PEMERIKSAAN JANTUNG

1. Anamnese : Baik + mengarah

2. Pemeriksaan Fisis
3. E K G
4. Foto toraks
5. Laboratorium
6. Tread Mill
7. Holter Monitor
8. Echo
9. Thallium Scanning
10. Kateterisasi

EKG
1.
2.
3.
4.
5.

6.
7.
8.
9.
10.

Ritme
Rate
P. Wawe
PR Interval
QRS Interval
QRS Complex
ST Sigment
T Wave
U Wave
QT Duration

ELEKTROKARDIOGRAM
12. LEAD EKG YANG KONVERSIONAL
TERDIRI DARI :
I .
BIPLAR LEADS :
1. L1
RA ------ LA
2. LII
RA ------ LL
3. LIII
LA ------ LL
II. AUGMENTED UNIPOLAR LEADS
1. LEAD AVR (RA LEAD)
2. L AVL (LA-LEAD)
3. L AVF (LL-LEAD)

III. UNIPOLAR CHEST LEADS V

V1 V6 : antara ICS IV V
V1 : ICS IV Para Sternal Kanan
V2 : ICS IV Para Sternal Kanan
V3 : Antara V2
- V4
V4 : ICS V MCL Kiri
V5 : ICS V Linia Axilaris Anterior
V6 : ICS V Linia Axilaris Media
V3 R, V4 R, V5 R, V6 R, Simetrisnya
V3, V4, V5, V6
Untuk mengetahui RVH
V7 V8 V9 direkam apabila QS
sampai V6

Sistem Konduksi
S.A node : sumber aktivitas listrik
pacemaker generator
pacu jantung
P-Cell
: Primary pacemaker cell
mengeluarkan impuls listrik.
4 x 10 mm (dewasa)
R.A dekat muara V.C.S
Lintasan internodal : anterior
tegak
gel P
pasterior EKG
A.V node : menerima impuls dari lintasan
internodal

Bundle of His 11/2 2 cm

R.B.B

I.B.B
Fasiculus anterior
pasterior
Serat-serat purkinye
(sangat halus, subendokardial)
Terminal Network

SISTEM KONDUKSI
JANTUNG

S.A. Node ( Sino Atrial Node)

Sumber aktivitas listrik
Pada R.A :
Bagian superior.
Pada pertemuan S.V.C & R.A
Ukuran : 10 x 4mm/dewasa
3 macam cell :
Pacemaker cell. (P.cell)
yang
mengeluarkan impuls listrik.
Sarcomere
Transitiona cell

Internodal tract/ interatrial.

Membawa impuls dari S.A
A.V.
S.A
R.A & L.A
Ukuran : 6 x 3 mm
Letak : Pada dasar R.A. kearah kiri. Antara
katup tricuspid med dengan muara S.C.
Bundle of HIS : Keluar dari A.V
Ke kiri & bawah
menembus I.V.S
pada
batas para membrano S.A dan para
muacularis
Cabang
R.B.B
L.B.B
Electroda :
Suatu metal berbentuk lempengan atau bulat
dapat menghantarkan aliran listrik dari tubuh

Arrhythmia Originatinating In The Sine

Atrial (S.A) Node
Sinus Tachycardia
Sinus Bradycardia, Sinus Arrhythmia.
Wandering Pacemaker. Sinus Atrial
Arrest (S.A Blook)

Disturbance of Impulse formation in the

S.A node
Pacemaker : S.A.node.
Normal : 60 100 times/minute
> 100/1 : Sinus tachycardia
< 60/1 : Sinus bradycardia
Does not discharge rhythmically sinus
arrhythmia

 Wander

from the S.A node :

Wandering pacemaker.
S.A. node fails to discharge an
impulse : Sinus Arreat.
S.A. node : Impulas formation under
control of sympathetic & para
symphatic ns.
Sympathetic dominant
H.R
Parasympatetic (vagal influence)

Sinus Tachycardia

Etiology :
S.A node discharge > 100/1
Sympaathetic system >
Fever
Anxiety
Physical activity.
Sinus tachycardia manifestation of
Heart faiure

Symptoms : palpitation
dyspnoe
E.C.G : sinus tachycardia >< fast rate
arrhythmia
Sinus tachycardia normal
gradually
Other tachycardia (-P.A.T)
Sinus rhytm : case abruptly

Sinus Bradycardia
S.A node discharge at rate < 60/1
First few hours after A.M.I; myocardial
ischemia, pain, drugs, other factors
Parasympathetic (vagal) dominance
Symptoms :
1. Seldom produce symptoms
Uniess the rate is slow enaugh CO
2. H.R : 40 60/1
Risk :
1. Sinus bradicardia
faster ectopic focus
to take over as pacemaker : serious
ventricular arrhythmia may develop

SINUS ARRHYTMIA
ETIOLOGI :
The Impulse : Arise from the S.A node but not in
regular rhytm
Dueto variation of vagal influences on S.A node
Related to the phase of respiration ( with
inspiration with exration)
SYMPTOMS :
1. The pulse is in regular but patient is unware
2. The diagnosis car only be verified an E.C.G.
TREATMENT :
No treatment is indicated

SINO ATRIAL ARREST ( and S.A.

Block)
ETIOLOGI :
Sino atrial arrest (disturbance of
impulse formation S.A node fails to
initiate an impulse at the expected
time.
In the absence of this impulse : neither
the atria nor ventricies are a imulated
PQRST complex drops out

S.A block : (disturbance of impuls

conduction)
Impulse is initiated normally biockes
within the node fails to reach atria
PQRS complex is absent.
Excessive vagal dominance, digitalis,
toxicity
Ischemic injury of the S.A node They
can not be clinically, distinguished
from one anather.

Clinical feature :
1. Patients : notice prolonged pause
unware
2. Physical finding :
prolonged pause
pulse/ listening to the
heart.
3. Oscar frequently : cerebral insuff/
syncope/vertigo.

Risk.
In A.M.I :
1. Infrequent S.A arrest
not of great
importance
2. Repeated /very prolonged pauses
suggest ischemic damage to S.A
node : potentially dangeraus.
3. Digitalis or quinidine overdosage
atrial stand still

Treatment :
1. Should be treated under the
following circumatances
a. CO (syncope, hypotension,
angina, H failure)
b. P.V.C (Premature Ventricular
Contraction) during the period of
bradycardia
c. Q.R.S rate < 50/1 : in elderly
person A.M.I

Atropine :
a. Blocks the vegal effec : on S.A
node
H.R
b. Should be the initil therapy.
3. Isoproterenol (isuprel) if atropine in
unsuccesfull : 1 mg in 500 ml
glucose solution (slow I.V infusion)
4. T.P.M may required if drug the rapy
fails
2.

Arrhythmia Originating In The Atria.

Premature Atrial Contraction
Paroxymal Atrial Tacycardia
Atrial Fiutter
Atrial Fibrillition
Atrial Standstill
The Atria
A.V node area
Potential
Ventricies
Capacity as
Pacemaker
S.A node : controis, discharges impulse factor

Same Reason :
A focus in the atrial walls initiates inpulses
Than S.A node
ectopic
Impulses replace the S.A node as pacemaker
for only beat :
Premature atrial contraction
Continiously : Atrial tachycardia
Atrial Flutter
Atrial Fibrillation
Irritabillity of the atrial muscie caused by
ischemia, over distention (stretching) of the
atrial wall,sss.

Atrial Tachycardia
Atrial rates : < 200/minutes
P. Wave visible but distorted in shape.
Each impulse
A.V node
ventricle

Normal QRB complex follow each

P.Wave.
Atrial Flutter
Atrial rates : 200 400/minutes
A.V node is unable to accept each
impulse atrial beat

Atrial Fibrillation
Atrial rates : 400 1000/minutes
Atrial muscle are not longer capable of
responding the repetitive impulse
individual fibera merely fibrillate atria
do not contract the P.Wave are not
seen
Chactic atrial activity
A.V node at
arapid, irragular rate
A.V node
blocks most of the impulses.
Ventricle at irregular intervala
Ventricular rhytm is irregular

Premature Atrial Contraction

Etiology.
Irritabillity of the atrial muscle
focus in the atrium
supersedes the S.A pacemaker.
Clinical Feature
1. Unaware of P.A.C.
Stethoscope : a beat the occus sooner than
expected beat.
2. Identifications : only by E.C.G.
3. In A.M.I : no particular significance do indicate
atrial irritability forewarn : serious atrial
arrhythmia : A.T. of A.F.
Treatment
1. P.A.C. : accur rarely
usually unnecessary
2.
In number of P.A.C
anti arrhythmiac drug

Paroxysma : Atrial Tachycardia

Etiology :
Focus within the atrium, outside
the S.A node originates impulses
: 150 250/minute displaces the
S.A node as pacemaker.
The ventricle is able to respond
to each atrial impulse
THE
ATRIA and VENTRICULAR RATE
are IDENTICAL

Clinical Feature :
1. Characteristic : P.A.T occure SUDDENLY
without warning/may precedec by P.A.C.
2. Most patient : aware of repid heart action
fluttering sensation in the chest,
headedness
3. Translent an and abruptly.
Hemodynamic concequence :
1. Increased H.R
short ventricular filling
time
S.V sustained
2. Increased H.R (ventricular rate)
o2
demand by myocardium
myocardialischemia or angina

Atrial Flutter.
Etiology :
The S.A node is replaced extramely irritable
focus within the atrial walls. Rate : 250
400/minute.
The A.V node is unable to conduct all
impulses, but every second
third
Impulse
fourth
reachthe
ventricle

Clinical Feature :
1. Symptoma depends on ventricular rate
QRS rate : 150/minute
palpitation
angina
dyspnoe
QRS rate : 80/minute (normal)
no
symptoma
2. Atrial flutter can be identified only by E.C.G
Hemodynamic Concequences :
1. Decreased S.V & CO.
2. If QRS rate normal : L.V performance is not
affected

Atrial Fibrilation
Etiology :
Ectopic fool troughtout the atrial. Discharge
impulse at a rate 400 100/minute
tiwiching of atrial wall.
(Not true atrial contraction)
Quivering tubes conneting the yreat veins
with the ventricle.
QRS rate : during A.F very : 40 180/minute.
QRS rate : > 100/minute : rapid
Uncontrolled

Clinnical Feature :
1. Aware of irregularrity/palpitation
2. Grossly irregular is characteristic of A.F.
3. Pulsus defisit : peripheral rate < H.R :
variation in the stroke volume.
4. Persistent rapid QRS rate
L.V
failure.
Hemodynamic Qoncequences :
1. Decreased C.O : rapid ventricle
response. Lose of atrial contraction
20% reducetion in C.O.

Treatment :
1. Terminate the arhythmia by reflex fagal
stimulation
2. Angina, L.V failure, blod pressure cardio
version
3. Adenosine : 6mg : rapid IV, push over 1-3s 1
2 min : 12 mg : rapid IV, push over 1-3s.
4. Verapamill 2,5 5 mg IV.
15 30
Verapamill 5 10 mg IV.
Consider : Digoxin, betablocker

Cardioversion

5. Repetitive P.A.T prophytactic.

anti arrhythmia :
(digoxin, amiodaron,
beta blocker).

Premature Junctional Contraction

Etiology :
1. Ectopic focus in the nodal area.
2. Premature : before impulse fom S.A
node transmitted downward
his urkinje system
P.J.C;
up ward atrial stimulation.
3. Irritabillity of the junctional tissue
secondary to ischemia

Clinical Features.
1. Symptoms are infrequent
2. Diagnosis can be estabilished only by
ECG.
3. May give rise to junctional tachycardia.
4. No significant effect on circulatory
efficiency
5. Sign of irritabillity in junctional tissue
maw reflect ischemic.
6. Minor arrhythmia
Tratment : is unnecassary

Passive Junctional Rhythm

Etiology :
1. A. focus in the A.V nodal area replaces the
S.A node as pacemaker.
2. Junctional impulses
downward
ventricle
Upward atria
3. Depression of the S.A node
Excessive vagal activity
Ischemic damage of S.A node
Digitalis toxicity

Hemodynamic Concequence :
Slow rate (40 60/minute)
ectopic fool with more rapid rates
take over the pacemaking function :
junctional tachycardia, ventricular
tachycardia.
2. Decressed CO
cerebral and
myocardial insufficiency.
3. Patential of serious ectopic rhythm

1.

Paroxysmal Junctional Tachycardia

Etiology :
1. An irritable center in the junctional
tissue discharges : impulse more
rapid > S.A node
2. Impulse
downward rapid
ventricular response (Q.R.S rate )
3. Secondary to ischemia of A.V node,
caecholamine secretion digitalis
intoxication

Clinical Feature :
1. The arrhythmia begin abruptly terminate
with suddenness
Paroxysmal action
P.A.T
P.V.T
2. Rapid ventricular rate (Q.R.S ) and
sustalned
Dyspnoe
Angina
3. Can not be distinguished from P.A.T the
diagnosis : only by E.C.G

1.

2.

3.

Hemodynamic Concequences
Rapid ventricular rate ( Q.R.S rate ) :
sustained :
C.O
L.V Failure
Myocardial
Cerebral ischemia
Junctional tachycardia ventricular
fibrillation (ventricular focus replace
junctional pacemaker)
Very dangerous arrhythmia warning of
impending iethal arrhythmia.

Treatment :
1. Junctional tachycardia
circulatory
insuff (L.V failure, angina, cerebral,
ischemia) precordial shock therapy
2. No overt symptom
drug therapy
Lidocaline : 1 mg/ kg IV (bolus)
2 3 mg/menit
Digitalis intoxication
stop
Dilantin inderal

Arrhytmias Originating In The Ventricies.

Premature Ventricular Contraction
Ventricular Tachycardia
Impuls Begins :
In the ventricles/below the level of A.V
Nodal area
Atria
supraventricular
A.V nodal area
arrhytmiation

P.V.C
Cischarge of an ectopic focus walls or
conduction pathway.
Premature
Myocardial irritabillity sec to ischemia :
frequency and degree of irritation
V.F degree consequence of myocardial
irritabillity: begins with P.V.C
Only in the cresence of ischemia : P.V.C are
likely to provoke V.F
Should not be resmed : all P.V.C are
potentially dangerous : V.T is an immediate
fore runner of V.F S.V
CO

Ventricular Fibrillation.
Death Producing
Arrhythmia.
1. V.F : most common cause of sudden
death in patient with C.H.D
2. V.F : is triggered by P.V.Cs or V.T can
arise spontaneously.
3. Once V.F develops : only hope for
survival is the application of
resuscitative techniques.
Etiology & Clinical Feature :
V.F :
Electrical focus within the ventricles

Stimulates the muscles at rate extremely rapid

recovery period disappears
muscle libers
twitch continuously but do not contract
Ineffective in propelling blood from the circulation
stop abruptly
death follows within minutes
V.F inconscious and conversions/inaduquate
cerebral oxygenation.
A.M.I myocardium is sensitized
minimal
electrical stimulus can initiate V.F.
Usual electrical stimulus P.V.Cs strikes during
vulnerable phase of the cardiac cycle (at the time
of the T - wave).
Primary V.F : in A.M.I who have no complication

Premature Ventricular Contraction (P.V.C)

Etiology : irritable focus within the ventricular
discharge before the anticipated
impulse.
Stimulate V directly
P.V.C
Clinical Features :
1. Palpitation
2. Compensatory pause
3. P.V.Cs indicate : myocardial irritabillity
initiate
4. V.T or V.F
5. P.V.C
V.T V.F occurs when P.V.Cs in
any of the five forms:

Occur frequently (5 8/minue)

b. Digeminy
c. R on T pattem
d. Multifocal P.V.Cs
e. Assur sequentially : 2 3 beats (short runs
of P.V.Cs)
4. Digitalis ovrdosage
P.V.C in digeminy
5. Hypokalemia (among patients treated with
diuretic)
Treatment :
In A.M.I : * Suppression of the irritable focus
* Lidocains 50 100mg/rapid IV
* Followed by (1 3) mg/minute
a.

Treatment :
1. 50% of all episode of V.T
and abruptly
(without treatment)
high risk of further episodes of V.T
High risk of sudden onset of V.F
2. Amiodaron (cordaron)
kemasan 1 ampuls berisi amiodaron 150 mg
Dosis : bolus 150mg diencerkan dalam 100
cc glucose 5% diberikan per infuse dalam
waktu 10 menit. Kemudian dilanjutkan 360
mg dalam 6 jam(1 mg/menit) : kemudian
dilanjutkan dengan 540 mg dalam 18 jam
(0,5 mg/menit). Dalam waktu 24 jam tidak
melebihi 1000 mg.

Lidocaine : 1 mg/ kg BW rapid injection iv

(1 3) mg/ minute
4. Failure to convert V.T
sinus with lidocaine
immedlate precordial shock.
5. V.T recurs despite lidocaine infusion
hypotalemia should be suspected
40 50 meg KCL in 1000 cc solution
(glucose 5%) empirically
6. V.T persist for > 5 minutes
lactic acidosis
can develop
sodium bicarbonate
3.