Download ECG in Ventricular arrhythmias

ECG in Ventricular
arrhythmias
Dr Mostafa Hekmat
Cardiologist
Electrophysiologist
A look at ventricular arrhythmias
• Ventricular arrhythmias originate in
the ventricles below the bundle of
His.
• They occur when electrical impulses
depolarize the myocardium using a
different pathway from normal
impulses
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A look at ventricular arrhythmias
• Ventricular arrhythmias appear on an
ECG in characteristic ways.
• The QRS complex is wider than
normal because of the prolonged
conduction time through the
ventricles
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A look at ventricular arrhythmias
• The T wave and the QRS complex deflect
in opposite directions because of the
difference in the action potential during
ventricular depolarization and
repolarization.
• P wave is absent because atrial
depolarization doesn’t occur
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No kick from the atria
• When electrical impulses are generated from
the ventricles instead of the atria, atrial kick is
lost
• Cardiac output decreases by as much as 30%.
• Patients with ventricular arrhythmias may
show signs and symptoms of cardiac
decompensation, including hypotension,
angina, syncope, and respiratory distress.
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Potential to kill
• Although ventricular arrhythmias may be
benign, they’re potentially deadly
because the ventricles are ultimately
responsible for cardiac output.
• Rapid recognition and treatment of
ventricular arrhythmias increases the
chance for successful resuscitation
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Premature ventricular contraction
• A PVC is an ectopic beat that may occur in
healthy people without causing problems.
• PVCs may occur singly, in clusters of two or
more, or in repeating patterns, such as
bigeminy or trigeminy
• When PVCs occur in patients with underlying
heart disease, they may indicate impending
lethal ventricular arrhythmias
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Premature ventricular contraction
• PVCs are usually caused by electrical
irritability in the ventricular
conduction system or muscle tissue.
• This irritability may be provoked by
anything that disrupts normal
electrolyte shifts during
cell depolarization and repolarization
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Premature ventricular contraction
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Electrolyte imbalances, such as hypokalemia, hyperkalemia,
hypomagnesemia, and hypocalcemia
Metabolic acidosis
Hypoxia
Myocardial ischemia and infarction
Drug intoxication, particularly cocaine, amphetamines, and tricyclic
antidepressants
Enlargement of the ventricular chambers
Increased sympathetic stimulation
Myocarditis
Caffeine or alcohol ingestion
Proarrhythmic effects of some antiarrhythmics
Tobacco use.
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Premature ventricular contraction
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PVCs are significant for two reasons.
1, they can lead to more serious
arrhythmias, such as ventricular tachycardia
or ventricular fibrillation.
The risk of developing a more serious
arrhythmia increases in patients with
ischemic or damaged hearts.
2,PVCs also decrease cardiac output,
especially if the ectopic beats are frequent
or sustained.
Decreased cardiac output is caused by
reduced ventricular diastolic filling time and
a loss of atrial kick
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PVC
• PVCs look wide and bizarre and appear as early
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beats causing atrial and ventricular irregularity.
The P wave is usually absent.
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Retrograde P waves may be stimulated by the PVC and
cause distortion of the ST segment.
• The PR interval and QT interval aren’t measurable
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on a premature beat,
QRS complex in the premature beat exceeds 0.12
second.
The T wave in the premature beat has a deflection
opposite that of the QRS complex.
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R-on-T
• When a PVC strikes on the downslope of the
preceding normal T wave it can trigger more
serious rhythm disturbances
• Because the cells haven’t fully repolarized, VT or
VF can result
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The pause that compensates
•Interval between two
normal sinus beats
containing a PVC equals
two normal sinus intervals.
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An interpolated PVC
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Multiform
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Couplet
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Bigeminy
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CLINICAL FEATURES
• The prevalence of premature complexes
increases with
• Age
• Male gender
• Hypokalemia
• PVCs are more frequent in the morning in
patients after MI
• This circadian variation is absent in patients with
severe left ventricular dysfunction.
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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
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Identifying idioventricular rhythm
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Accelerated idioventricular rhythm
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Torsades de pointes
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Torsades de pointes
• Is a special form of polymorphic
ventricular tachycardia
• The rate is 150 to 250 beats/minute,
usually with an irregular rhythm, and
the QRS complexes are wide with
changing amplitude.
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Torsades de pointes
• This arrhythmia may be paroxysmal,
starting and stopping suddenly, and may
deteriorate into ventricular fibrillation
• Reversible causes
• Amiodarone, ibutilide, erythromycin,
haloperidol, droperidol, and sotalol
• Myocardial ischemia and electrolyte
abnormalities, such as hypokalemia,
hypomagnesemia, and hypocalcemia
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Ventricular fibrillation
• Electrical activity in the ventricles
• Electrical impulses arise from many
different foci.
• It produces no effective muscular
contraction and no cardiac output.
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Ventricular tachycardia
• Three or more PVCs occur in a row and the
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ventricular rate exceeds 100 beats/minute
VT is an extremely unstable rhythm.
It can occur in short, paroxysmal bursts lasting
fewer than 30 seconds and causing few or no
symptoms.
Alternatively, it can be sustained, requiring
immediate treatment to prevent death, even in
patients initially able to maintain adequate cardiac
output
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Ventricular tachycardia
• Conditions that can cause ventricular tachycardia
include:
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MI
Coronary artery disease
Valvular heart disease
Heart failure
Cardiomyopathy
Electrolyte imbalances such as hypokalemia
Drug intoxication from digoxin (Lanoxin), procainamide,
Quinidine, or Cocaine
Proarrhythmic effects of some antiarrhythmics
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Unpredictable V-tach
• A patient may be stable with a normal pulse and
adequate hemodynamics or unstable with
hypotension and no detectable pulse.
• Because of reduced ventricular filling time and
the drop in cardiac output, the patient’s
condition can quickly deteriorate to ventricular
fibrillation and complete cardiac collapse
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Ventricular tachycardia
• The ventricular rate is usually rapid—100 to 250
beats/minute.
• The P wave is usually absent but may be
obscured by the QRS complex.
• Retrograde P waves may be present.
• The QRS complex is wide and bizarre, usually
with an increased amplitude and a duration of
longer than 0.12 second.
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VT + RBBB
• (1) the QRS complex is monophasic or
biphasic in V1, with an initial deflection
different from that of the sinus-initiated
QRS complex
• (2) the amplitude of the R wave in V1
exceeds the R′
• (3) a small R and large S wave or a QS
pattern in V6 may be present.
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Left Septal VT
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VT + LBBB
• (1) the axis can be rightward, with
negative deflections deeper in V1
than in V6,
• (2) a broad prolonged (more than 40
milliseconds) R wave in V1
• (3) a small Q–large R wave or QS
pattern in V6 can exist
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RVOT VT
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VT
• QRS duration exceeding 140 milliseconds
• In precordial leads with an RS pattern, the duration
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of the onset of the R to the nadir of the S exceeding
100
Fusion beat
Capture beat
AV dissociation has long been considered a
hallmark of VT
Retrograde VA conduction to the atria from
ventricular beats occurs in at least 25% of patients
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Supraventricular arrhythmia
with aberrancy
• (1) consistent onset of the tachycardia with a premature
P wave
• (2) very short RP interval (0.1 sec)
• (3) QRS configuration the same as that occurring from
known supraventricular conduction at similar rates
• (4) P wave and QRS rate and rhythm linked to suggest
that ventricular activation depends on atrial discharge
(an AV Wenckebach block)
• (5) slowing or termination of the tachycardia by vagal
maneuvers
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• A QRS complex in V1 - V6,  either all negative or all
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positive  favors a VT
The presence of a 2 : 1 VA block  VT
Positive QRS complex in V1 - V6
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Can also occur from conduction over a left-sided accessory
pathway.
• Supraventricular beats with aberration
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Triphasic pattern in V1
An initial vector of the abnormal complex similar to that of the
normally conducted beats
Wide QRS complex with long-short cycle sequence
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Treatment
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Treatment
•PVCs, even in the setting of an
acute MI, need not be treated
unless they directly contribute
to hemodynamic compromise
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Treatment
•Any wide QRS complex
tachycardia should be treated
as ventricular tachycardia until
definitive evidence is found to
establish another diagnosis
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Treatment
• Beta blockers are often the first line of therapy.
• If they are ineffective, class IC drugs seem
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particularly successful in suppressing PVCs,
Flecainide and Moricizine have been shown to
increase mortality in patients treated after MI
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Should be reserved for patients without coronary artery
disease or LV dysfunction
• Amiodarone
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Should be reserved for highly symptomatic patients and
those with structural heart disease.
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