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Physiological Approach of
Arrythmia
M. Saifur Rohman, dr SpJP, PhD. FICA
OUTLINE
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Membrane potential,
action potential,
impulse conduction,
type of arrhytmias,
cause of arrhytmias,
Electrical Activity of Heart
• Heart beats rhythmically as result of action
potentials it generates by itself (autorhythmicity)
• Two specialized types of cardiac muscle cells
– Contractile cells
• 99% of cardiac muscle cells
• Do mechanical work of pumping
• Normally do not initiate own action potentials
– Autorhythmic cells
• Do not contract
• Specialized for initiating and conducting action potentials
responsible for contraction of working cells
Jantung Rusak ?
Untuk Mengetahui Kelainan Jantung ?
Elektrokardiogram (EKG)
• Rekaman grafik potensial listrik yang
dihasilkan oleh jaringan jantung
Goldman & Goldschlager
Cara Perekaman EKG :
- Permukaan
- Epikardial
- Endokardial / intrakardial
Myocardium VS . AUTORYTMIC
Electro-Physiology of the Heart
• Electrophysiologic properties (regulates heart rate &
rhythm)
- Automaticity – ability of all cardiac cells to initiate
an impulse spontaneously & repetitively
- Excitability – ability of cardiac cells to respond to
stimulus by initiating an impulse (depolarization)
- Conductivity – cardiac cells transmit the electrical
impulses they receive
- Contractility – cardiac cells contract in response to
an impulse
- Refractoriness – cardiac cells are unable to
respond to a stimulus until they’ve recovered
(repolarized)
Electricity
Intrinsic Cardiac Conduction System
Approximately 1% of cardiac muscle cells are autorhythmic rather than contractile
70-80/min
40-60/min
20-40/min
Sinoatrial (SA) Node
•Normal cardiac impulse
originates here
•“Natural pacemaker”
•Inherent rate: 60-100 bpm
•Atrial depolarization occurs
cell to cell
•Four conduction pathways
transmit impulse to AV node:
Bachman’s Bundle and 3
internodal pathways (anterior,
middle & posterior tracts).
– Spreads impulse
throughout the atrium
Atriovenous (AV) Node
•Located inferiorly in RA
•All impulses initiated in atria
will be conducted to ventricles
via AV node alone.
•Impulse slows here to allow
diastolic filling time
•Inherent rate: 40-60 bpm
•Conduction delay at AV node
so that ventricular filling from
atrial contraction
Bundle of HIS
– Electrical impulses
conducted to ventricles
via Bundle of HIS &
purkinjie fibers
– Divides into bundle
branches
• Right
• Left
–Anterior Fascicle
–Posterior Fascicle
Purkinje Fibers
– Impulse stimulates
ventricular myocardial
cells
– Inherent rate: 20-40
bpm
Intrinsic Conduction System
• Autorhythmic cells:
– Initiate action potentials
– Have “drifting” resting potentials called pacemaker potentials
– Pacemaker potential - membrane slowly depolarizes “drifts” to
threshold, initiates action potential, membrane repolarizes to -60 mV.
– Use calcium influx (rather than sodium) for rising phase of the action
potential
Pacemaker Potential
• Decreased efflux of K+, membrane permeability decreases between
APs, they slowly close at negative potentials
• Constant influx of Na+, no voltage-gated Na + channels
• Gradual depolarization because K+ builds up and Na+ flows inward
• As depolarization proceeds Ca++ channels (Ca2+ T) open influx of Ca++
further depolarizes to threshold (-40mV)
• At threshold sharp depolarization due to activation of Ca2+ L channels
allow large influx of Ca++
• Falling phase at about +20 mV the Ca-L channels close, voltage-gated K
channels open, repolarization due to normal K+ efflux
• At -60mV K+ channels close
AP of Contractile Cardiac cells
PX = Permeability to ion X
PNa
1
+20
2
PK and PCa
0
Membrane potential (mV)
– Rapid depolarization
– Rapid, partial early
repolarization,
prolonged period of
slow repolarization
which is plateau
phase
– Rapid final
repolarization phase
-20
-40
3
0
PNa
-60
-80
PK and PCa
4
4
-100
0
Phase
100
200
Time (msec)
300
Membrane channels
0
Na+ channels open
1
Na+ channels close
2
Ca2+ channels open; fast K+ channels close
3
Ca2+ channels close; slow K+ channels open
4
Resting potential
AP of Contractile Cardiac cells
• Action potentials of cardiac
contractile cells exhibit
prolonged positive phase
(plateau) accompanied by
prolonged period of
contraction
– Ensures adequate ejection
time
– Plateau primarily due to
activation of slow L-type Ca2+
channels
Membrane Potentials in SA Node and Ventricle
Why A Longer AP In Cardiac Contractile Fibers?
• We don’t want Summation and tetanus in our myocardium.
• Because long refractory period occurs in conjunction with prolonged
plateau phase, summation and tetanus of cardiac muscle is impossible
• Ensures alternate periods of contraction and relaxation which are
essential for pumping blood
Refractory period
Action Potentials
Ion movement and channels
• The movement of specific ions across the cell
membrane serve as action potentials depends on :
• 1. Energetic favorability; concentration gradient
and transmembrane potential
• 2. Permeability of the membrane for the ion:
channels which is selective and gated
• Selective: manifestation of size and structure of its
pore
• Gated: pass through it specific channels only at
certain times; voltage sensitive gating (fast sodium
channel)
Action potential in autorhythmic
cells
Action Potential in contractile cells
Action Potential in contractile cells and ECG
Depolarization of atrium and ventricle
Electrical to mechanical response
• Excitation-contraction coupling
• During phase 2 of the action potential Ca enter
through L Type Ca Channel in the sarcolemma and T
tubule
• Ca triggers release much greater Ca from SR via
Ryanodine receptor into cytosol result in an increased
Ca in the cytosol
• Ca bind to Trop C and the activity of Trop I is inhibited
and induce conformational change of tropomyosin
result in unblock the active site between actin and
myosin
• Myosin head bind to actin causing interdigitating thick
and thin filament in ATP dependent reaction
Electrical Signal Flow - Conduction Pathway
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Cardiac impulse originates at SA node
Action potential spreads throughout
right and left atria
Impulse passes from atria into
ventricles through AV node (only point
of electrical contact between
chambers)
Action potential briefly delayed at AV
node (ensures atrial contraction
precedes ventricular contraction to
allow complete ventricular filling)
Impulse travels rapidly down
interventricular septum by means of
bundle of His
Impulse rapidly disperses throughout
myocardium by means of Purkinje
fibers
Rest of ventricular cells activated by
cell-to-cell spread of impulse through
gap junctions
Electrical Conduction in Heart
• Atria contract as single unit followed after brief delay by a
synchronized ventricular contraction
SA node
AV node
1
2
1 SA node depolarizes.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
AV node
A-V bundle
Bundle branches
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
4
Purkinje
fibers
5
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5 Depolarization wave
spreads upward from
the apex.
Purple shading in steps 2–5 represents depolarization.
Excitation-Contraction Coupling in Cardiac
Contractile Cells
• Ca2+ entry through L-type channels in T tubules
triggers larger release of Ca2+ from sarcoplasmic
reticulum
– Ca2+ induced Ca2+ release leads to cross-bridge cycling
and contraction
Heart Excitation Related to ECG
P wave: atrial
depolarization
START
P
The end
R
PQ or PR segment:
conduction through
AV node and A-V
bundle
T
P
P
QS
Atria contract.
T wave:
ventricular
Repolarization
Repolarization
R
T
P
ELECTRICAL
EVENTS
OF THE
CARDIAC CYCLE
QS
P
Q wave
Q
ST segment
R
R wave
R
P
QS
P
R
Ventricles contract.
Q
P
S wave
QS
Electrocardiogram (ECG)
• Record of overall spread of electrical activity through heart
• Represents
– Recording part of electrical activity induced in body fluids by
cardiac impulse that reaches body surface
– Not direct recording of actual electrical activity of heart
– Recording of overall spread of activity throughout heart during
depolarization and repolarization
– Not a recording of a single action potential in a single cell at a
single point in time
– Comparisons in voltage detected by electrodes at two different
points on body surface, not the actual potential
– Does not record potential at all when ventricular muscle is
either completely depolarized or completely repolarized
Electrocardiogram (ECG)
• Different parts of ECG record can be correlated to
specific cardiac events
EKG NORMAL
Batasan dan Pembagian Aritmia
Pada umumnya aritmia dibagi
menjadi 2 golongan besar :
I. Gangguan pembentukan impuls
II.Gangguan penghantaran impuls
Irama Sinus Normal
• Gelombang P :
- harus ada
- mendahului kompleks QRS
- positif di II, aVF
- inverted di aVR
• Interval PR :
- durasi 0,12- 0,20 detik dan konstan
• Kompleks QRS :
- durasi < 0,10 detik
• Frekuensi 60-100/menit
Irama Sinus Normal
Gangguan Pembentukan Impuls
a. Gangguan pembentukan
impuls di sinus
1. Takikardia sinus
2. Bradikardia sinus
3. Aritmia sinus
4. Henti sinus
Takikardia Sinus
Kriteria : irama sinus, rate > 100/menit
Bradikardia Sinus
Kriteria : irama sinus, rate < 60/menit
Aritmia Sinus
Pengaruh respirasi melalui stimulasi reseptor saraf vagus di paru
Akhir inspirasi : frekuensi > cepat, akhir ekspirasi frekuensi > lambat
Aritmia Sinus
Perbedaan rate maksimum dan minimum > 10 % atau > 120 mdet
Rate maks- rate min/ rate min > 10 %
Henti Sinus
Tak ada gelombang P dari sinus
Gangguan Pembentukan Impuls
b. Pembentukan impuls di atria
(aritmia atrial)
1. Ekstrasistol atrial
2. Takikardia atrial
3. Gelepar atrial
4. Fibrilasi atrial
Ekstrasistol Atrial
Kriteria : - gelombang P prematur dari atrium
- biasanya pause kompensasi tak lengkap
Tipe Ekstrasistol Atrial
Couplet : 2 EA, Takikardia atrial : 3 atau lebih EA
Bigemini : 1 kompleks sinus diikuti 1 EA
Trigemini : 2 kompleks sinus diikuti 1 EA
Atrial ekstrasistol unifokal, multifokal dan
wandering atrial pacemaker
Unifokal : satu fokus
ektopik
Multifokal : 2 atau
lebih fokus ektopik
Wandering PM : fokus
ektopik berbeda-beda
Fokus – fokus Re-entry pada
Takikardia Supraventrikular
a.
b.
Nodus SA
Miokard atrium
c. Nodus AV
d. Jalur bypass
Takikardia Atrial
Kriteria : 3 atau lebih ekstrasitol atrial berturutan
Gambaran EKG : - frekuensi biasanya 160-250 /menit
- sering P sukar dikenali karena bertumpuk pada T
- interval P-P dan R-R teratur
Takikardia Supraventrikular Paroksismal
AV Nodal Reentry Tachycardia ( AVNRT )
Fibrilasi Atrial
Gelombang f ( fibrilasi ) : gelombang-gelombang P yang tak teratur,
frekuensi 350-600/menit
Gelombang QRS tak teratur, frekuensi 140-200/menit
FA halus ( fine ) : defleksi gelombang P < 1 mm
FA kasar ( hoarse ) : defleksi gelombang P > 1 mm
Fibrilasi Atrial
Fluter Atrial
Denyut atria cepat dan teratur, frekuensi 250-350/menit
Gelombang fluter : seperti gergaji
Biasanya terdapat konduksi 2:1, karena simpul AV tak dapat
Meneruskan semua impuls dari atria
Gangguan Pembentukan Impuls
c. Pembentukan impuls di
penghubung AV
(aritmia penghubung)
1. Ekstrasistol penghubung AV
2. Takikardia penghubung AV
3. Irama lolos penghubung AV
Irama Junctional
Gelombang P prematur berasal dari penghubung AV :
vektor P lawan arus ( P negatif di II, III dan aVF )
Irama Junctional
Gangguan Pembentukan impuls
Pembentukan impuls di ventrikel
( aritmia ventrikular )
1. Ekstrasistol ventrikular
2. Takikardia ventrikular
4. Fibrilasi ventrikular
5. Henti ventrikular
6. Irama lolos ventrikular
Ekstrasistol Ventrikel
Gelombang QRS prematur, melebar dan bizarre ( tak teratur dan aneh )
P dari sinus tak terpengaruh oleh QRS ekstrasistol
( pause kompensasi lengkap )
Tipe Ekstrasistol Ventrikel
Couplet : 2 EV, Takikardia atrial : 3 atau lebih EV
Bigemini : 1 kompleks sinus diikuti 1 EV
Trigemini : 2 kompleks sinus diikuti 1 EV
Ekstrasistol Ventrikel
Fenomena R on T
QRS ekstrasitol jatuh sekitar puncak gelombang T
Takikardia Ventrikular
• Kriteria diagnosis :
- terdapat 3 atau lebih ekstrasistol ventrikel
yang berturutan
• Gambaran EKG :
- frekuensi biasanya 160-200/menit
- bila P dapat dikenali, maka P dan QRS
tidak berhubungan : disosiasi AV
- QRS melebar dan bizarre
Takikardia Ventrikel
Takikardia Ventrikel Polimorfik
Bentuk QRS berubah secara bergelombang melalui garis isoelektrik
Takikardia Ventrikel dan Torsade de Pointes
Fibrilasi Ventrikel
Gelombang QRS dan T menyatu menjadi undulasi
yang tidak teratur dan cepat
FV halus ( fine ) : gelombang f < 3 mm
FV kasar ( coarse ) : gelombang f > 3 mm
Fibrilasi Ventrikel
Fibrilasi dan Asistol Ventrikel
Asistol Ventrikel
II. Gangguan Penghantaran Impuls
Blok sino – atrial
Blok atrio – ventrikular
Blok intraventrikular
Gangguan Penghantaran Impuls
Pada umumnya suatu blok mempunyai
Beberapa derajat :
Blok derajat I :
impuls masih bisa diteruskan, tetapi dengan
lambat.
Blok derajat II :
sebagian impuls dapat diteruskan, dan
sebagian lagi terhenti.
Blok derajat III :
impuls tak bisa lewat sama sekali. Juga
disebut blok total.
Blok Atrio-Ventrikular
• Blok yang paling penting karena
menyebabkan gangguan pada koordinasi
antara atrium dan ventrikel sehingga
sangat mengganggu fungsi jantung
• Blok AV adalah blok yang paling sering
terjadi
Blok AV Derajat Satu
Dasar diagnosis :
Interval PR memanjang lebih dari
0.20 detik
Blok AV Derajat I
Blok AV Derajat Dua
Blok AV derajat dua dapat dibagi menjadi :
1. Blok AV tipe Wenckebach atau tipe
Mobitz I
2. Blok AV tipe Mobitz II
3. Blok AV lanjut atau derajat tinggi
Blok AV Tipe Wenckebach
Dasar diagnosis :
Interval PR makin memanjang, suatu
saat ada gelombang QRS yang hilang.
Blok AV Derajat II ( Tipe Wenckebach )
Blok AV Tipe Mobitz II
Dasar diagnosis :
Interval PR tetap, suatu saat ada
gelombang QRS yang hilang
Blok AV Derajat II Tipe Mobitz II
Blok AV Derajat II
Blok AV Derajat II
Blok AV Derajat Tinggi
Dasar diagnosis :
Blok AV dengan rasio konduksi 3:1
atau lebih. Misalnya blok AV 3:1, 4:1,
dan sebagainya
Blok AV Total
• Pada blok AV total, atria dan ventrikel
berdenyut sendiri-sendiri, yang disebut
disosiasi AV komplit.
• Gambaran EKG secara khas menunjukkan
letak gelombang-gelombang P yang tak ada
hubungannya dengan letak gelombanggelombang QRS.
Blok AV Derajat III
Blok AV Derajat III
Irama Pacing
Takikardia Nodal AV Paroksismal dan Non paroksismal
a. Paroksismal
b. Non paroksismal
Jalur Asesori
Sindrom Lown Ganong Levine
Sindrom Pre-eksitasi
Sindrom Pre-eksitasi
4 Mechanisms of Arrhythmia
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•
reentry (most common)
automaticity
parasystole
triggered activity
Reentry Requires…
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
Reentry Mechanism
Premature Beat Impulse
Repolarizing Tissue
(long refractory period)
Fast Conduction Path
Slow Recovery
Cardiac
Conduction
Tissue
Slow Conduction Path
Fast Recovery
1. An arrhythmia is triggered by a premature beat
2. The fast conducting pathway is blocked because of its
long refractory period so the beat can only go down the
slow conducting pathway
Reentry Mechanism
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
3. The wave of excitation from the premature beat
arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
Reentry Mechanism
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
4. On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
Reentry Circuits
AV Nodal Reentry
•SVT
Atrial Reentry
• atrial tachycardia SA Node
• atrial fibrillation
• atrial flutter
Atrio-Ventricular
Reentry
• WPW
• SVT
Ventricular Re-entry
• ventricular tachycardia
Reentry Requires…
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
Large reentry circuits, like a-flutter, involve the atrium.
Reentry in WPW involves atrium, AV node, ventricle
and accessory pathways.
Automaticity
• Heart cells other than those of the SA node
depolarize faster than SA node cells, and take
control as the cardiac pacemaker.
• Factors that enhance automaticity include:
 SANS,  PANS,  CO2,  O2,  H+,  stretch,
hypokalemia and hypocalcaemia.
Examples: Ectopic atrial tachycardia or multifocal
tachycardia in patients with chronic lung disease
OR ventricular ectopy after MI
Parasystole…
• is a benign type of automaticity problem
that affects only a small region of atrial or
ventricular cells.
• 3% of PVCs
Triggered activity…
• is like a domino effect where the arrhythmia is due
to the preceding beat.
• Delayed after-depolarizations arise during the
resting phase of the last beat and may be the cause
of digitalis-induced arrhythmias.
• Early after-depolarizations arise during the plateau
phase or the repolarization phase of the last beat
and may be the cause of torsades de pointes (ex.
Quinidine induced)
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