Arrhythmias and

Conduction Disorders
Professor V. Syvolap
 Standard ECG Components
By convention, the
ECG tracing is divided
into the
P wave,
PR interval,
QRS complex,
QT interval,
ST segment,
T wave, and
U wave
 Normal rhythm
 The resting sinus heart rate in
adults is usually 60 to 100
beats/min.

 Normally, a marked diurnal

variation in heart rate occurs,
with lowest rates just before
early morning awakening.
 Normal rhythm
 A slight increase in rate during
inspiration with a decrease in rate
during expiration (respiratory
sinus arrhythmia) is also normal;
 it is mediated by oscillations in
vagal tone and is particularly
common among healthy young
people.
 Normal rhythm
 The oscillations lessen but do not
entirely disappear with age.
 Absolute regularity of the sinus
rhythm rate is pathologic and
occurs in patients with autonomic
denervation (eg, in advanced
diabetes) or with severe heart
failure.
 Normal rhythm
 Most cardiac electrical activity is
represented on the ECG, although SA
node, AV node, and His-Purkinje
depolarization does not involve enough
tissue to be detected.
 The P wave represents atrial
depolarization. The QRS complex
represents ventricular depolarization,
and the T wave represents ventricular
repolarization.
 Normal rhythm
 The PR interval (from the
beginning of the P wave to the
beginning of the QRS complex) is
the time from the beginning of
atrial activation to the beginning
of ventricular activation. Much of
this interval reflects slowing of
impulse transmission in the AV
node.
 Normal rhythm
 The R-R interval (time between 2
QRS complexes) represents the
ventricular rate.
 Normal rhythm
 The QT interval (from the beginning of the QRS
complex to the end of the T wave) represents
the duration of ventricular depolarization.
 Normal values for the QT interval are slightly
longer in women; they are also longer with a
slower heart rate.
 The QT interval is corrected (QTc) for influence
of heart rate. The most common formula (all
intervals in sec) is:
 Sinus bradycardia

Slower rates (heart rate less then

60 b/m) occur in young people,
particularly athletes and during sleep.
 Sinus tachycardia

Faster rates (heart rate more then

100 b/m) occur with exercise, illness,
or emotion through sympathetic neural
and circulating catecholamine drive.
 Pathophysiology

Rhythm disturbances result from

 abnormalities of impulse formation,

 impulse conduction,

 or both.
 Bradyarrhythmias

result from decreased intrinsic

pacemaker function or blocks in
conduction, principally within the
AV node or the His-Purkinje
system.
 Tachyarrhythmias

Most tachyarrhythmias are caused

by
 reentry;

 some result from enhanced

normal automaticity
 or from abnormal mechanisms of
automaticity.
 Reentry

is the circular propagation of an

impulse around 2 interconnected
pathways with different conduction
characteristics and refractory periods
 Reentry
Two pathways
connect the same
points. Pathway A
has slower
conduction and a
shorter refractory
period. Pathway B
conducts normally
and has a longer
refractory period.
 Reentry
I. A normal impulse arriving at 1 goes down
both A and B pathways. Conduction through
pathway A is slower and finds tissue at 2
already depolarized and thus refractory. A
normal sinus beat results.
 Reentry
II. A premature impulse finds pathway B refractory and
is blocked, but it can be conducted on pathway A
because its refractory period is shorter. On arriving at 2,
the impulse continues forward and retrograde up
pathway B, where it is blocked by refractory tissue at 3.
A premature supraventricular beat with an increased PR
interval results.
 Reentry
III. If conduction over pathway A is sufficiently slow, a
premature impulse may continue retrograde all the way
up pathway B, which is now past its refractory period.
If pathway A is also past its refractory period, the
impulse may reenter pathway A and continue to circle,
sending an impulse each cycle to the ventricle (4) and
retrograde to the atrium (5), producing a sustained
reentrant tachycardia.
 Atrial premature beats
Atrial premature beats (APBs), or premature
atrial contractions (PACs), are common
episodic impulses.
They may occur in normal hearts with or
without precipitating factors (eg, coffee, tea,
alcohol, pseudoephedrine) or may be a sign
of a cardiopulmonary disorder.
They are common in patients with COPD.
 Atrial premature beats
Diagnosis is by ECG APBs may be normally,
aberrantly, or not conducted and are usually
followed by a noncompensatory pause.

Aberrantly conducted APBs (usually with

right bundle branch block morphology) must
be distinguished from premature beats of
ventricular origin.
 Atrial premature beats

In lead II, after the 2nd beat of sinus origin, the

T wave is deformed by an APB. Because the APB
occurs relatively early during the sinus cycle,
the sinus node pacemaker is reset, and a pause
—less than fully compensatory—precedes the
next sinus beat.
 Atrial tachycardia
Atrial tachycardia is a regular rhythm
caused by the consistent, rapid atrial
activation from a single atrial focus.
Heart rate is usually 150 to 200
beats/min; however, with a very rapid
atrial rate, nodal dysfunction, or
digitalis toxicity, atrioventricular (AV)
block may be present, and ventricular
rate may be slower.
 Atrial tachycardia
Mechanisms include enhanced atrial
automaticity and intra-atrial reentry.
Atrial tachycardia is the least common
form (5%) of supraventricular
tachycardia and usually occurs in
patients with a structural heart
disorder. Other causes include atrial
irritation (eg, pericarditis), drugs (eg,
digoxin), alcohol, and toxic gas
inhalation.
 Atrial tachycardia

Symptoms are those of other

tachycardias. Diagnosis is by ECG; P
waves, which differ in morphology
from normal sinus P waves, precede
QRS complexes but may be hidden
within the preceding T wave
 Atrial tachycardia
This narrow QRS tachycardia arises from an abnormal
automatic focus or intra-atrial reentry. P waves precede
the QRS complexes; it is a long RP tachycardia (PR <
RP).
 Nonparoxysmal
junctional tachycardia
Nonparoxysmal junctional tachycardia
is caused by abnormal automaticity in
the AV node or adjacent tissue, which
typically follows open heart surgery,
acute inferior MI, myocarditis, or
digitalis toxicity. Heart rate is 60 to
120 beats/min; thus, symptoms are
usually absent.
 Nonparoxysmal
junctional tachycardia
ECG shows regular, normal-appearing
QRS complexes without identifiable P
waves or with retrograde P waves
(inverted in the inferior leads) that
occur shortly before (< 0.1 sec) or
after the QRS complex. The rhythm is
distinguished from paroxysmal
supraventricular tachycardia by the
lower heart rate and gradual onset and
offset.
 Ventricular premature
beats (VPBs)
are single ventricular impulses
caused by reentry within the
ventricle or abnormal automaticity
of ventricular cells.
They are extremely common in
healthy patients and in patients
with a heart disorder.
VPBs may be asymptomatic or
cause palpitations. Diagnosis is by
ECG.
 Ventricular premature
beats
Ventricular premature beats (VPBs),
also called premature ventricular
contractions (PVCs), may occur
erratically or at predictable intervals
(eg, every 3rd [trigeminy] or 2nd
[bigeminy] beat).
VPBs may increase with stimulants
(eg, anxiety, stress, alcohol, caffeine,
sympathomimetic drugs), hypoxia, or
electrolyte abnormalities.
 Ventricular premature
beats
VPBs may be experienced as missed or skipped
beats; the VPB itself is not sensed but rather the
following augmented sinus beat.

When VPBs are very frequent, particularly when

they represent every 2nd heart beat, mild
hemodynamic symptoms are possible because the
sinus rate has been effectively halved.

Existing ejection murmurs may be accentuated

because of increased cardiac filling and augmented
contractility after the compensatory pause.
 Ventricular premature
beats
Diagnosis is by ECG showing a
wide QRS complex without a
preceding P wave, typically
followed by a fully compensatory
pause.
 Prognosis

VPBs are not significant in

patients without a heart disorder,
and no treatment is required
beyond avoiding obvious triggers.
Ventricular tachycardia

is ≥ 3 consecutive ventricular
beats at a rate ≥ 120 beats/min.
Symptoms depend on duration
and vary from none to
palpitations to hemodynamic
collapse and death.
Diagnosis is by ECG.
Ventricular tachycardia

Some experts use a cutoff rate of ≥

100 beats/min for ventricular
tachycardia (VT).
Repetitive ventricular rhythms at
slower rates are called accelerated
idioventricular rhythms or slow VT;
they are usually benign and are not
treated unless associated with
hemodynamic symptoms.
 Ventricular tachycardia
 Most patients with VT have a
significant heart disorder, particularly
prior MI or a cardiomyopathy.
 Electrolyte abnormalities (particularly
hypokalemia or hypomagnesemia),
acidemia, hypoxemia, and adverse
drug effects contribute.
 The long QT syndrome (congenital or
acquired) is associated with a
particular form of VT, torsades de
pointes.
Ventricular tachycardia

VT may be monomorphic or
polymorphic and nonsustained or
sustained.
Monomorphic VT results from a single
abnormal focus or reentrant pathway
and has regular, identical-appearing
QRS complexes.
Ventricular tachycardia

Polymorphic VT results from several

different foci or pathways and is thus
irregular, with varying QRS complexes.
Nonsustained VT lasts < 30 sec;
sustained VT lasts ≥ 30 sec or is
terminated sooner because of
hemodynamic collapse. VT frequently
deteriorates to ventricular fibrillation
and thus cardiac arrest.
 Symptoms and Signs

VT of short duration or slow rate

may be asymptomatic.
Sustained VT is almost always
symptomatic, causing
palpitations, symptoms of
hemodynamic compromise, or
sudden cardiac death.
Diagnosis VT is by ECG

Any wide QRS complex tachycardia (QRS ≥

0.12 sec) should be considered VT until
proved otherwise.
Diagnosis VT is by ECG

Diagnosis is supported by ECG findings

of dissociated P-wave activity, fusion
or capture beats, uniformity of QRS
vectors in the V leads (concordance)
with discordant T-wave vector
(opposite QRS vectors), and a frontal-
plane QRS axis in the northwest
quadrant.
 Diagnosis VT is by ECG

Differential diagnosis includes

supraventricular tachycardia
conducted with bundle branch block or
via an accessory pathway.
 Torsades de pointes
ventricular tachycardia
Diagnosis is by ECG showing an undulating
QRS axis, with the polarity of complexes
shifting around the baseline. ECG between
episodes shows a long QT interval after
correction for heart rate (QTc). Normal values
average about 0.44 sec, although they vary
among individuals and by sex. A family history
may suggest a congenital syndrome.
 Ventricular fibrillation
(VF)
is due to multiple wavelet reentrant
electrical activity and is manifested on
ECG by ultrarapid baseline undulations
that are irregular in timing and
morphology
 Ventricular fibrillation
(VF)
VF is the presenting rhythm for about
70% of patients in cardiac arrest and
is thus the terminal event in many
disorders. Overall, most patients with
VF have an underlying heart disorder
(typically ischemic, but also
hypertrophic or dilated
cardiomyopathies, arrhythmogenic
right ventricular dysplasia [ARVD], or
Brugada syndrome). Risk of VF in any
disorder is increased by electrolyte
abnormalities, acidosis, hypoxemia, or
ischemia.
Ventricular fibrillation
(VF)
 Atrial fibrillation

 is a rapid, irregularly irregular atrial

rhythm
Symptoms and Signs AF

AF is often asymptomatic, but many

patients have palpitations, vague chest
discomfort, or symptoms of heart
failure (eg, weakness, light-
headedness, dyspnea), particularly
when the ventricular rate is very rapid
(often 140 to 160 beats/min). Patients
may also present with symptoms and
signs of acute stroke or of other organ
damage due to systemic emboli.
Symptoms and Signs AF

The pulse is irregularly irregular with

loss of a waves in the jugular venous
pulse. A pulse deficit (the apical
ventricular rate is faster than the rate
palpated at the wrist) may be present
because left ventricular stroke volume
is not always sufficient to produce a
peripheral pressure wave at fast
ventricular rates.
 Diagnosis is by ECG

Findings include:
 absence of P waves,
 f (fibrillatory) waves between QRS
complexes (irregular in timing,
irregular in morphology; baseline
undulations at rates > 300/min not
always apparent in all leads),
 and irregularly irregular R-R intervals
Atrial fibrillation
 Atrial flutter

Atrial flutter is a rapid regular atrial

rhythm due to an atrial macro-
reentrant circuit.
 Atrial flutter
 Classical atrial flutter is due to a large
reentrant circuit involving most of the right
atrium. The atria depolarize at a rate of 250
to 350/min (typically 300/min). Because the
atrioventricular (AV) node cannot usually
conduct at this rate, typically ½ of the
impulses get through (2:1 block), resulting in
a regular ventricular rate of 150 beats/min.
Sometimes block varies from moment to
moment, causing an irregular ventricular
rhythm. Less commonly, a fixed 3:1, 4:1, or
5:1 block may be present.
 Atrial flutter
Symptoms and Signs
Symptoms depend primarily on ventricular
rate and the nature of any underlying heart
disorder. If ventricular rate is < 120
beats/min and regular, there are likely to be
few or no symptoms.
Faster rates and variable AV conduction
usually produce palpitations, and decreased
cardiac output may produce symptoms of
hemodynamic compromise (eg, chest
discomfort, dyspnea, weakness, syncope).
Close inspection of the jugular venous pulse
reveals flutter a waves.
 Atrial flutter
The diagnosis is by ECG, which shows continuous and regular
atrial activation with a sawtooth pattern, most obvious in leads
II, III, and aVF
Conduction Disorders
 Atrioventricular (AV)
block
is partial or complete interruption of
impulse transmission from the atria to
the ventricles. The most common
cause is idiopathic fibrosis and
sclerosis of the conduction system.
Diagnosis is by ECG; symptoms and
treatment depend on degree of block,
but treatment, when necessary,
usually involves pacing.
 First-degree AV block

First-degree AV block may be

physiologic in younger patients
with high vagal tone and in well-
trained athletes. First-degree AV
block is rarely symptomatic and no
treatment is required, but further
investigation may be indicated
when it accompanies another heart
disorder or appears to be caused
by drugs.
 First-degree AV block

All normal P waves are followed by

QRS complexes, but the PR interval is
longer than normal (> 0.20 sec)
 Second-degree AV block

Some normal P waves are

followed by QRS complexes, but
some are not. Three types exist:
 In Mobitz type I 2nd-degree AV
block,
 Mobitz type I 2nd-degree AV
block,
 High-grade 2nd-degree AV block
 Mobitz type I 2nd-degree
AV block
In Mobitz type I 2nd-degree AV block, the
PR interval progressively lengthens with
each beat until the atrial impulse is not
conducted and the QRS complex is
dropped (Wenckebach phenomenon); AV
nodal conduction resumes with the next
beat, and the sequence is repeated
 Mobitz type II 2nd-
degree AV block
In Mobitz type II 2nd-degree AV block,
the PR interval remains constant. Beats
are intermittently nonconducted and QRS
complexes dropped, usually in a
repeating cycle of every 3rd (3:2 block) or
4th (4:3 block) P wave
 High-grade 2nd-degree
AV block
In high-grade 2nd-degree AV block, every
2nd (or more) P wave is blocked
 Third-degree AV block

Heart block is complete.

There is no electrical communication between the
atria and ventricles and no relationship
between P waves and QRS complexes (AV
dissociation). Cardiac function is maintained by
an escape junctional or ventricular pacemaker.
Left Bundle Branch Block
(LBBB)

Left bundle branch block (LBBB) results

from conduction delay or block in any of
several sites in the intraventricular
conduction system, including the main left
bundle branch, in each of the two fascicles,
or, less commonly, within the fibers of the
bundle of His that become the main left
bundle branch.
The result is extensive reorganization of the
activation pattern of the left ventricle.
ECG ABNORMALITIES LBBB

 LBBB produces a prolonged QRS

duration,
 abnormal QRS complexes, and
 ST-T wave abnormalities.
 Commonly accepted
diagnostic criteria for LBBB
 Basic requirements include a prolonged QRS
duration to 120 msec or beyond;
 broad, sometimes notched R waves in leads
I and aVl and the left precordial leads;
 narrow r waves followed by deep S waves in
the right precordial leads; and absent septal
q waves.
 R waves are typically tall and S waves are
deep.
 Commonly accepted
diagnostic criteria for LBBB
 The mean QRS axis with LBBB is highly
variable; it can be normal, deviated to the
left or, less often, deviated to the right.
 Left axis deviation is associated with more
severe conduction system disease that
includes the fascicles as well as the main
left bundle, whereas right axis deviation
suggests dilated cardiomyopathy with
biventricular enlargement.
 Commonly accepted
diagnostic criteria for LBBB
 In addition to these features, some
electrocardiographers require a delayed intrinsicoid
deflection (60 msec or greater) to diagnose LBBB.
 ST-T wave changes are also prominent with LBBB.
In most cases, the ST wave and the T wave are
discordant with the QRS complex; that is, the ST
segment is depressed and the T wave is inverted in
leads with positive QRS waves (leads I, aVl , V5 ,
and V6 ), while the ST segment is elevated and the
T wave is upright in leads with negative QRS
complexes (leads V1 and V2 ).
ECG ABNORMALITIES
LBBB
CLINICAL SIGNIFICANCE LBBB

 LBBB usually appears in patients with

underlying heart disease.
 It is associated with significantly reduced
long-term survival and with 10-year survival
rates as low as 50 percent, probably
reflecting the severity of the underlying
cardiac disease.
CLINICAL SIGNIFICANCE LBBB

 Among patients with coronary artery

disease, the presence of LBBB correlates
with more extensive disease, more severe
left ventricular dysfunction, and reduced
survival rates.
 The duration of the QRS complex in LBBB
correlates inversely with left ventricular
ejection fraction. Patients with associated
left or right axis deviation have more severe
clinical manifestations.
CLINICAL SIGNIFICANCE LBBB

 In addition to the hemodynamic abnormalities

produced by these underlying conditions, the
abnormal ventricular activation pattern of LBBB itself
induces hemodynamic perturbations, including
abnormal systolic function with dysfunctional
contraction patterns, reduced ejection fraction and
lower stroke volumes, and abnormal diastolic
function; reversed splitting of the second heart
sound and functional mitral regurgitation are
common.
 ECG patterns of LBBB, including low R wave
amplitude in the midprecordial leads and ST-T wave
changes, can simulate anterior infarct patterns.
Right Bundle Branch Block
(RBBB)

Right bundle branch block is a result

of conduction delay in any portion of
the right-sided intraventricular
conduction system.
Right Bundle Branch Block
(RBBB)
The delay can occur in the main right
bundle branch itself, in the bundle of
His, or in the distal right ventricular
conduction system.
Right Bundle Branch Block
(RBBB)
The latter is the common cause of
RBBB after right ventriculotomy
performed, for example, to correct the
tetralogy of Fallot. The high
prevalence of RBBB corresponds to the
relative fragility of the right bundle
branch, as suggested by the
development of RBBB after minor
trauma produced by right ventricular
catheterization.
 ECG ABNORMALITIES
RBBB
As with LBBB, the QRS complex duration
exceeds 120 msec.
The right precordial leads show prominent
and notched R waves with rsr', rsR', or rSR'
patterns, while leads I, aVl , and the left
precordial leads demonstrate wide S waves
that are longer in duration than the
preceding R wave.
 ECG ABNORMALITIES
RBBB
Septal q waves are preserved because the
initial ventricular activation remains
unchanged.
The ST-T waves are, as in LBBB, discordant
with the QRS complex, so T waves are
inverted in the right precordial leads (and
other leads with a terminal R' wave) and
upright in the left precordial leads and in
leads I and AVl .
The mean QRS axis is not altered by RBBB.
RBBB
CLINICAL SIGNIFICANCE
RBBB is a common finding in the general
population, and many persons with RBBB
have no clinical evidence of structural heart
disease.
In the group without overt heart disease,
the ECG finding has no prognostic
significance.
However, the new onset of RBBB does
predict a higher rate of coronary artery
disease, congestive heart failure, and
cardiovascular mortality.
CLINICAL SIGNIFICANCE
When cardiac disease is present, the coexistence of
RBBB suggests advanced disease with, for example,
more extensive multivessel disease and reduced
long-term survival in patients with ischemic heart
disease.
An entity known as the Brugada syndrome has
been described in which a RBBB-like pattern with
persistent ST segment elevation in the right
precordial leads is associated with susceptibility to
ventricular tachyarrhythmias and sudden cardiac
death.