Life T hreatening Arrhythmia - PowerPoint Presentation

Slide1

Life

T

hreatening Arrhythmia

Slide2

VENTRICULAR

TACHYCARDIA

Slide3

Ventricular tachycardia can be caused by disorders of

impulse formation

(enhanced automaticity or triggered activity) and

conduction

(reentry

).

In

general, the specific type, prognosis, and management of VT depend on the presence of

underying

structural heart disease.

With

the

exception

of patients with inherited

VT

,

if structural heart disease is absent, the prognosis in patients with VT and PVCs is generally very good

,

whereas in those with structural heart disease, the subsequent risk

for SCD is

increased.

Slide4

Electrocardiographic Recognition

The

electrocardiographic

diagnosis

of VT is suggested by the occurrence of a series of

three or more consecutive

, abnormally shaped QRS complexes longer than

120ms,

with the ST-T vector pointing opposite the major QRS deflection.

The

R-R interval can be regular or varying.

Patients

can have VTs with multiple morphologies originating at the same or closely adjacent sites with different exits.

Others

have multiple sites of origin.

Slide5

Atrial

activity can be independent of ventricular activity (

AV dissociation

), or the atria can be depolarized retrogradely

(

VA

association

).

Depending

on the particular type of VT, rates range from 70 to 250 beats/min, and the onset can be

paroxysmal

(sudden) or

nonparoxysmal

.

QRS

contours during the VT can be unchanging (

uniform, monomorphic

) or can vary randomly (

multiform,

polymorphic

)

in a more or less repetitive manner (torsades de pointes), in alternate complexes (

bidirectional VT

), or in a stable but changing contour (i.e., right bundle branch contour changing to a left bundle branch contour).

Slide6

VT

can be

sustained

, defined arbitrarily as lasting longer than 30 seconds or requiring termination because of hemodynamic collapse, or

nonsustained

, when it stops spontaneously in less than 30 seconds.

Slide7

It is important to distinguish

SVT

with aberrancy from VT.

When

the QRS during tachycardia is narrow (≤120

ms

),

SVT is easily diagnosed.

However

, when the QRS during tachycardia is wide (>120

ms

),

electrocardiographic distinction can

be difficult because features of both arrhythmias overlap.

Slide8

Ventricular

complexes with an abnormal and prolonged configuration indicate only that conduction through the ventricle is abnormal, and such complexes can occur in supraventricular rhythms as a result of

preexisting

BBB

,

aberrant conduction during incomplete recovery of repolarization

,

conduction over accessory pathways

, and several other conditions.

Slide9

These complexes do not necessarily indicate the origin of impulse formation or the reason for the abnormal conduction.

Conversely, ectopic beats originating in the ventricle can infrequently have a fairly normal duration and shape.

However

, VT is the most common cause of tachycardia with a wide QRS complex in patients with

a past history of MI or heart failure

.

Slide10

During the course of a tachycardia characterized by wide QRS complexes, the presence of

fusion beats

and

capture beats

provides maximum support for the diagnosis of VT but occurs relatively

infrequently.

Fusion

beats indicate

activation

of the ventricle from two different foci, with the implication that one of the foci had a ventricular origin.

Capture

of the ventricle by the supraventricular rhythm with a normal configuration of the captured QRS

complex

at an interval shorter than the tachycardia in question indicates that the impulse has a supraventricular origin and thus excludes a supraventricular origin of the tachycardia.

Slide11

Slide12

AV

dissociation

has long been considered a hallmark of VT. However, retrograde VA conduction to the atria from ventricular beats occurs in at least 25% of patients, and therefore VT may not exhibit AV dissociation.

AV

dissociation can occur infrequently during SVTs.

Even

if a P wave appears to be related to each QRS complex, it is at times difficult to determine whether the P wave is conducted

anterogradely

to the next QRS complex (i.e., SVT with aberrancy and a long PR interval) or retrogradely from the preceding QRS complex (i.e., a VT).

As

a general rule, however, AV dissociation during tachycardia with a wide QRS complex is strong presumptive evidence that the tachycardia is of ventricular

origin

.

Slide13

Slide14

Differentiation

Between Ventricular and Supraventricular Tachycardia

Slide15

Slide16

Although

fusion

and

capture beats

and

AV dissociation

provide the strongest electrocardiographic evidence for differentiation of VT from SVT with aberrant conduction, these features are not always present.

Slide17

Other clues characterizing

supraventricular arrhythmia with aberrancy

include:

1) consistent

onset of the tachycardia with a

PAC

2

)

very short RP

interval (0.1 second), which often requires an esophageal recording or

invasive EPS

to visualize the P

waves

3

) QRS configuration

the same

as that occurring from known supraventricular conduction at similar

rates

4)

ventricular

activation depends on atrial discharge

(e.g., P-P interval changes preceding and therefore causing subsequent R-R intervals

)

5

) slowing or termination of the tachycardia by

vagal maneuvers

, although vagal maneuvers can terminate right ventricular outflow tract VTs

Slide18

Analysis of specific QRS contours can also be helpful in the diagnosis of VT and

localization

of its site of origin.

For

example, QRS contours suggesting VT include left axis deviation in the frontal plane and a QRS duration exceeding

140ms

with normal duration during sinus

rhythm.

In

precordial leads with an RS pattern, the duration of the onset of the R to the nadir of the S exceeding 100 milliseconds suggests VT as the diagnosis.

Slide19

During

VT with an RBBB

appearance:

the QRS complex

is monophasic or biphasic in V1, with an initial deflection different from that of the sinus-initiated QRS

complex

2

) the amplitude of the R wave in V1 exceeds that of

R′

3

) a small R and large S wave or a QS pattern in V6 may be present.

Slide20

With

a VT having an LBBB

contour:

1) the

axis can be rightward, with negative deflections deeper in V1 than in

V6

2) a

broad prolonged (>

40ms)

R wave can be noted in

V1

3

) a small Q–large R wave or QS pattern in V6 can exist.

A

QRS complex that is similar in V1 through V6, either all negative or all positive favors a ventricular origin, as does the presence of a 2 : 1 VA block.

Slide21

An

upright QRS complex in V1 through V6 can also occur as a result of conduction over a

left-sided accessory

pathway.

Supraventricular

beats with aberration often have a

triphasic

RSR′ pattern in V1, an initial vector of the abnormal complex similar to that of the normally conducted

beats.

Slide22

During

AF:

-fixed coupling

-short

coupling

intervals

-a

long pause after the abnormal

beat

-runs

of

bigeminy

rather than a consecutive series of abnormal complexes

all

favor a ventricular origin of the premature complex rather than a supraventricular origin with aberration.

A

grossly irregular, wide-QRS tachycardia with ventricular rates exceeding 200 beats/min should suggest AF with conduction over an accessory

pathway.

Slide23

Slide24

Slide25

In the presence of a preexisting

BBB,

a wide-QRS tachycardia with a contour different from the contour during sinus rhythm is most likely a VT.

On

the basis of these criteria, several algorithms to distinguish VT from SVT with aberrancy have been

suggested.

Exceptions

exist to all the aforementioned criteria especially in patients with preexisting conduction disturbances or

preexcitation

syndrome; when in doubt,

one must rely on sound clinical judgment

and consider the ECG as only one of several helpful ancillary tests.

Slide26

Slide27

Miller Criteria:

Initial R wave in aVR

→ VT

aVR

with initial r or q >40

ms

in duration → VT

aVR

with a notch on the descending limb of a negative-onset

and

predominantly negative QRS in

aVR

→ VT

In

aVR, mV of initial 40

ms

divided by terminal 40

ms

(vi/

vt

≤1) → VT

Slide28

Slide29

Slide30

Brugada

Criteria:

Absence

of RS complex in all precordial leads → VT

Longest

R/S interval >

100ms

in any precordial lead → VT

AV

dissociation → VT

If

RBBB

morphology:

monophasic

R or

qR

in V1 → VT

R

taller than R′ → VT

rS

in V6 → VT

if

LBBB

morphology:

initial

R >40

ms

in duration → VT

Slurred

or notched S in V1 or V2 → VT

Beginning

Q or QS in V6 → VT

Slide31

The VT origin or exit site can often be determined on the surface

ECG.

VTs

from the

LV

free wall typically exhibit an RBBB contour,

whereas

those from the

RV

or septum have an LBBB

contour.

Septal

VTs typically have narrower QRS complexes than free wall VTs.

Apical

VTs exhibit negative precordial lead concordance, whereas more basal sites typically have positive concordance.

Slide32

VTs from the posterior (inferior) left or right ventricle often have predominantly negative QRS complexes in leads II, III, and

aVF

,

whereas

outflow tract VTs frequently exhibit predominantly positive QRS complexes in these leads.

Epicardial

VTs have a delayed

intrinsicoid

(initial) deflection that slurs the early portion of the QRS complex;

an

intrinsicoid

deflection exceeding 55% of the QRS duration is likely to be

epicardial

.

Slide33

Clinical Features

Symptoms during VT depend on the ventricular

rate

,

duration

of the tachycardia, and the 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); or unstable runs, often resulting in hemodynamic collapse and degenerating into VF.

Slide34

VTs

initially non sustained can later become sustained.

Physical

findings depend in part on the

P-to-QRS

relationship

.

If

atrial activity is dissociated from the ventricular contractions, the findings of AV dissociation are present.

Slide35

Most patients treated for symptomatic recurrent VT have

ischemic heart disease

.

The

next largest group has

cardiomyopathy

,

with lesser percentages divided among those with primary electrical disease such as inherited ion channel

abnormalities,

idiopathic VT, congenital heart disease

,

and miscellaneous causes.

Coronary

artery spasm can cause transient myocardial ischemia with ventricular arrhythmias in some

patien

t

s

,

during ischemia

as well as during the apparent

reperfusion

period

.

Slide36

Many

patients resuscitated from

SCD

have CAD or cardiomyopathy.

Patients

with sustained VT are more likely to have a reduced EF, slowed intraventricular conduction and electrographic abnormalities (e.g., wide QRS), LV aneurysm, and previous MI.

In

patients with CAD, sustained VT displays a circadian variation,

with the peak frequency occurring in the morning

.

Slide37

prognosis

Inducibility

of VT

during

an

EPS

R

educed

LV

function

S

pontaneous

ventricular

arrhythmias

L

ate

potentials on a signal-averaged

ECG

QT-interval dispersion

T

wave

alternans

P

rolonged

QRS

duration

H

eart

rate

turbulence

D

ecreased

heart rate

variability

R

educed

baroreceptor

sensitivity

all

carry increased risk for total mortality and sudden death.

Slide38

Currently

, however, no technique reliably predicts outcome better than assessment of LV function.

LV

function

and

inducibility

of VT during EPS

are the two strongest predictors of a poor outcome.

In

general, the prognosis for patients with idiopathic

VT in

the absence of structural heart disease is good, and less

aggressive

treatment is warranted than for patients with structural heart disease.

Patients

with

inherited arrhythmia syndromes

are an exception to this

statement.

Slide39

Acute Management of Sustained

VT

VT

that does not cause hemodynamic decompensation can be treated medically to achieve acute termination by IV administration of

amiodarone

,

lidocaine

, or

procainamide

, followed by an infusion of the successful drug.

Lidocaine

is often ineffective; amiodarone and procainamide appear to be superior.

Slide40

patients

in whom procainamide is ineffective or may be problematic (severe heart failure, renal failure), IV amiodarone is frequently

effective.

In

general, an initial 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.

Slide41

If the VT does not terminate or if it recurs, a repeated loading dose can be given.

Rarely

, sinus bradycardia or AV block can be seen with IV amiodarone.

The hypotension associated with IV amiodarone does not seem to be a frequent problem and is usually related to the rate of infusion.

Slide42

If the arrhythmia does not respond to medical therapy,

electrical

DC

cardioversion

can be used.

VT

that precipitates hypotension, shock, angina,

CHF,

or symptoms of cerebral

hypoperfusion

should be treated promptly with DC

cardioversion.

Very

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

After

conversion of the arrhythmia to a normal rhythm, it is essential to institute measures to prevent recurrence.

Slide43

When a defibrillator is not readily available, striking the patient’s chest can infrequently terminate the VT.

However

, chest stimulation at the vulnerable period during the arrhythmia can accelerate the VT or possibly provoke VF, so backup defibrillation may be

necessary

.

In

some cases, such as VT associated with a remote MI (

which is caused by reentry

), ventricular

pacing

via a pacing catheter inserted into the

RV

or

transcutaneously

at rates faster than the tachycardia can terminate the tachycardia.

Slide44

This procedure incurs the risk of accelerating the VT to ventricular flutter or VF.

In

patients with recurrent VT,

overdrive

ventricular pacing can be used to prevent recurrences.

Intermittent VT, interrupted by several supraventricular beats, generally is best treated pharmacologically.

Slide45

A search for

reversible conditions

contributing to the initiation and maintenance of VT should corrected, if present.

For

example, VT related to ischemia, hypotension, or hypokalemia can at times be terminated by antianginal treatment, vasopressors, or potassium, respectively.

Correction

of heart failure can reduce the frequency of ventricular arrhythmias.

Slow

ventricular rates caused by sinus bradycardia or AV block can permit the occurrence of PVCs and ventricular

tachyarrhythmias

, which is

corrected by

transvenous

pacing

.

Rarely

,

SVT can initiate ventricular

tachyarrhythmias

and should be prevented if this is the observed mechanism of VT initiation.

Slide46

Long-Term Therapy for Prevention of Recurrences

Because

the goal of long-term therapy is to prevent SCD and recurrence of symptomatic VT, asymptomatic

nonsustained

ventricular arrhythmias in low-risk populations (i.e., preserved LV function) often need not be treated.

In

patients with

symptomatic

nonsustained

tachycardia, beta blockers may prevent recurrences.

In

patients refractory to beta blockers, class IC agents

sotalol

, or amiodarone can be effective.

Slide47

Sotalol

should be used cautiously because of its potential for prolonging the QT interval and producing torsades de pointes.

Patients

with

nonsustained

VT after MI and poor LV function are at significant risk for sudden death.

Slide48

For secondary prevention of sustained VT or cardiac arrest in patients with structural heart disease class I antiarrhythmic drugs (AADs) produce a worse outcome than do class III

AADs,

and ICDs provide better survival than amiodarone, particularly in patients with an LVEF less than

35%.

Therefore

, in patients who have survived cardiac arrest or who have sustained VT resulting in hemodynamic compromise and poor LV function an

ICD is the treatment of

choice

.

Slide49

In

patients who refuse an ICD, empiric amiodarone may be the next best

therapy

, although no reduction in mortality was found in SCD-

HeFT

.

The

optimal therapy for patients with CAD who have preserved LV function with sustained VT is not currently known.

Empiric

amiodarone appears to be the safest

therapy,

and ablation of monomorphic VT may be effective and preferable long-term

.

Slide50

Some patients who receive ICDs experience frequent shocks because of recurrent VT.

In

these patients, concomitant therapy with amiodarone or VT ablation may be required to reduce the frequency of VT or to slow the rate of the VT so that it can be pace-terminated.

Other drugs, such as

sotalol

, procainamide,

mexiletine

, and flecainide, may be required if amiodarone is not effective.

Slide51

On occasion, a combination of drugs can be effective when a single drug is not.

Ablation

can also be considered in this situation.

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.

In

addition, because of the significant mortality associated with these arrhythmias in patients with structural heart disease and depressed LV function, ablation is generally used as an adjunct to ICD placement to reduce the frequency of VT and ICD

shocks.

Slide52

However, in patients with well tolerated

postinfarction

VT and well-preserved LV function, or in patients refractory to drugs, ablation can be used as first-line therapy.

In patients with VT or VF, prophylactic ablation of the VT substrate can reduce future shocks.

Slide53

Specific Types of Ventricular Tachycardia

Slide54

Torsades de Pointes Electrocardiographic

Recognition

The

term torsades de pointes (TdP) refers to a VT characterized by QRS complexes of changing amplitude that appear to twist around the isoelectric line and occur at rates of 200 to 250 per

minute.

Originally

described in the setting of bradycardia caused by

CHB,

TdP usually connotes

a syndrome

, not simply an electrocardiographic description of the QRS complex of the tachycardia, characterized by prolonged ventricular repolarization with QT intervals generally exceeding 500

ms

.

The

U wave can also become prominent and merge with the T wave, but its role is not clear.

Slide55

Slide56

Relatively

late PVCs can discharge during termination of the long T wave and precipitate successive bursts of VT, during which the peaks of QRS complexes appear successively on one side and then on the other side of the isoelectric baseline; these peaks give the

typical twisting appearance

with continuous and progressive changes in QRS contour and

amplitude

.

Slide57

VT

that is similar morphologically to TdP and occurs in patients without QT prolongation, whether spontaneous or electrically induced, should generally be classified as

polymorphic VT, not as TdP

.

The

distinction has important therapeutic

implications.

Slide58

Electrophysiologic

Features

The

electrophysiologic

mechanisms responsible for TdP are not completely understood. Most data suggest that

EADs

are responsible

for

both long-QT syndrome and TdP, or at least its

initiation.

Perpetuation

can be caused by triggered activity, reentry resulting from dispersion of repolarization produced by the EADs, or abnormal automaticity.

However

, most data currently point to transmural

reentry

as the most likely mechanism of perpetuation.

Slide59

Clinical features depend on whether the TdP is caused by

acquired

or

congenital

(idiopathic)

lQT

syndrome.

Symptoms

from the tachycardia depend on its rate and duration, as with other VTs, and range from palpitations to syncope and death.

Women

, perhaps because of a longer QT interval, are at greater risk than men for TdP.

Slide60

Management

The

approach to management of VT with a polymorphic pattern depends on

whether it occurs in the setting of a prolonged QT interval.

For

this practical reason, and because the mechanism of the tachycardia can differ according to whether a long QT interval is present it is important to restrict the definition of torsades de pointes to the typical

polymorphic

VT in the setting of a long QT or U wave in the basal complexes.

In

all patients with TdP, administration of class IA, possibly some class IC, and class III AADs (e.g., amiodarone,

dofetilide

,

sotalol

) can increase the abnormal QT interval and worsen the arrhythmia.

Slide61

F

or

TdP from an acquired

cause:

IV

magnesium

is the initial treatment of choice

,

followed by temporary ventricular or atrial pacing.

Isoproterenol

, given cautiously because it may exacerbate the arrhythmia, can be used to increase the rate until pacing is instituted.

Lidocaine

,

mexiletine

, or

phenytoin

can be tried.

The

cause of the long QT should be determined and corrected, if possible.

Slide62

When the QT interval is normal,

polymorphic VT resembling TdP is diagnosed

, and

standard AADs

can be prescribed.

In

borderline cases the clinical context may help determine whether treatment should be initiated with AADs.

Slide63

For Torsades

de pointes resulting from congenital L

QT syndrome:

B

eta blockade

Pacing

ICDs

ECGs obtained from close relatives can help secure the diagnosis of long-QT syndrome in borderline cases.

Slide64

VENTRICULAR FLUTTER AND FIBRILLATION

Electrocardiographic Recognition

Ventricular

flutter and

VF

are arrhythmias that represent severe derangements of the heartbeat that can terminate fatally or produce significant brain damage within 3 to 5 minutes unless corrective measures are undertaken

promptly.

Ventricular

flutter is manifested as a sine wave in appearance—regular large oscillations occurring at a rate of 150 to 300 beats/min (usually about 200

).

Distinction

between

rapid VT

and

ventricular flutter

can be difficult and is usually of academic interest only

.

Hemodynamic

collapse is present with both.

Slide65

Slide66

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.

Slide67

Slide68

Mechanisms

VF occurs

in various clinical situations but most often in association with CAD and as a terminal

event.

Cardiovascular

events, including SCD from VF, occur most frequently

in the morning

.

VF

can occur during AAD administration, hypoxia, ischemia, or AF that results in very rapid ventricular rates in patients with

preexcitation

syndrome; after electrical shock administered during

cardioversion

or accidentally by improperly grounded equipment; and during competitive ventricular pacing to terminate VT.

Slide69

Clinical Features

Ventricular

flutter or VF results in faintness, followed by loss of consciousness, seizures, apnea, and eventually, if the rhythm continues untreated, death.

Blood

pressure is unobtainable, and heart sounds are usually absent.

The

atria can continue to beat at an independent rhythm for a time or in response to impulses from the fibrillating ventricles. Eventually, electrical activity of the heart

ceases.

Slide70

Management

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, ventricular flutter, and pulseless VT.

Cardiopulmonary

resuscitation is performed only until the defibrillation equipment is ready or if the “downtime” has been long.

Defibrillation

requires fewer joules if it is done early. If the circulation is markedly inadequate despite return to sinus rhythm, closed-chest massage should be instituted.

Slide71

The use of anesthesia during electrical shock is dictated by the patients condition but is not generally required.

After

conversion of the arrhythmia to a normal rhythm, it is essential to monitor the rhythm continuously and to institute measures to prevent recurrence.

Metabolic

acidosis quickly follows cardiovascular

collapse

.

If

the arrhythmia is terminated within 30 to 60 seconds, significant acidosis does

not

occur.

Slide72

Slide73