CHAPTER I

INTRODUCTION

Supraventricular tachycardia (SVT) is a type of heart rhythm disorder that can
be found in healthy children and adolescents as well as those with underlying heart
disease. Tachycardia refers to any heart rhythm where the heart beats faster than
normal for age and environmental factors. Supraventricular means above the
ventricles, thus describing any tachycardia that originates and or involves
structures above the ventricles of the heart. The term supraventricular tachycardia is
often used differently in different settings.
!
SVT (refers to paroymal SVT) is defined
as tachyarrhythmia (hear rate !"# $ %"#min) in which structure above the division
of the bundle of &is are essential for it maintenance and comprises atrial tachycardia
('T), atrial flutter ('()) and atrioventricular ('V) *unctional tachycardia include 'V
nodal reciprocating tachycardia ('V+,T), 'V reciprocating tachycardia ('V,T). -n
order to present a brief review we shall only discuss 'T and 'V+,T.
%
.any classifications have been used for SVT. /ne of the practical
classifications is to divide them according to the structures re0uired to initiate and
maintain the tachycardia. 1y this classification there are two types of SVT, those
which re0uire only atrial tissue for their initiation and maintenance, and those that
re0uire the atrioventricular ('V) *unction as the same with the definition above.
2
-n
term of medicine SVT classified into paro3ysmal and non paro3ysmal, in which
paro3ysmal SVT is applied to conditions presenting as a sudden episode that is
usually recurrent and non paro3ysmal refers to continuously recurring SVT that can
be episodic cause related to incidental triggers and non episodic (without precipitating
factor). The diagnosis of SVT is made primarily by using !% $ lead electrocardiogram
(456).
%,"
The incidence of SVT is high, is about 27 cases per !##.### persons per year,
and the prevalence is about %,%7 per !### (e3cluding atrial fibrillation, '(, and
multifocal 'T). SVTs are often recurrent, occasionally persistent, and the most
fre0uent cause of visits to emergency rooms and primary care physicians. SVT is
1
often caused by underlying heart disease but sometimes can be related to disease
processes of other organs. /ccasionally the underlying cause of the arrhythmia
cannot be determined. ,eentry arrhythmias are usually induced by premature atrial or
ventricular ectopic beats and precipitating factors such as e3cessive inta8e of
caffeine, alcohol, or recreational drugs and hyperthyroidism can increase the ris8 of
recurrence. 5ommon symptoms of SVT include palpitations, an3iety, light9
headedness, chest pain, pounding in the nec8 and chest, dyspnea, syncope and also
polyuria although it:s very rare. -n some people this condition can be cured itself but
for the others it needs some invasive procedure which is 8nown for its efficiency, it is
catheter ablation techni0ue.
%,7
.ost of patient with SVT have a normal life e3pectancy, but their 0uality of
life is fre0uently poor. The fre0uency and duration of attac8s, the need to see8
hospital treatment for the episodes, the impossibility of participating in certain sports
or professional activities and the feeling of prolonged tiredness after an episode all
determine the degree of impairment in the 0uality of life. -n some condition SVT can
lead to fatal circumstances if SVT continuously to V( and acute pulmonary oedema.
%
,egarding to the important matter of this disease to cardiovascular system and also
for its emergency status, so this topic is very interesting and important to be discussed
in detail through this paper.
2
CHAPTER II
CONTENT
2.1. PATOPHYSIOLOGY
The normal cardiac conduction system e3tends from atrium to the ventricular
myocardium. -n the normal heart, the atrial and ventricular myocardium are
electrically insulated from one another e3cept at the atrioventricular ('V) node and
bundle of &is. -mpulse generation originates in the sinus node, and impulse is
conducted through the atrial myocardium to the 'V node. The ma*or role of 'V node
is to allow conduction of the impulse to the ventricle, and the other important thing is
the inherent delay in the 'V node that slows conduction from the atrium to the
ventricle. This slowing allows ventricular filling. (rom 'V node, there is rapid
conduction via &is9;ur8in*e system with associated right and left branches that
intercalate to the ventricular myocardium
<
.
The normal heart rate varies between <# and !## beats per minutes. The rate
can increase up to !=# beats per minute in e3ercise or in e3ited condition, but it
0uic8ly returns to normal resting. -n SVT the heart races 0uite suddenly to rates as
high as %## beats per minute, and usually the rate is not slowing down
=
.
SVT are rapid rapid rhythm disturbance originating from the atria or the 'V
node. The SVT occurs as a result of three main mechanisms
>
, they are?
!. Triggered arrhythmia
Triggered arrhythmia depends on oscillations in the membrane potential that
closely follow an action potential. -n the absence of a new e3ternal electrical
stimulus, these oscillations, or after depolari@ations, cause new action
potential to develop. Thus, each new action potential results from previous
action potential. These arrhythmias can be produced by early or late after9
depolari@ation, depending on the timing of the first after9depolari@ation
relative to the preceding action potential
>
. -n early after-depolarization,
membrane repolari@ation is incomplete, which allows an action potential to be
initiated by subthreshold stimulus. This type is often associated with
3
electrolyte disturbance
>
. -n delayed after-depolarization, membrane
repolari@ation is complete, but an abnormal intracellular calcium load causes
spontaneous depolari@ation. The reason for high calcium level is unclear, but
it can be related to inhibition of the sodium pump by drugs such as digo3in. -n
either type of arrhythmia, the process may be repetitive and lead to a sustained
tachycardia
>
.
%. 'utomaticity
'utomaticity refers to spontaneous and repetitive firing from a single focus,
which may be either ectopic or may originate in the S' node. 'utomaticity
actually is an intrinsic property of all myocardial cells. -t has two
subcategories, they are enhanced automaticity and abnormal automaticity.
4nhanced automaticity is a focus that fires spontaneously and may originate in
the S' node, sudsidiary pacema8ers in the atrium including the 4ustachian
ridge, 1achmann bundle, coronary sinus, and 'V valve, the 'V node, his9
pur8in*e system, and the ventricle. 'bnormal automaticity is usually
secondary to a disease process causing alterations in ionic flow that produces
a lower (more positive) resting diastolic membrane potential. Threshold
potential is therefore more easily attained, thereby increasing the probability
of a sustained arrhythmia
>
.
2. +odal reentry impulses
There is repetitive pathway that consists of two limbs, one ta8es the impulse
away from, and one that carries it bac8 to the site of origin
2
. +odal reentry
tachycardia is the most common cause of SVT
A,!#
. Bnli8e an accessory
pathway, these e3tra connections are not visible histologically. +onetheless,
they provide the necessary substrate for reentry arrhythmias in a manner
similar to that seen with accessory connections
>
.
-n patient with 'V+,T, there are two different conduction pathways within the
'V node, as shown in figure !. /ne pathway is referred to as the fast pathway, and is
characteri@ed by rapid conduction velocity and relatively long refractory period. The
4
other pathway is slow pathway, characteri@ed by slow conduction velocity and slow
refractory period.
A,!#,!!

(igure !. ;athways on 'V node
!#
.
Curing sinus rhythm, conduction through the 'V node to the ventricles occurs
over the fast pathway. 'trioventricular nodal reentry is typically initiated by an atrial
premature depolari@ation that bloc8s anterogradely in the fast pathway (because of its
longer refractory period) while conducting slowly in the anterograde direction over
the slow pathway. -f anterograde conduction over the slow pathway is slow enough,
the refractory period in the fast pathway has enough time to end. This enables the
impulse to propagate retrogradely over the fast pathway bac8 to the atrium, thereby
completing the reentrant circuit
>
, as shown in the figure %.
(igure %. ,eentrant circuit in 'V+,T
!!
2.2. SIGN AND SYMPTOM
Signs and symptoms of SVT vary among people, especially according to age.
5hildren and young adults who have SVT usually don:t have signs and symptoms of
heart failure, because they or others such as parents or careta8ers 8now when the
heart is beating too fast (sometimes called palpitations or racing heart). 'lthough
5
older children and adolescents usually do not develop congestive heart failure, they
may complain of lightheadedness, di@@iness or fainting. These symptoms are more
li8ely during times of higherthanusual heart rates of SVT during strenuous e3ercise
when the person does not stop to rest when the SVT starts andor when dehydration
may e3ist.
<
5hildren and young adults can e3perience SVT at various times of the day or
during various activities. Some only have SVT during e3ercise, and some only will
have SVT during rest. .any times it is difficult to predict when or how often a person
will have SVT. The tendency for SVT can vary with stages of age, growth, and
development. (or e3ample, about half of babies with SVT will outgrow the problem
after one or two years of age. &owever, in those who appear to outgrow SVT, it can
return sometime in the future in about onethird of these children. 'nother e3ample?
for children who are first noted to have SVT at about 7 to = years of age, the SVT
probably will continue to recur in about ># percent.
=
2.3. DIAGNOSIS
The diagnosis of SVT is made primarily by using the !%9lead
electrocardiogram (456).
"
-f the patient is e3periencing SVT during the 456, a clear
diagnosis can be made.
!%
The usual presentation of SVT on electrocardiography (456) is as a narrow9
D,S9comple3 tachycardia (a D,S interval of less than !%# msec), but in some cases
(less than !# percent), wide9comple3 tachycardia is the manifestation of SVT. 'fter
the restoration of sinus rhythm, the !%9lead 456 should be e3amined for the presence
of delta waves, which indicate an accessory pathway.
7
The first step in diagnosing SVT is to categori@e the rhythm as narrow
comple3 (D,S E !%# milliseconds) or wide comple3 (D,SF !%# milliseconds) and
as regular (fi3ed ,9, cycle lengths) or irregular (variable ,9, cycle lengths). Some
tachycardias are represented in more than one category. The ne3t step is to loo8 for
evidence of atrial activity. -f a discrete ; wave is visible, the relationship of the ;
wave to the D,S comple3 should be evaluated. This relationship is characteri@ed as
6
either a GGshort9,; tachycardia:: or a GGlong9,; tachycardia.:: -n short9,; tachycardia,
the time from the ; wave to the preceding , wave is less than the time from the ;
wave to the following , wave (,; E ;,). -n long9,; tachycardia, the opposite is true
(,; H ;,).
"
-n addition to cycle regularity and D,S width, the following 456 criteria
may help differentiate the various types of SVT? heart rate during tachycardiaI
mechanism of initiationterminationI ; waveD,SST morphologyI changes in cycle
length with the appearance of bundle9branch bloc8I and 456 changes in response to
maneuvers such as carotid sinus massage or adenosine administration.
"
Atrial Tachycardia AT!
'T is initiated and sustained within the atria and is manifested by a single ;
wave morphology. The ; wave morphology depends of the site of origin of the
tachycardia. 'T may be caused by automaticity, triggered activity, or microreentry. 'T
is usually a long9,; tachycardia with an atrial rate usually less than %7# bpm and a
ventricular rate dependent on the presence or absence of 'V nodal bloc8. 'T caused
by abnormal automaticity often e3hibits a GGwarm9up:: phenomenon in which the
heart rate gradually speeds up before reaching a fi3ed pea8.
The diagnosis of 'T caused by triggered activity is often made in the
electrophysiology laboratory when the 'T can be initiated by pacing the atrium at a
critical rate. 'T caused by microreentry is often seen in patients who have structural
heart disease, usually is initiated by a premature atrial beat, and typically is
paro3ysmal.
(or 'T caused by abnormal automaticity, adenosine usually results in 'V
nodal bloc8 without terminating the 'T. /n the 456, this 'T is manifested as
discernible ; waves continuing at the 'T rate with occasionally conducted D,S
comple3es. -n contrast, triggered 'Ts usually are terminated with adenosine.
'lthough these general aspects of the different types of 'T can be useful in diagnosis,
significant overlap of these properties e3ists.
2
To help locali@e the origin of the 'T, one can begin by analy@ing the ; wave
polarity. To distinguish a right atrial from a left atrial location, aV) and V! are the
7
essential leads. ; waves that are positive in V! usually arise from the left atrium,
whereas ; waves that are positive in aV) usually arise from the right atrium or
occasionally from the right pulmonary vein. ;ositive ; wave polarity in leads --, ---,
and aV( predicts a superior originI negative ; wave polarity in these leads predicts an
inferior origin. The polarity of the ; wave may be difficult to interpret if the ; wave is
inscribed upon the ST segment or T wave. Thus, the ; wave morphology is
interpreted best when the heart rate or ventricular rate is slowed, such as after
adenosine administration.
7
(igure 2. (ocal atrial tachycardia with !?! conduction. +ote the narrow, regular
tachycardia. The ; waves are mar8ed with arrows (long9,; interval), and the ; wave
morphology differs from that of sinus rhythm.
7
Atri"#$%tric&lar N"d$ R$$%tra%t Tachycardia A'NRT!
-nitiation of 'V+,T is dependent on the presence of dual 'V node
physiology, with two pathways having differing conduction and refractory times.
'V+,T can be divided into typical and atypical forms, with the typical form being
more common. Typical 'V+,T, also 8nown as slow9fast 'V+,T, uses a slow 'V
nodal pathway for antegrade conduction and a fast pathway for retrograde
conduction.
2
8
There typically is a !?! 'V relationship in 'V+,T, but because the reentrant
circuit resides within the area of the 'V node, %?! 'V bloc8 can be seen. ,etrograde
'V nodal atrial bloc8 can occur also, although less commonly. Typical 'V+,T is
initiated with an atrial premature beat and terminates with a ; wave (antegrade slow
pathway). 'V+,T is terminated by adenosine (HA#J of the time) or vagal
maneuvers, which can be useful in ma8ing a diagnosis.
Typical 'V+,T is a short9,; tachycardia in which the earliest retrograde
atrial activity is detected on the septum, near the 'V node. The ,; interval is usually
less than =# milliseconds. 1ecause retrograde atrial activation occurs over a fast
pathway, the retrograde ; wave is superimposed on the D,S and appears as a pseudo
S wave (present during 'V+,T but not during normal sinus rhythm) that is best seen
in leads --, ---, and aV(. Similarly, a pseudo ,# may also be present in lead V!. These
456 findings are important because they are infre0uently seen in 'V,T. &aving a
pseudo S, a pseudo ,#, or both is A#J to !##J specific for typical 'V+,T and has
an >!J positive predictive value for typical 'V+,T. These criteria are only "%J
sensitive for typical 'V+,T.
!2
-n contrast to 'V,T, D,S alternans is an uncommon finding in 'V+,T and
may be related more to the rapidity of the heart rate than to the underlying SVT
mechanism. Ta8ing into account the pseudo S,# waves, the ,; interval, and the lac8
of significant ST depression in multiple leads (the Kaeggi algorithm), a correct
diagnosis of typical 'V+,T can be made by 456 analysis =<J of the time.
"
9
(igure ". Typical atrioventricular node reentrant tachycardia. +ote the rapid, regular,
narrow comple3es, the pseudo S waves in leads -,-- and aV( and the small pseudo ,
wave in lead V!.
7
2.(. DI))ERENTIAL DIAGNOSIS
(ollowing are the differential diagnosis of SVT.
!"
Atrial )i*rillati"%
'trial fibrillation occurs when the upper chambers of the heart, or atria,
fibrillate. This means that they beat very rapidly and irregularly. 1lood is not pumped
efficiently to the rest of the body which may cause you to feel wea8 or tired, or to
e3perience uncomfortable heart sensations li8e a racing or irregular heartbeat.
!7,!<
Si%&+ tachycardia
Sinus tachycardia, by far the most common SVT, is not a pathologic
arrhythmia (with the rare e3ception of inappropriate sinus tachycardia) but rather is
an appropriate cardiac response to a physiological event. Sinus tachycardia is gradual
in onset and recession. The heart rate is regular and classically does not e3ceed %%#
beats per minute minus the patient:s age. -n sinus tachycardia, ; waves precede the
D,S comple3.

Sinus Tachycardia secondary to dehydrationhypovolemia (most
common), fever, hypo3ia, anemia, shoc8, .-, pulmonary edema, hyperthyroidism,
10
hypocalcemia, or medications. Sinus tachycardia is present when a personLs heart rate
is over !## beats per minute. This is normal if there is a clear reason for the fast heart
rate, such as e3ercise, pain, or fever. Mith sinus tachycardia, the electrical system of
the heart is wor8ing normally.
!%,!=
Sinus tachycardia (heart rate over !## beats per minute) is not normal if there
is no apparent cause. -n this rare condition, the electrical system of the heart is
wor8ing normally. ;eople with inappropriate sinus tachycardia typically donLt have
any heart disease. -nappropriate sinus tachycardia with no heart disease may mean
your autonomic nervous system isnLt wor8ing right.
!7,!<
2.,. MANAGEMENT
The goal of any SVT treatment is its cessation, especially patients at
hemodynamic ris8 and cannot tolerate prolonged tacyarrythmias. Treatment of SVT is
divided into two groupsI short9term management and long9term management.
!>
The
algorithm of SVT can be seen in figure 7 and =, while the dosage in figure <.
Sh"rt-t$r. .a%a/$.$%t
+on9pharmacologic
+on9pharmacologic management typically use vagal maneuvers, including a
Valsalva maneuver, carotid sinus massage, bearing down, and immersion of the face
in ice water.
!2,!>
Vagal maneuvers increase vagal tone and bloc8 the atrioventricular
node by slowing its conduction.
!2,!>,!A
-t is also as first line treatment option for SVT
in younger patients who are hemodynamically stable and as diagnostic for nodal9
dependent SVT. This involves ta8ing a breath in and then Gstraining out:, with the
airway closed at the bac8 of the throat.
!>,%#
.eanwhile, carotid massage can be used
as a diagnostic and therapeutic toolI contraindicated in persons who may have
atherosclerotic pla0ue that could be dislodged as a result of such a techni0ue (i.e.,
history of carotid artery disease or carotid bruit). -f these methods fail to terminate the
SVT, or if the SVT soon relapses, pharmacologic therapy is used.
!>
;harmacologic
11
;harmacologic management typically includes intravenous adenosine or verapamil,
which are safe and effective treatment choices for terminating SVT.
!. 'denosine
'denosine is endogenous nucleotide that bloc8s atrioventricular nodal
conduction with a very short half9life (A9!% seconds). -t is highly effective in
terminates nearly all atrioventricular nodal reentrant tachycardias and
atrioventricular reciprocating tachycardias and is the first9line drug for acute
conversion of narrow comple3 SVT. 'denosine has the advantage of
temporarily slowing the rate enough to determine the underlying focus of the
rhythm (i.e., ventricular or supraventricular). -t should not be used in persons
with Molff9;ar8inson9Mhite syndrome and atrial fibrillation because this
rhythm can degenerate into ventricular fibrillation. Mhen administering
adenosine, ensure that resuscitation e0uipment is available in case the rare
complications of bronchospasm or ventricular fibrillation occur.
!2,!>,!A
%. Verapamil
Verapamil is a calcium channel bloc8er that may be used in SVT patients that
reoccur after adenosine therapy. 's a negative inotrope that bloc8 the
atrioventricular node and result in relative bradycardia and vasodilation, it is
used if patients have a significant decrease in cardiac output. -t may cause
hypotension and thus are not a first choice in the emergency setting.
!2, !>
4lectrical cardioversion is reserved for patients in unstable condition (such as
hypotension, unresponsivesness, chest pain, mental status changed, and new
onsetworsened heart failure) who are not having a response to adenosine and should
be readily availaible if the hemodynamic or symptomatic state worsens.
!2,%!

L"%/-t$r. .a%a/$.$%t
;harmacologic
;atients with infre0uent SVT episodes (not more than a few times per year,
but with episodes lasting one hour or longer) may only need pharmacotherapy on an
intermittent basis or what has been described as the pill9in9the9poc8et approach.
12
This approach re0uires an immediate9release medication with verapamil ("# $ !<#
mg), beta bloc8ers, flecainide (!## $ 2## mg) or propafenone (!7# $ "7# mg). -nitial
dose should be made under observation to assess tolerance. Typically done in patients
without pree3citation or a beta bloc8er in patients without chronic obstructive
pulmonary disease or asthma. -f the result is unsatisfactory, patients need
atrioventricular nodal bloc8ing agents (e.g., verapamil, diltia@em, beta bloc8ers,
digo3in), although in 'V+,T and 'V,T with retrograde conduction are only about
2# to <# percent effective. This relative lac8 of effectiveness can necessitate use of
two such agents or the addition of class -c or --- antiarrhythmics.
<,!>,%#,%!
5atheter ablation
'blative therapy of SVT is based on the observation that most arrhythmias
arise from a focal origin critically dependent on conduction through a defined ana9
tomic structure. -f the abnormal electrical connections that allow SVT to occur is
eliminated, the arrhythmia will no longer occurs spontaneously or with provocation.
1ecause of shorter procedure duration, lessened fluoroscopic e3posure, and increased
8nowledge in this area of cardiology, catheter ablation is becoming the first9line
treatment option for all patients with SVT, not *ust those with symptomatic
arrhythmias refractory to suppressive drug therapy or those who prefer a drug9free
lifestyle. 5atheter ablation provides a definitive management option for SVT and is
usually done under local anaesthesia as a day case. 5atheters capable of recording
electrical activation in the heart are inserted via the femoral vessels and manipulated
under 39ray guidance. ,adiofre0uency energy delivered via a catheter is used to
create small localised areas of scar.
<,!>,!A,%#

2.0. COMPLICATION
SVT has some complication which are e3plained below?
!. &ypo3ia
%. .yocardial -nfarction
Mhen SVT occurs in someone with significant coronary artery disease, the heart
may not receive enough blood to 8eep up with the demands of the increased heart
13
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>
rate. -f this occurs, the heart may not get enough o3ygen (ischemia), potentially
causing a heart attac8 (myocardial infarction).
%2,%"
2. &eart failure
SVT may result in heart failure, especially in people with diseases of the heart
valves (particularly aortic stenosis or mitral stenosis) or with a wea8ened heart
muscle (cardiomyopathy). 'nd if SVT persists for a long period of time, it may
cause a normal heart to wea8en and heart failure to develop (8nown as a
tachycardia9mediated cardiomyopathy), although it is often reversible if the SVT is
corrected.
%2,%"
2.1. PROGNOSIS
.ost episodes of SVT stop on their own. The duration ranges widely from
seconds to minutes and occasionally hours. -n some patients, an intervention is
re0uired to stop the SVT. .ost patients with SVT do not have any other significant
problems of the heart. ;atients who are born with specific heart conditions, called
congenital heart disease, prior heart surgery, or with heart valve problems are more
li8ely to have these arrhythmias.
%"
Bnless structural heart disease is present, the prognosis of patients with SVT
is e3cellent. 's mentioned above, SVT does not shorten life $ it does not lead to
death, stro8e or myocardial infarction. Should an episode of SVT arise while the
patient is sleeping, they will be awa8ened by the symptoms. &owever, SVT will recur
at some point in nearly all patients who do not die of another cause. (or patients who
have *ust e3perienced their first episode of SVT, it is impossible to say when the ne3t
episode will occur. (or this reason, many of such patients ta8e a wait and see
approach to their SVT. 's years and decades pass, nearly every patient e3periences
more fre0uent andor more long9lasting episodes. -t is also common for the patients to
feel worse physically with their SVT as they get older.
%7
CHAPTER III
14
CONCLUSION
Supraventricular tachycardia (SVT) is a type of heart rhythm disorder that can
be found in healthy children and adolescents. -t refers to any heart rhythm where the
heart beats faster than normal (N!"#9%"# beatsmin) for age and environmental
factors. -t named Gsupraventricular: because it originates and or involves structures
above the ventricles of the heart. There are three main mechanisms that cause SVT
such as triggered arrhythmia, automaticity and nodal reentry of impulses. Signs and
symptoms of SVT include poor feeding, breathing fast, sweating, irritability,
palpitation, di@@iness, paleness and shortness of breath or fainting. To diagnose SVT,
we should primarily perform electrocardiogram test. Me must differentiate SVT from
other heart disease especially atrial fibrillation and sinus tachycardia. Treatment of
SVT is divided into two groupsI short9term management and long9term management.
SVT itself can cause other complication such as hypo3ia, myocardial infarction and
heart failure. Bnless structural heart disease is present, the prognosis of patients with
SVT is e3cellent. 's mentioned before, SVT does not shorten life $ it does not lead to
death, stro8e or myocardial infarction.
15
ATTACHMENT
(igure 7. 'lgorithm of the short term management of SVT.
(456O4lectrocardiographyI -VOintravenousI VTOVentricular Tachycardia)
7
16
(igure <. Crugs used in treatment of SVT
%%
17
(igure =. 'lgorithm of long term management of SVT
7
18
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