Download ventricular ectopic beats and exercise

PVC’s 
DR MEHDY HASANZADEH.
MUMS.
MAY 2013
PREMATURE BEATS
Premature beats ,the most common
cause of irregular pulse , originated :
 Most commonly from the ventricles
 Less often from the atria and AVN
 Rarely from the sinus node

PREMATURE VENTRICULAR
CONTRACTIONS (PVC’S)
VENTRICULAR PREMATURE
BEATS (VPB’S)
VENTRICULAR ECTOPIC
BEAT’S
In terms of position in the cardiac cycle, 
ventricular extrasystoles are premature
ventricular depolarizations, which
originates from a source which is located
distal to the bifurcation of His fascicle
HOW COMMON
MULTIPLE RISK FACTOR
INTERVENTION TRIAL (MR FIT)
PVC’S ON A TWO MINUTE RHYTHM
STRIP ... 4.4% OF APPARENTLY
HEALTHY WHITE MEN
24 H HOLTER MONITORING OF
MALE MEDICAL STUDENTS ... 50 %
HAD AT LEAST ONE PVC, 2 % HAD
MORE THAN 50.
BY EXERCISE STRESS TESTING ... 7
- 20 %
VPB/PVC

VEBs have been described in 1% of
clinically normal people as detected by
standard ECG and 40–75% of apparently
healthy persons as detected by 24–48
hour ambulatory (Holter) ECG recording
STATISTICAL IMPLICATIONS
IN MR FIT 3 FOLD INCREASE IN
SCD AT 7 YR FOLLOW UP
IN A STUDY OF 45K VETERANS 3.8
% HAD PVC’S ON A RESTING EKG
AND A SIGNIFICANTLY HIGHER
MORTALITY (39 VS 22 %)
SIMILAR FINDINGS ELSEWHERE
SYMPTOMS
SKIPPED BEATS
EXTRA BEATS
MISSING BEATS
THUMPING
FORCEFUL BEATS
CHEST PAIN
DIZZINESS
EFFECTIVE BRADYCARDIA
RACING
On a healthy heart, ventricular extrasystoles
occur in the following situations: excessive
consumption of coffee, tobacco abuse,
emotions, stress;
 On a diseased heart: coronary artery disease,
cardiomyopathy, mitral regurgitation, left
ventricular arrhythmogenic dysplasia;
 Iatrogenic, ventricular extrasystoles appear: in
digoxin toxicity, after initiation of fibrinolytic
therapy in myocardial infarction and in
hypokalaemia

VENTRICULAR PREMATURE BEATS
1).The QRS complex is premature ,is 0.12second
or more wide ,and is aberrant , notched ,or
slurred .It is associated with a T wave that
usually point in a direction opposite to the main
deflection of the QRS complex.
2).The premature QRS complex is not preceded
by a P wave.
PVC
Extremely common throughout the population, 
both with and without heart disease
Usually asymptomatic, except rarely dizziness or 
fatigue in patients that have frequent PVCs and
significant LV dysfunction
PREMATURE VENT BEATS
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PVCs occur in association with various stimuli and
can be produced by direct mechanical, electrical,
and chemical stimulation of the myocardium.
Often, they are noted in patients with LV false
tendons, during infection, in ischemic or inflamed
myocardium, and during hypoxia, anesthesia, or
surgery.
They can be provoked by various medications,
electrolyte imbalance, tension states, myocardial
stretch, and excessive use of tobacco, caffeine, or
alcohol.
Both central and peripheral autonomic stimulation
have profound effects on the heart rate and can
produce or suppress premature complexes.
GRADING SYSTEM FOR VENTRICULAR
ECTOPY
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Grade Characteristic
1 Uniform ventricular premature beats
(fewer than 30/hour)
2 Uniform ventricular premature beats
(more than 30Ihour)
3 Multiform ventricular premature beats
4A Couplets (two consecutive ventricular premature
beats)
4B Triplets (three or more consecutive ventricular premature beats)
5 R-on-T phenomenon
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Ventricular extrasystoles can be:
Unifocal, QRS morphology is identical in all
leads;
Multifocal, QRS morphology is different in ECG
leads, which means that the QRS complexes
originate in one or more ectopic outbreaks;
Isolated, characterized by the occurrence of a
single ventricular extrasystole;
Systematized: the appearance of two or more
ventricular extrsystoles under the form of
bigeminy, trigeminy, etc
Based on Holter monitoring, Lown proposed the following
classification of ventricular extrasystoles:
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Class 0: absence ventricular extrsystoles at least 3 hours;
Class I: premature ventricular extrasystoles, monomorphic and
occasional, the occurrence is less than one ventricular
extrasystole per minute or less than 30 ventricular extrasystoles
per hour.
Class II: frequent monomorphic ventricular extrasystoles, more
than one ventricular extrasystole per minute or more than 30
ventricular extrasystoles per hour.
Class IIIa: polymorphic ventricular extrasystoles (multifocal).
Class IIIb: systematized ventricular extrasystoles (bigeminy,
trigeminy).
Class IVa: coupled repetitive ventricular extrasystoles (2
ventricular extrasystoles).
Class IVb: repetitive triplets of ventricular extrasystoles (3
ventricular extrasystoles).
Class V: R/T phenomena.
Classes I and II benefit from treatment of
the disease that lead to the appearance of
extrasystoles;
 Classes III, IV and V: monitoring,
determining of pathological substrate,
correcting electrolyte and acid-base
disorders, myocardial ischemia and other
factors incriminated that are causing the
ventricular extrasystoles. Administration of
beta blockers, amiodarone or lidocaine, all
intravenously

HTN AND PVC,S
in patients with systemic hypertension there is a
statistical relationship between VEBs and left
ventricular hypertrophy and the latter is related
to mortality, especially sudden death, in these
patients.
There is ongoing debate as to whether VEBs in
these conditions are genuinely specific markers
for malignant arrhythmias or simply markers for
the severity of the disease process, as in the
case for other structural heart diseases, such as
non‐ischaemic dilated cardiomyopathy.
VENTRICULAR ECTOPIC BEATS AND
EXERCISE

Although it was concluded that
exercise‐induced VEBs were not
associated with hard coronary heart
disease events, both infrequent and
frequent VEBs on exercise were
associated with an increase in all‐cause
mortality over 15 years of follow‐up.
IMPORTANCE OF PVC,S

The importance of PVCs depends on the
clinical setting. In the absence of
underlying heart disease, the presence
of PVCs usually has no impact on
longevity or limitation of activity;
antiarrhythmic drugs are not indicated.
Patients should be reassured if they are
symptomatic.
IMPORTANCE OF PVC,S /2
In some patients, frequent PVCs alone 
can cause heart failure that is reversed
when the PVC site is ablated.
IMPORTANCE OF PVC,S/3

Long runs of frequent PVCs in patients
with heart disease can produce angina,
hypotension, or heart failure. Frequent
interpolated PVCs actually represent a
doubling of the heart rate and can
compromise the patient's hemodynamic
status.
PVC,S AND MI

Before the widespread use of reperfusion
therapy, aspirin, beta blockers, and
intravenous nitrates in the management of
STEMI, it was believed that frequent
ventricular premature complexes (VPCs;
more than five/min), VPCs with multiform
configuration, early coupling (the R-on-T
phenomenon), and repetitive patterns in
the form of couplets or salvos presaged
ventricular fibrillation.
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In patients suffering from acute myocardial
infarction, PVCs once considered to presage the
onset of VF, such as those occurring close to the
preceding T wave, more than five or six per
minute, bigeminal or multiform complexes, or
those occurring in salvoes of two or three or
more, do not occur in about 50% of patients in
whom VF develops, and VF does not develop in
about 50% of patients who have these PVCs.
Thus, these PVCs are not particularly helpful
prognostically. The presence of 1 to 10 or more
ventricular extrasystoles per hour can identify
patients at increased risk for VT or sudden
cardiac death after myocardial infarction but is
similarly nonspecific.
PVCs are more frequent in the
morning in patients after myocardial
infarction, but this circadian variation
is absent in patients with severe left
ventricular (LV) dysfunction.

Because the incidence of ventricular
fibrillation in patients with STEMI seen in
CCUs over the past three or four decades
appears to be declining, the prior
practice of prophylactic suppression of
ventricular premature beats with
antiarrhythmic drugs no longer is
necessary, and its use may actually
increase the risk of fatal bradycardic and
asystolic events.
HOW DO PEOPLE PRACTICE
ELECTROPHYSIOLOGISTS PRACTICE WITH THE
FOLLOWING PRINCIPLES
1. EXCLUDE STRUCTURAL HEART DISEASE (LV
DYSFUNCTION ETC)
ELECTROPHYSIOLOGISTS PRACTICE WITH THE
FOLLOWING PRINCIPLES
1. EXCLUDE STRUCTURAL HEART DISEASE (LV
DYSFUNCTION ETC)
2. EXCLUDE CAD AND LOOK FOR VT WITH EXERCISE
ELECTROPHYSIOLOGISTS PRACTICE WITH THE
FOLLOWING PRINCIPLES
1. EXCLUDE STRUCTURAL HEART DISEASE (LV
DYSFUNCTION ETC)
2. EXCLUDE CAD AND LOOK FOR VT WITH EXERCISE
3. IS IT A TYPICAL BENIGN PVC? (REALIZING THAT A SMALL
PROPORTION OF THESE ARE LIFE THREATENING)
ELECTROPHYSIOLOGISTS PRACTICE
WITH THE FOLLOWING PRINCIPLES
1. EXCLUDE STRUCTURAL HEART DISEASE (LV
DYSFUNCTION ETC)
2. EXCLUDE CAD AND LOOK FOR VT WITH
EXERCISE
3. IS IT A TYPICAL BENIGN PVC? (REALIZING THAT
A SMALL PROPORTION OF THESE ARE LIFE
THREATENING)
4. IS THERE ANYTHINNG ELSE OBVIOUSLY
WRONG ( QT PROLONGATION ETC...)
WHO IS AT RISK?
LV DYSFUNCTION
CAD
CMP
QT PROLONGATION
SYNCOPE
SHORT COUPLED/FAST NSVT
HIGH PVC BURDEN
FHX SCD
HOW TO APPROACH
Patients with VEBs often describe “missing a
beat” or “feeling the heart has stopped”,
being aware of the compensatory pause
following VEBs, as well as “extra beats” or
“thumps”.
 The frequency and severity of these
symptoms should be assessed. The
presence, duration and frequency of any
fast palpitation should be noted and any
association with pre‐syncope or syncope
recorded.
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HOW TO APPROACH
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Patients should be asked about any triggering factors,
especially exercise.
The presence of ischemic or structural heart disease should
be considered, taking clues from past medical history and
other cardiac symptoms, especially those suggesting the
presence of heart failure.
Caffeine, alcohol, and drug intake should be noted as well
as smoking habits.
Family history may be relevant especially if there has been
sudden death or other clues towards a genetic syndrome or
cardiomyopathy.
Clinical examination should be aimed at identifying any
structural heart disease and/or heart failure.
HOW TO APPROACH
The morphology of VEBs should be
assessed in all the available rhythm
recordings including 12‐lead ECG, Holter
recording and ECG during ETT.
 It should be determined if the VEBs are
coming from a single focus (unifocal) or
from many sites (multifocal).
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HOW TO APPROACH
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Repetitive unifocal activity, especially associated
with exercise, is suggestive of triggered activity
primed by catecholamines, and the presence of
monomorphic VT, whether non‐sustained
(< 30 s) or sustained (> 30 s), should be sought.
VEBs which reduce in frequency on exercise are
generally regarded as “benign” while multifocal
VEBs provoked on ETT may signify an underlying
risk of cardiac disease even in the absence of
conventional ischaemic changes .
TREATING PATIENTS WITH VENTRICULAR
ECTOPIC BEATS: KEY POINTS
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Ventricular ectopic beats (VEBs) are frequently
seen in daily clinical practice and are usually
benign
Presence of heart disease should be sought
and, if absent, indicates good prognosis in
patients with VEBs
There is no clear evidence that caffeine
restriction is effective in reducing VEB
frequency, but patients with excessive caffeine
intake should be cautioned and appropriately
advised if symptomatic with VEB,S

In the absence of heart disease or significant risk
factors, patients with symptoms of VEBs that are
self‐limiting or respond to lifestyle modifications
may simply be reassured while patients with
ongoing or worsening symptoms should undergo
further investigations. These include a resting
12‐lead ECG, echocardiography, ambulatory Holter
recording and exercise tolerance test (ETT).
Echocardiography is important as both ventricular
function and the presence or absence of structural
heart disease are important considerations in
assessing the need for further intervention and
treatment
Unifocal VEBs arising from the right
ventricular outflow tract are common and
may increase with exercise and cause
non‐sustained or sustained ventricular
tachycardia. Catheter ablation is effective
and safe treatment for these patients
 β blockers may be used for symptom
control in patients where VEBs arise from
multiple sites. It should also be considered
in patients with impaired ventricular
systolic function and/or heart failure.
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Risk of sudden cardiac death from
malignant ventricular arrhythmia should
be considered in patients with heart
disease who have frequent VEBs.
Implantable cardioverter‐defibrillator
may be indicated if risk stratification
criteria are met
VEBs have also been shown to trigger
malignant ventricular arrhythmias in
certain patients with idiopathic
ventricular fibrillation and other
syndromes. Catheter ablation may be
considered in some patients as
adjunctive treatment
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In most patients, PVCs (occurring as
single PVCs, bigeminy, or trigeminy but
excluding nonsustained VT) do not need
to be treated, particularly if the patient
does not have an acute coronary
syndrome, and treatment is usually
dictated by the presence of symptoms
attributable to the PVCs
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Frequent PVCs, even in the setting of an
acute myocardial infarction, need not be
treated unless they directly contribute to
hemodynamic compromise, which is very
rare. If maximum dosages of lidocaine
are unsuccessful, intravenous
procainamide can be tried.
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Propranolol is suggested if other drugs
have been unsuccessful. Intravenous
magnesium can be useful. In most
patients, PVCs need not be treated, and
reassurance that they are benign in
those without structural heart disease
often is sufficient for most patients

Beta blockers are often the first line of
therapy. If they are ineffective, class IC
drugs seem particularly successful in
suppressing PVCs, but flecainide and
moricizine have been shown to increase
mortality in patients treated after
myocardial infarction and thus should be
reserved for patients without coronary
artery disease or LV dysfunction.

Amiodarone can be effective, but
because of its side effects, it should be
reserved for highly symptomatic patients
and those with structural heart disease
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For patients with significant symptoms,
particularly those with reduced cardiac
function, RF ablation of the PVC focus
can be effective and improve cardiac
performance. Low levels of serum
potassium and magnesium are
associated with higher prevalence rates
of ventricular arrhythmias
An approach to the treatment of patients with ventricular ectopic beats
Structural heart
disease
Frequent VEBs or
VT
Frequent
symptoms
Treatment
–
– (↓ on exercise)
–
Reassure
–
–
+
β blocker
–
+ (monomorphic) ±
Catheter ablation
+
–
1. Assess SCD
risk
±
2. β blocker
+
+
±
1. β blocker
2. ICD if high
SCD risk
ADENOSINE FOR SUSTAINED VT
BETA BLOCKERS EFFECTIVE IN 25 - 50
%
CALCIUM CHANNEL BLOCKERS
EFFECTIVE 25 - 30 %
COMBINATION OF BB AND CACB
SYNERGISTIC
DILT AND VERAPAMIL EQUALLY
EFFECTIVE
1C RX EFFECTIVE 25 - 50 %
SOTALOL AND AMIO MORE EFFECTIVE