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.

Studying for my cardiology boards and revisit this frequently. Thanks for the great explanation

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Great job!

Thanks 🙏 very helpful!

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.

Thanks sir

In phase 2 cells are in absolute refractory period and sodium channels are inactive and cells can not generate AP

thanks!