1. IN THE NAME OF GOD

2. Ventricular Tachyarrhythmia
Dr Amirhossein Azhari
Electrophysiologist

3. VENTRICULAR TACHYARRHYTHMIAS
VENTRICULAR TACHYCARDIA
VENTRICULAR FIBRILLATION

4. Underlying Arrhythmia of Sudden Death
Primary VF 8%
Torsades
de Pointes
13% VT
62%
Bradycardia
17%
Adapted from Bayés de Luna A. Am Heart J ;117:

5. DEFINITION
Occurrence of a series of three or more consecutive abnormaly shaped premature ventricular complexes,
WHOSE DURATION EXCEEDS 120 ms,
With the ST-T vector pointing opposite the major QRS deflection

7. Symptoms occurring during VT depend on
The ventricular rate,
Duration of tachycardia,
Presence and extent of the underlying heart disease and peripheral vascular disease.

8. VT can occur in several forms:
Short, asymptomatic, Nonsustained episodes;
Sustained,
Hemodynamically stable events, generally occurring at slower rates or in otherwise normal hearts;
Unstable runs, often degenerating into VF

9. VENTRICULAR TACHYCARDIAVT
NONSUSTAINED
SUSTAINED

10. NONSUSTAINED VT
Three or more consecutive ventricular premature depolarizations,
up to a maximum duration of 30 seconds before spontaeous termination

11. Importance of NSVT
Most tachyarrhythmias come to our attention because of the symptoms they produce
In contrast,most instances of NSVT do not cause symptoms
Rather it derives its importance from the prognostic significance it carries in some patient populations

12. SUSTAINED VT
MONOMORPHIC
UNIFORM
POLYMORPHIC
MULTIFORM ,PLEOMORPHIC

13. IN PATIENTS WITH NORMAL HEARTS
SUSTAINED VT
IN PATIENTS WITH
ORGANIC HEART DISEASE
IN PATIENTS WITH NORMAL HEARTS

14. VT in normal hearts 1-Idiopathic VT 2-long Q-T syndrome
3-Brugada syndrome
4-Catecholaminergic polymorphic VT
5-Short Q-T syndrome

15. IDIOPATHIC VT PROPRANOLOL ADENOSINE -SENSITIVE VT -SENSITIVE VT
AUTOMATICITY
ADENOSINE
-SENSITIVE VT
TRIGGERED ACTIVITY
VERAPAMIL
-SENSITIVE VT
INTRAFASCICULAR
REENTRY

16. IDIOPATHIC VT

17. ADENOSINE-SENSITIVE VT
CLINICAL CHARACTERISTICS
THE MOST COMMON FORM OF IDIOPATHIC VT(75-90%)
ORIGINATES FROM RIGHT VENTRICULAR OUTFLOW TRACT

18. USUALLY EXHIBITS ONE OF TWO PHENOTYPES
RVOT VT
USUALLY EXHIBITS ONE OF TWO PHENOTYPES
NONSUSTAINED REPETITIVE MONOMORPHIC VT(RMVT)
PAROXYSMAL EXERCISE INDUCED SUSTAINED VT

19. THERE IS A CONSIDERABLE OVERLAP BETWEEN THESE TWO PHENOTYPES OF ADENOSINE-SENSITIVE RVOT VT

20. RF ABLATION

21. Long QT
Acquired
Congenital

22. The acquired form has a long-QT interval caused by various drugs, such as
Quinidine, procainamide, sotalol, amiodarone, disopyramide, phenothiazines, tricyclic antidepressants, erythromycin, pentamidine, antimalarials, cisapride, and probucols

23. Electrolyte abnormalities, such as
Hypokalemia and hypomagnesemia;
The effects of a liquid protein diet and starvation;
Central nervous system lesions; significant bradyarrhythmias.

24. GENETIC BASIS OF LONG QT SYNDROME
DESIGNATION
GENE
GENE PRODUCT
ION CHANNEL
CHROMOSOME LOCUS
LQT1
KvLQT1
Iksα-subunit
Iks
11p15.5
LQT2
HERG
Ikr α-subunit
Ikr
7q35-36
LQT3
SCN5A
Na+ channel unit
INa
3q21-24
LQT4
ANKB
Ankyrin-B -
4q25-27
LQT5
Mink
Iks β-subunit
21q22.1-2
LQT6
LQT7
MiRP1
KCNJ2
Ikr β-subunit
IKl
21q22.1
17q23

25. CLINICAL MANIFESTATIONS
The principal symptoms are syncope and SCD,from TDP
Most often,TDP is self-terminating and cause a syncopal episode from which the patient quickly recovers
Cardiac arrest occurs if the TDP is more persistent,and SCD results if the rhythm does not return to normal spontaneously

26. QT Duration
A widely accepted method for correcting QT interval for rate is Bazett’s formula
Lead II is generally the best single lead for measuring QT interval.
Traditionally, QTc >440 msec were considered prolonged; however, values up to 460 msec may still be normal among females
Affected gene carriers can have a QTc of 410 msec or less and no normal person has a QTc of 470 or more (men) or 480 or more (women)

27. ECG MANIFESTATIONS
A QTC of 0.47 sec in men and 0.48 sec in women is 100% sensitive for LQTS
A QTC less than 0.40 sec in men and 0.42 sec in women is 100% specific for excluding LQTS

29. Treatment
Intravenous magnesium is the initial treatment of choice for torsades de pointes from an acquired cause, followed by temporary ventricular or atrial pacing.
In all patients with torsades de pointes, administration of class IA, possibly some class IC, and class III antiarrhythmic agents ( amiodarone, dofetilide, sotalol) can increase the abnormal QT interval and worsen the arrhythmia.

30. For patients who have idiopathic long-QT syndrome but
Not syncope,
Complex ventricular arrhythmias,
A family history of sudden cardiac death,
QTc no longer than 500 milliseconds
No therapy or treatment with a beta blocker is generally recommended

31. In patients with :
Syncope caused by ventricular arrhythmias or aborted sudden death,
An ICD is warranted

32. Brugada Syndrome
Brugada syndrome is a distinct form of idiopathic VF in which patients have right bundle branch block and ST-segment elevation in the anterior precordial leads, without evidence of structural heart disease
Mutations in genes responsible for the sodium channel (SCN5A) and calcium channel have been identified in many families with Brugada syndrome

33. Brugada Syndrome

34. Brugada Syndrome

35. Currently, no pharmacologic treatment reliably prevents VF in these patients. ICDs are the only effective treatment to prevent sudden death

37. Ischemic Cardiomyopathy
Patients with previous myocardial infarction are at risk for development of VT. In the setting of a remote myocardial infarction, the mechanism of VT is reentry, involving the infarct scar and in particular the border zone or other areas of the scar with deranged conduction. As a result, the VT in this setting is typically monomorphic

38. VT based on reentry

39. VT
1 sec

40. In general, ICDs are indicated to prevent sudden cardiac death from VT in this group of patients, especially in those with depressed LV function

41. VT IN DCM
BUNDLE BRANCH REENTRY MAY BE SEEN IN THIS POPULATION AND CAN BE TREATED BY ABLATING THE RBB

42. Pathology
Gross heart specimen from a patient with HCM showing characteristic asymmetric pattern of left ventricular hypertrophy with the ventricular septum (VS) bulging into the left ventricular cavity and thickened to a greater extent than the left ventricular free wall (FW).

43. RISK FACTORS FOR SCD IN HCM
VT IN HCM
RISK FACTORS FOR SCD IN HCM
CARDIAC ARREST(VF)
SUSTAINED VT
SYNCOPE PARTICULARLY IF RECURRENT AND EXERTIONAL
FAMILIAL SUDDEN HCM- RELATED DEATH IN FIRST DEGREE RELATIVES
NSVT ON HOLTER FREQUENT,REPETITIVE AND PROLONGED
ABNORMAL BP RESPONSE IN EXERCISE >20 mm HG
EXTREME LV HYPERTROPHY >30 mm

44. Acute Management of Sustained Ventricular Tachycardia
VT that does not cause hemodynamic decompensation can be treated medically to achieve acute termination by the intravenous administration of amiodarone, lidocaine, or procainamide, followed by an infusion of the successful drug

45. In general, amiodarone
loading dose of 15 mg/min is given during a 10-minute period.
This dose is followed by an infusion of 1 mg/min for 6 hours and then
a maintenance dose of 0.5 mg/min for the remaining 18 hours and for the next several days, as necessary

46. If the arrhythmia does not respond to medical therapy
Hypotension,Shock
Angina,
Congestive heart failure
Symptoms of cerebral hypoperfusion should be treated promptly with DC cardioversion.

47. Very low energies can terminate VT, beginning with a synchronized shock of 10 to 50 J.

48. The goal of long-term therapy is to prevent sudden cardiac death and recurrence of symptomatic VT.
Asymptomatic nonsustained ventricular arrhythmias in low-risk populations (preserved LV function) often need not be treated.
In patients with symptomatic nonsustained tachycardia, beta blockers are frequently effective in preventing recurrences.

49. In patients refractory to beta blockers, class IC agents, sotalol, or amiodarone can be effective.
However, class IC agents should be avoided in patients with structural heart disease, especially those with coronary artery disease because of the increased mortality associated with these drugs caused by proarrhythmia.

50. Sotalol should be used cautiously because of its potential for prolonging the QT interval and producing torsades de pointes.
Patients with nonsustained VT after myocardial infarction and poor LV function are at significant risk for sudden death

51. In patients who have survived a cardiac arrest or who have sustained VT resulting in hemodynamic compromise and poor LV function, an ICD is the treatment of choice.
In patients who refuse an ICD, empiric amiodarone may be the next best therapy

52. Amiodarone Toxicity Pulmonary fibrosis Hypo- or hyper-thyroidism
Liver failure
Bone marrow suppression
Renal failure
Photosensitivity
Corneal deposits
Side effects
Myalgias
Gait disturbance
Insomnia
Prolongation of coagulation time (PT) (need to reduce coumadin dosage)
Digoxin toxicity (need to reduce digoxin dosage)

53. Although RF ablation of certain types of idiopathic VT is very effective, ablation for postinfarction VT or that associated with dilated cardiomyopathy is somewhat less effective

54. VF
These arrhythmias represent severe derangements of the heartbeat that usually terminate fatally within 3 to 5 minutes unless corrective measures are undertaken promptly.

55. VF is recognized by the presence of irregular undulations of varying contour and amplitude . Distinct QRS complexes, ST segments, and T waves are absent.
Fine-amplitude fibrillatory waves (0.2 mV) are present with prolonged VF. These fine waves identify patients with worse survival rates and are sometimes confused with asystole.

56. VF occurs in various clinical situations but most commonly in association with coronary artery disease and as a terminal event
Ventricular flutter or VF results in faintness, followed by loss of consciousness, seizures, apnea, and eventually, if the rhythm continues untreated, death

57. In patients resuscitated from out-of-hospital cardiac arrest,
75% have VF.
Bradycardia or asystole, which can occur in 15% to 25% of these patients, is associated with a worse prognosis than VF and is usually associated with more advanced LV dysfunction

58. Management should follow
basic life support and
advanced cardiac life support guidelines.
Immediate nonsynchronized DC electrical shock using 200 to 400 J is mandatory therapy for VF and for ventricular flutter that has caused loss of consciousness.

59. Thanks for your
attention