type

subcat
egory

*
Norma
l sinus
rhyth
m

v rate

60 100

v
rhyth
m

reg

a rate

60 100

a
rhyth
m

qrs
durati
on

reg

usuall
y N,
may
be
regula
rly
abN

qrs
durati
on
consis
tency

qrs
shape

pw
prese
nce

pw
shape
consis
tency

pr
each
interv
al

alway
s in
front
of
QRS

N&
consis
tent
shape

b/w .
12 - .
20
secs

pr
interv
al
consis
tency

consis
tent

P:QRS
Ratio

characteristics
(description)

1:1

electrical impulse starts

at a regular rate and
rhythm in the sinus node
and travels through the
normal conduction
pathway

sinus
node

sinus
bradyc
a:
sinus
node
create
s an
impuls
e at a
slower
-thannorma
l rate

sinus
tachy:
sinus
node
create
s an
impuls
e at a
fasterthannorma
l rate

< 60

reg

< 60

reg

>
100,
< 200

Reg

>
100,
< 200

Reg

usuall
y N,
may
be
regula
rly
abN

usuall
y N,
may
be
regula
rly
abN

alway
s in
front
of
QRS

alway
s in
front
of
QRS,
but
may
be
burrie
d in
the
preced
ing T
w

N&
consis
tent
shape

b/w .
12 - .
20
secs

N&
consis
tent
shape

b/w .
12 - .
20
secs

consis
tent

consis
tent

1:1

1:1

All characteristics of
sinus bradycardia are the
same as those of normal
sinus rhythm, except for
the rate.
sinus node dysfx (>50
y/o) = decreased
exercise capacity,
fatigue, unexplained
confusion, or memory
loss may result

All aspects of sinus

tachycardia are the same
as those of
normal sinus rhythm,
except for the rate
does not start or end
suddenly
(nonparoxysmal)
As the
heart rate increases, the
diastolic filling time
decreases, possibly
resulting in reduced
cardiac output and
subsequent
symptoms of syncope
and low blood pressure.
If the rapid
rate persists and the
heart cannot compensate

causes

lower metabolic needs (eg,

sleep, athletic training,
hypothyroidism)
vagal stimulation (eg, from
vomiting, suctioning, severe
pain, extreme emotions) //
stimulation of vagus nerve
(e.g. bearing down, vomiting)
medications (eg, calcium
channel blockers, amiodarone,
beta-blockers)
idiopathic sinus node
dysfunction
increased intracranial
pressure (ICP)
myocardial infarction (MI),
especially of the inferior wall
Hs and the Ts: hypovolemia,
hypoxia, hydrogen ion
(acidosis), hypokalemia or
hyperkalemia, hypoglycemia,
and hypothermia; toxins,
tamponade (cardiac), tension
pneumothorax, thrombosis
(coronary or pulmonary), and
trauma (hypovolemia,
increased ICP)

Physiologic or psychological
stress (eg, acute blood loss,
anemia, shock, hypervolemia,
hypovolemia, heart failure,
pain, hypermetabolic states,
fever, exercise, anxiety)

Medications that stimulate the

sympathetic response (eg,
catecholamines,
aminophylline, atropine),
stimulants (eg, caffeine,
alcohol, nicotine), and illicit
drugs (eg, amphetamines,
cocaine, Ecstasy)
Enhanced automaticity of the

mgt

prevent
vagal
stimulation
witihhold
med

meds

assess ox to
etermine
hemodynamic effect +
possible cause of
dysrh
If the slow heart
rate causes significant
hemodynamic changes
resulting in shortness
of breath, acute
alteration of mental
status, angina,
hypotension, STsegment changes, or
premature ventricular
complexes, treatment
is directed toward
increasing the heart
rate.

Treatment of sinus
tachycardia is usually
determined by
the severity of
symptoms and
directed at identifying
and
abolishing its cause
Catheter ablation
(discussed
later in this chapter) of
the SA node may be
used in
cases of persistent
inappropriate sinus
tachycardia
unresponsive
to other treatments.

atropine, .
5mg rapid,
IV bolus, q
3-5 mins.
Max total
dose 3mg
(blocks vagal
stimulaxn ->
allow n hr to
occur
rare:
chateholami
ns,
emergency
transcutaneo
us pacing

Betablockers and
calcium
channel
blockers,
although
rarely used,
may be
administered
to reduce
the heart
rate quickly.

SA node and/or excessive

sympathetic tone with
reduced parasympathetic
tone, a condition called
inappropriate sinus
tachycardia

for the decreased

ventricular filling, the
patient may develop
acute
pulmonary edema.

Atrial

Sinus
arrhyt
hmia
occurs
when
the
sinus
node
create
s an
impuls
e at
an
irregul
ar
rhyth
m; the
rate
usuall
y
increa
ses
with
inspira
tion
and
decrea
ses
with
expira
tion
Prema
ture
atrial
compl
ex
Atrial
fluter:
occurs
becau
se of a
condu

60
100

75 150

Usuall
y n,
but
may
be
regly
abn

Irreg

Usuall
y reg,
but
may
be
ireg

250 400

reg

alway
s in
front
of
QRS

N,
consis
tent in
shape

b/w .
12 - .
20
secs

Sawtoothe
d
shape
= F
waves

Multipl
eF
waves
may
make
it

consis
tent

1:1

2:1,
3:1,
or 4:1

Autonomic dysfunction, which

results in a type of sinus
tachycardia called postural
orthostatic tachycardia
syndrome (POTS). Patients
with POTS have tachycardia
without hypotension within 5
to 10 minutes of standing or
with head-upright tilt testing.

Sinus arrhythmia does

not cause any significant
hemodynamic
effect and usually is not
treated.

Nonrespiratory causes include

heart disease and valvular
disease, but these are rare.

b/c atrial rate is faster

than the AV node can
conduct, not all
atrial impulses are
conducted into the
ventricle, causing a

often occurs in patients with

chronic obstructive pulmonary
disease, valvular disease, and
thyrotoxicosis, as well as
following open heart surgery
and repair

increased
fluid and
sodium
intake and
use of antiembolism
stockings
to prevent
pooling of
blood in the
lower
extremities.

Vagal maneuvers or
administration of
adenosine (Adenocard,
Adenoscan), which
causes sympathetic
block and slowing of

Adenosine
should be
rapidly
administered
intravenousl
y, followed

ction
defect
in the
atrium
and
causes
a
rapid,
regula
r atrial
rate,
usuall
y
betwe
en
250
and
400
times
per
minut
e
Atrial
fibrilla
tion:
uncoo
rdinat
ed
atrial
electri
cal
activat
ion
that
causes
a
rapid,
disorg
anized
,
and
uncoo
rdinat
ed
twitchi
ng of
atrial
muscu
lature

b/c of
a
chang
e in
AV
condu
cxn

120
200
(in
untrea
ted a
fib)
*
ventri
cular
rate
respo
nse is
depen
dent
on the
ability
of the
AV
node
to
condu
ct the
atrial
impuls
es,
the
level
of
sympa
thetic
and
parasy
mpath
etic
tone,
prese
nce of

Highly
irreg

300 600

Highly
irreg

Shape
&
durax
n
usuall
yN
but
may
be
abN

No
discer
nible P
waves
;
irregul
ar
undul
ating
waves
that
vary
in
amplit
ude
and
shape
are
seen
and
are
referr
ed to
as
fibrilla
tory
or f
waves

difficul
t to
deter
mine
the PR
interv
al

Cant
be
measu
red

many:
1

therapeutic block at the

AV node. This is an
important feature
of this dysrhythmia. If all
atrial impulses were
conducted
to the ventricle, the
ventricular rate would
also be 250 to 400,
which could result in
ventricular fibrillation, a
life-threatening
dysrhythmia

For example, regular RR

intervals in
atrial fibrillation may
indicate the presence of
complete AV
block, junctional
tachycardia, or
ventricular tachycardia.
Atrial fibrillation may be
transient, starting and
stopping
suddenly and occurring
for a very short time
(paroxysmal
dysrhythmia), or it may
be persistent, requiring
treatment
to terminate the rhythm
or to control the
ventricular rate.
The lack of consistency
in describing the pattern
of atrial
fibrillation has led to use
of numerous labels (eg,
acute,
chronic, paroxysmal,
persistent, permanent)
and difficulty
in comparative
assessment of
treatments
Atrial
fibrillation has been
linked to increased risk
of stroke and
premature death

of congenital cardiac defects

conduction in the AV
node, may allow
better visualization
of flutter waves.

by a 20-mL
saline flush
and
elevation of
the arm with
the IV line to
promote
rapid
circulation of
the
medication.

usually occurs in people of

advanced
age with structural heart
disease, such as valvular
heart disease
(most often mitral or
tricuspid), inflammatory or
infiltrative
disease (pericarditis,
myocarditis, amyloidosis),
coronary
artery disease, hypertension,
congenital disorder
(especially atrial septal
defect), and heart failure
(diastolic
or systolic) (Fuster, et al.,
2008). The dysrhythmia also
may
be found in people with
diabetes, obesity,
hyperthyroidism,
pheochromocytoma,
pulmonary hypertension and
embolism,
obstructive sleep apnea, and
acute moderate to
heavy ingestion of alcohol
(holiday heart syndrome),
as
well as following pulmonary or
open heart surgery
Neurogenic
atrial fibrillation that occurs
with subarachnoid
hemorrhage
and nonhemorrhagic stroke is

The clinical evaluation

of atrial fibrillation
should include
a history and physical
examination (to
identify pattern
of atrial fibrillation,
associated symptoms,
and any underlying
conditions); 12-lead
ECG (to identify
presence of ventricular
hypertrophy,
preexcitation from
accessory pathways,
intraventricular
conduction defects,
and history of MI);
echocardiogram (to
assess cardiac
chamber size,
thickness,
and function; to
identify potential
causes, such as
cardiomyopathy
or valvular
dysfunction; and to
identify the presence
of a thrombus); and
blood tests to assess
thyroid, renal, and
hepatic function
(Fuster, et al., 2008).
Additional tests may
include a chest x-ray
(to evaluate

Medications
that may be
administered
to achieve
cardioversio
n
to sinus
rhythm
include
flecainide,
propafenone,
or sotalol
(Fuster, et
al., 2008).
Other
choices
include
dofetilide
(Tikosyn),
amiodarone,
and ibutilide.
Because of
the incidence
of torsade de
pointes, a
ventricular
tachycardia,
the use of
ibutilide
warrants
ECG
monitoring
for at least 4
hours after
its
administratio
n.

access
ory
pathw
ays,
and
effects
of any
medic
ations

Sometimes atrial
fibrillation occurs in
people with no
underlying
pathophysiology (called
lone
atrial fibrillation)
A rapid and irregular
ventricular response
reduces the
time for ventricular
filling, resulting in a
smaller stroke volume.
Because atrial fibrillation
causes a loss in AV
synchrony
(the atria and ventricles
contract at different
times), the
atrial kick (the last part
of diastole and
ventricular filling,
which accounts for 25%
to 30% of the cardiac
output) is also
lost. This may lead to
irregular palpitations and
symptoms of
heart failure such as
shortness of breath,
fatigue, exercise
intolerance,
and malaise. Patients
may be asymptomatic or
experience
significant hemodynamic
collapse (hypotension,
chest pain, pulmonary
edema, and altered level
of consciousness),
especially if they also
have hypertension,
mitral
stenosis, hypertrophic
cardiomyopathy, or some
form of restrictive
heart failure. There is
usually a pulse deficit, a
numeric
difference between apical
and radial pulse rates.
The
shorter time in diastole
reduces the time
available for coronary
artery perfusion, thereby
increasing the risk of
myocardial
ischemia with the onset

caused by increased vagal or

sympathetic stimulation

pulmonary
vasculature),
exercise test (to
assess rate control as
well as myocardial
ischemia),
Holter or event
monitoring, and an EP
study. The
physical examination
may reveal an
irregular pulse,
irregular
jugular venous
pulsations, and
irregular S1 heart
sounds.
Treatment of atrial
fibrillation depends on
the cause, pattern,
and duration of the
dysrhythmia; the
ventricular
response rate; and the
patients symptoms,
age, and
comorbidities.
In many patients,
atrial fibrillation
converts
to sinus rhythm within
24 hours and without
treatment.
Hospitalization may
not be necessary.
Electrical cardioversion
is indicated for
patients with atrial
fibrillation that is
hemodynamically
unstable unless they
have digitalis toxicity
or hypokalemia.
Because of the high
risk of embolization
of atrial thrombi,
cardioversion of atrial
fibrillation
that has lasted longer
than 48 hours should
be avoided unless
the patient has
received warfarin
(Coumadin) for at
least 3 to 4 weeks
prior to cardioversion.
Alternatively, the
absence of a mural
thrombus can be

of chest discomfort. The

erratic
atrial contraction and the
atrial myocardial
dysfunction
promote the formation of
thrombi, especially
within the
atria, increasing the risk
of an embolic event.
In addition, a high
ventricular rate response
during atrial
fibrillation can lead to
dilated ventricular
cardiomyopathy.
The rapid ventricular rate
can also lead to mitral
valve dysfunction,
mitral regurgitation, and
intraventricular
conduction
delay. Controlling the
ventricular rate may
prevent
and correct these effects.

If the QRS is wide and

the ventricular rhythm is
very fast
and irregular, atrial
fibrillation with an
accessory pathway
should be suspected. An
accessory pathway is
congenital tissue
between the atria, His
bundle, AV node,
Purkinje fibers,
or ventricular
myocardium. This
anomaly is known as
Wolff-Parkinson-White or
WPW syndrome.

confirmed by
transesophageal
echocardiogram and
heparin can be
administered
immediately prior to
cardioversion. Because
atrial
function may be
impaired for several
weeks after
cardioversion,
warfarin is indicated
for at least 4 weeks
after the procedure.
Patients may be given
amiodarone
(Cordarone), flecainide
(Tambocor), ibutilide
(Corvert),
propafenone
(Rythmol), or sotalol
(Betapace) prior to
cardioversion to
prevent relapse of the
atrial fibrillation
Electrical
cardioversi
on
is the
treatment
of choice
for atrial
fibrillation
in
the
presence of
WPW
syndrome.
Medications
that block
AV
conduction
(eg, digoxin
[Digitek],
diltiazem
[Cardizem],
and
verapamil
[Calan])
should be
avoided.
Catheter
ablation is
performed
for
long-term
manageme
nt.

If the patient
is
hemodynami
cally
stable,
procainamid
e
(Pronestyl),
propafenone,
flecainide, or
ibutilide is
recommende
d to restore
sinus
rhythm
Other
medications
that may be
used include
sotalol,
quinidine
(Quinaglute)
,
disopyramid
e
(Norpace),
or
amiodarone.

To control
the heart
rate in
persistent
atrial
fibrillation,
an IV betablocker or a
nondihydrop
yridine
calcium
channel
blocker
(diltiazem
and
verapamil) is
recommende
d
(Fuster, et
al., 2006).
However,
people with
impaired
ventricular
function
should not
receive
verapamil,
those with
bronchospas
m should not
receive a
beta-blocker,
and those
with AV
block should
not receive
any of these
medications.
IV digoxin or
amiodarone
may be used
for rate
control in
patients with
heart failure
or left
ventricular
dysfunction
but without
an accessory
pathway. IV
procainamid
e or ibutilide
is an
alternative
for rate
control in
patients with

an
accessory
pathway. In
pregnant
women,
digoxin, a
betablocker,
or a
nondihydrop
yridine
calcium
channel
blocker
may be used
for rate
control. If
medications
fail to control
the heart
rate or cause
significant
side effects,
catheter
ablation
may be
indicated.
If
maintenance
of sinus
rhythm is
necessary to
maintain
quality of
life,
flecainide,
propafenone,
or sotalol
may be
prescribed
(Fuster, et
al., 2006).
Patients who
have been
observed
in the
hospital
while being
given a dose
of either
propafenone
or flecainide
to convert
atrial
fibrillation
may
be given the
medication
to selfadminister

outside the
hospital
if they have
a
recurrence,
an approach
called pill in
the pocket
(Fuster, et
al., 2008).
Several
approaches
are
used to
prevent the
occurrence
of
postoperativ
e atrial
fibrillation;
preoperative
administratio
n of a betablocker or
amiodarone
is the most
successful
(Fuster, et
al., 2006).
Pacemaker
implantation,
ablation, or
surgery may
be indicated
for patients
who do not
respond to
medications.
Although
control of
the rhythm
had been the
initial
treatment of
choice,
recent
studies have
found that
controlling
the heart
rate (resting
heart rate
less than 80)
is
equal to
controlling
the rhythm
in terms of
quality of

life,
frequency of
hospitalizatio
n for heart
failure, and
incidence
of stroke
(AFFIRM
Investigators
, 2002;
Fuster, et al.,
2006).
Antithrombot
ic therapy is
indicated for
all patients
with atrial
fibrillation.
The type of
therapy
should be
based on
the risks of
stroke and
bleeding
versus its
benefits in a
particular
patient.
Warfarin is
indicated if
the patient
with
atrial
fibrillation is
at high risk
for stroke
(ie, older
than 75
years of age
or has
hypertension
, diabetes,
heart failure,
or
history of
stroke)
(Fuster, et
al., 2008). If
immediate
anticoagulati
on
is necessary,
the patient
may be
placed on
heparin
until the
warfarin

level is
therapeutic,
usually
defined as
an
international
normalized
ratio (INR)
between 2
and 3. If a
patient
sustains an
ischemic
stroke or
develops a
systemic
embolization
during
treatment,
the
antithrombot
ic therapy
may be
increased
with the goal
of increasing
the INR to
between
3.0 and 3.5
(Fuster, et
al., 2006).
Although
aspirin
may be
substituted
for warfarin
in patients
with
contraindicat
ions
to warfarin
or those who
are at a high
risk of
bleeding,
warfarin is
generally
preferred
(Fuster, et
al., 2008). If
a
patient will
be
undergoing a
procedure
that carries
a risk of
bleeding,
anticoagulati

on therapy
may be
withheld for
up to
a week. If
more than a
week is
needed,
heparin may
be
given,
although its
efficiency is
unknown.
Patients with
atrial
fibrillation
who have a
coronary
artery stent
implanted
should
receive
clopidogrel
(Plavix), an
antiplatelet
agent, plus
warfarin for
1 to 12
months
following the
procedure
Juncti
onal

Prema
ture
junctio
nal
compl
ex
Juncti
onal/i
dionod
al
rhyth
m
Nonpa
roxys
mal
Juncti
onal
Tachyc
ardia
A
s
tr
u
io
p
v
r
e
a
n
v
tr
e
ic
n
ul
tr

ventri
cular

ic
ul
a
r
t
a
c
h
y
c
a
a
r
r
N
di
o
a
d
(
al
S
R
V
e
T
e
)
n
v
tr
e
y
n
T
tr
a
ic
c
ul
h
a
y
r
c
t
a
a
r
c
di
h
a
y
c
a
r
di
a
(
V
T
)
Prema
ture
Ventri
cular
Compl
ex
Ventri
cular
Tachyc
ardia:
three
or
more
PVCs
in a
row,
occurri
ng at
a rate

PVCs can occur in healthy

people, especially
with intake of caffeine,
nicotine, or alcohol. PVCs may
be
caused by cardiac ischemia or
infarction, increased workload
on the heart (eg, heart
failure, and tachycardia),
digitalis
toxicity, hypoxia, acidosis, or
electrolyte imbalances,
especially

excee
ding
100
bpm

hypokalemia. The Sleep Heart

Health Study found
that those people with sleep
disordered breathing (eg,
obstructive
sleep apnea) had a
significantly higher prevalence
of complex ventricular ectopy
and nonsustained ventricular
tachycardia during sleep
(Mehra, et al., 2006). The
implication
of the presence of PVCs
during and after exercise is
not
clear and remains
controversial

Ventri
cular
Fibrilla
tion
Idiove
ntricul
ar
Rhyth
m
Ventri
cular
Asysto
le
*
condu
ction
obNiti
es

FirstDegre
e
Atriov
entric
ular
Block
Secon
dDegre
e
Atriov
entric
ular
Block
Secon
dDegre
e
Atriov
entric
ular
Block,
Type
II
ThirdDegre
e
Atriov

Medical Management
of Conduction
Abnormalities.
Based on the cause of
the AV block and the
stability of the
patient, treatment is
directed toward
increasing the heart
rate
to maintain a normal
cardiac output. If the
patient is stable
and has no symptoms,
no treatment may be
indicated other
than decreasing or
eliminating the cause
(eg, withholding
the medication or
treatment). If the
causal medication is
necessary
for treating other
conditions and no
effective alternative
is available,
pacemaker
implantation may be

entric
ular
Block
**
pulsel
ess
electri
cal
activit
y

indicated.