This document provides guidance on the assessment and treatment of arrhythmias presenting in the emergency department. It outlines an approach of first determining hemodynamic stability, then distinguishing between narrow and wide complex tachycardias, and finally determining the specific arrhythmia and appropriate treatment. For unstable patients with any arrhythmia, synchronized direct current cardioversion is recommended. Further treatment is tailored based on whether the arrhythmia has narrow or wide QRS complexes and is regular or irregular.

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!

4. 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

5. Step 2
• Is it broad or narrow complex?

6. 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)

7. 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

8. 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

9. 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)

10. 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)

11. 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)

12. Narrow complex regular tachycardias

13. Sinus tachycardia

14. 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)

15. AVNRT

16. 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

17. AVNRT

18. AVNRT

19. 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

20. 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

21. AVRT (orthodromic)

22. AVRT (baseline)

23. 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.

24. AVRT

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

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

27. Atrial Flutter (fixed ratio 2:1)

28. 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

29. 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

30. Narrow complex irregular tachycardias

31. Atrial Fibrillation

32. 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)

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

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

35. 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

36. Atrial Fibrillation
• Consider need for anticoagulation
– CHA2DS2-VASc >1
• Recommend anticoagulation
– HASBLED >2
• Consult with cardiology before anticoagulating

37. Multifocal Atrial Tachycardia

38. 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

39. 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.

40. Atrial flutter (variable block)

41. Broad complex regular tachycardias

42. Monomorphic VT

43. 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.

44. 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)

45. Monomorphic VT

46. Monomorphic VT

47. 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

48. AVRT (antidromic)

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

50. AVRT (antidromic)

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

52. Sodium channel blockade

53. 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

54. Hyperkalaemia

55. 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

56. 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

57. Broad complex irregular tachycardias

58. Torsades de pointes

59. 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

60. AF + (L)BBB

61. AF + WPW

62. 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)

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

64. 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

66. 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