can produce a fall in cardiac output with fatigue, light-headedness, confusion, or syncope.

In such cases, any extrinsic provocative factors

should be corrected, and specic therapy, as
described in the next section, may be needed.

Sick Sinus Syndrome

Bradyarrythmias: HR < 60 bpm

Arrythmia
SA Node

Sinus Bradycardia

Clinical Presentation

Intrinsic SA node dysfunction that causes periods of inappropriate bradycardia is known as

sick sinus syndrome (SSS). This condition often
produces symptoms of dizziness, confusion, or
syncope. Patients with this syndrome (or any

Pathophysiology

EKG

Fatigue, Lightheadedness, Confusion

Syncope

280

Intrinsic SA Node Dysfunction

and aVF, indicating activation of the atria from

the inferior direction.
Ventricular escape rhythms are characCells in the atrioventricular (AV) node and
77237_ch12.indd 280
8/11/10
terized by even slower rates (30 to 40 bpm)
HisPurkinje system are capable of automaticand widened QRS complexes. The complexes
ity but typically have slower ring rates than
are wide because the ventricles are not dethe sinus node and are therefore suppressed
polarized by the normal rapid simultaneous
during normal sinus rhythm. However, if SA
Figure 12.2.
Bradyca
rdiatachycard
syndrom
brief irregular tachycardia
followed
slow sinus
over the is
right
andbyleft
bundle
node activity
becomes
impaired
or ifiathere
is e. Aconduction
node discharge.
branches but rather from a more distal point
conduction block of the impulse from the SA
in the conduction system. The morphology
node,
escape
rhythms can emerge from the
Chapter
12
and
aVF,
indicating
activation
of
the
atria
that the QRS shows depends on the site
offrom
more distal
latent
Escape
Rhythm
s pacemakers (Fig. 12.3).
the inferior
direction.
origin
of the escape
rhythm. For example, an
Junctional escape beats arise from the AV
Ventricular
escapefrom
rhythms
characCells
inorthe
atrioventricular
(AV)
and escape
rhythm originating
the leftare
bundle
node
proximal
bundle of His.
Theynode
are charterized
bycause
evena slower
ratesbranch
(30 toblock
40 bpm)
HisPurkinje
arenarrow
capableQRS
of automaticbranch
will
right bundle
acterized bysystem
a normal,
complex,
andpattern,
widened
QRS complexes.
The complexes
ityand
butwhen
typically
ring (termed
rates than
QRS
because
the impulse depolarizes
theyhave
occurslower
in sequence
a
the
ventricle
rst the
andPventricles
then spreads
more
areleftwide
are
not deescape
at a rate
thejunctional
sinus node
are therefore
suppressed
P and rhythm),
P appear
P
P because
through
ventricle
Conof 40 normal
to 60 bpm.
Therhythm.
QRS complexes
areifnot
polarized
by the
theright
normal
rapid(RV).
simultaneous
during
sinus
However,
SA slowly
an escape
originating
in the
preceded
by becomes
normal P impaired
waves because
im-is versely,
conduction
overrhythm
the right
and left
bundle
node
activity
or if the
there
Figure 12.4. First-degree AV block. The PR interval is prolonged.
bundlebut
branch
causes
theaQRS
to distal
appearpoint
pulse originates
below
the atria.from
However,
branches
rather
from
more
conduction
block of
the impulse
the SA right
a leftconduction
bundle branch
block con
retrograde
waves may
observed
as an
in the
system.
Theguration.
morphology
node,
escapeP rhythms
canbeemerge
from
the with
Escape
rhythms
that
originate
more
distally,
impulse
propagates
from
the more
distalrhythms
Junctional
ventricular
escape
antagonists,
digitalis,
other antiarrhythmic
that
the QRS
showsand
depends
on the in
site of
more
distal
latentand
pacemakers
(Fig.
12.3).pacethe
ventricular Structural
myocardium
itself,ofare
characmaker
backward
to the
atrium. Retrograde
protective
backup
mechanisms
that
mainmedications.
causes
rst-degree
origin
of the escape rhythm.
Forexample,
an
Jare
unctional
escape
beats
arise from
the
AV
terized
by even
widermyocardial
QRS complexes
because
Ptain
waves
typically
follow
theoutput
QRS complex
a
heart
rate
and
cardiac
when
the
AV
block
include
infarction
and
escape
rhythm
originating
from
the
left
bundle
node
orare
proximal
bundle
of His.
They
are
charsuch
impulses
are
conducted
outside
the
rapand
inverted
(negative
de
ection
on
the
sinus node
ornormal,
normal AV
conduction
fails. The
chronic degenerative
diseases
of the conduction
branch
will
cause
a
right
bundle
branch
block
acterized
by
a
narrow
QRS
complex,
idly
propagating
Purkinje bers.
electrocardiogram
[ECG])
in limbofleads
II, III,
clinical ndings and
treatment
bradycardia
system,
which commonly
occur with aging.

Escape Rhythms

Atria
AV Node
Dizziness, Confusion,
Syncope

Impulses initiated from AV Node or

Proximal Bundle of His. (Latent)

40-60bpm

Impaired SA Node, or conduction

block of SA Node impulse.

Prolongation of the delay between

atrial and ventricular depolarization

8:21:31 AM

Normal, Narrow QRS

No precedent P-waves
Inverted P waves after QRS: II, III, aVF
(retrograde
atrial
conduction
from
AV
Node)
QRS pattern,
because
the impulse
depolarizes
and when
they occur in sequence
(termed
a
associated with escape rhythms are identical
Generally, rst-degree AV block is a benign,

junctional escape rhythm), appear at a rate

to those of SSS described earlier.
of 40 to 60 bpm. The QRS complexes are not
preceded by normal P waves because the imAtriov
entricula
r Condthe
uction
System
pulse
originates
below
atria.
However,
retrograde
waves may
be observed
as AV
an
The AV Pconduction
system
includes the
impulse
the more
distal
node,propagates
bundle of from
His, and
the left
andpaceright
maker
backward
to Impaired
the atrium.
Retrograde
bundle
branches.
conduction
beP waves
typically
follow
the QRS
tween the
atria and
ventricles
can complex
result in
of AVde
conduction
block.
andthree
are degrees
inverted(types)
(negative
ection on
the
electrocardiogram [ECG]) in limb leads II, III,
Chapter 12
First-Degree AV Block

the left ventricle rst and then spreads more

asymptomatic condition that does not require
slowly through the right ventricle (RV). Contreatment. However, it can indicate disease in
versely,
an escape rhythm originating in the
the AV node associated with susceptibility to
right
causes
the QRS
to appear
higherbundle
degreesbranch
of AV block
if drugs
are adminwith
a left
block
conguration.
istered
thatbundle
further branch
impair AV
conduction,
or
Escape
rhythms that
originate
more distally, in
if the conduction
disease
progresses.
the ventricular myocardium itself, are characterized by even wider QRS complexes because
Second-Degree AV Block
such impulses are conducted outside the rapSecond-degree
AVPurkinje
block is bers.
characterized by
idly
propagating

Intermittent Failure of AV Node

Conduction

Anticholinergics: Atropine
-Agonists: isoproterenol
Permanent Pacemaker if
Chronic

Anticholinergics: Atropine
-Agonists: isoproterenol

Asymptomatic may not

require treatment

Mobitz I/ Wenchenbach: Progressive inc. in

PR interval, until a single QRS interval is
missed.

Mobitz I/ Wenchenbach:
benign in children and
athletes, people with high
vagal tone, esp. at night

Mobitz I: Tx not necessary

is asymptomic, Atropine if
symptomatic

the AV node associated with susceptibility to

P
P
P
higher
degrees
of AV block
if drugs are adminThe AV conduction system includes the AV
istered that further impair AV conduction, or
Figure
AV block:
The P-wave
rate is constant,
but
node, bundle
of12.5.
His,Second-degree
and the left
andMbitz
righttype I (W
if enckebach).
the conduction
disease
progresses.
77237_ch12.indd 281
8/11/10 8:21:32 AM
the PR interval progressively lengthens until a QRS is completely blocked (after fourth P wave).
bundle branches. Impaired conduction between the atria and ventricles can result in
Second-D
egree
AV
Block
three282
degrees (types) of AV conduction block.
Second-degree AV block is characterized by
Aspects
of conduction,
Cardiac Arrhythm
ias
intermittentClinical
failure
of AV
resultFirst-Degree AV Block
ing in some P waves not followed by a QRS
First-degree
complex. There are two forms of second77237_ch12.indd
282 AV block, shown in Figure 12.4,
8/11/10 8:21:32 AM
indicates prolongation of the normal delay
degree AV block. In Mbitz type I block
between atrial and ventricular depolarization,
(also termed Wenckebach block), shown in
such that the PR interval is lengthened ( 0.2
Figure 12.5, the degree of AV delay gradually
P
P
P
P
P
sec, which is 5 small boxes on the ECG). In
increases with each beat until an impulse is
this situation, the 1:1 relationship between P
completely blocked, such that a QRS does not
waves and
QRS
complexes
is preserved.
Thetype II.
follow
Pplex
wave
for a(after
single
Figure
12.6.
Second-degree
AV block: Mbitz
A QRS a
com
is blocked
the beat.
fourth PTherefore,
wave)
gradual is
lengthening
of the preceding
intervals.
hile the Q
width in this exam
ple
impairment
of without
conduction
usually within
the PRthe
ECG W
shows
aRSprogressive
increase
in the
is normal, it is often widened in patients with Mbitz type II block.
AV node itself and can be caused by a tranPR interval from one beat to the next until
sient reversible inuence or a structural defect.
a single QRS complex is absent, after which
in the conduction
is usually benign
dangerous
than Mbitz
type
Reversible
causes system).
include It
heightened
vagal
the PR interval
shortens
to Iitsblock.
initialMbitz
length,
and transient
may be seen
children,
trained
athletes,
type
II may
to third-degree
tone,
AV in
nodal
ischemia,
and
drugs
and the
cycleprogress
starts anew.
Mbitz typeblock
I block
anddepress
peopleconduction
with high vagal
tone,
particularly
without
warning;
therefore,
treatmentconducwith
that
through
the
AV node,
almost always
results
from impaired
during sleep.
It may also
occur
during an
acute
a
pacemaker
usually
warranted,
even
in
including
-blockers,
certain
calcium
channel
tion
in the AVisnode
(rather
than more
distally
myocardial infarction because of increased
asymptomatic patients.
vagal tone or ischemia of the AV node, but the
block is usually temporary. Treatment is typiThird-Degree AV Block
cally not necessary, but in symptomatic cases,
administration of intravenous atropine or isoThird-degree AV block, also termed complete
proterenol usually improves AV conduction
heart block (Fig. 12.8), is present when there
transiently. PPlacement ofP a permanent
isP complete failure
of conduction
between the
P paceP
P
maker is required for a symptomatic block that
atria and ventricles. In adults, the most com-

Atrioventricular
SystemP
P Conduction
P

High-Grade: Conduction Block

beyond AV Node (His or Purkinje)

Anticholinergics: Atropine
-Agonists: isoproterenol

Reversible: 1) inc. vagal tone,

2) transient AV Node
ischemia, 3) drugs blockers, and Ca2+-Channel
Blockers, Digitalis
Structural: 1)MI, 2) chronic
degenerative disease

ure 12.3.and
Escap
e rhythms. No
waves are evident. A.system,
J unctional
escapecommonly
rhythm with norm
al-width
igndings
treatment
ofPbradycardia
which
occur
withQRS
aging.
Mobitz I/ Wenchenbach: AV delay clinical Fcom
plexes. B. Wide QRS complexes typical of a ventricular escape rhythm.
with escape rhythms are identical
Generally, rst-degree AV block is a benign,
gradually increases, until an impulse isassociated
to those of SSS described earlier.
asymptomatic condition that does not require
treatment. However, it can indicate disease
281in
completely blocked

Mobitz II: Conduction block beyond

AV Node
(His or Purkinje)

Treatment

P-waves are lengthened. (>0.2sec, >5 small

boxes)

intermittent failure of AV conduction, resulting in some P waves not followed by a QRS

First-degree AV block, shown in Figure 12.4,
complex. There are two forms of secondindicates prolongation of the normal delay
degree AV block. In Mbitz type I block
Figure 12.3. Escape rhythms. No P waves are evident. A. J unctional escape rhythmwith normal-width QRS
between
atrial and ventricular depolarization,
(also termed Wenckebach block), shown in
complexes. B. Wide QRS complexes typical of a ventricular escape rhythm.
such that the PR interval is lengthened ( 0.2
Figure 12.5, the degree of AV delay gradually
sec, which
on the ECG).P In
increases Pwith each beat until
an impulse is
P is 5 small boxes
P
P
281
this situation, the 1:1 relationship between P
completely blocked, such that a QRS does
not
waves and QRS complexes is preserved. The
follow a P wave for a single beat. Therefore,
impairment of conduction
is usually
within
theblock.the
showsisaprolonged.
progressive increase in the
Figure 12.4.
First-d
egree AV
TheECG
PR interval
AV node itself and can be caused by a tranPR interval from one beat to the next until
sient reversible inuence or a structural defect.
a single QRS complex is absent, after which
77237_ch12.indd 281
8/11/10 8:21:32 AM
J unctional
ventricular
rhythms
antagonists,
digitalis,
antiarrhythmic
Reversible and
causes
include escape
heightened
vagal
the
PR interval
shortensand
to other
its initial
length,
tone,
transient
AV
nodal
ischemia,
and
drugs
and
the cycle starts
anew. Mbitz
I block
are protective backup mechanisms that mainmedications.
Structural
causestype
of
rst-degree
that
depress
through
thewhen
AV node,
almost
always
resultsmyocardial
from impaired
conduc- and
tain a
heart
rateconduction
and cardiac
output
the
AV block
include
infarction
-blockers,
calcium
channel
tion
in the
AV node (rather
than of
more
sinusincluding
node or normal
AVcertain
conduction
fails.
The
chronic
degenerative
diseases
thedistally
conduction

Conduction Block:
First-Degree Block

Conduction Block:
Second-Degree
Block

Elevated Vagal Tone (athletes,

pain/fear)
Aging
Disease of the Atrium
Meds: -Blockers, Ca2+Figure 12.1. Sinus bradycardia. The P wave and QRS complexes are normal but the rate is 60 bpm.
Channel Blockers
Figure 12.2. Bradycardiatachycardia syndrome. A brief irregular tachycardia
is
followed
by
slow
sinus
Clinical Aspects of Cardiac Arrhythmias
node discharge.
Bradycardia-tachycardia
syndrome:
Intrinsic SA Node Dysfunction
Clinical Aspects of Cardiac Arrhythmias

Bradycardia-tachycardia syndrome:
Tachycardia followed by profound
sinus bradycardia. Common in elderly.
Atrial Fibrosis impairs SA Node.

Sick Sinus
Syndrome (SSS)

Junctional Escape
Rhythm

Causes

Normal P-wave and QRS-complex, <60bpm

<60bpm
Dizziness, Confusion,
Syncope

tachycardias (SVTs), most commonly atrial

brillation (AF). This combination is known
as the bradycardiatachycardia syndrome
(Fig. 12.2) and is thought to result from atrial
brosis that impairs function of the SA node
and predisposes to AF and utter. During the
tachyarrhythmia, overdrive suppression of the
SA node occurs, and when the tachycardia terminates, a period of profound sinus bradycardia may ensue. Treatment generally requires
the combination of antiarrhythmic drug therapy to suppress the tachyarrhythmias plus a
permanent pacemaker to prevent bradycardia.

Mobitz II: Extensive MI

Mobitz II: loss of AV conduction w/o gradual

lengthening of PR interval

High-Grade: Extensive MI

Mobitz II: Pacemaker

High-Grade: Pacemaker

grade AV block (Fig. 12.7). Mbitz type II

block is usually caused by conduction block
beyond the AV node (in the bundle of His or
more distally in the Purkinje system), and the
QRS pattern often is widened in a pattern of
right or left bundle branch block. This type of
block may arise from extensive myocardial infarction involving the septum or from chronic
degeneration of the HisPurkinje system. It
usually indicates severe disease and is more

rate that is not related to the intervals at which

QRS complexes appear. Depending on the site
of the escape rhythm, the QRS complexes may
be of normal width and occur at 40 to 60 bpm
(originating from the AV node) or may be widened and occur at slower rates (originating
from the HisPurkinje system). As a result of
the slow rate, patients frequently experience
light-headedness or syncope. Permanent pacemaker therapy is almost always necessary.

High-Grade: Missed QRS complex for 2

beats. QRS may be widened with pattern of
Clinical Aspects of Cardiac Arrhythmias
RBBB or LBBB

Figure
h-grade
AV block. Sequential
comirregular
plexes are
blocked (after
the
third
Figure12.7.
12.2. Hig
Bradycard
iatachycardia
syndromeQ
. RS
A brief
tachycardia
is follow
edsecond
by slowand
sinus
Pnode
waves).
discharge.

Complete failure of conduction

between atria and ventricles
Conduction Block:
Third-Degree
Block, Complete
Heart Block

aVF, indicating activation

of the atria from Acute MI
No relationship betweenandP-waves
and QRS
Escape Rhythms
283
the inferior direction.
Ventricular escape rhythms are charac- Chronic Degenerative
Cells incomplexes
the atrioventricular (AV) node and
terized
by
even
slower
rates
(30
to
40
bpm)
HisPurkinje system are capable of automaticQRS:
Widened.
40-60bpm
if from
AV Node,
Disease
and widened
QRS complexes.
The complexes
ity but
typically have
slower ring rates
than
are wide because the ventricles are not dethe sinus node and are therefore suppressed
longer
if
from
His-Purkinje
Chapter
12
polarized by the normal rapid simultaneous
during normal sinus rhythm. However, if SA

77237_ch12.indd 283

Ventricles
30-40bpm

Ventricular Escape
Rhythm

Ventricles are depolarized from distal

point in conduction system:
1) Left Bundle Branch
2) Right Bundle Branch
3) Ventricular Myocardium

8/11/10 8:21:33 AM

conduction over the right and left bundle

node activity becomes impaired or if there is
branches but rather from a more distal point
conduction block of the impulse from the SA
in the conduction system. The morphology
node, escape rhythms can emerge from the
that the QRS shows depends on the site of
more distal latent pacemakers (Fig. 12.3).
origin of the escape rhythm. For example, an
J unctional escape beats arise from the AV
escape rhythm originating from the left bundle
node or proximal bundle of His. They are charP
P
P
P
P
P
P
P
branch will cause a right bundle branch block
acterized by a normal, narrow QRS complex,
QRS pattern, because the impulse depolarizes
and when they occur in sequence (termed a
ventricle
rst and of
then
more
junctional
rhythm),
appear
aPrate
Figureescape
12.8. Third-deg
ree AV
block.at
The
wave andthe
QRSleft
rhythm
s are independent
one spreads
another. The
com
plexesThe
are widened
as they originate
within the
distalthrough
ventricular
conduction
system, not
at the
slowly
the
right ventricle
(RV).
Conof 40 Q
toRS60
bpm.
QRS complexes
are not
bundle
His. ThePsecond
and
fourth P the
waves
are superim
posedan
on norm
al T rhythm
waves. originating in the
versely,
escape
preceded
byofnormal
waves
because
imright bundle branch causes the QRS to appear
pulse originates below the atria. However,
a left bundle
branch
block con
guration.
retrograde
waves
may be observed
as an
The term PAV
dissociation
is a general
de- with
arrhythmias
are
categorized
into
those that
Escape
thatventricles
originate more
distally, in
impulsethat
propagates
from
the
more distal
pacescription
refers to
any
situation
in which
arise rhythms
above the
(supraventricular)
the ventricular myocardium itself, are characto thebeat
atrium.
Retrograde
themaker
atria backward
and ventricles
independently,
and those that arise within the ventricles.
terized by even wider QRS complexes because
P waves typically follow the QRS complex
without any direct relationship between P
such impulses are conducted outside the rapand are inverted (negative deection on the
waves and QRS complexes. Third-degree AV idly propagating Purkinje bers.
electrocardiogram [ECG]) in limb leads II, III,
Supraventricular Arrhythmias

QRS Complexes: Widened

Escape Rhythm from Left Bundle: widened

QRS in RBBB configuration
Figure (Rabbit
12.9 presents a Ears)
schema to help organize

block is one example of AV dissociation.

the common supraventricular tachyarrythmias

presented in this section.

TACHYARRHYTHMIAS

Escape Rhythm from Right Bundle:

Sinus Tachycardia (Broad
widened QRS in LBBB configuration
Sinus tachycardia is characterized by an SA
notch)
node discharge rate 100 bpm (typically 100

When the heart rate is 100 bpm for three

beats or more, a tachyarrhythmia is present.
Tachyarrhythmias result from one of the three
mechanisms: enhanced automaticity, reentry,
or triggered activity (see Chapter 11). Tachy-

Supraventricular
Tachyarrhythmias
Figure 12.3. Escape rhythms. No P waves are evident. A. J unctional escape rhythm with normal-width QRS
complexes. B. Wide QRS complexes typical of a ventricular escape rhythm.
Regular rhythm

Irregular rhythm

(constant P-P inter val) myocardium: wider QRS

Ventricular
complexes
3 P wave
shapes

Multifocal atrial
tachycardia

No distinct
P waves

281

Atrial
fibrillation

77237_ch12.indd 281

8/11/10 8:21:32 AM

Atrial
rate (bpm)

P-wave
morphology

Response to carotid
sinus massage

Sinus tachycardia

100180

Normal

Atrial rate
may slow

Reentrant SVTs

140250

Hidden or
retrograde

May abruptly
terminate

Focal atrial
tachycardia

130250

Difers from
normal P

AV block may
increase; doesnt
usually revert

Atrial flutter

180350

Saw-toothed

AV block may
increase

(e.g., AVNRT, ARVT)

Figure 12.9. Differentiation of common supraventricular tachyarrhythmias.

284

77237_ch12.indd 284

Permanent Pacemaker
Therapy

8/11/10 8:21:33 AM

Anticholinergics: Atropine
-Agonists: isoproterenol

to 180 bpm) with normal P waves and QRS

complexes (Fig. 12.10). This rhythm most
often results from increased sympathetic and/
or decreased vagal tone. Sinus tachycardia is
an appropriate physiologic response to exercise. However, it may also result from sympathetic stimulation in pathologic conditions,
including fever, hypoxemia, hyperthyroidism,
hypovolemia, and anemia. In disease states,
sinus tachycardia is usually a sign of the severity of the primary pathophysiologic process and treatment should be directed at the
underlying cause.

Tachyarrthmias: >100bpm
Arrythmia
SA Node

Clinical Presentation
Palpations

Pathophysiology

EKG

SA Node Discharge >100bpm

Normal P-wave and QRS-complex, >100bpm

Atrial Premature Beats

Inc. sympathetic tone/ dec.

parasympathetic tone

Sinus Tachycardia

Atria
Asymptomatic, may
have palpations

Atrial Premature
Beats

Automaticity in an atrial focus outside

of SA Node
Reentry in an atrial focus outside of
SA Node
Blocked APB: abnormal atrial impulse
encounters refractory AV Node
APB with Aberrant Conduction:
abnormal atrial impulse later in
diastole, conducts through AV Node,
encounters refractory His-Purkinje,
slow conduction though ventricular
myocites

Atrial Flutter

Atrial Fibrillation

Predispose to atrial
thrombus
Avg. Ventricular Rate:
140-160bpm

Atrial activity often meets refractory AV

Node, and does not conduct to
ventricles slower ventricular rate.
Reentry of large anatomically fixed
circuit. Atrial tissue along tricuspid
valve.

Multiple wandering reentrant circuits.

Rapids ventricular rates
compromise cardiac
output
Hypotension
Pulmonary congestion
Esp. in those with L.
vent. hypertrophy (loss
of atrial contraction
impairs ventricular filling)
Promotes thrombus,
esp. in atrial appendage:
stroke

P-Wave: earlier than expected. Abnormal

Shape.
QRS complex: follows P-wave, normal
including
fever, hypoxemia,
hyperthyroidism, conduction
diastole, it may conduct through the AV node
unimpaired
ventricular
hypovolemia, and anemia. In disease states,
but encounter portions of the HisPurkinje
sinus tachycardia is usually a sign of the severity of the primary pathophysiologic process and treatment should be directed at the
underlying cause.

Paroxysmal: sudden, initiated by

rapid foci firing into pulmonary veins
Often associated with R. or L. Atrial
enlargement

Predisposition:
Caffeine
Alcohol
Adrenergic Stimulation
(emotional stress)

system that are still refractory. As a result, the

impulse is conducted through those territories
and to the ventricular myocytes more slowly
than normal, producing QRS complexes that
are abnormally wide (termed an APB with abAPB
errant conduction).
Atrial Premature Beats
APBs require treatment only if they are
Figure 12.11. Atrial premature beat (APB). The P wave occurs earlier than expected, and its shape is
Atrial premature beats (APBs) are common in
symptomatic. Because caffeine, alcohol, and
abnormal.
healthy as well as diseased hearts (Fig. 12.11).
adrenergic stimulation (e.g., emotional stress)
They originate from automaticity or reentry in
can all predispose to APBs, it is important
an atrial focus outside the SA node and are
to address these factors. -Blockers are the 285
often exacerbated by sympathetic stimulation.
initial preferred pharmacologic treatment if
APBs are usually asymptomatic but may cause
needed.
palpitations. On the ECG, an APB appears
as an earlier-than-expected P wave with an
Clinical Aspects of Cardiac Arrhythmias
Atrial Flutter
abnormal shape (the impulse does not arise
8/11/10
from the SA node, resulting in abnormal conAtrial utter is characterized by rapid, regutherapy. First, the ventricular rate is slowed
P waves are not visible on the ECG, the baseduction through the atria). The QRS complex
lar atrial activity at a rate of 180 to 350 bpm
by drugs that increase AV block: -blockers,
line shows low-amplitude undulations punctuthat
follows
the P blockers
wave is(e.g.,
usually
normal, ated
(Fig.
Many of these
impulses reach
calcium
channel
verapamil,
by12.12).
QRS complexes
and Tfast
waves.
resembling
theorQRS
duringOnce
sinusthe
rhythm,
the
AVmechanism
node during
and
diltiazem),
digoxin.
rate beis
The
of its
AFrefractory
probably period
involves
cause
ventricular
conduction
not made
impaired.
do not conduct
to the
ventricles,
resulting
in a
Chapter
effectively
12
slowed,
attemptsis are
to
multiple
wandering
reentrant
circuits
within
However,
if therhythm
abnormal
focus res the
slower
rate,
often the
an even
fraction
restore sinus
usingatrial
antiarrhythmic
atria, ventricular
and in some
patients,
rhythm
re-

Blocked APB: P-wave not followed by QRS

complex
APB with Aberrant Conduction: QRS
abnormally wide
P-waves: sawtooth, or sinusoidal

Antiarrhythmics may exacerbate by

allowing recovery of AV node, and
thereby transmission of rapid impulses
to ventricles. (220bpm)

P-waves: indiscernible
QRS complex: irregular rate

Low amplitude undulations punctuated by

QRS complexes and T-waves

77237_ch12.indd 287

-blockers in symptomatic
patients

8:21:33 AM

Areas of large atrial scarring:

1) MI, 2) cardiac surgery, 3)
prior ablation

8:21:33 AM

Diseases that promote atrial

enlargement:
Heart Failure
Hypertension
Coronary Artery Disease
Pulmonary Disease
Predispose:
Thyrotoxicosis
Alcohol

8/11/10 8:21:34 AM

286

77237_ch12.indd 286

Arrythmia

Physiologic response
Sympathetic Stimulation in
pathologies: fever,
hypoxemia, hyperthyroidism,
hypovolemia (reflex tach.),
and anemia

drugs that slow conduction or prolong

petitively shifts between brillation and atrial
the refractory period of the atrial myocarutter. When brillation is paroxysmal (i.e.,
dium (class IA, IC, or III agents; see Chapsudden, unpredictable episodes), it is often
ter 17). Should these drugs fail to convert
initiated by rapid ring of foci in sleeves of
the rhythm, electrical cardioversion can be
atrial muscle that extend into the pulmonary
undertaken. Once sinus rhythm has been
veins. To sustain AF, a minimum number of
APB
restored, class IA, IC, or III antiarrhythmic
reentrant circuits is needed, and an enlarged
drugs may be administered chronically to
atrium increases the potential for this to occur.
Figure 12.11. Atrial premature beat (APB). The P wave occurs earlier than expected, and its shape is
prevent
recurrences.
Thus, AF is often associated with right or left
abnormal.
atrial enlargement. Accordingly, diseases that
4. When chronic therapy is required to preFigure
12.12.
Atrial
fl
utter
is
typifi
ed
by
rapid
saw-toothed
activity
(arrow
s).promote AF,
increase
atrial atrial
pressure
and
size
vent recurrences, catheter ablation is often
285
including heart failure, hypertension, coroa better alternative than pharmacologic
nary artery disease, and pulmonary disease.
approaches. In this method, an electrode
ofcatheter
the atrialisrate.
Thus,into
if the
rate is
300 Thyrotoxicosis
dangerous by allowing
the AV
node more time
and alcohol
consumption
can
inserted
theatrial
femoral
vein,
bpm
and
2:1
block
occurs
at
the
AV
node
(i.e.,
to
recover
between
impulses.
In
this
situaprecipitate
AF
in
some
people.
passed via the inferior vena cava to the
every
atrial
nds theand
AV caunode
tion,
node maydangerous
begin to conduct
in a
AF the
is aAV
potentially
arrhythmia
rightother
atrium,
andimpulse
used tolocalize
77237_ch12.indd 285
8/11/10
refractory),
the ventricular
rate is 150
bpm.
1:1 fashion,
producing
very rapid
because:
(1) rapid
ventricular
ratesventricular
may comterize (ablate)
part of the reentrant
loop
to
Because
vagal interrupt
maneuvers
carotid
sinus
rates. For
example,
a patient
with in
atrial
utter
promise
cardiac
output,
resulting
hypotenpermanently
the(e.g.,
utter
circuit.
massage) decrease AV nodal conduction, they
at a and
rate of
280 bpm congestion
and 2:1 conduction
block
sion
pulmonary
(especially
in
increase the degree of block, temporarily slowat
the
AV
node
would
have
a
ventricular
rate
patients with a hypertrophied or stiff left
ing the ventricular rate, which allows better
of 140 bpm.
If the atrial
slows to
220
ventricle
in whom
the rate
loss then
of normal
atrial
Atrial
Fibrillation
visualization
of the underlying atrial activity.
bpm, the AVcan
node
maycantly
be able
to recover
sufcontraction
signi
reduce
left venIn is
general,
atrial
utterwith
is caused
by rate
reentry
cientlybetween
to and
conduct
AF
a chaotic
rhythm
an atrial
so
tricular
lling anddepolarizations
stroke volume),
(2)
over
a
large
anatomically

xed
circuit.
In
the
every
atrial
impulse,
causing
the
ventricular
fast (350 to 600 discharges/ min) that disthe absence of organized atrial contraction
common
form
ofnot
atrial
utter, this
circuit
rate to accelerate
to 220
In patients
with
tinct
P waves
are
discernible
on the
ECGis
promotes
blood stasis
inbpm.
the atria,
increasing
the atrial
tissue
along
the tricuspid
valveof
annulimited
cardiac
reserve,
this acceleration
may
(Fig.
12.13).
As with
atrial
utter, many
the
the
risk of
thrombus
formation,
particularly
in
lus: the
circulating
depolarization
wave
proparesult
a profound
reduction
of cardiac
atrial
impulses
encounter
refractory
tissue
at
the
leftin
atrial
appendage.
Embolization
of outleft
gates
the interatrial
septum,
across
roof
put and
hypotension.
Atrial utter
also
predisthe
AVup
node,
allowing only
some
of thethe
depoatrial
thrombi
is an important
cause
of stroke.
and
down
the
free
wall
of
the
right
atrium
poses
to
atrial
thrombus
formation.
larizations to be conducted to the ventricles in
Thus, treatment of AF considers three aspects
along
the oor
of the right
Several
approaches
to the treatment
of atrial
aand
verynally
irregular
fashion
(indicated
by aatrium
charof the
arrhythmia:
(1) ventricular
rate control,
between irregularly
the tricuspid
valve rhythm).
annulus The
and
utter
are available:
acteristic
irregular
(2)
consideration
of methods to restore sinus
inferiorventricular
vena cava.rate
Because
large parts
ofapthe rhythm, and (3) assessment of the need for
average
in untreated
AF is
1. For symptomatic patients with recent-onset
atrium
are
depolarized
throughout
the
cycle,
P
proximately 140 to 160 bpm. Because discrete
anticoagulation
prevent
atrial utter,tothe
most thromboembolism.
expeditious therapy
waves often have a sinusoidal or sawtooth
is electrical cardioversion to restore sinus
appearance. Large utter circuits can occur in
rhythm. This technique is also used to reother parts of the right or left atrium as well,
vert chronic atrial utter that has not reusually associated with areas of atrial scarring
sponded to other approaches.
from disease, prior heart surgery, or ablation
2. Flutter can be terminated by rapid atrial
procedures.
stimulation (burst pacing) using a tempoAtrial utter generally occurs in patients
rary or permanent pacemaker (see Chapwith preexisting heart disease. It may be parter 11). This procedure can be used when
oxysmal and transient, persistent (lasting for
temporary atrial pacing wires are already
days or weeks), or permanent. Symptoms of
present, as in the days following cardiac
atrial utter depend on the accompanying
Figure 12.13. Atrial fibrillation is characterized by chaotic atrial
activity
ithout organized
Pw
aves and
by
surgery.
In waddition,
certain
types
of perventricular
rate. If the rate is 100 bpm, the
irregularity of the ventricular (QRS) rate.
manent pacemakers and implanted debrilpatient may be asymptomatic. Conversely,
lators can be programmed to perform burst
faster rates often cause palpitations, dysppacing
automatically
when
atrial

utter
287
nea, or weakness. Paradoxically, antiarrhythoccurs.
mic medications that reduce the rate of atrial
utter by slowing conduction in the atrium
3. Patients without an immediate need for
may paradoxically make the rhythm more
cardioversion can begin pharmacologic

Chaotic Rate: 350-600 discharges/min

Causes

Atrial premature beats (APBs) are common in

healthy as well as diseased hearts (Fig. 12.11).
They originate from automaticity or reentry in
an atrial focus outside the SA node and are
often exacerbated by sympathetic stimulation.
APBs are usually asymptomatic but may cause
palpitations. On the ECG, an APB appears
Figure 12.10. Sinus tachycardia. The P wave and QRS complexes are normal, but the rate is 100 bpm.
as an earlier-than-expected P wave with an
Atrial Flutter
abnormal shape (the impulse does not arise
180
normalinP abnormal
waves andconQRS
very soon
afteristhe
previous beat,by
therapid,
impulse
fromto
the
SAbpm)
node,with
resulting
Atrial
utter
characterized
regucomplexes (Fig. 12.10). This rhythm most
may encounter an AV node that is refractory to
duction through the atria). The QRS complex
lar atrial activity at a rate of 180 to 350 bpm
often results from increased sympathetic and/
excitation, resulting in a blocked impulse that
that or
follows
the P wave is usually normal,
(Fig.
12.12). Many of these fast impulses reach
decreased vagal tone. Sinus tachycardia is
does not conduct to the ventricles. The preresembling
the QRSphysiologic
during sinus
rhythm,
bethe
AV Pnode
an appropriate
response
to exermature
waveduring
is then its
not refractory
followed byperiod
a QRS and
causecise.
ventricular
not impaired.
do
not conduct
to the ventricles,
resulting
However,conduction
it may alsoisresult
from symcomplex
and is termed
a blocked APB.
Simi- in a
However,
if stimulation
the abnormal
atrial focus
res
slower
ventricular
rate,res
often
even
fraction
pathetic
in pathologic
conditions,
larly, if the
ectopic focus
justan
a bit
later
in

77237_ch12.indd 285

Rapid, regular atrial

activity: 180-350bpm
Palpations, dyspnea,
weakness
Hypotension, profound
dec. in cardiac
output
May be paroxysmal,
transient, persistent
(days-weeks),
permanent

very soon after the previous beat, the impulse

may encounter an AV node that is refractory to
excitation, resulting in a blocked impulse that
does not conduct to the ventricles. The premature P wave is then not followed by a QRS
complex and is termed a blocked APB. Similarly, if the ectopic focus res just a bit later in
diastole, it may conduct through the AV node
but encounter portions of the HisPurkinje
system that are still refractory. As a result, the
impulse is conducted through those territories
and to the ventricular myocytes more slowly
than normal, producing QRS complexes that
are abnormally
wide (termed an APB with abClinical Aspects of Cardiac Arrhythmias
errant conduction).
APBs require treatment only if they are
symptomatic. Because caffeine, alcohol, and
adrenergic stimulation (e.g., emotional stress)
can all predispose to APBs, it is important
to address these factors. -Blockers are the
initial preferred pharmacologic treatment if
needed.

8/11/10 8:21:34 AM

Electrical cardioversion
Pacemaker
1) Slow Vent. Rate:
-blockers
Ca2+-Channel Blockers
Digoxin
2) Restore Sinus Rhythm:
IA: Moderate Na+-channel
blockers
IC: Na+-channel blockers
III: K+-channel blockers
1) Slow ventricular rate by
inc. AV block:
-blockers
Ca2+-Channel Blockers
(Digoxin NOT effective)
2) Restore Sinus Rhythm:
Antiarrhythmics
IA: Moderate Na+-channel
blockers
IC: Na+-channel blockers
III: K+-channel blockers
3) Anticoagulants
Maze Procedure
Percutaneous catheter

ablation
Paroxysmal
Supraventricular
Tachycardias
(PSVT) - See
AVNRT & AVRT

1) Sudden onset, 2) atrial rates of 140250bpm, 3) narrow (normal) QRS

complexes
Automaticity of an Atrial Ectopic Site
Reentry

Focal Atrial
Tachycardia

Antiarrhythmic drug treatment of AF is

Because the efcacies and toxicities of ansimilar to that of atrial utter. -Blockers or
tiarrhythmic drugs have been disappointing,
certain Ca channel antagonists (diltiazem,
nonpharmacologic options for the manageverapamil) are administered to promote block
ment of AF have been devised. For example,
at the AV node and to reduce the ventricular
the surgical maze procedure places multiple inrate. Digitalis is less effective for this purcisions in the left and right atria to prevent the
pose, although it may be useful in patients
formation of reentry circuits and is sometimes
with accompanying impairment of ventricular
performed in patients who undergo cardiac
contractile function. For those who remain
surgery for coronary artery or valve disease
symptomatic despiteadequateratecontrol, conwho also have AF. A less invasive approach
version to sinus rhythm is usually attempted,
is percutaneous catheter ablation. In this apas described in the next paragraph. AF that
proach, areas of the left atrium around the
has been present for more than 48 hours may
pulmonary veins are cauterized to interrupt
predispose to atrial thrombus formation, and
potential reentry circuits and foci that initiate
systemic anticoagulation (for at least 3 weeks)
AF. It requires extensive catheter manipulais usually warranted prior to cardioversion to
tion and ablation in the left atrium, and risks
reduce the risk of thromboembolism. Alterof the procedure includes stroke from systemic
natively, a transesophageal echocardiogram
thromboembolism and cardiac perforation that
can be performed to evaluate for the prescan cause tamponade. Thus, catheter ablation
Chapter
ence
of12thrombus; if none is found, cardiofor AF is usually reserved for patients who
version may proceed directly, with minimum
remain symptomatic despite pharmacologic
thromboembolic risk.
approaches.
Cardioversion to sinus rhythm can be atWhen sinus rhythm cannot be maintained
tempted chemically by administration of class
and the heart rate cannot be controlled adeIA, IC, or III antiarrhythmic drugs (see Chapquately with medications, catheter ablation of
ter 17). Alternatively,
cardioversion
P
P electrical
P
P
P
P thePAV node
P is another
P
P available procedure.
can be undertaken. Following successful
This method intentionally creates complete
conversion
to12.18.
sinus
rhythm,
heart
block
as QaRSmeans
tobypermanently
slow
Figure
Multifocal
atrialantiarrhythmic
tachycardia. The rhythm is
irregular
and each
is preceded
aP
wave
of varying
morphology.in an attempt to
drugs are
often
continued
the ventricular rate. As a consequence, a perprevent recurrences. Note that these drugs
manent pacemaker is also required to generate
action
the ECG, arate.
VPB appears as
An isoelectric
(i.e.,
at) serious,
baseline sometimes
between
have
the capacity
to
cause
anpotential.
adequateOn
ventricular
a widened QRS complex, because the impulse
P waves distinguishes MAT from the chaotic
lethal,
side effects (see Chapter 17). Thus, in
travels from its ectopic site through the ventribaseline of AF. This rhythm is likely caused
patients with asymptomatic AF, it is often ap- cles via slow cell-to-cell connections rather
by either abnormal automaticity in several foci
Paroxysmal Supraventricular Tachycardias
propriate
simply
controlactivity
the ventricular
than through the normal rapidly conducting
within thetoatria
or triggered
and ocrate
continue
therapy HisPurkinje
Paroxysmal
tachycardias
system.supraventricular
Furthermore, the ectopic
curs and
most often
in the anticoagulation
setting of severe pulmochronically,
rather
than
to
pursue
cardioverare manifested
by (1)
sudden onset and
beat(PSVTs)
is not related
to a preceding
P wave.
nary disease and hypoxemia. Because patients
sion.
an approach
supported
bythe
clini- VPBs
termination,
(2) atrial
rates between
can also occur
in repeating
patterns.140 and
with Such
this rhythm
are oftenis
critically
ill from
When
every
alternate
beat
is a VPB,
the rhythm
underlying
mortality
rate is
high,
cal
trials ofdisease,
AF thatthe
have
assessed
long-term
250
bpm,
and (3)
narrow
(normal)
QRS compis termed
When
two aberrant
normal beats
and treatment
is aimed at the causative disorclinical
outcomes.
lexes bigeminy.
(Fig. 12.14),
unless
conduction

P-wave: before each QRS, morphology

different from sinus rhythm

Digitalis Toxicity (worsened by

hypokalemia)
Elevated Sympathetic Tone
(illness, exertion)

Abnormal Automaticity in multiple atrial P-waves:

foci.
Irregular rhythm
Atrial rate > 100bpm
At least 3 different morphologies
Isoelectric (flat) baseline

Multifocal Atrial
Tachycardia

AV Node
Teenagers, and Young
Adults
Palpations
Light-headedness
Dyspnea

Paroxysmal
Reentrant
Tachycardia: AV
Node (AVNRT)

Chapter 12

Elderly, Underlying
Heart Disease
Syncope
Angina
Pulmonary Edema

Severe Pulmonary Disease

Hypoxemia

1) Sudden onset, 2) atrial rates of 140- Common AVNRT:

250bpm, 3) narrow (normal) QRS
QRS complex: normal, narrow
complexes
P-waves:
1) hidden, superimposed on QRS
Common AVNRT:
2) Inverted at terminal end of QRS: Leads
every VPB, trigeminy is present. Conder. The calcium channel blocker verapamil is
4) Spontaneous ABP
II, III, aVF (retrogradeprecede
atrial
activation)
Clinical
Aspects of to
Cardiac
Arrhythmias
secutive VPBs
are referred
as couplets
(two
often effective at slowing the ventricular rate
5) APB encounters refractory Fast
in a row) or triplets (three in a row).
as a temporizing measure.
and do not require other specic intervenVentricular Pre-excitation Syndrome
VPBs are not dangerous by themselves, and
tions. Frequent symptomatic episodes, particPath. (unidirectional block)
inInpatients
patientswithout
with ventricular
heart disease,
pre-excitation
they confer
ularly when
requiring
Ventricular
Arrhythm
iasvisits to the emergency (also termed WolffParkinsonWhite [WPW]
6) APB conducts down Slow Path
department for treatment, warrant preventive no added risk of a life-threatening arrhythmia.
syndrome;
see Chapter
11),
atrial impulses
They
can, however,
be an
indication
of an unThe common
arrhythmias
(1)
therapy: ventricular
oral -blockers,
calcium are
channel
can passcardiac
in an anterograde
direction
to added
the
disorder and
take on
premature
beats
(VPBs),
(2) ventric-for derlying
7) At distal AV Node, APB propagates ventricular
blockers,
or digoxin
are
often successful
ventricles through both the AV node and
ular tachycardia
(VT),
and (3)
ventricular
brilthis purpose.
Catheter
ablation
of the slow
AV signicance in that case. For example, in pathe
accessory
pathway.
Because
conduction
distally (His-Purkinje) and
is also
an effective
but tients with structural heart disease, VPBs genlationnodal
(VF). pathway
Ventricular
arrhythmias
areoption
usually
through the accessory pathway is usually
is
associatedthan
with supraventricular
a small risk ( 2%)rhythm
of heart erally increase in frequency in relation to the
dangerous
than
that
via theby
AV
node,
ventricles
retrograde up recovered Fast Path more
Figureto12.14.
Paroxysm
al supra
ventricula
rfaster
tachyca
rdia
caused
AV
nodathe
l reentry.
blockand
owing
unintended
damage
the severity
of depressed
ventricular
contractility.
disorders
are responsible
for this
many
oftothe
are
stimulated
earlier
by normal
P waves
examplethat
occur sim
ultaneously
with,
andthan
are hidden
in,conducthe
fast AV Retrograde
nodal pathway,
a in
complication
They
havethe
been
with
anrhythm,
increased
approximately
sudden
cardiac deaths
tion over
AV associated
node. During
sinus
QR300,000
S complexes.
8) Retrograde impulse meets atria
requires permanent pacemaker implantation.
risk
of sudden
death
in patients
with
heart failthat occur
every year in the United States.
activation
of the
ventricle
from the
accessory
Chronic class IA or IC antiarrhythmic drugs
ure
or prior
myocardial
infarction.
pathway
causes
a characteristic
ECG appear9) Reenters Slow Path, completing
Uncommon
AVNRT:
are also effective, but are often less desirable
ance:
(1) the PR interval
short ( 0.12
sec)
In otherwise
healthyis persons,
treatment
288 than catheter ablation, because of associated
Ventricular
Premature
circuit tachycardia
Inverted
atBeats
terminal end ofof
QRS:
Leads
II,
III,
because
ventricular
stimulation
begins
earlier
VPBs
mainly involves
reassurance
and, if
potential drug toxicities.
than normal
through the
accessory
needed,
symptomatic
control
usingpathway,
-blockers.
Similar to APBs, VPBs are common even
aVF
(retrograde
atrial
activation)
(2)
the
QRS
has
a
slurred
rather
than
a
sharp
In patients with advanced structural heart
among
healthy people
and are
often asymptoAtrioventricular
Reentrant
Tachycardias
upstroke (referred to as a delta wave) because
disease
with features that place them at risk
matic and benign (Fig. 12.19). A VPB arises
Uncommon AVNRT:
Atrioventricular reentrant tachycardias (AVRTs)
the initial ventricular activation by the accesof life-threatening ventricular arrhythmias,
whenare
ansimilar
ectopic
ventricular focus res an
to AVNRTs except that in the former,
sory pathway is slower than activation over
Anterograde conduction in Fast Path,
one limb of the reentrant loop is constituted by an
the Purkinje system, and (3) the QRS complex
accessory pathway (bypass tract), rather than by
is widened because it represents fusion of two
and retrograde conduction back up
separate fast and slow pathways within the AV
excitation wave fronts through the ventricles,
node itself. As described in Chapter 11, an accesone from the accessory pathway and one from
Slow Path
sory pathway is an abnormal band of myocytes
the normal HisPurkinje system (Figs. 12.16
spans the AV groove and connects atrial to
and 12.17).
One limb of reentrant circuit is an
1)that
Wolf-Parkinson-White
Syndrome /
ventricular tissue separately from the normal conPatients with WPW syndrome are predisduction system (see Fig. 11.10). Approximately 1
posed to PSVTs because the accessory pathway
Accessory Pathway
Ventricular
Pre-Excitation
in 1,500 people has such a pathway.
provides a potential limb of a reentrant loop.
Accessory
pathways allow an impulse to
The most common PSVT in these patients is
1) Wolf-Parkinson-White
Sinus
Rhythm
igure 12.19.
Ventricular prem
ature beats (arrow
s). During this tachycardia,
conduct from atrium toFventricle
(anterograde
orthodromic
AVRT.
conduction),
from ventricle
to atrium (retroan impulse (early
travels anterogradely
down the AV
Syndrome / Ventricular Pre PR
Interval
is short:
<0.12sec
venticular
grade conduction), or in both directions. Denode to the ventricles and then retrogradely up
294
pending on the characteristics of the pathway,
the accessory
tract back to the atria (see Fig.
Excitation
stimulation
via
accessory
path)
one of two characteristic entities can result:
12.17B). Because the ventricles in this situation
(1) the ventricular pre-excitation syndrome, or
are depolarized exclusively via the normal conSinus Rhythm
Delta
Wave: slurred upstroke
in QRS complex
(2) PSVT resulting from a concealed accessory
duction system (through the AV node and the
pathway.
Some
pathways
do
not
conduct
imbundle of His), there is no delta wave during the
Atrial impulses pass anterograde
Widened
QRS
complex:
fusion
ofthetwo
pulses at rates sufcient to cause tachycardias
tachycardia and
width of the QRS is usually
and cause no symptoms at all.
normal. Retrograde P waves are often visible
through Accessory Path (faster)
excitation waves
and AV Node (slower)
Earlier ventricular conduction
Orthodromic AVRT
Anterograde down AV Node
Retrograde up Accessory Pathway
77237_ch12.indd 288

Paroxysmal
Reentrant
Tachycardia:
Atrioventricular
(AVRT)

77237_ch12.indd 294

291

77237_ch12.indd 291

8/11/10 8:21:37 AM

Acute Therapy: Terminate

tachycardia via AV block:
Valsalva maneuver, or
Carotid massage
Adenosine
-blockers
Ca2+-Channel Blockers
Preventive Therapy:
-blockers
Ca2+-Channel Blockers
Digoxin

8/11/10 8:21:34 AM

8/11/10 8:21:38 AM

Figure 12.16. WolffParkinsonWhite syndrome. The delta wave (arrow) indicates pre-excitation of the
ventricles. Note the shortened PR interval.

-blockers
Ca2+-Channel Blockers
Antiarrhythmics
IA: Moderate Na+-channel
blockers
IC: Na+-channel blockers
III: K+-channel blockers
Verapamil: Ca2+-Channel
Blockers

1) Wolf-Parkinson-White
Syndrome / Ventricular
Pre-Excitation
Antiarrhythmics
IA: Na+-channel blockers,
e.g., Procainamide
IC: Na+-channel blockers
III: K+-channel blockers, e.g.,
ibutilide
Digitalis, -blockers, and
Ca2+-channel blockers are
ineffective; do not slow
conduction over accessory

Antidromic AVRT
Orthodromic AVRT
Anterograde down AccessoryChapter
Pathway
No Delta Wave: normal conduction of
12
ventricles via AV Node
Retrograde up AV Node
Chapter 12
QRS complex: Normal width
AF or Atrial Flutter
Conduction over fast Accessory Path P-waves: Inverted at terminal end of QRS
Chapter 12
(retrograde atrial activation via accessory
Ventricular rates up to 300bpm
path) P P P
VFib and Cardiac Arrest
P
P
P
P
P
P
P
*Lown-Goanon-Levine Syndrome:
Figure 12.18. Multifocal atrial tachycardia. The rhythm is irregular and each QRS is preceded by a P
wave of varying morphology.
AV Nodal Reentry: enhanced
conduction through normal AV Node An isoelectric (i.e., at) baseline between action potential. On the ECG, a VPB appears as

pathway

a widened QRS complex, because the impulse

P waves distinguishes MAT from the chaotic
travels from its ectopic site through the ventribaseline of AF. This rhythm is likely caused
cles via slow cell-to-cell connections rather
by either abnormal automaticity in several foci
than through the normal rapidly conducting
within the atria or triggered activity and ocHisPurkinje system. Furthermore, the ectopic
curs most often in the setting of severe pulmobeat is not related to a preceding P wave.
nary disease and hypoxemia. Because patients
Figure
WolffPa
rkinsonW
syndthe
rome. A. During
sinus
rhythm
the shortened
PR interval, delta wave,
VPBsnorm
canalalso
occur
in, repeating
patterns.
with
this12.17.
rhythm
are often
criticallyhite
ill from
and
w
idened
Q
RS
com
plex
indicate
fusion
of
ventricular
activation
via the AV
node
accessory
pathway. B. An atrial
When
every alternate
beat
is aand
VPB,
the rhythm
underlying disease, the mortality rate is high,
prem
ature beatiscan
trigger
icdisoratrioventricular
reentrant
tachycardia,
in which
impulses
are conducted anterois termed
bigeminy.
When
two normal
beats
and
treatment
aimed
at an
theorthodrom
causative
gradely down the AV node and retrogradely up the accessory pathway. Retrograde P waves are visible immediately after the
precede
every
VPB,
trigeminy
is
present.
Conder.
channel
blocker
verapamil
is
QRSThe
comcalcium
plex. There
is no delta
wave
because anterograde
ventricular stimulation passes exclusively through the AV node.
secutive
VPBs
areare
referred
to asanterogradely
couplets (two
often
effective
at slowing thereentrant
ventricular
rate
C. Antidrom
ic atrioventricular
tachycardia
in
which im
pulses
conducted
down the accessory
in is
a row)
or triplets
(three
a row). are stimulated by abnormal
astract
a temporizing
measure.
and retrogradely
up the AV node. The QRS complex
very widened
because
theinventricles
conduction through the accessory pathway. SA, sinoatrial.
VPBs are not dangerous by themselves, and
in patients without heart disease, they confer
Ventricular Arrhythmias
riskPR
ofinterval,
a life-threatening
Figure 12.17. WolffParkinsonWhite syndrome. A. During normal sinus rhythm,no
theadded
shortened
delta wave, arrhythmia.
and widened QRS complex
indicate
ofQRS
ventricular
activation
via
AV node
andcan,
accessory
pathway.
B.
atrial
They
however,
be over
anAn
indication
of an un-pathway when
The
common
ventricular
arrhythmias
arethe
(1)
soon
afterfusion
each
complex
because
the
atria
conduction
the accessory
premature beat can trigger
an orthodrom
ic atrioventricular
reentrant
tachycardia, in
which impulses
aredisorder
conductedand
anteroderlying
cardiac
take on added
ventricular
premature
beats
(VPBs),
(2)
ventricareand
stimulated
from
below pathw
via retrograde
conatrial
utter
gradely down the AV node
retrogradely up
the accessory
ay. Retrograde P
waves are AF
visibleor
imm
ediately
after
the is present. Some accessigniexclusively
cance in through
that case.
Fornode.
example, in patachycardia
(VT),
and (3) ventricular
brilQRS complex. There is ular
no
delta
wave
because
anterograde
ventricular
stim
ulation passes
the AV
duction
through
the
accessory
pathway.
sory pathways
have short refractory periods
tients
with structural
disease, VPBs genlation (VF).
Ventricular
arrhythmias
are
usually
C. Antidromic atrioventricular
reentrant
tachycardia
in which im
pulses
are conducted
anterogradely
down heart
the accessory
InAV
fewer
than
10%
patients
with
AVRT
that
allow
faster
of ventricular
stimulatract and retrogradely up
the
node. The
QRS com
plexof
is very
widened
because
the
ventricles
are stim
by abnorm
al
erally
increase
inulated
frequency
inrates
relation
to the
more
dangerous
than
supraventricular
rhythm
conduction through the
accessory and
pathw
ay. SA,
sinoatrial.
involving
anare
pathway,
the
reentrant
tion
than
the AV
node. Thus, during AF
severity
of
depressed
ventricular
contractility.
disorders
many
of ,the
Figure 12.17. WolffParkinsonW
hite syndrom
e.accessory
A.responsible
During norm
alfor
sinus
rhythm
the
shortened
PR interval,
delta wdoes
ave,
and widened QRS complex indicate
fusion of ventricular
activation
the AVdeaths
node
and accessory
pathw
ay.
B. associated
Anatrial
They have
with an increased
approximately
arrhythmia
travels
300,000
sudden
in thevia
cardiac
opposite
direction.
orbeen
atrial
utter, ventricular
rates as fast as 300
premature beat can trigger an orthodrom
ic atrioventricular
tachycardia,
which im
pulses
conducted
anterorisk
of are
sudden
death
inresult.
patientsSuch
with heart
that
occur
every year
inreentrant
the United
States.
Impulses
anterogradely
downPinthe
accesbpm
may
ratesfailare poorly tolergradelysoon
down the
AV node
retrogradely
uptravel
the accessory
wavesover
are visible
imm
ediately
after
the when
after
eachand
QRS
complex
because
thepathw
atriaay. Retrograde
conduction
accessory
pathway
urethe
or prior
myocardial
infarction.
QRS complex. There is no delta w
ave because
pathway
and retrogradely
ventricular stimulation
uporthe
passes
AVexclusively
node
through
ated
the
and
AV node.
can
lead
ventricular brillation
are stimulated fromsory
below
viaanterograde
retrograde
conAF
atrial
utter
isdow
present.
Some
acces-to treatment
In otherwise
healthy
persons,
C. Antidromic atrioventricular reentrant tachycardia in which impulses are conducted anterogradely
n the accessory
(see
Fig. 12.17C).
antidromic
AVRT,
and cardiac
arrest, even in a young, otherwise
V
entricular
Prem
atureTermed
Beats
duction
through
accessory
sory pathways
short
refractory
tract and
retrogradely
up thethe
AV node.
The QRSpathway.
complex is very widened because
the ventricles
are
stim
ulated
by abnorm
al periods
ofhave
VPBs
mainly
involves
reassurance and, if
itspathw
ECG
isVPBs
characterized
a
wide
QRS
healthy
patient.
conductionIn
through
thethan
accessory
SA,
sinoatrial.
fewer
10%
of ay.
patients
with
AVRT
thatbyallow
faster
ratessymptomatic
of ventricular
stimulaneeded,
control
using -blockers.
Similar
topattern
APBs,
are common
even
complex
because
the ventricles
are
activated
Pharmacologic
management
involving an accessory
pathway,
the
reentrant
tion
than
doesIn
thepatients
AV node.
Thus,
duringstructural
AF
with
advanced
heartof arrhythmias
people
are often
asymptoFigure 12.17. WolffParkinsonWhite syndrome. among
A. During healthy
normal sinus
rhythm,and
the shortened
PR interval,
delta wave,
entirely
from
anterograde
conduction
the
in patients
withas
the
WPWatsyndrome
requires
arrhythmia
in activation
the
direction.
atrial
utter,
disease
ventricular
with
rates
features
as fast
that
place
300them
risk
and widened QRS complex
indicate fusiontravels
of ventricular
matic
andopposite
benign
via the
AV
(Fig.
node 12.19).
and accessory
A or
VPB
pathway.
arises
B
. over
An
atrial
soon
after
each
QRS
complex
because
the
atria
conduction
over
the
accessory
pathway
when
premature beat can trigger an orthodromic atrioventricular
reentrant
tachycardia,
in which impulses
are
conducted
anteroof Such
life-threatening
ventricular
arrhythmias,
when
an
ectopic
ventricular
focus
res
an
Impulses
travel
anterogradely
down
the
accesbpm
may
result.
rates
are
poorly
toleraccessory
pathway.
From
the
ECG
alone,
such
greater
caution
than
those
with AVNRTs. Algradely down the
AVstimulated
node and retrogradely
the accessory
pathway. Retrograde
are visible
immediately
after the
are
fromup
below
via retrograde
con-P wavesAF
or atrial
utter
is present. Some accesQRS complex. There is nosory
delta wave
becauseand
anterograde
ventricular up
stim
ulation
passes
exclusively
through
the
AV
node.lead to though
pathway
re
trogradely
the AV
node
ated
and
can
ventricular
brillation
antidromic
tachycardia
is pathways
dif
cult
to
distindigitalis,
-blockers, and certain calduction
through
the
accessory
pathway.
sory
have
short
refractory
periods
C. Antidromic atrioventricular reentrant tachycardia in which impulses are conducted anterogradely down the accessory
(see
Fig.
12.17C).
Termed
antidromic
AVRT,
and cardiac
arrest, evencium
in a young,
otherwise
guish
tachycardia
(described
channel
tract and retrogradely
the AVthan
node. The
QRS com
is veryfrom
widened
because
are
stimulated
by abnorm
In up
fewer
10%
of plex
patients
withventricular
AVRTthe ventricles
that
allow
faster
ratesal of ventricular
stimula-blockers are effective at blocking
conduction through the accessory
SA, is
sinoatrial.
its ECGpathway.
pattern
characterized
by a wide QRS
healthy patient.
later inthe
thereentrant
chapter).
conduction
through the AV node, they do not
involving an accessory pathway,
tion than does the AV node. Thus,
during AF
complex because the A
ventricles
are
activated
Pharmacologic
management
of
arrhythmias
thirddirection.
type of arrhythmia
in rates
slow
conduction
arrhythmia travels in the opposite
or atrial encountered
utter, ventricular
as fast
as 300 over most accessory pathways.
entirely from
anterograde
conduction
over the
in patients
with
the WPW syndrome requires
soon after each
QRS complex
the patients
atriadown
conduction
over the
accessory
pathway
whenrates are
with
WPW
syndrome
anterograde
Sometimes
these drugs actually shorten the
Impulses
travelbecause
anterogradely
the accesbpm
may is
result.
Such
poorly toleraccessory
pathway.conFrom the ECG
alone, such
greater
caution
than those with AVNRTs. Alare stimulated
from
below via
retrograde
is present.
Some
sory
pathway
and
retrogradely up AF
the or
AVatrial
nodeutterated
and can
leadaccesto ventricular brillation
antidromic
tachycardia
is
dif
cult
to
distinthough
digitalis,
-blockers,
and
certain calduction through the accessory pathway.
sory pathways have short refractory periods
(see Fig. 12.17C). Termed antidromic
AVRT,
and cardiac arrest, even in a young, otherwise
In fewer than 10%
of patients
with AVRT
that allow (described
faster rates of ventricular
stimulaguish
from ventricular
cium channel
blockers are effective at blocking
292 tachycardia
its ECG pattern
is characterized
bytion
a wide
QRS
healthy patient.
involving an accessory
pathway,
the reentrant
than does the AV node.
Thus, during
AF
later
in the chapter).
conduction
through
the AV node, they do not
complex
because
thedirection.
ventricles are
activated
Pharmacologic
of(arrow
arrhythmias
Figure
12.19.
Ventricular
ature beats
s).
arrhythmia travels
in the
opposite
or atrial
utter, ventricular
rates
fast management
asprem
300over
A third
type
of arrhythmia
encountered
in
slowas
conduction
most accessory pathways.
entirely
from
anterograde
conduction
over
the
in
patients
with
the
WPW
syndrome requires
Impulses travel anterogradely down the accesbpm may result. Such rates are poorly tolerpatients with WPW syndrome is anterograde
Sometimes these drugs actually shorten the
accessory
pathway.
From
the ECGated
alone,
cautionbrillation
than those with AVNRTs. Alsory pathway
and retrogradely
up the
AV node
andsuch
can leadgreater
to ventricular
294
(see Fig. 12.17C).
Termedtachycardia
antidromic AVRT,
andto
cardiac
arrest, though
even in adigitalis,
young, otherwise
antidromic
is difcult
distin-blockers, and certain calits ECG pattern
is characterized
by a wide
QRS 292 healthy
patient.
77237_ch12.indd
8/11/10
guish
from
tachycardia
(described
cium channel blockers are effective at blocking
292 ventricular
complex because
thethe
ventricles
are activated
Pharmacologic management
arrhythmias
later in
chapter).
conductionofthrough
the AV node, they do not
entirely from anterograde conduction over the
in patients with the WPW syndrome requires
A third type of arrhythmia encountered in
slow conduction over most accessory pathways.
accessory pathway. From the ECG
alone, such
greater caution than those with AVNRTs. Al77237_ch12.indd 294
8/11/10 8:21:38 AM
patients with
WPW
anterograde
drugs
shorten
the
Clinical
Aspects
of Cardiac Arrhythmias
antidromic tachycardia
is dif
cult syndrome
to distin- isthough
digitalis, Sometimes
-blockers, andthese
certain
cal- actually

Chapter 12
2) PSVT from concealed
accessory
pathway
Orthodromic AVRT: only retrograde
conduction in Accessory Pathway.

2) PSVT from concealed

accessory pathway:
Terminate tachycardia via
AV block
Valsalva maneuver, or
Carotid massage
Adenosine
-blockers
Ca2+-Channel Blockers

Antidromic AVRT
QRS complex: wide (myocyte conduction via
accessory path)

*Lown-Goanon-Levine Syndrome: short PR

interval; normal, narrow QRS complex (no
delta wave)

Ventricles
Often asymptomatic and
benign.

Ventricular
Premature Beats

Ventricular
Tachycardia

Sudden Death in
patients with Heart
Failure, or prior MI

Rate: 100-200 bpm

Sustained VT: VT that
persists for 30 sec or
more
Syncope
Pulmonary Edema
Cardiac Arrest
Nonsustained VT: selfterminating VT

Ectopic ventricular focus fires and

action potential. Slower impulse
conduction via cell-to-cell connections
rather than His-Purkinje

QRS Complex: Widened (slower conduction)

Bigeminy: every alternating beat is a

VPB
Trigeminy: two normal beats precede
a VPB
Couplets: 2 consecutive VPBs
Triplets: 3 consecutive VPBs
Series of 3 VPB guish from ventricular tachycardia (described Monomorphic
VT: at blocking
cium channel blockers are effective
292
later in the77237_ch12.indd
chapter).
292
A third type of arrhythmia encountered in
patients with WPW syndrome is anterograde

Monomorphic VT: QRS at regular

rate.
292
Structural abnormality that supports
reentrant circuit (MI scar).
Idiopathic from ectopic focus

conduction through the AV node, they do not

slow conduction over most accessory pathways.
Sometimes these drugs actually shorten the

77237_ch12.indd 292

8/11/10 8:21:37 AM

8/11/10 8:21:37 AM

Chapter
12
placement
of an implantable cardioverter-

pointes (discussed later in the chapter) and

acute myocardial ischemia or infarction are
the most common causes of polymorphic VT.
Rare, inherited predispositions to polymorphic
Ventricular Tachycardia
VT and sudden death arise from abnormaliVT is a series of three or more VPBs
ties of cardiac ion channels or calcium han(Fig. 12.20). VT is divided arbitrarily into two
dling (e.g., the LQTS, the Brugada syndrome,
categories. If it persists for more than 30 sec,
familial catecholaminergic polymorphic VT),
produces severe symptoms such as syncope,
as described in Box 12.1. Sustained polymoror requires termination by cardioversion or
phic VT usually degenerates to VF.
administration
andes
antiarrhythmic
it polym
is orphicThe
of onstrate
VT varya depending
Figure 12.21. of
Torsa
de pointes. Thedrug,
widened
QRSsymptoms
complexes dem
waxing and on the
designated
waning pattern.
as sustained VT; self-terminating
rate of the tachycardia, its duration, and the
episodes are termed nonsustained VT. Both
underlying condition of the heart. Sustained VT
forms of VT are found most commonly in
can cause low cardiac output resulting in the
patients
with structural
heart
disease,
includ- Torsades
loss of de
consciousness
(syncope), pulmonary
used
to distinguish
VT from
SVT
with aberPointes
ing myocardial
ischemia is
and
infarction,
heart
edema, or progress to cardiac arrest. These
rancy,
but the distinction
often
very dif
Torsades
de pointes (twisting
of the
points)
failure,
ventricular
hypertrophy,
primary
severe consequences
of VT are
most
likely in
cult. Most patients with wide QRS tachycardia
is
a
form
of
polymorphic
VT that
presents
electrical
diseases as
(e.g.,
long-QT
patients who have underlying
depressed
conshould
be managed
though
they syndromes
have VT
varying
amplitudes
of the QRS,
as if theVT
[LQTS];
seeotherwise.
Box 12.1), valvular heart diseases, astractile
function.
Conversely,
if sustained
until
proven
complexes
were
about
the
base-be
and congenital cardiac abnormalities.
is relatively
slowtwisting
(e.g., 130
bpm),
it may
line
(Fig.
12.21).
It
can
be
produced
by
early
The ent
QRS
complexes
well tolerated and cause only palpitations.
Managem
of Patients
withofVTVT are typically
wide ( 0.12 sec) and occur at a rate of 100 afterdepolarizations (triggered activity), particularly in patients who have a prolonged
Sustained
episodes
of VT are
dangerous
beto 200 bpm
or sometimes
faster.
VT is further
Distinguishing Monomorphic VT from
cause
they canaccording
produce syncope
deteriorate
categorized
to its or
QRS
morphol- QT interval. QT prolongation (which indiSupraventricular
Tachycardia
a lengthened
action potential duration)
into
VF,When
whichevery
is fatalQRS
if not
quickly appears
corrected.the cates
ogy.
complex
from electrolyte
disturbances
(hy-by
Acute
usually
consistsit of
sametreatment
and the rate
is regular,
is electrical
referred to can
VTresult
can usually
be distinguished
from SVT
pokalemia
hypomagnesemia),
cardioversion.
Intravenous
administration
of
as monomorphic
VT (see
Fig. 12.20). Susthe width or
of the
QRS complex: it persistent
is routinely
drugs
block
certain
such indicates
as amio- a bradycardia,
tainedantiarrhythmic
monomorphic drugs,
VT usually
wide in the and
former
and that
narrow
(i.e.,cardiac
normal)
potassium
currents,
including
many
antidarone,
procainamide,
be
structural
abnormality or
thatlidocaine,
supports can
a reentry
in the latter. However, under certain circumagents (particularly
the class
III
considered
if the
patient is
hemodynamically
circuit, most
commonly
a region
of myocardial arrhythmic
stances, arrhythmias
that originate
from sites

Polymorphic VT:

debrillator (ICD) is typically recommended.

Polymorphic VT: continually changing

QRS complexes
Torsades de pointes
Acute MI or Infarction
Inherited (LQTS, Brugada Syndrome,
familial catecholinergic
polymorphic VT)
Sustained polymorphic VT usually
degenerates to VF

Otherwise Normal Patients:

-blockers
Patients with Underlying
Disease: implantable
cardioconverter-defibrillator
(ICD)

8:21:37 AM

Structural Heart Disease

MI
Heart Failure
Ventricular Hypertrophy
Primary Electrical Disease
(long-QT Syndrome)
Valvular Diseases
Congenital Cardiac Diseases
Polymorphic VT:
Torsades de pointes
Acute MI or Infarction
Inherited (LQTS, Brugada
Syndrome, familial
catecholinergic
polymorphic VT)

8/11/10 8:21:37 AM

Figure 12.20. Monomorphic ventricular tachycardia.

77237_ch12.indd 292

Structural Heart Disease: inc.

frequency indicates severity of
depressed ventricular
contractility.

Acute VT: Restore Sinus

Rhythm
Electric Cardioversion
Amiodarone
Procainamide
Lidocaine

Syncope, Lightheadedness

Triggered Activity: Early

Afterpolarizations in those with
prolonged QT interval

Torsades de
Pointes

Immediate, Lifethreatening
Ventricular
Fibrillation

Cessation of cardiac
output, and death

Disordered, rapid ventricular

stimulation with no coordinated
contractions.
Multiple, small wavelets of reentry.

During Polymorphic VT, then Look to Normal segment of EKG:

If Long QT, then likely Torsades de Pointes.

If Normal QT, then likely ischemia/MI

VT vs SVT
VT typically has widened QRS complexes;
whereas, SVT does not.
SVT w/ Aberrancy (widened QRS):
1) Patients with prior MI, CHF, or L. ven.
Dysfunction = VT.
2) Effective Vagal Maneuvers = SVT
Chapter 12
Twisting of the Points

QT Prolongation:
Hypokalemia or
Hypomagnesemia
Persistant bradycardia
Drugs that block cardiac
Figure 12.21. Torsades de pointes. The widened polymorphic QRS complexes demonstrate a waxing and
potassium currents
waning pattern.
o
Class III: sotalol,
used to distinguish VT from SVT with aberTorsades de Pointes
ibutilide, dofetilide
rancy, but the distinction is often very difTorsades de pointes (twisting of the points)
o
Some Class I:
cult. Most patients with wide QRS tachycardia
is a form of polymorphic VT that presents
should be managed as though they have VT
as varying amplitudes of the QRS, as if the
quinidine,
until proven otherwise.
complexes were twisting about the baseline (Fig. 12.21). It can be produced by early
procainamide,
Management of Patients with VT
afterdepolarizations (triggered activity), pardisopyramide
ticularly in patients who have a prolonged
Sustained episodes of VT are dangerous beQT interval. QT prolongation (which indicause they can produce syncope or deteriorate
cates a lengthened action potential duration) Erythromycin
into VF, which is fatal if not quickly corrected.
can result from electrolyte disturbances (hyAcute treatment usually consists of electrical
pokalemia or hypomagnesemia), persistent Phenothiazines
cardioversion. Intravenous administration of
bradycardia, and drugs that block cardiac
certain antiarrhythmic drugs, such as amiopotassium currents, including many anti- Haloperidol
darone, procainamide, or lidocaine, can be
arrhythmic agents (particularly the class III
considered if the patient is hemodynamically
drugs sotalol, ibutilide, and dofetilide and Methadone
stable.
some class I drugs, including quinidine,
After sinus rhythm is restored, a patient
procainamide, and disopyramide). Many Congenital QT prolongation
who has had sustained VT requires careful

medications administered for noncardiac illevaluation to dene whether underlying strucnesses can also prolong the QT interval and
tural heart disease is present and to correct
linical
Aspects
Cardiac Arrhythm
ias
predispose C
to
torsades
deofpointes,
including
any aggravating factors, such as myocardial
erythromycin, phenothiazines, haloperidol,
ischemia, electrolyte disturbances, or drug toxand methadone. A rare group of hereditary
icities. Patients who have suffered VT in the
ion channel abnormalities produces congenisetting of structural heart disease have a high
tal QT prolongation, which can also lead to
risk of recurrence and sudden cardiac death;
torsades de pointes (see Box 12.1).
implantation of an ICD is usually warranted to
Torsades de pointes is usually symptomatic,
automatically and promptly terminate future
causing light-headedness or syncope, but is
episodes.
frequently self-limited. Its main danger results
Patients who experience VT in the absence
from degeneration into VF. When it is drug or
of underlying structural heart disease are usuFigure
12.22.
Ventricular
electrolyte
fibrillation.
induced, correcting the underlying
ally found to have idiopathic VT.
This
type
cause abolishes recurrences. In other cases,
of arrhythmia tends to originate from foci in
administration of intravenous magnesium
the right ventricular outow tract or in the
often suppresses repeated episodes. Additional
septal portion of the left ventricle. It is rarely
preventive
an
lifearti
threatening.
cial pacemaker.
-Blockers,
When
calcium
torsades
channel
de
S
UMMARY strategies are aimed at shortening
the QT interval by increasing the underlyblockers,
or catheter
ablation are
commonly
pointes
results
from congenital
prolongation
1.
formation
and
ingDisorders
heart rate of
withimpulse
intravenous
-adrenergic
effective
control -blocking
symptomatic
episodes
of
of
the QT to
interval,
drugs
are often
conduction
result(e.g.,
in bradyarrhythmias
stimulating
agents
isoproterenol) or
idiopathic
VT.of choice, because sympathetic
the
treatment
and tachyarrhythmias. Through careful
stimulation actually aggravates the arrhythanalysis of the ECG, it is usually possible
mia in many such individuals. An implant298
to distinguish individual rhythm disorable debrillator is often appropriate for these
ders so that appropriate therapy can be
patients.
administered.
2. When evaluating a patient with a slow
Ventricular Fibrillation
heart rhythm (Figs. 12.112.8), two key8/11/10
77237_ch12.indd 298
questions should be addressed:
VF is an immediately life-threatening arrhythmia (Fig. 12.22). It results in disordered, rapid
a. Are P waves present?
stimulation of the ventricles with no coordib. What is the relationship between the
nated contractions. The result is essentially
P waves and the QRS complexes?
cessation of cardiac output and death if not
3. Differentiation of tachyarrhythmias requires
quickly reversed. This rhythm most often ocassessment of:
curs in patients with severe underlying heart
a. The width of the QRS complex (normal
disease and is the major cause of mortality in
or wide).
acute myocardial infarction.
b. The morphology and rate of the P waves.
VF is often initiated by an episode of

Chaotic, irregular appearance without discrete

QRS waveforms

VT, which degenerates, it is believed, by

the breakup of excitation waves into multiple smaller wavelets of reentry that wander
through the myocardium. On the ECG, VF is
characterized by a chaotic irregular appearance without discrete QRS waveforms.
Untreated, VF rapidly leads to death. The
only effective therapy is prompt electrical
debrillation. As soon as the heart has been
converted to a safe rhythm, the underlying
precipitant of the arrhythmia (e.g., electrolyte
imbalances, hypoxemia, or acidosis) should
be sought and corrected to prevent further
episodes. Intravenous antiarrhythmic drug
therapy may be administered to prevent immediate recurrences. If no reversible inciting
precipitant is found, survivors of VF usually
receive an ICD.

Often initiated by VT

8:21:38 AM

c. The relationship between the P waves

and the QRS complexes.
d. The response to vagal maneuvers (see
Fig. 12.9).
Each of the ECG texts listed at the end of
Chapter 4 provides many additional examples
of the rhythm disorders presented in this
chapter.

Acknowledgments
Contributors to the previous editions of this chapter
were Hillary K. Rolls, MD; Wendy Armstrong, MD;
Nicholas Boulis, MD; J ennifer E. Ho, MD; Marc S.
Sabatine, MD; Elliott M. Antman, MD; Leonard I.
Ganz, MD; William G. Stevenson, MD; and Leonard
S. Lilly, MD.

299

77237_ch12.indd 299

8/11/10 8:21:39 AM

Shorten QT interval:
-adrengeric agonists (e.g.,
isoproterenol)
Congenital Prolonged-QT:
-blockers

Prompt electric defibrillation