Why is there always an Indian doctor (and despite the accent being much more difficult to understand) who explains every medical matter in a perfect way? Thank you very much.
this is amazing. ive always been bothered with HOW and WHY the ST elevation and depression happens and this is the perfect explanation. Medschool just simply tells us about STEMI and NSTEMI but doesn't explain the physiology behind it. thank you very much!
I am a medical student from India and this is The best explanation of st dep. And ele. ever!!!! It cleared my most of the doubts. May god bless this admin!
@@ThePhysiologyChannel do you have any video of explaining t wave changes of electrolyte imbalances. I didn't find any proper video on t wave changes by its ionic basis.
@@ThePhysiologyChannel You are amazing! I would like to ask a question Doctor. What's the reason why the ST segment is the only one going back to the isoelectric line while the others have fluctuations? I know in the ECG it seems to appear that the ST is the one that depresses or elevates. But why doesn't the QRS for instance goes in the same level with respect to the ST during that time? Thanks in advance Doctor 🙏🏾
Thank you very much for this video! I have one question: Why in subendocardial ischaemia the injury current flows left, if there is more healthy tissue and more "resting pluses" at the right side of the heart (septum and RV)?
This video is very impressive, it was all perfectly clear and the graphics are great! Thank you very much! The only thing that I still don't get is in transmural infarction, why the dipole vector points toward the endocardium? Since there are 2 normal regions on each side (over and under the affected region in the drawing), and no healthy tissue in between the infarction and the electrode, wouldn't the net vector just be cancelled?
It's my understanding that the only true isoelectric segment happens after the T-wave. There is electrical activity during all other periods and thus traveling action potential from the beginning of the P wave until then as it progresses thru the heart from SA, Atrium,AV, Ventricle.
Ischemia causes interstitial hyperkalemia in the affected cardiac tissue. The mechanisms are not clearly understood but some mechanisms contributes to that are 1. decrease in ATP levels affects NaKATPase and ATP sensitive ion channels 2. Changes in pH affecting membrane transporters 3. Decreased washing out of extracellular metabolites. K+ equilibrium potential (around -90mV) is the major determinant of negative membrane potential. If extracellular K+ increase then its Equilibrium potential becomes less negative, therefore the membrane potential also becomes less negative
Such a great video I understood so much ! But why is the segment isoelectric if the atria are not in the same state as the ventricles ? why do we only take into account the ventricles when considering the iso electric level ?
That’s a good question! The answer is atria and ventricles are electrically separated! No significant current is generated from potential differences between atria and ventricles due to insulation in between them. Atria acts as a separate dipole and ventricles acts as a separate dipole.
At 10:50 you said the vector is moving from endocardium to epicardium but in subendocardial Ischemia all the current is moving from epicardium to endocardium (pos to neg) that's why it is depressed.
Great video sir thank you!! I Have a doubt. Regarding the current flow, current flow direction is conventionally taken to be in direction of flow of positive charges(opp to direction of e- flow). Ecg sense the current flow in ecf. When depolarization wave travels; the positive charges travel inside the cell and negative charges flow in ecf simultaneously. For example the negative charges flow towards + terminal of lead2 during depolarization ( major ventricular depolarization) which produces positive deflection. But in a galvanometer when positive charges flow towards positive electrode it shows positive deflection. How does this relate sir? Please help
Hi Nawin! In ECG we are recording potential difference between two points. ECF around cells at Resting membrane potential (RMP) are positive charged and depolarized cells are negatively charged. During R wave base of ventricles depolarized(ECF side negative) which is near the negative electrode of lead 2. Apex is at RMP so positive outside, which is close to positive electrode of lead 2. The potential difference is recorded positive because, positive charges near positive electrode and negative charges near negative electrode. This video will help to imagine ruclips.net/video/T616yKzJkO8/видео.html
thank you very much for this,studying medicine in australia and by far this is a very amazing explanation. I have one doubt - what actually occurs in the heart to produce initial hyper acute T waves, and then an inverted T wave later? additionally what happens to produce the pathological Q waves? thank you sir
Those pathological Q waves depends on the direction of current of injury and lead placement only as we know q wave points towards septal Depolarization if the direction of Depolarization is more obtuse even with the direction of septal depolarization then pathological q waves occur
Great lecture sir. But what if there is subendothelial/transmural damage on the wall of right ventricle rather than left ventricle, Will results change?
Thanks for watching!! Though the principles are same in all parts of heart, the Lead in which the changes are seen will vary. I’m making a video on ‘ localization of MI’, will post soon.
Irreversible Ischamia-anaeribic resp - atp depletion- failure NaK Atpase , accumulates Na+ . Disrupted Membrane permeability - leak of K+ , H+. Disruption of organelles due to release of Ca All adds to build of positive charges intracellulary. How does voltage gated Na channels deactivate.please explain sir. Trying to find actual Concept of This topic for so long and this video helped very much .thank u so much
The NaV will get inactivated when the membrane potential becomes less negative. More on Sodium channel in this video. ruclips.net/video/h7wHS7IOT4M/видео.html As the RMP gets closer to 0 mV the, Action potential gradually decrease in magnitude and duration due to inactive NaV and cease completely. Thanks
Sir thank you for the amazing video cleared all concepts! But sir in Harrison the direction of waves are oritented exactly opposite to what is drawn here, it is towards the leads in case of transmural leading to ST elevation and away from the leads in case of subendocardial leading to ST depression. Please explain sir!!!
Same concept but different approach! In Harrison they have explained in terms of resultant ST vector and ST elevation/ depression due to it. But in my explanation it was Injury current vector acting throughout the ECG except during the ST segment. We are talking about different vectors, so directions are opposite. In other words, Harrison explains it as true ST elevation due to resultant ST vector towards the lead, but I explained that True changes are seen in entire ECG getting depressed due to injury current vector going away from lead and ST appears to be elevated. (Resultant vector = normal cardiac current vector + injury current vector)
Thank you so very much sir! I finally understood this! Can you please also tell me the variation in T waves in subendocardial and transmural ischemia? Please sir!!
T wave morphology changes due to changes in the re-polarization vector. The normal vector is from Endocardium to epicardium since epicardium repolarizes first. This results in positive T wave. Sub endocardial ischemia/ infarction causes endocardium to repolarize earlier due to shorter action potentials. This causes a inward vector and T wave inversion but sometimes it could be biphasic. transmural acute STEMI causes Tall T waves and during resolving stages a inverted T wave .
Current of injury refers only to the current generated due to potential difference between ischemic/infarct area and normal cardiac tissue. Here I have shown how the current of injury is superimposed over the normal ECG and cause ST segment changes.
Thank you for your explanation. It was very helpful. I have a few queries 1. If subendocardial ischemia occurs in the right side instead of left, current of injury would be negative and ST segment would be elevated wouldn't it? So why do we look at it only from perspective of ischemia in the left side and not considering right side? 2. Why do we only look at lead 1 and not at others? Same current of injury will produce different results in the ST segment depending on which lead we look at. So why do we ignore them while classifying the ischemia as ST segment elevated or depressed?
Please watch my video on STEMI location and ECG Changes. ruclips.net/video/ruwL2U-N4m4/видео.html if you have further queries after watching that, leave it in comment, I’ll be glad to answer.
Depolarization difference is due to differences in their activation time which is influenced by conduction velocity of the cardiac impulse! Repolarization time differences are due to differences in the duration of action potentials which is due to differences in the properties of ion channels in these sub regions
I'm a medical student from Australia, and this is the best explanation I could find on RUclips. Liked and subscribed. Well done and thanks!!
Glad to hear. Welcome to the channel.
Why is there always an Indian doctor (and despite the accent being much more difficult to understand) who explains every medical matter in a perfect way? Thank you very much.
Couldnt have said it better myself
Indian are genius ❤ I appreciate them
It literally blew my mind, sir you are truly a genius.
I had never understood this concept in such a basic way.
Thank you.
I’m so happy that it helped. Happy Learning!!
this is amazing. ive always been bothered with HOW and WHY the ST elevation and depression happens and this is the perfect explanation. Medschool just simply tells us about STEMI and NSTEMI but doesn't explain the physiology behind it. thank you very much!
I am a medical student from India and this is The best explanation of st dep. And ele. ever!!!! It cleared my most of the doubts. May god bless this admin!
Thanks
@@ThePhysiologyChannel do you have any video of explaining t wave changes of electrolyte imbalances. I didn't find any proper video on t wave changes by its ionic basis.
Wow!! The best explanation I found after trying to think so much on it. 👍
Hats off Sir !!!!!!!!!This is the most Satisfying Explanation So far😍😍😍😍😍😍😍😍😍😍
suma v bhat Thanks for the comment
Thank You doctor! Great video, the clearest I’ve watched so far
Thanks for the feedback!
Thanks for explaining the NET effect and difference of ischemia ST segment, really helped me a lot!
You are welcome
✨st elevation/depression explanation must needed. Thank you.
You are welcome
best explanation i have ever seen for that confusing topic ...many thanks
You’re welcome!
Thank you for explaining this so clearly, I really enjoyed listening to your video
Glad to hear. Thanks for watching
Excellent and thorough explanation. Thank you
You’re welcome, Thanks for the feedback
Beautiful ❤️❤️
You are the real professor
😊Thanks Arun
This was amazing Doc keep up the good work
Thanks for the motivation!!
doc, youre a lifesaver!!!
Haha! Thank you so much. Stay tuned!
This is the best explanation I have watched! Thanks so much for this.
Thanks
@@ThePhysiologyChannel You are amazing! I would like to ask a question Doctor. What's the reason why the ST segment is the only one going back to the isoelectric line while the others have fluctuations? I know in the ECG it seems to appear that the ST is the one that depresses or elevates. But why doesn't the QRS for instance goes in the same level with respect to the ST during that time? Thanks in advance Doctor 🙏🏾
Because only during the ST segment the ventricle is completely depolarized including the ischemic tissue. Everything is isoelectric!
amazing!
Thank you, best explanation
Best explanation for this topic
Thanks
Thank you very much for the clear explanation! It helped a lot!
You are welcome
That is an amazing explanation.
I'm glad you think so. Thanks.
Amazing explanation, thanks a lot!! really makes a lot of sense.
You are welcome!
Thank you very much ❤️❤️
Thanks a lot
Wow! that was good. Thank you ❤
Thank you very much for this video! I have one question: Why in subendocardial ischaemia the injury current flows left, if there is more healthy tissue and more "resting pluses" at the right side of the heart (septum and RV)?
Thank You Dr.
You are welcome!!
great explanation .. thank you sir
You are welcome Zainab
Medical student from Italy, thank u
Prego
Best explanation ❤❤thankyou so much
You are Welcome
This video is very impressive, it was all perfectly clear and the graphics are great! Thank you very much!
The only thing that I still don't get is in transmural infarction, why the dipole vector points toward the endocardium? Since there are 2 normal regions on each side (over and under the affected region in the drawing), and no healthy tissue in between the infarction and the electrode, wouldn't the net vector just be cancelled?
It's my understanding that the only true isoelectric segment happens after the T-wave. There is electrical activity during all other periods and thus traveling action potential from the beginning of the P wave until then as it progresses thru the heart from SA, Atrium,AV, Ventricle.
THANK YOU!
You’re welcome
Wow!! Thank u for this ...
I’m glad it helped
Thank you so much!!
You are welcome!
thanks very much
great explanation
fro srilanka
amazing lecture!!!!
Thanks
Really nyc explanation sir! Tysm
I’m glad it helped!
Great video mate
Thanks
12:07 that’s the point thanks alot
Appreciated❤️
You’re welcome
My ecg said mild st elevation and the ecg before that said poor r wave leads 2 and 3. Is this bad ?
Why does ischemia cause local hyperkalemia and the membrane potential becomes less negative when potassium leaves the cell?
Ischemia causes interstitial hyperkalemia in the affected cardiac tissue. The mechanisms are not clearly understood but some mechanisms contributes to that are 1. decrease in ATP levels affects NaKATPase and ATP sensitive ion channels 2. Changes in pH affecting membrane transporters 3. Decreased washing out of extracellular metabolites.
K+ equilibrium potential (around -90mV) is the major determinant of negative membrane potential. If extracellular K+ increase then its Equilibrium potential becomes less negative, therefore the membrane potential also becomes less negative
Thnks dear really really helpful.You helped me understand this concept.
Glad to hear that! Thanks for the comment!
Thanks sir, very helpful video ..
You are welcome
Thank you sir ...
You’re welcome!
Well said sir.
Thanks
Great lecture👍
🙏
excellent sir
Thanks Syed
Such a great video I understood so much ! But why is the segment isoelectric if the atria are not in the same state as the ventricles ? why do we only take into account the ventricles when considering the iso electric level ?
That’s a good question! The answer is atria and ventricles are electrically separated! No significant current is generated from potential differences between atria and ventricles due to insulation in between them. Atria acts as a separate dipole and ventricles acts as a separate dipole.
@@ThePhysiologyChannel Thank you !
At 10:50 you said the vector is moving from endocardium to epicardium but in subendocardial Ischemia all the current is moving from epicardium to endocardium (pos to neg) that's why it is depressed.
nice work! couple of changes in the beginning would be great. the build up and climax are excellent!
tq
Please make a similar conceptual video of ELECTROLYTES AND ITS EFFECTS ON ECG.
Will try! Thanks
Great video sir thank you!! I Have a doubt. Regarding the current flow, current flow direction is conventionally taken to be in direction of flow of positive charges(opp to direction of e- flow). Ecg sense the current flow in ecf. When depolarization wave travels; the positive charges travel inside the cell and negative charges flow in ecf simultaneously. For example the negative charges flow towards + terminal of lead2 during depolarization ( major ventricular depolarization) which produces positive deflection.
But in a galvanometer when positive charges flow towards positive electrode it shows positive deflection.
How does this relate sir? Please help
Hi Nawin! In ECG we are recording potential difference between two points. ECF around cells at Resting membrane potential (RMP) are positive charged and depolarized cells are negatively charged. During R wave base of ventricles depolarized(ECF side negative) which is near the negative electrode of lead 2. Apex is at RMP so positive outside, which is close to positive electrode of lead 2. The potential difference is recorded positive because, positive charges near positive electrode and negative charges near negative electrode. This video will help to imagine ruclips.net/video/T616yKzJkO8/видео.html
@@ThePhysiologyChannel thanks for the explanation sir. I'll check the video
🥺🥺👍🏻👍🏻 well explained
Thanks 😊
Thank U from Bangladesh
You are welcome!
Phase 2 is ST Segment
Of course, Yes. I misspoke once at 3:02, But the arrow was correctly shown from phase 2. Thanks for watching and pointing out the error.
The rest of the Video is really good Sir
thank you very much for this,studying medicine in australia and by far this is a very amazing explanation. I have one doubt - what actually occurs in the heart to produce initial hyper acute T waves, and then an inverted T wave later? additionally what happens to produce the pathological Q waves? thank you sir
Those pathological Q waves depends on the direction of current of injury and lead placement only as we know q wave points towards septal Depolarization if the direction of Depolarization is more obtuse even with the direction of septal depolarization then pathological q waves occur
What lead is that?
Great lecture sir. But what if there is subendothelial/transmural damage on the wall of right ventricle rather than left ventricle, Will results change?
Thanks for watching!! Though the principles are same in all parts of heart, the Lead in which the changes are seen will vary. I’m making a video on ‘ localization of MI’, will post soon.
ruclips.net/video/ruwL2U-N4m4/видео.html
Irreversible Ischamia-anaeribic resp - atp depletion- failure NaK Atpase , accumulates Na+ . Disrupted Membrane permeability - leak of K+ , H+. Disruption of organelles due to release of Ca All adds to build of positive charges intracellulary. How does voltage gated Na channels deactivate.please explain sir. Trying to find actual Concept of This topic for so long and this video helped very much .thank u so much
Also please make video on ecg changes due to hyperkalemia sir!
The NaV will get inactivated when the membrane potential becomes less negative. More on Sodium channel in this video. ruclips.net/video/h7wHS7IOT4M/видео.html As the RMP gets closer to 0 mV the, Action potential gradually decrease in magnitude and duration due to inactive NaV and cease completely. Thanks
@@ThePhysiologyChannel thank you sir
@@cmnaveenmusic Thanks for the request.
Plz tell me answer of this q that what is difference between this and current of injury
Sir thank you for the amazing video cleared all concepts!
But sir in Harrison the direction of waves are oritented exactly opposite to what is drawn here, it is towards the leads in case of transmural leading to ST elevation and away from the leads in case of subendocardial leading to ST depression. Please explain sir!!!
Same concept but different approach! In Harrison they have explained in terms of resultant ST vector and ST elevation/ depression due to it. But in my explanation it was Injury current vector acting throughout the ECG except during the ST segment. We are talking about different vectors, so directions are opposite. In other words, Harrison explains it as true ST elevation due to resultant ST vector towards the lead, but I explained that True changes are seen in entire ECG getting depressed due to injury current vector going away from lead and ST appears to be elevated. (Resultant vector = normal cardiac current vector + injury current vector)
Thank you so very much sir! I finally understood this! Can you please also tell me the variation in T waves in subendocardial and transmural ischemia? Please sir!!
T wave morphology changes due to changes in the re-polarization vector. The normal vector is from Endocardium to epicardium since epicardium repolarizes first. This results in positive T wave. Sub endocardial ischemia/ infarction causes endocardium to repolarize earlier due to shorter action potentials. This causes a inward vector and T wave inversion but sometimes it could be biphasic. transmural acute STEMI causes Tall T waves and during resolving stages a inverted T wave .
why does subendocardial ischemia has a net vector totally different than transmural ?! :// Literally in the opposite direction :/// ??????
Why in hypokalemia st depression occur
Best best best
Thanks
I want to ask a question what is difference between this and current of injury
Current of injury refers only to the current generated due to potential difference between ischemic/infarct area and normal cardiac tissue. Here I have shown how the current of injury is superimposed over the normal ECG and cause ST segment changes.
@@ThePhysiologyChannel can st segment changes occur without current of injury
@@ThePhysiologyChannel and thanks for reply and sorry I still have confusion plz reply
Yes there are many non ischemic causes for ST segment abnormalities
@@ThePhysiologyChannel thanks
Thank you for your explanation. It was very helpful. I have a few queries
1. If subendocardial ischemia occurs in the right side instead of left, current of injury would be negative and ST segment would be elevated wouldn't it? So why do we look at it only from perspective of ischemia in the left side and not considering right side?
2. Why do we only look at lead 1 and not at others? Same current of injury will produce different results in the ST segment depending on which lead we look at. So why do we ignore them while classifying the ischemia as ST segment elevated or depressed?
Please watch my video on STEMI location and ECG Changes. ruclips.net/video/ruwL2U-N4m4/видео.html if you have further queries after watching that, leave it in comment, I’ll be glad to answer.
Also please tell why Repolarization from epi towards endocardium
And Depolarization from endo towards epicardium.
Depolarization difference is due to differences in their activation time which is influenced by conduction velocity of the cardiac impulse! Repolarization time differences are due to differences in the duration of action potentials which is due to differences in the properties of ion channels in these sub regions
@@ThePhysiologyChannel this mean epicardium has more duration of action potential than endo?
Cardiac muscle near Epicardium has the shortest Action potential. That’s why they repolarize first
Okay I got it.
Possible to have french translate, I will be very happy if u can....
Slight st coming in ecg report
ST segment could be elevated in many conditions other than MI. Symptoms, Clinical examination and other changes in ECG could help the diagnosis.
I got more confused😂
It's not completely accurate, specially when describing vectors in subendocardial ischemia