Physiological Approach of

Arrythmia
M. Saifur Rohman, dr SpJP, PhD. FICA
OUTLINE
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 theyve 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:
Bachmans 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
Rapid depolarization
Rapid, partial early
repolarization,
prolonged period of
slow repolarization
which is plateau
phase
Rapid final
repolarization phase
Phase Membrane channels
P
X
= Permeability to ion X
+20
-20
-40
-60
-80
-100
M
e
m
b
r
a
n
e

p
o
t
e
n
t
i
a
l

(
m
V
)

0
0 100 200 300
Time (msec)
P
K
and P
Ca

P
Na

P
K
and P
Ca

P
Na

Na
+
channels open
Na
+
channels close
Ca
2+
channels open; fast K
+
channels close
Ca
2+
channels close; slow K
+
channels open
Resting potential
1
2
3
0
4
4
0
1
2
3
4
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 Ca
2+

channels

Membrane Potentials in SA Node and Ventricle
Why A Longer AP In Cardiac Contractile Fibers?
We dont 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

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 to mechanical response
Electrical Signal Flow - Conduction
Pathway
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

THE CONDUCTING SYSTEM
OF THE HEART
SA node
AV node
Purkinje
fibers
Bundle branches
A-V bundle
AV node
Internodal
pathways
SA node
SA node depolarizes.
Electrical activity goes
rapidly to AV node via
internodal pathways.
Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
Depolarization wave
spreads upward from
the apex.
1
4
5
3
2
1
4
5
3
2
1
Purple shading in steps 25 represents depolarization.
Excitation-Contraction Coupling in Cardiac
Contractile Cells
Ca
2+
entry through L-type channels in T tubules
triggers larger release of Ca
2+
from sarcoplasmic
reticulum
Ca
2+
induced Ca
2+
release leads to cross-bridge cycling
and contraction

Heart Excitation Related to ECG
P wave: atrial
depolarization
START
Atria contract.
PQ or PR segment:
conduction through
AV node and A-V
bundle
P
P
Q
Q wave
R wave
P
Q
R
S wave
Q
S

R
P
ELECTRICAL
EVENTS
OF THE
CARDIAC CYCLE
Repolarization
ST segment
Ventricles contract.
P
Q
R
S
The end
T wave:
ventricular
Repolarization
P
Q
S

R
T
P
Q
S

R
T
P
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
b. Pembentukan impuls di atria
(aritmia atrial)
1. Ekstrasistol atrial
2. Takikardia atrial
3. Gelepar atrial
4. Fibrilasi atrial



Gangguan Pembentukan Impuls
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
Multifokal : 2 atau
lebih fokus ektopik
Unifokal : satu fokus
ektopik

Wandering PM : fokus
ektopik berbeda-beda
Fokus fokus Re-entry pada
Takikardia Supraventrikular
a. Nodus SA
b. 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 gelombang-
gelombang 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
reentry (most common)
automaticity
parasystole
triggered activity
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Reentry Requires
Electrical Impulse
Cardiac
Conduction
Tissue
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.
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
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
Repolarizing Tissue
(long refractory period)
Reentry Mechanism
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
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
Reentry Mechanism
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

Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
Reentry Mechanism
Atrial Reentry
atrial tachycardia
atrial fibrillation
atrial flutter
Atrio-Ventricular
Reentry
WPW
SVT
Ventricular Re-entry
ventricular tachycardia
AV Nodal Reentry
SVT
Reentry Circuits
SA Node
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, CO
2
, O
2,
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)
Terima Kasih