Thankyou sir

Thank you very much sir🙏

thankyou sooo much this was awesome

sir where can i get this presentation ppt?

@Shyam Kothari Dear sir if you are reading this message please 🙏 drop your mail ID here. My father Anil Kumar (Baidyanath dham , Jharkhand) was being treated by you from the past 20 year. Past 1 year we are searching for you every where on the internet since you have left AIIMS. Even in AIIMS no one has given any information about you. Please help us,🙏🙏

Great sir

Mam m apse milna chahta hu par kase milu samjh me nahi aa raha hai apni 2 saal ki beti ke liye jiske dil me 6 mm ka chhed h bahut jagah gaya ab aap hi hamari akhiri ummeed h agar hamara msg aap tak pahuche to please reply jarur kariye 🙏🙏🙏🙏🙏🙏🙏🙏🙏🙏🙏🙏🙏

Excellent class madam -thank you

what is full form of PVRI

Amazing story sir! Very inspiring.

Case was good but candidate shud be a liitle more softspoken and less overconfident

Fantastic talk. Thank you 🙏🏼

Nicen

Murli sir 🙏

Inspiring

L

Marvelous sir,you are always

I'm gone through rhd.. and I done double valve replacement surgery at aiims Delhi

Nice lecture, very informative

To the question on apical-carotid delay in Aortic stenosis - The values are : Normal = 70 ms , AS = 130 ms. This is described in ancient studies done with an apexcardiogram and carotid pulse. The main caveat for this is, we have to. interpret. this with caution. So many conditions may affect this: 1) young [brisk upstroke] vs old 2) Carotid artery disease 3) LV dysfunction 4) Associated infarct at apex 5) Associated valve disease [MR, AR] 6) Tachycardia or AF 7) Others - COPD, chest wall causes. So, practically it is a useless entity ! I am surprised people are interested in this medicine practiced on Egyptian mummies.

To the question, which has higher more mortality Acute MR vs AR? This is not a valid comparison. Its like asking which one is worse CKD or CCF. Because Acute MR and AR are due to a cause and this cause dictates the prognosis. We have data about acute MR in SHOCK registry [PMD MR] here 39% died in hospital. There is another series of acute MR that says 30 day mortality is 22% with degenerative MR doing better. So, we have some data with MR. In acute AR, we have data for Aortic dissection [short term mortality = 31%] and Endocarditis. In IE in two large series it is around 20-30%. I dont know much about BMV, a JIPMER series of 2018 says 30 day mortality after BMV is about 4 or 5%. This sounds lower than MI related MR. So, I would say mortality depends on etiology and generalization is not useful.

Event rates for sarcoid = 7.1%/year.

It is a well known fact that GCM and Sarcoidosis are extremely hard to distinguish on HPE. This fulminant presentation and "loose" granulomas, No conduction abnormalities and no lymph nodes should be diagnosed as Giant cell and not Sarcoid.

To the question of why we have a wide split S2 in RCM and CCP ? RCM and CCP are known to have a wide split of S2 [not related to RBBB]. This split is a phonocardiographic phenomenon and infrequently perceived clinically. When observed clinically it is perceived in. the first two beats of inspiration. The mechanism of this has been described in 60s. - Due to the sharp initial movement of the A2 component towards the R wave, while the R-P2 remains constant. (Basically its an early A2) In other words the abbreviation of LV stroke volume, the mechanism of which also causes Pulsus paradoxus is responsible for this. We hardly observe RBBB in CCP so attributing it to RV electrical delay is not a feasible explanation.

Simple anemia can also present with a similar picture !

ACHD, Bicuspid Aortopathy is a forefront DD after history and patient presenting in late second decade with dyspnea and palpitations.