内科学心律失常课件.ppt

Arrhythmia,Zhu wen- qing,Dep. Of Cardiology, Zhong-Shan Hospital, Fu Dan University. Shanghai. China.,ArrhythmiaZhu wen- qingDep.,Conduction and anatomy of heart,Conduction and anatomy of hear,Conduction system,Conduction system,Stable SVT is generally well tolerated in patients without underlying heart disease!?but may lead to myocardial ischemia or congestive heart failure in patients with coronary disease, valvular abnormalities, and systolic or diastolic myocardial dysfunction. Ventricular tachycardia, if lasting 1030 secs, often results in hemodynamic compromise and is more likely to deteriorate into ventricular fibrillation.,RATE & RHYTHM,Stable SVT is generally well,RATE & RHYTHM,slow heart rates produce symptoms at rest or on exertion depends upon whether cerebral perfusion can be maintained, which is generally a function of whether the patient is upright or supine and whether left ventricular function is adequate to maintain stroke volume. If the heart rate abruptly slows, as with the onset of complete heart block or sinus arrest, syncope or convulsions may result.,RATE & RHYTHMslow heart rates,RATE & RHYTHM,Arrhythmias are detected either because they present with symptoms or detected during the course of monitoring. Arrhythmias causing sudden death, syncope, or near syncope require further evaluation and treatment unless they unlikely to recur (eg, electrolyte abnormalities or acute myocardial infarction).Controversy over when and how to evaluate and treat rhythm disturbances that are not symptomatic but are possible markers for more serious abnormalities ( eg, nonsustained ventricular tachycardia).,RATE & RHYTHMArrhythmias are d,MECHANISMS OF ARRHYTHMIAS,Electrophysiologic studies have greatly increased our understanding of the mechanisms underlying most arrhythmias. These include(1) disorders of impulse formation or automaticity(2) abnormalities of impulse conduction,(3) reentry, and (4) triggered activity. Altered automaticity is the mechanism for sinus node arrest, many premature beats, and automatic rhythms as well as an initiating factor in reentry, arrhythmias.,MECHANISMS OF ARRHYTHMIASElect,MECHANISMS OF ARRHYTHMIAS,Abnormalities of impulse conduction can occur at the sinus or atrioventricular node, in the intraventricular conduction system, and within the atria or ventricles. These are responsible for sinoatrial exit block, for atrioventricular block at the node or below, and for establishing reentry circuits.,MECHANISMS OF ARRHYTHMIASAbnor,MECHANISMS OF ARRHYTHMIAS,MECHANISMS OF ARRHYTHMIAS,MECHANISMS OF ARRHYTHMIAS,Triggered activity occurs when afterdepolarizations (abnormal electrical activity persisting after repelarization) reach the threshold level required to trigger a new depolarization. This may be the mechanism of ventricular tachycardia in the prolonged QT syndrome and in some cases of digitalis toxicity.,MECHANISMS OF ARRHYTHMIAS Trig,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Electrocardiographic MonitoringThe ideal way of establishin,g a causal relationship between a symptom and a rhythm disturbance is to demonstrate the presence of the rhythm during the symptom, Unfortunately, this is not always easy because symptoms are usually sporadic.,TECHNIQUES FOR EVALUATING,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Electrocardiographic MonitoringPatients with SD and recent or recurrent syncope are often monitored in the hospital. Outpatients. When episodes are infrequent, use of an event recorder is preferable to 24-hour continuous monitoring. Exercise testing may be helpful when the symptoms are associated with exertion or stress. Further electrophysielogic studies may be useful in evaluating ventricular tachyarrhythmias.,TECHNIQUES FOR EVALUATING,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Electrocardiographic Monitoring,TECHNIQUES FOR EVALUATING,Electrocardiographic Monitoring,Electrocardiographic Monitorin,Electrocardiographic Monitoring,Electrocardiographic Monitorin,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,ECG MonitoringIn many cases, symptoms are due to a different arrhythmia or to noncardiac causes. For instance, dizziness or syncope in older patients may be unrelated to concomitantly observed bradycardia, sinus node abnormalities, and ventricular ectopy. Ambulatory monitoring is frequently used to quantify ventricular ectopy and detect asymptomatic ventricular tachycardia in post-myocardial infarction or heart failure patients. Unfortunately, while asymptomatic ventricular arrhythmias have negative prognostic implications, there are few-data to support specific therapeutic intervention. Thus, monitoring in asymptomatic individuals is usually not indicated.,TECHNIQUES FOR EVALUATING,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Heart rate Variablityseveral studies have indicated that greater heart rate variability is associaled with a better prognosis and fewer life threatening arrhythmias in a variety of cardiac conditions.RR cycle length variability to provide indices of the relative balance between parasympathetic and sympathetic activity, with being considered to confer a better prognosis. postinfarction and patients with symptomatic arrhythmias, these Indices have had some prognostic value. However, adequate data are not yet available to support routine use of this technique in clinical practice.,TECHNIQUES FOR EVALUATING,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Signal-Averaged ECGSignal averaged ECG is new technique . To record 300 consecutive beats during basal conditions, Using appropriate electrical filtering and computer averaging of the signal, very law frequency signals called late potentials can be identified in the period following the QRS complex. Abnormal late potentials are considered markers for potential Ventricular Arrhythmia,TECHNIQUES FOR EVALUATING,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Electrophysiology Test Evaluation of recurrent syncope of possible cardiac origin, when the ambulatory ECG has not provided the diagnosis; Differentiation of SVT from VA; Evaluation of therapy in patients with accessory atrioventricular pathways; Evaluation of the efficacy of pharmacotherapy in survivors of sudden death or other patients with symptomatic or life threatening VT; Evaluation of patients for catheter ablation procedures or antitachycardia devices.,TECHNIQUES FOR EVALUATING,Autonomic Testing ( Tilt Table Testing )with recurrent syncope or near Syncope, arrhythmias are no cause. This is particularly true when the patient has no evidence of associated heart disease by history, examination, ECG, or noninvasive testing. Syncope may be neurocardiogenic in origin, mediated by excessive vagal stimulation or an imbalance between sympathetic and parasympathetic autonomic activity.,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Autonomic Testing ( Tilt Tabl,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,Autonomic Testing ( Tilt Table Testing ),60 - 80,TECHNIQUES FOR EVALUATING,TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES,TECHNIQUES FOR EVALUATING,Antiarrhythmia drug,Antiarrhythmic drugs have limited efficacy and frequent side effects. They are often divided into four classes.Class I agents block membrane sodium channels. Three subclasses are further defined by the effect of agents on the Purkinje fiber action potential Class la drugs slow the rate of rise of the action potential (Vmax) and prolong its duration, thus slowing conduction and increasing refractorineas. Class lb agents shorten action potential duration, they do not affect conduction or refractoriness. Class Ic agents prolong Vmax and slow repolarization, thus slowing conduction and prolonging refractoriness, but more so than class la drugs,Antiarrhythmia drugAntiarrhyth,Antiarrhythmia drug,Class II agents -beta-blockersDecrease automaticity, Prolong AV conduction,Prolong refractoriness.,Antiarrhythmia drugClass II ag,Antiarrhythmia drug,Class III agents Block potassium channels Prolong repolarization, widening the QRS and prolonging the QT interval. Decrease automaticity and conduction and prolong refractoriness.,Antiarrhythmia drugClass III a,Antiarrhythmia drug,Class IV agents - slow calcium channel blockers Decrease automaticity andAtrioventricular conduction,Antiarrhythmia drugClass IV ag,Drugs,DrugsWilliams分类法：I：II：III：IV：A,Antiarrhythmia drug-Risk,The risk of antiarrhythmic agents has been highlighted by the Coronary Arrhythmia Suppression Trial (CAST). Two class Ic agents (flecainide, encairfide) and a clam la agent (moficizine) increased mortality rates in patients with asymptonlatic ventricular ectapy after myocardial infarction. Therefore, these agents (any antiarrhythmic drug) should not be used except for life-threatening ventricular arrhythmias and symptomatic supraventricular tachyarrhythmias.,Antiarrhythmia drug-RiskThe r,Radiofrequency Ablation,Ablation has become the primary modality of therapy for many symptomatic SVTIncluding AVNRTAVRT -involving accessory pathways, paroxysmal atrial tachycardia, inappropriate sinus tachycardia, junctional tachycardia, Many laboratories have achieved reasonable success rates in preventing atrial flutter with rediofrequency techniques, and experience with atrial fibrillation is accumlating as well.,Radiofrequency AblationAblatio,Radiofrequency Ablation,Catheter ablation of VA has proved more difficult. Three specilic forms of VA proved to be amenable to radiofrequeney ablation. bundle branch reentry,VT originating in right ventricuiar outflow tract, VT originating in the left side of the interventricular septum. Other forms of VT, may be amenable to ablation, but experience thus far is limited.,Radiofrequency AblationCathete,Radiofrequency Ablation,In addition, some procedures involve transseptal or retrograde left ventricular catheterization, with the attendant potential complications of aortic perforation, damage to the heart valves, or left-sided emboli. These procedures are generally safe, though there is a low incidence of perforation of the atria or right ventricle that results in pericardial tamponade and sufficient damage to the atriovantricular node to require permanent cardiac pacing.,Radiofrequency AblationIn addi,内科学-心律失常课件,内科学-心律失常课件,内科学-心律失常课件,AVRT ablation,AVRT ablation,内科学-心律失常课件,AVNRT Ablation,AVNRT Ablation,Atrial tachycardia-ablation,Atrial tachycardia-ablation,Atrial fibrillation accounts for 1/3 of all patient discharges with arrhythmia as principal diagnosis.,2% VF,Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.,34% Atrial Fibrillation,18% Unspecified,6% PSVT,6% PVCs,4% Atrial Flutter,9% SSS,8% Conduction Disease,3% SCD,10% VT,Atrial fibrillation accounts f,SUPRAVENTRICULAR ARRHYTHMIAS sinus bradycardia,Causes of Slow Rhythms:HypoxiaHyperkalemiaAcute MIHeart DiseaseIncreased parasympathetic toneDrug effects from narcotics, benzodiazepines, digoxin, beta blockers, propranolol, or calcium channel blockers,SUPRAVENTRICULAR ARRHYTHM,Sinus Bradycardia,Decrease in the rate of atrial depolarizationRhythm is regularRate 60P waves uniform and one in front of each QRS complexPR interval and QRS complex is normal,Sinus BradycardiaDecrease in t,Sinus Bradycardia,severe sinus bradycardia may be an indication of sinus node pathology especially in elderly patients and individuals with heart disease. It may cause weakness, confusion, or syncope if cerebral perfusion is impaired. Atrial and ventricular ectopic rhythms are more apt to occur with slow sinus rates. Pacing may be required if symptoms correlate with the bradycardia.,Sinus Bradycardiasevere sinus,Sinus Bradycardia,Treatment:If accompanied by hypotension, syncope or light headedness:Stop procedureAtropine IVTranscutaneous pacingdopamine, epinephrine and transvenous pacemaker,Sinus BradycardiaTreatment:,Fast Rhythms:Sinus Tachycardia and Supraventricular Tachycardia,Causes:HypoxiaEmotional and physical stresscaffeine, smokingexercisefatiguealcoholpaininfectioncardiomyopathy,Fast Rhythms:Sinus Tachycardi,Sinus Tachycardia,Sinus node is still the pacemaker, but the rate is acceleratedRhythm is regularRate 100 beats/minP wave, PR interval, and QRS complex are all normal,Sinus TachycardiaSinus node i,Sinus Tachycardia,Treatment:Alleviate the underlying causeinappropriate sinus tachycardia that may be very symptomatic or lead to LV contractile dysfunction. Radiofrequeney modification of the sinus node has mitigated this problem,Sinus TachycardiaTreatment:,ATRIAL PREMATURE BEATS,APB occur before the next sinus node impulse or a reentry_ circuit is established. P wave usually differs from the patients normal. R-R cycle length is usually unchanged or only slightly prolonged. premature beats occur in normal hearts and are never a sufficient basis heart disease. Speeding of the heart rate by any means usually abolishes most premature beats. Early APB may cause aberrant QRS complexes or may be nonconducted to the ventricles because the latter are still refractory.,ATRIAL PREMATURE BEATSAPB occu,Variability of Ventricular Ectopy with Age,Effect of age on probability (%) of having more than a given number ofPVCs per 24 hours in subjects with normal hearts.,10-29,30-39,40-49,50-59,60-69,Data from Kostis JB. Circulation. 1981;63(6):1353.,Age,Variability of Ventricular Ect,VENTRICULAR BEATS,Distinction can be very difficult in patients with a wide QRS; it is important because of the differing prognostic and therapeutic implications of each type. ventricular origin include atrioventricular dissociation; a QRS duration exceeding 0.14 s; capture or fusion beats (infrequent); left axis deviatinn with right bundle branch block morphology; monophasic (R) or biphasic (qR, QR., or RS) complexes in V1,; and (6) a qR or QS complex in V6.,VENTRICULAR BEATS Distinction,VENTRICULAR BEATS,Supraventricular origin is favorecl by a triphasic QRS complex, especially if there was initial negativity in leads I and V6; ventricular rates excceeding 170/min; QRS duration longer than 0.12 s but not longer than 0.14 s: the presence of preexcitation syndrome.,VENTRICULAR BEATSSupraventricu,A single irritable focus within the ventricle fires prematurely giving rise to an ectopic beat. QRS is wideIf every other beat is PVC ventricular bigeminyIf every third beat is a PVC ventricular trigeminyIf every fourth beat is PVC ventricular quadrigeminyA PVC that falls on the T wave precipitates VT or VF,VENTRICULAR BEATS,A single irritable focus withi,VENTRICULAR BEATS,Treatment: PVCs which need to be treated are:MultifocalOccur in coupletsFall on or after the T waveThat occur greater than 6 per minute,VENTRICULAR BEATSTreatment:,Premature Ventricular Contraction,Treatment Continued:In the setting of an acute MI, PVCs need to be aggressively treated with nitroglycerine, aspirin, morphine and oxygen. Lidocaine is the drug of choice to diminish PVCs, but does little to the underlying pathology.,Premature Ventricular Contract,SUPRAVENTRICULAR TACHYCARDIA,the commonest paroxysmal tachycardia and often occurs in patie