Cardiac Arrhythmias

Prof Dr P T Thomas

27 Oct 2011

CVS Year 2

What is arrhythmia?

• Arrhythmias are disorders of cardiac impulse formation and impulse propagation

• Broadly divided into tachyarrhythmias and bradyarrhythmias

The cardiac conduction system. Depolarisation starts in the sinoatrial node and spreads through the atria (blue arrows), and then through the AV node (black arrows). Depolarisation

then spreads through the bundle of His and the bundle branches to reach the ventricular muscle (red arrows). Repolarisation is in the opposite direction (green arrows).

PQRST - The upper limit of the normal range for each interval is given in brackets.

The sequence of activation of the ventricles. Activation of the septum occurs first (red arrows), followed by spreading of the impulse through the left ventricle (blue arrows) and

then the right ventricle (green arrows).

The sequence of activation of the ventricles. Activation of the septum occurs first (red arrows), followed by spreading of the impulse through the left ventricle (blue

arrows) and then the right ventricle (green arrows).

Normal appearance of the ECG from different leads in the frontal plane..

Premature complexes (ectopic beats)

• Supraventricular ectopics

– Does not originate in sinoatrial node

– Originates either in left atrium or right atrium, then transmits to AV node and down to ventricles – QRST is normal

• Ventricular ectopics

– Originate in left or right ventricle and spread to ventricles – QRST is broad

Atrial ectopic beats. The first, second and fifth

complexes are normal sinus beats. The third, fourth and sixth complexes are atrial ectopic beats with identical QRS

complexes and abnormal (sometimes barely visible) P waves.

Ventricular ectopic beat

Sinus node dysfunction

• Sick sinus syndrome

• Bradycardia-tachycardia syndrome

• Sinus arrest / SA block

Sinoatrial disease (sick sinus syndrome). A continuous rhythm strip from a 24-hour ECG tape recording illustrating periods of

sinus rhythm, atrial ectopics, junctional beats, sinus bradycardia, sinus arrest and paroxysmal atrial fibrillation.

Supraventricular arrhythmias

• Sinus tachycardia - physiological

• Sinus bradycardia – physiological

• Supraventricular ectopics

• Atrial fibrillation – common arrhythmia

• Atrial flutter – paroxysmal, persistent

– Cardioversion

– Control ventricular rate

Atrial fibrillation

• Common arrhythmia

• Seen in conditions with atrial dilatation

• Worsens heart failure

• Predisposes to thromboembolism

• Indication for anticoagulation

• P wave absent, varying R-R intervals and QRS voltage

Atrial fibrillation

Two examples of atrial fibrillation. The QRS complexes are irregular and there are no P waves. There is usually a fast ventricular rate, often between 120 and 160/min, at the onset of atrial fibrillation. In chronic atrial fibrillation the ventricular rate may be much slower due to the effects of medication and AV nodal fatigue.

Atrial flutter. Simultaneous recording showing atrial flutter with 3:1 atrioventricular block;

flutter waves are only visible in leads II and III.

Paroxysmal SVT

• Reentry in vast majority of cases

• AV nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT)

• Regular, narrow QRS complexes (120-250/min). Initiated by atrial ectopic beat

• Carotid sinus massage may terminate an episode

• Adenosine IV, radiofrequency ablation

• Multifocal atrial tachycardia (MAT)

Supraventricular tachycardia. The rate is 180/min and the QRS complexes are normal.

Mechanism of re-entry. Re-entry can occur when there are two alternative pathways with different conducting properties (e.g. the AV node and an accessory pathway, or an area of normal tissue and an area of ischaemic tissue). In this example, pathway A conducts slowly and recovers quickly while pathway B conducts rapidly and recovers slowly. (1) In sinus rhythm each impulse passes down both pathways before entering a common distal pathway. (2) As the pathways recover at different rates a premature impulse may find pathway A open and B closed. (3) Pathway B may recover while the premature impulse travels selectively down pathway A. The impulse may then travel retrogradely up pathway B, setting up a closed loop or re-entry circuit. (4) This may initiate a tachycardia that will continue until the circuit is interrupted by a change in conduction rates or electrical depolarisation.

Wolff-Parkinson-White (WPW) syndrome

• AV bypass tract present, leading to recurrent arrhythmias

• Preexcitation – delta waves, short PR interval with broad QRS on ECG during sinus rhythm

• Risk of SVT, VF, VT

• Radiofrequency ablation of abnormal tracts

Wolff-Parkinson-White syndrome. In this condition there is a strip of accessory conducting tissue that allows electricity to bypass the AV node and spread from the atria to the ventricles rapidly and without delay. When the

ventricles are depolarised through the AV node (1) the ECG is normal, but when the ventricles are depolarised through the accessory conducting tissue (2) the ECG shows a very short PR interval and a broad QRS complex. Sinus rhythm. In sinus rhythm the ventricles are partly depolarised through the AV node, and partly through the accessory pathway, producing an ECG with a short PR interval and broadened QRS complexes; the characteristic slurring of the

upstroke of the QRS complex is known as a delta wave. The degree of pre-excitation (the proportion of electricity passing down the accessory pathway) and therefore the ECG appearances may vary a lot, and at times the ECG can look normal. Orthodromic tachycardia. This is the most common form of tachycardia in WPW. The re-entry circuit

passes antegradely through the AV node and retrogradely through the accessory pathway. The ventricles are therefore depolarised in the normal way, producing a narrow-complex tachycardia that is indistinguishable from

other forms of SVT. Antidromic tachycardia. Occasionally, the re-entry circuit passes antegradely through the accessory pathway and retrogradely through the AV node. The ventricles are then depolarised through the accessory

pathway, producing a broad-complex tachycardia. Atrial fibrillation. In this rhythm the ventricles are largely depolarised through the accessory pathway, producing an irregular broad-complex tachycardia which is often more

rapid than the example shown.

Ablative therapy for arrhythmias • Non-surgical approach to map the abnormal

tract and destroy it using radiofrequency energy

• Usually used in WPW syndrome with SVT

Ventricular ectopic beats. There are broad bizarre QRS complexes (arrows) with no preceding P wave in

between normal sinus beats. Their configuration varies, so these are multifocal ectopics.

Ventricular tachycardia

• Structural heart disease, MI, cardiomyopathy, long QT

• Most episodes of VF begins with VT

• Wide-complex QRS, regular

• Paroxysmal VT is usually initiated by a VPC

• Cardioversion, ICD implantation, RFA

Ventricular tachycardia: rhythm strip. Typical broad bizarre QRS complexes with a rate of 160/min.

Ventricular tachycardia: fusion beat (arrow). In ventricular tachycardia there is independent atrial and ventricular

activity. Occasionally a P wave is conducted to the ventricles through the AV node. This may produce a normal sinus beat in the middle of the tachycardia (a capture beat); however,

more commonly the conducted impulse fuses with an impulse from the tachycardia (a fusion beat). This

phenomenon can only occur when there is AV dissociation and is therefore diagnostic of ventricular tachycardia.

Torsades de pointes

• VT with polymorphic QRS

• Associated with QT prolongation

• Hypokalaemia, hypomagnesaemia

• Quinidine, phenothiazines, tricyclics, III degree AV block, congenital

Torsades de pointes. A bradycardia with a long QT interval is followed by polymorphic ventricular

tachycardia that is triggered by an R on T ectopic.

Ventricular fibrillation

• Most common after acute MI

• Side effect of antiarrhythmia drugs

• Long QT and Tdp

• WPW syndrome with AF

• Electric shock

• Treat with – DC defibrillation

– Implanted cardioverter/defibrillator

Ventricular fibrillation. A bizarre chaotic rhythm initiated in this case by two ectopic beats in rapid succession.

Heart blocks (AV blocks)

• Escape rhythm – when SA node does not fire

• His bundle has a rate of 40-60/min

• His-Purkinje system rate 25-45/min, wide QRS and unstable

• First-degree AV block – PR >0.20 s

• Second-degree – Mobitz type I (Wenckebach phenomenon) in inferior MI, digoxin, -blockers

• Mobitz type II – His-Purkinje system disease

First-degree heart block. The PR interval is prolonged and measures 0.26 seconds.

Second-degree atrioventricular block (Mobitz type I-Wenckebach's phenomenon). The PR interval progressively

increases until a P wave is not conducted. The cycle then repeats itself. In this example, conduction is at a ratio of 4:3, leading to groupings of three ventricular complexes in a row.

Second-degree atrioventricular block (Mobitz type II). The PR interval of conducted beats is normal but some P waves are not conducted. The

constant PR interval distinguishes this from Wenckebach's phenomenon.

Complete heart block

• III degree AV block – congenital in AVN, lower blocks require pacing

• AV dissociation

• Atropine and isoprenaline IV

• Cardiac pacemaker: temporary and permanent

Complete (third-degree) atrioventricular block. There is complete dissociation of atrial and ventricular

complexes. The atrial rate is 80/min and the ventricular rate is 38/min.

Right bundle branch block. Note the wide QRS complexes with 'M'-shaped configuration in leads V1

and V2 and a wide S wave in lead I.

Left bundle branch block. Note the wide QRS complexes with the loss of the Q wave or

septal vector in lead I and 'M'-shaped QRS complexes in V5 and V6.