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Cardiac arrhythmias y2 oct 2010

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Cardiac arrhythmias y2 oct 2010

  1. 1. Cardiac Arrhythmias Prof Dr P T Thomas 27 Oct 2011 CVS Year 2
  2. 2. What is arrhythmia?• Arrhythmias are disorders of cardiac impulse formation and impulse propagation• Broadly divided into tachyarrhythmias and bradyarrhythmias
  3. 3. The cardiac conduction system. Depolarisation starts in the sinoatrial node and spreadsthrough 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.
  4. 4. The sequence of activation of the ventricles. Activation of the septum occurs first (redarrows), followed by spreading of the impulse through the left ventricle (blue arrows) and then the right ventricle (green arrows).
  5. 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. 6. Normal appearance of the ECG from different leads in the frontal plane..
  7. 7. 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
  8. 8. Atrial ectopic beats. The first, second and fifthcomplexes are normal sinus beats. The third, fourth and sixth complexes are atrial ectopic beats with identical QRScomplexes and abnormal (sometimes barely visible) P waves.
  9. 9. Ventricular ectopic beat
  10. 10. Sinus node dysfunction• Sick sinus syndrome• Bradycardia-tachycardia syndrome• Sinus arrest / SA block
  11. 11. Sinoatrial disease (sick sinus syndrome). A continuous rhythmstrip from a 24-hour ECG tape recording illustrating periods of sinus rhythm, atrial ectopics, junctional beats, sinus bradycardia, sinus arrest and paroxysmal atrial fibrillation.
  12. 12. Supraventricular arrhythmias• Sinus tachycardia - physiological• Sinus bradycardia – physiological• Supraventricular ectopics• Atrial fibrillation – common arrhythmia• Atrial flutter – paroxysmal, persistent – Cardioversion – Control ventricular rate
  13. 13. 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
  14. 14. Atrial fibrillation
  15. 15. Two examples of atrial fibrillation. The QRS complexes areirregular and there are no P waves. There is usually a fastventricular rate, often between 120 and 160/min, at theonset of atrial fibrillation. In chronic atrial fibrillation theventricular rate may be much slower due to the effects ofmedication and AV nodal fatigue.
  16. 16. Atrial flutter. Simultaneous recording showing atrial flutter with 3:1 atrioventricular block;flutter waves are only visible in leads II and III.
  17. 17. 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)
  18. 18. Supraventricular tachycardia. The rate is180/min and the QRS complexes are normal.
  19. 19. Mechanism of re-entry. Re-entry can occur when there are two alternative pathways withdifferent conducting properties (e.g. the AV node and an accessory pathway, or an area ofnormal tissue and an area of ischaemic tissue). In this example, pathway A conducts slowlyand recovers quickly while pathway B conducts rapidly and recovers slowly. (1) In sinusrhythm each impulse passes down both pathways before entering a common distalpathway. (2) As the pathways recover at different rates a premature impulse may findpathway A open and B closed. (3) Pathway B may recover while the premature impulsetravels selectively down pathway A. The impulse may then travel retrogradely up pathwayB, setting up a closed loop or re-entry circuit. (4) This may initiate a tachycardia that willcontinue until the circuit is interrupted by a change in conduction rates or electricaldepolarisation.
  20. 20. 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
  21. 21. 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 depolarisedthrough the accessory conducting tissue (2) the ECG shows a very short PR interval and a broad QRS complex. Sinusrhythm. In sinus rhythm the ventricles are partly depolarised through the AV node, and partly through the accessorypathway, 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 theaccessory 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.
  22. 22. 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
  23. 23. Ventricular ectopic beats. There are broad bizarreQRS complexes (arrows) with no preceding P wave in between normal sinus beats. Their configuration varies, so these are multifocal ectopics.
  24. 24. 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
  25. 25. Ventricular tachycardia: rhythm strip. Typical broad bizarre QRS complexes with a rate of 160/min.
  26. 26. Ventricular tachycardia: fusion beat (arrow). In ventricular tachycardia there is independent atrial and ventricularactivity. Occasionally a P wave is conducted to the ventriclesthrough 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.
  27. 27. Torsades de pointes• VT with polymorphic QRS• Associated with QT prolongation• Hypokalaemia, hypomagnesaemia• Quinidine, phenothiazines, tricyclics, III degree AV block, congenital
  28. 28. Torsades de pointes. A bradycardia with a long QT interval is followed by polymorphic ventriculartachycardia that is triggered by an R on T ectopic.
  29. 29. 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
  30. 30. Ventricular fibrillation. A bizarre chaotic rhythm initiated in this case by two ectopic beats in rapid succession.
  31. 31. 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
  32. 32. First-degree heart block. The PR interval is prolonged and measures 0.26 seconds.
  33. 33. Second-degree atrioventricular block (Mobitz type I- Wenckebachs phenomenon). The PR interval progressively increases until a P wave is not conducted. The cycle thenrepeats itself. In this example, conduction is at a ratio of 4:3,leading to groupings of three ventricular complexes in a row.
  34. 34. Second-degree atrioventricular block (Mobitz type II). The PR interval of conducted beats is normal but some P waves are not conducted. Theconstant PR interval distinguishes this from Wenckebachs phenomenon.
  35. 35. 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
  36. 36. 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.
  37. 37. Right bundle branch block. Note the wide QRScomplexes with M-shaped configuration in leads V1 and V2 and a wide S wave in lead I.
  38. 38. 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.

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