Tachydysrhythmias

1. Tachydysrhythmias August 2, 2001 Gavin Greenfield Bryan Young

2. Outline • Basic Science • Mechanisms of Tachydysrhythmias • impulse formation or impulse conduction • Anti-dysrhythmics • Classification • Management of Specific Tachydysrhythmias • Diagnosing Etiology of Wide-Complex Tachycardia • Practice EKG’s • Revised ACLS Tachycardia Algorithm

3. Basic Science - Anatomy • 3 basic types of myocardial cells • contractile, conductive, pacemaker • 99% of cardiac muscle cells are contractile • Innervation • sympathetic via ~T1-T5 • neurotransmitter? receptor? • parasympathetic via vagus nerve • neurotransmitter? • both innervate cells of both the contractile and conductive systems

4. Basic Science - Electrophysiology • Depolarization • common to contractile and conductive cells • Action Potential • Resting Membrane Potential

5. Basic Science - Electrophysiology Resting Membrane Potential

6. Basic Science - Depolarization

7. Basic Science - Depolarization • Differences between contractile cells and those involved in conduction

8. Basic Science – Effect of Autonomic Nervous System on Depolarization • Sympathetic stimulation increases slope of phase 4 depolarization • Parasympathetic stimulation decreases slope of phase 4 depolarization • parasympathetic stimulation also hyperpolarizes membrane (potential starts from lower value)

9. Basic Science – Sequence of Excitation • SA node is dominant pacemaker – why? • Blood supply to SA node? • Pathway of action potential from SA node to AV node? • Blood supply to AV node? • AV node to bundle of His to R and L BB’s to Purkinje fibers • Purkinje fibers rapidly distribute impulse to contractile cells in ventricles

10. Basic Science – Refractory Period • Refractory Period definition • Cardiac muscle cells have long refractory period (this prevents tetanic contractions and therefore allows filling)

11. Mechanisms for Tachydysrhythmia Formation • Altered automaticity increased automaticity in normal (enhanced automaticity) or ectopic (abnormal automaticity) site

12. Mechanisms for Tachydysrhythmia Formation • Reentry in normal or accessory pathway

13. Mechanisms for Tachydysrhythmia Formation • Triggered Dysrhythmias

14. Pharmacology of Anti-dysrhythmics

15. Pharmacology of Anti-dysrhythmics • 4 Broad Classes • based on effect on action potential and impulse conduction • Classification system ignores multiple overlapping properties of drugs • agents classified according to major effect • Class I – sodium channel blockers • Class II – beta-adrenergic blockers • Class III – antifibrillatory agents • Class IV – calcium channel blockers

16. Pharmacology of Anti-dysrhythmics • Class I (Sodium Channel Blockers) • Which part of action potential is therefore inhibited? • phase 0 is inhibited resulting in slowed depolarization and therefore slowed conduction and membrane stabilization (therefore prominent anti-ectopic effects) • varying effects on repolarization • 3 subclasses 1A, 1B, 1C

17. Pharmacology of Anti-dysrhythmicsClass I – sodium channel blockers • Class 1A • Procainamide • Quinidine • Disopyramide • Specific Effects • moderately slow depolarization and conduction • prolong repolarization and action potential duration • clinically results in slowed conduction through atria, AV node, and His-Purkinje system • also decreases conduction in accessory pathways

18. Pharmacology of Anti-dysrhythmicsClass I – sodium channel blockers • Class 1B • lidocaine • phenytoin • tocainide, mexiletine, moricizine, aprindine • Specific Effects • minimally slow depolarization and conduction • shorten repolarization and action potential duration (1A and 1C prolong)

19. Pharmacology of Anti-dysrhythmicsClass I – sodium channel blockers • Class 1C • Propafenone (also some 1A properties) • Flecainide, Encainide, Lorcainide • Specific Effects • profoundly slow depolarization and conduction • prolong repolarization and action potential duration

20. Pharmacology of Anti-dysrhythmicsClass II – Beta adrenergic blockers • Metoprolol, Esmolol, Acebutolol, Nadolol, Propranolol • Specific Effects (think of NE and Beta 1 actions on depolarization and contractility) • slow SA node impulse formation, slow AV conduction, prolong action potential and can depress conduction in ischemic tissue • depress myocardial contractility

21. Pharmacology of Anti-dysrhythmicsClass III – antifibrillatory agents • Amiodarone • Bretylium • Sotalol (shares activity with Class II) • Ibutilide (shares activity with Class II) • Specific Effects • prolong action potential duration and refractory period duration thus exhibiting antifibrillatory properties

22. Pharmacology of Anti-dysrhythmicsClass IV – Calcium (slow) channel blockers • Diltiazem, Verapamil • Specific Effects • block calcium entry to cells thus causing depression of anterograde conduction through AV node and suppression of other calcium-dependent dysrhythmias

23. Pharmacology of Anti-dysrhythmicsMiscellaneous • Adenosine • naturally occurring purine nucleoside • causes concentration dependent slowing of AV conduction and slowing of both anterograde and retrograde paths of a reentrant circuit • at antidysrhythmic doses has peripheral vasodilatory properties

24. Pharmacology of Anti-dysrhythmicsMiscellaneous • Digoxin • positive inotrope • variable electrophysiological effects on myocardial cells – can divide into excitant and depressant (therapeutic effects are result of depressant actions) • Excitant – increase in altered automatic and triggered ectopic impulses • Depressant – depresses conduction and lengthens refractoriness in AV node

25. All anti-dysrhythmics are pro-arrhythmics

26. Amiodarone • Effects • complex drug with effects on sodium, potassium, and calcium channels • alpha adrenergic and beta adrenergic blocking properties • prolongs action potential duration and refractory period • slows automaticity in pacemaker cells • slows conduction in AV node • causes smooth muscle relaxation

27. Amiodarone – “ARREST” Trial • Kudenchuk et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation, NEJM 341(12), 871-8, September 16, 1999. • prospective trial of VF/pulseless Vtach after first 3 shocks, intubation and 1 mg Epi • Amiodarone vs placebo followed by routine antiarrhythmic drugs • statistically significant increase in survival to hospital admission in amiodarone group • trial lacked statistical power to detect differences in survival to hospital discharge, which differed only slightly between the two groups

28. Tachydysrhythmia Classification • Several ways to classify tachydysrhythmias: • mechanism of formation • anatomic • EKG appearance • stable vs. unstable

29. Tachydysrhythmia ClassificationDecision Point 1 • Stable vs. Unstable: How do we differentiate? • unstable condition must be related to tachycardia • chest pain suggestive of myocardial ischemia • shortness of breath / pulmonary edema / congestive heart failure • shock / decreased LOC / hypotension • If unstable it doesn’t matter what the rhythm is – just sedate and cardiovert

30. Specific Dysrhythmias • Narrow QRS (supraventricular tachys) • Sinus tachycardia • Ectopic atrial tachycardia • Multifocal atrial tachycardia • Atrial fibrillation • Atrial flutter • AV nodal reentrant tachycardia • Atrioventricular reentrant tachycardia • Junctional tachycardia

31. Specific Dysrhtyhmias • Wide QRS • ventricular tachycardia • ventricular fibrillation • any supraventricular tachycardia with aberrant conduction

32. Narrow-Complex TachycardiasSinus Tachycardia • from acceleration of SA Node discharge rate • Atrial rate usually between 100 and 160 • sinus tachycardia is a response to: 1. physiologic stress (exertion, anxiety, etc.) 2. pharmacologic influence (caffeine, nicotine, alcohol, sympathomimetics) 3. pathologic (fever, anemia, hypoxia, hypotension, etc.) • Treat underlying condition

33. Narrow-Complex TachycardiasAtrial Tachycardia • from any nonsinus focus above AV Node • each QRS preceded by P’ • if no old EKG difficult to differentiate from sinus tachycardia

34. Narrow-Complex TachycardiasMultifocal atrial tachyardia • subset of atrial tachycardia aka wandering pacemaker • irregular rhythm, often confused with afib • at least three foci of impulse formation, therefore 3 distinctly different P waves • often associated with pulmonary disease and hypoxemia

35. Treatment of Atrial and Multifocal Atrial Tachycardia • causes: • include electrolyte and acid-base disturbances, drug toxicity, fever, hypoxemia • MFAT classically associated with pulmonary disease and hypoxemia • Treat underlying disorder • if pt symptomatic can treat with Beta blocker or Calcium channel blocker or Amiodarone • Magnesium second line agent • Procainamide and digoxin can also be used • specific antiarrhythmic therapy is rarely indicated

36. Narrow Complex TachycardiasSVT • regular rapid rhythm that arises from either reentry or ectopic pacemaker in area above bifurcation of bundle of His • reentrant variety often presents as PSVT • 60% have reentry within AV node • 20% have reentry involving bypass tract • remainder have reentry in other sites

37. Mechanisms for Tachydysrhythmia Formation • Reentry in normal or accessory pathway

38. SVT • 2 types of reentry SVT • AV Nodal Reentrant Tachycardia (AVNRT) • dual AV nodal pathways • initiated with ectopic atrial impulse encountering AV node during partial refractory period • 2nd type of reentry is Atrioventricular reentry (AVRT) • What is AVRT dependent upon?

39. SVTAtrioventricular reentrant tachycardia (AVRT) • seen in patients with bypass tracts • What is classic example? • second connection (other than AV node) present between atria and ventricles • like AVNRT, AVRT usually initiated by ectopic extrasystole • 2 types of conduction

40. SVTWPW • 2 types of conduction • orthodromic conduction (85% of WPW) • impulse conducted anterogradely down AV node and retrogradely up bypass tract • produces narrow QRS • antidromic conduction (15% of WPW) • impulse conducted anterogradely down accessory tract and up AV node • wide QRS – difficult to differentiate from vtach

42. SVT • etiology of reentrant SVT • can occur in normal heart, or in association with rheumatic heart disease, acute pericarditis, MI, mitral valve prolapse, or one of the pre-excitation syndromes (WPW) • with compromised heart can get • anginal chest pain, dyspnea, pulmonary edema from decreased diastolic filling

43. SVT Treatment • can treat by impeding conduction through one limb of reentry circuit • sustained reentry then impossible and sinus node can take over • increase vagal tone – “vagal maneuvers” • carotid sinus massage (Munro NC, McIntosh S, Lawson J, et al: Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc 1994;42:1248-1251 )  • Valsalva – most effective vagal maneuver • facial immersion in cold water

44. SVT Treatment • Pharmacologic • Hood MA, Smith WM: Adenosine versus verapamil in the treatment of supraventricular tachycardia: A randomized double-crossover trial. Am Heart J 1992;123:1543-1549 • Taylor DM - Am J Emerg Med - 1999 Mar; 17(2): 214-6 • Brady WJ Jr. DeBehnke DJ. Wickman LL. Lindbeck G. Treatment of out-of-hospital supraventricular tachycardia: adenosine vs verapamil. [see comments]. [Journal Article] Academic Emergency Medicine. 3(6):574-85, 1996 Jun. • Adenosine • MOA? • dose? • side effects? • Verapamil • 0.075 to 0.15 mg/kg (3-10 mg) IV over 15-60 sec • repeat dose in 30 min if necessary • associated with hypotension • Diltiazem, Beta blockers, digoxin • Consider procainamide, amiodarone, sotalol (2000 ACLS)

45. Atrial Flutter • Definition (Rosen) • regular atrial depolarization rate of 250 to 350 bpm; classically 300 • distinct EKG manifestations of abnormal atrial depolarization in a sawtooth appearance • common association with a 2:1 block (ventricular rate of 150 or 4:1 block) • can see irregular rhythm with variable conduction (sometimes profound bradycardia) • pathophysiology thought to be reentry and or abnormal automaticity

46. Atrial Flutter • often associated with underlying heart disease • IHD, CHF, valvular dysfunction, PE • metabolic derangements

47. Atrial Flutter - Treatment • Of course, cardioversion if unstable • low energy required – start at 25-50 J • treat underlying cause (if known) • Pharmacologic (Rate Control) • ventricular rate control with calcium channel blocker (Diltiazem or Verapamil) or beta blocker • if preexisting CHF (EF < 40%) consider diltiazem, digoxin, amiodarone (ACLS 2000) • can think of using adenosine to unmask flutter waves if diagnosis uncertain

48. Atrial Flutter - Treatment • Pharmacologic (Conversion) • Class 1A (procainamide), Class 1C (propafenone, flecainide), Class III (amiodarone, ibutilide) – ACLS 2000 • consider amiodarone if CHF (EF < 40%) (ACLS 2000)

49. Atrial Fibrillation • Causes (heart, PE, metabolic) • IHD, acute MI • valvular heart disease (esp. mitral) • hypertensive heart disease • pericarditis • myocardial contusion • cardiomyopathy • cardiac surgery • congestive heart failure • sick sinus syndrome • acute ethanol intoxication (“holiday heart”) • catecholamine excess • hyperthyroidism • accessory pathway (WPW) • pulmonary embolism • idiopathic

50. Atrial Fibrillation • completely irregular rhythm because of irregular ventricular response • loss of coordinated atrial activity and potentially rapid ventricular response can lead to decreased cardiac output (reduced diastolic filling) • paroxysmal or chronic • fibrillatory waves best seen inferiorly and V1 • multiple atrial microreentry circuits results in “atrial rate” of 300-600