Approach to Ventricular

tachyarrythmias and complications of

STEMI

ABNET

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Outline

Introduction
Mechanisms of arrhythmias
Specific ventricular arrhythmias
Unique ventricular syndrome
Classification
Clinical symptoms
Algorithm of approach
Differential diagnosis
Treatment
Complications STEMI
Long-term management of STEMI

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INTRODUCTION

• Ventricular arrhythmias ranges from asymptomatic

ventricular premature beats (VPBs) to ventricular fibrillation
(VF)
• Are common in patients with heart failure (HF) and
cardiomyopathy
• These arrhythmias fall into two broad categories:
• Malignant or potentially lethal arrhythmias
• sustained ventricular tachycardia (VT) and VF
• Nonsustained or hemodynamically tolerated arrhythmias
• VPBs, nonsustained ventricular tachycardia (NSVT), and accelerated idioventricular
rhythm (AIVR).

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Mechanisms of tachyarrythmias

• Tachycardias are due to abnormalities of

• Impulse formation and/or
• Impulse propagation

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 Abnormalities in Impulse Formation
1. Increase in automaticity
a. Increase in the slope of phase 4
depolarization
b. Reduced threshold for AP
depolarization
APCs and VPCs & ATs.
Pacing does not provoke
automatic rhythms.

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 Abnormal impulse formation
2. Triggered activity
• Related to cellular
afterdepolarizations
• Attributable to an ↑intracellular
Ca accumulation
• EAD-phase 3
• responsible for the VPCs TDP
• LAD- phase 4
• Responsible for atrial,
junctional, and fascicular
tachyarrhythmias &
catecholamine-sensitive VT

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Abnormalities in Impulse Propagation

• Reentry appears to be the basis

for most abnormal sustained SVTs
and VTs.
• reentry can be due to
• anatomically driven (fixed)
based on the
• presence of "extra" pathways,
natural anatomic barriers of
conduction
• extensive fibrosis

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Reentry circuit

• Two potentially conduction pathways or more.

• Unidirectional block must occur in one
pathway
• An activation front that passes around the
zone of unidirectional block over the alternate
pathway.
• Activation of the myocardium distal to block
with delay.
• The activation wavefront to activate the block
by retrogradely and reexcite the tissue where
the actviation wavefront originated.
• For reentry to occur the wavefront should
find the tissue to be excitable in the direction
of its propagation.

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Ventricular Premature Complexes
(VPCs)

Originates at sites remote from the Purkinje

network
Produces slow ventricular activation( a wide QRS
complex >140 ms)
Increase with age and the presence of structural
heart disease
Occur in 70 to 95 percent of patients with HF

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• In general there is no P wave identified before a premature QRS
complex. However, there may be a normal sinus P wave present if
the PVC is very late; in this situation, there is a long coupling interval
(from the prior QRS complex), the P wave is not conducted, and the
PR interval is shorter than the native sinus beat.
• The QRS complex of a PVC is widened, often notched, and with a QRS
duration usually >0.16 seconds . It will have a morphology that
resembles a right or left bundle branch block depending upon the
location of origin, but its morphology is generally not the same as a
typical bundle branch block. It is assumed that the PVC originates in
the left ventricle when it has a positive deflection or tall R wave in V1
(right bundle branch block configuration), while a negative complex
with a deep S wave in V1 (resembling a left bundle branch block
morphology) originates in the right ventricle. Other findings on the
ECG include marked repolarization abnormalities, manifested as ST
segment and T wave abnormalities

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• .Retrograde activation of the atrium is variably present; it depends
upon the location of the premature beat, the time necessary for
impulse conduction to the atrioventricular (AV) node, the coupling
interval to the prior sinus beat, and the ability of the node to conduct
retrograde to the atrium. When present, there is a retrograde P
wave, usually seen within or slightly before the T wave. The interval
from the previous P wave to the retrograde P wave is, however,
shorter than the underlying sinus PP interval, reflecting the
premature activation of the atrium.  

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 Patterns of VPC
1.Bigeminy:every sinus beat is followed by a VPC
2.Trigeminy: two sinus beats are followed by a VPC
3.Quadrigeminy :a premature complex that follows
three normal beats
4.Multiformed VPCs :may have different
morphologies
5.Pairs or couplets : Two successive VPCs

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DDx

APCs with aberrant ventricular

conduction may also create a
wide and early QRS complex..
QRS pattern for a VPC does not
appear to follow a typical RBBB
or LBBB pattern as the QRS and
can be quite bizarre.
VPCs are associated with a "fully
compensatory pause" [i.e., the
duration between the last QRS
before the PVC and the next QRS
complex is equal to twice the
sinus rate

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 Treatment:VPCs
• Dictated by the presence of symptoms attributable to
the PVCs.
• Both fast and slow heart rates can provoke the
development of PVCs.
• PVCs accompanying slow ventricular rates
• Atropine or isoproterenol or by pacing,
• Slowing of the heart rate in some patients with sinus
tachycardia can eradicate PVCs.
• Iv lidocaine/procainamide/amiodarone
• Propronalol
• Intravenous magnesium can be useful.
• RF ablation
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ACCELERATED IDIOVENTRICULAR
RHYTHM  —
•  An accelerated idioventricular rhythm (AIVR) is a repetitive
ventricular rhythm occurring at a rate between 60 and 100 beats per
minute . It may be the result of an accelerated ventricular focus
which generates an impulse faster than the sinus node and therefore
assumes control. There may or may not be AV dissociation; if
dissociation is present, the atrial rate is slower than the ventricular
rate and the PP intervals are longer than the RR intervals. On the
other hand, if the idioventricular rhythm represents an escape
rhythm (generally the result of third degree AV nodal block), the P
waves are dissociated from the QRS impulses and the atrial rate is
faster than the ventricular rate. In the setting of acute ischemia, AIVR
may be a marker of spontaneous or induced reperfusion.

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Accelerated Idioventricular Rhythm (AIVR)

• Ventricular rhythm that is

characterized by ≥ 3 complexes at
a rate 40-120bpm
• It is due to abnormal automaticity
 Has a characteristic gradual onset
and offset and more variability in
cycle length.
• Commonly associated with
– Acute MI , cocaine intoxication,
acute myocarditis, digoxin
intoxication, and postoperative
cardiac surgery
 commonly occurs at the moment
of reperfusion of a previously
occluded coronary artery

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AIVR

• Sustained forms of AIVR can exist

– Acute MI(50%) and postop
– Hemodynamic compromise can occur because of the loss of AV synchrony.
• Bradyarrhythmias & the hemodynamic
consequences of AIVR are associated with RV
infarction
• Acceleration of the atrial rate either by atropine or
atrial pacing
• Most episodes of AIVR are transient and require no
treatment.

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DDx

• Slow sustained VT
• can manifest rates between 90 and 120 beats per minute
• marked warm up in rate and the marked cycle-length oscillations seen less
likely
• occur in the setting of chronic infarction or cardiomyopathy
• initiated with programmed stimulation

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Ventricular Tachycardia

• Originates below the bundle of His at a rate >100 bpm

• Most VT patients have rates >120 beats per minute
• Obviously, significant overlap rates may exist b/n AIVR and Slow VT
• ECG characteristics and the clinical circumstance sometimes can be
used to distinguish the two forms of tachycardia.

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• Ventricular tachycardia  — 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 wav

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• VT is the most common cause of WCTs, particularly in patients with a history
of cardiac disease. In series of unselected patients, VT accounted for up to
80 percent of cases of WCT. VT frequency can exceed 90 percent in patients
with structural heart disease (eg, a prior MI) 
• 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:
• 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 (eg, 21 percent of cases in one series)

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• Preexcitation syndrome — In the preexcitation 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 (AV
• 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

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• 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.

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• Among patients with a pacemaker or an ICD, further possibilities
need to be considered in addition to the usual differential diagnosis
of a WCT. These include:
• 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.

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• 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.
• Artifact mimicking VT  — ECG artifact, particularly when observed on
a rhythm strip, may be misdiagnosed as VT and can result in
unnecessary invasive procedures . The presence of narrow-complex
beats that can be seen to "march" through the supposed WCT at a
fixed rate strongly supports the diagnosis of artifact

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patients are categorized as follows:

• 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

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• Patients who become unresponsive or pulseless are considered to
have a cardiac arrest and are treated according to standard
resuscitation algorithms.
• 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:
• History of heart disease — The presence of structural heart disease,
especially coronary heart disease and a previous MI, strongly
suggests VT as an etiology . In one report, over 90 percent of patients
with a WCT and a previous MI had VT. It is also important to establish
whether a cardiac arrhythmia has occurred in the past and, if so,
whether the patient is aware of the etiology.

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• Presence of a pacemaker or ICD — The patient should be asked about the
presence of pacemaker or ICD. Patients are instructed to carry identification
cards providing information about such devices, which can facilitate device
interrogation. 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.
• 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 (positive predictive value 70 percent). 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

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• 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

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• 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.
• Although AV dissociation is typically diagnosed on the ECG (see 'AV dissociation' ,
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. 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.

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• 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.

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• 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.
• The diagnostic implications of the responses to certain medications include:
• 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 adenosinestrongly 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.

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• 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

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• 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. 

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QRS

Wellens and colleagues (1978) found

that approximately 70% of VTs have a QRS duration longer
than 140 milliseconds in patients with a right bundle branch
block pattern. VTs with a left bundle branch pattern generally
have a QRS duration longer than 160 milliseconds. Generally,
a VT with right bundle branch block morphology (predominantly
positive QRS complex in lead V1) suggests an LV origin,
whereas a VT with left bundle branch block morphology
(predominantly negative QRS in lead V1) suggests right ventricular

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(RV) origin . VT with a right bundle branch block
pattern will not have a typical RS wave. The R wave is single or
biphasic (QR or RS) or triphasic (with initial R wave taller than
the smaller r´ and an S wave in between that crosses the baseline).
V6 typically demonstrates small r and large S waves. In VT
with a left bundle branch block pattern, the duration of the
initial R wave exceeds 30 milliseconds, and the beginning of the
QRS to the nadir of the S wave exceeds 70 milliseconds

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. The S
wave may be notched or slurred. Since SVT with aberration is
due to a functional bundle branch block, the QRS should resemble
a typical bundle branch block, and the S wave is neither
notched or slurred. If V6 is used, a qS pattern suggests VT.
Though sometimes useful, these findings have limited sensitivity
and specificity.

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Change in the frontal plane QRS axis of more than 40
degrees, especially toward the “Northwest quadrant” between –90
and –180 degrees (normal is –30 to 90 degrees), is highly
suggestive of VT. The presence of a qS pattern in lead V6 favors
VT as a cause of wide-complex tachycardia. Concordance refers
to uniform direction of the QRS complexes in the precordial
leads, either all positive or all negative; for example, in VT with
right bundle branch block pattern, the QRS is upright in all
precordial leads

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• 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

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• 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 

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•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.

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• 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

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• 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 [ 21 ]. 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.
• The following findings are helpful in establishing the presence of AV dissociation.

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• Dissociated P waves  — P waves are said to be dissociated if they are not
consistently coupled to the QRS complexes, as evidenced by the following:
• PP and RR intervals are different
• PR intervals are variable
• There is no association between P and QRS complexes
• The presence of a P wave with one, but not all, QRS complexes
• During a WCT, P waves are often difficult to identify. If P waves are not
evident on the surface ECG, direct recordings of atrial activity (eg, with an
esophageal lead or an intracardiac catheter) can reveal AV dissociation
During a WCT, P waves are often difficult to identify. If P waves are not evident
on the surface ECG, direct recordings of atrial activity (eg, with an
esophageal lead or an intracardiac catheter) can reveal AV dissociation

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• Fusion beats  — Fusion occurs when one impulse originating from
the ventricle and a second supraventricular impulse simultaneously
activate the ventricular myocardium. The resulting QRS complex has
a morphology intermediate between that of a sinus beat and a
purely ventricular complex . Intermittent fusion beats during a WCT
are diagnostic of AV dissociation and therefore of VT.
• Capture beats  — Capture beats, or Dressler beats, are QRS
complexes during a WCT that are identical to the sinus QRS complex .
The term "capture beat" implies that the normal conduction system
has momentarily "captured" control of ventricular activation from
the VT focus.
• Fusion beats and capture beats are more commonly seen when the
tachycardia rate is slower

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48
• 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
• This distinction does not, by itself, make the diagnosis, but additional
features favor VT in either RBBB-like or LBBB-like WCTs.
• V1 positive (RBBB) pattern — In the patient with a WCT and positive
QRS polarity in lead V1, the following associations have been made

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• RBB-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

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• 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.

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Brugada criteria  — The Brugada criteria are a
stepwise approach in which four criteria for VT
are sequentially assessed
The steps are as follows:
•Leads V1-V6 are inspected to detect an RS complex. If there are no RS
complexes, concordance is present and the diagnosis of VT can be
made. 
•If an RS complex is present, the interval between the onset of the R
wave and the nadir of the S wave (RS interval) is measured. If the
longest RS interval in any lead is >100 msec and the R wave is wider
than the S wave, the diagnosis of VT can be made. This reflects the fact
that aberration is due to a terminal delay and a wider terminal portion
of the QRS complex (ie, S wave), while with VT even the initial portion
of the QRS complex (ie, R wave) is wide and abnormal.
•If the longest RS interval is <100 msec, the presence or absence of AV
dissociation is assessed. If AV dissociation is seen, the diagnosis of VT is
made. 

56
57
• If the RS interval is <100 msec and AV dissociation cannot clearly be
demonstrated, the QRS morphology criteria for V1-positive and V1-
negative wide QRS complex tachycardias are considered
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.

58
• An alternative algorithm uses a stepwise approach similar to the
Brugada criteria, but includes different ECG features . Two unique
features of this algorithm include an initial R wave in aVR (diagnostic
of VT), and the Vi:Vt ratio. Vi and Vt are the magnitude of voltage
change in the initial and terminal 40 msec of a QRS, respectively. A
Vi:Vt ratio ≤1 is diagnostic of VT.
• A Bayesian approach utilizes likelihood ratios (LR) for six ECG criteria .
Patients are presumed to start with a "prior odds ratio" of 4.0 (4:1) in
favor of VT. As each criterion is evaluated sequentially, the
associated LR is multiplied by the prior odds ratio to calculate the
new probability of VT. The final odds ratio (posterior probability) is
considered consistent with VT if the value is ≥1.0, and SVT if the
value is <1.0.

59
60
• For cases in which preexcitation is thought to be likely (such as a young
patient without structural heart disease, or a patient with a known accessory
pathway), a separate algorithm was developed by the Brugada group. Their
second algorithm consists of the following three steps:
• 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.

61
62
• Unstable patient  — Hemodynamic compromise may occur with any
WCT, regardless of the etiology. Furthermore, patients who initially
appear stable may deteriorate rapidly.
• When a patient with a WCT is unstable, but still responsive with a
discernible blood pressure and/or pulse, we recommend the
following approach:
• 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

63
• 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]).
• 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.

64
• Ventricular tachycardia  — In stable patients with VT or an uncertain
diagnosis that is being managed with the presumed diagnosis of VT ,
the following approach is recommended:
• 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.

65
• Any associated conditions should be treated, including cardiac ischemia,
heart failure, electrolyte abnormalities, or drug toxicities.
• 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. 
• However, given the risk for hemodynamic deterioration following the
administration of these medications, an external defibrillator should be
immediately available prior to administration. Furthermore, the decision to
use these medications in this setting, particularly if there is any uncertainty
regarding the diagnosis, should be made in conjunction with a cardiologist
who is experienced in arrhythmia management. If such expertise is not
immediately available, electrical cardioversion is generally preferred

66
• If the SVT is likely to be AVNRT or AVRT, or if the specific SVT
diagnosis is uncertain, the following treatments are recommended:
• 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. 

67
• Adenosine has a very short half-life (less than 10 seconds), reducing the risk
of an untoward reaction. However, adenosine can cause degeneration to VF,
particularly in patients with coronary artery disease. Thus, an external
defibrillator should be immediately available if adenosine is given.
• 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.

68
• 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 or a WCT of uncertain etiology, we
recommend the following:
• 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 amiodaronethat 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

69
• 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.

70
Classification(cont…. )

71
72
73
74
75
76
77
Difference of MVT,PVT

MONO MORPHIC VT POLYMORPHIC VT

1. Stable tachycardia Unstable, dynamic

2. Reproducible, recurrent phenomenon Less reproducible

3. Initiated by pacing ,programmed Not reliably initiated

ventricular stimulation
4. Normal hearts./structural heart Acute ischemia ,myocarditis,drugs
disease
5. Reentry circuit Pause dependent VT,TRIGERRING

6. Hemodynamically stable Not so

7. MVT—PVT—VF/VFL PVT—VF/VFL

8. Catheter ablation,pacing,AAD Bbs ,pacing…/ablation?

78
Diagnosis

• Asymptomatic individuals with or without electrocardiographic

abnormalities
• Symptoms potentially attributable to ventricular arrhythmias
alpitations
P

Dyspnea
Chest pain
Syncope and presyncope
Cannon a waves
Absent pulse
Hypotension
Variable S1

79
Diagnosis

• Algorithm based
• ECG –12 Lead with long rhythm strip of lead II.
• 24 hr holter monitoring in case of transient episode
• Echocardiography
• Electrophysiologic testing
• Routine investigations
• Serum electrolytes--calcium,magnesium
• ABG

80
 Daignosis

S.No SUPRAVENTRICULAR TACHYCARDIA VENTRICULAR TACHYCARDIA

1. Abberant QRS pattern that matches exactly not in morphology of

that of the wide complex rhythm. LBBB,RBBB,wide complexes
present
2. Presence of p wave before QRS complex P waves and QRS complexes are
dissociated.

3. Preexcited QRS pattern on SR ECG indicates Bizzare QRS complex

atrial arryhthmia.—AFL,focal AT,antidromic
macroreentrant tachycardia.

4. Responds to vagal Manuevre:-carotid Not so

massage ,valsalva,adenosine admin

5. Verapamil effective Worsens the LV dysfunction

81
82
83
 Management
• Sustained PVT, ventricular flutter, and VF
 Emergency asynchronous defibrillation (200-J monophasic or 100-J
biphasic shock)
Intravenous lidocaine and/or amiodarone
• Monomorphic wide complex rhythm that results in
hemodynamic compromise, a prompt R-wave synchronous
shock is required

84
Management

NON SUSTAINED VT :
• No treatment in absence of heart disease.
• Look for reversible factors.
• In termination of episodes –IV BBs can be used.
• For preventing recurrences –oral BBs /CCB s.

85
MONOMORPHIC VT with hemodynamic
compromise

Severity of underlying structural heart disease

Ventricular rate
Origin of arryhthmia
LVD
Hypotension,pulmonary edema,MI.
Synchronised R wave shock is given. With appropriate
sedation.100j—200-300-360 j
After SR rhythm lidocaine 2-4 mg/min iv infusion.

ACC/AHA/ESC guidelines 2006 for ventricular arrythmias/STEMI

86
MONOMORPHIC VT with hemodynamic
compromise
• Wide-QRS tachycardia should be presumed to be VT if the diagnosis
is unclear (IC)
• DC cardioversion with appropriate sedation (IC)

87
Sustained monomorphic VT ,stable

• DC cardioversion –effective in termination

• IV antiarryhthmic drugs can also be used—no response—
cardioversion.
Presence /abscence LVD
1. Preserved LVF: only one drug to be used.
1. IV PROCAINAMIDE---class IIaB recommendation
• More effective than amiodarone in termination.
• <50 mg/min---1-4 mg/min
• Preferred over other drugs.
• Rapid infusion causes hypotension.

88
Sustained monomorphic VT ,stable

2. IV AMIODARONE :can be given in presence of LVD also

(IIaB)
• Refractory to electrical cardioversion,
• Unstable or recurrent VT inpsite of IV procainamide.
• 150mg IV given as bolus with in 10 min –repeat after 10-15 min.
• Infusion of 1 mg/min*6 hrs,0.5mg/min*18 hrs.
• Max dose is 2.2 gms in 24 hrs.
3. Transvenous catheter pace termination:class IIaC
• Refractory cases to cardioversion or recurrent despite AAD
4. IV LIDOCAINE :due to acute myocardial ischemia --class II
b
• IV bolus at 1mg/min—0.5-0.75mg/min---1-4mg/min

89
Sustained monomorphic VT ,stable

2.In presence of LVD –

• LVD EF <40%-- amiodarone/lignocaine
• Dose is same .

90
SUSTAINED POLYMORPHIC VT

Usually hemodynamically unstable if sustained.

 Should be given asynchronous defibrillation(IB)
 Minimal is 200 j monophasic /100 j biphasic.
 Asynchronous to avoid delay related to sensing of QRS complex.
 If persists repeat shocks with -200j—300j-360j
Pharmacological therapy depending upon QT interval is
normal/prolonged
Normal QT interval or suspect myocardial ischemia
 IV beta blockers
 Recurrent VT(IB)
 IV amiodarone ( IC) if recurrent
 IV lidocaine class II b recommendation in case of MI
 Coroanry angio,IABP(IC)

91
SUSTAINED POLYMORPHIC VT
Torsades de pointes:
 Correction of electrolyte abn.(IA)
 Remove offending drugs (IA)
 Antiarrhythmic agents:class IA and class III are avoided.
 Lidocaine—does not prolong QT interval
 Acute and long-term pacing(IA)
 Torsades de pointes due to heart block and symptomatic bradycardia
 IV Magnesium sulfate –class IIaB ,
 1-2gm of mgso4 diluted in 5% D loading dose—rapidly—10-20 gm
in 24 hrs
 Isoproterenol ---bridge befor temporary pacemaker(IIaB)
 Recurrent pause-dependent
 Do not have congenital LQTS
 2-10 mcg/min
 Temporary pacemaker—pause dependent
 BB combined with pacing (IIaC)
 TDPs with sinus bradycardia

92
Incessant Ventricular Tachycardia

• Revascularization and beta blockade followed by IV

antiarrhythmic drugs such as procainamide or amiodarone
are recommended for patients with recurrent or incessant
polymorphic VT due to acute myocardial ischemia. (Class
IC)
• IV amiodarone or procainamide followed by VT ablation
can be effective in the management of patients with
frequently recurring or incessant monomorphic VT. (Class
IIaB)

93
PREVENTION OF VT

• ICD + antiarryhthmic drug

• Sotalol /amiodarone –monomorphic VT/polymorphic VT
• Evaluate the patient in case of nonsustained VT in presence of
structural heart disease.
• Sotalol--20-120 mg (0.5-1.5 mg/kg) given by inj over 10 min,
may repeat every 6 hr if needed.

94
Catheter ablation

• Cure rate > 90 % in absence of structural heart disease

• Use both endocardial and epicardial pacing
• Recurrent VT (eliminate the requirement for toxic drug)
• For prevention of ICD shocks(being actively investigated )

95
VT storm

Defn
 >2 episodes of VT in 24 hrs
 Repeated VT episodes requiring external cardioversion/defibrillation or
repeated ICD shcok therapy.
Recurrent polymorphic VT ,no QT prolongation-- IV
amiodarone/IV lignocaine
QT prolonged VT –removal of offending drug ,correction of ele.
Pause dependent Tdps--emergency pacing
Brugada syndrome –IV quinidine ,IV isoproterenol
Acute ischemia –IABP or coronary angioplasty
VPC s –ablation
Monomorphic VT ---empirical treatment
Catheter ablation---eliminate frequent recurrent or incessant VT
and frequent ICD shocks

96
97
98
Prognosis

• Risk of SCD can be decreased by ICD implantation in

structurally heart disease patients.
• Malignant VT,risk of SCD –prolonged QTc, BRUGADA, ARVD
—ICD
• Most common cause of death in acute MI

99
ICDs

100
UNIQUE VT SYNDROMES

101
Idiopathic outflow tract VT

• No structural heart disease

• RV 80%,LV 20%
• More in women(hormonal triggers)
• Not associated with SCD.
• Symptoms on exercise,stress, caffeine ingestion.
• Vagal manuevres ,adenosine,BBs terminate the VTs .
• Calcium dependent triggered activity.
• Large monophasic R waves in inferior leads.
• LBBB pattern in V1 –RVOT
• RBBB pattern in V1 ---LVOT

102
Treatment

• Hemodynamically stable and nonsustained..no Rx

• IV bb s useful in termination
• BBs and CCBs --chronic therapy
• Class Ia,Ic,sotalol
• Catheter ablation in resistant cases…site by 12 lead ECG
• Efficacy of therapy by treadmill testing and ECG monitoring.
• EPS only when the diagnosis is in question or to perform
catheter ablation.

103
Idiopathic LV septal /fascicular VT

• 2nd most common.

• Macroreentry involving calcium dependent slow response
fibres/automaticity.
• Narrow RBBB+ LAD ---posterior fascicles
• Narrow RBBB+RAD – anterior fascicles
• Unique nature –suppression by verapamil
• Catheter ablation therapy effective.

104
VT assosciated with LV DCM

• Monomorphic/polymorhic VT can occur.

• Mitral and aortic areas involved.
• Drug therapy ineffective
• After ICD implantation –sotalol/amiodarone
• Less amenable to catheter ablation of endocardium
• VT origin is from epicardium ---accessed by percutaneous
pericardial puncture
• EF <30% --prophylactic ICD

105
Bundle branch reentrant tachycardia

• Macro reentry circuit

• Antegrade direction down the right branch
• Retrograde up the left posterior or anterior fascicles/LBB
• Mimic RV pacing with LBBB pattern,leftward superior axis.
• Opposite occurrence then RBBB
• Readily amenable to catheter ablation therapy.
• Coupled with ICD due to risk of SCD.
• Occurs in nonischemic cardiomyopathy or valvular
cardiomyopathy.

106
VT assosciated with HOCM

• ICD is usually indicated in presence of HOCM,

• h/o sustained VT/VF,unexplained syncope,a strong family history of
SCD,LV septal thickness >30 mm –risk of SCD.

• VT Associated with Other Infiltrative CMP and NMDs

• AV conduction disturbances exist
• High frequency of VT/VF in sarciodosis,amyloidosis,kearne
sayre syndrome, Emery-Dreyfuss muscular dystrophy, Limb-
girdle muscular dystrophy
• ICD implantation

107
Arrythmogenic RV dysplasia

• Genetically determined dysplastic process or after a

suspected viral myocarditis.
• Sporadic nonfamilial nondysplastic is more common.

108
Bidirectional VT

The QRS complexes are varying in their morphology and axis

cannot be determined

109
OTHERS

• VT after operation of fallot repair

• Fascicular tachycardia caused by digoxin toxicity.
Genetically determined are :
• Long QT syndrome
• Acquired LQTS
• Short QT syndrome
• Brugada syndrome
• Catecholaminergic polymorphic VT

110
Complications of STEMI

111
 Left Ventricular Failure
THE single most important predictor of mortality
after AMI
Characterized by either systolic dysfunction alone or
both systolic and diastolic dysfunction
Increased clinical manifestations as the extent of the
injury to the LV increases
Mortality increases with the severity of the
hemodynamic deficit
The development of HF after STEMI is an indication
for angiography with intent to proceed with
revascularization if not previously performed
112
113
 Killip classification
class I -- mortality rate is abt 5%
No signs of pulmonary or venous congestion
class II--moderate heart failure- 10–20%
Basal rales,S3 gallop, tachypnea signs of Rt. side HF
class III--severe HF with pulmonary edema
 expected mortality rate 35–45%
class IV– 85–95% expected mortality rate
shock with SBP <90 mmHg
 evidence of peripheral vasoconstriction, peripheral cyanosis, mental confusion,
and oliguria

114
Left Ventricular Failure

Treatment:
• Diuretics
• Nitroglycerin
• Vasodilators-- ACE inhibitors
• Digitalis???
• positive inotropic agents

115
 RV infarction
• Complicates the course of ~1/3rd of patients with inferior STEMI
• Most often due to proximal occlusion of the right coronary artery
• Is associated with a higher mortality risk
• Clinical triad of hypotension, clear lung field & ↑ JVP.
• EKG --1-mm ST elevation in lead V1 and V4R -- most sensitive ECG
marker

116
RV infarction

• AV synchrony should be achieved and bradycardia should

be corrected
• RV preload should be optimized with volume challenge in
patients with hemodynamic instability if JVP is normal or
low
• Inotropic support if no response
• Delay CABG for 4wks to allow recovery

117
 Cardiogenic shock
onset is bimodal; most cases occur within 24 hrs.
For those with pump failure, 15% of cases occur at time of
presentation, and 85% develop during hospitalization
Cause
Extensive LV infarction (>40%)
Mechanical complications
Papillary muscle rupture
Ventricular septal rupture
Free-wall rupture with tamponade
RV infarction

118
 Treatment of Cardiogenic Shock

I IIa IIb III

Emergency revascularization with either PCI or CABG is
recommended in suitable patients with cardiogenic shock due to
pump failure after STEMI irrespective of the time delay from MI
onset.

I IIa IIb III

In the absence of contraindications, fibrinolytic therapy should be
administered to patients with STEMI and cardiogenic shock who
are unsuitable candidates for either PCI or CABG.

119
 Treatment of Cardiogenic Shock

I IIa IIb III

The use of intra-aortic balloon pump counterpulsation can be
useful for patients with cardiogenic shock after STEMI who do
not quickly stabilize with pharmacological.

I IIa IIb III

Alternative LV assist devices for circulatory support may be
considered in patients with refractory cardiogenic shock.

120
Arrhythmias

• The incidence of arrhythmias after STEMI is higher

• The mechanisms responsible for infarction-related
arrhythmias
• ANS imbalance
• Electrolyte disturbances
• Ischemia
• Slowed conduction in zones of ischemic myocardium.
• The prompt management of arrhythmias constitutes a
significant advance in the treatment of STEMI.

121
Ventricular Tachycardia and Fibrillation

• Within the first 24 h of STEMI, ventricular tachycardia and

fibrillation can occur without prior warning arrhythmias
• Routine prophylactic antiarrhythmic drug therapy is no
longer recommended

122
123
Supraventricular Arrhythmias
Sinus tachycardia is the most common supraventricular arrhythmia
Rx –
 primary problem should be treated
first.
beta blocker
Atrial flutter and atrial fibrillation
Often secondary to LV failure.
HFDigoxin
No HF beta blockers, verapamil, or
diltiazem
124
Supraventricular Arrhythmias

 If the abnormal rhythm persists for >2 h with a

ventricular rate >120 bpm, or
 If tachycardia induces heart failure, shock, or ischemia
(as manifested by recurrent pain or ECG changes),
 Rx a synchronized electroshock (100–200 J
monophasic wave form)
 Accelerated junctional rhythms ---inferoposterior
infarction.
 In severely compromised LV function, the loss of
appropriately timed atrial systole results in a marked
reduction of cardiac output
 Right atrial or coronary sinus pacing is indicated

125
• SINUS BRADYCARDIA  — Sinus bradycardia, defined as less than 50 to
60 beats/min, occurs in 15 to 25 percent of patients after acute MI . It has the
following clinical characteristics :
• It is frequently seen with inferior wall infarctions, since the right coronary artery
supplies the sinoatrial node (SA) in approximately 60 percent of people.
• It is most often transient, particularly for sinus bradycardia occurring within the
first six hours; such arrhythmias typically resolve within 24 hours.
• It is usually caused by increased vagal tone, often seen with inferior MI. Other
causes include ischemia of the SA node and as a reperfusion arrhythmia
following fibrinolysis .
• It is due to medications (beta-blockade).
• Treatment  — If therapy is necessary due to hemodynamic compromise or
ischemia, sinus bradycardia following an acute MI usually responds well to
intravenous atropine (0.6 to 1.0 mg in the majority of cases) . Persistent
bradycardia with hemodynamic compromise despite intravenous atropine
warrants consideration of temporary cardiac pacing . Atrial or sequential
atrioventricular pacing is superior to ventricular pacing, particularly if there is an
associated right ventricular MI

126
• Permanent pacing is not typically necessary in patients with sinus
bradycardia after an MI, because in most cases the bradyarrhythmia
is transient . Any decision to implant a permanent cardiac pacemaker
should be delayed for several days of observation.
• Mortality as a result of periinfarction sinus bradycardia is rare. Its
significance is related to the associated reduction in cardiac output
and coronary perfusion, thereby exacerbating ischemia, and to the
possible development of an escape rhythm with possible AV
dissociation causing hemodynamic compromise

127
 Sinus Bradycardia
• Symptomatic sinus bradycardia
• Iv Atropine in doses of 0.5 mg initially
• If the rate remains <50–60 bpm, additional doses of 0.2 mg, up to a total of 2.0
mg, may be given
• Persistent bradycardia (<40 bpm) despite atropine --electrical pacing
• Isoproterenol should be avoided.

128
NONPAROXYSMAL JUNCTIONAL
TACHYCARDIA  — 
• Junctional tachycardia (or an accelerated junctional tachycardia) is an
arrhythmia arising from a discrete focus within the AV node or His bundle.
The mechanism is thought to be one of enhanced automaticity rather than
reentry. In adults, this rhythm, generally called nonparoxysmal junctional
tachycardia, and is an uncommon arrhythmia associated with acute MI . The
same arrhythmia may also be seen with digitalis intoxication .
• Atrial activity during junctional tachycardia is variable. Retrograde atrial
activation may occur, with a P wave that either follows each QRS complex or
is concealed in the QRS complex, as with AVNRT. If retrograde conduction
does not occur, independent atrial activity may be seen, with complete AV
dissociation that must be distinguished from AV dissociation due to
complete heart block (in complete heart block, the atrial rate exceeds the
ventricular rate, while with an accelerated junctional tachycardia the atrial
rate is slower than the ventricular rate).
• Nonparoxysmal junctional tachycardia is typically transient, occurring within
the first 48 hours of infarction and developing and terminating gradually. No
specific antiarrhythmic therapy is indicated

129
Atrioventricular and Intraventricular Conduction
Disturbances

• Bradycardia due to AV block--Temporary electrical pacing

• Retrospective studies suggest that permanent pacing may reduce the
long-term risk of sudden death due to bradyarrhythmias in the rare
patient who develops combined persistent bifascicular and transient
3rd -degree heart block during the acute phase of MI.

130
 Pacing in STEMI

I IIa IIb III

Temporary pacing is indicated for symptomatic bradyarrhythmias
unresponsive to medical treatment.

131
Pericarditis

• Pericardial friction rubs and/or pericardial pain radiating to either

trapezius muscle is helpful, because such a pattern of discomfort is
typical of pericarditis but rarely occurs with ischemic discomfort.
• Anticoagulants potentially could cause tamponade & should not be
used
• Complication can usually be managed with aspirin (650 mg 4 times
daily).

132
 Management of Pericarditis After
STEMI
I IIa IIb III
Aspirin is recommended for treatment of pericarditis after STEMI.

I IIa IIb III

Administration of acetaminophen, colchicine, or narcotic
analgesics may be reasonable if aspirin, even in higher doses, is
not effective.

I IIa IIb III

Glucocorticoids and nonsteroidal antiinflammatory drugs are
potentially harmful for treatment of pericarditis after STEMI.
Harm

133
Thromboembolism

• In 10% of cases, but embolic lesions are found in 20% of necropsy

series,
• Cause of death in 25% of patients with STEMI
• Predisposing factor -large infarcts (especially anterior), CHF, and a LV
thrombus
• 2D –ECHO -reveals LV thrombi in about one-third of patients with
anterior wall infarction.
• Systemic anticoagulation-3-6 months
Arterial emboli originate from LV mural thrombi, while most
pulmonary emboli arise in the leg veins. The incidence of arterial
embolism from a clot originating in the ventricle at the site of an
infarction is small but real

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 Anticoagulation

I IIa IIb III

Anticoagulant therapy with a vitamin K antagonist is reasonable
for patients with STEMI and asymptomatic LV mural thrombi.

I IIa IIb III

Anticoagulant therapy may be considered for patients with
STEMI and anterior-apical akinesis or dyskinesis.

I IIa IIb III

Targeting vitamin K antagonist therapy to a lower international
normalized ratio (e.g., 2.0 to 2.5) might be considered in patients
with STEMI who are receiving DAPT.

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Mitral Regurgitation

• Mitral regurgitation after STEMI occurs via

• papillary muscle rupture
• postinfarction LV remodeling
• displacement of the papillary muscles, leaflet
tethering, and annular dilatation.

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Mitral Regurgitation

Acute severe MR
• Pulmonary edema and/or shock
• systolic murmur may not always be appreciated.
• Rx
• Temporary stabilization with medical therapy and IABP
• Mitral valve replacement > MV repair
Ischemic (functional)MR
• Rx
• timely reperfusion, diuretics, and after load reduction.

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 Ventricular septal rupture
• Occurs most often within the first 24 hrs
• Emergency surgical repair is necessary
• Percutaneous closure is a less invasive ??.
• transcatheter closure
• Temporary medacal Rx
• Inotropic and vasodilator agents, IABP when needed
• surgical mortality rate remains high(20% to 87%)
• Mortality risk is higher for patients with inferior-basal
defects than for those with anteriorapical defects.

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Free Wall Rupture

Features that characterize free wall rupture:

• Elderly
• HTN
• More frequently occurs in left ventricle
• Seldom occurs in atria
• Usually involves the anterior or lateral walls
• Usually associated with a relatively large transmural infarction involving
atleast 20% of the left ventricle
• It occurs between 1 day and 3 weeks, but most commonly 1 to 4 days after
infarction
• Most often occurs in patients without previous infarction

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Free Wall Rupture

Usually leads to hemopericardium and death from

cardiac tamponade
Occasionally, rupture of the free wall of the
ventricle occurs as the first clinical manifestation in
patients with undetected or silent MI, and then it
may be considered a form of “sudden cardiac
death”

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Free Wall Rupture

The coarse of rupture can vary from catastrophic,

with an acute tear leading to immediate death, to
subacute, with nausea, hypotension, and pericardial
type of discomfort
Survival depends on the recognition of this
complication, on hemodynamic stabilization of the
patient, and most importantly, on prompt surgical
repair

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 LV Aneurism
Described as dyskinesis or local expansile paradoxical wall motion
The complications of LV aneurysm do not usually occur for weeks to
months after STEMI; CHF, arterial embolism, and ventricular
arrhythmias.
Apical aneurysms
 most common
most easily detected by clinical examination
P/E -double, diffuse, or displaced apical impulse.
Ventricular aneurysms detected by 2d- echo --reveal a mural thrombus
in an aneurysm.
Because a pseudoaneurysm often ruptures spontaneously, it should be
surgically repaired if recognized.

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LV Aneurism

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Long term management

144
• Smoking -Complete cessation
• Blood pressure-< 140/90 mm Hg
• Physical activity-Minimum goal is 30 minutes 3 to 4 days per week, optimally
daily
• Weight management- Goal BMI 18.5 to 24.9 kg/m2, Waist circumference-
Women: < 35 in,Men: < 40 in.
• Diabetes management-Appropriate hypoglycemic therapy to achieve near-
normal HbA1c.

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Lipid management
• Start dietary therapy in all patients (< 7% of total calories as
saturated fat and < 200 mg/d cholesterol, trans fatty acids)
• Adding plant stanol/sterol(2gm/day)and /or viscous fiber
(>10gm/d).
• Promote physical activity and weight management.
• Encourage increased consumption of omega-3 fatty acids in
form of fish or capsules 1gm/d.

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• Assess fasting lipid profile in all patients,
preferably within 24 hours of STEMI.
• Add drug therapy according to the following
guide
• LDL-C should be < 100 mg/Dl
• Further reduction to <70mg/dl is reasonable

• LDL-C ≥ 100 mg/dL

• LDL-C–lowering therapy

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If TGs are ≥ 150 mg/dL or HDL-C is < 40 mg/dL
Emphasize weight management and physical
activity. Advise smoking cessation.
If TG is 200 to 499 mg/dL
After LDL-C–lowering therapy, consider adding
fibrate or niacin.
If TG is ≥ 500 mg/dL
Consider fibrate or niacin before LDL-C–lowering
therapy

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warfarin

• Managing warfarin to INR 2 to 3 in patients when

clinically indicated(AF or LV thrombus)

• when used in conjunction with antiplatelets should

be monitored closely

• INR of 2 to 2.5 is recommended in such patients

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 REFFERENCES

2013 ACCF/AHA Guideline for the

Management of ST-Elevation
Myocardial Infarction

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Thank you !

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