Frank-Starling mechanism | Circulatory system physiology | NCLEX-RN | Khan Academy
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- เผยแพร่เมื่อ 14 ต.ค. 2024
- Carefully follow 5 different preload scenarios to see how each one will have a different effect on how actin and myosin line up. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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You are an excellent teacher and make things simple and easy to remember! Thank you
If i become a great doctor you are one of the reasons :)
Nelly Hoffman same 😂
I am just living it by the hour now
just entered med school hehe any updates? :)
Soooooo hi doctor :)
*When
updates?
Not quite. Check out the video on active contraction vs. passive recoil.
Great video, thanks alot for explaining the Frank Starling in an easy yet still in debt way. Btw your mouse drawing skills are impressive!
These videos are just AMAZING!
Very clear explanation of an otherwise confusing concept. Thank you for your help in teaching my team.
But from my understanding of basic histology shouldn't the myosin and actin not overlap during relaxation? Like the first drawing I'm pretty sure it's how contraction looks with the actin closer and overlapping the H zone and it's definitely not relaxation
off topic but u sound like pewdiepie when he's serious lol
7 minutes in... still waiting to see how this is about starling forces >__
All of this is relevant. Extrapolate.
Exactly! It is hard to say if the makers of some Khan Academy videos are themselves dumb or they make these videos for blockheads. Too much actin overlap here - a straightforward explanation that should have taken less than 5 min can get extended to almost 15 min... Unbelievable!
This is NOT the video for starling forces...I don't know where the hell you got that idea from.
This was immensely helpful.
5th myosin actin would be drawn according to graph giving maximum pressure
This is true but it's not the whole mechanism. Increased cardiac muscle length also increases calcium release from the sarcoplasmic reticulum.
It's normal due to increase of diameter and sarcomeres of cardiac muscle fibers , therefore have much sarcoplasmic reticulum ----> increase release of Calcium.
With the increasing cardiac muscle length you have an increase in contractility of the heart. When with increasing contractility you increase heart rate that in turn increased the number of action potentials. Increasing the number of action potentials you increase intracellular Ca2+ content and you increase the inward movement of Ca2+ current.
You are correct but this description of the Frank-Starling mechanism is still incomplete. Although stretch does not directly lead to more Ca2+ being released, it increases the sensitivity of the myocytes to Ca2+ as the troponin C has a higher affinity for it. The mechanism for this increased sensitivity is yet to be determined but it does contribute to the Frank-Starling concept
@@janerosiecurran Yes!
Wonderful explanation, thank you.
شكرًا
Thank you so much for helping me 😊
Shout out to Frank & Sterling
Thank you so much sir
Thank u so much for crystal clear explaination👏👏👍
Absolutely gorgeous illustration /// thank you so much
Thank you so much.
thank you thank you thank you thank you thank you thank you
AMAZING! Thank you:)
thanks very much guys
Thank you very much. You make these subjects seem easy learning.
They're talking about one heartbeat and what's happening during the 0.08 seconds it takes to complete a cycle.
Myosin & actin are motor proteins. They help muscles move.
I'm a paramedic. Cardiac care is my area of special interest.
It might be 0.8 seconds rather than 0.08. Anyway, there's an 8 in it and that's how I remember that the "golden hour" for cardiac collapse is no more than 8 minutes to arrive on the scene and start care.
AWESOME!!!!! Very helpful. Thanks! :)
what software is it? (drawing)
Thanks. This really helped
good !!!
amazing, thanks!
Really good & helpful
That's why hypertrophy leads to reduced force of contraction ultimately..
Actually what I didn't get, is whether the condition no 1 normally present in myocardium.??
Excellent.
This is the basis of heart failure, I learned this back in pathophysiology and then forgot. Came back to remember this stuff and holy fuck it clears things up, thanks.
well explained! thank you for sharing useful information for heart failure
Best❤
Nice
Is this a spring force? F = k*x where k is a spring constant and x is the distance of stretch.
so good!
Shout out lol... Nice!
the drawing is so satisfying
this helps me a lot!!
thankyou! :)
thanx
عشت حجي
:DDDDDDDDDDD
At step 5, there is no force, right? I kind of imagine preload as a rubber band being stretched out. So at step 5, is this the point at which the rubber band breaks? or the ventricle wall breaks at this point leading to no force?
Thank you so much dude ! you're doing a great job,
that was really helpful, thanks for the new creative way of learning, as i was watching this vid, i wonder what future projects do you have? what new dreams do you wanna accomplish? what new semiological lessons do you want to make? but that's not the think, isn't it ? it all about time, time is precious, so precious that we would want to study them carefully, taking as much time as planning a holiday, or party... :) good luck
So does the heart normally start somewhere between situation one and two?
That was super helpful.
great video 👌
what causes to get the myocytes goes to 5th stage in frank-starling law? in other word what causes the myocytes overstretched and can't give force?
"STARLING LAW"
" WATER GAIN "
' THEORY '
I like to get all my books up please.
What's the situation like between scenario 4 and 5?
1:43 Preload is Stress? Is it not the Volume? (Preload = LVEDV)
does the tropomyosin, troponin C, and g-actin play a role in the Frank/Starling Mechanism?
Thank you for your great helpful videos.... I am a fan of you
সহজ বাংলায় এবং প্রনবন্ত উপস্থাপনার মাধ্যমে,ফ্রাঙ্ক স্টার্লিং ম্যাকানিজম সম্পর্কে জানতে,ক্লিকঃ
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বি.দ্রঃচ্যানেলটি একদমই নতুন!নিয়মিত লেকচার পেতে সাবসক্রাইব করে,বেল আইকনটি বাজিয়ে দিন!
Watch in 2x. Still was not clear about preload and after load. Due to auto regulation, (calcium sensitivity to troponin is increased) increase in after load and increase in preload, both increase stroke volume, right? Is this true with regards to Frank-Starling law?
Have my exams, would like to clarify before it.
What is the relation of this to heterometric and homeometric reserve?
Why is the graph flipped the other way???
So when senerio 5 happens, we get congestive heart failure ?!
Overall poor example of Frank Starling, should use a Frank Starling curve to explain this, not a pressure volume graph. Try looking at a book on Cardiac Physiology
Imagine being rude to a guy who’s offering free help on the internet. Wow!
hey
hello
Enoch Starling
Are you left-handed?
There are so many things wrong with this video. Myosin cross bridges and force of contraction do not happen the way he is saying here. My professor at UCSF tells me that thin filament does not cross over each other under physiological or any condition because of other structural elements that prevent shortening of sarcomere the way Rishi is showing. My prof thinks that medical doctors do not try to understand or update how Frank-Starling mechanism works and they keep parroting text book information.
dont know what there talking bout
Like it
They're talking about cardiac output and cardiac volume. It has to do with the beating of the heart and how much blood is going through the heart during a heartbeat and what the pressure of the blood is.
I'm a paramedic, and cardiac care is my area of special interest.
I'm also an EKG (aka ECG) Technician.
Your Videos are such a good recap! Thanks alot!! Will give you credit in my physio final ;)