Transcript Ventricular arrhythmia

Mehdi Bakhshi
MSN.PhD
Take home points

PVCs are very common arrhythmias that can
occur in healthy or diseased hearts with
multiple features on ECG

VT and VF are dangerous arrhythmias that
can lead to sudden cardiac death

Not all wide complex tachyarrhythmias arise
from the ventricles

Distinguish between VT and SVT with aberrancy
because the treatment and prognosis of each is
very different
Ventricular arrhythmias

Commonly occur as
a result of ectopic
focus/foci distal to
the bundle of His

Most common one is
the premature
ventricular
contraction (PVC)

Most are benign but
can be lethal
Mechanisms of ventricular arrhythmias

Impulse Formation Disorders
 Abnormal Automaticity
○ Discharge from a pathologic ectopic ventricular focus
 Triggered beats
○ Afterdepolarizations (AD): Abnormal depolarizations of
myocytes that interrupt phase 2, 3, or 4 of the AP

Impulse Conduction Disorders
 Delayed conduction
○ Delayed SA/AV nodal impulse allows initiation of inherent
ventricular impulse
 Re-entry
○ Creation of a circuit that leads to 2 or more depolarizations in
surrounding tissue
Afterdepolarization
Early afterdepolarization (EAD)
occurs with abnormalities during phase 2 (interrupted due to augmented opening of Ca
channels) or phase 3 (opening of Na channels)
Delayed afterdepolarization (DAD)
begin during phase 4 - after repolarization is completed, but before another action
potential would normally occur. Due to elevated cytosolic Ca concentrations (digoxin
toxicity)
medresidents.stanford.edu/TeachingMaterials/EKGs%20and%20Arrhythmias/Arrythmias%20and%20EKGs%203.ppt
Types

Premature ventricular contraction (PVC)
 Bigeminy, trigeminy, couplets, interpolated,
monomorphic, multimorphic, fusion beat






Idioventricular rhythm/ accelerated
idioventricular rhythm
Ventricular parasystole
Ventricular tachycardia (VT)
Torsades de pointes
Ventricular flutter
Ventricular fibrillation (VF)
Premature Ventricular Contractions (PVCs)

Epidemiology
 Very common; occur in healthy people &
pts with cardiac disease

Etiology
 Cardiac: CAD, post-MI, MVP, CHF,
rheumatic heart disease, congenital
arrhythmias
 Non-cardiac: acid-base disturbance,
electrolyte abnormalities, meds, caffeine,
anxiety

Symptoms

Physical exam findings
 Palpitations, “skipped beats”
 Chest or neck discomfort
 Presence of premature beat
 Hypotension
 Decreased or absent peripheral pulses
(radial)
ECG Characteristics of PVCs




Ectopic beat originating from ventricles occurring
before next expected beat (premature)
Usually not proceeded by P wave
Wide QRS: at least > 0.12 sec, usually 0.16-0.2
with bizarre morphology
Large T wave in the opposite direction of the major
QRS deflection
ECG Characteristics of PVCs

Full Compensatory Pause
 Follows most PVCs
 PVCs usually do not conduct
retrograde to the atria, thus
SA nodal rhythm not
disturbed
 When SA node discharges,
the ventricles are still
refractory from the PVC and
don’t depolarize in response
to the impulse
 The interval between the first
sinus beat and the PVC plus
the interval between the PVC
and the next sinus beat = 2
normal sinus intervals
ECG Characteristics of PVCs

Interpolated PVCs




No compensatory pause
PVC occurs between 2 normal sinus beats
No change in the R-R interval
Usually seen when the HR is slow
ECG Characteristics of PVCs

Fusion beats
 Simultaneous activation of the ventricle from supraventricular impulse
and a PVC
 Ventricular depolarization occurs simultaneously in two directions
 QRS complex that has the characteristics of the PVC and the QRS
complex of the underlying rhythm

Captured beats (Dressler beats)


QRS complexes during a WCT that are identical to the sinus QRS
complex.
Implies that the normal conduction system has momentarily "captured"
control of ventricular activation from the VT focus.
ECG Characteristics of PVCs

R on T phenomenon
 PVC begins during mid/late T wave
 Associated with vulnerable ventricles often predisposing to polymorphic
VT or VF, especially in acute ischemia
PVC Patterns

Bigeminy
 PVC every other beat
 “Rule of bigeminy”: often
becomes selfperpetuating

Trigeminy
 PVC every 3rd beat

Couplets
 Two successive PVCs

Triplets
 Tree successive PVCs
 Rate <100bpm
PVC Morphology

Monomorphic

Polymorphic
 PVCs originate from a
 PVCs origniate from
single ventricular
ectopic focus
 Single wave
morphology
multiple ventricular
ectopic foci
 ≥ 2 morphologies
PVC Prognosis and Treatment

Prognosis

Post MI PVCs and
Lown’s class 3-5 are
associated with ↑ risk for
VT/VF and sudden
death

Treatment
 Lown Classification
○ Class 1: <30PVC/hr
○ Class 2: >30 PVC/hr
○ Class 3: Multiform
PVCs
○ Class 4a: PVC
couplets
○ Class 4b: PVC triplets
or greater
○ Class 5: R on T
 No changes in mortality
with PVC suppressive tx
 Asx, healthy:
reassurance
 Sx: B-Blockers
Idioventricular (Escape) rhythm

Escape rhythm due to failure
of SA/AVN ventricular
activation or complete
conduction block

Inherent 20-40bpm takes over
since it is no longer
suppressed

Regular wide QRS

Etiologies
 Post-MI, CM, digoxin toxicity
Accelerated Idioventricular Rhythm (AIVR)
Sinus bradycardia





AIVR
May result from accelerated ventricular focus that is faster
than the prevailing sinus rate and takes
over or can occur
rd
as escape rhythm ( generally with 3 degree AVN block)
Usually 60-100 bpm (differentiates from VT)
Regular wide QRS
Associated with post-MI (especially inferior wall MI),
reperfusion tx, digoxin toxicity, or after a PVC
Usually self limited, rarely see progression to VT/VF
Ventricular parasystole
Independent ectopic ventricular rhythm competing with the
sinus rhythm
 May or may not activate the ventricles
 Rate slower than sinus, but NOT overdriven because of
entrance block

 Sinus rhythm unable to enter the ectopic site and reset its timing
Unifocal PVCs with a variable coupling intervals
 Interectopic intervals are multiple of the basic rate (e.g. R-R)

Ventricular Tachycardia (VT)

Life threatening arrhythmia
 May lead to VF and sudden death

Etiologies
 Heart disease (prior MI, CAD, CM, valvular dz)

ECG findings
 ≥3 consecutive PVCs with a rate of 100-250 bpm
 No P waves
 QRS axis -30° to -180°
 AV dissociation
 Fusion beats and captured beats
 Duration
○ Non-sustained: <30sec
○ Sustained: >30 sec or requiring termination because of
hemodynamic collapse
Ventricular Tachycardia
Monomorphic VT
Polymorphic VT
VT Treatments
IV procainimide, amiodarone
 DC cardioversion

 Severe, symptomatic VT

Implanted ICD
 Indicated with decreased LV function

Radiofrequency ablation
Torsades de Pointes

“twisting of points” : changing axis of polymorphic QRS VT

Associated with congenital or acquired long QT, severe bradycardia, hypoK, hypoMg,
meds (TCAs, procainimide, quinidine)

ECG findings


Wide QRS complexes of changing amplitudes that appear to twist about the isoelectric line

Ventricular rate 200-250 bpm

Usually initiated by a long RR interval (like post PVC compensatory pause) followed by a short RR cycle
( e.g. R on T)
Treatment

Acquired: IV Magnesium + ventricular or atrial pacing

Congenital: B-blockers

Anti-arrhythmia drugs prolong the QT interval and worsen the arrhythmia
Long QT syndrome




Associated with Torsades and sudden death
Seen in young people whose ECG is normal except
for long QT interval
Rhythm abnormality can be precipitated by a startle
reaction
Two types
 Jarvell-Lange-Neilson syndrome- deafness
 Romano-Ward syndrome- without deafness


QTc >500ms in pts with LQT syndrome is
associated with an increased risk of sudden death
QTc>430ms with FHx makes LQTS gene defect
likely
Ventricular Fibrillation

Disordered ventricular impulses with no coordinated ventricular contraction

No cardiac output occurs & pt immediately loses consciousness

Can occur with any type of cardiac disease, electrolyte imbalance, hypoxemia,
acidosis, shock, drugs (epi, cocaine)

ECG findings


Chaotic, irregular complexes; no discrete QRS waveforms

Rate: 350-450 bpm

Can occur spontaneously or preceded by PVCs or VT
Treatment

Immediate defibrillation followed by anti-arrhythmic drugs to suppress further ventricular ectopy
Brugada syndrome






Associated with VT/ VF and sudden death
If symptomatic, mortality risk up to 10% per
yr
AD inheritance pattern, SCN5A gene
mutation
Endemic in SE Asia
Arrhythmia start in 30-40’s, often during
sleep or rest
May be triggered by fever, sodium channel
blocker, or spontaneous
ECG change in Brugada


RV conduction delay or block morphology V1
Unusual ST elevation segments in http://en.ecgpedia.org/wiki/Brugada_Syndrome
V1-V3
www.ojrd.com/content/1/1/35/figure/F1
Wide complex tachyarrhythmias
QRS greater or equal to 0.12 sec and rate
>100 bpm
 Not all are of ventricular origin
 Differential

 Ventricular tachycardia
 Supraventricular tachycardia with aberrancy
(conduction block) or presence of an accessory
pathway with antegrade conduction (WPW
syndrome)
 Artifact
VT vs SVT with Aberrancy


Both manifest as wide complex tachycardias on ECG
Distinguishing ECG findings:
 SVT with aberrant conduction
○ QRS > 0.14
○ Rhythm onset with premature P wave
○ PR interval <100msec
○ P wave and QRS are linked
○ Vagal maneuver slows/terminates rhythm
 Monomorphic VT
○ QRS >0.14 msec
○ AV dissociation with fusion or capture beats
○ Absence of RS complex in precordial leads
○ Extreme axis deviation
 If above findings fail to be detected, morphologic criteria used: if
QRS in V1 does NOT look like typical R or L conduction block
VT vs SVT with Aberrancy
Clinical importance

Misdiagnosing VT as SVT can lead to fatal
error

Treating VT as SVT with verapamil,
diltiazem, and adenosine can precipitate
ventricular fibrillation, even if initially stable.

All wide complex tachyarrhythmia should be
considered VT until proven otherwise
Take home points

PVCs are very common arrhythmias that can
occur in healthy or diseased hearts with
multiple features on ECG

VT and VF are dangerous arrhythmias that
can lead to sudden cardiac death

Not all wide complex tachyarrhythmias arise
from the ventricles

Distinguish between VT and SVT with aberrancy
because the treatment and prognosis of each is
very different
Reference






Previous Harvey Hand out
Up to date
ECG learning center
http://library.med.utah.edu/kw/ecg/ecg_outline
ECG pedia org http://en.ecgpedia.org
Lilly: Pathophysiology of Heart Disease. 3rd
edition, 2003.
Google images