医学精品课件：心律失常课件英文班

1、Cardiac Arrhythmia,INTRODUCTION,Arrhythmia: abnormalities of cardiac rhythm and conduction Arrhythmias can be lethal (sudden cardiac death ) , symptomatic ( syncope , near syncope dizziness , or palpitations ) , or asymptomatic . They are dangerous to the extent that they reduce cardiac output , so

2、that perfusion of the brain or myocardium is impaired , or tend to deteriorate into more serious arrhythmias with the same consequences,Anatomy of cardiac conduction system,Category of Arrhythmia,Abnormalities of impulses generating Abnormalities of impulses conduction,Abnormalities of impulses gene

3、rating,Sinus arrhythmias: sinus bradycardia, sinus tachycardia, sinus arrest,Abnormalities of impulses generating,Ectopic rhythm: 1.Passive abnormalrhythm: escape beat, escape rhythm (atrial, AV junctional, ventricular) 2.Initiative abnormal rhythm: premature beat(atrial, AV junctional, ventricular)

4、 paroxysmal tachycardia(atrial, AV junctional,ventricular) atrial flutter, atrial fibrillation ventricular flutter, ventricular fibrillation,Abnormalities of impulses conduction,1.physiologic 2.pathologic: sinoatrial block, intra-atrial block, atrial ventricular block, bundle branch block, intra-ven

5、tricular block. 3.abnormal pathway conduction: preexcitation syndrome,MECHANISMS OF ARRHYTHMIAS,Most arrhythmias can be classified as (1) disorders of impulse formation or automaticity (2) abnormalities of impulse conduction (3) reentry (4) triggered activity,Altered automaticity is the mechanism fo

6、r sinus node arrest , many premature beats , and automatic rhythms as well as an initiating factor in reentry 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

7、 responsible for sinoatrial exit block at the node or below , and for establishing reentry circuits,Reentry is the underling mechanism for many arrhythmias , including premature beats , most paroxysmal supraventricular tachycardias , and atrial flutter . For reentry to occur , there must be an area

8、of unidirectional block with an appropriate delay to allow repeat depolarization at the site of origin . Triggered activity occurs when afterdepolarizations ( abnormal electrical persisting after repolarization ) reach the threshold level required to trigger a new depolarization . This may be the me

9、chanism of ventricular tachycardia in the prolonged QT syndrome and in some cases of digitalis toxicity,DIAGNOSIS,History: palpitations , syncope , near syncope, dizziness To determine; existene and category; precipitate factors（stress, caffeine, alcohol）;onset and termination mode; affection; effic

10、acy of pharmacotherapy Physical examination: heart rate and rhythm ECG, Holter ECG monitoring, Exercise testing , Electrophysiologic testing Electrophysiologic testing is useful in the diagnosis and management of complex arrhythmias,ANTI-ARRHYTHMIA AGENTS,Antiarrhythmic drugs are often divided into

11、four classes based upon their electropharmacologic actions,Class I agents block membrane sodium channels . Three subclasses are further defined by the effect of agents on the Purkinje fiber action potential . Class Ia drugs slow the rate of rise of the action potential (Vmax ) and prolong its durati

12、on , thus slowing conduction and increasing refractoriness . e.g Quindine Class Ib agents shorten action potential duration ; they do not affect conduction or refractoriness . e.g Lidocaine, Mexiletine Class Ic agents prolong Vmax and slow repolarization , thus slowing conduction and prolonging refr

13、actoriness , but more so than class Ia drugs . e.g Propafenone,Class agents are the blockers , which decrease automaticity , prolong atrioventricular conduction , and prolong refractoriness .e.g Metoprolol,Class agents block potassium channels and prolong repolarization , widening the QRS and prolon

14、ging the QT interval . They decrease automaticity and conduction and prolong refractoriness . e.g Amiodarone, Sotalol,Class agents are the calcium channel blockers , which decrease automaticity and atrioventricular conduction . e.g Verapamil, Diltiazem,NON-DRUG TREATMENT OF ARRHYTHMIA,Non-Drug Treat

15、ment of arrhythmia mainly include radiofrequency ablation pacemaker , ICD and several others,Sinus Arrhythmia,Sinus Tachycardia,Normal sinus rhythm: the P wave appear regularly, the P wave is upright in lead I, II, AVF and negative in lead AVR, P-R interval 120-200ms.60-100bpm,Sinus Tachycardia,ECG

16、Sinus Tachycardia is defined as a heart rate faster than 100 beats / min with sinus rhythm, frequency between 100-150bpm. P wave have a normal contour and appear before each QRS complex with a stable P-R interval . Stimulate vagal nerve,Sinus Tachycardia,Causes: it occurs with fever , exercise , emo

17、tion , pain ,anemia , heart failure , shock , thyrotoxicosis , or in response to many drugs . Alcohol ,tea, caffeine and alcohol withdrawal are common causes of sinus tachycardia. Treatment: therapy should be directed primary disease; use beta blockers if needed,Sinus bradycardia,ECG: sinus rhythm E

18、CG, heart rate slower than 60 beats /min .sinus arrhythmia,Sinus bradycardia,Causes: Physiological:young adults, atheletes, during sleep. Pathological: hypothermia, raised intracranial pressure, hypothyroidism, jaundice, AMI affecting the SA node, drugs(e.g. beta-blockers), fibrosis of SA node. Trea

19、tment: Atropine, Pacing may be required if symptoms correlate with the bradycardia,Sinus arrest,ECG: pauses between the P wave are longer than 2s and are not a multiple of the basic PP interval.escape beat. Causes: AMI affecting the SA node, drugs, fibrosis of SA node. drugs-digitalis,CCB Treatment:

20、 see SSS,Sinoatrial block,ECG: mobitz type Iprogressive shorting of the PP interval prior to a pause. mobitz type II - pauses between the P wave are longer than 2s and are exact multiples of the basic PP interval,Sinoatrial block,Causes: AMI affecting the SA node, drugs( digitalis , calcium channel

21、blockers), fibrosis of SA node. Treatment: see SSS,Sick Sinus Syndrome,Causes: Sick sinus syndrome occurs most commonly in elderly patients . The pathologic changes are usually nonspecific , characterized by fibrosis of the sinus node and cardiac conduction system . Coronary disease is an uncommon c

22、ause . amyloidosis,typhoid fever,Sick Sinus Syndrome,Cinical manifestation: Most patients with electrocardiographic evidence of sick sinus syndrome are asymptomatic , but severe individuals may experience syncope , dizziness , confusion , palpitations , heart failure , or angina,Sick Sinus Syndrome,

23、ECG: persistent sinus bradycardia(50bpm); sinus arrest , sinoatrial block; sinoatrial block and atrialventricular block exist at the same time; bradycardia-tachycardia syndrome(sinus bradycardia, atrial tachycardia, atrial flutter, atrial fibrillation alternatively,Sick Sinus Syndrome,Treatment :asy

24、mptomatic patients dot need treatment. Pharmacologic therapy for sick sinus syndrome has been difficult . Most symptomatic patients will require permanent pacing,Atrial Arrhythmia,Atrial Premature Beats,Derivation Holter Organic heart disease Premonitory sign,Atrial Premature Beats,ECG:A premature P

25、 wave ,the contour of the P wave usually differs from the patient s normal complex . followed by a prolonged PR interval .blocked PAC,aberrant conduction,complete or incomplete compensatory pause,Atrial Premature Beats,Treatment is not indicated unless the patient is very symptomatic in which case b

26、eta blockers may be of some help,Atrial tachycardia,Automatic atrail tachycardia Reentrant atrail tachycardia Chaotic atrail tachycardia,Automatic atrail tachycardia,Cause : digitalis intoxication ,MI,COPD Behaviour ECG:150-200bpm ,AVF upright 2:1AVB equipotential line stimulate vagal nerver acceler

27、ation phenomena,Automatic atrail tachycardia,Treatment Digitalis intoxication withdraw drugs K+ normal ,supply K+, 5g/30 min po. K+ increase, lidocarin, beta blockers ,CCB non- digitalis intoxication therapy should be directed to primary disease. digitalis, beta blockers ,ccb class ia, ic, iii antia

28、rrhythmic agents radiofrequency ablation therapy,Reentrant atrail tachycardia,Cause : scar, anatomic structure ECG: the contour of the P wave usually differs from the patient s normal complex followed by a prolonged PR interval,Atrial Flutter,Causes:Atrial flutter occurs most often in patients with

29、chornic obstructive pulmonary disease (COPD) but may be seen also in those with rheumatic or coronary heart disease , congestive heart failure , thyrotoxicosis, alcohol,Atrial Flutter,ECG 1.Regular sawtooth atrial flutter wave (F wave),rates of 250300 beats/min; 2 transmission of every second ,third

30、 , or fourth impulse through the atrioventricular node to the ventricles .3.narrow or wide QRS complex. Atrial flutter with wide QRS complex aberrant ventricular conduction bundle branch block accessory pathway anterograde conduction,Atrial Flutter,Cinical manifestation:Severity of the symptoms depe

31、nds on the ventricular response rate (a rapid ventricular response is likely to cause palpitations, angina, cardiac failure,Atrial Flutter,Treatment: Therapy should be directed to primary disease. Electrical cardioversion back to sinus rhythm is the best treatment, with as little as 2550 J . Class I

32、a, Ic, III (Amioderone) antiarrhythmic agents is probably the pharmacologic agent of choice for cardiovert to sinus rhythm and maintain sinus rhythm. Rate control :beta blockers, CCB, digitalis Precardioversion anticoagulation is not necessary for atrial flutter of less than 48 hours duration. Radio

33、frequency ablation Overdrive pacing,Atrial Fibrillation,Atral fibrillation is the commonest chronic arrhythmia , with an incidence and prevalence that rise with age , so that it affects nearly 1% of individuals over age 60 years ,10% over age 80 years. Category of Atral fibrillation Paroxysmal AF（24

34、h7days） Persistent AF（ 7days 1year ） Permanent AF（ 1year,Atrial Fibrillation,Causes: rheumatic and other forms of valvular heart disease , coronary heart disease, dilated cardiomyopathy , hypertensive heart disease , pulmonary disease, thyrotoxicosis ,emotional stress or following surgery, acute alc

35、oholic intoxication. patients with no apparent cardiac disease.-lone atral fibrillation Patients with bradycardia-tachycardia syndrom,Atrial Fibrillation,Cinical manifestation: Atrial fibrillation itself is rarely life-threatening ; however , it can have serious consequences if the ventricular rate

36、is sufficiently rapid to precipitate hypotension , myocaridial ischemia , or tachycardia-induced myocardial dysfunction .It happens ,HR 150 Perhaps the most serious consequence of atrial fibrillation is the propensity for thrombus formation due to stasis in the atria and consequent embolization,Atri

37、al Fibrillation,The first cardiac sound is variable and cardiac rhythm is irregular. Not all ventricular beats produce a palpable peripheral pulse . The difference between the apical rate and the pulse rate is the “pulse deficit ” ; Cardiac rhythm is regular cardioverter to sinus rhythm cardioverter

38、 to atrial tachycardia cardioverter to atrial flutter cardioverter to junctional , ventricular tachycardia (digitalis intoxication) complete AVB(digitalis intoxication,Atrial Fibrillation,ECG: no P waves and irregular baseline with a irregular ventricular response , ventricular response ranges 100-1

39、60bpm,can be slower or faster,Atrial Fibrillation,Treatment: Therapy should be directed to primary disease and precipitating factors. Newly Diagnosed Atrial Fibrillation(Acute Atrial Fibrillation) Subsequent Management (Chronic Atrial Fibrillation,Atrial Fibrillation,Newly Diagnosed Atrial Fibrillat

40、ion(Acute Atrial Fibrillation) Initial Managemnt Up to two-thirds of patients experiencing a first episode of atrial fibrillation will spontaneously revert to sinus rhythm within 24 hours . The approach to the initial management of atrial fibrillation depends on the clinical presentation . If , as i

41、s often the case-particularly in older individuals the patient presents without symptoms , hemodynamic stability hospitalization is usually not necessary,Atrial Fibrillation,In contrast , if the patient is hemodynamically unstable-usually as a result of a rapid ventricular rate or associated cardiac

42、 or noncardiac conditions-hospitalization and immediate treatment of atrial fibrillation are required,Atrial Fibrillation,Urgent cardioversion chronic theraphy Drugs(A C ) Rate control Electrical cardioversion Anticoagulation Ratiofrequency ablation,Atrial Fibrillation,Urgent cardioversion is usuall

43、y indicated in patients with shock or severe hypotension , pulmonary edema , or ongoing myocardial infarction or ischemia . An initial shock with 100 200 J is administered in synchrony with the R wave,Atrial Fibrillation,Drugs cardioversion A quinidine,procainamide C propafenone aminodarone,Atrial F

44、ibrillation,In less unstable patients, a strategy of rate control is appropriate . 1.Digoxin is less risky , is rather slow. 2.In the setting of myocardial infarction or ischemia , -blockers are the preferred agent . The most frequently used agents are either metoprolol or esmolol .,Atrial Fibrillat

45、ion,3 If hypertension is present or -blockers are contraindicated , calcium channel blockers are immediately effective . Diltiazem is the preferred calcium blocker if hypotension or left ventricular dysfunction is present .Otherwise , verapamil may be used,Atrial Fibrillation,4 Aminodarone , even wh

46、en administered intravenously , has a relatively slow onset but is often a useful adjunct when rate control with the previously cited agents is incomplete or contraindicated or when cardioversion is planned in the near future . 0.2 Q8h 1 week 0.2 Q12h 1 week 0.2 Q24h 5-7 days/week 3mg/kg iv 10min; 1

47、mg/min ivgtt 6 hours;0.5mg/min ivgtt 24-48hours,Atrial Fibrillation,Subsequent Management (Chronic Atrial Fibrillation) If atrial fibrillation persists or has been present for more than a week , spontaneous conversion is unlikely . Management consists of rate control and anticoagulation,Atrial Fibri

48、llation,Rate control is usually relatively easy to achieve with -blockers , rate-slowing calcium blockers , and digoxin , used as single agents or more often in combination . Good rate control should consist of a ventricular rate between 60and 80 beats/min with usual daily activities and a ventricul

49、ar rate not exceeding 110 beats /min except with moderate to strenuous activity,Atrial Fibrillation,Anticoagulation with warfarin to an INR target of 2.03.0 should be established and maintained as long as the patient is in atrial fibrillation . Cardioversion , if planned( when atrial fibrillation pe

50、rsists 24hanticoagulation should be performed at least 3 weeks before cardioversion and must be maintained for at least 4 weeks following cardioversion,Atrial Fibrillation,However , patients with signifingly obstructive valvular disease , chronic heart failure or left ventricular dysfunction , diabe

51、tes , hypertension , or age over 75 years and those with a history of prior embolic events are at substantially higher risk. Patients with one or more of these risk factors for stroke should be treated with warfarin,Atrial Fibrillation,Patients below the age of 6065 years without any of these stroke

52、 risk factors (“lone atrial fibrillation ” ) may be treated with aspirin or no antithrombotic therapy . Ablation therapy for cure of AF is generally employed for patients with paroxysmal AF,Atrioventricular junctional arrhythmia premature beats escape beats rhythm tachycardia,Premature atrioventricu

53、lar junctional beat,Derivation Impuls transmission directions Treatment,Premature atrioventricular junctional beat,ECG Premature retrograde P P waves inverted in leads ,III,and aVF P wave may be observed after the QRS complex or before the QRS complex,or may not seen PR0.12s，RP0.20s normal-appearing

54、 QRS complexes Most of them with complete compensatory pause,AV junctional escape beat and AV junctional rhythm,The escape rhythm may arise from AV junctional area, in which case its rate will tipically be 40-60bpm. SAN frequency deceleration SAN conduction block,AV junctional escape beat and AV jun

55、ctional rhythm,1.the most common escape rhythm 2. QRS wave is characterized the performance of junctional beats 3.rate will tipically be 40-60bpm,AV junctional escape beat and AV junctional rhythm,Cause Mostly due to sinus arrest, 。AVB Increased vagus nerve tension Protective rhythm,AV junctional es

56、cape beat and AV junctional rhythm,Sign The first cardiac sound is variable Jugular venous pulse huge wave Treatment,nonparoxysmal atrioventricular junctional tachycardia,Mechanism : Triggered activity Increased automaticity Causes: often occurs in patients with digitalis intoxication, inferior wall

57、 MI,myocarditis,rheumaric heart disease,nonparoxysmal atrioventricular junctional tachycardia,ECG : The onset of nonparoxysmal tachycardia is usually gradual, with a warm-up period prior to stabilization of the rate. nonparoxysmal junctional tachycardia range from 70-150bpm and is perfectly regular

58、. QRS complexes are narrow shows P wave and the R waves are independent from each other,nonparoxysmal atrioventricular junctional tachycardia,Treatment asymptomatic patients dont need treatment. digitalis has been used withdraw drugs K+ normal ,supply K+, 5g/30 min po. K+ increase, lidocarin, beta b

59、lockers class Ia, Ic, III antiarrhythmic agents,Paroxysmal Supraventricular Tachycardia(PSVT,Sinoatrial reentrant tachycardia Atrioventricular nodal reentrant tachycardia(AVNRT) Atrial reentrant tachycardia Atrioventricular reentrant tachycardia(AVRT) AVNRT and AVRT 90,Atrioventricular nodal reentra

60、nt tachycardia(AVNRT,Causes: often occurs in patients without structural heart disease . Cinical manifestation: Attacks begin and end abruptly and may last a few seconds to several hours or longer . Patients may be asymptomatic except for awareness of rapid heart action , but some experience palpita