1. Disorders of heart rhythm D.D., Professor Denefil Olha Volodymyrivna

2. ETIOLOGYETIOLOGY Functional violations and influences - ANS activity changes - Physical load - Body’s t 0 change (fever; hyperthermia, hypothermia) - Hormone’s blood concentration changes - Intracranial pressure increase - Infection (flu, typhoid) - breathing (in children)

4. Organic factors - inflammation of myocardium (infection, uninfection) - myocardial dystrophy (hypoxia, ischemia, amyloidosis) - myocardial necrosis ETIOLOGYETIOLOGY

6. Toxic influences - alcohol - medicines (beta-adrenoblockers) - catecholamine - glucocorticoids - bacterial toxins - phosphor organic substances ETIOLOGY

7. D.D., Professor Denefil O.V.

8. Hormone balance violation - Hyperthyroidism - Hypothyroidism - suprarenal glands hyperfunction - suprarenal glands hypofunction ETIOLOGY

9. ETIOLOGY Ions imbalance - changes of K, Na, Ca, Mg, Cl cardiomyocytes concentration (because long time using diuretics, uncontrolled using mineral water) Organism more sensitive to К + deficit than to АТP one

10. Mechanical influences - catheter using (for diagnosis and for treatment) - operation - chest trauma ETIOLOGY

11. Injury of conductive system different parts No electrical homogenous of myocardium No electrical functional stable of myocardium (violation of MRP) PATHOGENESIS (pathological condition of the heart)

12. Electricity of injury (No electrical homogenous of myocardium) Zone of injury Normal tissue membrane is partly depolarized membrane is completely depolarized (MRP = 0 mV or +20 mV) (MRP = -90 mV) potential difference appears between both these zones and ectopic driver activates PATHOGENESIS (ARRHYTHMIAS THEORIES)

13. Ectopic rhythm driver activation (electrical functional unstable myocardium ) Subthreshold oscillations : unstable MRP causes low amplitude fluctuation, which can cause early depolarization (hypoxia, K + deficit, heart distention) PATHOGENESIS (ARRHYTHMIAS THEORIES)

14. Ectopic rhythm driver activation (electrical functional unstable myocardium ) Overthreshold oscillations : appears at retardation or at breaking of repolarization (MAP cann’t be transformed in to MRP and new action potential arrears and as a result - ectopic rhythm) PATHOGENESIS (ARRHYTHMIAS THEORIES)

15. “Re-entry” Nature: repeat or multiple impulses enter in some area of conductive system of the heart or in contractile myocardium Condition: There are 2 conductive ways, which are separated functionally or structurally There is block of impulses transmission thought the one conductive way Impulses transmission is possible only in reverse route PATHOGENESIS (ARRHYTHMIAS THEORIES)

17. Automatism violations Conduction violations Combined violations (automatism, conduction and excitability) ARRHYTHMIAS CLASSIFICATION

18. * Nomotopic (violation of impulses formation in sinus node) 1. Sinus tachycardia 2. Sinus bradycardia 3. Sinus arrhythmia (respiratory) * Heterotopic rhythms (dominance of ectopic area activity) 1. Tardy ectopic rhythm (vicarious, passive) 2. Unparoxismal tachycardia 3. Migration of supraventricular rhythm driver Automatism violation

19. Nomotopic Automatism violation Sinus tachycardia Reasons: physical load, emotional stress, heart failure, myocardium ischemia or infarction, myocardium dystrophy ECG: sinus rhythm, HR 90-180 /min, R-R duration<0,60 c

20. Reasons: n. Vagus high activity (sportsmen, flu, typhoid), intracranial pressure increase (results from irritation of n.Vagus nucleas) ECG: sinus rhythm, HR 59-40 /min, R-R duration>1,0 с Nomotopic Automatism violation Sinus bradycardia

21. Reasons: breathing (in children), after viruses infections, neurocirculative dystonia ECG: sinus rhythm, difference between the shortest R-R and longest R-R >0,15 sec Nomotopic Automatism violation Sinus (respiratory) arrhythmia

22. Source: atrium, AV node, ventricle Meaning: protection of the heart at long time asystole (at SA node arrest) Kinds: - atrial -аtrial- ventricular - Ventricular (HR <40/min) Heterotopic rhythms Tardy (slowly) ectopic rhythm (vicarious, passive)

23. Source: atrium, AV node, ventricle ECG: - HR 90-130/min - progressive beginning and finishing - regular ventricle rhythm Heterotopic rhythms accelerated ectopic rhythm Unparoxismal tachycardia

24. Heterotopic rhythms Migration of supraventricular pacemaker Gradual removal of pacemaker from SA node to AV node ECG: P wave configuration violation Change of P-Q duration Arrhythmia

25. Conduction violations heart block - Sinus atrial - (or SA node arrest) - Intra Atrial - Atrial-ventricular - ventricular pre-excitation ventricular syndrome 1. WPW syndrome (Kent bundle) 2. CLC syndrome (James bundle)

26. Conduction violations Sinus atrial block (arrest) Violation of impulses transmission from SA-node to atriums (most often - noncomplete) ECG : PQRST complex is absent compensatory pause is equal 2 (R-R) Some time 3-4 PQRST complexes fall out and tardy ectopic rhythm (vicarious, passive) appears

27. Violation of impulses transmission through the atrium conductive system ECG : Р duration >0,11 sec, Р - deformed (two waved) Conduction violations Atrial block

28. Conduction violations АV-block Violation of impulses transmission through the AV node 1 degree 2 degree: Mobitz type I, Mobitz type II, type III (high degree AV block) 3 degree (complete AV block )

29. ECG : PQ>0,2 sec Conduction violations АV-block 1 degree

30. * Mobitz type I (period of Venkebah) - Progressive increase of PQ duration (Venkebah’s pariods) with after fall out QRST * Mobitz type II - PQ are prolonged or N but their length is constant QRST fall out (periodicity is 2:1, some time 3:1, 4:1) * type III (high degree AV block) - QRST fall out (periodicity is 2:1, 3:1, 4:1) bradycardia ( tardy ectopic rhythm arrears ) Symptoms: dizziness, unconsciousness Conduction violations АV-block 2 degree

32. * Absolute stop impulses conduction from atriums to ventricles * Independent excitation and contraction of the atriums and ventricles ECG : Р amount > QRS amount, P waves and QRS complexes appear independently, some time Р are masked by QRS or T and that causes their deformation Conduction violations АV-block 3 degree (complete)

33. Complete AV block

34. Stokes-Adams’s syndrome Reasons: - long time asystole (more than 10-20 seс) (occurs at transition of АV-block 2 degree type III into complete АV-block - long time asystole at АV-block 3 degree (complete) - long time asystole at ventricles fibrillation because АV-block 3 degree Signs: unconsciousness, convulsions (because: decreased heart output and brain hypoxia) Prognosis: at every attack patient can die Conduction violations АV block

35. Violation of impulses conduction in ventricle conductive system Giss’s bundle branches block * block of 1 branche * block of 2 branches * block of 3 branches * local intraventricle block ECG : QRS deformation Conduction violations ventricle block

36. Giss’s bundle left branche block

37. WPW (Wolff-Parkinson-White) syndrome Reason: additional Kent’s bungle (impulses don’t transmit through the AV node but through Kent’s brunch) ECG : PQ<0,12 sec, QRS is deformed and wide because Δ-wave, ST и T are localized dyscordly, pre-excitation of the ventricles Conduction violations Pre-excitation syndrome wave

38. WPW (Wolff-Parkinson- White) syndrome

39. CLC (Clerk-Levy-Critesco) syndrome (syndrome of short PQ) Reason: additional Jaims’s bungle (impulses came to ventricles earlier than through the AV node) ECG : PQ<0,12 sec, QRS unchanged Conduction violations Pre-excitation syndrome

40. Complications Pre-excitation of any area in ventricle Y Formation of electrical unstable myocardium Y “Re-entry” mechanism activation Y Ectopic driver appearens Y extrasistole paroxysmal tachycardia ventricle flutter (ventricular tachycardia) Conduction violations Pre-excitation syndrome

41. Arrhythmias in the result of combined violations (automatism, conduction and excitability) Extrasistole Paroxysmal tachycardia Atrium flutter Atrium fibrillation Ventricle flutter (ventricular tachycardia) Ventricle fibrillation

42. extraordinary systole in the result of ectopic pacemaker activation Reason: * Membrane’s high oscillative activity * “re-entry” mechanism Types, ECG signs: - atrial (Р deformed) - atrial-ventricular (Р appears after QRS) - ventricular (no Р before QRS, QRS deformation, complete compensatory pouse) Extrasistole

43. ECG signs: Р deformation Extrasistole (atrial)

44. ECG signs: Р appears after QRS Extrasistole (from AV node)

45. ECG signs: no Р before QRS, deformation of QRS, complete compensatory pause Extrasistole (ventricular)

46. Attack of the heart contractions (140-250/min), which sudden onset and offset at regular rhythm Mechanisms:- “re-entry”, ectopic driver activation Types, ECG signs : - atrial (Р deformed) - atrial-ventricular (Р appears after QRS) - ventricular (no Р before QRS, QRS is deformed and wide) Duration – from some seconds to some minutes Paroxysmal tachycardia

47. Paroxysmal tachycardia (ventricle)

50. rapid and regular atrial contructions with a rate from 240 to 450/min Mechanisms: re-entry, ectopic driver activation ECG : regular and rapid F-waves (sawtooth pattern), QRS unchanged Atrium flutter

51. Atrium fibrillation rapid and unregular atrial contractions with frequency 350-700/min Mechanisms: re-entry, ectopic driver activation ECG : unregular and rapid f-waves (sawtooth pattern), complexes QRS appear irregular

52. Flutter – frequent (200-300/min) regular excitation and contraction of the ventricles because impulses from ectopic driver circulates constantly (“re- entry”) ECG : no P, QRS is wide Fibrillation – frequent (200-500/min), inregular and haotic excitation and contraction of cardiomyocyte’s separated groups in ventricles (finally ventricles don’t contract) ECG : changed shape and amplitude of the waves without any intervals Ventricle flutter and fibrillation

62. Premature Ventricular Contractions

63. Premature Atrial Contractions

64. Junctional rhythms Accelerated junctional rhythms

66. Thank you for attention !