Presentasi berjudul: "Physiological Approach of Arrythmia"— 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 cellsContractile cells99% of cardiac muscle cellsDo mechanical work of pumpingNormally do not initiate own action potentialsAutorhythmic cellsDo not contractSpecialized for initiating and conducting action potentials responsible for contraction of working cells
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)
11 Intrinsic Cardiac Conduction System Approximately 1% of cardiac muscle cells are autorhythmic rather than contractile70-80/min40-60/minApproximately 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
12 Sinoatrial (SA) Node Normal cardiac impulse originates here “Natural pacemaker”Inherent rate: bpmAtrial depolarization occurs cell to cellFour 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 timeInherent rate: bpmConduction delay at AV node so that ventricular filling from atrial contraction
14 Bundle of HISElectrical impulses conducted to ventricles via Bundle of HIS & purkinjie fibersDivides into bundle branchesRightLeftAnterior FasciclePosterior Fascicle
16 Intrinsic Conduction System Autorhythmic cells:Initiate action potentialsHave “drifting” resting potentials called pacemaker potentialsPacemaker 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 PotentialDecreased efflux of K+, membrane permeability decreases between APs, they slowly close at negative potentialsConstant influx of Na+, no voltage-gated Na + channelsGradual depolarization because K+ builds up and Na+ flows inwardAs 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+ effluxAt -60mV K+ channels close
18 AP of Contractile Cardiac cells Rapid depolarizationRapid, partial early repolarization, prolonged period of slow repolarization which is plateau phaseRapid final repolarization phasePhaseMembrane channelsPX = Permeability to ion X+20-20-40-60-80-100Membrane potential (mV)100200300Time (msec)PK and PCaPNaNa+ channels openNa+ channels closeCa2+ channels open; fast K+ channels closeCa2+ channels close; slow K+ channels openResting potential1234
19 AP of Contractile Cardiac cells Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contractionEnsures adequate ejection timePlateau primarily due to activation of slow L-type Ca2+ channels
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 impossibleEnsures alternate periods of contraction and relaxation which are essential for pumping blood
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 potential2. Permeability of the membrane for the ion: channels which is selective and gatedSelective: manifestation of size and structure of its poreGated: pass through it specific channels only at certain times; voltage sensitive gating (fast sodium channel)
30 Electrical to mechanical response Excitation-contraction couplingDuring phase 2 of the action potential Ca enter through L Type Ca Channel in the sarcolemma and T tubuleCa triggers release much greater Ca from SR via Ryanodine receptor into cytosol result in an increased Ca in the cytosolCa 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 myosinMyosin head bind to actin causing interdigitating thick and thin filament in ATP dependent reaction
31 Electrical Signal Flow - Conduction Pathway Cardiac impulse originates at SA nodeAction potential spreads throughout right and left atriaImpulse 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 HisImpulse rapidly disperses throughout myocardium by means of Purkinje fibersRest 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 contractionTHE CONDUCTING SYSTEMOF THE HEARTSA nodeAV nodePurkinjefibersBundle branchesA-V bundleInternodalpathwaysSA 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.14532Purple shading in steps 2–5 represents depolarization.
33 Excitation-Contraction Coupling in Cardiac Contractile Cells Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulumCa2+ induced Ca2+ release leads to cross-bridge cycling and contraction
34 Heart Excitation Related to ECG P wave: atrialdepolarizationSTARTAtria contract.PQ or PR segment:conduction throughAV node and A-VbundlePQQ waveR waveRS waveQSELECTRICALEVENTSOF THECARDIAC CYCLERepolarizationST segmentVentricles contract.SThe endT wave:ventricularT
35 Electrocardiogram (ECG) Record of overall spread of electrical activity through heartRepresentsRecording part of electrical activity induced in body fluids by cardiac impulse that reaches body surfaceNot direct recording of actual electrical activity of heartRecording of overall spread of activity throughout heart during depolarization and repolarizationNot a recording of a single action potential in a single cell at a single point in timeComparisons in voltage detected by electrodes at two different points on body surface, not the actual potentialDoes 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 dibagimenjadi 2 golongan besar :Gangguan pembentukan impulsGangguan penghantaran impuls
39 Irama Sinus Normal Gelombang P : - harus ada - mendahului kompleks QRS - positif di II, aVF- inverted di aVRInterval PR :- durasi 0,12- 0,20 detik dan konstanKompleks QRS :- durasi < 0,10 detikFrekuensi /menit
55 Fibrilasi AtrialGelombang f ( fibrilasi ) : gelombang-gelombang P yang tak teratur,frekuensi /menitGelombang QRS tak teratur, frekuensi /menitFA halus ( fine ) : defleksi gelombang P < 1 mmFA kasar ( hoarse ) : defleksi gelombang P > 1 mm
65 Fenomena R on TQRS ekstrasitol jatuh sekitar puncak gelombang T
66 Takikardia Ventrikular Kriteria diagnosis :- terdapat 3 atau lebih ekstrasistol ventrikelyang berturutanGambaran EKG :- frekuensi biasanya /menit- bila P dapat dikenali, maka P dan QRStidak berhubungan : disosiasi AV- QRS melebar dan bizarre
74 II. Gangguan Penghantaran Impuls Blok sino – atrialBlok atrio – ventrikularBlok intraventrikular
75 Gangguan Penghantaran Impuls Pada umumnya suatu blok mempunyaiBeberapa 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 jantungBlok AV adalah blok yang paling sering terjadi
77 Blok AV Derajat SatuDasar diagnosis :Interval PR memanjang lebih dari 0.20 detik
86 Blok AV Derajat TinggiDasar diagnosis :Blok AV dengan rasio konduksi 3:1 atau lebih. Misalnya blok AV 3:1, 4:1, dan sebagainya
87 Blok AV TotalPada 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.
97 4 Mechanisms of Arrhythmia reentry (most common)automaticityparasystoletriggered activity
98 Reentry Requires…Electrical ImpulseCardiac Conduction TissueFast Conduction PathSlow RecoverySlow Conduction PathFast Recovery2 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.
99 Reentry Mechanism Repolarizing Tissue (long refractory period) Premature Beat ImpulseCardiac Conduction TissueRepolarizing Tissue (long refractory period)Fast Conduction PathSlow RecoverySlow Conduction PathFast Recovery1. An arrhythmia is triggered by a premature beat2. The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway
100 Reentry Mechanism Fast Conduction Path Slow Recovery Cardiac Conduction TissueFast Conduction PathSlow RecoverySlow Conduction PathFast Recovery3. 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
101 Reentry Mechanism Fast Conduction Path Slow Recovery Cardiac Conduction TissueFast Conduction PathSlow RecoverySlow Conduction PathFast Recovery4. 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
103 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.
104 AutomaticityHeart 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
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)
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