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Physiological Approach of Arrythmia M. Saifur Rohman, dr SpJP, PhD. FICA.

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Presentasi berjudul: "Physiological Approach of Arrythmia M. Saifur Rohman, dr SpJP, PhD. FICA."— Transcript presentasi:

1 Physiological Approach of Arrythmia M. Saifur Rohman, dr SpJP, PhD. FICA

2 OUTLINE Membrane potential, action potential, impulse conduction, type of arrhytmias, cause of arrhytmias,

3 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

4 Jantung Rusak ?

5 Untuk Mengetahui Kelainan Jantung ?

6 Elektrokardiogram (EKG) Rekaman grafik potensial listrik yang dihasilkan oleh jaringan jantung Goldman & Goldschlager Cara Perekaman EKG : -Permukaan -Epikardial -Endokardial / intrakardial

7 Myocardium VS. AUTORYTMIC

8 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)


10 Electricity

11 Intrinsic Cardiac Conduction System Approximately 1% of cardiac muscle cells are autorhythmic rather than contractile 70-80/min 40-60/min 20-40/min

12 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

13 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

14 Bundle of HIS – Electrical impulses conducted to ventricles via Bundle of HIS & purkinjie fibers – Divides into bundle branches Right Left – Anterior Fascicle – Posterior Fascicle

15 Purkinje Fibers – Impulse stimulates ventricular myocardial cells – Inherent rate: 20-40 bpm

16 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

17 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

18 AP of Contractile Cardiac cells – Rapid depolarization – Rapid, partial early repolarization, prolonged period of slow repolarization which is plateau phase – Rapid final repolarization phase PhaseMembrane channels P X = Permeability to ion X +20 -20 -40 -60 -80 -100 Membrane potential (mV) 0 0100200300 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

19 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

20 Membrane Potentials in SA Node and Ventricle

21 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

22 Refractory period

23 Action Potentials

24 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)

25 Action potential in autorhythmic cells

26 Action Potential in contractile cells

27 Action Potential in contractile cells and ECG


29 Depolarization of atrium and ventricle

30 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

31 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

32 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 2–5 represents depolarization.

33 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

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

35 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

36 Electrocardiogram (ECG) Different parts of ECG record can be correlated to specific cardiac events


38 Batasan dan Pembagian Aritmia Pada umumnya aritmia dibagi menjadi 2 golongan besar : I. Gangguan pembentukan impuls II. Gangguan penghantaran impuls

39 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

40 Irama Sinus Normal

41 Gangguan Pembentukan Impuls a. Gangguan pembentukan impuls di sinus 1. Takikardia sinus 2. Bradikardia sinus 3. Aritmia sinus 4. Henti sinus

42 Takikardia Sinus Kriteria : irama sinus, rate > 100/menit

43 Bradikardia Sinus Kriteria : irama sinus, rate < 60/menit

44 Aritmia Sinus Pengaruh respirasi melalui stimulasi reseptor saraf vagus di paru Akhir inspirasi : frekuensi > cepat, akhir ekspirasi frekuensi > lambat

45 Aritmia Sinus Perbedaan rate maksimum dan minimum > 10 % atau > 120 mdet Rate maks- rate min/ rate min > 10 %

46 Henti Sinus Tak ada gelombang P dari sinus

47 b. Pembentukan impuls di atria (aritmia atrial) 1. Ekstrasistol atrial 2. Takikardia atrial 3. Gelepar atrial 4. Fibrilasi atrial Gangguan Pembentukan Impuls

48 Ekstrasistol Atrial Kriteria : - gelombang P prematur dari atrium - biasanya pause kompensasi tak lengkap

49 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

50 Atrial ekstrasistol unifokal, multifokal dan wandering atrial pacemaker Multifokal : 2 atau lebih fokus ektopik Unifokal : satu fokus ektopik Wandering PM : fokus ektopik berbeda-beda

51 Fokus – fokus Re-entry pada Takikardia Supraventrikular a.Nodus SA b.Miokard atrium c. Nodus AV d. Jalur bypass

52 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

53 Takikardia Supraventrikular Paroksismal

54 AV Nodal Reentry Tachycardia ( AVNRT )

55 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

56 Fibrilasi Atrial

57 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

58 Gangguan Pembentukan Impuls c.Pembentukan impuls di penghubung AV (aritmia penghubung) 1. Ekstrasistol penghubung AV 2. Takikardia penghubung AV 3. Irama lolos penghubung AV

59 Irama Junctional Gelombang P prematur berasal dari penghubung AV : vektor P lawan arus ( P negatif di II, III dan aVF )

60 Irama Junctional

61 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

62 Ekstrasistol Ventrikel Gelombang QRS prematur, melebar dan bizarre ( tak teratur dan aneh ) P dari sinus tak terpengaruh oleh QRS ekstrasistol ( pause kompensasi lengkap )

63 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

64 Ekstrasistol Ventrikel

65 Fenomena R on T QRS ekstrasitol jatuh sekitar puncak gelombang T

66 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

67 Takikardia Ventrikel

68 Takikardia Ventrikel Polimorfik Bentuk QRS berubah secara bergelombang melalui garis isoelektrik

69 Takikardia Ventrikel dan Torsade de Pointes

70 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

71 Fibrilasi Ventrikel

72 Fibrilasi dan Asistol Ventrikel

73 Asistol Ventrikel

74 II. Gangguan Penghantaran Impuls Blok sino – atrial Blok atrio – ventrikular Blok intraventrikular

75 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.

76 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

77 Blok AV Derajat Satu Dasar diagnosis :  Interval PR memanjang lebih dari 0.20 detik

78 Blok AV Derajat I

79 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

80 Blok AV Tipe Wenckebach Dasar diagnosis :  Interval PR makin memanjang, suatu saat ada gelombang QRS yang hilang.

81 Blok AV Derajat II ( Tipe Wenckebach )

82 Blok AV Tipe Mobitz II Dasar diagnosis :  Interval PR tetap, suatu saat ada gelombang QRS yang hilang

83 Blok AV Derajat II Tipe Mobitz II

84 Blok AV Derajat II


86 Blok AV Derajat Tinggi Dasar diagnosis :  Blok AV dengan rasio konduksi 3:1 atau lebih. Misalnya blok AV 3:1, 4:1, dan sebagainya

87 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.

88 Blok AV Derajat III


90 Irama Pacing

91 Takikardia Nodal AV Paroksismal dan Non paroksismal a. Paroksismal b. Non paroksismal

92 Jalur Asesori

93 Sindrom Lown Ganong Levine

94 Sindrom Pre-eksitasi



97 4 Mechanisms of Arrhythmia reentry (most common) automaticity parasystole triggered activity

98 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.

99 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

100 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

101 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

102 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

103 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.

104 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

105 Parasystole… is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells. 3% of PVCs

106 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)

107 Terima Kasih

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