TachyarrhythmiaNADHI FONSEKA
Reference
LifeintheFastlane
Tintinally’s emergency Medicine
Uptodate
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
Classification-Anatomical
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
Atrial Tachyarrhythmia
Sinus Tachycardia
SNRT
Atrial fibrillation
Atrial Tachycardia
-Focal Atrial Tachycardia
-Macro-re-entrant atrial tachycardia = Atrial flutter
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
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
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
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
Ectopic atrial tachycardia
Rate 120
Abnormal P waves
Atrial flutter with 3:1 block
Sinus tachycardia
P waves hidden within T [camel hump appearance]
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
Atrioventricular tachyarrhythmia
Depends on activation between atria and ventricles or AVN
AVNRT
AVRT
Junctional tachycardia
[commonly called SVT]
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
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
Pathophysiology
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
P waves seen as Pseudo R waves
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
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
ECG-WPW
In SR
Short PR < 120
Delta wave [positive /negative]
QRS – wide > 110
ST and T discordant changers
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
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.
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)
After treatment Shows Underlying WPW in SR
Age 5 with WPW
Antidromic AVRT
Broad complex
difficult to distinguish from VT.
> 95% of broad complex tachycardia in children are SVT with aberrancy.
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).
AF in WPW
Shows intermittent pre-excitation-Produce delta waves
Other impulses are transmitted via the AV node, producing narrow QRS complexes.
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
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
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
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.
Ventricular Tachyarrhythmia
Contained completely in the ventricle
VT
-Monomorphic VT
-Polymorphic VT [Eg-torsades de pointes]
VF
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
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
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)
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
R only
S only
RS complexes
If RS complexes present measure RS interval
RS > 100 – VT if not go to next step
Look for hidden P waves
If P present in a different rate to VR – VT
If not go to next step
Look for morphological criteria for VT
In V1-2 and V6
V1 – Dominant R - RBBB like morphology
Dominant S - LBBB like morphology
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
LBBB morphology- VT is indicated by
In V6- QS waves &/or qR pattern
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
Hyperkalaemia
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
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
For Drug induced QT prolongation- Predicting risk of TdP
TdP
Secondary to Severe Hypokalaemia
U waves
Long QU interval
R on T -beat 9 on rhythm strip
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.
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
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)
Management
Tachycardia with Pulse
Stable
IVC
ECG
Unstable
Sync-Cardioversion
IVC/ECG/Sedate if possible
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
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
Broad Complex tachycardia -If in Doubt treat as VT
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
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
https://youtu.be/qrhWH2_KKOY