#According to UW in diagnosis of sever aortic stenosis, In most cases the valve area is ≤1 cm2, but valve area is NOT considered for diagnosis. It's diagnosed based on: aortic jet velocity >_4.0 m/sec or mean transvalvular pressure gradient >_40 mm Hg Great lecture thought!!
This is great revision. I request, if you can attach the scripts of this audio in the link. This will help us to activate listening and reading at the same time for effective concentration. Thanks.
One thing to note: Kussmal sign isn't seen in cardiac tamponade because even though the increase in pericardial pressure exerts inward force compressing the entire heart during inspiration, the increase in negative intrathoracic pressure is still able to be transmitted to the right side of the heart and subsequent increase in blood flow to R.A ensues.
We have to differentiate acute from chronic cardicac tamponade. In acute causes/cases, the pericardial sac doesn't have time to stretch and accommodate the fluid, so even like 100mls of fluid is a MAJOR issue and very uncomfortable for the patient. In chronic causes/cases, given the time, the pericardial sac can accommodate LITRES of fluid. Hence, acute cases will behave more like constrictive pericarditis than chronic ones. We see similar stuff with Ascites. Rapid = intolerable, dangerous, etc. Chronic = maybe can accommodate upto 10 Litres of fluid even, and can still breathe.
Initially it is LVH, longstanding it leads to DCM as well. Think of LVH as initial compensation to overcome the increase in Afterload, and DCM as being the exhaustion/failing stage.
Treatment of pericarditis now is combination of NSAIDs and colchicine since it results in significantly better rates of remission and recurrence than treatment with NSAID alone. Don't get tripped up with the NSAID alone choice like I did :)))
Do ace inhibitor still have a mortality benefit or is it just made up blockers and aspirin? The last time that I studied this I only saw beta blockers and aspirin listed.
Question he mentioned metformin as a contraindication in heart failure patients however isn't this information since been revised that It improves cv outcomes and reduces mortality in type 2 diabetes & heart failure?
Deidre Cline not only is the heart having problems relaxing due to the deposits but it also weakens the muscle from contracting optimally, therefore it has a reduced EF. Hope that helps. It's unique because it has mixed features.
Me too! It's especially in sections where he'd normally have put mnemonnics or memorizing shortcuts I think. But he's years past doing this, so while he videos are still helpful, I doubt they'll ever get fixed.
When you talked about PAD causing acute limb ischemia - you said thrombosis. So do you see thrombosis in acute limb ischemia in PAD vs. embolus in acute limb ischemia following an MI? Or is embolus more common in both acute MI and PAD causing acute limb ischemia?
From uworld: Although ALI is often due to thrombosis (eg, plaque), it can also be caused by embolism (eg, thrombus). Given this patient's recent anterior ST-segment elevation myocardial infarction (STEMI), his ALI is most likely due to embolization of a left ventricular (LV) mural thrombus
Nitrates is contraindicated in Right sided MI not inferior MI, inferior MI effects the RCA which can lead to right sided MI if the proximal RCA is occluded but that does not always happen. The RV is supplied by the proximal RCA and its right marginal branch. ST elevation in V4R-V6R is a contraindication to nitrates because it implies an RV infarction
You're editing the phrases halfway. Seems very unnatural. If you don't remember something, just say emm and repeat it, or cut the whole sentence out and repeat it
I’ve watched this multiple times. Always helpful.
Same
@@alexroitburt323 same
#According to UW in diagnosis of sever aortic stenosis, In most cases the valve area is ≤1 cm2, but valve area is NOT considered for diagnosis.
It's diagnosed based on:
aortic jet velocity >_4.0 m/sec
or
mean transvalvular pressure gradient >_40 mm Hg
Great lecture thought!!
It's been 4 yrs since this video release so I think it's understandable
Hi, just want to thank you for these videos. So helpful for my past exam!
This is great revision. I request, if you can attach the scripts of this audio in the link. This will help us to activate listening and reading at the same time for effective concentration.
Thanks.
@@AHLGREN6 thanks. I bought it already. And it helped me to pass one examination. Thanks again to him and you for kind words.
Thank you so very much! Truly appreciate it! This was SUPER helpful. I wish you all the best!
Thank you so much, you don’t know how helpful this is!!!
One thing to note: Kussmal sign isn't seen in cardiac tamponade because even though the increase in pericardial pressure exerts inward force compressing the entire heart during inspiration, the increase in negative intrathoracic pressure is still able to be transmitted to the right side of the heart and subsequent increase in blood flow to R.A ensues.
At 15.16 he is saying that kusumauls sign is seen in CT , but in Uw they mentioned it only for constrictive pericarditis
We have to differentiate acute from chronic cardicac tamponade. In acute causes/cases, the pericardial sac doesn't have time to stretch and accommodate the fluid, so even like 100mls of fluid is a MAJOR issue and very uncomfortable for the patient.
In chronic causes/cases, given the time, the pericardial sac can accommodate LITRES of fluid.
Hence, acute cases will behave more like constrictive pericarditis than chronic ones.
We see similar stuff with Ascites. Rapid = intolerable, dangerous, etc. Chronic = maybe can accommodate upto 10 Litres of fluid even, and can still breathe.
At 16 he mentioned AS,HTN in longrun becoming DCM, in Uw it says concentric hypertrophy; where as DCM causes eccentric
Initially it is LVH, longstanding it leads to DCM as well.
Think of LVH as initial compensation to overcome the increase in Afterload, and DCM as being the exhaustion/failing stage.
Treatment of pericarditis now is combination of NSAIDs and colchicine since it results in significantly better rates of remission and recurrence than treatment with NSAID alone. Don't get tripped up with the NSAID alone choice like I did :)))
Do ace inhibitor still have a mortality benefit or is it just made up blockers and aspirin? The last time that I studied this I only saw beta blockers and aspirin listed.
I I have been thinking of the day you have been a long long to get back into
Awesome videos! By the way I love your shirt!!
Question he mentioned metformin as a contraindication in heart failure patients however isn't this information since been revised that
It improves cv outcomes and reduces mortality in type 2 diabetes & heart failure?
9:34. Can you explain the decreased ejection fraction. Thank you
Deidre Cline not only is the heart having problems relaxing due to the deposits but it also weakens the muscle from contracting optimally, therefore it has a reduced EF. Hope that helps. It's unique because it has mixed features.
is it just me thats getting black screens sometimes during the video?
stop blinking
Me too getting the black screen
I think it’s just u
Me too
Me too! It's especially in sections where he'd normally have put mnemonnics or memorizing shortcuts I think.
But he's years past doing this, so while he videos are still helpful, I doubt they'll ever get fixed.
in restrictive cardiomyopathy the PfEf i mean these preserved ejection fracture unless it occur with dilated
Hey man Im confused about something. I thought diastolic HF had a preserved EF?
At first yes
Pulsus paradoxus also could be caused by COPD😊
And asthma!
Croup also
Thank u 💯💯🤙🏽
When you talked about PAD causing acute limb ischemia - you said thrombosis. So do you see thrombosis in acute limb ischemia in PAD vs. embolus in acute limb ischemia following an MI? Or is embolus more common in both acute MI and PAD causing acute limb ischemia?
Acute limb wud be due to an embolus....
From uworld: Although ALI is often due to thrombosis (eg, plaque), it can also be caused by embolism (eg, thrombus). Given this patient's recent anterior ST-segment elevation myocardial infarction (STEMI), his ALI is most likely due to embolization of a left ventricular (LV) mural thrombus
Ie, empiric , Vancouver. Amino
Thank you so much 💓
I want notes 📝 with this video please 😭
Yes, they are available on Amazon! Link is in the description
Nitrates is contraindicated in Right sided MI not inferior MI, inferior MI effects the RCA which can lead to right sided MI if the proximal RCA is occluded but that does not always happen. The RV is supplied by the proximal RCA and its right marginal branch. ST elevation in V4R-V6R is a contraindication to nitrates because it implies an RV infarction
Hero we need.
Urgency oral meds,emergency if .
Thank you bro
I love your videos🥰
Angina 0:10
Please, I want to talk to you very urgently.
wooooooow !
Ali, pe give heparin first. Plz.
Holo mr, tr, vsd
You're editing the phrases halfway. Seems very unnatural. If you don't remember something, just say emm and repeat it, or cut the whole sentence out and repeat it
this is boring. Its better to have a visual aid instead of someone who speaks with no punctuation speaking
ok rude and unnecessary negativity
I agree