1-what factors determine QT interval? how come sometimes medications which widen QRS do not change QT interval? is not QRS complex a part of QT?
2-all class1 antiarrytmics block sodium channels at phase 0,then should not we expect all class1s widen QRS? then why i just read class1a and 1c,but not 1B widen qrs?and again we have long QT with class1A but not with 1c,how come?
I will try and answer these questions, i may not be correct so hopefully someone more knowledgeable will correct it here.
During AP in Nodal tissues, there are three states of Na channel, active state, inactive state and transition state. The three different classes act on three of these states. This has been explained well by Dr.Lionel Raymond in Kaplan Pharmacology videos. Like when you block active Na channel, then you prolong the APD (Action Potential Duration). This active channel after some time goes back to being inactive until a next impulse comes, one of the class I drugs (i don't remember which specifically but i think its I B) blocks it rendering it inactive for transition into active state on the impulse arrival. This is how they have slightly different modes of action. This in turn, i presume explains different actions on QRS.
I am sorry if i haven't been coherent in my explanation but this is what i remember from the lectures. However on UW and USMLE Consult, the things that they check your knowledge is drugs and their effects on APD, their side effects profile and not really the mechanism why they prolong the QRS interval.
2-all class1 antiarrytmics block sodium channels at phase 0,then should not we expect all class1s widen QRS? then why i just read class1a and 1c,but not 1B widen qrs?and again we have long QT with class1A but not with 1c,how come?
I will try and answer these questions, i may not be correct so hopefully someone more knowledgeable will correct it here.
During AP in Nodal tissues, there are three states of Na channel, active state, inactive state and transition state. The three different classes act on three of these states. This has been explained well by Dr.Lionel Raymond in Kaplan Pharmacology videos. Like when you block active Na channel, then you prolong the APD (Action Potential Duration). This active channel after some time goes back to being inactive until a next impulse comes, one of the class I drugs (i don't remember which specifically but i think its I B) blocks it rendering it inactive for transition into active state on the impulse arrival. This is how they have slightly different modes of action. This in turn, i presume explains different actions on QRS.
I am sorry if i haven't been coherent in my explanation but this is what i remember from the lectures. However on UW and USMLE Consult, the things that they check your knowledge is drugs and their effects on APD, their side effects profile and not really the mechanism why they prolong the QRS interval.
