VENTRICULAR TACHYCARDIA 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 ID: 775334
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Slide1
Life
T
hreatening Arrhythmia
Slide2VENTRICULAR
TACHYCARDIA
Slide3Ventricular 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.
Slide4Electrocardiographic 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.
Slide5Atrial
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).
Slide6VT
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.
Slide7It 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.
Slide8Ventricular
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.
Slide9These 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
.
Slide10During 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.
Slide11Slide12AV
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
.
Slide13Slide14Differentiation
Between Ventricular and Supraventricular Tachycardia
Slide15Slide16Although
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.
Slide17Other 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
Slide18Analysis 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.
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.
Slide20With
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.
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.
Slide22During
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.
Slide23Slide24Slide25In 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.
Slide26Slide27Miller 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
Slide28Slide29Slide30Brugada
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
Slide31The 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.
Slide32VTs 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
.
Slide33Clinical 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.
Slide34VTs
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.
Slide35Most 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
.
Slide36Many
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
.
Slide37prognosis
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.
Slide38Currently
, 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.
Slide39Acute 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.
Slide40patients
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.
Slide41If 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.
Slide42If 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.
Slide43When 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.
Slide44This 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.
Slide45A 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.
Slide46Long-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.
Slide47Sotalol
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.
Slide48For 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
.
Slide49In
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
.
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.
Slide51On 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.
Slide52However, 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.
Slide53Specific Types of Ventricular Tachycardia
Slide54Torsades 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.
Slide55Slide56Relatively
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
.
Slide57VT
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.
Slide58Electrophysiologic
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.
Slide59Clinical 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.
Slide60Management
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.
Slide61F
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.
Slide62When 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.
Slide63For 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.
Slide64VENTRICULAR 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.
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.
Slide67Slide68Mechanisms
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.
Slide69Clinical 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.
Slide70Management
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.
Slide71The 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.
Slide72Slide73