ARRHYTHMIAS. Zuzana Charvátová

Transcription

1 ARRHYTHMIAS Zuzana Charvátová

2 ARRHYTMIAS = abnormalities of heart rhythm presence of any heart rhythm different from physiologic sinus rhythm various spectrum of clinical importance

3 A. myocardial reasons: ischemia (IHD) myocarditis cardiomyopathy Etiology amyloidosis, scar after AMI electric remodelation B. hemodynamic reasons volume and pressure overload (disorders of valves) C. extracardial reasons change of tonus VNS disorders of electrolytes (K +, Ca 2+, acidosis) endocrinopathy (hypertyreosis) hypoxia drugs (digitalis, antiarrhythmics) toxins (alcohol, cofee, narcotics) genetic reasons (mutations of ion channels)

4 Pathophysiologic Consequences of Arrhythmias hemodynamic manifestations decreased CO shortening of diastolic filling period coronary flow ischemia of myocardium disorders of left ventricle contractility

5 Signs and symptoms palpitation: an awareness of an abnormal heartbeat skipped beats or accelerated heart rate low cardiac output signs: dyspnea lung congestion weakness, decreased tolerance to physical activity mental alteration hypoperfusion of the brain stenocardia temporary or persistent circulation failure signs: (presyncope, syncope, persistent circulatory arrest ) arterial embolia (when intracardial trombus released)

6 Diagnosis excellent method is ECG standard 12 leads Holter monitoring episodic ECG recorder (loop or event) electrophysiologic maping

7 Overview of leads in ECG 12 leads ECG 3 bipolar limb leads I, II, III 3 unipolar augmented leads avr, avl, avf 6 unipolar chest leads V 1-6 I avr avl II III earth + + avf

8 Position of the chest leads V9 V8 V7 V6 V5 V4R V3R V1 V2 V3 V4

9 The normal electrocardiogram (waves and intervals)

10 Physiologic ECG

11 Arrhythmias clasification 1. electric processes: abnormalities of impulse generation impulse propagation combination of both 2. localization: supraventricular (narrow QRS complex) ventricular (wide QRS complex) 3. velocity (hemodynamic effect): bradyarrhytmias - rate < 60/min tachyarrhytmias - > 100/min (4). context heart pathology: primary pure electrophyziologic origin secondary hemodynamic and methabolic influences

12 Mechanisms of arrhythmias development 1. abnormality of impulse generation enhanced automaticity reduced automaticity pacemaker failure triggered activity abnormal repolarization leads to subsequent depolarization 2 forms: early afterdepolarization (EAD) delayed afterdepolarization (DAD) 2. abnormality of impulse propagation reentry blockades (A-V blockades, bundle blocks) 3. combination of the two above 3 arytmogenic mechanisms: abnormal automaticity, triggered activity, re-entry

13 Triggered activity abnormal repolarization leads to subsequent depolarization ( afterdepolarization ) Before the end of repolarization (phase 3) new depolarization occurs due to opening of channels for Na + and Ca ++. Ca 2+ overload releasing from SR

14 Reentry there develops a self-perpetuating rapid and abnormal activation (circus movement) conditions necessary for reentry include a combination of unidirectional block and slowed conduction Exerpted from pp of Grauer K, Cavallaro D: ACLS: Comprehensive Review (Vol. 2) - 3rd Edition, Mosby Lifeline, St. Louis

15 OVERVIEW OF ARRHYTHMIAS

16 Sinus Tachycardia = sinus rhytm with frequence 100/min at rest Physiologic: infants, physical and psychical stress, emotions, increased tonus of symphatetic system Pathologic: fever, hyperthyreosis, anemia, hypovolemia, shock, Pharmacologic: foodstuffs (alcohol, nicotin, coffein), adrenalin derivates, atropin,..

17 fr.: 60/min fr.: 125/min

18 Sinus Bradycardia = sinus rhytm with frequence < 60/min at rest Physiologic: in sleep, athletes, vagal tone Pathologic: hypotyreosis, hypotermia, intracranial hypertension Pharmacologic: β-blockers, antiarrhythmics, digitalis

19 fr.: 60/min fr.: 48/min

20 Sick Sinus Syndrome (tachy brady syndrome) sinus bradycardia insufficient increase in HR during exercise sinoatrial blocks paroxysmal supraventricular tachycardia or atrial fibrillation

21 Atrial Flutter Coordinated atrial response at the same rate ( /min) In favourable leads the continous series of P (F) waves gives a characteristic saw-tooth appearance

22 Atrial Fibrillation The rate is extremly rapid ( /min) No coordinated atrial excitation is possible P wave are replaced by a rapid irregular series of oscilations known as f waves Irregular ventricular complexes (non stable R-R)

23 Atrial Fibrillation

24 Premature Ventricular Complexes PVCs (extrasystoles) ectopic impulses originating from an area distal to the His Purkinje fibres unifocal PVCs are triggered from a single site in the ventricle complexes have different configurations > 0.11s in width is usually followed by a complete compensatory pause

25 Compensatory pause Incomplete compensatory pause (supraventricular arrhythmia) Complete compensatory pause (ventriclular extrasystole)

26 Ventricular Extrasystoles - Bigeminy repeated sequence of one ventricular premature complex followed by one normal beat.

27 PVCs groups of subsequent extrasystoles

28 Ventricular Tachycardia 5 or more subsequent wide QRS complexes ( 0.12s) monotopic (unifocal) x polytopic (multifocal)

29 Torsades des Pointes ventricular polymorphic tachycardia, characteristic ECG picture mostly associated with LQT syndrome

30 Ventricular Fibrilation chaotic ventricular activity ceases blood circulation medical emergency

31 Ventricular Fibrilation

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33 First degree AV block permanent prolonged PQ interval above 0.2 s

34 Second degree AV block Mobitz I (Wenckebach type) cyclic variation in A-V conduction time ECG shows an increasing P-R interval in successive beats until a ventricular complex is dropped altogether cycle then recurs; ratio is n: (n-1), e.g. 3:2, 4:3, 5:4 etc.

35 Second degree AV block Mobitz II Only a proportion of the impulses reaching the A-V node are transmitted, usually every second, third or fourth.

36 Complete (third) AV block the ventricular myocardium is completely isolated from supraventricular stimuli (AV dissociation) P-P constant, R-R constant

37 Left bundle branch block delays conctraction of the left ventricle leads recording the direction of the delayed ventricle display a predominantly positive M-shaped QRS complex exceeding 0.12 s, followed by S-T segment depression and T wave inversion (leads I, avl, V5,6)

38 Right bundle branch block delayed activation of the right ventricle (QRS 0,12) In right-sided chest leads (V1,V2) - doubled R waves followed by S-T segment depression and T wave inversion.

39 Wolf-Parkinson-White syndrome (preexcitation) atrioventricular tachycardia using accessory pathways PQ < 0,12s, delta wave ( early ventricular activation)

40 Therapy (basic principles) I causal therapy according to etiology antiarrhythmic drug therapy influence on ion channels Class I agents interfere with the sodium (Na + ) channel. Class II agents are anti-sympathetic agents. Most agents in this class are beta blockers. Class III agents affect potassium (K + ) efflux. Class IV agents affect calcium channels and the AV node. Class V agents work by other or unknown mechanisms. electroimpulsotherapy cardioversion, defibrillation, cardiostimulation (temporary or permanent), ICD radiofrequency catheter ablation produces necrotic lesions (substrate of arrhythmia) by heating tissue three-dimensional electroanatomic mapping can find the substrate of an arrhythmia

41 Therapy (basic principles) II surgery - nowadays when cathetrization is not successfull supportive therapy psychotherapy, regimen arrangement, vagal maneuvers

42 Cardiac Resynchronization Therapy in patient with congestive heart failure suboptimal sequence of atrioventricular activation or intraventricular conduction delay dyssynchronious contraction biventricular cardioverter-defibrillator

43 Cardiostimulation an artificial electronic pacemaker

44 Stimulated rhytm sharp short-time waves in all leads = spikes

45 Electroanatomic mapping

46 Electroanatomic mapping

47 Thank you for your attention

48 Types of Cardiomyocytes aprox. 99 % cells of working myocardium aprox. 1 % cells of conductive system

49 Changes of ions during AP cells of working myocardium (AP with rapid depolarization)

50 Changes of ions during AP cells of conduction systém (SA and AV node; AP with slow depolarization) mv spontaneous diastolic repolarization (RP less negative) 0 - depolarization slower (Ca2+ specific channels opening)

51 AP in the heart

52 Heart Conduction System Sinus node: the main pacemaker of the heart because its rate of rhythmical discharge is faster than that of any other part of the heart (AV node, Purkinje fibers )