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Do you know the mechanism of typical atrial flutter (AFL)? 1/
Typical AFL is a macroreentrant circuit with the activation wavefront rotating clockwise or counterclockwise around the tricuspid annulus and using the CTI as an essential part of the circuit.
2/ Conduction across the CTI is relatively slower than the rest of the atrium (likely due to the anisotropic fiber orientation), which provides the protected zone of relatively slow conduction necessary for the flutter reentry circuit.
3/
Key to the development of typical AFL is formation of a line of transverse conduction block in the RA free wall, which acts as a critical lateral boundary that prevents short-circuiting of the flutter wavefront around the IVC and, hence, extinguishes (see video).
4/ This line of block (as indicated by the presence of double potentials on the map) is usually functional, often related to the normal anisotropic and geometric properties of crista terminalis (note the normal voltage in the region of conduction block in this video).
5/ A run of transitional rhythm (e.g., AFib) of variable duration is often required to create this functional line of block and induce AFL in otherwise normal atria.
6/ The intercaval line of block line can be fixed (e.g., atriotomy scar). Then, antecedent AF may not be necessary to induce AFL. In fact, in this setting, typical AFL is more common than peri-atriotomy macroreentrant AT.
6/ The intercaval line of block line can be fixed (e.g., atriotomy scar). Then, antecedent AF may not be necessary to induce AFL. In fact, in this setting, typical AFL is more common than peri-atriotomy macroreentrant AT.
7/ Wavefront rotation in the RA free wall should not be misinterpreted as a macroreentrant circuit (especially given the inherent annotation pitfalls of some mapping systems and with incomplete maps). Entrainment mapping from the CTI helps in the DDx.
8/ It is important note that the CTI is not the “diseased” tissue that causes the AFL. We ablate the CTI just because it happens to be the easiest target to eliminate typical AFL, and not because it is arrhythmogenic substrate.
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“Aberration” describes transient bundle branch block (BBB) and does not include persistent QRS abnormalities caused by persistent BBB, preexcitation, or the effect of drugs.
Acceleration-dependent BBB (aka “phase 3 block” or “voltage-dependent block”) occurs when an impulse arrives at tissues that are still refractory due to incomplete repolarization (during phase 3 of the action potential [AP]).
3/9
Aberration secondary to phase 3 block tends to be in the form of RBBB when premature excitation (and Ashman phenomenon) occurs during normal baseline heart rates and in the form of LBBB when it occurs during fast heart rates.
Impedance and RF ablation:
Part 2: How does RF ablation affect impedance?
1/9 As tissue temperature rises during RF energy application, ions within the tissue being heated become more mobile, resulting in a decrease in impedance to current flow.
2/9 There are currently 2 methods to measure impedance: Generator Impedance (GI) & Local Impedance (LI).
3/9 Lack of impedance drop during RF energy application can reflect inefficient energy delivery to the tissue due to poor tissue contact, lack of catheter stability, or inadequate power delivery.
Impedance & RF ablation:
Part 1: How does impedance affect RF lesion formation?
1/8 During RF ablation, system impedance = impedance of genera¬tor + transmission lines + catheter + electrode-tissue interface + skin patch interface + interposed tissues.
2/8 IMPEDANCE & POWER
The magnitude of RF current delivered by the generator is determined by impedance btwn ABL electrode and ground pad. Ablation at lower impedance yields higher current output (and tissue heating) compared with ablation at a similar power & higher impedance.
3/8 IMPEDANCE OF ELECTRICAL CONDUCTORS
Currently used electrical conductors from the generator to the patient and from the ground pad back to the generator are designed to have low electrical resistance to help minimize power loss within those conductors.
1/8 ECG patterns that mimic 2°AVB are often related to atrial ectopy, concealed junctional ectopy, or AVN echo beats. Distinguishing physiologic from pathologic AVB is important.
2/8 In 2°AVB, sinus P-P interval is fairly constant (except for some variation caused by ventriculophasic arrhythmia), the nonconducted P wave occurs on time as expected, and P wave morphology is constant. With ectopy, P waves occur prematurely & often have different morphology.
3/8 Early PACs can arrive at the AVN during the refractory period and conduct with long PRI or block (physiologic rather than pathologic block) and can mimic Mobitz I or Mobitz II 2°AVB.
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What Is the Gap Phenomenon? 1/4 “PROXIMAL DELAY ALLOWS DISTAL RECOVERY” is the fundamental concept of gap phenomenon. This requires a distal site with a long effective refractory period (ERP) and a proximal site with a shorter ERP.
2/4 During gap phenomenon, initial block occurs distally (due to longer ERP). Earlier impulses encroach on the relative refractory period (RRP) of proximal site where conduction delay is encountered, which allows for expiration of the ERP of the distal site, enabling conduction.
3/4 Any pair of structures in the AV conduction system that has the appropriate EP physiological relationship can exhibit the gap phenomenon (e.g., atrium–AVN, proximal AVN–distal AVN, AVN–HPS, HB-distal HPS). Gap can occur in the anterograde or retrograde direction.
1/7 Concealed conduction can be defined as "the propagation of an impulse within the conduction system that can be recognized only from its effect on the subsequent impulse, interval, or cycle."
2/7 Impulse propagation in the conduction system generates too small electrical current to be recorded on ECG. If this impulse travels only a limited distance (incomplete penetration) in the conduction system, it can interfere with formation or propagation of another impulse.
3/7 Irregular Ventricular Response During AF:
AVN is expected to conduct at regular intervals when its RP expires after each conducted AF impulse. Irregular response is caused by incomplete penetration of some AF impulses into AVN, variably resetting its refractoriness.