Tachyarrhythmias

Tachyarrhythmias

1. Laughter Electricity is the best medicine Tim Cook Tachyarrhythmias

2. Basic stuff Haemodynamic stability Chest pain / syncope Hx of Cardiac Disease PPM / ICD Signs / symptoms of heart failure OLD ECGS!

3. Step 1 Are they unstable? Decreased GCS SBP <90mmHg Significant chest pain / signs of heart failure If so, perform synchronised DCCV Up to 3 attempts May also give Amiodarone

4. Step 2 Is it broad or narrow complex?

5. Step 3 Do something about it! Narrow complex regular Empirically treat as AVNRT Vagal manoeuvres Adenosine +/- CCB If not responding to above (or visible underlying flutter waves) then likely atrial flutter Consider rate control (or rhythm control)

6. Step 3 Do something about it! Narrow complex irregular Empirically treat as Atrial Fibrillation If onset >48hr Rate control with IV beta blocker / CCB (+/- digoxin ) If onset <48hr Consider rhythm control ( Amiodarone loading or DCCV) or rate control Consider need for anticoagulation

7. Step 3 Do something about it! Wide complex regular Empirically treat as Ventricular Tachycardia Amiodarone loading *Caveat being known History of SVT + BBB Consider vagal manoeuvres / adenosine

8. Step 3 Do something about it! Wide complex irregular Dependant on underlying cause: AF + BBB Treat as per AF AF + pre-excitation (DCCV or) consider amiodarone * Polymorphic VT Magnesium (+/- DCCV)

9. Narrow complex tachycardia Regular Sinus tachycardia AVNRT AVRT ( orthodromic ) Atrial tachyardia Atrial flutter (fixed ratio) Junctional tachycardia Irregular Sinus tachycardia with PACs/PJCs/PVCs Atrial fibrillation Multifocal atrial tachycardia Atrial flutter (variable block)

10. Wide complex tachycardia Regular Ventricular Tachycardia ( monomorphic VT) AVRT ( antidromic ) Sodium channel blockade Hyperkalaemia Any regular tachyarrhythmia with aberrancy (BBB) / pre-excitation (accessory pathway) Irregular Torsades de pointes (polymorphic VT) Any irregular tachyarrhythmia with aberrancy (BBB) / pre-excitation (accessory pathway)

11. Narrow complex regular tachycardias

12. Sinus tachycardia

13. Sinus tachycardia ‘Normal’ p wave before every QRS Narrow QRS complex (assuming no aberrancy / accessory pathway) Rough guide to maximum predicted rate ~220 – age but variable Regular rhythm and gradual variation Treat the underlying cause ( hypovolaemia , shock, sepsis, PE, anaemia , exercise, drug intoxication/withdrawal, hyperthyroidism, pain/anxiety etc)

14. AVNRT

15. AVNRT 3:1 female to male ratio Abrupt onset Rate: regular and usually 140-260bpm Narrow QRS complex (assuming no BBB / accessory pathway) Retrograde P wave usually buried in QRS complex (and may not be visible) Pseudo R’ wave may be seen in V1/V2 Pseudo S waves may be seen in inferior leads

16. AVNRT

17. AVNRT

18. AVNRT Vagal manoeuvres Adenosine 6mg -> 12mg ->12mg Verapamil 2.5-5mg / Diltiazem 15-20mg Other options could include: beta blockers or amiodarone but rarely needed

19. REVERT Trial Modified valsava manoeuvre in pSVT Improved success rate from 17% to 43% No serious adverse events Patient positioned in semi-recumbent position generating 40mmHg pressure for 15 sec then repositioned in supine position with passive leg raise immediately post valsalva

20. AVRT ( orthodromic )

21. AVRT (baseline)

22. AVRT A re-entry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement. During tachyarrythmias the accessory pathway forms part of the re-entry circuit. AVRT often triggered by premature atrial or premature ventricular beats. AVRT are further divided into orthodromic or  antidromic  conduction based on direction of re-entry conduction and ECG morphology.

23. AVRT

24. AVRT ( orthodromic ) Rate usually 200 – 300 bpm P waves usually retrograde and often buried in the ST segment Narrow QRS complex

25. AVRT ( orthodromic ) Vagal manoeuvres Adenosine or calcium-channel blockers Other options could include: beta blockers or amiodarone DCCV if non-responsive to medical therapy

26. Atrial Flutter (fixed ratio 2:1)

27. Atrial Flutter (fixed ratio) Caused by a re-entrant circuit in the right atrium and usually results in an atrial rate of ~300bpm Ventricular response dependent on AV conduction ratio; most commonly resulting in 2:1 block but can be other ratios or variable Treated as per Atrial Fibrillation (see later) Generally more sensitive to DCCV

28. Atrial Flutter (fixed ratio) Narrow complex tachycardia Flutter waves  (saw-tooth pattern) best seen in inferior leads Flutter waves are often difficult to see when 2:1 block is present, but be suspicious with HR of ~150 and little rate variability Flutter waves in V1 may resemble P waves Loss of the  isoelectric baseline

29. Narrow complex irregular tachycardias

30. Atrial Fibrillation

31. Atrial Fibrillation Irregular rhythm rAF often associated with a ventricular rate ~110 – 170bpm No P waves Fibrillatory waves may be present Absence of an isoelectric baseline Narrow QRS complex (assuming no BBB / accessory pathway)

32. Atrial Fibrillation Look for and treat reversible causes: Electrolyte disturbances Hyperthyroidism Sepsis Recreational drug / alcohol binge Peri/ myocarditis ACS / PE Digoxin toxicity

33. Atrial Fibrillation If onset >48hr Rate control Beta blocker / CCB / amiodarone (+/- digoxin ) Consider TOE guided DCCV Consider elective DCCV after 3/53 of anticoagulation

34. Atrial Fibrillation If onset <48hr Rate control if: age >65, untreated reversible cause ( eg sepsis) or recent CVA / TIA Consider rhythm control ( Amiodarone loading or DCCV) if age <65, no obvious reversible cause, WPW, heart failure or unacceptable symptoms ‘Wait and see’ approach (if onset <24hr) Return in <24hrs for re-review 60% will spontaneously revert within 48hrs of onset

35. Atrial Fibrillation Consider need for anticoagulation CHA 2 DS 2- VASc >1 Recommend anticoagulation HASBLED >2 Consult with cardiology before anticoagulating

36. Multifocal Atrial Tachycardia

37. Multifocal Atrial Tachycardia A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria Most commonly seen in elderly, unwell patients with severe COPD / CCF Poor prognostic marker, associated with a 60% in-hospital mortality & mean survival of just over one year. Death occurs due to the underlying illness; not the arrhythmia itself Tends to resolve following treatment of the underlying disorder

38. Multifocal Atrial Tachycardia Heart rate usually 100-150 bpm May be as high as 250 bpm Irregular rhythm with varying PP, PR and RR intervals. At least 3 distinct P-wave morphologies in the same lead Isoelectric baseline between P-waves (i.e. no flutter waves). Absence of a single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent PACs). Some P waves may be non-conducted; others may be aberrantly conducted to the ventricles.

39. Atrial flutter (variable block)

40. Broad complex regular tachycardias

41. Monomorphic VT

42. Monomorphic VT vs SVT + Aberrancy Absence of typical RBBB or LBBB morphology Extreme axis deviation - “northwest axis” Very broad complexes (>160ms) AV dissociation (P and QRS complexes at different rates) Capture beats —when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration. Fusion beats —when a sinus and ventricular beat coincides to produce a hybrid complex. Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen. Brugada’s sign - The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms in any of the chest leads Josephson’s sign – Notching near the nadir of the S-wave RSR’ complexes with a taller left rabbit ear. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.

43. Monomorphic VT vs SVT + Aberrancy Other suggestive factors: Age > 35 Structural heart disease / Cardiomyopathy Ischaemic heart disease / Previous MI Congestive heart failure Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)

44. Monomorphic VT

45. Monomorphic VT

46. Monomorphic VT DCCV if haemodynamically unstable +/- amiodarone (300mg over 20-60min) Consider lignocaine (1-1.5mg/kg over 2min), particularly for VT associated with myocardial ischaemia

47. AVRT ( antidromic )

48. AVRT ( antidromic ) Much less common than orthodromic AVRT Rate usually 200 – 300 bpm Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway.

49. AVRT ( antidromic )

50. AVRT ( antidromic ) If in doubt treat as VT Stable patients may respond to drug therapy including amiodarone or procainamide , but may require DCCV

51. Sodium channel blockade

52. Sodium channel blockade Tachycardia: this is often a sinus tachycardia with a grossly prolonged PR interval, such that the P wave is hidden in the previous T wave or QRS complex Broad QRS complexes. Right axis deviation of the terminal QRS positive R’ wave in aVR , deep S wave in lead I Give bicarb and intubate / hyperventilate

53. Hyperkalaemia

54. Hyperkalaemia Widening/flattening then loss of p wave Peaked T waves Development of a sine-wave appearance Usually slower rather than fast heart rate Give calcium and agents to reduce / shift the potassium

55. Other WCT differentials Sinus tachycardia + BBB (constant or rate-related) Sinus tachycardia + WPW Pacemaker mediated tachycardia If unsure; treat as VT! Overall, VT accounts for: 80% of cases of WCT >90% of cases of WCT in patients with structural / ischaemic heart disease

56. Broad complex irregular tachycardias

57. Torsades de pointes

58. Torsades de pointes Ventricular tachyarrhythmia associated with prolonged QT interval (congenital or acquired) Cease QT prolonging agents (inc amiodarone ) and correct electrolyte abnormalities Initially Magnesium Sulphate 2g over 10 min DCCV if needed Consider pacing / isoprenaline to prevent relapse

59. AF + (L)BBB

60. AF + WPW

61. AF + WPW Rate > 200 bpm Irregular rhythm Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway QRS Complexes change in shape and morphology Axis remains stable (unlike TDP)

62. AF + WPW Don’t give AV nodal blocking drugs eg : Adenosine / CCB / Beta blockers etc DCCV usually preferred Some suggest considering procainamide

63. Side note Can consider the S5 / Lewis Lead if having difficulty identifying suspected atrial activity Will highlight atrial activity and diminish ventricular activity Read off Lead I

64. References Australian Resuscitation Council Guideline 11.9 – Managing Acute Dysrhyhmias https://resus.org.au/guidelines/ Life In The Fast Lane Deranged Physiology UpToDate REVRT trial http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)61485-4/abstract