Hi WBDR! I think it would have been very interesting to see an ECG strip with an arrythmia example that be an indication for each class of anti-arrythmia drug. Then see how the action potential changes from the drug would translate to the ecg waveform.
Thanks for checking out the video! It has to do with the degree of their potassium channel blockade! More potassium channel blockade equates to more prolonged ERP! Does that make sense?
![Class II Anti-Arrhythmic - The Beta Blockers [Explained Clearly]](http://i.ytimg.com/vi/gNxo15IdGtU/mqdefault.jpg)
Hi WBDR! I think it would have been very interesting to see an ECG strip with an arrythmia example that be an indication for each class of anti-arrythmia drug. Then see how the action potential changes from the drug would translate to the ecg waveform.
Excellent lecture
Thanks for checking out the video and for the kind words!
Why do class1b drugs shorten ERP and why do class1c not affect ERP? what is the mechanism?
Thanks for checking out the video! It has to do with the degree of their potassium channel blockade! More potassium channel blockade equates to more prolonged ERP! Does that make sense?
If class 1B had almost no effect on na channels why was phase 0 so slow?
You are correct, our drawing isn’t spot on. The class 1B slope should be less steep than class 1a and then class 1c. Thank you for pointing that out!