Well described ❤️🙏 With respect Sir Increase in ATP in smooth muscles leads Vasodilation, so ideally Thiamine should Vasodilate but due to it's inhibiting controll effect on release of Nitrous oxide Thiamine prevents VD. ☺️
So let’s see if I understand this correctly? - T3/T4 increase metabolism which increases metabolic waste products I.e. CO2 etc. - this increase in waste products cause systemic vasodilation and an initial decrease in BP - Baroreceptors sense this initial drop, and signal to the heart to increase HR - BP maintained but continuous elevation in metabolism leads to even more waste products and vasodilation (positive feed back loop) - HR increases further to compensate thereby reducing diastole period and thus perfusion to it’s own tissues - eventually the hearts demand is so high and it’s supply is so compromised that it fails? *My question... - where does the RAAS response come in to maintain BP? Where is the SNS/catecholamine response come in? Wouldn’t they help offset some of this vasodilation and thus reduce some of the stress off the heart (so it wouldn’t have to work alone in maintain BP)? Also, wouldn’t this significant increase vasodilation lead to like systemic edema, pleural effusions etc? Don’t the capillaries get excessively leaky as they dilate that much?
he never said capillary ...its arterioles not capillary that should solve the vasodilation issue as for RAAS query lets say it kicked in will normalize the bp but still to treat this thing you need to treat the cause behind it in ur case thyroid supplementation .......even after bp normal the tissue will continue to sec co2 in blood which will again cause vasodiln more RAAS more fluid ...repeat the process....ultimately the this will exceed the body`s capacity to hold fluid and heart would not be able to pump againt those press generated after multiple cycle of fluid reabs.....and heart failure which was caused bcz of high cardiac output
fistulas are simple same thing just difference is in lets say in case of increase thyroid .....more waste causes vasodiln and more preload but in av fistulae there is a direct bipass bw arteries and veins and bcz of resistance being lower in veins that is easy for blood to go through
so with this could we expect hypotension or HTN? i get confused when you say the vessels dilate, but the heart beats at a faster demand because of the low output to the body. if the heart is beating increasingly fast to compensate, how would this affect the BP? what would be some tips to lookout for in the prehospital setting?
Good question. Let's break down the sequence of events. First the vessels dilate. This leads to a fall in the BP. However, heart will start beating fast to maintain the BP. If you see this patient you will observe almost normal BP with increased heart rate. You won't see increased BP though. If the situation isn't corrected then the heart will start filling leading to a progressive drop in the BP.
thank you so much! complex concept just became clear in a second
Such a brilliant explanation for difficult topic.. thank u
You are very welcome. Glad the topic became clear 🎉🎉🎉
Amazing! helps me alot with my cardiology exam.
Well described ❤️🙏 With respect Sir Increase in ATP in smooth muscles leads Vasodilation, so ideally Thiamine should Vasodilate but due to it's inhibiting controll effect on release of Nitrous oxide Thiamine prevents VD. ☺️
Good point, thanks!
Wonderful lecture sir, good presentation, nice and concise talk..really informative..
Awesome! Thank you for teaching 😁_ It makes my readings for HIGH output make sense!
Thanks Dr from somalia
You are most welcome. Cheers from the USA.
Ty, you helped me understand in your first minute!
Your lecture is adorable Dr. And you look like ravish Kumar
Thank you dear. Who is ravish Kumar?
@@DrBeenMedicalLectures .ravish kumar is a Indian journalist and managing editor of ND TV. He received Roman magsaysay award recently.
What happens in anaemia..?? How does it less to high output cardiac failure..?? Btw ..very nice video.
So let’s see if I understand this correctly?
- T3/T4 increase metabolism which increases metabolic waste products I.e. CO2 etc.
- this increase in waste products cause systemic vasodilation and an initial decrease in BP
- Baroreceptors sense this initial drop, and signal to the heart to increase HR
- BP maintained but continuous elevation in metabolism leads to even more waste products and vasodilation (positive feed back loop)
- HR increases further to compensate thereby reducing diastole period and thus perfusion to it’s own tissues
- eventually the hearts demand is so high and it’s supply is so compromised that it fails?
*My question... - where does the RAAS response come in to maintain BP? Where is the SNS/catecholamine response come in? Wouldn’t they help offset some of this vasodilation and thus reduce some of the stress off the heart (so it wouldn’t have to work alone in maintain BP)?
Also, wouldn’t this significant increase vasodilation lead to like systemic edema, pleural effusions etc? Don’t the capillaries get excessively leaky as they dilate that much?
he never said capillary ...its arterioles not capillary that should solve the vasodilation issue
as for RAAS query lets say it kicked in will normalize the bp but still to treat this thing you need to treat the cause behind it in ur case thyroid supplementation .......even after bp normal the tissue will continue to sec co2 in blood which will again cause vasodiln more RAAS more fluid ...repeat the process....ultimately the this will exceed the body`s capacity to hold fluid and heart would not be able to pump againt those press generated after multiple cycle of fluid reabs.....and heart failure which was caused bcz of high cardiac output
I like your presentation n I have liked the video becos I like it.😂
Very well explained sir
Sir,
As in wet beriberi, the heart muscle is already weak.. So how can it pumps more blood like how it's making more output???
omg excellent video!!! but where can i find the rest of it? i wanted to understand about fistulas
fistulas are simple same thing just difference is in lets say in case of increase thyroid .....more waste causes vasodiln and more preload but in av fistulae there is a direct bipass bw arteries and veins and bcz of resistance being lower in veins that is easy for blood to go through
Very well explained!
Thank you so much this helped me a lot!
great video and very helpful, but i came here specifically for anemia :/
amazing, thank you so much dr!
Hi sir good information
Thank you
Very nice!!
Thank you
I didn't understand the part where you said diastolic is from aorta and systolic is due to arteriolar constrictions
Nice, thx
so with this could we expect hypotension or HTN? i get confused when you say the vessels dilate, but the heart beats at a faster demand because of the low output to the body. if the heart is beating increasingly fast to compensate, how would this affect the BP? what would be some tips to lookout for in the prehospital setting?
Good question. Let's break down the sequence of events. First the vessels dilate. This leads to a fall in the BP. However, heart will start beating fast to maintain the BP. If you see this patient you will observe almost normal BP with increased heart rate. You won't see increased BP though. If the situation isn't corrected then the heart will start filling leading to a progressive drop in the BP.
@@DrBeenMedicalLectures Thank you!
Sir,...How vasodilation will cause increase in venous return..........rather than causing blood stasis???????
How do Beta blockers effect the dynamics?
Omg thank you !!!!!!!
You are most welcome!
Hi doc hw r u?
I am doing great. You?
How are you
Thank you!!