A word about the diagnostic framework - specifically the category of "hypoxemia". This is an oversimplification of the pathophysiology, since most pathologies listed in this category result in dyspnea via multiple mechanisms (e.g. reduced lung compliance in heart failure and ILD), of which hypoxemia may not be the most important.
I have discussions tomorrow and this will help me more more than my teacher does after I learned , you make it together all , 🥰✋🏻 thnz best teacher 👨🏫 keep it
Hi doctor strong medicine Thanks for converting theoretical knowledge into practical approaches by your videos.one request plz Can there b a video showing clinical approach to investigate pancytopenia with underlying cause
Firstly, thank you for your video. It's very informative and helpful. However, I have a question, I really curious about how you decide to categorise the causes of acute dyspnea by the pathophysiology. I know that you had explained a little bit about it in the video but i still find it unclearly abt the reason why.
I'm so sorry - just seeing your comment now! I largely chose to categorize the etiologies of acute dyspnea by pathophysiology to provide some variety since the etiologies of chronic dyspnea in the corresponding video are categorized by organ system.
Hi doctor Thanks for your amazing lectures. I was wondering whether carbon monoxide poisoning could also be on the differentials list for acute dyspnea?
Carbon monoxide poisoning does not stimulate the respiratory center because the mechanism involves neither hypoxemia, hypercapnia nor acidosis. That is why it is called a silent killer.
What is the possible cause of chronic dyspnea at rest without any other associated symptoms in a pt who is hypertensive (well controlled) and all his cardiac a pulmonary and blood tests are normal . And he is not stressed out
Very instructional video again, thank you so much! Why is "upper airway obstruction" listed in Miscellaneous? Doesn't it lead to Hypoxemia as well and could therefore be listed there? Thanks so much!
Upper airway obstruction will first lead to dyspnea by causing increased airway resistance, which mechanically loads the respiratory system before it causes hypoxemia. A patient with an upper obstruction can eventually develop related hypoxemia, but it is a late consequence that implies either profound obstruction, exhaustion of the muscles of respiration, or both. The same phenomenon can be seen in asthma in which an asthma exacerbation accompanied by hypoxemia is extremely concerning for an imminent respiratory arrest.
Yes. The presence of hypoxemia in an asthma exacerbation suggests either a very severe (i.e. life-threatening) exacerbation, or the presence of a concurrent problem such as pneumonia or mucus plugging.
A WELL PRESENTED GOOD CONCISE REVIEW. However, it seems to me that a few minor inaccuracies exist. In particular, coarse crackles are considered to be of upper (central) airway origin and result from inspiratory airflow through airway related secretions. They are not regarded to be characteristic of interstitial and alveolar edema that present as late fine inspiratory crackles or rales that is inconsistent with this presentation. Another example is the application of ultrasound imaging of the IVC for increased width or congestion with its noted advantages over naturetic peptides (ie BNP) in reference to heart failure as the possible etiology of acute dyspnea. Evidence does exist for the argument of the application of IVC assessment in terms of comparable accuracy when compared to naturetic peptides (ie BNP, pro-NT-BNP) and the benefit of significantly reduced time to investigate a cardiac origin of dyspnea. However, to my knowledge, this is not implemented in major guidelines for heart failure. Once again, I found that the overall brief review to be quite good.
![Noob To Max With DRAGON REWORK In Blox Fruits [FULL MOVIE]](http://i.ytimg.com/vi/LnBMOinoOvA/mqdefault.jpg)
A word about the diagnostic framework - specifically the category of "hypoxemia". This is an oversimplification of the pathophysiology, since most pathologies listed in this category result in dyspnea via multiple mechanisms (e.g. reduced lung compliance in heart failure and ILD), of which hypoxemia may not be the most important.
Finding your channel for my Cardiology and Pulmonology OSCE prep is my PA School Miracle!
Thank you so very much!!!
I just want to say thank you for all your works
Thanks for this fast, dense, helpful explanation
damn one of the best videos ive come across thank you sir
I have discussions tomorrow and this will help me more more than my teacher does after I learned , you make it together all , 🥰✋🏻 thnz best teacher 👨🏫 keep it
Excellent video with simple explanations! Thank you!
Thank you Dr. Strong for making these videos!
Thanks for your great informative videos
Thank you so much. Please make videos on approach to young stroke, myaesthenia gravis, guillaine barre syndrome and myelopathy
great videos. plss keep posting
waooo thnx for such precious videos...looking fwd to abdominal pain approch
Great and clear explanation, keep it up.
Hi doctor strong medicine
Thanks for converting theoretical knowledge into practical approaches by your videos.one request plz
Can there b a video showing clinical approach to investigate pancytopenia with underlying cause
thanks i was diagnosed with acute dyspnea yesterday
Awesomely informative and perfectly explained! Thank you so much! 😊😊 15/9/2019
That's awesome ....tq so much sir
Thank you sir for the informative video.How does one differentiate alveolar vs interstitial opacities on a chest x ray?
The whole linked video focuses on this question, but is summarized near the end here: ruclips.net/video/mNLd4DKtGs4/видео.html
@@StrongMed thank you sir for the immediate reply .
Is there any of your traditional videos coming soon?
I'm eagerly waiting for them ...
Firstly, thank you for your video. It's very informative and helpful. However, I have a question, I really curious about how you decide to categorise the causes of acute dyspnea by the pathophysiology. I know that you had explained a little bit about it in the video but i still find it unclearly abt the reason why.
I'm so sorry - just seeing your comment now! I largely chose to categorize the etiologies of acute dyspnea by pathophysiology to provide some variety since the etiologies of chronic dyspnea in the corresponding video are categorized by organ system.
Great Work Sir👍
Do you have any references? pls
Would a diaphragma paralysis also be a cause? Is that then neuromuscular?
Million thx...can u please make a video about approach to dysphagea
thanks alot sir i wish you were my teacher
thank you dr Strong.
Hello sir I'm struggling to finding a book explaining the symptoms as topics in details, do u have any suggestions or website..?
Hi doctor
Thanks for your amazing lectures.
I was wondering whether carbon monoxide poisoning could also be on the differentials list for acute dyspnea?
Carbon monoxide poisoning does not stimulate the respiratory center because the mechanism involves neither hypoxemia, hypercapnia nor acidosis. That is why it is called a silent killer.
Course crepitations only in bronchiectasis and resolving pneumonia....while fine crepitations are found in acute pulmonary edema and ILD..
Thank you so much for this!!!
Thanks!
What is the possible cause of chronic dyspnea at rest without any other associated symptoms in a pt who is hypertensive (well controlled) and all his cardiac a pulmonary and blood tests are normal . And he is not stressed out
very great lecture thanks alot
Hey, is the Chronic dyspnea video out yet?
Not yet. In about 2 weeks...
Strong Medicine This video was fantastic BTW!
Strong Medicine Any plans of making a new video regarding resources for the USMLE exam, as an update to the previous one?
I'm sorry, but no immediate plans for that specific topic. It's hard to keep up to date on USMLE resources.
Very instructional video again, thank you so much! Why is "upper airway obstruction" listed in Miscellaneous? Doesn't it lead to Hypoxemia as well and could therefore be listed there? Thanks so much!
Upper airway obstruction will first lead to dyspnea by causing increased airway resistance, which mechanically loads the respiratory system before it causes hypoxemia.
A patient with an upper obstruction can eventually develop related hypoxemia, but it is a late consequence that implies either profound obstruction, exhaustion of the muscles of respiration, or both. The same phenomenon can be seen in asthma in which an asthma exacerbation accompanied by hypoxemia is extremely concerning for an imminent respiratory arrest.
Kindly make videos on approach to other symptoms as well ct head,chest and abdomen
Hi Dr. Eric .. Is it unusal for asthma exacerbations to cause isolated hypoxemia ?
Yes. The presence of hypoxemia in an asthma exacerbation suggests either a very severe (i.e. life-threatening) exacerbation, or the presence of a concurrent problem such as pneumonia or mucus plugging.
Thank you
Hello sir What will be the immediate care for such patients
It depends on the cause of the dyspnea.
Thank you so much
any one can explain why some people dislike these videos, especially this one?
Except for a deadhead
Thank you .
Tq verymuch sir ♥️
Superb
beautiful
It seems that my previous comment contains a minor oversight. "pro-NT BNP" should be NT-proBNP.
Great!
A WELL PRESENTED GOOD CONCISE REVIEW. However, it seems to me that a few minor inaccuracies exist. In particular, coarse crackles are considered to be of upper (central) airway origin and result from inspiratory airflow through airway related secretions. They are not regarded to be characteristic of interstitial and alveolar edema that present as late fine inspiratory crackles or rales that is inconsistent with this presentation. Another example is the application of ultrasound imaging of the IVC for increased width or congestion with its noted advantages over naturetic peptides (ie BNP) in reference to heart failure as the possible etiology of acute dyspnea. Evidence does exist for the argument of the application of IVC assessment in terms of comparable accuracy when compared to naturetic peptides (ie BNP, pro-NT-BNP) and the benefit of significantly reduced time to investigate a cardiac origin of dyspnea. However, to my knowledge, this is not implemented in major guidelines for heart failure. Once again, I found that the overall brief review to be quite good.
Well said, fine crackles, rales and crepitations are found in cardiogenic pulmonary edema. Thanks for the video, excellent presentation.
🥰
I can't fucking breathe help
Hindi
Thank you so much
Thank you.