Physiological Approach of Arrythmia
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Transcript of Physiological Approach of Arrythmia
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Physiological Approach of Arrythmia
M. Saifur Rohman, dr SpJP, PhD. FICA
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OUTLINE
• Membrane potential, • action potential, • impulse conduction, • type of arrhytmias,• cause of arrhytmias,
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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
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Jantung Rusak ?
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Untuk Mengetahui Kelainan Jantung ?
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Elektrokardiogram (EKG)
• Rekaman grafik potensial listrik yang dihasilkan oleh jaringan jantung
Goldman & Goldschlager
Cara Perekaman EKG :- Permukaan- Epikardial- Endokardial / intrakardial
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Myocardium VS . AUTORYTMIC
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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)
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Electricity
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Intrinsic Cardiac Conduction SystemApproximately 1% of cardiac muscle cells are autorhythmic rather than contractile
70-80/min
40-60/min
20-40/min
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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
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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
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Bundle of HIS– Electrical impulses conducted to
ventricles via Bundle of HIS & purkinjie fibers
– Divides into bundle branches• Right• Left
–Anterior Fascicle–Posterior Fascicle
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Purkinje Fibers
– Impulse stimulates ventricular myocardial cells
– Inherent rate: 20-40 bpm
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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
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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
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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
PX = Permeability to ion X
+20
-20
-40
-60
-80
-100
Mem
bran
e po
tenti
al (m
V)
0
0 100 200 300Time (msec)
PK and PCa
PNa
PK and PCa
PNa
Na+ channels open
Na+ channels close
Ca2+ channels open; fast K+ channels close
Ca2+ channels close; slow K+ channels open
Resting potential
1
2
30
4 4
0
1
2
3
4
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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
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Membrane Potentials in SA Node and Ventricle
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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
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Refractory period
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Action Potentials
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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)
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Action potential in autorhythmic cells
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Action Potential in contractile cells
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Action Potential in contractile cells and ECG
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Depolarization of atrium and ventricle
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• 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
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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
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Electrical Conduction in Heart
• Atria contract as single unit followed after brief delay by a synchronized ventricular contraction
THE CONDUCTING SYSTEMOF THE HEART
SA nodeAV node
Purkinjefibers
Bundle branchesA-V bundle
AV node
Internodalpathways
SA node
SA node depolarizes.
Electrical activity goesrapidly to AV node viainternodal pathways.
Depolarization spreadsmore slowly acrossatria. Conduction slowsthrough AV node.
Depolarization movesrapidly through ventricularconducting system to theapex of the heart.Depolarization wavespreads upward fromthe apex.
1
4
5
3
2
1
4
5
3
2
1
Purple shading in steps 2–5 represents depolarization.
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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
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Heart Excitation Related to ECG
P wave: atrialdepolarizationSTART
Atria contract.
PQ or PR segment:conduction throughAV node and A-Vbundle
P
P
Q
Q wave
R wave
P
Q
R
S wave
QS
R
P
ELECTRICALEVENTSOF THE
CARDIAC CYCLE
Repolarization
ST segment
Ventricles contract.
P
Q
R
S
The end
T wave:ventricular
Repolarization
P
QS
R
T
P
QS
R
T
P
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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
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Electrocardiogram (ECG)• Different parts of ECG record can be correlated to
specific cardiac events
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EKG NORMAL
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Batasan dan Pembagian Aritmia
Pada umumnya aritmia dibagi menjadi 2 golongan besar :
I. Gangguan pembentukan impulsII.Gangguan penghantaran impuls
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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
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Irama Sinus Normal
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Gangguan Pembentukan Impuls
a. Gangguan pembentukan impuls di sinus
1. Takikardia sinus 2. Bradikardia sinus 3. Aritmia sinus 4. Henti sinus
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Takikardia Sinus
Kriteria : irama sinus, rate > 100/menit
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Bradikardia Sinus
Kriteria : irama sinus, rate < 60/menit
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Aritmia Sinus
Pengaruh respirasi melalui stimulasi reseptor saraf vagus di paruAkhir inspirasi : frekuensi > cepat, akhir ekspirasi frekuensi > lambat
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Aritmia Sinus
Perbedaan rate maksimum dan minimum > 10 % atau > 120 mdetRate maks- rate min/ rate min > 10 %
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Henti Sinus
Tak ada gelombang P dari sinus
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b. Pembentukan impuls di atria (aritmia atrial)
1. Ekstrasistol atrial2. Takikardia atrial3. Gelepar atrial4. Fibrilasi atrial
Gangguan Pembentukan Impuls
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Ekstrasistol Atrial
Kriteria : - gelombang P prematur dari atrium - biasanya pause kompensasi tak lengkap
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Tipe Ekstrasistol Atrial
Couplet : 2 EA, Takikardia atrial : 3 atau lebih EA Bigemini : 1 kompleks sinus diikuti 1 EATrigemini : 2 kompleks sinus diikuti 1 EA
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Atrial ekstrasistol unifokal, multifokal dan wandering atrial pacemaker
Multifokal : 2 ataulebih fokus ektopik
Unifokal : satu fokus ektopik
Wandering PM : fokus ektopik berbeda-beda
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Fokus – fokus Re-entry pada Takikardia Supraventrikular
a. Nodus SAb. Miokard atrium
c. Nodus AVd. Jalur bypass
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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
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Takikardia Supraventrikular Paroksismal
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AV Nodal Reentry Tachycardia ( AVNRT )
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Fibrilasi Atrial
Gelombang f ( fibrilasi ) : gelombang-gelombang P yang tak teratur,frekuensi 350-600/menitGelombang QRS tak teratur, frekuensi 140-200/menitFA halus ( fine ) : defleksi gelombang P < 1 mmFA kasar ( hoarse ) : defleksi gelombang P > 1 mm
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Fibrilasi Atrial
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Fluter Atrial
Denyut atria cepat dan teratur, frekuensi 250-350/menitGelombang fluter : seperti gergajiBiasanya terdapat konduksi 2:1, karena simpul AV tak dapatMeneruskan semua impuls dari atria
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Gangguan Pembentukan Impuls
c. Pembentukan impuls di penghubung AV (aritmia penghubung)1. Ekstrasistol penghubung AV2. Takikardia penghubung AV3. Irama lolos penghubung AV
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Irama Junctional
Gelombang P prematur berasal dari penghubung AV : vektor P lawan arus ( P negatif di II, III dan aVF )
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Irama Junctional
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Gangguan Pembentukan impuls
Pembentukan impuls di ventrikel ( aritmia ventrikular )
1. Ekstrasistol ventrikular2. Takikardia ventrikular4. Fibrilasi ventrikular5. Henti ventrikular6. Irama lolos ventrikular
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Ekstrasistol Ventrikel
Gelombang QRS prematur, melebar dan bizarre ( tak teratur dan aneh )P dari sinus tak terpengaruh oleh QRS ekstrasistol ( pause kompensasi lengkap )
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Tipe Ekstrasistol Ventrikel
Couplet : 2 EV, Takikardia atrial : 3 atau lebih EV Bigemini : 1 kompleks sinus diikuti 1 EVTrigemini : 2 kompleks sinus diikuti 1 EV
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Ekstrasistol Ventrikel
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Fenomena R on T
QRS ekstrasitol jatuh sekitar puncak gelombang T
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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
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Takikardia Ventrikel
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Takikardia Ventrikel Polimorfik
Bentuk QRS berubah secara bergelombang melalui garis isoelektrik
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Takikardia Ventrikel dan Torsade de Pointes
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Fibrilasi Ventrikel
Gelombang QRS dan T menyatu menjadi undulasi yang tidak teratur dan cepatFV halus ( fine ) : gelombang f < 3 mmFV kasar ( coarse ) : gelombang f > 3 mm
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Fibrilasi Ventrikel
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Fibrilasi dan Asistol Ventrikel
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Asistol Ventrikel
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II. Gangguan Penghantaran Impuls
Blok sino – atrialBlok atrio – ventrikularBlok intraventrikular
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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.
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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
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Blok AV Derajat Satu
Dasar diagnosis :Interval PR memanjang lebih
dari 0.20 detik
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Blok AV Derajat I
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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 II3. Blok AV lanjut atau derajat tinggi
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Blok AV Tipe Wenckebach
Dasar diagnosis :
Interval PR makin memanjang, suatu saat ada gelombang QRS yang hilang.
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Blok AV Derajat II ( Tipe Wenckebach )
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Blok AV Tipe Mobitz II
Dasar diagnosis :Interval PR tetap, suatu saat
ada gelombang QRS yang hilang
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Blok AV Derajat II Tipe Mobitz II
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Blok AV Derajat II
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Blok AV Derajat II
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Blok AV Derajat Tinggi
Dasar diagnosis :Blok AV dengan rasio konduksi 3:1
atau lebih. Misalnya blok AV 3:1, 4:1, dan sebagainya
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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.
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Blok AV Derajat III
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Blok AV Derajat III
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Irama Pacing
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Takikardia Nodal AV Paroksismal dan Non paroksismal
a. Paroksismal b. Non paroksismal
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Jalur Asesori
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Sindrom Lown Ganong Levine
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Sindrom Pre-eksitasi
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Sindrom Pre-eksitasi
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4 Mechanisms of Arrhythmia
• reentry (most common)• automaticity• parasystole • triggered activity
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Fast Conduction PathSlow Recovery
Slow Conduction PathFast 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.
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Fast Conduction PathSlow Recovery
Slow Conduction PathFast 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
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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 PathSlow Recovery
Slow Conduction PathFast Recovery
Cardiac Conduction Tissue
Reentry Mechanism
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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 PathSlow Recovery
Slow Conduction PathFast Recovery
Cardiac Conduction Tissue
Reentry Mechanism
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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
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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.
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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
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Parasystole…
• is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells.
• 3% of PVCs
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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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Terima Kasih