Ventricular Arrhythmias

1. Ventricular Arrhythmias Claire B. Hunter, M.D.

2. Objectives • To know the implication and management of PVC • To know the diagnosis and acute treatment of VT and VF • To know the common etiologies of Torsades de pointes • To understand the implication of accelerated ventricular rhythm • To know the major indications of implantable cardioverter-defibrillators (ICD)

3. Origin of Ventricular Arrhythmias

4. Normal Action Potential

5. Action Potential – ECG Correlation

6. Mechanisms of Cardiac Arrhythmias • Abnormal impulse formation • Increased normal automaticity • Abnormal automaticity • Triggered activity due to early afterdepolarization (EAD) • Triggered activity due to delayed afterdepolarization (DAD) • Abnormal impulse conduction • reentry

7. Increased Automaticy

8. Abnormal Automaticity

9. Early Afterdepolarization (EAD) Stim. Triggered activities Stim.

10. Delayed Afterdepolarization (DAD) Triggered activities

11. Reentry Simple reentry Figure of 8 reentry

12. Premature Ventricular Contraction (PVC): ECG coupling interval Compensatory pause (2100 ms) Full compensation (2100 ms)

13. PVC Bigeminy v v v v v v v

14. PVC Trigeminy v v v v

15. PVC Couplet

16. Polymorphic PVCs PVC A PVC B

17. Interpolated PVC

18. Parasystole

19. Premature Ventricular Complex (PVC) • Prevalence: PVC is the most common cardiac arrhythmia, observed in about 50% of healthy medical students, 60% of healthy adult male, and 80% of patients with previous MI. • Mechanism: Probably reentry in majority, increased automaticity in some (parasystole). The role of triggered activities remains uncertain.

20. PVC: Etiology • No identifiable heart diseases in many patients. • Some known causes: ischemia, myocarditis, cardiomyopathy, some medications, conditions associated with increased blood catecholamines, alcohol, caffeine, and others.

21. PVC: Clinical Presentation • Most patients have no symptoms. • In symptomatic patients, it is mostly reported as “skipped heart beats”, or “irregular heart beats” – palpitation.

22. PVC: Implications • PVC alone may not indicate heart diseases or cause heart damage. • Frequent PVCs are associated with an increased mortality in patients with cardiac dysfunction – a risk marker. • PVCs may trigger VT or VF in some patients with underlying heart diseases.

23. PVC: Evaluation • Careful history and physical examination are generally sufficient to rule out significant cardiovascular diseases. • ECG is important to correlate symptoms with PVCs. • PVC frequency may increase or decrease during exercise.

24. PVC: Treatment • Reassurance: the treatment of choice. • Drug therapy: only for a few patients with severe symptoms that are persistent after reassurance. Low dose -blocker is the first line drug. • Goal of therapy: to improve symptoms, not to eliminate PVCs. • Suppression of PVCs by class I antiarrhythmic drugs in patients with MI and LV dysfunction may increase mortality!

25. CAST (Cardiac Arrhythmia Suppression Trial) • Study patients: post MI, left ventricular dysfunction, frequent PVCs that were suppressed by flecainide or encainide. • Randomization: flecainide/encainide vs. placebo • Result: The flecainide/encainide group had a higher mortality than the placebo group!

26. Ventricular Tachycardia (VT): Definitions • VT: ectopic ventricular rhythm >100 bpm. • Monomorphic VT: QRS morphology remains the same. • Polymorphic VT: QRS morphology changes. • Sustained VT: VT duration  30 sec or requires immediate intervention because of hemodynamic instability. • Nonsustained VT: VT from 3 beats to 30 sec.

27. MonomorphicVT: Etiologies • Coronary disease is the most common cause, particularly after MI. Acute ischemia is unlikely the direct cause of monomorphic VT. • Any other heart diseases that are associated with myocardial scar or slow conduction (cardiomyopathy, RV dysplasia, valvular disease, congenital heart disease). • Idiopathic in a small number of patients w/o structural heart disease (RV outflow tract VT, idiopathic left ventricular VT).

28. VT mechanism - reentry

29. Monomorphic VT: Presentation • Symptoms are variable, from palpitation to syncope or cardiac arrest. Dizziness and dyspnea are common. • Blood pressure can be normal, reduced or un-measurable. • Heart rate can vary from 100 to 300 beat/minute.

30. Monomorphic VT: Diagnosis • ECG is very useful. The major challenge is to differentiate VT from SVT with bundle branch block (BBB) or aberrancy. • Evidences supporting VT: • A-V dissociation or fusion beats • Positive or negative concordance on V1 to V6. • “Pseudo-delta waves”

31. VT - AV Dissociation &Negative Concordance

32. VT - Positive Concordance

33. VT - Pseudo-delta Waves

34. MonomorphicVT: Treatment • Stable: iv antiarrhythmic drug  DC cardioversion if drug fails. • Unstable (hypotension or pulmonary edema): DC cardioversion first  iv antiarrhythmic drug  repeat DC cardioversion if VT recurs.

35. Example of VT Cardioversion shock Never shock an awake patient!

36. VT Treatment: Antiarrhythmic drugs • Drugs: lidocaine, procainamide, amiodarone. First choice varies according to patient profile and physician preference but lidocaine is no longer recommended as the first choice. • Lidocaine (class Ib): fast action but not very effective. Acute side effects mainly neurological. • Procainamide (class Ia): fast action and quite effective. Acute side effects mainly hypotension. • Amiodarone (class III): very slow action but very effective. Acute side effects mainly hypotension. • Avoid iv verapamil or diatilzem

37. Ventricular Fibrillation (VF) • VF: sustained, rapid (>300 bpm) and irregular ventricular rhythm. • Venticular flutter (VFL): sustained, rapid (>300 bpm) and regular ventricular rhythm. • VFL and rapid sustained monomorphic VT are arbitrarily defined. • Sustained polymorphic VT and VF are also arbitrarily defined. • VF is the most important cause of sudden death!

38. Example of VF

39. VF: Etiologies • Any terminal disease • Ischemia, myocarditis, cardiomyopathy. • Electrolyte or metabolic disturbances, drugs. • Electrocution/trauma. • Genetic disorders (Brugada syndrome) • Others

40. VF: Mechanism

41. Management of VF • Shock ASAP! • Asynchronized DC shocks • CPR (cardiopulmonary resuscitation) while waiting for shocks. • Search and treat underlying etiologies after successful defibrillation.

42. Example of Ventricular Defibrillation Shock

43. Nonsustained VT with normal QT

44. Nonsustained VT with Normal QT • Presentation: • No symptoms • Palpitation • Dizziness • Syncope

45. Nonsustained VT with Normal QT: Management • Search and treat underlying etiology • Asymptomatic with LV dysfunction: refer for consideration of implantable cardioverter-defibrillator (ICD) for prevention of sudden death. • Asymptomatic with normal LV function: follow-up only. • Symptomatic with normal LV function: antiarrhythmic drugs for symptom relief.

46. Nonsustained VT with QT prolongation (Torsades de pointes) R on T Recorded 10 minutes after iv ibutilide 1 mg for atrial fibrillation conversion.

47. Nonsustained VT with QT prolongation (Torsades de pointes) 29F, alcoholic, K2.9.

48. Nonsustained VT with QT prolongation (Torsades de pointes) 90F, sinus node dysfunction.

49. Treatment of Torsades de pointes • Search and treat etiology • KCl:only slow iv infusion is allowed, unlikely to see immediate effect. • MgSO4:1 g iv over 2-5 min, may repeat 1 dose, may see immediate effect. • Isoproterenol:Start from 1 mcg/patient/min, titrate up (1 mcg increment) until VT suppression, or 5 mcg/patient/min. A HR up to 120 bpm may be necessary to suppress VT. Never use this drug if you are not sure if the VT is true torsade de pointe! • Overdrive pacing

50. Example of torsades de pointes suppression By Overdrive Pacing