Dr nigat

A widened QRS (≥120 msec)- occurs when ventricular
activation is abnormally slow, most commonly because
the arrhythmia originates outside of the normal
conduction system (eg, ventricular tachycardia), or
because of abnormalities within the His-Purkinje
system (eg, supraventricular tachycardia with
aberrancy) or pre-excitation with SVT.
.WCTs most often result from:
-ventricular tachycardia (VT)
-SVT with aberrant conduction
-SVT with pre-excitation
-SVT with ventricular pacing
-some types of artifact mimicking WCT

A wide complex tachycardia that is regular could
be Vtach, SVT with aberrancy, pre-excited
tachycardia or a v-paced rhythm. A wide complex
tachycardia that is irregular may be atrial
fibrillation with aberrancy, pre-excited atrial
fibrillation, polymorphic vtach or torsades de
pointes.

Diagnosing the WCT is difficult — Although most
WCTs are due to ventricular tachycardia (VT), the
differential diagnosis includes a variety of
supraventricular tachycardias (SVTs). Diagnostic
algorithms are complex and imperfect.
Urgent therapy is often required — Patients may
be unstable at the onset of the arrhythmia or
deteriorate rapidly at any time. Therapeutic
decisions are further complicated by the risks
associated with giving therapy for an SVT to a
patient who actually has VT.

Much less common are pre-excited tachycardias; -
---these are supraventricular tachycardias with
antegrade conduction over an accessory pathway
into the ventricle. This only occurs in a minority of
patients with pre-excitations syndromes (Wolff-
Parkinson-White Syndrome).
There is no single criterion or combination of
criteria that provides complete diagnostic
accuracy in evaluating a WCT.

VT accounts for up to 80 percent of cases of WCT
in unselected populations, and more than 90
percent of cases in patients with a prior
myocardial infarction (MI).
Treatment of VT as if it were SVT (eg, adenosine ,
calcium channel blockers, or beta blockers), which
can precipitate cardiac arrest in patients with VT.
Treatment of SVT as if it were VT (eg, with IV
amiodarone , procainamide , lidocaine , or
external countershock) is safe and frequently
effective in restoring sinus rhythm.

The presence of hemodynamic stability should not be
regarded as diagnostic of SVT. VTs usually originate
within the ventricular myocardium, outside of the
normal conduction system. Compared to a normally
conducted supraventricular beat, ventricular activation
during VT is slower and proceeds in a different
sequence. Thus, the QRS complex is wide and
abnormal . As there may be slight changes of the
activation sequence during the VT, reflecting the
abnormal pathway of impulse conduction, there may
be subtle changes in QRS complex morphology of in the
ST-T waves.

VT may be either monomorphic (having a uniform and a
fairly stable QRS morphology during an episode) or
polymorphic (having a continuously varying QRS complex
morphology and/or axis during an episode).
Supraventricular tachycardia — When an SVT conducts
to the ventricles via the normal atrioventricular (AV)
node and His-Purkinje system, the activation wavefront
spreads quickly through the ventricles and the QRS is
usually narrow. However, any SVT (eg, atrial tachycardia,
atrial fibrillation, atrial flutter, or an atrioventricular nodal
reentrant tachycardia) can also produce a widened QRS
by a number of mechanisms.

1) Aberrant conduction — The conduction of a
supraventricular impulse can be delayed or blocked in
the bundle branches or in the distal Purkinje system,
resulting in a wide, abnormal QRS. This phenomenon is
referred to as aberrancy. Aberrant conduction is the
most common reason for a widened QRS during an SVT,
but an aberrantly conducted SVT is still much less
common than VT. In some cases, the baseline ECG
during sinus rhythm will have a left bundle branch
block (LBBB), right bundle branch block (RBBB), or a
nonspecific intraventricular conduction delay.

In such patients any SVT will have a widened QRS. Thus,
if time allows, review of a baseline ECG can be helpful
in differentiating VT from SVT with aberrancy.
Alternatively, conduction may be normal during sinus
rhythm but aberrant during the tachycardia. There are
several reasons why this might occur. The most
common is rate-related aberration (functional bundle
branch block), in which rapidly generated impulses
reach the conducting fibers before they have fully
recovered from the previous impulse. Such a delay in
recovery may be the result of underlying disease of the
His-Purkinje system, hyperkalemia, or the actions of
antiarrhythmic drugs, particularly the class IC agents
(eg, flecainide , propafenone ).

2)Pre-excitation syndrome — In the pre-
excitation syndromes, AV conduction can occur over
the normal conduction system and also via an
accessory AV pathway . These two pathways create the
anatomic substrate for a reentrant circuit, facilitating
the development of a circus movement or reentrant
tachycardia known as AV reentrant tachycardia (AVRT).
AVRT can present with a narrow or a wide QRS
complex:
If antegrade conduction to the ventricles occurs over
the AV node and retrograde conduction back to the
atria is over the accessory pathway, the QRS complex
will be narrow. This narrow complex AVRT is known as
an orthodromic AVRT

if antegrade conduction occurs over an accessory
pathway and retrograde conduction occurs over
the AV node or a second accessory pathway, the
QRS complex will be wide. This is known as an
antidromic AVRT .
Antidromic AVRT is a relatively uncommon cause
of WCT . It is difficult to differentiate from VT,
because ventricular activation starts outside the
normal intraventricular conduction system in both
types of tachycardia.

In addition, patients with an accessory pathway may
develop a different SVT (eg, atrial tachycardia, atrial
fibrillation, or atrial flutter). In such cases, the QRS
could be either narrow or wide, depending upon
whether ventricular activation occurs over the normal
conduction system, the accessory pathway, or both.
Pacemakers and defibrillators — When the
ventricles are activated by a pacing device, the QRS
complex is generally wide. Most ventricular pacemakers
pace the right ventricular apex, causing a wide QRS complex of
the LBBB type. Most importantly, there is a broad R wave in lead
I, which is an R to L bipolar lead. Impulses directed toward the
left produce a positive deflection.

Pacemakers used in cardiac resynchronization
therapy (CRT) usually pace both ventricles.
Although CRT generates a QRS complex that is
narrower than the patient's baseline (a chronically
widened QRS is one of the components of the
indication for CRT), it is still usually longer than
120 msec. The important finding indicating CRT is
the presence of a Q wave or QS complex in lead I,
indicating activation going from left to right. Most
contemporary ICDs also have pacemaker (or CRT)
capabilities; pacing will create a wide QRS
complex similar to those devices.

Recognizing that a QRS complex is due to
ventricular pacing can be challenging, particularly
during a tachycardia. In addition to characteristic
QRS morphology, a pacing "spike" or stimulus
artifact can often be identified. The stimulus
artifact is a narrow electrical signal too rapid to
represent myocardial depolarization. With
unipolar pacemakers (more common in older
devices), the spike is large and easily seen.
However, bipolar pacemakers produce a smaller
stimulus artifact, which is often difficult to detect
on the surface ECG.

Thus, the presence of the pacemaker, if not
known from the patient's history and physical
examination, may not always be identifiable by
examination of the ECG alone. Among patients
with a pacemaker or an ICD, further possibilities
need to be considered in addition to the usual
differential diagnosis of a WCT. In the presence of
sinus tachycardia or some SVTs (eg, an atrial
tachycardia, atrial flutter, or atrial fibrillation), the
device may "track" the atrial impulse and pace
the ventricle at the rapid rate, resulting in a WCT.

However, two features of device programming reduce
the likelihood of this occurring. First, most devices are
programmed to "track" atrial activity only up to a
certain heart rate (usually 120 to 130 beats per
minute). At faster atrial rates, the ventricle will usually
be paced at the upper programmed limit, but below
the atrial rate, and AV dissociation may be detected.
Second, most pacemakers recognize very fast atrial
rates as abnormal, and will automatically switch to a
mode that does not track such rates.

A WCT can result if ventricular paced beats are
conducted retrograde (backward) through the AV
node to the atrium, resulting in an atrial signal,
which the pacemaker senses and tracks with
another ventricular stimulus. This ventricular
paced beat is also conducted retrograde, and the
cycle repeats indefinitely, a process termed
pacemaker mediated tachycardia or endless loop
tachycardia. The first priority when evaluating a
patient with a WCT is an assessment of patient
stability.

Assessment of stability — Immediate
assessments of the patient's vital signs and the
level of consciousness are of primary importance.
Stable — This refers to a patient showing no
evidence of hemodynamic compromise despite a
sustained rapid heart rate. Such patients should
have continuous monitoring and frequent
reevaluations due to the potential for rapid
deterioration.
The presence of hemodynamic stability should
not be regarded as diagnostic of SVT.

. Misdiagnosis of VT as SVT based upon hemodynamic
stability is a common error that can lead to
inappropriate and potentially dangerous therapy.
Unstable — This term refers to a patient with
evidence of hemodynamic compromise, but who
remains awake with a discernible pulse. In this setting,
emergent synchronized cardioversion is the treatment
of choice regardless of the mechanism of the
arrhythmia.
Findings consistent with hemodynamic instability
requiring urgent cardioversion include hypotension,
angina, altered level of consciousness, and heart
failure.

Diagnosis of WCT
History — When evaluating the stable patient with a
WCT, the following historical features may be help to
determine the likely etiology and/or guide therapy. The
presence of structural heart disease, especially
coronary heart disease and a previous MI, strongly
suggests VT as an etiology. The presence of either a
pacemaker or an ICD raises the possibility of a
device-associated WCT. More importantly, the
presence of an ICD implies that the patient is
known to have an increased risk of ventricular
tachyarrhythmias and suggests strongly (but does
not prove) that the patient's WCT is VT.

Some patients with a WCT have few or no
symptoms (palpitations, lightheadedness,
diaphoresis), while others have severe
manifestations including chest pain or angina,
syncope, shock, seizures, and cardiac arrest.
Age — A WCT in a patient over the age of 35 years
is likely to be VT (positive predictive value 85
percent in one series). SVT is more likely in
younger patients. However, VT must be
considered in younger patients, particularly those
with a family history of ventricular arrhythmias or
premature sudden cardiac death.

Duration of the tachycardia — SVT is more likely if
the tachycardia has recurred over a period of
more than three years . The first occurrence of
the tachycardia after an MI strongly implies VT.
Medications — Many medications have
proarrhythmic effects, and obtaining a medication
history is among the first priorities in the
evaluation of a patient with a WCT.
QT prolonging drugs — The most common drug-
induced WCT is a form of polymorphic VT called
torsades de pointes (TdP).

This arrhythmia is associated with QT interval
prolongation when the patient is in sinus rhythm.
Frequently implicated agents include
antiarrhythmic drugs such as sotalol and
quinidine and certain antimicrobial drugs such as
erythromycin and the quinolones.
Class I antiarrhythmic drugs — The class I
antiarrhythmic drugs can cause both aberrancy
during an SVT and also VT. These drugs, especially
class IC agents, slow conduction and have a
property of "use-dependency" (a progressive
decrease in impulse conduction velocity at faster
heart rates).

As a result, these drugs can cause rate-related aberration
and a wide QRS complex during any SVT. However, they
can also cause VT with a very wide, bizarre QRS, which
may be incessant.
Digoxin — Digoxin can cause almost any cardiac
arrhythmia, especially at plasma concentrations above
2.0 ng/mL (2.6 mmol/L). Digoxin-induced arrhythmias are
more frequent at any given plasma concentration if
hypokalemia is also present.
Diuretics — Diuretics are a common cause of
hypokalemia and hypomagnesemia, which may
predispose to ventricular tachyarrhythmias, particularly
TdP. The risk of TdP in the presence of hypokalemia
and/or hypomagnesemia is greatest in patients taking
antiarrhythmic drugs.

Physical examination — As with the history, the initial
physical examination should focus upon evidence of
underlying cardiovascular disease which can impact the
likelihood that the WCT is VT. Signs of acute or chronic
heart failure. A healed sternal incision as evidence of
previous cardiothoracic surgery. The sequelae of
peripheral artery disease or stroke. A pacemaker or
ICD. These devices are usually palpable and are in the
left or, less commonly, right pectoral area below the
clavicle; some earlier ICDs are found in the anterior
abdominal wall.

During AV dissociation, the normal coordination of
atrial and ventricular contraction is lost, which may
produce characteristic physical findings. The presence
of AV dissociation strongly suggests VT.
AV dissociation is typically diagnosed on the ECG
characteristic physical examination findings include:
Marked fluctuations in the blood pressure because of
the variability in the degree of left atrial contribution to
LV filling, stroke volume, and cardiac output.
-Variability in the occurrence and intensity of heart
sounds (especially S1) ("cacophony of heart sounds"),
which is heard more frequently when the rate of the
tachycardia is slower. Cannon "A" waves upon
examination of the jugular pulsation in the neck.

3rd degree Av block requires the presence of AV
dissociation in which the ventricular rate is slower
than the sinus or atrial rate.

Cannon waves are intermittent and irregular jugular
venous pulsations of greater amplitude than normal
waves. They reflect simultaneous atrial and ventricular
activation, resulting in contraction of the right atrium
against a closed tricuspid valve. Prominent A waves can
also be seen during some SVTs. Such prominent waves
result from simultaneous atrial and ventricular
contraction occurring with every beat.
Carotid sinus pressure — Carotid sinus pressure
enhances vagal tone and therefore depresses sinus and
AV nodal activity. Examples of how various arrhythmias
respond to carotid pressure include:

-Sinus tachycardia will gradually slow with carotid sinus
pressure and then accelerate upon release.
During atrial tachycardia or atrial flutter, the ventricular
response will transiently slow (due to increased AV nodal
blockade). The arrhythmia itself, which occurs within the
atria, is unaffected.
-A paroxysmal SVT (either AVNRT or AVRT) frequently
terminates with carotid sinus pressure.
-VT is generally unaffected by vagal maneuvers such as
carotid sinus pressure or valsalva, although these
maneuvers may slow or block retrograde conduction. In
some cases, this response exposes AV dissociation by
altering the sinus rate (or PP intervals). Rarely, VT
terminates in response to carotid sinus pressure.

Pharmacologic interventions — The
administration of certain drugs can provide
diagnostic information. However, some drugs
used for the diagnosis or treatment of SVT (eg,
verapamil , adenosine , or beta blockers) can
cause severe hemodynamic deterioration (often
the result of hypotension) in patients with a VT
that is initially hemodynamically tolerated and
can provoke ventricular fibrillation (VF) and
cardiac arrest. Thus, these medications are
generally reserved for the treatment of patients in
whom the diagnosis of SVT is already known; they
are rarely used for diagnostic purposes for a WCT.

Termination of the arrhythmia with lidocaine
suggests, but does not prove, that VT is the
mechanism. Infrequently an SVT, especially AVRT,
terminates with lidocaine.
Termination of the arrhythmia with digoxin ,
verapamil , diltiazem , or adenosine strongly
implies SVT. However, VT can rarely terminate
after the administration of these drugs.
Termination of the arrhythmia with procainamide
or amiodarone does not distinguish between VT
and SVT.

Additional tests — A number of additional tests may
provide further insight to the mechanism of the
tachycardia and the presence of associated conditions.
Laboratory tests — The plasma potassium and
magnesium concentrations should be measured as part
of the initial evaluation, since hypokalemia and
hypomagnesemia both predispose to the development
of ventricular tachyarrhythmias. Hyperkalemia can
cause a wide QRS complex rhythm with the loss of a
detectable P wave, although this usually has a slow rate
(so-called "sinoventricular rhythm"). In patients taking
digoxin , quinidine , or procainamide , plasma
concentrations of these drugs should be measured to
assist in evaluating possible toxicity.

Chest x-ray — A chest x-ray can provide evidence
suggestive of structural heart disease, such as
cardiomegaly. Evidence of previous cardiothoracic
surgery and the presence of a pacemaker or ICD can
also be detected.
Electrophysiologic study — Electrophysiologic testing
allows definitive diagnosis of a WCT, but is rarely
feasible in the acute setting.
The electrocardiogram (ECG) can provide a probable
diagnosis for a WCT in many patients. However,
definitive diagnosis is not always possible and may be
time-consuming, especially for clinicians unfamiliar
with the criteria for distinguishing VT from SVT.

Basic features — The standard initial approach
includes an assessment of rate, regularity, axis, and
QRS duration.
Rate — The rate of the WCT is of limited use in
distinguishing VT from SVT. When the rate is
approximately 150 beats per minute, atrial flutter with
aberrant conduction should be considered, although
this diagnosis should not be accepted without other
supporting evidence.
Regularity — VT is generally regular, although slight
variation in the RR intervals is sometimes seen.

Slight irregularity suggests VT as opposed to
most SVTs, which are characterized by
uniformity of the RR intervals. When the
onset of the arrhythmia is available for
analysis, a period of irregularity ("warm-up
phenomenon"), suggests VT. More marked
irregularity of RR intervals occurs in
polymorphic VT and in atrial fibrillation (AF)
with aberrant conduction.

Axis — The QRS axis in the frontal plane can
be useful in distinguishing SVT from VT. A
right superior axis (axis from -90 to ±180º),
sometimes called an indeterminate or
“northwest" axis, is rare in SVT and strongly
suggests VT . One exception to this rule is an
antidromic AVRT seen with the Wolff-
Parkinson-White (WPW) syndrome
(ventricular preexcitation).

In this situation there is direct activation of the
ventricular myocardium, bypassing the normal His-
Purkinje system, and the QRS complex may have an
indeterminate axis. Compared to the axis during sinus
rhythm, an axis shift during the WCT of more than 40º
suggests VT .
In a patient with a RBBB-like WCT, a QRS axis to the left
of -30º suggests VT.
In a patient with an LBBB-like WCT, a QRS axis to the
right of +90º suggests VT.

QRS duration — In general, a wider QRS favors VT. In a
RBBB-like WCT, a QRS duration >140 msec suggests VT;
while in a LBBB-like WCT, a QRS duration >160 msec
suggests VT. In an analysis of several studies, a QRS
duration >160 msec was a strong predictor of VT
(likelihood ratio >20:1) . However, a QRS duration >160
msec is not helpful in some settings, including SVT with
an AV accessory pathway ,the presence of drugs
capable of slowing intraventricular conduction, such as
class I antiarrhythmic drugs, and in association with
hyperkalemia.

A QRS duration <140 msec does not exclude VT, since
VT originating from the septum or within the His-
Purkinje system (as opposed to the myocardium) may
be associated with a relatively narrow QRS complex.
Concordance — Concordance is present when the QRS
complexes in all six precordial leads (V1 through V6) are
monophasic with the same polarity. They can either all
be entirely positive with tall, monophasic R waves, or
all be entirely negative with deep monophasic QS
complexes. If any of the six leads has a biphasic QRS
(qR or RS complexes), concordance is not present.

Negative concordance is strongly suggestive of VT but
is not definitive. Rarely, SVT with LBBB aberrancy will
demonstrate negative concordance, but there is almost
always some evidence of an R wave in the lateral leads.
Positive concordance is most often due to VT but can
also occur in the relatively rare case of antidromic AVRT
with a left posterior accessory pathway. While the
presence of concordance strongly suggests VT (>90
percent specificity), its absence is not helpful
diagnostically.
Fusion and capture beats -are diagnostic for VT.

AV dissociation — AV dissociation is characterized
by atrial activity that is independent of ventricular
activity .
In a WCT with AV dissociation, an atrial rate
slower than the ventricular rate strongly suggests
VT. An atrial rate that is faster than the ventricular
rate is seen with some SVTs, such as atrial flutter
or an atrial tachycardia with 2:1 AV conduction. In
these settings, however, there is a consistent
relationship between the P waves and the QRS
complexes, so there is not true AV dissociation.

While the presence of AV dissociation largely
establishes VT as the diagnosis, its absence is not as
helpful for two reasons:
AV dissociation may be present but not obvious on the
ECG.
In some cases of VT, the ventricular impulses conduct
backwards through the AV node and capture the
atrium (referred to as retrograde conduction),
preventing AV dissociation. If the ECG demonstrates 2:1
retrograde conduction (a P wave after every other QRS)
VT is likely but not certain since AVNRT with aberrancy
and 2:1 retrograde conduction can also be seen, but it
is uncommon.

Such a pattern does, however, rule out AVRT since with
this arrhythmia there needs to be a 1:1 relationship
between P wave and QRS complex.
QRS morphology — Frequently, the above criteria do
not provide a definitive diagnosis. Further ECG
evaluation involves assessment of the morphology of
the QRS complex.
Diagnostic criteria — A number of criteria have been
developed to facilitate the evaluation of QRS
morphology. However, the value of these morphologic
criteria is subject to several limitations.

Morphologic criteria favoring VT can be present in
patients with an intraventricular conduction delay
during sinus rhythm, limiting their applicability in these
cases. Morphologic criteria tend to misclassify
antidromic AVRT as VT. Most of these approaches
involve classifying the WCTs as having one of two
patterns:
An RBBB-like pattern — QRS polarity is positive in leads
V1 and V2
An LBBB-like pattern — QRS polarity is negative in leads
V1 and V2

V1 positive (RBBB) pattern — In the patient with a WCT
and positive QRS polarity in lead V1, the following
associations have been made. -Findings in lead V1 — A
monophasic R or biphasic qR complex in lead V1 favors
VT. A triphasic RSR' or RsR' complex (the so-called
"rabbit-ear" sign) in lead V1 usually favors SVT. As an
exception, if the left peak of the RsR' complex is taller
than the right peak, VT is more likely. -Findings in lead
V6 — An rS complex (R wave smaller than S wave)
in lead V6 favors VT . In contrast, an Rs complex (R
wave larger than S wave) in lead V6 favors SVT. V1
negative (LBBB) pattern — In the patient with a
WCT and negative QRS polarity in lead V1, the
following associations have been made.

-Findings in lead V1 or V2 — A broad initial R
wave of 40 msec duration or longer in lead V1 or
V2 favors VT. In contrast, the absence of an initial
R wave or a small initial R wave of less than 40
msec in lead V1 or V2 favors SVT. Two other
findings that favor VT are a slurred or notched
downstroke of the S wave in lead V1 or V2, and a
duration from the onset of the QRS complex to
the nadir of the QS or S wave of ≥60 msec in lead
V1 or V2. In contrast, a swift, smooth downstroke
of the S wave in lead V1 or V2 with a duration of
<60 msec favors SVT.

In an analysis of several studies, the presence of any of
these three criteria (broad R wave, slurred or notched
downstroke of S wave, and delayed nadir of S wave)
was a strong predictor of VT. Findings in lead V6 — The
presence of any Q or QS wave in lead V6 favors VT . In
contrast, the absence of a Q wave in lead V6 favors SVT.
Variation in QRS and ST-T shape — Subtle, non-rate-
related fluctuations or variations in QRS and ST-T wave
configuration suggest VT and may reflect variations in
the VT reentrant circuit within the myocardium as well
as a subtle difference in the activation sequence of the
myocardium reflecting activation that bypasses the
normal conduction system.

AV dissociation can cause variability in the ST segment
and T wave morphology. In contrast, SVT, because it
follows a fixed conduction pathway to and through the
ventricular myocardium, is characterized by uniformity
of QRS and ST-T shape unless the rate changes.
ALGORITHMS FOR WCT DIAGNOSIS
Brugada criteria- QRS morphology criteria consistent
with VT must be present in leads V1 or V2 and in lead
V6 to diagnose VT. If either the V1-V2 or the V6 criteria
are not consistent with VT, an SVT is assumed. An
exception is an antidromic AVRT in Wolff-Parkinson –
White (WPW) syndrome.

VT versus AVRT — Differentiation between VT
and an antidromic AVRT is particularly difficult.
Because ventricular activation begins outside of
the normal conduction system in both
tachycardias, many of the standard criteria are
not able to discriminate antidromic AVRT from VT.
The clinical significance of this problem is often
limited, however, because preexcitation is an
uncommon cause of WCT (6 percent in one series)
. This is particularly true if other factors (eg, age,
underlying heart disease) suggest VT.

The predominant polarity of the QRS complex in
leads V4 through V6 is defined either as positive or
negative. If predominantly negative, the diagnosis
of VT can be made.
If the polarity of the QRS complex is predominantly
positive in V4 through V6, the ECG should be
examined for the presence of a qR complex in one
or more of precordial leads V2 through V6. If a qR
complex can be identified, VT can be diagnosed.

If a qR wave in leads V2 through V6 is absent, the AV
relationship is then evaluated (AV dissociation). If a 1:1
AV relationship is not present and there are more QRS
complexes present than P waves, VT can be diagnosed.
MANAGEMENT for unstable patient- Emergent
synchronized cardioversion — Initial cardioversion is
performed with a synchronized shock of 100 to 200
joules (monophasic) or 50 to 100 joules (biphasic), with
titration of the energy upward as needed. If the QRS
complex and T wave cannot be distinguished accurately,
a synchronized shock may not be possible. Such patients
should be treated with immediate defibrillation (ie,
unsynchronized shock using 360 joules [monophasic] or
200 joules [biphasic]).

Summary to differentiate VT from SVT

The cautious use of intravenous analgesics or sedatives
may be appropriate. However, the use of such agents
must be balanced against the risks of further
hemodynamic deterioration.
Stable patient- Ventricular tachycardia- Urgent or
elective cardioversion is usually appropriate. Following
appropriate conscious sedation, an initial synchronized
shock of 100 to 200 joules (monophasic) or 50 to 100
joules (biphasic) is administered. Repeated shocks at
higher energies may be performed as necessary.
Class I and III antiarrhythmic drugs are generally
reserved for refractory or recurrent arrhythmias.

For patients with one of the known syndromes of
VT in structurally normal hearts, calcium channel
blockers or beta blockers may be used,
particularly if the patient has been successfully
treated in the past with such medications. These
drugs can be used either to terminate the
arrhythmia, or after cardioversion to suppress
recurrences.
Supraventricular tachycardia - Vagotonic
maneuvers — We recommend carotid sinus
pressure (if no carotid bruits are present) or
valsalva maneuver as the initial intervention.

Adenosine — Adenosine (6 mg IV over 1-2
seconds) is highly effective in terminating many
SVTs (eg, AVNRT, AVRT), and for others (eg, AF,
atrial flutter), adenosine may facilitate the
diagnosis by slowing the ventricular response to
allow clearer assessment of atrial activity. If the
initial dose is ineffective, a 12 mg dose may be
given and repeated once if necessary.

Calcium channel blockers or beta blockers —
Intravenous verapamil (2.5 to 5 mg IV), or beta
blockers (eg, metoprolol 5 to 10 mg IV) may be
given if the SVT persists after adenosine
administration. These medications can terminate
AVNRT or AVRT, as well as some atrial
tachycardias. If the specific SVT diagnosis remains
unknown, these drugs may slow the ventricular
response and facilitate diagnosis.

Cardioversion — Cardioversion is rarely necessary
in patients with a stable SVT. However, if AVNRT
or AVRT persist after the above interventions,
synchronized cardioversion is usually effective in
restoring sinus rhythm. Following appropriate
conscious sedation, an initial synchronized shock
of 100 to 200 joules (monophasic) or 50 to 100
joules (biphasic) is administered.

If the arrhythmia is known to be AF, atrial flutter, or an
atrial tachycardia, management options include rate
control and cardioversion (ie, rhythm control).
Recurrent or refractory WCT — If the WCT recurs or
persists following initial attempts at cardioversion,
suppression of the arrhythmia by pharmacologic means
should be attempted and further evaluation should
focus upon the presence of arrhythmia triggers (eg,
ischemia, electrolyte abnormalities, and drug toxicity).
Cardioversion or defibrillation should be repeated as
necessary in patients who are hemodynamically
unstable.

For patients with recurrent VT :
. Amiodarone (150 mg IV over 10 minutes followed by
an infusion of 1 mg/minute for 6 hours, then 0.5
mg/minute) is recommended in most settings, due to
its efficacy in the suppression of both atrial and
ventricular arrhythmias.
.Procainamide (15 to 18 mg/kg administered as slow
infusion over 25-30 minutes, followed by 1-4
mg/minute by continuous infusion) is an alternative to
amiodarone that also suppresses both SVTs and VT. In
addition, because of its ability to suppress conduction
over a bypass tract, procainamide is recommended if
antidromic AVRT or an SVT conducting over a bypass
tract is suspected.

Intravenous lidocaine (1 to 1.5 mg/kg over 2 to 3
minutes) may be useful, particularly if cardiac
ischemia is suspected. In some cases lidocaine,
may actually slow conduction in the accessory
pathway and terminate an antidromic AVRT.
In a patient with a stable blood pressure and
recurrent arrhythmias, the cautious use of beta
blockers (eg, metoprolol 5 to 10 mg IV) may be
initiated. Due to the possibility of precipitating
hemodynamic deterioration, beta blockers should
be administered in a setting where urgent
defibrillation can be performed, if necessary.

For patients with a known SVT that recurs or persists,
intravenous verapamil , diltiazem , or beta blockers may
be used.
Multiple recurrences of WCT should raise concern
about cardiac ischemia, hypokalemia, digitalis toxicity,
and polymorphic VT with or without QT prolongation,
all of which have specific appropriate therapy.
Presence of a pacemaker — If the WCT is the result of
the pacemaker tracking an underlying atrial arrhythmia
or the result of a pacemaker mediated tachycardia, the
appropriate therapy is the placement of a magnet over
the pacemaker.

Presence of an ICD — There has been a dramatic
increase in use of ICDs for both the primary and
secondary prevention of sudden cardiac death. The
presence of an ICD has a number of unique
implications for patients with a WCT. Although patients
with an ICD should receive device therapies for a WCT,
such therapies are usually delivered within the first
minutes of the arrhythmia. In a patient with a
persistent or recurrent WCT, the ICD should not be
relied upon to provide definitive management.
If an individual with expertise in device evaluation and
management is available, the device should be
interrogated. If the patient is stable, the device may be
evaluated during the WCT.

Electrical storm/ arrhythmic storm
- refers to multiple recurrences of ventricular
arrhythmias over a short period of time.
-In most instances polymorphic VT and
ventricular fibrillation (VF) can also result in
electrical storm.
-Incessant VT is defined as hemodynamically
stable VT which persists for longer than one
hour.

DEFINITION — a state of cardiac electrical
instability characterized by multiple episodes of
VT/ VF within a relatively short period of time.
In patients without ICD electrical storm has been
variously defined as :
-The occurrence of three or more
hemodynamically stable ventricular
tachyarrhythmias within 24 hours
-VT recurring soon after (within five minutes)
termination of another VT episode.
-Sustained and non-sustained VT resulting in a
total number of ventricular ectopic beats greater
than sinus beats in a 24-hour period

.In patients with an ICD
Three or more appropriate therapies for
ventricular tachyarrhythmias, including
antitachycardia pacing or shocks, within 24
hours.
When electrical storm is defined by >2
VT/VF episodes requiring device
intervention over a 24-hour period.

TRIGGERS OF ELECTRICAL STORM
-Drug toxicity
-Electrolyte disturbances ( ↓K and ↓Mg)
-New or worsened heart failure
-Acute myocardial ischemia
-Thyrotoxicosis
-QT prolongation
DIAGNOSIS
Electrical storm is dxed by Three or more
confirmed episodes of VF/VT resulting in
symptoms ICD therapy within a 24-hour
period.

The diagnosis of incessant VT is made by
confirming the presence of continuous VT for
greater than one hour.
Initial treatment is based on hemodynamic
stability assessment:
.Hemodynamically unstable
-electrical cardioversion
.Hemodynamically stable
-IV amiodarone And
beta blocker ( metoprolol IV/PO)
-urgent coronary revascularization in AMI
-Catheter ablation

Management of refractory cases
-Left ventricular aneurysmectomy.
-Insertion of an intraaortic balloon pump
-Cardiac transplantation.
-Thoracic epidural anesthesia and/or general
anesthesia.
-Cardiac sympathetic denervation (CSD)
-Stellate ganglion block (usually left-sided).
-Renal artery denervation (RDN)
-stereotactic body radiation therapy

Dr nigat

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Dr nigat

Similar to Dr nigat (20)

Recently uploaded

Recently uploaded (20)

Dr nigat