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Arrhythmias

1. Arrhythmia 1 BY DR ADEDOKUN T.A 1

2. Outline 2

3. Introduction Normal cardiac function relies on the flow of electric impulses through the heart in an exquisitely coordinated fashion. This pathway is made up of 5 elements: The sino -atrial (SA) node The atrioventricular (AV) node The bundle of His The left and right bundle branches The Purkinje fibres 3

4. Normal cardiac conduction pathway 4

5. PATHWAY OF CONDUCTION 5

6. Arrhythmia 1 Disorders of heart rhythm resulting from alterations of impulse formation , impulse conduction , or both. Cardiac arrhythmia (or dysrhythmia) describes any abnormality of cardiac rhythm. Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all. Broadly divided into two Slow heart rhythms are termed bradycardias (or bradyarrhythmias ). Fast rhythms are known as tachycardias (or tachyarrhythmias). 6

7. Arrhythmia Bradyarrhythmias result from decreased automaticity or conduction block. Tachyarrhythmias result from enhanced automaticity, reentry, or triggered activity. Tachycardias are further characterized 1. Supraventricular when they involve the atrium or atrioventricular (AV) node. 2. Ventricular when they originate from the His–Purkinje system or ventricles. 7

8. Cardiac excitation-contraction coupling Describes the physiological process by which electrical stimulation of the cardiomyocytes (the action potential) results in a mechanical response (muscle contraction). The contraction of a cardiac myocyte is governed primarily by intracellular Ca 2+ concentration. 8

9. Myocardial action potential 9

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11. Cardiac action potential Phase 0 - depolarization from the SA node brings the membrane potential to the threshold, opening voltage-activated sodium channels. Phase 1 - early rapid repolarization then results from the activation of the fast and slow transient outward potassium currents Phase 2 - prolonged plateau resulting from a balance between the inward currents mediated by the L-type Ca 2+ channel and Na + –Ca 2+ exchanger and outward currents mediated by delayed rectifier K + channels 11

12. Cardiac action potential Phase 3 - Calcium channels become inactivated; outward potassium currents predominate  further repolarization  membrane potential moves towards the potassium equilibrium potential. Phase 4 - Membrane potential returns to its resting value after full repolarization (-90mV) The repolarization phase of pacemaker cells results from both the inactivation of the open calcium channels and the opening of voltage-gated potassium channels that permit the efflux of potassium from the cells. The resting state is maintained mainly by K + inward rectifier current & weak inward rectifying ATP-dependent K + channels 12

13. Cardiac action potentials The distinct populations of automatic cells in the specialized conduction pathway have different intrinsic rates of firing. These rates are determined by three variables that influence how fast the membrane potential reaches the threshold condition: (1) Rate (i.e., the slope) of phase 4 spontaneous depolarization (2) Maximum negative diastolic potential (3) The Threshold potential 13

14. NODAL ACTION POTENTIAL 14

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16. Cardiac Arrhythmia Cardiac tissue is composed of electrically coupled cells operating as a syncytium. As myocytes depolarize and the electrical activity rapidly propagates from one cell to the next with minimal resistance, spreading through a large mass of tissue. Electrical impulse formation in the heart arises from the intrinsic automaticity of specialized cardiac cells. Automaticity refers to a cell’s ability to spontaneously depolarise to a threshold voltage to generate an action potential. 16

17. Cardiac Arrhythmia The cells of the specialized conducting system do possess natural automaticity and are therefore termed pacemaker cells. The specialized conducting system includes the sinoatrial (SA) node, the AV nodal region, and the ventricular conducting system. The latter comprises the bundle of His, the bundle branches, and the Purkinje fibres . Although atrial and ventricular myocytes do not have this property under normal conditions, In pathologic situations, they may also acquire automaticity 17

18. Pacemakers of the heart 18

19. Etiology of cardiac arrhythmias Hypertension, Diabetes, CADx Structural heart dx: HHD, valvular, congenital ht dx Degenerative dx: Lev’s & Lenegres Metabolic abnormalities: hyperthyroidism, pheochromocytoma, Hypokalemia, hypomagnesaemia Acute or chronic alcohol abuse Drugs Adrenergic overdrive Cardiac catherization , cardiothoracic surgery, oesophageal disease 19

20. Pathophysiology The heart has intrinsic pacemaker activity SAN depolarizes more rapidly than other cells in Conducting System Cardiac myocytes are excitable cells Rate of depolarization is dependent on: location, autonomic, pathologic & pharmacologic states of the cells 20

21. Pathophysiology 21

22. Pathophysiology 22

23. Mechanisms of arrhythmia 23

24. Mechanisms of Arrhythmia 24

25. Automaticity 25

26. Mechanisms of cardiac arrhythmia 26

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28. Effect of sympathetic and parasympathetic (cholinergic) stimulation on pacemaker current channels. 28

29. Causes of Increased automaticity 1)Increased sympathetic stimulation Hypovolaemia Hypoxia- anaemia , lung dx Sympathomimetic drugs- cocaine, amphetamine Pain Anxiety 2)Increased metabolic activity Fever Hyperthyroidism 29

30. Causes of decreased automaticity 1)Increased vagal tone Sleeping Athletes Pathological- inferior wall MI 2)Slow AV conduction- beta-blockers, calcium channel blockers, digoxin 3)Decreased metabolic activity Hypothermia Hypothyroidism 4) Electrolyte imbalance – hyperkalemia 5)Raised ICP 30

31. Triggered Activity Occurs when depolarizing oscillations of the membrane potential occur during or after an action potential in which one oscillation is strong enough to trigger a new potential. These oscillations are called afterdepolarizations 31

32. Triggered activity 32

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34. Early after depolarization EAD occur during the plateau phase of the action potential, prior to repolarization, and are more evident at slow heart rates, particularly in the presence of hypokalaemia and hypomagnesaemia. Mutations in cardiac Na+ or K+ channels, or drugs that prolong myocardial repolarization by inhibiting one or more components of the outward potassium current, IK, (class IA and class III antiarrhythmics, tricyclic antidepressants, antihistamines, organophosphorus insecticides, and many others) can predispose to the appearance of early after-depolarizations. 34

35. Delayed after depolarization These are subthreshold depolarisations occurring after full repolarization of the action potential. Their amplitude is increased by tachycardia or intracellular calcium overload and may reach a threshold at which an action potential is generated, potentially initiating sustained tachycardia. Delayed after-depolarizations can be induced experimentally by digitalis overload and are the likely mechanism of digitoxic arrhythmias. 35

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37. Reentry 37

38. Re-entry 38

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40. Reentry 40

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42. Reentry Reentry can be subdivided into 2 categories based on whether the reentrant circuit is large enough to be mapped via catheter Macroreentry –Circuit is large enough to be mapped ( e.g Atrial flutter, AVRT) Microreentry - Circuit is too small to be mapped e.g atrial fibrillation, intraatrial reentrant tachycardia 42

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44. Categorization of tachyarrhythmias by mechanism 44

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46. THANK YOU FOR YOUR ATTENTION 46