IN THE NAME OF GOD

Ventricular Tachyarrhythmia

Dr Amirhossein Azhari Electrophysiologist

VENTRICULAR TACHYARRHYTHMIAS

VENTRICULAR TACHYCARDIAVENTRICULAR FIBRILLATION

Underlying Arrhythmia of Sudden Death

VT62% Bradycardia

17%

Torsadesde Pointes

13%

PrimaryVF8%

Adapted from Bayés de Luna A. Am Heart J. 1989;117:151-159.

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

Symptoms occurring during VT depend on

The ventricular rate,

Duration of tachycardia,

Presence and extent of the underlying heart disease and peripheral vascular disease.

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

VENTRICULAR TACHYCARDIA

VT

NONSUSTAINED SUSTAINED

NONSUSTAINED VT

Three or more consecutive ventricular premature depolarizations,

up to a maximum duration of 30 seconds before spontaeous termination

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

SUSTAINED VT

MONOMORPHIC UNIFORM

POLYMORPHICMULTIFORM ,PLEOMORPHIC

SUSTAINED VT

IN PATIENTS WITH NORMAL HEARTS

IN PATIENTS WITH ORGANIC HEART DISEASE

VT in normal hearts

1-Idiopathic VT2-long Q-T syndrome3-Brugada syndrome4-Catecholaminergic polymorphic VT5-Short Q-T syndrome

IDIOPATHIC VT

ADENOSINE-SENSITIVE VT

TRIGGERED ACTIVITY

VERAPAMIL-SENSITIVE VT

INTRAFASCICULAR REENTRY

PROPRANOLOL-SENSITIVE VT

AUTOMATICITY

IDIOPATHIC VT

ADENOSINE-SENSITIVE VT

CLINICAL CHARACTERISTICS

THE MOST COMMON FORM OF IDIOPATHIC VT(75-90%)

ORIGINATES FROM RIGHT VENTRICULAR OUTFLOW TRACT

RVOT VT

USUALLY EXHIBITS ONE OF TWO PHENOTYPES

NONSUSTAINED REPETITIVE MONOMORPHIC VT(RMVT)

PAROXYSMAL EXERCISE INDUCED SUSTAINED VT

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

RF ABLATION

Long QT

Acquired

Congenital

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

Electrolyte abnormalities, such as

Hypokalemia and hypomagnesemia;

The effects of a liquid protein diet and starvation;

Central nervous system lesions; significant bradyarrhythmias.

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 Iks 21q22.1-2

LQT6LQT7

MiRP1KCNJ2

Ikr β-subunit

IKl

Ikr

IKl

21q22.117q23

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

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)

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

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.

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

In patients with :

Syncope caused by ventricular arrhythmias or aborted sudden death,

An ICD is warranted

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

Brugada Syndrome

Brugada Syndrome

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

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

VT based on reentry

VT

1 sec

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

VT IN DCM

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

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

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

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

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.

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

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.

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.

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

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

AmiodaroneToxicity– 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)

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

VF

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

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.

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

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

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.

Thanks for your

attention