course intended for B Sc cardiac technology students

1. VENTRICULAR
ARRYTHMIA
DR.S.R.Sruthi Meenaxshi

2. PREMATURE VENTRICULAR
CONTRACTIONS
• Premature ventricular complexes/contractions (PVC; also referred to as premature
ventricular beats or premature ventricular depolarizations)are early occurring,
widened QRS complexes originating from the left or right ventricle that have a
distinct morphology (resembling neither a typical left nor right bundle branch block)
that is markedly different from the sinus QRS complex.
• Unifocal PVCs all have a single morphology. Multiple different QRS morphologies
are termed "multifocal PVCs" and usually originate from different locations in the
ventricles.

3. • 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,
though this is not a strict rule.

4. • Other findings on the electrocardiogram (ECG) include marked repolarization
abnormalities, manifested as ST segment and T wave abnormalities.
• 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 a retrograde P wave is present, it is 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. This
retrograde P wave is usually negative in leads II, III, and aVF.

6. • There can be many sinus node responses to a PVC. Most commonly, a full compensatory pause
follows the PVC; thus, the RR interval between the QRS complexes before and after the
premature beat is twice the RR interval between two successive sinus beats.
• The pause is due to retrograde AV nodal penetration of the PVC, which causes the AV node to
be refractory to the next on-time sinus impulse, which is blocked.
• The subsequent sinus impulse after this does conduct through the AV node to stimulate the
ventricle. In this situation, a normal appearing P wave may be seen, often buried in the ST
segment or T wave of the PVC, with no QRS following it.
• Other cases may have retrograde activation of the atrium with an inverted P wave in the inferior
leads and resultant delay of sinus node impulse generation. In this situation, the RR interval
between the QRS complex before and after the PVC may be less than two sinus beats.

7. • On occasion, the PVC may be interpolated.
• It occurs between two normal sinus QRS complexes, and the PP interval between
the QRS complex prior to and after the premature beat is the same as the
underlying sinus PP interval, due to lack of retrograde penetration into the AV
node.
• If the ventricular myocardium is no longer refractory from the PVC, it is capable of
again being stimulated from the next sinus beat.
• There also may be concealed retrograde conduction of the PVC into the AV node,
rendering it partially refractory and leading to a longer PR interval of the first sinus
beat following the premature complex.

9. • Ventricular bigeminy — Ventricular bigeminy is present when a premature
ventricular complex follows every sinus beat
• Ventricular bigeminy may become self-perpetuating, a situation known as the rule
of bigeminy.
• This occurs because the long cycle length after the prior PVC tends to precipitate
the next PVC after a sinus beat.

11. • Ventricular trigeminy — Ventricular trigeminy is present when there are
two sinus beats followed by the PVC. Thus, every third beat is a PVC

12. • Ventricular couplets — Ventricular couplets are defined as two PVCs in a
row
• There is often a compensatory pause after the second premature beat.
• The two premature beats may have an identical morphology (unifocal
couplet), or their morphology may differ (multifocal couplet).
• The RR interval between the two successive PVCs varies widely.

14. VENTRICULAR ESCAPE COMPLEXES
OR RHYTHM
• An escape ventricular beat or rhythm occurs when there is failure of the sinus and
atrioventricular (AV) node to generate an impulse.
• There is an absence of P wave activity, associated with a widened QRS complex that
resembles a premature ventricular complex/contraction (PVC; also referred to as premature
ventricular beats or premature ventricular depolarizations) and occurs after a pause of
variable duration (but always greater than the normal sinus RR interval).
• Persistence of this activity leads to multiple successive ventricular complexes, representing
an escape ventricular rhythm with a rate that is slower than the normal sinus rhythm.
• In cases of complete heart block in which there is sinus node activity but failure of
conduction through the AV node, there are P waves dissociated from the ventricular
complexes with a rate faster than the ventricular rate (AV dissociation)

16. VENTRICULAR PARASYSTOLE
• Ventricular parasystole represents an independent ectopic ventricular rhythm that
has no relationship to the sinus rhythm.
• It appears on the electrocardiogram (ECG) as a unifocal premature ventricular
complex/contraction (PVC; also referred to as premature ventricular beats or
premature ventricular depolarizations) with a variable coupling cycle (the interval
between the prior sinus beat and the premature beat varies)
• The interval between two successive PVCs is always constant or some integer of the
underlying rate of the ectopic focus.

18. • Ventricular parasystole is the result of an ectopic focus within the ventricular myocardium
or ventricular conduction system that manifests spontaneous automaticity and has a rate that
is slower than the underlying sinus rate.
• This focus is not suppressed or overdriven by the normal ventricular conduction because of
entrance block into the area of the ectopic focus; it is protected from suppression.
• However, the ectopic focus may or may not activate the ventricular myocardium and result
in a PVC, depending on the ability of the rest of the ventricular myocardium to be
stimulated, which in turn is determined by its state of refractoriness.
• Thus, there may also be intermittent exit block from this focus, and the PVC does not
appear at the expected time.

19. VENTRICULAR TACHYCARDIA
• Ventricular tachycardia (VT) is defined as three or more successive ventricular
complexes at a rate greater than 100 beats per minute.
• Nonsustained VT is a series of at least three consecutive ventricular beats that have
a duration of less than 30 seconds or do not require emergency intervention.
• Sustained VT lasts for more than 30 seconds or requires termination early because
of hemodynamic impairment.
• The rhythm is usually regular in monomorphic VT and irregular with polymorphic
VT.

20. • The morphology of the QRS complex during VT is usually different when
compared to the sinus beat.
• Additionally, it does not resemble either a typical left or right bundle branch block,
as ventricular activation is not via the normal His-Purkinje conduction system, but is
through direct ventricular myocardial activation.
• The QRS axis may be deviated to the left or to the right. The width of the QRS
complex is generally >0.16 sec when in a left bundle branch block pattern and
>0.14 sec when in a right bundle branch block pattern. Other useful features of
ventricular tachycardia include:

21. ●Atrioventricular (AV) dissociation, which is the hallmark of ventricular tachycardia. Subtle differences
in ST-T wave morphology representing possible superimposed P waves should be assessed.
●Presence of fusion or capture beats.
●Absence of an RS complex in all of the precordial leads.
●Longest R to S interval >100 ms in any precordial lead.
●Concordance of the QRS complex across the precordial leads (eg, only R waves or S waves in leads
V1-V6). However, this may be seen in any situation in which there is direct myocardial activation,
including Wolff-Parkinson-White pattern or a paced complex. Negative concordance is less useful, as
this may be seen with a left bundle branch block.
●A monophasic Rr' pattern in lead 1 (termed rabbit ears) with a taller left ear. This is often associated
with an rS or QS complex morphology in leads V5-V6.

22. • ●An indeterminate axis (between -90 and -180º). However, this may be seen in any situation in
which there is direct myocardial activation including a paced rhythm (especially biventricular
pacing) or Wolff-Parkinson-White pattern.
• ●In lead II, time from beginning of the QRS to first change of polarity ≥50ms, regardless of
whether the QRS change is positive or negative.
• ●In lead aVR, an initial R wave, width of the r or q wave >40ms, and/or notch on the
descending limb of a predominantly negative QRS.
• The VT is monomorphic when all of the QRS complexes of an episode are identical .
• However, monomorphic VT often displays subtle changes of the QRS complexes with regard to
morphology and width as a result of variable changes in the electrophysiologic properties of the
ventricular myocardium.

25. • When the QRS complexes within each episode display changing morphologies, often with grossly
irregular RR intervals, the VT is called polymorphic
• The differences in QRS morphology result from changes in the direction (vector) of myocardial
activation due to marked heterogeneity of the electrophysiologic characteristics of the ventricular
myocardium.
• The rate is usually between 100 and 330 beats per minute.
• If the polymorphic VT is associated with a baseline QRS complex that has a normal QT
interval, the most common etiology is ischemia.
• If the polymorphic VT is associated with a QRS complex on the baseline electrocardiogram
(ECG) that has QT prolongation, then it is termed "torsades de pointes." The QT prolongation
may be acquired, due to medications that prolong the QT interval

26. • The presence of AV dissociation is a very important finding and is usually
diagnostic of VT.
• However, it is not always present, or if present may not be easily recognized,
especially when the ventricular rate is very rapid (the RR cycle length is short).
• The P waves are not distinctive in these cases, but may alter the QRS complexes or
be superimposed upon the ST and T waves, causing irregular changes in their
morphology.

27. • AV dissociation occurs as a result of retrograde VA conduction that enters, but blocks, within the AV node
(concealed conduction).
• The retrograde concealed conduction into the node causes the node to be refractory to antegrade
stimulation, thereby blocking conduction from the atrium to the ventricle.
• If the tachycardia does not lead to antegrade AV block, fusion or capture beats may be present, as described
below. In some cases of VT, there is retrograde conduction through the AV node to the atria.
• There may be a variable degree of retrograde block (2:1, 3:1, or even Wenckebach); on occasion, there may
be 1:1 retrograde activation of the atrium and therefore no AV dissociation with a fixed RP interval.
• Dissociation is more obvious when the tachycardia rate is relatively slow. The P waves occur at a slower rate
than the QRS complexes, and there is no relationship between them.

28. • Other features of AV dissociation include:
• ●Fusion beats, which occur with a QRS complex that has features resembling a combination of the both the
sinus QRS and that of the VT.
• These result from simultaneous activation of the ventricles from the VT exit site as well as via a sinus beat
travelling down the normal AV nodal-His Purkinje pathway.
●Capture beat , which are intermittently captured QRS complexes that are identical to sinus complexes.
• They are preceded by a P wave, indicating that there is intermittent capture of the ventricles by the sinus
node via the normal AV nodal-His Purkinje pathway
• However, the occurrence of intermittent capture of the ventricle from above does not alter the VT or affect
its focus of origin.

29. • A fusion beat occurs when a supraventricular and a ventricular impulse coincide to
produce a hybrid complex. It indicates that there are two foci of pacemaker cells
firing simultaneously: a supraventricular pacemaker (e.g. the sinus node) and a
competing ventricular pacemaker (source of ventricular ectopics).
• The fusion beats are of intermediate width and morphology to the supraventricular
and ventricular complexes.
• Originally described by William Dressler in 1952.

33. • Idiopathic monomorphic ventricular tachycardia — Idiopathic monomorphic VT
occurs in those with no structural heart disease.
• It most frequently originates from the right ventricular outflow tract (RVOT) just inferior to
the pulmonary valve, but less frequently may occur in the left ventricular outflow tract,
sinuses of Valsalva, papillary muscles, moderator band, or other areas of the heart.
• RVOT VT has the ECG appearance of a left bundle branch block pattern with an inferiorly
directed axis. In general, these have a benign prognosis.

34. • Ventricular flutter — Ventricular flutter is a monomorphic VT that occurs
at a very rapid rate, usually around 300 beats per minute
• Often no distinctive T waves are discernible. There is no isoelectric interval
between QRS complexes. P waves or evidence of atrial activity are absent
since the ventricular rate is rapid.

36. • Torsades de pointes — Torsades de pointes is a rapid and distinct form of
polymorphic VT associated with a baseline prolonged QT interval. It means
"twisting of points," a name that refers to the continuously changing axis of
polymorphic QRS morphologies that are observed during each episode .
• The typical form is initiated by bradycardia or is pause dependent, with a short-
long-short coupling interval, ie, a PVC (short RR interval), a compensatory pause
(long RR interval), and second PVC (short RR interval)
• If the baseline QTc interval is normal, the rhythm is referred to as polymorphic VT
and not torsades de pointes.

39. ACCELERATED IDIOVENTRICULAR
RHYTHM
• An accelerated idioventricular rhythm (AIVR) occurs at a rate between 60 and 100 beats per
minute
• It is an accelerated ventricular focus that generates an impulse faster than the sinus node and
therefore assumes control.
• There may or may not be atrioventricular (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.

41. VENTRICULAR FIBRILLATION
• Ventricular fibrillation is identified by the complete absence of properly
formed QRS complexes and no obvious P waves .
• There is no uniform activation of the ventricular myocardium and the QRS
complexes have markedly different morphology, axis, and amplitude.
• The rate is irregular and usually greater than 300 beats per minute. When the
fibrillation is recent onset, the amplitude is usually high, but as time passes,
the fibrillatory waves become finer and may resemble asystole.
• Ventricular fibrillation leads promptly to cardiac arrest.

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