Tachyarrhythmia Management

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