You stated that BNP is specific and not sensitive. The opposite is true. BNP has high SENSITIVITY but is relatively NONSPECIFIC. Elevated BNP levels are an indicator of cardiac myocyte strain, and are also elevated in conditions such as renal failure, PE, pulm HTN, chronic hypoxia, etc. (hence, nonspecific). To further clarify, in studies using LOW cutoff levels of BNP @ 100pg/nl, sensitivity is 96% and specificity is only 26%. To increase the specificity, raise cutoff level to 400pg/nl, and that results in specificity of 74% but with a decline in sensitivity to 87%. USMLE gold mine for a clinical/biostats question..
+Allyson Stone agreed characterization of circulating proBNP, BNP, and NT-proBNP forms is necessary to define the relevant standard for assay standardization. Until then, assays should be designed to detect the total amount of the circulating analyte to achieve optimal sensitivity. The identification of possible disease effects on proBNP, BNP, and NT-proBNP metabolism could pave the way for the development of more disease specific assays in the clinical setting. Of course any lab in a university setting or otherwise utilize NT-proBNP.
Hats off for you Dr. Paul. such an amazing approach and easy to understand and memorize :) ... I'm basically watching every other video in your channel at the moment :D ... But, it would be absolutely amazing if you made a video in the future about Infective Endocarditis, I'd really appreciate it :) Greetings from Egypt
I appreciate your lectures, they have been an excellent supplement to school! I especially appreciate your review of medications with conditions! NP students use your videos also, and I am sure that PA's do as well! Keep up the good work! Take care and God bless!
so my question to is, does this all apply to those of us who have CHF not related to heart disease, instead related to cardiomyopathy and valve insufficiency? How does this info apply to the new Cardiac Contractility Modulation device?
You stated that BNP is specific and not sensitive. The opposite is true. BNP has high SENSITIVITY but is relatively NONSPECIFIC. Elevated BNP levels are an indicator of cardiac myocyte strain, and are also elevated in conditions such as renal failure, PE, pulm HTN, chronic hypoxia, etc. (hence, nonspecific). To further clarify, in studies using LOW cutoff levels of BNP @ 100pg/nl, sensitivity is 96% and specificity is only 26%. To increase the specificity, raise cutoff level to 400pg/nl, and that results in specificity of 74% but with a decline in sensitivity to 87%. USMLE gold mine for a clinical/biostats question..
+Allyson Stone agreed
characterization of circulating proBNP, BNP, and NT-proBNP forms is necessary to define the relevant standard for assay standardization. Until then, assays should be designed to detect the total amount of the circulating analyte to achieve optimal sensitivity. The identification of possible disease effects on proBNP, BNP, and NT-proBNP metabolism could pave the way for the development of more disease specific assays in the clinical setting.
Of course any lab in a university setting or otherwise utilize NT-proBNP.
Updated version from 2021: ua-cam.com/video/lIWpuaAOhk4/v-deo.html
Hats off for you Dr. Paul. such an amazing approach and easy to understand and memorize :) ... I'm basically watching every other video in your channel at the moment :D ... But, it would be absolutely amazing if you made a video in the future about Infective Endocarditis, I'd really appreciate it :) Greetings from Egypt
I appreciate your lectures, they have been an excellent supplement to school! I especially appreciate your review of medications with conditions! NP students use your videos also, and I am sure that PA's do as well! Keep up the good work!
Take care and God bless!
11:39 at some point when you have a really big heart, it'll harming yourself lol
Helped alot to understand and to get a good introduction to heart failure, Thnx Paul
Love it. But, why is your heart upside down?
greetings from Sweden Dr..... your videos helps ...
Great presentation! Thanks and keep up the good work! :)
so my question to is, does this all apply to those of us who have CHF not related to heart disease, instead related to cardiomyopathy and valve insufficiency? How does this info apply to the new Cardiac Contractility Modulation device?
+Starla Jones good question, but this is just education. This is not to hypothesize. That's what you are supposed to do. write us a paper.
Thank you brother :)
At 16min,in a-fib those are called f waves
well explained
Can someone please explain to me why a decreased LVEF leads to an increased afterload (force heart has to work against)?
Thanks
it's the other way round! the Increased SVR leads to decreased lvef
Thank you!
Ty v much. Great info.gbu.
Gracias!
good yor good
Anti quack