Physiological Approach of Arrythmia

transcript

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 they’ve recovered (repolarized)

Electricity

Intrinsic Cardiac Conduction SystemApproximately 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

– 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

0 100 200 300Time (msec)

PK and PCa

Na+ channels open

Na+ channels close

Ca2+ channels open; fast K+ channels close

Ca2+ channels close; slow K+ channels open

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

• 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 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.

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: atrialdepolarizationSTART

Atria contract.

PQ or PR segment:conduction throughAV node and A-Vbundle

Q wave

R wave

S wave

ELECTRICALEVENTSOF THE

CARDIAC CYCLE

Repolarization

ST segment

Ventricles contract.

The end

T wave:ventricular

Repolarization

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 impulsII.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 paruAkhir inspirasi : frekuensi > cepat, akhir ekspirasi frekuensi > lambat

Aritmia Sinus

Perbedaan rate maksimum dan minimum > 10 % atau > 120 mdetRate maks- rate min/ rate min > 10 %

Henti Sinus

Tak ada gelombang P dari sinus

b. Pembentukan impuls di atria (aritmia atrial)

1. Ekstrasistol atrial2. Takikardia atrial3. Gelepar atrial4. 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 EATrigemini : 2 kompleks sinus diikuti 1 EA

Atrial ekstrasistol unifokal, multifokal dan wandering atrial pacemaker

Multifokal : 2 ataulebih fokus ektopik

Unifokal : satu fokus ektopik

Wandering PM : fokus ektopik berbeda-beda

Fokus – fokus Re-entry pada Takikardia Supraventrikular

a. Nodus SAb. Miokard atrium

c. Nodus AVd. 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/menitGelombang QRS tak teratur, frekuensi 140-200/menitFA halus ( fine ) : defleksi gelombang P < 1 mmFA kasar ( hoarse ) : defleksi gelombang P > 1 mm

Fibrilasi Atrial

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

c. Pembentukan impuls di penghubung AV (aritmia penghubung)1. Ekstrasistol penghubung AV2. Takikardia penghubung AV3. 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 ventrikular2. Takikardia ventrikular4. Fibrilasi ventrikular5. Henti ventrikular6. 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 EVTrigemini : 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 cepatFV halus ( fine ) : gelombang f < 3 mmFV kasar ( coarse ) : gelombang f > 3 mm

Fibrilasi Ventrikel

Fibrilasi dan Asistol Ventrikel

Asistol Ventrikel

II. Gangguan Penghantaran Impuls

Blok sino – atrialBlok atrio – ventrikularBlok 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 II3. 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 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

Irama Pacing

Takikardia Nodal AV Paroksismal dan Non paroksismal

a. Paroksismal b. Non paroksismal

Jalur Asesori

Sindrom Lown Ganong Levine

Sindrom Pre-eksitasi

4 Mechanisms of Arrhythmia

• reentry (most common)• automaticity• parasystole • triggered activity

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.

Premature Beat Impulse

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

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

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, 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)

Terima Kasih

Physiological Approach of Arrythmia

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