Been a physician assistant 20 years. Worn in critical care. Everything falls back on Frank Starling. Present or does a fabulous job teaching the subject tied in WUH clinical examples. Loved it.
End diastolic volume (EDV) affects preload. They aren't the same thing, but are closely related. An increase in EDV (which itself is affected by end diastolic pressure and compliance) will cause preload (the filling pressure) to increase, which increases the stroke volume (and therefore cardiac output). Sorry i went on a bit there, trying to cement this idea in my head too! Hope it helps :)
I don't understand how the contractility can be a factor on its own, when it is already intrinsically included in afterload. Afterload is directly characterized by the systolic tension of the myocardium and indirectly by the peripheral resistance. (Definition of the Pschyrembel, the most recognized german medical dictionary. So if you have a high tension of the myocardium the afterload, which is the stroke resistance, decreases. I am conscious about the fact, that I equate the contractility with the tension of the myocardium. Is that right? If it isn't, is that my error in thinking?
Best video on the subject... This video > my 3 hour cardiodynamics lecture.
Been a physician assistant 20 years. Worn in critical care. Everything falls back on Frank Starling. Present or does a fabulous job teaching the subject tied in WUH clinical examples. Loved it.
সহজ বাংলায় এবং প্রনবন্ত উপস্থাপনার মাধ্যমে,ফ্রাঙ্ক স্টার্লিং ম্যাকানিজম সম্পর্কে জানতে,ক্লিকঃ
ua-cam.com/video/Efjr_mjrNBM/v-deo.html
বি.দ্রঃচ্যানেলটি একদমই নতুন!নিয়মিত লেকচার পেতে সাবসক্রাইব করে,বেল আইকনটি বাজিয়ে দিন!
This and other videos like it has taught me more than my £50 cardiology book I have been struggling with. Thank you!!
Hey, thanks this video really helps. You explained it better than my hour long lecture today.
This video is great! It's straight to the point.....
Awesome Vid!!!
End diastolic volume (EDV) affects preload. They aren't the same thing, but are closely related. An increase in EDV (which itself is affected by end diastolic pressure and compliance) will cause preload (the filling pressure) to increase, which increases the stroke volume (and therefore cardiac output).
Sorry i went on a bit there, trying to cement this idea in my head too! Hope it helps :)
love the enthusiasm!
Great!
easy and simple explaination !!! good job
Awesome video.
Great job.
This realy helped me. Thank you!
awesome - thank you so much!
lifesaver, thanks!
thanks! just made my life easier
Thanks! Very helpful.
May Allah bless you brother, thanksss
thanks so much:) your videos really helped alot
awesome! Thanks!
Thank You Sir.!
Great! Thanks!
we can say more in more out ?
best vidio sir ,
can you upload more questions, like does in last 3 minutes meanwhile like isoprotenol and hydrazine need other more examples
I don't understand how the contractility can be a factor on its own, when it is already intrinsically included in afterload.
Afterload is directly characterized by the systolic tension of the myocardium and indirectly by the peripheral resistance. (Definition of the Pschyrembel, the most recognized german medical dictionary.
So if you have a high tension of the myocardium the afterload, which is the stroke resistance, decreases.
I am conscious about the fact, that I equate the contractility with the tension of the myocardium. Is that right? If it isn't, is that my error in thinking?
Yo, thanks!
thank u
i love you
Wonderful, thanks a lot.
gold, gold, gold, gold, gold
is the preload the same as the end diastolic volume?
Isn't it that isoproterenol is already obsolete?