Cardiac Arrhythmia)

Dr. Li JingboDepartment of cardiology, affiliated 6th peoples hospital, Shanghai Jiao Tong University

Property of cardiac elctrophysiologyExcitability)(automaticity)(Conductivity)

ExcitabilityElectrical activity which takes place when myocardial cell is stimulatedElectrical activity of single myocardial cell is called action potential(AP)

ExcitabilityComposition and features of APThere are five phase01234Electrophysiological phenomena during APRefractory periodAbsolute, Effective, RelativeSuperconductive

0-60-90+20Threshold voltagemv01234ARPERPRRPSuper-conductive period

ConductivityElectrical impulse can conduct in myocardial tissue bidirectionallyNormal conduction pathwaysinus nodeintranode bundle atrioventricula node and intraatrial bundleHis bundleright and left bundle branch(including left anterosuperior and posteroinferior)Purkinje fibermyocardium

automaticityProperty of spontaneously discharging cells(spotaneous AP, diastolic depolarization)Automaticity increases from high to low as follows:Physiological statusSNAVNHISPurkinjepathologicaldiseased myocardial and conductive tissue, etc.

Property of normal rhythmImpulse from SNHeart rate is within 60100/minRegular rhythmPP interval0.12sPR interval is between 0.120.20sQRS complex duration0.10sFrontal axis within -30110 It is considered as arrhythmia if any item above is not matched

Classification of cardiac arrhythmiasClassified on property of electrical activityAbnormality of impulse and conductionClassified on heart rate, rapid or slowRapid or slow arrhythmiasClassified on clinical manifestation, mild or severFatal or nonfatalHigh risk or low risk

Method of diagnosing arrhythmia and its evaluation Symptom Caused by abnormal contractilepalpitation, discomfort, beating stop, etc. Induced by cardiac output decreasingchest compressing and pain, dizziness, presyncope, syncope, short of breathlessFactors related to symptom: medications, diet, emotion, infection, etc.

Method of diagnosing arrhythmia and its evaluationSignChanging of rhythm : increasing or decreasing,regular or irregularChanging of heart soundS1 muffle or loudcannon soundRelation between carotid vein wave pulse and ventricle contraction

Method of diagnosing arrhythmia and its evaluationElectrocardiogramMost valuable: evaluating arrhythmia type, property, prognosis, etc.Dynamic Electrocardiogram(Holter)Most valuable: assessing arrhythmia type, numbers, distribution, property, prognosis. Evaluating clinical significance, effects of treatment, etc.

Method of diagnosing arrhythmia and its evaluationEsophagus ElectrocardiogramDifferentiating SVT from VTunderstanding mechanism of SVT. Semi-invasive.

Method of diagnosing arrhythmia and its evaluationElectrophysiologic study(EPS)Classical way of researching arrhytnmias. InvasiveAssessing function of SNSinus node recovery time, SNRTSinoatrial conduction time, SACTAssessing AV conduction Analyzing mechanisim of tachyarrhythmiasEvaluating unknown syncope

Method of diagnosing arrhythmia and its evaluationExercise ElectrocardiogramSuitable for some of arrhythmias, such as VTOthers Average signal techniquesuch as late potential(LP), QT dispersion, used for evaluating prognosis of AMI

Mechanisms of arrhythmogenesisReentryprerequisite of reentry Conduction inconsistency of anatomy or physiology Single directional conduction blockingDelayed conductionInitial blocking area recovers excitability (reentry cycle length great than refractory period of the blocking )

Mechanisms of arrhythmogenesisIncreased automaticity Endogenous or exogenous catecholamine increasingAbnormality of acid, basic , electrolyte balance Ischemia, hypoxia Mechanical stretch drugsDisturbance of nerve and liquid modulation

Mechanisms of arrhythmogenesisTriggered activityDepolarizing oscillations of membrane voltage induced by abnormal inward Na+ current (one or more preceding AP)during earlier or later reporlarization, ie, After depolarizationEarly depolarizationDelayed depolarization

Mechanisms of arrhythmogenesisAutomatic cells diminish or malfunction, such as sick sinus syndromeDysfunction of conductive tissues, such as sinoatrial block, atrioventricular block or bundle branch block

Specific arrhythmiasRapid arrhythmias Premature contractionAtrial, junctional, ventricularTachyarrhythmias Sinus, atrial, supraventricular, junctional, ventricular, atrial flutter and fibrelationBradyarrhythmiasDisease of sinus, AV node or bundle branch

Specific arrhythmiasTwo syndromes Preexciting syndromeRelated with rapid arrhythmiasSick sinus syndrome(SSS)Related with slow arrhythmias

sinus arrhythmias

Sinus tachycardiaFeatures of ECGSame as it from sinus node, but heart rate is more than 100 beats per minute(pbm), often between 100~160 bpm

Sinus tachycardiaClinical featuresVery common. Almost having reasons e.g. nervous, excise, excite infection, blood loss, hypoxia, heart failure, etc. Palpitation or chest discomfort are often complanedTreatment of etiology

Sinus bradycardiaFeatures HR 0.12 s sometimesRhythm is slightly irregularIt is common in healthy personUsually, no need treating

Sinus standstillFeatures PP interval elongates abruptly, basically at sinus bradycardia, which is not common multiples of basic PP intervalEscape beat or rhythm is common seenSymptoms is depend on whether standstill is too long or notNo effective drugs, pacemaker is ultimate choice

sinoatrial blockClassification of ECGFirst degree SAB can`t be seen on ECGThird degree SAB can`t be differentiated from sinus standstillSecond degree SAB is divided into two subtype, i.e. type I and type II second degree SAB Symptoms and therapy are same as sinus standstill

Type I Second degree SABFeatures of ECGPP interval progressively shortens prior to the pausePP interval before the pause < it after the PP intervalThe duration of the pause is < two basic PP cycles

Type secondary degree SABFeatures of ECGP wave is lost, and the pause consequently follows itThe duration of the pause equals 2, 3, 4, times the normal PP cycleEscape beat or rhythm is common seen

Sick sinus syndromeFeatures of ECGSerious bradycardia (often

Sick sinus syndromeFeatures of ECGFrequent sinus arrest or exit block with slow HRBoth of sinoatrial and AV node are diseased escape interval > 2s, or slow and persistent AF, or slow escape rhythm

Sick sinus syndromeEtiology Intrinsic sinus node itself is involved, e.g. ischemia, regressive degeneration, infiltration of other cells or tissues Extrinsic high vagal tone, hyperkalemia, antiarrhythmics most frequent etiology are regressive degeneration and CHD

Sick sinus syndromeSymptoms Ischemia of brain, heart, kidneyAdams-Stokes syndromeDiagnosis Typical ECG patternsSymptoms is related with ECG changingsHolter, provoking test, treadmill and finally electrophysiological study for the suspected. Holter is most valuable

Management of Sick sinus syndromeNo specific drugs, or symptomatic treatment Ultimately, Permanent pacemaker is last choice of therapy

Indication of implantation of permanent pacemaker in SSSSymptoms caused by SSS, such as syncope, heart failure, etc.Brady-tachy syndrome with or without long pause, in which therapy of rapid arrhythmias is at risk to induce serious bradycartdiasLong pause >4s or sinus node recover time >3.5s

Atrial arrhythmias

Premature atrial contractionFeatures of ECGPremature P wave followed by near QRS complexQRS complex is similar to it from sinus node one with incomplete compensatory pause Sometimes, PR interval is prolonged, Premature P wave not conduct to the ventricles, or aberration in ventricle, full compensatory pause can be seen

Premature atrial contractionClinical features Common seen, provoked by variety of factors, e.g. infection, inflammation, ischemia, tobacco, alcohol etc. it is more common in the elderlySymptom is related to prolonged compensatory pause, increased contraction, frequent PAC and sensitivity of patientsOn auscultation, irregular beating, longer interval, increased S1Treatment aim for etiology except obvious symptom

Automatic atrial tachycardiaFeatures Less common. Most have underlying diseases,HR is around 130 bpm, >200 bpm less seenP wave is not as same as sinus one, PR interval changing with slightly irregular rhythmWarm-up can be seen at its initial attackTherapy aim to factors caused, RF also play role

chaotic atrial tachycardiaFeatures Rare, most having basic diseaseHR is between 100-130 bpm, at lest two kind P Wave seenPR and PP interval are changing, P not conducting sometimes, isoelectrical line between PP interval can be seen, precursor of atrial fibrillationTreating etiologiesmedication refer to STV with caution

Atrial flutter(AFL)Features of ECGP wave disappears, substituted by regular saw-like F wave with its rate being between 220350 bpmVentricular response(AV ratio) is usually 2:1, sometimes 4:1 or irregularStimulation of vagus nerve or exercise may decrease or increase AV ratio in multiplication

Atrial flutter(AFL) Clinical featuresHR is usually around 150 bpm which represents AV ratio is 2:1may having underlying diseasesTiny and rapid jugular pulses can be seen with its rate beyond 300 bpmSimilar manifestation to it in atrial fibrillation(AF)DC cardioversion is the best choice for ceasing it, refractory one need controlled rate with drugs, e.g. amiodarone

Atrial fibrillation(AF)Features of ECGNo P wave, replaced by rapid, chaotic and tiny atrial beating with its rate in 350600 bpmVentricle response is irregularly irregular with normal QRS complex, but individual QRS complex may slightly different

Atrial fibrillation Clinical featuresVery common with underlying diseases in majority cases. There are characteristics of three P in clinical, i.e. paroxysmal, persistent and permanent AF Symptoms severity depends on whether HR is too fast , or AF duration too long, or underlying heart disease too severe

Atrial fibrillationPredisposed to have thrombus and sequent embolism May have long cardiac arrest after AF stops, which could induce cerebral ischemia With stethoscope, palpating artery pulse and watching jugular pulse, near all most of AF can be diagnosed surely

Management of AFTerminating AF or keeping sinus rhythmDC cardioversionmedicationamiodarone, properfenone, sotalol, disropyramide, quinidine, etc. success rate is about 50%Controlling or lowing HR same above plus calcium antagonist, blocker, digitalis, etc.

Management of AFPreventing AF recurrent medication amiodarone, properfenone, sotalol, disropyramide, quinidine, etc.Surgical intervention or catheter ablationPacemaker, including ICDPreventing embolism eventsAnticoagulation Anti-platelet

Management of AFChronic atrial fibrillationRestoring sinus rhythm as far as possible if patient condition is availableControlling HR and preventing embolism if can not restore sinus rhythm Methods of cardioversionFirst choice: DC cardioversion with >90% successmedication: amiodarone, properfenone, sotalol, disropyramide, quinidine

Indication of chronic AF cardioversionDuration of chronic AF less than 6 monthsAF is in the early stage Still persistent AF after surgical or catheter intervention 2 weeks laterNo disadvantage factors of restoring AF, such as EF less than 0.4 or 0.3, left atrium more than 60mm in diameter, possible thrombus in the atrium, etc.

Indication of chronic AF cardioversionAF secondary to diseases which have been already cured or controlledRapid ventricle respond at AF can not be diminished with antiarrhythmicsAF recurred, which were restored and can keep sinus rhythm for 36 months

Junctional arrhythmias

Junctional premature contractionFeatures of ECGPremature retrograde P wave(may not seen)The P usually in front of QRS complex ( may follows QRS one), PR

Junctional premature contraction Clinical features Rather common. Most occurred with organic heart diseaseSimilar findings to atrial one on auscultationSymptom is similar to that of atrial onesTreatment is not necessary unless obvious symptom

Nonparoxysmal junctional tachycardiaFeatures Less common. Most have underlying diseases, digitalis side effect Attack gradually, AV dissociation common, QRS complex usually normalHR between 70-130 bpm, hemodynamics relatively changing less Main therapy is for causes, antiarrhythmics is not emphaized

Supraventricular paroxysmal tachycardiaFeatures of ECGHR between 160250bpm, absolute regular, QRS complex narrowing (exception of aberration)Occasionally, retrograde P wave seenReentry(AV node, AV) is majority of mechanism

Supraventricular paroxysmal tachycardia Clinical featuresMost without organic heart disease, common seenAttack with sudden initiation and termination, maintaining short for minutes or long for hours. Palpation is mainstream of symptomHypotension, collapse is far less than VT Good reaction to treatment, e.g. vagal maneuvers, antiarrhythmics. Radiofrequace can cure them

Managements of SVTVagal maneuversCarotid sinus massage, pressing eye ball, Valsalva maneuver.Medication Adenosine, calcium antagnist, properfenone and other antiarrhythmics, digitalis, -blocker, pressor drugsDirect current cardioversionRadiofrequence

Pre-excitation or Wolf-Parkinson-white(WPW) syndromeFeatures of ECGPR interval < 0.12 s or normal, wave in onset of QRS complex which result in widened QRS complex followed by secondary ST-TchangePR interval is

Features of Preexcitation syndrome P-R=0.12s, wave Secondary ST-T change STV often seen

Preexcitation syndromeClnical featuresPart of patients have onset of SVT, AF, AFL, its mechanism is reentryThere are several types of preexcitation, e.g. persist, intermittent, latent, concealedIt is predisposed to sudden death if refractory period of accessory pathway is

Ventricular arrhythmias

Ventricular premature contractionFeatures of ECGPremature QRS complex with no preceding related P wave QRS complex is bizarre in shape with full compensatory pause( insert one exception)AV dissociation can be seen

Ventricular premature contraction Clinical featuresMost common. Seen at organic heart diseases, some of it in AMI or myocardiopathy can induce fatal arrhythmiaSimilar features to other premature complex on auscultation.Palpitation is a common complainTreatment regimen on basis of clinical manifestation

Ventricular paroxysmal tachycardiaFeatures of ECGHR between 150200 bpmregular rhythmQRS complex bizarre and widenAV dissociation, ventricular fusion and capture

Ventricular paroxysmal tachycardiaClinical features Often with organic diseases, inducing hemodynamics deterioration causing remarkable symptomsBoth sustained and non-sustained VT seen in clinical It should be stopped as soon as possible(with antiarrhythmics or DC cardioversion)Varapamil, adenosine, -blocker are effective for some specific VT

Torsade de pointes(TDP)Features Congenital (recurrent syncope, deafness, long QT, i.e long QT syndrome)Acquired (drugs e.g. quinidine, electrolyte disturbance, high degree AVB, etc.), at least 80% is acquired in clinicalLong QT is common, often VPC at late diastole inducing TDPTDP displays as peak of QRS complex reverses along isoelectric line, causing patients syncopeTDP, most of it, terminating spontaneously with several sec.

Torsade de pointes(TDP)Treatment During attack Increasing HRatropine, pacing, isoproterenol Infusion of magnesium, potassium, lidocaine useful only in a few patients During reliefe-blocker, calcium antagonist, antiepileptic drugsLeft side cervicothoracic symppathetic ganglionectomy or implantation of cardioverter-defibrillator in some refractory cases

Accelerated idoventricular rhythmFeatures Common in AMI, myocarditis, digitalis intoxication HR between 60120bpm, regular, QRS complex bizarreBoth onset and ceasing are gradualMild effect on hemodynamics changingAim for causes, caution to using antagonist

Heart blocking

atrioventricular block AVBClassification Acute and chronic AVBThe acute is mainly due to myocarditis, AMI, electrolyte abnormality and some drugs impactThe chronic is mainly caused by regressive degenerative fibrosis or a consequence of the acute one

1st degree AVBFeatures of ECG PR interval > 0.20s in adults or > 0.18s in children Most of it is in 0.210.35s

2nd typeAVB(Wenchebach block)Features of ECGProgressive PR interval prolongation occurs, resulting in a nonconduction P wave( the pause), the duration of the pause is < two basic RR cyclesRR interval progressively shortensFirst PR interval after the pause is shortest, AV conduction ratios usually are 3:2 or 4:3

2nd type AVBFeatures of ECG PR interval is usually normal and no changeP wave do not conduct suddenly or periodically, making the long pauseThe long pause is multiples of basic cycles

3rd degree AVBFeatures of ECGAV conduction fails completely with AV dissociationVentricular activity is maintained by an escape rhythm arising from site distal to His bunduleAtrial rate > ventricular rateQRS complex is broad if pace site distal to His, otherwise it is nearly normalAdvanced AVB refer to that only a few P wave conducts to the ventricles, getting its same clinical significant as it in III AVB

Features of AVB first degree AVBSeen at inflammation(myocarditis, AMI), drugs, trauma, fibrosis, increased vagus tone, etc.No symptoms

Manifestation of AVB Second degree typeAVBSeen at high vagal tone, drugs myocarditis, AMI, etc.No remarkable hemodynamics change, may have wild symptomsA few cases may progress worse into severe AVB

Manifestation of AVBSecond degree type II AVBAlmost has underlying heart diseasesHR is slow and sometimes unstableThose whose blocking level is distal to His bundle are predisposed to progress into third AVBSymptoms are prominent

Manifestation of AVBThird degree AVBAlmost has underlying heart diseasesHR is slow and unstableThose whose blocking level is distal to His bundle are predisposed to turn into cardiac asystole or TDP, which could cause recurrent syncope or Adams-Stokes syndrome

Manifestation of AVBThird degree AVBOn auscultation, intensity of S1 varies due to loss of AV synchrony, cannon sound(wave), S3S4 can be heardSyncope, presyncope, chest compression heart failure, etc. are seen frequently. With high risk of sudden death

Management of AVBFirst or second degree type I AVBAim for etiology and symptoms, follow up AV conduction changing Second degree type AVBAim for etiology and symptoms, close investigation of clinical manifestationPatients with symptomatic bradyarrhythmia should receive a permanent pacemaker

Management of AVBThird degree AVBThere is evidence that pacing can improve prognosis in these patient no matter symptomatic or asymptomatic, in acute stage, temporary pacemaker, chronic permanent

Bundle branch block(BBB)Right BBB(complete, incomplete)Left BBB (complete, incomplete)Left anterior fascicular blockRBBB plus Left anterior fascicular blockIntraventricular block(nonspecific intraventricular conduction defect)Left posterior fascicular block

Right bundle branch blockFeatures of ECGDuration of QRS complex >0.12sVAT(ventricle activity time) at right precordial leads >0.07sQRS complex in lead V1 is in pattern of rSR`in V5 with a blunt, prolonged and shallow S wave, with secondary ST-T changingQRS complex measured is

Left t bundle branch blockFeatures of ECGDuration of QRS complex >0.12sVAT(ventricle activity time) at left precordial leads >0.07sQRS complex in lead V1 is in pattern of rSin V5 is a high, blunt, widen R wave, with secondary ST-T changingQRS complex measured is

Left anterior fascicular blockFeatures of ECG QRS complex is in pattern of qR or R in lead , aVL , and rS in lead , aVFQRS axis is left deviation, >-45 degreeQRS complex widens slightly

Left posterior fascicular block Features of ECG QRS complex is in pattern of rS in lead , aVL , and qR in lead , aVFQRS axis is rignt deviation, >+110 degreeQRS complex widens slightlyRare in clinical

Bilateral bundle branch blockFrequent combinatonRBBB and left anterior divisional blockBundle branch block alternant Bundle branch block with prolongation of PR interval

Intraventricular blockFeatures of ECGQRS complex widen, often >0.12s, however no characteristic patter of either RBBB or LBBB or other divisional block could be seen

Clinical significance of BBBBBB per se have no significant effect on hemadynamicsBBB may not deteriorate at long term follow-up in patients who have no underlying heart diseasesNew BBB in AMI or myocarditis signifies clinical deterioration

Clinical significance of BBBMost of bilateral BBB will develop complete heart blockNo particular treatment unless there is indication of pacing

Management of arrhythmias MedicationNon medicationCatheter based Ablation(electric, radiofrequecy, cryoablation, chemoablation)Programmed electric stimulation

Management of arrhythmiasNon medicationpacemakerFor bradycardiaFor tachycardiaSurgical operationCut off, excision, Fox operation, CABG, etc. othersDC cardioversion, stimulation of vagus nerve, transesophageal pacing

Strategy Evaluating risk of arrhythmiasDeciding to Treating it or not Which therapy should be chosenWhat is the endpoint of therapy

Evaluation of risk Recognition of malignant arrhythmiasVentricular flutter or fibrillationSustained or non sustained VTAdvanced or complete AVB

Evaluation of riskRecognition of malignant arrhythmiasAF or AFL with rapid ventricle response VPC are Multilocal, polymorphic, couplet, triplet and R on TSevere SSS

Evaluation of riskSerious heart diseasesAMIserious myocarditis, myocardiopathy, hear failure, taking digitalis Hemodynamics unstableBlood pressure decrease, shock, heart failure or heart failure deterioration when on onset of arrhythmias

Evaluation of riskLife quality is decreased, which is caused by arrhythmias

Suggest worse prognosis when the arrhythmia

Attitude of mamagementEmergency Urgent activePalliative

Emergency treatmentFatal arrhythmiasSustained VT, VFL, VFExtremely slow and unstable bradycardia, asystole will happen at any timeHemodynamics deterioration or shockVT, rapid AF or AFL, extreme and/or bradycardias, etc.

Urgent mamagementWith serious heart diseases(myocarditis, myocardiopathy)With acute coronary ischemiaWith remarkable depressed cardiac function or decompensate heart failureOn digitalisAbnormality of acid, basic , electrolyte balance

Active treatmentToo much complain, life quality decrease, may induce complication, but relatively normal heartSuch as frequent premature contraction, AF, SVT

palliate treatmentAsymptomatic arrhythmias with normal or relatively normal heart

Principles of managementAim for removal of provocative factorsCorrection of anoxia, ischemia, disturbance of elctrolyte, acid and basic Control of heart failure, infection, inflammation, diminishing side-effects of drugs relevant to arrhythmias

Principle of managementMedication IV administration in emergencyCombination of antiarrhythmics in necessary, in which effect would be good but possible side effects also increaseType Ia is not used with type Ib, if so, side effects may increase dramatically

Principle of managementNon medicationDC cardioversion, pacing are usually used in emergency or urgentPacemaker, RF, surgical operation are used in cases who have no or little response or tolerance to medical treatment

Endpoint of managementElimination of malignant arrhythmiasElimination of symptomatic arrhythmiasrelieve symptomsPrevention of recurrent rrhythmias

Classification of antiarrhythmic drugs( Vaughan-Willianms)Class I : inhibiter of fast sodium channelClass Ia: in addition prolong refractoriness, QT interval, e.g. quinidine, procainamide, disopyramideClass Ib: less potent inhibiting Na channel, shorten AP, e.g. lidocaine, mexiletineClass Ic: potent Na channel inhibiter with no effect on AP, e.g. propafenone, flecainide, ethmosine

Classification of antiarrhythmicClass II : -adrenoceptor antagnistPropranolol, metroprolol, atenolol, l-sotalolClass III: inhibitor of potassium channel with prolaongation of AP, e.g. amiodarone, d-sotalol, ibutilide, dofetilideClass IV: slow calcium channel antagonist, e.g. varapamil, diltiazemOthers:adenosine, digitalis glycosides