OMG....I have never heard anyone explain the biophysical basis for ST depression and elevation so clearly and simply! Some of us learn better by learning the mechanism of things, but that not how things are taught generally in medical education, where instead it’s often “this is what you beed to know. Dont worry about why, unless you become an electrophysiologist.” Thank you!
I had to come to the comments to write how amazing Dr. Mustache is to actually get me to UNDERSTAND the why's behind this. This video was beyond helpful.
I just have been sent this video in the 5th week of my CVS block and man this was such a helpful and eye opening lecutre. Thank you so much for putting this much effort into making these videos so great. Your way of explaning and creative use of the board is outstanding! Keep doing what you do, you deserve 100 times the amount of subscribers you have! Thank you once again and I wish you all the success in the future.
And my med school only have one lecture on ECG with NO teaching about cardiac pathology. We have to learn everything ourselves. Online resources like this is a god savior.
in a nutshell >> its the shift of isoelectric point, either high(in ST depression) or low (in ST elevation) makes it appear as ST elevation/Depression. ST elevation- subendocardial ischemia ST depression- transmural ischemia/infarct thank you man, thats pretty simple, lots of love...❤
Sir, if electrical activity is going on before QRS complex so, why is iso electric line is straight? Electrodes are sensing the vectors(thats why iso electric line is elevating or depressing) but as electrical activity is going on why there is no any deflection why the iso electric line is straight?
No dr Mike you do not understand I have been looking for this explanation for the past 3 days day and night and it has been driving me crazy. Like thank you so freaking much my Australian professor
Thank you thank you! This was beyond helpful it helped bridge the gap between what it means when I see it and what is actually occuring to make it that way. Can't say thanks enough
I didn’t quite get why would a resting membrane potential of -50 lead to the fast acting sodium channels not opening up (they were supposed to open up at above -70 so they should be open). Also didn’t understand why would the repolarization happen earlier.
So is it spontaneous depolarization in absence of SAN impulse in NSTEMI? or do we still need SAN impulse before depolarization but it just happens faster and repolarizes faster?
Thank you. I’m a nurse. Not cardiac- HH wound ostomy care. Cardiology beyond basics is French to me. Thanks for the clear explaination of all I forgot since nursing school! I was dx today w ST depressions symptomatic but nothing but ST depressions 1.5mm on stressEKG during nuclear med test. Other findings normal. If family hx of widow maker (my dad) mom CHF, brother stents at 35. I’m 58 cardiologist gave me the choice to take meds and watch… wait and see if it resolved or angiogram- came to the hospital yesterday morning w chest pain and troponin was .97. An hour later .96 then last one .58 CT at that time showed mild pericarditis and effusion- got steroids IV then prednisone 30mg tabs daily- at stress test fluid and inflammation was already not apparent echo and nuclear stress WNL Except the ST depressions- I’m opting for the angiogram and feel good w that after watching your video on it. Thank you. I don’t need to be a ticking time bomb and wait and watch on meds that have side effects (already ill w/ Crohn’s). I’d rather find out what’s causing it and move on. Hopefully w no meds no blockage but I don’t see if there is no blockage how it won’t lead to one eventually w ischemia already.
Man, that was informative. I like the fact that you describe it in a way I need it: from an engineering perspective. I now understand, in part, what I am facing. I now would like to know which electrode detected the ischemia (is that the right word?). It sounds like the depression event if not treated will eventually become a elevation event which, according to your diagram, is a more problematic situation. BTW, I get electrodes all over my chest but none on my back. Why?
By far the best Ive seen so far, but as a man with weak facial hair growth, that magnificent mustche is making it hard to focus. Cheers to the down under from the northern parts of Scandinavia!
What type of Myocardial Infarctions present this way? The video was amazing, I'm just a bit confused on what types of MI you're talking about and also how it would show up differently on an ECG if the MI happened in a different region of the heart? Thanks!!
For that you have to understand the different leads. Leads I/avL/V5/V6 are for lateral part of the heart which represents the left circumflex artery issues. Leads II/III/aVF are for inferior part of the heart, which is supplied by the right coronary artery. V1-V4 leads are supplied by the Left anterior descending artery, for the anteroseptal part of the heart
Omg, sounded right but is wrong. The watershed area may seem like the subendocardium, but it is actually the inferior/posterior region. Assuming lesion is left coronary, if not, it is also inferior posterior but right sided in rca. Also, depolarisation and flow is wrong, the leads pick up potential difference, you can’t have a single lead, you need 2 leads to make a lead reading. Lead II is left arm and left leg as the negative, and right arm and leg as the positive, hence if the electrical potential state is positive to the right, then it deflects negatively, but if it is positive to the left, it deflects positively. And no, though you are right in saying that ischaemia results in potassium leaking, ST segment changes happen only after hours from proper ischaemia, in the early phase, there is potentially NO st segment changes, maybe a T wave deflection and usually negative and deep suggesting a temporal delay in repolarisation between sub endocardium and epiendocardium. You have confused T inversion into negative with deepening with posterior/inferior infarcts that would actually result in ST depression. If you stuck the leads on the back or reverse side, you will get the classic ST elevation. That is posterior or right sided (or even septal/infero septal) infarcts. Since it is not a proximal coronary lesion, the majority of the heart should still function. If an anterior lesion occurred, you will lose 75% of cardiac function, that is the widowmaker lesion in proximal lad or LMCA, that is the classic stemi on classical lead placements The st elevation should always be assessed from the appropriate lead. Treat ST depression as reverse side ST elevations and it would make more sense. Sub endocardial lesions would make sense if it was a very proximal stenosis resulting in general watershed flow reduction everywhere and the last to receive flow would be the endocardium, but since all of the endocardium or the posterior endocardium would be affected first, an st depression should still result. The problem with using your model is that you didn’t take into account realistic coronary perfusion direction and area and realistic coronary artery anatomy, but isolated it to some small sub branch from the main coronary arteries hence giving some strange hard to interpret ecg but then trying to link back to common anatomical real ecgs. A theoretical sub endocardial ecg that fails to depolarise from the small area indicated would barely make a difference in the overall QRST. You’ll need a bigger area. Perhaps the issue is also thinking that ecg leads existed in isolation, and that they measured flow of charge, which they do not. So hence it made the explanation also wrong to follow.
How about the S is four blocks below Baseline j point starts two blocks above there then it upsloping to the top of the T most there is no visible j point no ST segment.. just an s 4 blocks below base line then an up slope to the top of the t hump.. I went through 2 years of permanent afib the last 5 months it effected the ventricles hart rate jumped from 60 to 120 - 135 constant 24 hours a day 7 days a week so says the zio patch and readings from my kardia ekg device during that time the s was like 6 blocks below base line they finally do catheter oblation now when I lay flat and do the kardia ekg there is pretty much only Q R S and a base line no atria activity
you have K+ leaking out because of lack of ATP, but you somehow still have enough K+ to put the cell into a more positive charge??? it makes so sense. if it's leaking, there should be less K+ making it more negative, no???
It leaked due to opening of K channels due to ischaemia but when the concentration of Potassium outside = Potassium inside the Concentration gradient got less so no leak hereafter
There is a problem with this explanation:If the K goes out of the cell shouldn't it hyperpolarise ? I don t get how it could lead to faster depolarisation
initially yes, but over time you have excess K+ outside to the point less K+ leaves the cell so we have a higher EP inside the cell. Earlier at -90mV a lot of K+ was leaving and now less K+ is leaving as the gradient is weaker.
I am still confused about the part about NSTEMI. So do the ischaemic tissues self depolarize as they have reached the threshold needed for the activation of the Calcium channels. So this in turn causes depolarization of the affected ventricle before SAN stimuli? @@mariaiorgulescu7109
That was lit. However, the lead 2 is placed on the 4th intercostal space (left side of the sternum), so this lead does not monitor the apex of the heart, right?
You're thinking of V2. Lead 2 is different. It's a limb lead vs a precordial lead, and it's not placed on the chest wall. Lead 2 though not placed at apex, does "aim" it's view toward the inferior region of the heart (bottom, apex).
one question : i wanna know TP segment mechanism when STE and STD following your lecture TP segment is down when STD and TP segment is up when STE what is right..? some books say pre QRS complex and after repolization moving together, when STE and STD give some advice for me thank u very much ur lecture very very helpful to me
In case of Transmural or complete occlusion of Coronary arteries-> No ATP -> Na-K ATPase malfunctioning-> improper Depolarization of ischaemic cells in contrast to Normal cells so it's creates potential difference that drives the vector away from ischemic cells towards the healthy cells at TP segment only Ventricular Repolarization reaches its final state of RMP by using Na-K ATPase but here since the TP Segment is taken as Baseline and due to Transmural it causes to push up so STE
is it transmural ischaemia always away from the lead? therefore isoelectric lower down, st segment look elevated? st segment elevated indicate transmural?
Because Outside also u have potassium but concentration of K+ Outside is less than Inside that's why it leaks out here due to ischaemia the tissue got exposed and so there will be increased permeability to ions so always in depolarized state even at rest too and More depolarized means -ve outside and +ve inside and less or no depolarization means +ve outside and -ve inside and here even though K+ leaks due to opening of K+ channels by ischaemia but now the concentration outside matches or reaches the limit so Concentration gradient got decreased so no K+ leaks out further so its +ve inside
OMG....I have never heard anyone explain the biophysical basis for ST depression and elevation so clearly and simply! Some of us learn better by learning the mechanism of things, but that not how things are taught generally in medical education, where instead it’s often “this is what you beed to know. Dont worry about why, unless you become an electrophysiologist.” Thank you!
this may be the single best video I have ever watched
Thank you 🙏
God bless this mustached man helping me understand how to do my essay.
😂😂😂
Amen! Lol
I had to come to the comments to write how amazing Dr. Mustache is to actually get me to UNDERSTAND the why's behind this. This video was beyond helpful.
🤣🤣🤣🤣 you make me laugh by moustache
Moustachioed - lovely word !
I just have been sent this video in the 5th week of my CVS block and man this was such a helpful and eye opening lecutre. Thank you so much for putting this much effort into making these videos so great. Your way of explaning and creative use of the board is outstanding! Keep doing what you do, you deserve 100 times the amount of subscribers you have! Thank you once again and I wish you all the success in the future.
I'm having a serious case of mustache envy at the moment. I feel the sudden need to overcompensate. Good video by the way. Very informative.
I was quite upset as none of the books provide an explanation for this phenomenon. Thank you for your wonderful presentation.
YES. So many resources only tell you what the ECG indicates but not WHY or the pathophysiology behind.
And my med school only have one lecture on ECG with NO teaching about cardiac pathology. We have to learn everything ourselves. Online resources like this is a god savior.
@@rebeccawan3088 Yup, same here in India
I know right! Lol!
Dr. Mike, what a wonderful presentation. Thank you sooooo much!!! Please, can you do a video on how to read an EKG and 12-lead EKG printouts?
Spent half an hour om this video and now I understand it. Thanks so much!
Great explanation Dr. Mike! Have been looking everywhere as to why subendocardial ischemia leads to initial elevation of the isoelectric point..
Wow. So simple! A question I’ve had for years finally answered. Thank you!
I'm a medical student and I was struggling to understand this, thank you so much!
in a nutshell >>
its the shift of isoelectric point, either high(in ST depression) or low (in ST elevation) makes it appear as ST elevation/Depression.
ST elevation- subendocardial ischemia
ST depression- transmural ischemia/infarct
thank you man, thats pretty simple, lots of love...❤
I’m worried that I’m becoming addicted to your videos. Brilliant explanation. Thank you.
Wow, I finally understand it! This is a really wonderful explanation. Thank you so much.
Oh how i wish you were my nursing instructor. You explained that so well! Thank you so much 💓
thank you so much this finally started to make sense after weeks of trying to get my head around it thank you again
Sir, if electrical activity is going on before QRS complex so, why is iso electric line is straight? Electrodes are sensing the vectors(thats why iso electric line is elevating or depressing) but as electrical activity is going on why there is no any deflection why the iso electric line is straight?
Fully depolarized means it wont record any potential
No dr Mike you do not understand I have been looking for this explanation for the past 3 days day and night and it has been driving me crazy.
Like thank you so freaking much my Australian professor
BRILLIANT EXPLANATION, thank you!!
i had no idea! I was looking for this video for a while and I m glad that I found it! thank you so much
Thank you thank you! This was beyond helpful it helped bridge the gap between what it means when I see it and what is actually occuring to make it that way. Can't say thanks enough
you save my license test, how lucky i am can come across this video. thanks way more a lot
Another great video... thank you 🙏
Your videos make things easier to understand
I didn’t quite get why would a resting membrane potential of -50 lead to the fast acting sodium channels not opening up (they were supposed to open up at above -70 so they should be open). Also didn’t understand why would the repolarization happen earlier.
So THAT'S how it works! Great lecture!
So is it spontaneous depolarization in absence of SAN impulse in NSTEMI? or do we still need SAN impulse before depolarization but it just happens faster and repolarizes faster?
I finally understand this! Thank you.
Amazing!please make more videos like this,basic is explained so nicely!
Thank you I was looking for this concept
Thank you. I’m a nurse. Not cardiac- HH wound ostomy care. Cardiology beyond basics is French to me. Thanks for the clear explaination of all I forgot since nursing school! I was dx today w ST depressions symptomatic but nothing but ST depressions 1.5mm on stressEKG during nuclear med test. Other findings normal. If family hx of widow maker (my dad) mom CHF, brother stents at 35. I’m 58 cardiologist gave me the choice to take meds and watch… wait and see if it resolved or angiogram- came to the hospital yesterday morning w chest pain and troponin was .97. An hour later .96 then last one .58
CT at that time showed mild pericarditis and effusion- got steroids IV then prednisone 30mg tabs daily- at stress test fluid and inflammation was already not apparent echo and nuclear stress WNL Except the ST depressions- I’m opting for the angiogram and feel good w that after watching your video on it. Thank you. I don’t need to be a ticking time bomb and wait and watch on meds that have side effects (already ill w/ Crohn’s). I’d rather find out what’s causing it and move on. Hopefully w no meds no blockage but I don’t see if there is no blockage how it won’t lead to one eventually w ischemia already.
Thank you sir for teaching me this concept😊
Man, that was informative. I like the fact that you describe it in a way I need it: from an engineering perspective. I now understand, in part, what I am facing. I now would like to know which electrode detected the ischemia (is that the right word?). It sounds like the depression event if not treated will eventually become a elevation event which, according to your diagram, is a more problematic situation.
BTW, I get electrodes all over my chest but none on my back. Why?
By far the best Ive seen so far, but as a man with weak facial hair growth, that magnificent mustche is making it hard to focus. Cheers to the down under from the northern parts of Scandinavia!
this was AMAZING - better than my medical school. WOW!
Yes SIR! Thank you so much!
What type of Myocardial Infarctions present this way? The video was amazing, I'm just a bit confused on what types of MI you're talking about and also how it would show up differently on an ECG if the MI happened in a different region of the heart? Thanks!!
For that you have to understand the different leads. Leads I/avL/V5/V6 are for lateral part of the heart which represents the left circumflex artery issues. Leads II/III/aVF are for inferior part of the heart, which is supplied by the right coronary artery. V1-V4 leads are supplied by the Left anterior descending artery, for the anteroseptal part of the heart
Hell yeah this is a great explanation, thank you!
Thank you for such an amazing explanation ❤️❤️
Thank you so much for the brilliant explanation Dr. Mike! nice mustache by the way.
Awesome! Thank you very much
That was an amazing explanation. Thank you.
Oh my god i feel like a third eye is open now.. thank you
Thank you doctor for you great video 🙌❤
Aweeeeesome! God Bless!
Amazing explanation. Thanks in advance
Wooow, excellent explanation 🎉❤
Thank you so much this help me a lot 👏👏👏
This was Awesome!!!
Great explanation
Thank you !
Thanks so much for this!
Awesome video...!!please make video series on ECG basics and interpretation. Thanks alot 😄😄
You are amazing ... You solved My 1 yr doubt in just 16 minutes ...❤
Omg, sounded right but is wrong. The watershed area may seem like the subendocardium, but it is actually the inferior/posterior region. Assuming lesion is left coronary, if not, it is also inferior posterior but right sided in rca.
Also, depolarisation and flow is wrong, the leads pick up potential difference, you can’t have a single lead, you need 2 leads to make a lead reading.
Lead II is left arm and left leg as the negative, and right arm and leg as the positive, hence if the electrical potential state is positive to the right, then it deflects negatively, but if it is positive to the left, it deflects positively.
And no, though you are right in saying that ischaemia results in potassium leaking, ST segment changes happen only after hours from proper ischaemia, in the early phase, there is potentially NO st segment changes, maybe a T wave deflection and usually negative and deep suggesting a temporal delay in repolarisation between sub endocardium and epiendocardium.
You have confused T inversion into negative with deepening with posterior/inferior infarcts that would actually result in ST depression.
If you stuck the leads on the back or reverse side, you will get the classic ST elevation. That is posterior or right sided (or even septal/infero septal) infarcts. Since it is not a proximal coronary lesion, the majority of the heart should still function.
If an anterior lesion occurred, you will lose 75% of cardiac function, that is the widowmaker lesion in proximal lad or LMCA, that is the classic stemi on classical lead placements
The st elevation should always be assessed from the appropriate lead. Treat ST depression as reverse side ST elevations and it would make more sense.
Sub endocardial lesions would make sense if it was a very proximal stenosis resulting in general watershed flow reduction everywhere and the last to receive flow would be the endocardium, but since all of the endocardium or the posterior endocardium would be affected first, an st depression should still result.
The problem with using your model is that you didn’t take into account realistic coronary perfusion direction and area and realistic coronary artery anatomy, but isolated it to some small sub branch from the main coronary arteries hence giving some strange hard to interpret ecg but then trying to link back to common anatomical real ecgs.
A theoretical sub endocardial ecg that fails to depolarise from the small area indicated would barely make a difference in the overall QRST. You’ll need a bigger area.
Perhaps the issue is also thinking that ecg leads existed in isolation, and that they measured flow of charge, which they do not. So hence it made the explanation also wrong to follow.
But what about the inverted T wave?
How about the S is four blocks below Baseline j point starts two blocks above there then it upsloping to the top of the T most there is no visible j point no ST segment.. just an s 4 blocks below base line then an up slope to the top of the t hump.. I went through 2 years of permanent afib the last 5 months it effected the ventricles hart rate jumped from 60 to 120 - 135 constant 24 hours a day 7 days a week so says the zio patch and readings from my kardia ekg device during that time the s was like 6 blocks below base line they finally do catheter oblation now when I lay flat and do the kardia ekg there is pretty much only Q R S and a base line no atria activity
Awesome video. Thanks
Thanku very much
You explained it in a lot simpler way❤️
you have K+ leaking out because of lack of ATP, but you somehow still have enough K+ to put the cell into a more positive charge??? it makes so sense. if it's leaking, there should be less K+ making it more negative, no???
It leaked due to opening of K channels due to ischaemia but when the concentration of Potassium outside = Potassium inside the Concentration gradient got less so no leak hereafter
thank you so much
thank you so much for the very clear explanation! ❤️
Amazing explanation thank you
This was great man
Thank you so much.
Is this the same mechanism of cardioplegia by increasing the K+ during cardiopulmonary bypass?
This was GREAT!! 👏🏻👏🏻👏🏻
Perfect explanation. Thanks...
If k+ is leaking out it means inside the cell is being more negative. So from 90mv won't it become hyperpolarised? I m confused.
When it leaks out sodium calcium are coming in right so it will become depolarized
There is a problem with this explanation:If the K goes out of the cell shouldn't it hyperpolarise ? I don t get how it could lead to faster depolarisation
initially yes, but over time you have excess K+ outside to the point less K+ leaves the cell so we have a higher EP inside the cell. Earlier at -90mV a lot of K+ was leaving and now less K+ is leaving as the gradient is weaker.
it depolarizes faster as our resting potential is above the required for Voltage gated Ca+ to open
@@peppapig934 thank You, i think i finally got it
I am still confused about the part about NSTEMI. So do the ischaemic tissues self depolarize as they have reached the threshold needed for the activation of the Calcium channels. So this in turn causes depolarization of the affected ventricle before SAN stimuli?
@@mariaiorgulescu7109
To be honest, i dont think many people understand the concept properly. I am finding many questions than answers. Video is not clear enough
Is there any simpler way to describe this?
thank you very much for this video, it’s sooooo informative
I would like to know if potassium has something to do with the swollen nasal turbinates.Thanks dear bro !
Can you explain muscular hypertrophy too?
I have!! Check my muscle/musculoskeletal playlists.
thank you very very much brother
10/10 amazing! Thank you so much!!
This is BRILLIANT> now I believe in the evolution of human intelligence....
Excellent
That was lit. However, the lead 2 is placed on the 4th intercostal space (left side of the sternum), so this lead does not monitor the apex of the heart, right?
You're thinking of V2. Lead 2 is different. It's a limb lead vs a precordial lead, and it's not placed on the chest wall. Lead 2 though not placed at apex, does "aim" it's view toward the inferior region of the heart (bottom, apex).
@@vulpine174 You're right.
what about the T waves
Thanks man
Why does ischemic tissue depolarize early?
Because of damage they will get exposed so Increased permeability to ions so always in depolarized state even at rest too
Amazing
If potassium from inside only came outside then how come it is still positive inside?
Not all potassium left out
Well explained 👏 Thank you
i will never forget this concept ...hatsoff thankyu so very much
Can you have an MI without troponin elevation?
Yes that's called NSTEMI
AMAZING
Is there a way to determine how long an individual has had an ST depression?
Thank you✨
thanks so much i finally understood
Can you use a IV bolus of Heparin for STEMI's or ST Depression? (not a heparin drip)
one question : i wanna know TP segment mechanism when STE and STD
following your lecture TP segment is down when STD and TP segment is up when STE
what is right..?
some books say pre QRS complex and after repolization moving together, when STE and STD
give some advice for me
thank u very much ur lecture
very very helpful to me
In case of Transmural or complete occlusion of Coronary arteries-> No ATP -> Na-K ATPase malfunctioning-> improper Depolarization of ischaemic cells in contrast to Normal cells so it's creates potential difference that drives the vector away from ischemic cells towards the healthy cells at TP segment only Ventricular Repolarization reaches its final state of RMP by using Na-K ATPase but here since the TP Segment is taken as Baseline and due to Transmural it causes to push up so STE
finally got it :))))
Thank you!!!
based on the location of the lead that Dr Mike drew, is it lead 3? because left arm and left leg? anyone know?
is it transmural ischaemia always away from the lead? therefore isoelectric lower down, st segment look elevated? st segment elevated indicate transmural?
Good stuff
Thanks a lot sir !
love you..
If potassium moved out of cell then inside cell should become more negative becuse positive charge left why it become postive
Because Outside also u have potassium but concentration of K+ Outside is less than Inside that's why it leaks out here due to ischaemia the tissue got exposed and so there will be increased permeability to ions so always in depolarized state even at rest too and More depolarized means -ve outside and +ve inside and less or no depolarization means +ve outside and -ve inside and here even though K+ leaks due to opening of K+ channels by ischaemia but now the concentration outside matches or reaches the limit so Concentration gradient got decreased so no K+ leaks out further so its +ve inside
I it means it's in depolarized state and no K+ leaks out hereafter so will be In depolarized state -ve outside and Positive inside
I am Escanor, the Lion sun of pride🌞
oooookkeeeeyy look at this circle at 00:42 not perfect but still annoyingly satisfying
I will build a statue of your moustache one day