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Physiological Approach of Arrythmia

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.

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Physiological Approach of Arrythmia

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  1. Physiological Approach of Arrythmia M. SaifurRohman, drSpJP, 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)

  9. Electricity

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

  11. 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

  12. 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

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

  14. Purkinje Fibers • Impulse stimulates ventricular myocardial cells • Inherent rate: 20-40 bpm

  15. 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

  16. 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

  17. PX = Permeability to ion X PNa 1 +20 2 PK and PCa 0 -20 PK and PCa 3 0 -40 Membrane potential (mV) PNa -60 -80 4 4 -100 0 100 200 300 Time (msec) Phase Membrane channels 0 Na+ channels open 1 Na+ channels close 2 Ca2+ channels open; fast K+ channels close 3 Ca2+ channels close; slow K+ channels open 4 Resting potential AP of Contractile Cardiac cells • Rapid depolarization • Rapid, partial early repolarization, prolonged period of slow repolarization which is plateau phase • Rapid final repolarization phase

  18. 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

  19. Membrane Potentials in SA Node and Ventricle

  20. 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

  21. Refractory period

  22. Action Potentials

  23. 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)

  24. Action potential in autorhythmic cells

  25. Action Potential in contractile cells

  26. Action Potential in contractile cells and ECG

  27. Depolarization of atrium and ventricle

  28. 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

  29. 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

  30. 1 1 SA node AV node 2 1 THE CONDUCTING SYSTEM OF THE HEART SA node depolarizes. 2 Electrical activity goes rapidly to AV node via internodal pathways. SA node 3 Internodal pathways 3 Depolarization spreads more slowly across atria. Conduction slows through AV node. AV node 4 Depolarization moves rapidly through ventricular conducting system to the apex of the heart. A-V bundle 4 Bundle branches Purkinje fibers Depolarization wave spreads upward from the apex. 5 5 Purple shading in steps 2–5 represents depolarization. Electrical Conduction in Heart • Atria contract as single unit followed after brief delay by a synchronized ventricular contraction

  31. 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

  32. P wave: atrial depolarization START P The end R PQ or PR segment: conduction through AV node and A-V bundle T P P QS Atria contract. T wave: ventricular Repolarization ELECTRICAL EVENTS OF THE CARDIAC CYCLE Repolarization R T P QS Q wave P Q ST segment R R wave P R Q S P R Ventricles contract. Q P S wave QS Heart Excitation Related to ECG

  33. 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

  34. Electrocardiogram (ECG) • Different parts of ECG record can be correlated to specific cardiac events

  35. EKG NORMAL

  36. Batasan dan Pembagian Aritmia Pada umumnya aritmia dibagi menjadi 2 golongan besar : • Gangguan pembentukan impuls • Gangguan penghantaran impuls

  37. 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

  38. Irama Sinus Normal

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

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

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

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

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

  44. HentiSinus Tak ada gelombang P dari sinus

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

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

  47. Tipe EkstrasistolAtrial Couplet : 2 EA, Takikardia atrial : 3 atau lebih EA Bigemini : 1 kompleks sinus diikuti 1 EA Trigemini : 2 kompleks sinus diikuti 1 EA

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

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