Class 1b - penelope24

[ArchivalUser]

I dont understand the class 1B antiarrhythmics mechanism:

If they decrease AP duration and decrease ERP, how does they treat arrythmias?

Thank you

[ArchivalUser]

I meant how do*

[ArchivalUser]

Do you remember slow conduction in those ischemic tissue here where the arrhythmia healthy tissue that firing fast and working fine vs hypoxic tissue in next door & ischemic heart so you can think like balancing it in life with evil & good.
Blocking channel that is already close ( or simple word black the door that paralyzed to begin with)? Imagine blocking Inactivated (imagine blocking/preventing any Na channel to return to cell bz the channel indeed is closed as you holing the channel handcuff* -> what you preventing go -> back to “resting” -> AP firing back ( keeping those cell in hypoxic tissue refractory )
The most important about 1B -> shorten the APD by blocking slow NA window current heart tissue & dissociate from those channel with rapid kinetics if you recall & that domino effect of DIASTOLE & buying more time for recovery-> shorting the AP & QT interval and slowing conduction & prolonging QRS interval happen @ QRS at fast HR and as you know class 1B AV nodal conduction have immunity /or muscle cell contractility.

Sorry bit drunk hope justifiable to your understanding I will try post few Q later.