Arrhythmias and Devices Module 1

1. Arrhythmias and DevicesModule 1

2. Objectives • Recognize typical rhythms and rhythm disorders

3. Arrhythmias and DevicesOverview • The Conduction System • Normal Conduction • Automaticity & Action Potential • Causes of Rhythm Disorders • Rhythm Disorders • Categories • Disorders of Impulse Formation • Disorders of Impulse Conduction • Mechanisms • Arrhythmia Recognition and Classification • Bradycardias • Tachycardias

4. The Heart’s ‘Natural Pacemaker’ Rate of 60-100 bpm at rest Cardiac ConductionSinus Node Sinus Node (SA Node)

5. Receives impulses from SA node Delivers impulses to the His-Purkinje System Delivers rates between 40-60 bpm if SA node fails to deliver impulses Cardiac ConductionAV Node Atrioventricular Node (AV Node)

6. Begins conduction to the ventricles AV Junctional Tissue: Rates between 40-60 bpm Cardiac ConductionHIS Bundle Bundle of His

7. Bundle Branches and Purkinje Fibers Moves the impulse through the ventricles for contraction Provides ‘Escape Rhythm’: Rates between 20-40 bpm Cardiac ConductionPurkinje Fibers Purkinje Network

8. Normal Sinus Rhythm

9. Impulse Formation in SA Node

10. Atrial Depolarization

11. Delay at AV Node

12. Conduction through Bundle Branches

13. Conduction through Purkinje Fibers

14. Ventricular Depolarization

15. Plateau Phase of Repolarization

16. Final Rapid (Phase 3) Repolarization

17. Normal ECG Activation This pattern of depolarization results in efficient mechanical contraction – which is the purpose – to pump blood.

18. Horizontal axis – time: Each small square = 40 ms Each block = 200 ms (5 ea. 40 ms squares) Converting this to a rate in bpm: 1 min = 60,000 ms, so: 60,000/ms = bpm 60,000/600ms = 100 bpm Pacemakers and ICDs calculate intervals (ms), not in rates (bpm) Reading ECG Squares Intervals and Timing

19. ECGs Annotation Normal Ranges in Milliseconds: • PR Interval 120 – 200 ms • QRS Complex 60 – 100 ms • QT Interval 360 – 440 ms

20. This ECG shows a QRS duration of about 100 ms – a normal duration. If this represents efficient ventricular contraction… …then what effect could a QRS duration of 200 ms have on mechanical efficiency and cardiac output? Status Check Click for Answer Inefficient contraction

21. Status Check Match the term on the left with the description on the right • P-R Interval • AV Node • Purkinje Network • Bundle Branches Click for Answer Escape rate is 40-60 bpm Connect His bundle to Purkinje network Normally 120-200 ms Depolarizes the Ventricles

22. We’ve Seen How the Normal Pattern of Conduction Occurs But: • What triggers the depolarization – what causes that first cell to depolarize? • If a cell depolarizes, why does it result in depolarization in other cells?

23. Cardiac Cells are unique because they spontaneously depolarize Upper (SA Node) 60-80 bpm Middle (AV Junction) 40-60 bpm Lower (Purkinje Network) 20-40 bpm Automaticity

24. Automaticity Once a pacemaker cell initiates an impulse, its neighboring cells follow suit – like dominos.

25. 5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Action Potential of a Cardiac Cell

26. 5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Action Potential of a Cardiac Cell

27. 5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Action Potential of a Cardiac Cell

28. 5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Action Potential of a Cardiac Cell

29. 5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Action Potential of a Cardiac Cell

30. 5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Action Potential of a Cardiac Cell

31. Refractory Periods ERP - Effective Refractory Period AKA: Absolute Refractory Period Phases 0, 1, 2, and early Phase 3 A depolarization cannot be initiated by an impulse of any strength RRP - Relative Refractory Period Late Phase 2 and early Phase 3 A strong impulse can cause depolarization, possibly with aberrancy “R on T” phenomena Action Potential of a Cardiac Cell

32. Congenital Present at birth due to genetics, or conditions during the peri-natal environment Cardiac and other diseases Myocardial Infarction, high blood pressure, cardiomyopathy, valvular heart disease Acquired Medications (even anti-arrhythmic Rx), diet pills, cold remedies, illegal drugs, caffeine and/or alcohol abuse, tobacco use... Causes of Rhythm Disorders

33. Causes of Rhythm Disorders Secondary to other conditions • Hyper-Thyroid • Neurocardiogenic Syncope - Hypersensitive Carotid Sinus Syndrome (CSS) - Vasovagal Syncope (VS)

34. Rhythm Disorders2 Categories Impulse Formation • Abnormal Automaticity • Triggered Activity Disorders of Impulse Conduction

35. Rhythm Disorders2 Categories Impulse Formation • Abnormal Automaticity • Triggered Activity Bradycardia: Abnormally slow rates usually due to disease Tachycardia: Excessively rapid rates due to ANS

36. Rhythm Disorders2 Categories Impulse Formation • Abnormal Automaticity • Triggered Activity Depolarization occurring in Phase 3 or 4 of the action potential can trigger arrhythmias

37. Mechanisms of Rhythm DisordersTriggered Activity Early Afterdepolarization • Potential Causes: - Low potassium blood levels - Slow heart rate - Drug toxicity (ex. Quinidine causing Torsades de Pointes type of VT) • Late Afterdepolarization • Potential Causes: • - Premature beats • - Increased calcium blood levels • - Increased adrenaline levels • - Digitalis toxicity

38. Rhythm DisordersTwo Categories Impulse Formation • Abnormal Automaticity • Triggered Activity Impulse Conduction • Slow or Blocked Conduction • Reentry

39. Mechanisms of Rhythm Disorders Slowed or Blocked Conduction • Impulse generated normally • Impulse slowed or blocked as it makes its way through the conduction system

40. Rhythm DisordersTwo Categories Impulse Formation • Abnormal Automaticity • Triggered Activity Impulse Conduction • Slow or Blocked Conduction • Reentry

41. Mechanisms of Rhythm DisordersReentry Model • Conduction paths are “mirrored” • Pathway A: • Slow conduction but short (fast) refractory • Pathway B: • Fast conduction but long (slow) refractory period

42. Mechanisms of Rhythm DisordersReentry Model A premature event occurs, which is conducted down the slow pathway. During this “antegrade” conduction, the fast or “retrograde” pathway is still refractory A premature event occurs, which is conducted down the slow pathway. During this “antegrade” conduction, the fast or “retrograde” pathway is still refractory. By the time the slow antegrade conduction is complete, the fast pathway is no longer refractory, allowing retrograde conduction to occur. This “circus” mechanism is maintained as long as the relationship between fast and slow conduction, and fast/slow refractoriness persists.

43. A-V Intervals ms V-V Intervals ms Mechanisms of Rhythm DisordersReentry Model These are sometimes referred to as “circus tachycardias.” This mechanism explains one common arrhythmia seen in the EP lab: AV node re-entrant tachycardia. Note the almost simultaneous depolarization of the atria and ventricles.

44. Terminating Reentry • Spontaneous termination • Another premature beat that disturbs the underlying conduction/refractoriness relationships • Pace the heart at a rate above the tachycardia rate • Abruptly stop pacing • This is how implantable cardioverter-defibrillators can stop VT without a shock (ATP)

45. Impulse Formation Impulse Conduction Bradycardia Classifications Disorders of

46. Impulse Formation Impulse Conduction Bradycardia Classifications • Sinus Arrest • Sinus Bradycardia • Brady/Tachy Syndrome

47. Sinus Arrest • Failure of sinus node discharge • Absence of atrial depolarization • Periods of ventricular asystole • May be episodic as in vaso-vagal syncope, or carotid sinus hypersensitivity • May require a pacemaker

48. Sinus Bradycardia • Sinus Node depolarizes very slowly • If the patient is symptomatic and the rhythm is persistent and irreversible, may require a pacemaker

49. Brady/Tachy Syndrome • Intermittent episodes of slow and fast rates from the SA node or atria • Brady < 60 bpm • Tachy > 100 bpm • AKA: Sinus Node Disease • Patient may also have periods of AF and chronotropic incompetence • 75-80% of pacemakers implanted for this diagnosis

50. Sinus Arrest Impulse Formation • Sinus Bradycardia • Brady/Tachy Syndrome Impulse Conduction Bradycardia Classifications • Exit Block • 1st Degree AV Block • 2nd Degree AV Block • 3rd Degree AV Block • Bi/Trifascicular Block