Electrophysiology of dysrhythmias (tachyarrhythmias) Flashcards
How can a re-entrant tachycardia be terminated?
- By prolongation of the refractory period (e.g. by drugs)
- electrically induced ventricular depolarization during the excitable gap (which is the region in the circuit not yet activated by the circulating wavefront)
- increase the conduction velocity in the slow pathway
- decrease the length of the re-entrant circuit (so that the next wavefront will reach the slow pathway in refractory period)
What is the mechanism of ANVRT?
- 30% of population has dual AVN physiology with a fast pathway (long refractory period) and a slow pathway (with a short refractory period)
- In sinus rhythm: the electrical impulse travels down the fast pathway. The slow pathway is in refractory from the previous normal beat, hence no retrograde conduction is observed.
- An early atrial extrasystole happens and is only conducted via the slow pathway since the fast pathway is still in refractory. Once it traveled through the slow pathway, the fast pathway is no longer in refractory hence retrograde conduction is observed.
- The slow pathway is the antegrade limb and the fast pathway is the retrograde limb of the reentry.
What is the mechanism of orthodromic AV reentrat tachycardia?
AV node: slow pathway
Accessory pathway: fast pathway
- An AVRT often starts with a VPB. When a VPB triggers it can´t go up the AVN since it is still in refratory period, but it can travel up the accessory pathway (retrograde conduction through the accessory pathway) The AVN is now ready to receive another impulse and the electrical wavefront goes down the AVN again (antegrade conduction via AVN).
What is the mechanism of atrial tachycardia?
- Atrial tachycardia can be generated in any part of the atrium and is usually focal. If there is re-entry it is localized “focal” area.
- Different P wave morphology on ECG
- Atrial rate usually between 150-200 bpm.
- Narrow QRS (similar to intrinsic) due to conduction through AVN.
What is the mechanism of atrial fibrillation?
Two possible mechanisms that can coexist:
1) Multiple wavelets: of depolarization within the atria coalescing and extinguishing each other as they travel in a random fashion seeking tissue that is excitable
2) single or small number of high-frequency “drivers” of “micro-reentry” primarily located at the left atrium - pulmonary vein junction
- F waves have a rate of 300-500 bpm
Dual chamber EGMs: discrimination of tachycardia with 1:1 conduction
- SVT with 1:1 conduction: normally sinus tachycardia accelerates gradually with stable PR intv.
- VT with 1:1 retrograde VA conduction (2-3% of VTs detected by ICDs): VT may exhibit a few beats of AV dissociation before stable VA conduction becomes established.
- A short PP interval favors SVT
- A short RR interval favors VT
In tachycardia with 1:1 conduction:
a transient AV block indicates SVT
VA block during ATP is diagnostic of VT
How to discriminate VT vs SVT with response to ATP?
No termination of tachycardia with ATP: Highly suggestive of AT if atrial rate remains the same or if there is preserved A-AV response with acceleration of the atrial rate
Termination of tachycardia by ATP: Not AT
Name the possible causes for wide QRS tachycardias?
1) VT
2) SVT with aberrant conduction (BBB)
3) Antidromic AVRT
4) Orthodromic AVRT with aberrant conduction (BBB)
5) AF with aberrant conduction over an accessory pathway
6) Antidromic AVRT via Mahaim fibers (atriofascicular accessory pathway between right atrium and RBB)