Cardiac Arrhythmias. For Pharmacists

Transcription

1 Cardiac Arrhythmias For Pharmacists

2 Agenda Overview of the normal Classification Management Therapy Conclusion

3 Cardiac arrhythmias Overview of the normal

4 Arrhythmia: definition From the Greek a-, loss + rhythmos, rhythm = loss of rhythm Any variation from the normal rhythm of the heartbeat encompassing abnormalities of: Rate: too slow (bradycardia) or too fast (tachycardia) Regularity Site of impulse origin Sequence of activation Any rhythm that is not normal sinus rhythm

5 Normal sinus rhythm

6 Temporal sequence of activation

7 Temporal sequence of activation

8

9 Shape of action potential

10 Normal cardiac automaticity

11 Normal cardiac automaticity All cardiac cells have property of self-excitation ie INTRINSIC RHYTHMICITY They can therefore spontaneously depolarize Pacing of the heart will be carried out by cells with the fastest natural rate ie OVERDRIVE SUPPRESSION

12 Currents responsible for ventricular AP. Length of the arrows shows the relative size of each ionic current. E: Equilibrium potential ECF: extracellular fluid ICF: intracellular fluid.

13 Cardiac arrhythmias Classification

14 Arrhythmias: classification Site of origin Mechanism Duration Clinical significance

15 Site of origin Supra-ventricular: Sinus node Atria Atrio-ventricular junction (above bifurcation of HB) Ventricular: Bundle branches Purkinje fibres Working myocardium

16 Mechanism Abnormal impulse initiation Abnormal automaticity Triggered activity Abnormal impulse conduction Slow or blocked conduction Re-entry Most clinically important arrhythmias are due to re-entry

17 Re-entry

18 Re-entry

19 Duration Paroxysmal or non-sustained Persistent or sustained Permanent or chronic

20 Clinical significance Benign No independent increase in risk Significant Independent increase in risk Potentially lethal Can lead to proximate fatality if left untreated

21 Cardiac arrhythmias Management

22 Management 1. Precise diagnosis + assessment Must precede any intervention!! 2. Eliminate precipitants Drugs: digoxin, beta-blockers CHF, TTX, anxiety Hypokalaemia, hypoxia, acidosis

23 Management 3. Assess risk High risk Moderate risk Low risk

24 Low risk arrhythmias Do not have potential to produce death Need not be suppressed Treat only if they produce disruptive symptoms

25 High risk arrhythmias Potentially life-threatening Must be suppressed Treat always even if symptoms are minor

26 Moderate risk arrhythmias Problematic! No clear cut treatment of choice

27 Management strategies Termination Conversion of SVT to SR Amelioration Increasing AVB in AF Pacing AVB Prevention Decrease or abolish arrhythmia attacks Cure Ablation of irritable focus or accessory pathway

28 Management strategies Termination Conversion of SVT to SR Amelioration Increasing AVB in AF Pacing AVB Prevention Decrease or abolish arrhythmia attacks Cure Ablation of irritable focus or accessory pathway

29 Management strategies Termination Conversion of SVT to SR Amelioration Increasing AVB in AF Pacing AVB Prevention Decrease or abolish arrhythmia attacks Cure Ablation of irritable focus or accessory pathway

30 Management strategies Termination Conversion of SVT to SR Amelioration Increasing AVB in AF Pacing AVB Prevention Decrease or abolish arrhythmia attacks Cure Ablation of irritable focus or accessory pathway

31 Management modalities Autonomic manoeuvers External electric therapy Anti-arrhythmic drugs Non-pharmacologic therapy

32 Management modalities Autonomic manoeuvers External electric therapy Anti-arrhythmic drugs Non-pharmacologic therapy

33 Management modalities Autonomic manoeuvers External electric therapy Anti-arrhythmic drugs Non-pharmacologic therapy

34 Management modalities Autonomic manoeuvers External electric therapy Anti-arrhythmic drugs Non-pharmacologic therapy

35 Management modalities Non-pharmacologic therapy Radio-frequency ablation Arrhythmia surgery Implantable devices

36 Cardiac arrhythmias Pharmacotherapy

37 Bradyarrhythmias

38 Bradyarrhythmias Identify and treat the cause eg hypothyroidism Atropine (anti-cholinergic) Decreases vagal tone Decreases AV block and increases SA rate Sympathomimetics: isoprenaline or adrenaline Increase heart rate and contractility: ß1 adrenergic effect

39 Bradyarrhythmias

40 Bradyarrhythmias

41 Bradyarrhythmias

42 Tachyarrhythmias

43 Aims of drug treatment 1. Afford symptomatic relief 2. Prevent onset of arrhythmias producing major haemodynamic sequelae 3. Prevent recurrent life-threatening arrhythymias

44 Ideal anti-arrhythmic drug 1 Wide range of therapeutic activity against atrial, junctional and ventricular arrhythmias 2 Available in parenteral and oral form 3 Pharmacokinetic properties to allow predictable long term plasma level 4 No pro-arrhythmic, no depressant haemodynamic effects or significant non-cardiac side-effects

45 Ideal anti-arrhythmic drug 1 Wide range of therapeutic activity against atrial, junctional and ventricular arrhythmias 2 Available in parenteral and oral form 3 Pharmacokinetic properties to allow predictable long term plasma level 4 No pro-arrhythmic, no depressant haemodynamic effects or significant non-cardiac side-effects

46 Torsades de pointes

47

48 Once upon a time Back in 1986

49 Back in 1986

50 Back in 1986

51 CAST A causes B PVCs in post-mi patients increase mortality C reduces A AAD (encainide, flecainide, and moracizine) can successfully reduce PVCs C therefore reduces B AADs in post-mi patients with PVCs reduces mortality

52 CAST Prophylactic treatment of PVCs in post-mi patients

53 CAST Drugs used: encainide, flecainide, and moracizine Successful reduction in the amount of PVCs BUT: led to more arrhythmia-related deaths

54 CAST Total mortality was significantly higher in actively treated group compared to placebo Excess mortality was attributed to proarrhythmic effects of the agents

55 AFFIRM Rate or rhythm control in AF

56 AFFIRM How do you interpret this?

57

58 Classification of AADs No good classification scheme exists!! Vaughan Williams (1970) Effect on the action potential of cardiac cells Sicilian Gambit (1990) Effect on the ionic currents of cardiac cells

59

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61 General considerations Continuing imperfections of current AADs and rapidly expanding technologies have led to: Rapid expansion in use of devices and ablation techniques for treatment of arrhythmias Rapid disappearance of many AADs (some of which are no longer manufactured!!)

62 Cardiac arrhythmias Non-pharmacological therapy

63 EPS

64 RF Ablation RF energy is delivered to a localised area of cardiac tissue from the tip of a steerable electrode catheter

65 RF Ablation Arrhythmia trigger/substrate is modified: Initiating foci are destroyed Conducting pathways are interrupted No painful skeletal muscle contraction occurs Can be carried out under LA Serious complications seldom occur Non reversible, permanent cure Uniformly high success rate (depends on arrhythmia type)

66 RF Ablation lesions

67 RF Ablation Useful for: AVNRT and AVRT Atrial tachycardia Atrial flutter Bundle branch re-entry VT in normal hearts

68 Conclusions Remember..

69 Conclusions - 1 An arrhythmia is any rhythm that is not sinus rhythm Ionic flows through membrane channels determine automaticity, conduction and excitability

70 Conclusions - 2 Arrhythmias may be classified by: Site of origin Mechanism Duration Clinical significance

71 Conclusions - 3 Management depends on: Precise diagnosis Elimination of precipitants Risk assessment

72 Conclusions - 4 Pharmacotherapy is: Imperfect May be dangerous RF ablation and devices are rapidly becoming the mainstay of treatment

73 Confidential for internal use only Thank you for your attention!

74 Confidential for internal use only Any questions?