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

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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 Approximately 1% of the cardiac muscle cells are autorhythmic rather than contractile. * These specialized cardiac cells don’t contract but are specialized to initiate and conduct impulses through the heart to coordinate its activity. * These constitute the intrinsic cardiac conduction system. These autorhythmic cells constitute the following components of the intrinsic conduction system: * the sinoatrial (SA) node, just inferior to the entrance of the superior vena cava into the right atrium, * the atrioventricular node (AV) node, located just above the tricuspid valve in the lower part of the right atrium, * the atrioventricular bundle (bundle of HIS), located in the lower part of the interatrial septum and which extends into the interventricular septum where it splits into right and left bundle branches * which continue toward the apex of the heart and the purkinje fibers * which branch off of the bundle branches to complete the pathway into the apex of the heart and turn upward to carry conduction impulses to the papillary muscles and the rest of the myocardium. Although all of these are autorhythmic, they have different rates of depolarization. * For instance, the SA node * depolarizes at a rate of 75/min. * The AV node depolarizes at a rate of 40 to 60 beats per minute, * while the rest have an intrinsic rate of around 30 depolarizations/ minute. * Because the SA node has the fastest rate, it serves as the pacemaker for the heart. * 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 +20 -20 -40 -60 -80 -100 Membrane potential (mV) 100 200 300 Time (msec) 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 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 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 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 Internodal pathways 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 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 Atria contract. PQ or PR segment: conduction through AV node and A-V bundle P Q Q wave R wave R S wave QS ELECTRICAL EVENTS OF THE CARDIAC CYCLE Repolarization ST segment Ventricles contract. S The end T wave: ventricular T

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 : Gangguan pembentukan impuls 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 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 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 : Blok AV tipe Wenckebach atau tipe Mobitz I Blok AV tipe Mobitz II 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

Reentry Requires… Electrical Impulse Cardiac Conduction Tissue Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery 2 distinct pathways that come together at beginning and end to form a loop. A unidirectional block in one of those pathways. Slow conduction in the unblocked pathway.

Reentry Mechanism Repolarizing Tissue (long refractory period) Premature Beat Impulse Cardiac Conduction Tissue Repolarizing Tissue (long refractory period) Fast Conduction Path Slow Recovery 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 Fast Conduction Path Slow Recovery 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 Fast Conduction Path Slow Recovery 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 Ventricular Re-entry ventricular tachycardia Atrial Reentry atrial tachycardia atrial fibrillation atrial flutter SA Node Atrio-Ventricular Reentry WPW SVT

Reentry Requires… 2 distinct pathways that come together at beginning and end to form a loop. A unidirectional block in one of those pathways. 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. 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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