内科学课件：22 心律失常讲稿

1、Arrhythmia Dep. Of Cardiology, Zhong-Shan Hospital, Fu Dan University. Shanghai. China. Conduction and anatomy of heart Conduction system Heart Beat Anatomy Sinus Node (SA Node) The Hearts Natural Pacemaker - 60-100 BPM at rest SINUS NODE Sinus Node (SA Node) Heart Beat Anatomy AV NODE Sinus Node (S

2、A Node) Atrioventricular Node (AV Node) Receives impulse from SA Node Delivers impulse to the His- Purkinje System 40-60 BPM if SA Node fails to deliver an impulse Heart Beat Anatomy BUNDLE OF HIS Sinus Node (SA Node) Atrioventricular Node (AV Node) Bundle of His Begins conduction to the Ventricles

3、AV Junctional Tissue: 40-60 BPM Heart Beat Anatomy Atrioventricular Node (AV Node) Sinus Node (SA Node) Bundle of His Bundle Branches Purkinje Fibers Bundle Branches Purkinje Fibers Moves the impulse through the ventricles for contraction Provides Escape Rhythm: 20-40 BPM THE PURKINJE NETWORK Normal

4、 Sinus Rhythm Click heart to view animation * Animation Impulse Formation In SA Node Atrial Depolarization Delay At AV Node Conduction Through Bundle Branches Conduction Through Purkinje Fibers Ventricular Depolarization Plateau Phase of Repolarization Final Rapid (Phase 3) Repolarization Normal EKG

5、 Activation Reading EKGs Normal Ranges in Milliseconds: PR Interval 120 200 ms QRS Complex 60 100 ms QT Interval 360 440 ms Intervals and Timing Reading EKG Squares 4Each square = 40 ms 4Each interval = 200 ms Intervals and Timing Stable SVT is generally well tolerated in patients without underlying

6、 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 d

7、eteriorate into ventricular fibrillation. Symptom Sign (Fast) Symptom Sign (Slow) slow heart rates produce symptoms Aat 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 ventricula

8、r function is adequate to maintain stroke volume. A If the heart rate abruptly slows, as with the onset of complete heart block or sinus arrest, syncope or convulsions may result. Symptom Sign 4Arrhythmias are detected either because they present with symptoms or detected during the course of monito

9、ring. 4Arrhythmias causing sudden death, syncope, or near syncope require further evaluation and treatment unless they unlikely to recur (eg, electrolyte abnormalities or acute myocardial infarction. 4Controversy over when and how to evaluate and treat rhythm disturbances that are not symptomatic bu

10、t are possible markers for more serious abnormalities ( eg, nonsustained ventricular tachycardia). MECHANISMS OF ARRHYTHMIAS uElectrophysiologic studies have greatly increased our understanding of the mechanisms underlying most arrhythmias. These include udisorders of impulse formation uabnormal of

11、impulse conduction (reentry and triggered activity). uAltered automatlcity is the mechanism for sinus node arrest, many premature beats, and automatic rhythms as well as an initiating factor in reentry, arrhythmias. Abnormally Slow = Bradycardia 4Failure due to disease Excessively Rapid = Tachycardi

12、a 4Due to sympathetic nervous system Mechanisms of Rhythm Disorders Abnormal impulse Phase 1 Early rapid repolarization with transient onward movement of potassium ions 4Phase 0 Rapid upstroke depolarization with an influx of sodium ions into the cell 4Phase 2 Plateau Phase: Continued Influx of Sodi

13、um Differentiation of SVT from VA; Evaluation of therapy in patients with accessory atrioventricular pathways; E v a l u a t i o n o f t h e e f f i c a c y o f pharmacotherapy in survivors of sudden death or other patients with symptomatic or life threatening VT; Evaluation of patients for catheter

14、 ablation procedures or antitachycardia devices. 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. Syn

15、cope may be neurocardiogemc in origin, mediated by excessive vagal stimulation or an imbalance between sympathetic and parasympathetic autonomic activity. Techniques for Evaluating Rhythm Techniques for Evaluating Rhythm 4Autonomic Testing ( Tilt Table Testing ) 60 - 80 Techniques for Evaluating Rhy

16、thm Antiarrhythmia Drug MAntiarrhythmic drugs have limited efficacy and frequent side effects They are often divided into four classes. MClass I agents block membrane sodium channels. Three subclasses are further defined by the effect of agents on the Purkinje fiber action potential Antiarrhythmia D

17、rug MClass la drugs Slow the rate of rise of Action Potential (Vmax) Prolong its duration, Slowing conduction Increasing refractorineas. Antiarrhythmia Drug MClass lb agents Shorten action potential duration Not affect conduction or Refractoriness. Antiarrhythmia Drug MClass Ic agents Prolong Vmax a

18、nd Slow repolarization, thus Slowing conduction and Pprolonging refractoriness, (but more so than class la drugs) Antiarrhythmia drug 4Class II agents -beta-blockers Decrease automaticity, Prolong AV conduction, Prolong refractoriness. Antiarrhythmia drug Class III agents ABlock potassium channels A

19、Prolong repolarization, Widening the QRS and Prolonging the QT interval. Decrease automaticity and conduction and Prolong refractoriness. Antiarrhythmia drug Class IV agents - slow calcium channel blockers Decrease automaticity and Atrioventricular conduction Drugs WilliamsWilliams分类法：分类法： I：II：III：

20、IV： a：Quinidinec： Flecainide PropranololAmiodaroneVerapamil ProcainamideEncainideMetoprololSotalolDiltiazem Changrolin PropafenoneEsmololBretyliumBepridil b：Lidocaine Atenolol Mexiletine Tocainide Moricizine Phenytoin Antiarrhythmia drug-Risk 4The risk of antiarrhythmic agents has been highlighted b

21、y the Coronary Arrhythmia Suppression Trial (CAST). 4Two class Ic agents (flecainide, encairfide) and a clam la agent (moficizine) increased mortality rates in patients with asymptonlatic ventricular ectapy after myocardial infarction. 4Therefore, these agents (any antiarrhythmic drug) should not be

22、 used except for life- threatening ventricular arrhythmias and symptomatic supraventricular tachyarrhythmias. Radiofrequency Ablation 4Ablation has become the primary modality of therapy for many symptomatic SVT 4Including AVNRT 4AVRT -involving accessory pathways, paroxysmal atrial tachycardia, ina

23、ppropriate 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 Ablation 4Catheter ablation of VA has proved more

24、 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. 4Other forms of VT, may be amenable to ablation, but experience thus far

25、is limited. Radiofrequency Ablation 4In 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. 4These procedures are generally safe, though there

26、 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. AVRT ablation AVNRT Ablation Atrial tachycardia-ablation ARRY Ensite 3000 Atrial fibrillation accounts for

27、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 Causes of Rhythm Disorders Congenital Present at b

28、irth due to genetics, environment Heart Disease Myocardial Infarction, Cardiomyopathy, High Blood Pressure Chemically Induced 4Diet Pills, Cold Medicine, Illegal Drugs, Caffeine, Tobacco, Alcohol Causes of Rhythm Disorders Secondary to other conditions 4Hyper-Thyroid 4Neurocardiogenic Syncope - Hype

29、rsensitive Carotid Sinus Syndrome (CSS) - Vasovagal Syncope (VS) SUPRAVENTRICULAR ARRHYTHMIAS sinus bradycardia 4Causes of Slow Rhythms: Hypoxia Hyperkalemia Acute MI Heart Disease Increased parasympathetic tone Drug effects from narcotics, benzodiazepines, digoxin, beta blockers, propranolol, or ca

30、lcium channel blockers Sinus Bradycardia 4severe sinus bradycardia may be an indication of sinus node pathology especially in elderly patients and individuals with heart disease. 4It may cause weakness, confusion, or syncope if cerebral perfusion is impaired. 4Atrial and ventricular ectopic rhythms

31、are more apt to occur with slow sinus rates. 4Pacing may be required if symptoms correlate with the bradycardia. Sinus Bradycardia (1) Sinus rhythm ;Rhythm is regular (2) Heart rate 1.0 sec ) P waves uniform and one in front of each QRS complex PR interval and QRS complex is normal Sinus Bradycardia

32、 Sinus Bradycardia Sinus Bradycardia Sinus arrhythmia 4 Sinus rhythm and PR interval, 4 Difference of P-P interval 0.12sec in the same lead Sinus arrhythmia sinus arrest Sinus arrest The P wave missed for a short time Sinus Bradycardia Treatment: If accompanied by hypotension, syncope or light heade

33、dness: Stop procedure Atropine IV Transcutaneous pacing dopamine, epinephrine and transvenous pacemaker Fast Rhythms: Sinus Tachycardia and Supraventricular Tachycardia A Causes: AHypoxia AEmotional and physical stress Acaffeine, smoking Aexercise Afatigue Aalcohol Apain Ainfection Acardiomyopathy S

34、inus Tachycardia Sinus node is still the pacemaker, but the rate is accelerated Rhythm is regular Rate 100 beats/min P wave, PR interval, and QRS complex are all normal Sinus rhythm features : (1) Every P wave is following by a QRS complex; (2) P wave is upright in lead I, II, aVF, V4-V6, inverse in

35、 aVR; (3) P-R interval 0.12sec; (4) Normal rate is 60-100 beats/min Sinus Tachycardia (1) Sinus rhythm, rate 100 bpm The R-R interval (or the P-P interval) 0.12s. (3) There may be a noncompensatory pause. Premature Beats Premature Atrial Contraction (PAC) Origin:Atrium (outside the Sinus Node) Mecha

36、nism:Abnormal Automaticity Characteristics: An abnormal P-wave occurring earlier than expected, followed by compensatory pause Atrial Premature Contractions Atrial Premature Contractions Atrial Premature Contractions Atrial Premature Beats 4Treatment 4Ia Drug; /Ic; / II; /III; /IV Premature junction

37、al contraction (1)A premature normal-appearing QRS complex. (2)The junctional P wave (P) may be appear before, in, and after the QRS. (3)Usually a complete compensatory pause. Premature Junctional Contraction Origin:AV Node Junction Mechanism:Abnormal Automaticity Characteristics:A normally conducte

38、d complex with an absent p-wave, followed by a compensatory pause Premature Beats Junctional Premature Beats 4Treatment 4Ia Drug; /Ic; / II; /III; /IV Variability of Ventricular Ectopy with Age 4Effect of age on probability (%) of having more than agiven number of PVCs per 24 hours in subjects with

39、normal hearts.10-29 30-39 40-49 50-59 60-69 Data from Kostis JB. Circulation. 1981;63(6):1353. Age VENTRICULAR BEATS 4Distinction 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 inclu

40、de 4 atrioventricular dissociation; 4 a QRS duration exceeding 0.14 s; 4capture or fusion beats (infrequent); 4 left axis deviatinn with right bundle branch block morphology; 4 monophasic (R) or biphasic (qR, QR., or RS) complexes in V1,; and (6) a qR or QS complex in V6. Premature Ventricular Contr

41、actions (PVCs) Origin:Ventricles Mechanism: Abnormal Automaticity Characteristics: A broad complex occurring earlier than expected, followed by a compensatory pause Premature Beats PVC Patterns Bigeminy -Every other beat Trigeminy -Every third beat Quadrigeminy -Every fourth beat Origin:Varies withi

42、n the Ventricle Mechanism: Abnormal Automaticity Characteristics: Each premature beat changes axis; implies a different focus origin for each beat Multifocal PVC VENTRICULAR BEATS Treatment: 4PVCs which be treated are: Multifocal Occur in couplets Fall on or after the T wave(R on T) That occur great

43、er than 6 per minute Premature Ventricular Contraction 4Treatment 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. SUPRAVENT

44、RICULAR TACHYCARDIA 4the commonest paroxysmal tachycardia and often occurs in patients without structural heart disease. 4Attacks begin and end abruptly and may last a few ,seconds to several hours or longer. 4Hr may be 140-240/mia (usually 160-220/min) and is perfectly regular (despite exercise or

45、change in position). 4P wave usually differs in contour from shins beats. 4Asymptomatic, but some experience mild chest pain or shormess of breath, especially when episodes are prolonged, even in the absence of associated cardiac abnormalities. 4PSVT may result from digitalis toxicity and then is co

46、mmonly associated with atrioventricular block. Accelerated Idio-Junctional Rhythm Origin:AV Node or Junctional Tissue Mechanism: Abnormal Automaticity Characteristics: Occurs when cells depolarize at a rate faster than the Sinus Node 4Paroxysmal Ectopic focus, sudden onset, abrupt cessation 4Sustain

47、ed Duration of 30 seconds Requires intervention to terminate 4Non-Sustained At least 6 beats or 100 BPM Mechanism: Abnormal Automaticity ATRIAL TACHYCARDIA ATRIAL TACHYCARDIA 房性心动过速房性心动过速（Ablation） 房性心动过速房性心动过速（Ablation） 房性心动过速房性心动过速（Ablation） 房性心动过速房性心动过速（Ablation） VENTRICULAR ARRHYTHMIAS -VENTRICU

48、LAR PREMATURE BEAT 4Diagnosis: ECG/ Ambulatory monitoring 4Treatment: Drugs / Ablation 4If no associated cardiac disease is present and asymptomatic, no therapy is indicated. 4 may exacerbate serious arrhythmias in 520% of patients. Therefore, to avoid using class I or III antiarrhythmic agents in p

49、atients without symptoms. VENTRICULAR ARRHYTHMIAS - VENTRICULAR TACHYCARDIA 4VT is defined as three or more consecutive ventricular premature beats. The usual rate is 160- 140/mm and is moderately regular but less so than atrial tachycardia. 4Diagnosis: ECG / Monitor / EPS VENTRICULAR ARRHYTHMIAS -V

50、T 4VT causes hypotension,heart failure, or myocardial ischemia,synchronized DC cardioversion with 100-360 J should be performed immediately. 4Patientis stable IV lidocaine / procainamide/ amiodarone. 4VT aim be terminated and Prevent recurrent. Ventricular tachycardia 4Origin: Ventricles (Single Foc

51、us) 4Mechanism:Reentry Initiated by abnormal Automaticity or Triggered activity 4Characteristics:Rapid, wide, and regular QRS EKG Characteristics Monomorphic VT * Animation 4Origin: Ventricles (Wandering Single Focus) 4Mechanism:Reentry with movement in the circuit Initiated by Abnormal Automaticity

52、 or Triggered activity 4Characteristics:Wide and irregular QRS Complex that changes in axis Polymorphic VT * Animation Origin:Ventricle Mechanism:Reentry (movement in focus) Rate: 200 250 BPM Characteristics: Associated with Long QT interval; QRS changes axis this phenomenon is almost always due to

53、abnormal conduction within the atrioventricularnode. Mabitz type II 4Third degree (complete heart block, in which no supraventricular impulses are conducted to tile ventricles). His bundle system. First Degree A-V Block 4Prolonged P-R interval: P-R interval 0.20sec. in adults (varies with heart rate

54、) First Degree A-V Block First-Degree AV Block 4PR interval 200 ms 4Delayed conduction through the AV Node - Example shows PR Interval = 320 ms 4Progressive prolongation of the PR interval until there is failure to conduct and a ventricular beat is dropped Known as Wenckebach Block Second-Degree AV

55、Block - Mobitz I * Animation Second Degree A-V Block (Morbiz I)Morbiz I) 4Regularly dropped ventricular beats Ex: 2:1 block (2 P-waves to 1 QRS complex) Atrial rate = 75 BPM Ventricular rate = 42 BPM Second-Degree AV Block Mobitz II Mobitz type II Third Degree A-V Block (Complete heart block) Third Degree A-V Block (Complete