Within about 14 minutes I quite clearly was able to fully comprehend the relation between the mechanism of the drugs and the relation with ECG changes ,which I couldn't even after refering 3 textbooks.your video is my platform to master antiarrythmic drugs. Thanks a million time
These lectures are pure gems! My first aim is to reinforce mai understanding of antiarrhythmics but the second is definitely to learn how to deliver a presentation.
Thanks. I'm glad someone noticed it! Whenever I mention Floyd to my students today and they respond with blank stares, I feel like I die a little inside...
Thank you so much, and fantastic timing. We just started our anti-arrhythmic lectures today :) Thank you for your hard work, I will be recommending your video to my cohort.
Thank you so much for your great explanation, I bet you were at least a substitute teacher at one point in your life. I will recommend your channel to the rest of my classmates.🙏🙏🙏
I have a question about your explanation of the “slow response” action potential in the SA and AV nodes at 9:40.. you're saying that the slow diastolic depolarization (phase 4) is caused by inward Na+ and K+ currents.. but I thought that K+ currents would oppose membrane depolarization? After all, the maximum diastolic potential in the SA and AV nodes doesn't reach below the equilibrium potential for potassium, so how could there be in an inward potassium current (even though these are inward rectifier channels)?
Or maybe I misunderstood the concept of inward rectifier potassium channels? As far as I understand it, these channels are blocked at more positive potentials due to Mg2+ and polyamines blocking the channels.. but these channels (e.g., the IK1 current in ventricular myocytes) are important for stabilizing the resting potential of myocytes, but by not conducting at more depolarized potentials, they allow the plateau with calcium influx, which then allows calcium-induced calcium release..
Could anyone explain why class 2 and 4 slow the sinus and PR interval? Calcium comes into play during early depolarization so shouldn’t it also prolong QT interval. Having trouble differentiating these in my head from class 3 effects bc it’s depolarization.
thank you perfect video can someone answer this : slowing down the influx of sodium ions into cardiac muscle cells causing a decrease in the excitability of the cells it has a beta adrenergic blocker which can cause bradycardia and bronchospasm : sotalol propafenone verapamil mexitilene
Simple, precise, essential - as usual you are showing great understanding of the subject derived from clinical experience and remarkable teaching skills. The only thing I might contest is a pain reflex arc described in your analogy - it's one of more simple arc consisting of two or three neurons connecting on the level of spine. No brain involed... I could be wrong though - I attended physiology classes in 2002. PS Marry Christmas and thanks for your effort!
you're the uttermost of what we call a teacher. Love your logic in presenting ideas in a clear simple way
Within about 14 minutes I quite clearly was able to fully comprehend the relation between the mechanism of the drugs and the relation with ECG changes ,which I couldn't even after refering 3 textbooks.your video is my platform to master antiarrythmic drugs.
Thanks a million time
A doctor from china learn a lot from your online lesson, thank you for your excellent lecture.
Never seen such a wonderful lesson! You're incredibly CLEAR!!!
These lectures are pure gems! My first aim is to reinforce mai understanding of antiarrhythmics but the second is definitely to learn how to deliver a presentation.
Finally, someone that explains the effects on EKG.
This series is such a FANTASTIC refresher for Step 2/fourth year rotations. THANK YOU!
Enjoyed "the dark side of the moon" reference. Thank you for all the great videos you have made!!
Thanks. I'm glad someone noticed it! Whenever I mention Floyd to my students today and they respond with blank stares, I feel like I die a little inside...
@@StrongMed You shouldn't die I was very happy to see the Dark side too!
I was about to leave a comment on that reference and noticed someone already did 3 years ag :D Greetings from Berlin, Germany
Oh how i wish our books were as simple in explaining these concepts as you
Thank you so much, and fantastic timing. We just started our anti-arrhythmic lectures today :) Thank you for your hard work, I will be recommending your video to my cohort.
Just yesterday I was wondering about new videos from you! Thank you so much for the lectures Dr. Strong!
Seems like I've hit a jackpot !! I'm so thankful for these valuable videos Thank you Dr Strong 🙏
Thanks a lot sir. That is the one of the simple yet best explanation I have ever watched in You Tube overall.
Dr Strong is a diva!!
Thank you so much for your great explanation, I bet you were at least a substitute teacher at one point in your life. I will recommend your channel to the rest of my classmates.🙏🙏🙏
Thanks
Thank you!
Thank you Dr Strong, crucial lecture indeed.
Such a beautiful presentation!
I have a question about your explanation of the “slow response” action potential in the SA and AV nodes at 9:40.. you're saying that the slow diastolic depolarization (phase 4) is caused by inward Na+ and K+ currents.. but I thought that K+ currents would oppose membrane depolarization? After all, the maximum diastolic potential in the SA and AV nodes doesn't reach below the equilibrium potential for potassium, so how could there be in an inward potassium current (even though these are inward rectifier channels)?
Or maybe I misunderstood the concept of inward rectifier potassium channels? As far as I understand it, these channels are blocked at more positive potentials due to Mg2+ and polyamines blocking the channels.. but these channels (e.g., the IK1 current in ventricular myocytes) are important for stabilizing the resting potential of myocytes, but by not conducting at more depolarized potentials, they allow the plateau with calcium influx, which then allows calcium-induced calcium release..
Your videos are definitely the BEST !
one of my favorite Bach pieces btw
Thank you Dr Eric for your great videos :)
From Cambodia 🇰🇭 , thanks you so much.
Could anyone explain why class 2 and 4 slow the sinus and PR interval? Calcium comes into play during early depolarization so shouldn’t it also prolong QT interval. Having trouble differentiating these in my head from class 3 effects bc it’s depolarization.
Fantastic video😍🎉
very much helpful
😊😊 thank u sir
Thank you 10000x. This is a great lesson
thanks a lot sir... so beautiful explanation .. enjoying medicine much more than ever... thanks a lots sir...
thank you perfect video can someone answer this :
slowing down the influx of sodium ions into cardiac muscle cells causing a decrease in the excitability of the cells it has a beta adrenergic blocker which can cause bradycardia and bronchospasm :
sotalol
propafenone
verapamil
mexitilene
Excellent video thank you!
Thank you for the excellent videos!
Simple, precise, essential - as usual you are showing great understanding of the subject derived from clinical experience and remarkable teaching skills.
The only thing I might contest is a pain reflex arc described in your analogy - it's one of more simple arc consisting of two or three neurons connecting on the level of spine. No brain involed... I could be wrong though - I attended physiology classes in 2002.
PS Marry Christmas and thanks for your effort!
Are the rest of the videos far away ?? this is great
Posting 1 video a day for the next week.
Thank you so much for this ❤️
when will the next video of this series be available?
Will be posted tomorrow. I'll be posting 1 video/day for the next week (i.e. the whole antiarrhythmics series).
STRONG WORK!
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ok this was just woooooow
You are really good, keep going.
Which book ?
crystal clear
6:08
Never thought Dr. Eric is that cute XD
Nice video sir😊
Thank u
Nice video!
this guy is so fucking boring, but he is the presents this topic in the most organized way, so here we are, folks.
great