Keypoints of video: Premature activation by afterdepolarization. Early or delayed. Reasons: opening of the L type Ca2+ channels. Leads to membrane depolarization. bradycardia, hypoxia, acidosis, low K+ also contribute. Delayed afterdepolarization is result of too much Ca2+ in cell. Digoxin and ischeamia contribute too. The oscilation may trigger depolarization of new cells. Afterdepolarization leads to: premature beats, tachyarrhythmia, tachycardias. might induce reentry mechanisms.
@rishikahdevi92403 жыл бұрын
thank youuuu
@MarcKatzMD2 жыл бұрын
Studying for my cardiology boards and revisit this frequently. Thanks for the great explanation
@SaraMicallef Жыл бұрын
im in my first year of medschool so why thE fuckS this shit in my syllabus.
@umniah_105 жыл бұрын
You are greatttt, and awesome , just complete what you are doing. We are supporting you here! 🍀🍀🍀
@MrJayPuff10 ай бұрын
Great job!
@offrednatalie78874 жыл бұрын
Thanks 🙏 very helpful!
@itsmejulia1 Жыл бұрын
Stupid question probably, but I'll just throw it out: - Why exactly does high intracellular Ca2+ cause delayed afterdepolarizations? Is it because of decreased resting potential? (I was also about to ask what's the mechanism behind Digoxin being a risk factor for DAD, but since it raises intracellular Ca2+ it's basically the same question as before) Not studying for boards, in my defense. Just interested student.
@nyleshamsi4465 Жыл бұрын
Calcium has to be pumped out in order for the contractile cell to stop contracting. If calcium doesn't leave and stays in the cell longer than instructed, then it will hang around in the cytosol and will therefore cause a small depolarisation because it is a positive charge when the cell is trying to get back down to the negative resting potential. This random depolarisation is seen on an ECG as arrhythmia (a lot of small contractions)
@abdullahwahid601 Жыл бұрын
Thanks sir
@user-bp9od4km6p2 жыл бұрын
In phase 2 cells are in absolute refractory period and sodium channels are inactive and cells can not generate AP