I dont understand the class 1B antiarrhythmics mechanism:
If they decrease AP duration and decrease ERP, how does they treat arrythmias?
Thank you
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.