta blockers c. calcium channel blocker eg verapamilii. Antiarhythmic drug eg amiodarone for chemical

conversion to sinus rhythmiii. Restoration of cardiac rhythm by direct current

cardioversion

Atrial Fibrillation is the most common sustained cardiac arrhythmias. Patients suffering from AF have higher risk of strokes.

AF is characterized by presence of multiple, interacting re-entry circuits looping around the atria.

i. The atrial contractions are irregular , disorganized, chaotic and very rapid. The atria may contract at a rate of 400-600 beats/ min.

ii. The irregular pulses reach the AV node at rapid succession, but not all of them can make it past the AV node. Therefore the ventricle beat slower, often at a rate of 110-180 beats/min in an irregular rhythm.

iii. This results into rapid, irregular heart beat, irregularly irregular pulse and often a sensation of fluttering in the chest.

Atrial Fibrillation may be of following types1. Paroxysmal or intermittent self limiting episodes

lasting from seconds to days.2. Persistent prolonged episodes requiring medical

treatment to end episodes.3. Permanent where the heart is always in of atrial

fibrillation. Conversion into sinus rhythm is not possible or not appropriate

for medical reason (eg acute cardiac ischemia or impending hemodynamic collapse).

S/Si. Patient may be asymptomaticii. Common symptoms include palpitation, sensation

of rapid and irregular heart beat or fluttering sensation in the chest.

There nay be weakness, lightheadedness, dyspnea and chest pain.

Common causes of AF are i. CADii. Valvular heart diseaseiii. Hypertensioniv. Sinoatrial diseasev. Hyperthyroidismvi. Excess alcohol intake (holiday heart)vii. Cardiomyopathy viii. Congenital heart diseaseix. Pulmonary embolismx. Pericarditisxi. Infectious diseases

ECG shows i. Irregular rhythmii. Discrete P waves are absent,

undulating fibrillatory (f) waves are present.

Other investigations include echocardiogram and thyroid function test.

Treatmenti. Rate control by beta blockers,

calcium channel blockers and digoxin

ii. Anticoagulant eg warfarin to prevent stroke

iii. Electric conversion to sinus rhythm

Cardioversion is a procedure where an electric shock is delivered to the heart to convert an abnormal heart rhythm back to a normal rhythm.

Elective or non-emergency cardioversions are performed to treat atrial flutter or atrial fibrillation, benign heart rhythm disturbances originating in the atria.

Emergency cardioversion is performed to correct rapid abnormal rhythm associated with faintness, low BP, chest pain, dyspnea or loss of consciousness.

Cardioversion can bei. Chemical: by the use of antiarrhythmic drugsii. Electrical: by direct current delivered for a split sec

through the chest wall to the heart through the special electrodes or paddles, that are applied to the skin of the chest and back.

Supraventricular tachycardia (SVC) is a rapid heart beat originating in the atria and setting up abnormal electric impulses. The heart beats so fast that the heart muscles cannot relax between contractions. It originates in the atria or in the AV node.

Supraventricular tachycardia can be found in healthy young children, in adolescents and in people with underlying heart disease.

Paroxsysmal or sporadic supraventricular tachycardia (PSVT) usually occur without other symptoms. It is often associated with a number of medical conditions like

atherosclerosis, heart failure, hyperthyroidism, chronic lung disease, pulmonary emboli, pericarditis, emotional stress, structural abnormalities, alcohol and cocaine abuse, side effects of digitalis and bronchodilators.

Symptoms may appear suddenly last a few minutes to 2-3 days and then disappear without treatment. The symptoms are typical with rapid pulse of 140-250 beats /min.

The symptoms include anxiety, dizziness, shortness of breadth, palpitation and chest pain.

ECG shows tachycardia with normal QRS complexes and occasionally rate dependent bundle branch block.

Treatment is not always necessary. It may be treated by

i. Valsalva manoeuvre (forcibly exhaling while keeping the nose and the mouth closed) or application of carotid sinus pressure.

ii. Intravenous adenosine (cause transient heart block in the AV node) or verapril restore sinus rhythm.

iii. DC cardioversion may be required when there is severe hemodynamic compromise.

Wolf-Parkinson-White syndrome is a congenital abnormality involving the presence of abnormal conductive tissue between the atria and the ventricles that is often associated with supraventricular tachycardia. It involves the activation of the ventricles that occurs earlier than anticipated (pre excitation), because of the conduction of an atrial impulse not by means of the normal conduction system, but an extra atrioventricular (AV) muscular connection, termed as accessory pathway, that bypasses the AV node.

Classical ECG findings of WPW syndrome includei. Presence of short PR interval (<120ms or 0.12s)ii. Wide QRS complex longer than 120 msiii. Slurred onset of the QRS waves producing delta

wavesiv. Secondary ST-T changes

Pathophysiology:An abnormal band of conducting tissue called

accessory tract (bypass tract, Kent fibers) connects the atria to the ventricles. Physiologically it resembles the Purkinje fibers but differ by having

i. more rapid conducting properties ii. different refractory period iii. lack of rate limiting properties of the AV node.Some accessory (bypass) pathways cannot conduct

impulses in ante grade fashion and conducts in the retrograde direction (from ventricles to atria). These are called concealed pathways (ie concealed WPW syndrome). Although no evidence of the pathway is evident in sinus rhythm (ie no pre excitation) tachycardia is present. However when the heart rate more than 200 beats per min a retrograde P wave is visible following the QRS complex, a concealed pathway may be dangerous.

In other cases shorter refractory period in the accessory pathway may cause block of an ectopic atrial impulse in the normal pathway, with antegrade conduction down the accessory tract during sinus rhythm. Then there is retrograde reentry of the normal pathway. It is called the manifest accessory pathway.

If atrial fibrillation occur in a case of WPW syndrome, it will produce dangerously rapid ventricular rate and may cause collapse, syncope and even death. The condition should be treated as emergency by DC cardioversion.

ECG shows--short PR interval--delta waves or slurring of QRS complex during sinus

rhythmSuch tachycardia is difficult to differentiate from

ventricular tachycardia.

Treatment;i. Carotid sinus pressureii. Intravenous adenosineiii. DC cardioversion in case of emergencyiv. Catheter ablation of accessory

pathwayv. Pophylactic treatment to slow the

conduction rate and prolong refractory period of the bypass tract by antiarrhythmic drugs like beta blockers, calcium channel blockers, digoxin amiodarone etc.

Catheter ablation is an invasive procedure to remove a faulty electrical pathway from the heart in cases of cardiac arrhythmias such as atrial fibrillation, atrial flutter, supraventricular tachycardia and Wolff-Parkinson-White syndrome.

By ablation, normal rhythm of the heart is restored by destroying small, carefully selected part of the heart that cause tachycardia.

Several flexible catheters are introduced into femoral vein, internal jugular vein or subclavian vein to reach the heart. High frequency electrical impulses are used to induce arrhythmias, the abnormal tissue identified and destroyed.

Although there are several ways of ablation, the two most common are radiofrequency ablation and cryoablation.

Radiofrequency ablation uses radio energy to heat and destroy the defective tissues and is the most common form of ablation.

Cryoablation uses intense cold to freeze and destroy tissue, it causes tiny ice crystals in and around the abnormal tissue and destroys these cells.

A. Ventricular ectopic beats (extrasystoles, premature beats) are ectopic impulses originating from an area distal to the HIS Purkinje system.

Ventricular premature complexes are common and do not indicate a problem in otherwise healthy people without heart disease. They are prominent in rest and disappear with exercises.

However if a person has aortic stenosis, heart failure or previous heart attack, VEBs may be followed by ventricular tachycardia and fibrillation which can lead to sudden death.

Common mechanisms for VPCs arei. Automaticity: development of a new site of

depolarization in non-nodal ventricular tissue. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium.

ii. Reentry: occur when slow conducting tissue eg infarcted myocardium is present adjacent to normal tissue.

iii. Triggered activity:

ECG shows i. Wide and bizarre QRS complexesii. No preceding premature P wavesVentricular ectopics can occur in

patterns such as bigeminy (every other beat), trigeminy (every third beat) or quadrigeminy (every fourth beat). They may also occur in sequence such as couplets, triplets, salvos (4-7) or episodes (eight or more).

Causes includei. Cardiac causes --acute myocardial infarction --valvular disease --cardiomyopathy --cardiac contusionii. Non-cardiac causes --electrolyte disturbances --hypokalemia --hypocalcemia --hypomagnesaemia --medicines like digoxin, aminophylline, tricyclic

antidepressants, pseudoepinephrine etc. --infection --stress

Treatment i. Asymptomatic patients require no

treatment.ii. Symptoms are treated with anxiolytic

drugs, beta blockers, calcium channel blockers

iii. Treatment of underlying heart disease

B. Ventricular tachycardia (VT) refers to any rhythm faster than 100 beats per min arising distal from the bundle of HIS. The rhythm may arise from ventricular myocardium and or the distal conduction system.

Important symptoms are palpitation, dyspnea and syncope.

Pathophysiologyi. Rapid rhythm faster than 100-120 beats per min

arise in the ventriclesii. Severity of the clinical symptoms determines the

urgency of treatment.iii. Due to rapid heart rate and lack of properly timed

and co-ordinated atrial contraction, cardiac output is reduced.

iv. Hemodynamic collapse is likely when underlying left ventricular dysfunction is present or with very rapid rates.

v. Diminished cardiac output may cause diminished myocardial perfusion, onset of ventricular fibrillation and sudden death.

ECG showsi. No P wavesii. QRS complexes are greater than

160 per minute.Treatmenti. Intravenous amiodarone, lidocaineii. Betablockers iii. DC cardioversion if BP is less than

90 mm of Hg

C. Torsades de Pointes literally meaning twisting points, is distinctive point of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QT complexes around the isoelectric line. Torsades is associated with a prolonged QT interval, which may be congenital or acquired. It usually terminates spontaneously but frequently recurs and may degenerate into sustained VT and ventricullar fibrillation.

Pathophysiology;The abnormality underlying both

acquired and congenital long QT syndromes is in the ionic current flow during repolarization, which affects the QT interval. The prolongation of the repolarization delays the inactivation of the ion channels responsible for the inward flow of positive depolarizing currents. This leads to further delay in the repolarization and causes early after depolarization and triggers torsade.

S/S Recurrent episodes of palpitation,

dizziness and syncope.Sudden cardiac death may occur in

first episode.Risk factors i. Congenital and acquired long QT

syndromes.ii. Bradycardiaiii. Female sex

Causes of long Qt syndromes i. Congenital --Romano-ward syndrome, a familial

autosomal dominant abnormality --Jerval and Lange-Nielson syndrome

with congenital deafness and inherited cardiac abnormality

ii. Acquired --use of antiarrhythmic drugs like

quinidine, satalol, and rarely amiodarone

--antibiotics like erythromycin, claritheomycin

--tricyclic and tetracyclic antidepressant --electrolyte abnormalities like

hypokalemia, hypomagnesemia, hypocalcemia

iii. Cardiac conditions --myocardial ischemia, myocardial

infarction, complete AV blockiv. Intracranial condition --subarachnoid hge, cerebrovascular

accidents, encephalitis, head injury.

ECG showsi. Paroxysm of 5-20 beats, with a heart rate faster

than 200 bpm, occasionally sustained episodes can be seen

ii. Progressive change in polarity of QRS about the isoelectric line occurs

iii. Complete 1800 twist of QRS complexes in 10-12 beats present

iv. A prolonged QT interval and pathological U waves are present

v. A short-long-short sequence between the PR interval occurs before the trigger response.

( U wave is usually very small and represents late repolarization of the Purkinji fibers in the ventricle and is more often not shown on a rhythm strip)

Treatment1. Short term treatment --DC cardioversion in stable patients --defibrillation if there is ventricular fibrillation --discontinuation of offending drugs --suppression of early depolarization by intravenous magnesium -- Temporary transvenous spacing. Based on the fact

that QT interval shortens with faster heart rate, pacing can be effective in terminating torsade.

a. atrial spacing to suppress arrhythmias by rate-dependent shortening of QT interval.

b. in patients with AV block, ventricular spacing is done

c. pacing should be instituted at a rate of 90-110 bpm until the QT interval is normalizes.

2. Long term treatment --permanent spacing --implantable cardioverter-defibrillators

(ICD) is used as last resort.

Sudden cardiac death is defined as unexpected non-traumatic death in clinically well stable patients who die within 1 hr after onset of symptoms. The causative rhythm in most cases is ventricular fibrillation, which is usually preceded by ventricular tachycardia except in the case of acute ischemia or myocardial infarction. Complete heart block or sinus node arrest may also cause sudden death.

Most of the victims of sudden cardiac death have severe CAD,

Other conditions predisposing sudden death include LVH, hypertrophic cardiomyopathy, congestive cardiomyopathy, aortic stenosis, pulmonary stenosis, cyanotic congenital heart disease, mitral valve prolapse, conduction system disease etc.

Sinus arrhythmias is a cyclic increase in the normal heart rate with inspiration and decrease with expiration. It occurs due to normal parasympathetic activities on normal pacemaker and disappears with breadth holding, or increase of heart rate, and has no clinical significance.

Sinus bradycardia is a heart rate slower than 50 beats/min due to increased vagal influence on the normal pacemakers or organic disease of the sinus node. In healthy individuals, sinus bradycardia to a rate of 50 beats /min or lower is a normal finding. However severe sinus bradycardia especially in elderly patients and individuals with heart disease may indicate sinus node pathology. If cerebral perfusion is impaired, weakness, confusion or syncope may occur.

Sinus tachycardia is defined as heart rate faster than 100 beats /min and is caused by rapid impulse formation from the SA node. It occurs with fever, exercise, emotion, pain, anemia, heart failure, shock, thyrotoxicosis or in response to some drugs. Alcohol and alcohol withdrawal are common causes of sinus tachycardia and supraventricular arrhythmias.

Essentials of diagnosis are Most patients are asymptomatic More common in elderly population May have recurrent supreventricular

arrhythmia and bradyarrhythmia Frequently seen in patients with

concomitant atrial fibrillation May be caused by drug therapy eg

digitalis, calcium channel blockers, beta blockers etc

Def: Sick sinus syndrome is a group of abnormal heart rhythms (arrhythmias) causing malfunction of the sinus node. The SA node beats abnormally causing slow heart rate, rapid heart rate or in alternating slow and fast rhythm.

Symptoms:a. Most people are asymptomaticb. S/S may come and go and include i. Fatigue ii. Dizziness or lightheadedness iii. Fainting iv. Shortness of breadth v. Chest pain vi. Disturbance of sleep vii. Confusion or impaired memory viii.

Palpitation

Causes include i. Patchy fibrosis of SA node and cardiac

conduction systemii. Degenerative changesiii. Ischemia of the SA nodeiv. Intake of drugs like Ca++ channel

blockers and beta blockers to control hypertension

v. Cardiomyopathies

Atrioventricular blockAV block occurs when the atrial

depolarization fail to reach the ventricles and when the atrial depolarization is conducted with a delay. 3 degrees of Av block are recognized.

First degree block consists of prolongation of the PR interval (>20s in adults and >16s in children). All atrial impulses reach the ventricles in the first degree AV block, but conduction is delayed in the AV node.

Second degree AV block is characterizes by trial impulses (generally occurring at regular rate) failing to conduct to the ventricles in one of the following ways.

1. Morbitz type I second degree AV block (Wenckebach’s phenomenon) consists of progressive prolongation of the PR interval with progressive shortening of R-R interval. Ultimately atrial contraction fails to conduct and a QRS complex is not generated, resulting in a pause. The cycle then repeats itself. This is usually due to impaired conduction in the AV node itself.

3 rules of ‘classic AV Wenchebach’ are i. increasing PR interval until a nonconducted P wave

occursii. PR interval of the pause is more than preceding two

PR intervalsiii. the PR interval after the pause is less than PR

interval just prior to the pauseHowever there are many examples of atypical forms.

2. Morbitz II second-degree AV block is characterized by a constant PR interval followed by a sudden failure of a P wave to be conducted to the ventricles, such that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked) and so on.

Usually caused by disease of the HIS-Purkinje system.

3. High-grade AV block consists of at least 2 or more P waves in a row that do not conduct and are blocked. The conduction ratio can be 3:1 or more and the PR interval of the conducted beats is constant. It is differs from the complete AV block in that, the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P wave and the QRS complexes.

Third degree AV block are diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent of QRS wave complexes. The QRS complexes represent escape rhythm, either junctional or ventricular.

The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats per minute.

Escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats per min.

No relationship exists between rhythm of P waves and the rhythm of QRS complexes. Frequency of P wave (atrial rate) is higher than the frequency of QRS complexes (ventricular rate).

First-degree heart block and second-degree Morbitz I AV block are usually caused by a delay at the AV nodal level.

Second-degree Morbitz II AV block is generally caused by blockage in the HIS bundle or lower in the conduction system.

Third-degree AV block is caused by conduction disturbances in the AV node or the HIS-Purkinje system.

In complete AV block, an escape rhythm originate from the ventricles, with wide QRS complexes at a low regular rate of 30-40 bpm.

A higher anatomic location of the block results in a higher location of escape rhythm pacemaker, a faster escape rhythm (40-60 bpm in the region of the HIS bundle), and a narrow QRS duration.

Causes of heart block are i. Myocardial infarctionii. Cardiomyopathies iii. Valvular heart diseaseiv. Coronary artery diseasev. After heart surgeryTreatment of heart blocki. Permanent pacing in symptomatic

bradyarrhythmias, asymptomatic Morbitz II AV block and complete heart block.

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and can occur in presence of intact AV conduction.

Independence between atrial and

ventricular beats is called AV dissociation

Stokes-Adams attacks are a type of syncope (fainting) of cardiac origin, usually lasting less than a minute and resulting from a sudden reduction of the blood flow from the heart to the brain. Syncope results when the patient’s pulse suddenly becomes exceptionally low or fast. Stokes-Adams occur in more frequently in patients with complete AV block and pulse of 40 or less per min.

Causes are i. Inadequate blood flow to the brainii. Arrhythmias (<30 and >180 bpm) --sick sinus syndrome, AV block or tachyarrhythmiasS/Si. Abrupt and transient (lasting for seconds to a few

minutes) loss of consciousnessii. Prompt recovery of full consciousnessiii. Convulsion may occur if there is prolonged asystole.

ECG Resting ECG may showa. Arrhythmiasb. Evidences of accessory pathwaysc. Prolonged QT intervalsd. Other signs of heart diseases like

infarction or hypertrophy.

The two main bundles of conducting fibers in the heart conducting impulses through the ventricles are the Right bundle and the Left bundle (which has an anterior and posterior fascicle).

The possible abnormalities are --Right bundle branch block (usually

considered a normal finding)--Left bundle branch block--anterior hemiblock--posterior hemiblock--bifascicular block (any two of these- right

bundle, left anterior or left posterior)

Causes:i. May be found in individuals with otherwise normal

heartii. More commonly found in organic heart disease

Right bundle branch block is found in --Normal individuals--Congenital heart disease--Myocardial infarction--Pulmonary heart disease--Drugs and electrolyte imbalances

Left bundle branch block is found in--myocardial infarction--left ventricular outflow obstruction--cardiomyopathy--fibrosis of the conducting system

Progression Block in either of the ventricular conduction

system produces a de-coordination of the contraction of the two ventricles. The right bundle branch block results in delayed right ventricular contraction and left bundle branch block causes delayed left ventricular contraction. They may progress to complete heart block.

Treatment --mild partial bundle branch block requires

no treatment --severe arrhythmias may require permanent

pacing --treatment of the underlying cause

QRS complex prolonged >120ms

RSR1 pattern Dominant R1 in

V1 &V2 Inverted T waves

in V1 and sometimes in V2-V3

Deep and wide S waves in leads I & V6

QRS duration > 120ms

M pattern in V6 and sometimes in V4-V5 due to secondary R waves

No septal Q waves Inverted T wave in

V5-V6 Left axis deviation

may be seen

Left ant. hemiblock ie marked left axis with deep S waves in II and III

RBBB