7. Supraventicular Tachycardias
Generally used to mean any tachyarrythmia with abrupt onset and offset
involving a re-entrant pathway:
Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular re-entry tachycardia (AVRT) – orthodromic, antidromic
AVNRT
Anatomy of the AV node: fast & slow fibres. Results in a functional re-entrant
circuit within the AV node.
Narrow complex, rates of 140-280. Heart is structurally normal. More common in
women. Sudden onset / offset. May respond to vagal manoeuvres.
8. AVNRT
Typically initiated by a PAC.
Different subtypes (google LITFL…)
ECG findings – narrow complex tachy, QRS alternans, retrograde conduction of
P waves
Management: vagal manoeuvres, adenosine, other anti-arrythmics (CCB, BB,
amiodarone). Rarely requires DCCV*
10. AVRT
Pre-excitation syndromes seen on ECG when patient in sinus rhythm (WPW
changes). These are lost when AVRT is established
Short PR, delta wave, widened QRS
Anatomical re-entrant pathway (Bundle of Kent). Circus movement between
the AV node and accessory pathway.
May be triggered by PAC or PVC
Circus movement may by orthodromic or antidromic
13. Orthodromic AVRT
ECG features: rate 200-300 bpm; buried or retrograde P waves, narrow
complex*, QRS alternans, TWI, ST depression.
Treatment – is pt stable? Can try vagal, adenosine, CCB. If pt compromised
DCCV!
14. Antidromic AVRT
Antegrade conduction via the accessory pathway, retrograde conduction via
AV node.
ECG features: rate 200-300, wide QRS (abnormal depolarisation of ventricles)
Likely to be mistaken for VT. Treatment: DCCV
16. Summing up the SVTs
AVNRT – most common
Narrow complex*, rate up to 240, regular, responds to adenosine
Structurally normal heart – functional re-entrant pathway
AVRT – seen in pre-excitation syndromes (WPW)
Anatomical re-entrant pathway due to presence of accessory bundle
Orthodromic via AV node and back up (retrograde) via the bundle. Results in
narrow complex tachy up to 300bpm, regular
Antidromic via accessory pathway and retrograde via the AV node. Results in
broad complex tachy up to 300bpm, regular.
19. Ventricular Tachycardia
Ventricular tachycardia, rates up to 300bpm
Sustained / non-sustained; monomorphic, polymorphic
VT should be regular (sustained irregularity think SVT w BBB e.g. AF)
SVT with aberrancy vs VT
Pt can be stable or unstable
Features more suggestive of VT:
Age > 35
Pre-existing ischaemic heart disease
Previous VT
Absence normal BBB morphology
Hx structural disease, CCF, cardiomyopathy
FHx sudden cardiac death
20. SVT with aberrancy
Looks like VT!
Broad complex tachycardia originating above Bundle of His. Becomes broad due to
pre-existing BBB. This will be seen on the baseline ECG!
Some clues to distinguish
North west axis
Concordance of QRS complexes in praecordial leads
Left rabbit ear > right in V1 (very specific for VT)
Fusion & capture beats; AV dissociation
Brugada & Josephson’s signs
Q wave in V6
Very broad complex
http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/ for examples of above
28. Multi Focal Atrial Tachycardia
Associated w severe
respiratory disease,
hypoxia
High mortality –
survival at 1 yr is
20%
Treat the
underlying
condition, not the
tachycardia
Must have 3 P wave
morphologies
Baseline is
isoelectric!!!
34. Other causes of broad complex tachys
Don’t forget
Metabolic derangements e.g. hyperkalaemia
Toxidromes e.g. TCA poisoning
Pacemaker related
36. Summing it up…
Tachyarrhythmias can be regular, irregular, narrow or broad complex
May be the result of functional or anatomical re-entrant circuits, or increase
automaticity
Treatment may depend on underlying cause and on whether the patient is
haemodynamically stable
VT and SVT with aberrancy can be difficult to distinguish, when in doubt,
cardioversion
Physiological e.g. exercise
In response to stressors e.g. catecholamine surg, anxiety, infection, fever
Treat the underlying cause.
Can have ‘inappropriate sinus tachycardia’ – persistent HR > 100 otherwise NSR at rest. Typically seen in young women.
This is 4:1 block, suggests treatment with nodal blocking drug. Clearly demonstrates saw toothed appearance of P waves.
Re-entry circuit established in right atrium.
Very rapid flutter can resemble other forms of SVT (e.g. AVNRT), but tends not to revert with adenosine of vagal manoeuvres. May slow so flutter waves become more obvious facilitating diagnosis..
Can have fixed or variable block. Should suspect if the ventricular rate is bang on 150.
AV node comprised of two bundles of fibres – fast and slow.
Fast fibres depolarise rapidly, but have a long refractory period. Slow fibres taking longer to depolarise but have a shorter refractory period. This can set the stage for re-entrant tachy-arrhythmias.
Normally, Impulse reaches AV node, travels down both fast and slow fibres. Fast impulse propagated to ventricles, then begins up slow pathway and meets refractory tissue. Impulse is terminated.
PAC arrives at AV node when the fast tissue is still refractory (remember, long refractory period – the normal physiology for AV delay), but the slow pathway is no longer refractory, so the impulse travels down slow pathway, meets the fast tissue, which is no longer refractory and impulse travels retrograde to establish a re-entrant circuit. Impulses can also be conducted back up to the atria, which is the basis for retrograde P waves that can either be buried in the QRS or appear after the QRS (esp V1). These P waves will resolve one NSR is restored.
*Can required DCCV especially in a pt who has had previous and failed ablation.
Narrow complex, normal QRS morphology
Regular
Rate 145 (ranges between 120 and 250bpm)
Retrograde P waves seen in V1 (can be inverted in the inferior leads), just after QRS. Can be buried in QRS because atria and ventricles have simultaneous depolarisation.
Can have ST and T wave changes related to rate.
These changes resolve with reversion to NSR
Short PR as there is no delay via the AV node.
Slurring of QRS upstroke as the accessory bundle beings to depolarise the ventricles prior to the normal conduction pathway (pre-excitation of the ventricles), and this causes widening of the QRS.
Thought to be other variants e.g ?Levon Gown – not proven to exist.
Baseline ECG
Short PR interval
Delta wave
Broad complex QRS
AVRT can be established by two types of circus movement:
Orthodromic – conduction is anterograde (i.e. toward the ventricle) via the AV node and then travels retrogradely towards the ventricles via the accessory bundle. This establishes a circus loop. Because the bundles are depolarised via the AV node, this results in a narrow complex tachycardia
Antidromic – conduction is anterograde (toward the ventricles) via the accessory pathway. The venticles therefore undergo abnormal depolarisation. Impulse travels retrogradely toward ventricles by the AV node causing the loop. This results is a broad complex tachycardia.
*any narrow complex rhythm can be broad complex in the presence of aberrancy or pre-existing BBB.
Can be extremely difficult to differentiate from AVNRT
?pre-excitation features on baseline ECG
Antidromic AVRT
Broad complex, regular due to abnormal depolarisation of the ventricles via the accessory bundle.
Note: can have narrow complex VT if established high at the Bundle of His.
VT can also be slow (e.g. in setting of medications such as anti-arrythmics)
VT should be the default diagnosis.
Can use Brugada criteria to help establish, but largely a theoretical exercise as these patient should be treated as VT until proven to be SVT.
Brugada sign – Distance from onset of QRS to nadir of S wave is >100 msec
Josephson sign – notching of the S wave near the nadir
Very broad complex
Negative concordance
North west axis
QS complex in V6
Consistent with VT
Broad, but relatively narrow QRS
Normal axis
No AV dissocation
Non concordant
LBBB pattern
Consistent with SVT (AVNRT) with BBB.
An old ECG would demonstrate pre-existing LBBB.
Rhythm vs rate control
May be regular or irregular or regularly irregular or irregularly irregular….
Can have variable block
Rare
Associated with severe respiratory disease (COPD) and hypoxia
Requires at least 3 different P wave morphologies on same rhythm strip (numerous different atrial pacemakers)
High mortality – survival at 1 yr after an episode of MAT is 20%
Do not treat the rhythm, but the underlying cause of the rhythm e.g. COPD.
Must have HR >100
3 distinct P wave morphologies in the same lead (different ectopic foci)
Baseline must be isoelectric (to distinguish from AF)
Differing P-P, PR and R-R intervals
Whitney Houston – I will always love you, the Bodyguard
Gloria Estefan – the rhythm will get you
Beach Blanket Bingo – theme song from Beach Blanet Bingo
The real tacky brady syndrome…
Other forms of polymorphic VT e.g. bidirectional VT (rare)
Irregular chaotic activity does not produce an output.
Shockable rhythm
Irregular AF impulses travel down the accessory pathway – abnormal depolarisation of ventricles results in broad complex. No AV nodal delay so can have very rapid rates up to 300bpm.
Features of pre-excitation are absent
Can occasionally have a capture beat
Pt’s are haemodynamically compromised and require DCCV – admit!
