Thanks for the kind words! More videos in this series are definitely coming. I'm currently taking a break due to travel and a large non-medical DIY project (that will hopefully be featured on my other RUclips channel once finished).
@@StrongMed Excellent! Best of luck with your project! I'm starting Perfusion school in a month and I've been reviewing cardiothoracic content on your channel. Top-level content, all around. Again, thank you 👍
thanks for the video. I am considering getting my masters in Math with a biology track and cardiac mechanics is one class I may have to take. This helped shed some light on the subject.
Amazing clear explanation of difficult cardiac physiology and pathophysiology concepts, excellent correlation with clinically relevant parameters and their limitations. Thank you.
Thank you for pointing out that preload and afterload doesn’t have universally same definition Because I have spent more time to understand this Now onwards my first go for cardiology for clinical practice will be Strong Medicine
Thank you Doctor Strong. I just re watched and better understood. Your lecture is the best place . Oh may be if you have time , you could make another video regard to Covid , new vaccines , and the end game of Covid ect ….
I don't understand why in your explanation of afterload, wall tension and afterload are interchangeable. (when talking about the law of Laplace, "afterload is proportional to the LV pressure and the LV radius"). Thank you for the video
Cardiomyocytes have mechanosenstive ion channels that are permeable to caclium. These channels open as a function of cell cortex-membrane tension. This results in a flux of calcium from intracellular stores.
I am a med studnet and we really appreciate your efforts. I really like your videos and you made me fall in love with cardiology and internal medicine. I love how you explain things at great details, especially in the heart sounds series. You make us really understand things, rather than memorize. Any videos you make are definitly helpful, no matter what topic it is. Please keep it up. We appreciate your efforts. Thank you from Egypt!
As a physiology TA I thank you for the Frank-starling and EF section, I knew hearth failure would "flatten" the graph, but i'd never put that much tought to how this was because due to changes on contractility, nevermind how afterload could manage to make the same changes, i'd never even heard someone say that preload and afterload status would change EF evaluation, this puts the whole HFpEF/HFrEF situation in a whole other light, makes me question a single EF measurment as an addecuate indicator of how should one treata patient. Do you have a recommended source to expand on this subject?
The best resource for advanced physiology topics that I know of (particularly for cards & pulm) is the website, Deranged Physiology (derangedphysiology.com/main/home) run/written by Alex Yartsev, an Australian critical care doc. It's much better than any single physiology textbook I've found to date.
It would seem, based on your list of factors influencing afterload, that increased preload is itself going to increase afterload, since chamber diameter would be increased, and thus increasing wall tension, right? Yet physiology texts I've seen state that the effects of afterload, (e.g. on the force-velocity relationship) can be offset by increasing EDV (i.e. preload). Can you please clarify?
Hello Dr. Strong. I am fascinated by u and ur great lectures. I have developed interest in internal medicine. Sir don't u think with advent of lots of superspecialities and again subspecialities within superspecialities the job of a internal medicine doctor has restrained to treatment only a few diseases ?
Yes and no. A few years ago, I moved from a VA hospital (where everything non-surgical was admitted to medicine) to Stanford (where we have separate neurology, gen cardiology, heart failure, EP, oncology, hematology, hepatology, and pulm hypertension services). So on one hand, I see a more narrow range of primary problems, but those problems I do see can be far more complex than what I saw before. Your comment also seems very closely related to the video I posted this morning, in which I argued that the conventional organ system model that serves as the rough basis for the division of medicine into subspecialties is itself inherently flawed. There can be disease that might end up on a subspecialty service (e.g. cardiac amyloidosis, neurosarcoidosis, Wilson's disease presenting with hepatic failure, etc...) in which a complete understanding of the person's pathology can require someone whose perspective isn't biased by 3+ years of subspecialty training on just one organ. Are there days where I wish I saw more cardiology and maybe even completed a cards fellowship? Yeah, I have those days. But on the whole, I think I am more satisfied being better able to see the forest for the trees (no shade intended towards subspecialists).
Hello doctor strong, may I ask a question? If the preload can also be defined by law of laplace, then I think the difference between preload and afterload is very confusing. If the venous return increased, not only the end-diastolic volume increase, but the systolic volume also increase ; moreover, if the systolic vascular resistance increase, then the transmural pressure during end-diastole will also increase, which will also lead to an increase of preload. I came across this question when studying arterial and venous vasodilator, which decrease systolic pressure and increase venous return respectively.
Thanks you Dr.Strong! Currently, I have made some videos with Vietnamese subtitles from your videos. Could I do that with your permission? Thank you so much. Best regard.
Is decreasing SVR dangerous? I understand the pressure will go down but will not CO go up which is what really matters in terms of oxygen delivery to the organs. So why is anaphylactic/septic chock dangerous? (I understand the blood volume leakage is dangerous but if you just account for lower SVR)
This is a really fascinating question that I remember having myself as I was a resident in the ICU. Part of the issue with lowering SVR to increase CO is that when SVR drops too much due to medications, sepsis, or anaphylaxis, you lose the ability to autoregulate the perfusion to specific vascular beds. Normally, through a combination of autonomic input, varying expression of hormone receptors in different parts of the body, and the effect of local mediators, our bodies have the ability to alter vascular tone to preferentially direct blood to specific sites (e.g. brain, kidneys, skin, gut, skeletal muscle, etc...). If something interferes with the ability to preferentially vasoconstrict some vascular beds but not others, the body is no longer able to redirect the cardiac output where it's needed most. So even if the CO is increased overall, the CO to a specific organ (e.g. kidneys) might end up reduced. For example, in sepsis, this is why the skin is usually warm and flushed - there is too much blood being redirected to the skin rather than to internal organs. Without specifically looking into it at the moment, I suspect there is also an issue specifically with cerebral perfusion. For most organs, blood flow is partially determined by the difference between mean arterial pressure and venous pressure. Changes in both position and hydration affect both those values in the same direction (though not necessarily to the same degree). But for the brain, blood flow is determined by the difference between mean arterial pressure and intracranial pressure. So even if cardiac output is increased by lowering SVR, the drop in MAP will lead to an even bigger problem with blood getting shunted away from the brain. If anyone else has additional thoughts on this, feel free to share!
Yes! Cardiovascular physiology. Unfortunately, the videos take longer than my average to make, so I'll be releasing them interspersed with other topics or else my video frequency would drop significantly.
I'm sorry, I honestly don't. I made that series using a different workflow which doesn't allow the quick export of images in pdf format the way many of my other videos do.
If you have questions about the video content, you are welcome to post them here. However, I don't answer personal questions, and I am unable to provide specific individualized medical advice. (Not saying that's what you are asking about, but it is the most common reason viewers track me down off RUclips, and unfortunately, I usually am unable to help them.)
Done (assuming you mean English subtitles). If you are asking for subtitles in a different language, unfortunately, I don't currently have the resources/support to provide that. (EDIT: I sincerely wish I could!)
Salute you r kind and present things in soft patable way
Hoping to see this series continued! These three video presentations that currently comprise it are phenomenal. Thanks so much 😊😊
Thanks for the kind words! More videos in this series are definitely coming. I'm currently taking a break due to travel and a large non-medical DIY project (that will hopefully be featured on my other RUclips channel once finished).
@@StrongMed Excellent! Best of luck with your project! I'm starting Perfusion school in a month and I've been reviewing cardiothoracic content on your channel. Top-level content, all around. Again, thank you 👍
thanks for the video. I am considering getting my masters in Math with a biology track and cardiac mechanics is one class I may have to take. This helped shed some light on the subject.
Amazing clear explanation of difficult cardiac physiology and pathophysiology concepts, excellent correlation with clinically relevant parameters and their limitations. Thank you.
thank you Dear Mr Eric strong for the best prsentation as I ever watched in this field on youtube be successfull be strong
Very good animation of the 3d method of disks, outstanding
After watching your ECG videos directly liked the video without seeing it
Thanks😊
So glad to have this online course during the pandemic in Taiwan…thank you!
Thank you, Dr. Strong! I’d love to watch the rest of the series and would be very interested in further in-depth lectures on this topic.
Thanks doc , ur every video is really good . The way you explain every topic with fine details shows ur commitment. hats off to u sir
it was splendid talk on the basics of physiology in cardiology!...thank you so much sir!
Thank you Doctor Strong ❤️
Many thanks for these world class vedios Sir. Good bless you 🙏🙏
Thank you very much Doctor Strong. Very good lecture. I learn new thing from you. Probably need to re watch also. Your lecture is superb.
Thank you for pointing out that preload and afterload doesn’t have universally same definition
Because I have spent more time to understand this
Now onwards my first go for cardiology for clinical practice will be Strong Medicine
Thank you so much Dr. Eric for a wonderful video and Explanation.
I just found this , and it's very helpful. Thank you very much.
Thank u Dr. Strong❤❤❤
Thank you Doctor Strong. I just re watched and better understood. Your lecture is the best place . Oh may be if you have time , you could make another video regard to Covid , new vaccines , and the end game of Covid ect ….
Thank You Sir .. waiting for next
It's coming soon! Was working on it earlier today.
@@StrongMed Thank You so much Sir from the depths of my heart... Love and Respect
Thanks you Dr
Symptomatology
Doctor a tension pneumothorax could another example for increased intrathoracic pressure?
I don't understand why in your explanation of afterload, wall tension and afterload are interchangeable. (when talking about the law of Laplace, "afterload is proportional to the LV pressure and the LV radius"). Thank you for the video
Cardiomyocytes have mechanosenstive ion channels that are permeable to caclium. These channels open as a function of cell cortex-membrane tension. This results in a flux of calcium from intracellular stores.
Thanks Dr. Strong. Helpful as always.
u r really good teacher
Yes, Dr. STRONG. AGREED WITH ACHMED. THANK STRONG MEDICINE SO MUCH-NEEDED!
Sir, please continue similar videos on different systems. Thaaaaaaaaaanks!
I hope to, but CV is going to keep me busy for a while!
I am a med studnet and we really appreciate your efforts. I really like your videos and you made me fall in love with cardiology and internal medicine. I love how you explain things at great details, especially in the heart sounds series. You make us really understand things, rather than memorize. Any videos you make are definitly helpful, no matter what topic it is. Please keep it up.
We appreciate your efforts. Thank you from Egypt!
@@youssefrefaat1594 Thank you for the kind words!
@@StrongMed hi sir pls do video on leukaemia plsss???
Please we need à video about long covid and treatment 🙏
As a physiology TA I thank you for the Frank-starling and EF section, I knew hearth failure would "flatten" the graph, but i'd never put that much tought to how this was because due to changes on contractility, nevermind how afterload could manage to make the same changes, i'd never even heard someone say that preload and afterload status would change EF evaluation, this puts the whole HFpEF/HFrEF situation in a whole other light, makes me question a single EF measurment as an addecuate indicator of how should one treata patient.
Do you have a recommended source to expand on this subject?
The best resource for advanced physiology topics that I know of (particularly for cards & pulm) is the website, Deranged Physiology (derangedphysiology.com/main/home) run/written by Alex Yartsev, an Australian critical care doc. It's much better than any single physiology textbook I've found to date.
Thanks
It would seem, based on your list of factors influencing afterload, that increased preload is itself going to increase afterload, since chamber diameter would be increased, and thus increasing wall tension, right? Yet physiology texts I've seen state that the effects of afterload, (e.g. on the force-velocity relationship) can be offset by increasing EDV (i.e. preload). Can you please clarify?
Thank you dr Eric for your lectures. I would like to ask you why positive pressure ventilation decrease afterload ? I expected the opposite
ruclips.net/video/plcrzGTOBmw/видео.html 03:23
Thank you!
Hello Dr. Strong. I am fascinated by u and ur great lectures. I have developed interest in internal medicine. Sir don't u think with advent of lots of superspecialities and again subspecialities within superspecialities the job of a internal medicine doctor has restrained to treatment only a few diseases ?
Yes and no.
A few years ago, I moved from a VA hospital (where everything non-surgical was admitted to medicine) to Stanford (where we have separate neurology, gen cardiology, heart failure, EP, oncology, hematology, hepatology, and pulm hypertension services). So on one hand, I see a more narrow range of primary problems, but those problems I do see can be far more complex than what I saw before. Your comment also seems very closely related to the video I posted this morning, in which I argued that the conventional organ system model that serves as the rough basis for the division of medicine into subspecialties is itself inherently flawed. There can be disease that might end up on a subspecialty service (e.g. cardiac amyloidosis, neurosarcoidosis, Wilson's disease presenting with hepatic failure, etc...) in which a complete understanding of the person's pathology can require someone whose perspective isn't biased by 3+ years of subspecialty training on just one organ.
Are there days where I wish I saw more cardiology and maybe even completed a cards fellowship? Yeah, I have those days. But on the whole, I think I am more satisfied being better able to see the forest for the trees (no shade intended towards subspecialists).
@@StrongMed I see what you did with the last phrase. Great play of words!
Looking forward to watching this...I think you mean contractility (title)
Yes, thank you! (Those are the silly errors that happen when I post videos at 4am!)
Hello doctor strong, may I ask a question? If the preload can also be defined by law of laplace, then I think the difference between preload and afterload is very confusing. If the venous return increased, not only the end-diastolic volume increase, but the systolic volume also increase ; moreover, if the systolic vascular resistance increase, then the transmural pressure during end-diastole will also increase, which will also lead to an increase of preload. I came across this question when studying arterial and venous vasodilator, which decrease systolic pressure and increase venous return respectively.
AWESOME!
Thanks you Dr.Strong!
Currently, I have made some videos with Vietnamese subtitles from your videos.
Could I do that with your permission?
Thank you so much.
Best regard.
Master sword. Nice
Is decreasing SVR dangerous? I understand the pressure will go down but will not CO go up which is what really matters in terms of oxygen delivery to the organs. So why is anaphylactic/septic chock dangerous? (I understand the blood volume leakage is dangerous but if you just account for lower SVR)
This is a really fascinating question that I remember having myself as I was a resident in the ICU. Part of the issue with lowering SVR to increase CO is that when SVR drops too much due to medications, sepsis, or anaphylaxis, you lose the ability to autoregulate the perfusion to specific vascular beds. Normally, through a combination of autonomic input, varying expression of hormone receptors in different parts of the body, and the effect of local mediators, our bodies have the ability to alter vascular tone to preferentially direct blood to specific sites (e.g. brain, kidneys, skin, gut, skeletal muscle, etc...). If something interferes with the ability to preferentially vasoconstrict some vascular beds but not others, the body is no longer able to redirect the cardiac output where it's needed most. So even if the CO is increased overall, the CO to a specific organ (e.g. kidneys) might end up reduced. For example, in sepsis, this is why the skin is usually warm and flushed - there is too much blood being redirected to the skin rather than to internal organs.
Without specifically looking into it at the moment, I suspect there is also an issue specifically with cerebral perfusion. For most organs, blood flow is partially determined by the difference between mean arterial pressure and venous pressure. Changes in both position and hydration affect both those values in the same direction (though not necessarily to the same degree). But for the brain, blood flow is determined by the difference between mean arterial pressure and intracranial pressure. So even if cardiac output is increased by lowering SVR, the drop in MAP will lead to an even bigger problem with blood getting shunted away from the brain.
If anyone else has additional thoughts on this, feel free to share!
@@StrongMed thank you very much for the explaination!
👏👏
Need a ‘strong’ cardiac & vascular function curves video
I know - don't worry, it's coming! (Unfortunately, I haven't yet had any bandwidth for making videos this summer)
is this a part of another/new series?
Yes! Cardiovascular physiology. Unfortunately, the videos take longer than my average to make, so I'll be releasing them interspersed with other topics or else my video frequency would drop significantly.
Sir do u have chest x ray series notes?
I'm sorry, I honestly don't. I made that series using a different workflow which doesn't allow the quick export of images in pdf format the way many of my other videos do.
Him: “if we cut the sphere in half we can see the interior cavity”
Me: is that a MASTER SWORD???!!
Yes. Yes it is. ;)
Yaaassss
Sir how to contact you to clarify my doubts ?
If you have questions about the video content, you are welcome to post them here. However, I don't answer personal questions, and I am unable to provide specific individualized medical advice. (Not saying that's what you are asking about, but it is the most common reason viewers track me down off RUclips, and unfortunately, I usually am unable to help them.)
@@StrongMed sir I have assigned myself as ur student, I don't need ur help for personal medical advice but for building my career. Please help .
Please give a subtitle
Done (assuming you mean English subtitles). If you are asking for subtitles in a different language, unfortunately, I don't currently have the resources/support to provide that. (EDIT: I sincerely wish I could!)