Supraventricular

Tachycardia
Presenter: Ahmad Randy
Supervisor: dr. Pendrik Tandean, Sp.PD

PATIENT IDENTITY
Name : Mr. AL
No.MR : 209.769
Age
: 33 y.o
Gender
: Male
Address
: BTN Pepabri, blok E No.
1 Makassar
Date of admittance : 25th March 2009

HISTORY
Chief complaint : out of breath
It has been felt since four day continuously.
Oppressed increases if the patient has been
cough. There is cough since approximately 1
year ago. Mucus there are white colour, blood is
not exist, bleeding cough history is exist. Chest
pain is exist, once in a while if coughs it firm.
Chest pain is not disseminates to other arm or
other area. His heart felt palpitates. Nausea and
vomit is not exist, heart burn is not exist. Fever
is not exist. Body weight declines in a few this
last month. Urinate & defecate were normal.

PAST MEDICAL HISTORY

Hypertension (-)
Diabetes mellitus (-)
Cardiovascular disease (SVT on

January 2009)
Pulmonary disease (TB on treatment)

PHYSICAL EXAMINATION
Status present : Moderate-illness/Underweight/Composmentis
Vital Sign :

Blood pressure
: 120/80mmHg
Pulse
: 160x/min
Inspiratory rate
: 32x/min
Body temperature : 36.5oC

Head Examination :

Eyes : there was anemis, no icterus

Lip : no cyanosis
Neck : JVP R-2 cmH2O, there were no mass & tenderness

Thoracal Examination :

Inspection
: Symmetric
Palpation : No mass; no tenderness
Percussion
: Sonor
Auscultation
: Breath Sound : bronchovesicular
Additional sound : ronchi +/+ apeks; wheezing -/-

PHYSICAL EXAMINATION
Cardiac Examination :

Inspection
Palpation
Percussion
Auscultation

: ictus cordis was invisible

: ictus cordis was impalpable
: deaf
: sound of I/II heart sound; no murmur

Abdominal Examination :

Inspection
Palpation
Percussion
Auscultation

: normal
: no mass; no tenderness
: tympani
: peristaltic sound (+); normal

Extremities : swelling (-)

ADDITIONAL EXAMINATION
Laboratory test

Random glucose : 95 mg/dl

Complete blood
WBC
RBC
HGB
HCT
PLT

: 8,8 x 103 /mm3 ()

: 4,24x 106 /mm3
: 10,9 g/dl
: 35.8 %
: 352x 103 /ul

: 114 mmol/l ( )
: 4,4 mmol/l
: 106 mmol/l ( )

Cardiac enzymes
CK
CKMB

SGOT

: 18 U/l

SGPT

: 15 U/l

Cholesterol total : 133 mg/dl

Cholesterol HDL: 62 mg/dl
Cholesterol LDL : 81 mg/dl

Blood electrolytes
Natrium
Kalium
Chloride

Blood chemistry

: 73
: 22

Triglyseride

: 91 mg/dl

Ureum

: 12 mg/dl

Creatinin

: 0,26 mg/dl

ELECTROCARDIOGRAPHY
Interpretation
:
- Sinus
takikardi
- Normoaxis
- None Pwave (II, III,
aVF)

Echocardiografi
Interpretation:
- Within normal

CHEST X-RAY
Interpretation:
- KP duplex lama
aktif
- efusi pleura
dextra

DIAGNOSE
- Supraventricular tachycardia
- TB pulmo

- Dietary high callory high protein

- IVFD RL:D 5% 1:1 20 dpm
- Bed rest
- O2 4-6 L/i
- Alprazolam 0,5mg 0-0-1
- Cordaron 450mg/24j/sp
- Aspilet 80mg 0-1-0

Discussio
n

Discussion
Supraventricular tachycardia (svt) is any
tachyaritmia that requires only atrial and/or
atrioventricular (av) nodal tissue for its
initiation and maintenance.
The most common mechanism identified is
reentry

Reentry can be happen in:

- SA node (sinus nodal reentrant tachycardia).
Very rare
- Atrium (atrial tachycardia)
- AV node (AVNRT and AVRT)

Sinus nodal reentrant tachycardia (SNRT)

SNRT is due to reentry circuit, either in or
near the sinus node. Therefore, it has an abrupt
onset and offset. The heart rate is usually 100150x/I and ECG tracings usually demonstrate
normal sinus P-wave morphology.

SNRT

The QRS complexes are narrow and regular. The patient's heart rate is
approximately 135 beats per minute. P waves are normal in morphology

Atrial Tachycardia
Atrial tachycardia is an arrhythmia originating
in the atrial myocardium. The heart rate is
regular and is usually 120-250x/i.

Atrial Tachycardia

Atrial tachycardia. The patient's heart rate is 151 beats per minute. P waves are upright in lead
V1

AVNRT (AV nodal reentrant tachycardia)

- The most common cause of PSVT is AVNRT.
AVNRT is diagnosed in 50-60% of patients who
present with regular narrow QRS tachyarrhythmia.
- The heart rate is 150-250 bpm and is typically quite
regular
- AVNRT may occur in healthy, young individuals, and
it occurs most commonly in women. Most patients
do not have structural heart disease. However,
occasionally these individuals may have an
underlying heart condition such as rheumatic heart
disease, pericarditis, myocardial infarction or mitral
valve prolapse

AVNRT

The patient's heart rate is approximately 146 beats per minute with a normal axis. Note the
pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR.
These deflections represent retrograde atrial activation.

- The AV node is functionally divided into 2 longitudinal

pathways that form the reentrant circuit. In the majority of

patients, during AVNRT, antegrade conduction occurs to the
ventricle over the slow (alpha) pathway and retrograde
conduction occurs over the fast (beta) pathway
- The tachycardia is initiated when an appropriately timed atrial

premature complex is blocked in the fast pathway (longer

period) and conducts in the slow pathway (shorter period).
- While the impulse conducts to the ventricle in the slow

pathway (antegrade conduction), the fast pathway recovers so

that the impulse can conduct retrograde up the fast pathway to
the atrium and the atrial end of the slow pathway (retrograde
conduction).

AV reentrant tachycardia (AVRT)

- AVRT is the second most common form of SVT. The

incidence rate of AVRT in the general population is

0.1-0.3%. AVRT is more common in males than in
females
- in AVRT, 1 or more accessory pathways connect the
atria and the ventricles. The accessory pathways may
conduct impulses in an anterograde manner, a
retrograde manner, or both

Sex:
Most series of catheter ablation reflect a higher
proportion of female patients with AVNRT than
male patients. In a population-based study, the
risk of developing SVT was twice as high in
women compared to men.
Age:
The prevalence of SVT increases with age.

Clinical finding:
Common presenting symptoms of SVT and their frequency
rates are as follows:
Palpitation (> 96%)
Dizziness (75%)
Shortness of breath (47%)
Syncope (20%)
Chest pain (35%)
Fatigue (23%)
Diaphoresis (17%)
Nausea (13%)

Physical finding:
Generally limited to cardiovascular and respiratory

systems. Patients often appear quite distressed.

Tachycardia may be the only finding in patients who
are otherwise healthy.
Patients who have limited hemodynamic reserve may
be tachypneic and hypotensive. Crackles may be
auscultated secondary to heart failure. An S3 may be
present, and large jugular venous pulsations may also
be visualized.

Management:
- Vagal maneuver (cough, vomit)
- Valsalva maneuver
- Compressing sinus carotis

Short-term medical management

Short-term management involves intravenous

adenosine or calcium channel blockers. Adenosine is a

short-acting drug that blocks AV node conduction; it
terminates 90% of tachycardias due to AVNRT or
AVRT.
Other alternatives include calcium channel blockers
like verapamil, diltiazem or beta-blockers like
metoprolol or esmolol. Verapamil is a calcium channel
blocker that also has AV blocking properties.

Long-term medical management

- Patients with SVT may initially be treated with

calcium channel blockers, digoxin, and/or betablockers. Class IA, IC, or III antiarrhythmic agents
are used less frequently because of the success of
radiofrequency catheter ablation
- Radiofrequency ablation is cost-effective for patients
who have frequent episodes of SVT

Terima
Kasih