Tachyarrhythmia Management

1. Tachyarrhythmia
NADHI FONSEKA

2. Reference
 LifeintheFastlane
 Tintinally’s emergency Medicine
 Uptodate

3. Mechanism
 Increased automaticity in a normal or ectopic site
Usually gradual in onset and termination
 Re-entry in a normal or accessary pathway
Abrupt onset and termination.
Triggered by Ectopics
 After depolarization causing triggered rhythms

4. Classification-Anatomical

6.  Tachycardia Narrow or Wide QRS
Narrow Wide
Regular Irregular Regular Irregular
Sinus AF VT Polymorphic VT
AVRT MAT Antidromic AVRT
AVNRT AF with Variable Narrow complex tachy with aberrancy
Aflutter block

7. Atrial Tachyarrhythmia
 Sinus Tachycardia
 SNRT
 Atrial fibrillation
 Atrial Tachycardia
-Focal Atrial Tachycardia
-Macro-re-entrant atrial tachycardia = Atrial flutter

8. Sinus Tachycardia
 Physiological[exercise/emotion] or pathological
-look for underlying cause
-If no underlying cause found consider SNRT or focal Atrial tachycardia
-Sinus tachycardia in a normal heart with no underlying cause is called
inappropriate sinus tachycardia

9. Atrial fibrillation
 Most common sustained cardiac arrhythmia
 Usually associated with some underling heart disease
Atrial enlargement, elevated atrial pressure , inflammation
 Multiple ectopic foci continuously discharging with no uniform atrial
depolarization or contraction
 Fibrilatory waves best seen in V1-3 and aVF
 Irregularly irregular ventricular contractions 110-160

10. Atrial tachycardia
Regular atrial rhythm with P rate > 100
 Focal atrial tachy
-from a automatic focus in atria firing faster than SAN.
-different P wave morphology and axis

11. Atrial Flutter
 Caused by re-entry circuit over a large area of a atrium[R/L]
 Atrial rate >240[usually 300]. AV block 2:1 usually or more occasionally
 1:1 if sympathetic stimulation or Accessary pathway[unstable/VF]
 Ventricular rate usually 125-175
 Narrow complex tachycardia
 Flutter waves best seen in leads II, III, aVF
 Flutter waves in V1 may resemble P waves
 Irregular with variable AV block
 Loss of isoelectric baseline

13. Ectopic atrial tachycardia
 Rate 120
 Abnormal P waves

15.  Atrial flutter with 3:1 block

17.  Sinus tachycardia
 P waves hidden within T [camel hump appearance]

19. Regular narrow-complex tachycardia at 250-300 bpm.
-Flutter waves not clear
-undulation to the baseline in the inferior leads –Could be flutter with a 1:1 block.
-Or SVT

20. Atrioventricular tachyarrhythmia
Depends on activation between atria and ventricles or AVN
 AVNRT
 AVRT
 Junctional tachycardia
[commonly called SVT]

21.  60% of SVT is re-entry within AVN
 20% re-entry involving a bypass tract
 In a normal heart SVT at the typical rates of 160-200 is often tolerated
for hours to days
 Produce narrow complex tachycardia unless aberrant conduction is present
 Abrupt onset and offset

22. AVNRT
 Occur in normal hearts or hearts with disease
 Commonest cause of palpitations in structurally normal hearts
 Paroxysmal . Could be spontaneous or provoked
 Can terminate spontaneously or may needs intervention

23. Pathophysiology

24. ECG
 Regular tachycardia [140-280]
 Narrow QRS [<120] –unless known BBB, accessory pathway or rate related aberrant
conduction
 P waves
-Not visible usually
-if visible inverted in 11,111,aVF or as pseudo s waves
-May be seen as a Pseudo R wave after QRS V1-2
 ST depression with or without CAD-rate related

25.  P waves seen as Pseudo R waves

26. AVRT
 Re-entry circuit with 2 parallel limbs
-AVN and a Bypass tract
 Re-entry can occur either direction
-usually anterograde through AVN and retrograde through bypass tract
orthodromic-Narrow complex tachycardia
-If Antidromic – Wide complex tachycardia resembling VT
 Triggered by PAC or PVC

27. WPW
 Congenital AV accessory pathway –commonest is bundle of Kent
 Incidence 0.3-1 per 1000
 Small risk of SCD
 Accessory pathway can usually conduct both directions
 Tachyarrhythmia can occur from
a re-entry circuit –AVRT
Can completely bypass AVN –AF or Atrial Flutter in WPW

28. ECG-WPW
In SR
 Short PR < 120
 Delta wave [positive /negative]
 QRS – wide > 110
 ST and T discordant changers

29. AF and Atrial flutter in WPW
 Accessory pathway allows rapid conduction to Ventricles bypassing AVN
 Rapid Ventricular rate can degenerate into VF/VT
 Rate > 200 bpm
 Irregular rhythm in AF
 Wide QRS complexes
 QRS Complexes change in shape and morphology
 Axis remains stable unlike TdP
In Flutter rate is regular

31. WPW
 SR
 very short PR interval (< 120 ms)
 Delta wave
 Tall R waves and inverted T waves in V1-3 mimics RVH — these changes
are due to WPW and do not indicate underlying RVH.

33. Orthodromic AVRT
 Regular, narrow complex tachycardia at 225 bpm
 No visible P-waves
 The QRS complexes are narrow because impulses are being transmitted in an
orthodromic direction (A -> V) via the AV node
 This rhythm is indistinguishable from AV-nodal re-entry tachycardia (AVNRT)

35.  After treatment Shows Underlying WPW in SR

37.  Age 5 with WPW
 Antidromic AVRT
 Broad complex
 difficult to distinguish from VT.
 > 95% of broad complex tachycardia in children are SVT with aberrancy.

39. AF with WPW
 Rapid and irregular
 broad complex tachycardia
 This could easily be mistaken for AF with LBBB.
 However, the morphology is not typical of LBBB, the rate is too rapid (up to 300 bpm in
places, i.e. too rapid to be conducted via the AV node) and there is a subtle beat-to-beat
variation in the QRS width which is more typical of WPW (LBBB usually has fixed width
QRS complexes).

41. AF in WPW
 Shows intermittent pre-excitation-Produce delta waves
 Other impulses are transmitted via the AV node, producing narrow QRS complexes.

42. Junctional Tachycardia
 Arise from AVN or bundle of His
Junctional pace maker rate > SAN
 Impulses spread retrograde to Atria and antegrade to Ventricles
 Atria may activate before, during or after ventricles
 If no retrograde conduction and faster Junctional pace maker rate [than
SAN ]can cause AV dissociation
 Uncommon in healthy hearts
 Seen with CHF, IHD and Digoxin Toxicity

43. Can be classified by rate
 Junctional escape rhythm : 40 – 60 bpm
SAN discharge slow or fail to reach AVN
No retrograde conduction – QRS with no P waves seen
 Accelerated Junctional rhythm : 60 – 100 bpm
Sinus Node overridden

44. ECG-Junctional Rhythms
 Narrow complex
 Ventricular rate usually 60-100
 Retrograde P waves before , during or after QRS
 P – inverted in inferior leads and upright aVR and V1

46.  Junctional tachycardia 115 bpm
-Narrow complex
-Retrograde P waves — inverted in II, III and aVF; upright in V1 and aVR
 Short PR interval (< 120 ms) indicates a junctional rather than atrial focus.

47. Ventricular Tachyarrhythmia
Contained completely in the ventricle
 VT
-Monomorphic VT
-Polymorphic VT [Eg-torsades de pointes]
 VF

48. VT
 Commonest is Monomorphic VT-Regular BC Tachycardia
 Sustained – if Duration > 30 secs or needs intervention secondary to
hemodynamic instability
 Non-sustained – 3 or more beats terminating spontaneously < 30 sec
 Clinically could be stable or unstable
 Shows common features to any broad complex tachycardia
Wide QRS
Increased rate

49. Features suggestive of VT
 Very broad >160ms
 No typical RBBB or LBBB pattern
 Extreme axis deviation
 Capture beats and fusion beats
 Positive or negative concordance with no RS complexes
 Brugada sign
 Taller Left rabbit ear[V1]
 Josephson’s sign
 AV dissociation

51. DD – Wide complex tachycardia
 Ventricular Tachycardia
 SVT with aberrant conduction due to bundle branch block
 SVT with aberrant conduction due to the Wolff-Parkinson-White syndrome
 Pace-maker mediated tachycardia
 Metabolic derangements e.g. hyperkalaemia
 Poisoning with sodium-channel blocking agents (e.g. tricyclic
antidepressants)

52. VT vs SVT with Aberrancy
Broad Complex Tachycardia could be-
 VT
 SVT with aberrant conduction due to bundle branch block
 SVT with aberrant conduction due to the Wolff-Parkinson-White syndrome
Identification important as AVN blocker can cause precipitous instability in VT

54.  R only
 S only
 RS complexes

55.  If RS complexes present measure RS interval
 RS > 100 – VT if not go to next step

56.  Look for hidden P waves
 If P present in a different rate to VR – VT
 If not go to next step

57.  Look for morphological criteria for VT
In V1-2 and V6
 V1 – Dominant R - RBBB like morphology
Dominant S - LBBB like morphology

58.  RBBB morphology – VT is indicated by
Smooth monophasic R V1 QS in V6
Taller L/rabbit ear V1
R/S < 1 V6 –probably VT
QR in V1
QR pattern V1

59.  LBBB morphology- VT is indicated by
 In V6- QS waves &/or qR pattern

61.  RVOT tachycardia
VT is very rare in normal hearts
Commonest cause is IHD
RVOT is a VT seen in normal hearts and considered benign VT
-causes paroxysms of palpitations related to exercise
-Adenosine sensitive
-Broad complex , LBBB morphology with Rightward/inferior axis with AV dissociation

63. Hyperkalaemia

64. Torsades de pointes- QT and Polymorphic VT
 A polymorphic VT
 QRS axis swings from positive to negative in one lead
 Usually short runs of 5-15 seconds-self limiting
 Rate 200-240 bpm
 Seen with congenital LQTS, myocardial disease with long QT in ECG
or drug/disease/electrolyte induced QT prolongation
 Can cause instability / degenerate to VF

66.  Long QT precipitates Early after depolarizations – Tall U waves / PVC
 If a PVC occurs on a preceding T [ R on T ] TdP can be initiated
 Onset is often after a long-short-long R-R interval [Pause dependent]
 Bigemini with long QT– High risk of TdP
 Rate > 220 – High risk of VF

67. For Drug induced QT prolongation- Predicting risk of TdP

69. TdP
Secondary to Severe Hypokalaemia
 U waves
 Long QU interval
 R on T -beat 9 on rhythm strip

71. Digoxin Toxicity
 Bidirectional ventricular tachycardia (BVT) is a rare ventricular dysrhythmia
characterised by a beat-to-beat alternation of the frontal QRS axis.
 In the example above, you can see the QRS axis shifts 180 degrees from
left to right with each alternate beat.

72. VF
 Lose CO immediately
 If no immediate ALS – Fatal
 If Prolonged degenerate in to asystole
 Chaotic irregular rhythm
 No P,QRS or T
 Rate 150-500

73. Causes
 IHD
 Electrolyte abnormalities
 Cardiomyopathy
 Long QT (acquired / congenital) causing TdP –> VF
 Brugada
 Drugs (e.g. verapamil in patients with AF+WPW)
 Environmental – electrical shocks, drowning, Hypothermia
 PE
 Tamponade
 Blunt trauma (Commotio Cordis)

74. Management

75. Tachycardia with Pulse
Stable
IVC
ECG
Unstable
Sync-Cardioversion
IVC/ECG/Sedate if possible

76. Stable Narrow-complex
Tachycardia
Regular
Vagal
Adenosine 6-12-12
Converts
Probably AVNRT / AVRT
May need AVN blocking Agent
Dose not Convert
Possible Aflutter/EAT/Junctional
Control Rate CCB or BB
Irregular
Possible AF/Flutter/MAT
Rate Control CCB/BB

77. Stable Wide-Complex
Tachycardia
Regular
VT/Uncertain Rhythm
-Amiodarone
-Prepare for Cardioversion
-If Known SVT with Aberrancy
Give Adenosine
Irregular
-If Pre-excitation with AF[AF+WPW]
NO AVN Agents[ Adenosine/CC/BB]
Consider
Antiarrhythmic[Amiodarone/Procanamide
-TdP- Mg 1-2 g over 5-60 min
-Polymorphic VT
Sync Cardioversion
-AF with Aberrancy
Follow Narrow-complex Irregular Protocol

78. Broad Complex tachycardia -If in Doubt
treat as VT

79. Adenosine
 Do not use –
-broad complex irregular tachycardia[AF+WPW]/ Polymorphic tachycardia
-flutter in WPW
-VT –Precipitous instability
 Can be used in RVOT
 Can be used in Narrow Complex Tachycardia – WPW/AF/Flutter/SVT

80. AF
 Loan AF is Unlikely to present with instability
 Treat underlying causes [ Sepsis/Hypovolemia/IHD]
 Adenosine, BB, CCB, Digoxin and Amiodarone –Contraindicated in AF+WPW

81. https://youtu.be/qrhWH2_KKOY