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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
Cardiac arrhythmias y2 oct 2010
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).
Cardiac arrhythmias y2 oct 2010
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
Cardiac arrhythmias y2 oct 2010
Atrial fibrillation
Cardiac arrhythmias y2 oct 2010
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.
Cardiac arrhythmias y2 oct 2010
Cardiac arrhythmias y2 oct 2010
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.
Cardiac arrhythmias y2 oct 2010
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.
Cardiac arrhythmias y2 oct 2010
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
Cardiac arrhythmias y2 oct 2010
First-degree heart block. The PR interval is
 prolonged and measures 0.26 seconds.
Cardiac arrhythmias y2 oct 2010
Cardiac arrhythmias y2 oct 2010
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
Cardiac arrhythmias y2 oct 2010
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.
Cardiac arrhythmias y2 oct 2010

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Cardiac arrhythmias y2 oct 2010

  • 1. Cardiac Arrhythmias Prof Dr P T Thomas 27 Oct 2011 CVS Year 2
  • 2. What is arrhythmia? • Arrhythmias are disorders of cardiac impulse formation and impulse propagation • Broadly divided into tachyarrhythmias and bradyarrhythmias
  • 4. 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.
  • 5. 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).
  • 6. 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).
  • 8. Normal appearance of the ECG from different leads in the frontal plane..
  • 9. 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
  • 10. 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.
  • 12. Sinus node dysfunction • Sick sinus syndrome • Bradycardia-tachycardia syndrome • Sinus arrest / SA block
  • 13. 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.
  • 14. Supraventricular arrhythmias • Sinus tachycardia - physiological • Sinus bradycardia – physiological • Supraventricular ectopics • Atrial fibrillation – common arrhythmia • Atrial flutter – paroxysmal, persistent – Cardioversion – Control ventricular rate
  • 15. 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
  • 19. 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.
  • 20. Atrial flutter. Simultaneous recording showing atrial flutter with 3:1 atrioventricular block; flutter waves are only visible in leads II and III.
  • 21. 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)
  • 22. Supraventricular tachycardia. The rate is 180/min and the QRS complexes are normal.
  • 23. 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.
  • 24. 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
  • 25. 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.
  • 28. 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
  • 29. 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.
  • 30. 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
  • 31. Ventricular tachycardia: rhythm strip. Typical broad bizarre QRS complexes with a rate of 160/min.
  • 32. 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.
  • 33. Torsades de pointes • VT with polymorphic QRS • Associated with QT prolongation • Hypokalaemia, hypomagnesaemia • Quinidine, phenothiazines, tricyclics, III degree AV block, congenital
  • 34. 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.
  • 36. 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
  • 37. Ventricular fibrillation. A bizarre chaotic rhythm initiated in this case by two ectopic beats in rapid succession.
  • 39. 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
  • 41. First-degree heart block. The PR interval is prolonged and measures 0.26 seconds.
  • 44. 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.
  • 45. 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.
  • 46. 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
  • 48. 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.
  • 49. 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.
  • 50. 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.