#IssaTweetorials
How does drug therapy affect atrial flutter (AFL)?
1/8
- Typical AFL is an intra-atrial peritricuspid macroreentry that is independent of the AVN.
- Drugs used in AFL affect the atrial action potential, the AVN action potential, or both.
#EPeeps
How does drug therapy affect atrial flutter (AFL)?
1/8
- Typical AFL is an intra-atrial peritricuspid macroreentry that is independent of the AVN.
- Drugs used in AFL affect the atrial action potential, the AVN action potential, or both.
#EPeeps
2/8
For AFL reentry to sustain, the wavelength of the reentrant wavefront (conduction velocity x ERP) should be shorter than the reentry pathlength.
This can be achieved by:
- Slowing wavefront velocity.
- Shortening ERP
- Enlarging anatomic length of the reentry circuit.
For AFL reentry to sustain, the wavelength of the reentrant wavefront (conduction velocity x ERP) should be shorter than the reentry pathlength.
This can be achieved by:
- Slowing wavefront velocity.
- Shortening ERP
- Enlarging anatomic length of the reentry circuit.
3/8
ß-blockers, Diltiazem, Verapamil:
- Prolong AVN conduction time and refractoriness = Reduce ventricular rate & unmask flutter waves.
- No significant effects on atrial action potential = No effect on atrial rate, and these drugs do not terminate AFL.
ß-blockers, Diltiazem, Verapamil:
- Prolong AVN conduction time and refractoriness = Reduce ventricular rate & unmask flutter waves.
- No significant effects on atrial action potential = No effect on atrial rate, and these drugs do not terminate AFL.
4/8
Adenosine:
- Suppress AVN conduction = Reduce ventricular rate & unmask flutter waves.
- Shorten atrial ERP = accelerate atrial rate during AFL & may convert AFL into AFib.
- Termination of a tachycardia with Adenosine is inconsistent with AFL & suggests SVT rather than AFL.
Adenosine:
- Suppress AVN conduction = Reduce ventricular rate & unmask flutter waves.
- Shorten atrial ERP = accelerate atrial rate during AFL & may convert AFL into AFib.
- Termination of a tachycardia with Adenosine is inconsistent with AFL & suggests SVT rather than AFL.
5/8
Class III AADs:
-Prolong atrial ERP = Prolong wavelength + shorten excitable gap in AFL circuit = AFL reentry circuit becomes vulnerable to termination.
-No major effect on atrial conduction velocity = Slowing of atrial rate during is not prominent.
Class III AADs:
-Prolong atrial ERP = Prolong wavelength + shorten excitable gap in AFL circuit = AFL reentry circuit becomes vulnerable to termination.
-No major effect on atrial conduction velocity = Slowing of atrial rate during is not prominent.
6/8
Class Ic AADs:
- Reduce excitability and suppress atrial conduction velocity + small effects on ERP.
- If atrial conduction block develops = AFL terminates.
Class Ic AADs:
- Reduce excitability and suppress atrial conduction velocity + small effects on ERP.
- If atrial conduction block develops = AFL terminates.
7/8
Class Ic AADs:
- If atrial conduction slowing (not block) develops = Shorten wavelength = Promote AFL reentry (proarrhythmogenic)+ Decrease atrial rate during AFL.
- No effects on AVN = Slower atrial rate may allow 1:1 AV conduction and paradoxically faster ventricular rates
Class Ic AADs:
- If atrial conduction slowing (not block) develops = Shorten wavelength = Promote AFL reentry (proarrhythmogenic)+ Decrease atrial rate during AFL.
- No effects on AVN = Slower atrial rate may allow 1:1 AV conduction and paradoxically faster ventricular rates
8/8
Class Ic AADs:
- Suppress HPS conduction velocity (especially at faster rates; ie, use-dependent effects) = QRS widening can develop during AFL with 1:1 AV conduction, mimicking VT.
- Therefore, treatment with class Ic AADs should be combined with AVN blocking drugs.
Class Ic AADs:
- Suppress HPS conduction velocity (especially at faster rates; ie, use-dependent effects) = QRS widening can develop during AFL with 1:1 AV conduction, mimicking VT.
- Therefore, treatment with class Ic AADs should be combined with AVN blocking drugs.
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