This is how my father died today. He has been dealing with kidney failure and simply refused to do his peritoneal dialysis treatment. He did not want to live anymore due to all of the pain it caused him. He was very delirious, weak, tired and cold throughout the ordeal. He went into cardiac arrest in the ambulance and died upon arrival to the hospital. High potassium is deadly and anyone dealing with hyperkalemia should take it very seriously.
My issue is: Why aren't we warned earlier than Stage 3 that our potassium is inching up each time we have lab work? Many patients in my support group are VERY angry that we aren't notified as soon as any increase in potassium, phosphorous, A1c, etc., shows an ongoing increase even if a little bit. All they ever warn us about is B/P and want to prescribe statins. No mention of anything else.
At 5:44, you write "adrenal failure (Cushings Disease)". I think it should be Addisons disease? To my knowledge, Cushings is the opposite to adrenal failure; the cortices are hyperactive, leading to high levels of cortisol and aldosterone, which in turn leads to hypOkalemia, not hyper.
Excellent video! But still I have a question. At 11:03, did you mention the membrane excitability will DECREASE? If hyperkalemia elevated the baseline potential, shouldn't the excitability be INCREASED? Thankyou.
Increased potassium levels cause a sustained increase in membrane potential and it becomes less negative. One would expect that this would make depolarization easier and the cell hyperexcitable BUT actually sustained increase in membrane potential closes the deactivation gate of sodium channels and this prevents sodium influx and action potential cannot be generated. This is called ACCOMMODATION.
Great video! I was a little confused at the end, does hyperkalemia result in the heart cell being more easily depolarized or more difficult to depolarize?
But why do we have a high and fast repolarisation if the extracellular K+ -Concentration is already so high?? I thought also repolarisation will happen very slowly?
One of the potassium currents (Ikr), located on the myocyte cell membrane, is mostly responsible for the potassium efflux seen during phases 2 and 3 of the cardiac action potential.10 For reasons that are not well understood, these Ikr currents are sensitive to extracellular potassium levels, and as the potassium levels increase in the extracellular space, potassium conductance through these currents is increased so that more potassium leaves the myocyte in any given time period.10 This leads to an increase in the slope of phases 2 and 3 of the action potential in patients with hyperkalemia and therefore, to a shortening of the repolarization time. This is thought to be the mechanism responsible for some of the early electrocardiographic manifestations of hyperkalemia, such as ST-T segment depression, peaked T waves, and Q-T interval shortening from: www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/
I think der r some errors here.. Firstly..tendency to depolarise increases initially bcz K conc outside the cell becomes high nd hence its difficult fr K to leave the cell nd hence the polarity inside bcmz more postve nd towrds the threshold potential..bt then free flow of Na should happen and it wont happen bcz f increased postve charge inside the cell..this will actually delay the depolarisation.Now during the repolarisation, initially der s a plateau phase where K efflux and Ca influx happens simultaneously..but since K does not leave as easily as expected bcz f reduced gradient,there will be prolongation in the repolarisation which is evident from the delayed or wide QRS..Eventually leading to absent atrial depolarisation and sine wave pattern nd ventricle fires at its own rate and produce ventricular fibrilations nd cardiac arrest @ d end evidenced by asystole in ECG
Other than Angiotensin II and adrenocorticotropic hormone, what else triggers the adrenal gland to secrete mineralocorticoids? I didn't even think adrenocorticotropic hormone did this, I thought it only stimulated the release of cortisol. Please explain thank you
See the whole series at www.medcram.com along with other top quality videos including reviews in pulmonary, cardiology, infectious disease, and hematology!
it is said that hyperkalaemia is often associated with metabolic acidosis.... yet the only cause in which acidosis and hyperkalaemia occur is addison's disease. other causes of metabolic acidosis ( DKA, acetazolamide, diarrhea, and renal tubular acidosis are associated with hypokalaemia. would you like to explain that please??
+Nada Dwiddar this is because acidosis itself causes hyperkalemia. Protons in the serum go into the cell in exchange for potassium which comes out of the cell causing hyperkalemia.
+Nada Dwiddar yes as the blood pH goes down this causes protons in the blood to go into the cells. Potassium then comes out of the cells to balance it and this causes hyperkalemia. The opposite occurs when the blood pH goes up.
![[#2024MAMA] G-DRAGON - 무제(Untitled, 2014)+POWER+HOME SWEET HOME+뱅뱅뱅+FANTASTIC BABY | Mnet 241123 방송](http://i.ytimg.com/vi/Ox29z5Nf1Uk/mqdefault.jpg)
This is how my father died today. He has been dealing with kidney failure and simply refused to do his peritoneal dialysis treatment. He did not want to live anymore due to all of the pain it caused him. He was very delirious, weak, tired and cold throughout the ordeal. He went into cardiac arrest in the ambulance and died upon arrival to the hospital. High potassium is deadly and anyone dealing with hyperkalemia should take it very seriously.
My issue is: Why aren't we warned earlier than Stage 3 that our potassium is inching up each time we have lab work? Many patients in my support group are VERY angry that we aren't notified as soon as any increase in potassium, phosphorous, A1c, etc., shows an ongoing increase even if a little bit. All they ever warn us about is B/P and want to prescribe statins. No mention of anything else.
Cushing’s was an error, he meant Addison’s disease.
Thank you for your video.
+megaroozi correct Addisons is the disease when the adrenal gland is less secretory not Cushings
Could you please unlock the treatment video? It’s currently listed as private. Thank you
I am a student here in the Philippines.. thanks for this video.. it helps me a lot for my discussion..
Thanks for watching in the Philippines. Best wishes with your studies and thanks for the comment
We had this topic last Spring and this video was a great refresher. Thank you!
wvllanner4 Good to hear- thank you
At 5:44, you write "adrenal failure (Cushings Disease)". I think it should be Addisons disease? To my knowledge, Cushings is the opposite to adrenal failure; the cortices are hyperactive, leading to high levels of cortisol and aldosterone, which in turn leads to hypOkalemia, not hyper.
Watch at 1.5 speed... you're welcome
Excellent video!
But still I have a question. At 11:03, did you mention the membrane excitability will DECREASE?
If hyperkalemia elevated the baseline potential, shouldn't the excitability be INCREASED? Thankyou.
Increased potassium levels cause a sustained increase in membrane potential and it becomes less negative. One would expect that this would make depolarization easier and the cell hyperexcitable BUT actually sustained increase in membrane potential closes the deactivation gate of sodium channels and this prevents sodium influx and action potential cannot be generated. This is called ACCOMMODATION.
How does a less negative resting potential cause a spike T wave though? there should be less electrical potential to drive a large influx of K.
I am a student and your videos help me. All your videos are so clear and interesting !! Thank you so much !!
+Abdelhamid Benzerroug Thank you for the feedback
I would add rapid infusion or overdosing of IV Potassium as a cause of hyperkalemia. Thank you for the video!
Thank you Dr. Seheult.
thanks for posting these! very helpful in anesthesia applications!
I see how this works. A loss leader video to buy video 2 on the websight.
Can you do a lecture on hypokalemia?
+Hashim Ismail Thanks for the suggestion
seconded
We are waiting :) Thanks so much!
Preferably before my nephrology exam on the 31st of August, please :P
PLease did you do it ?
Can you explain how the narrow and peak T wave happen?
What happened to the treatment video of Hyper K?? There was a video explaining treatment interactions at a physiological level.
I discovered another helpful channel
Thank you so much !!! I would love if you completed the series with Hypokalemia !! Thanks Again !!!
At 12:20 I think you meant to say Addison's disease. Thanks for your videos.
Ron Norris Thanks for catching this- you are correct. I've made a note on the video that I should have wrote Addison's.
Clear, interesting and easy to follow....Thank You!
exteremly good and simple to understand thanks
Can you please complete this series by adding Hypokalemia?
Thank You!
Thanks Dr. Seheult. Explained clearly. Could you make some video about magnesium, another essential element for our body.
Thank you medcram
Great video! I was a little confused at the end, does hyperkalemia result in the heart cell being more easily depolarized or more difficult to depolarize?
It really is explained clearly! Thanks
excellent videos. you do indeed explain things clearly. This is great review for a practicing RN.
+Navid Aliaghai Good to hear- thanks so much for the comment
But why do we have a high and fast repolarisation if the extracellular K+ -Concentration is already so high??
I thought also repolarisation will happen very slowly?
alsh123am yes same question here.#Medcram plz solve it @medcrAm
One of the potassium currents (Ikr), located on the myocyte cell membrane, is mostly responsible for the potassium efflux seen during phases 2 and 3 of the cardiac action potential.10 For reasons that are not well understood, these Ikr currents are sensitive to extracellular potassium levels, and as the potassium levels increase in the extracellular space, potassium conductance through these currents is increased so that more potassium leaves the myocyte in any given time period.10 This leads to an increase in the slope of phases 2 and 3 of the action potential in patients with hyperkalemia and therefore, to a shortening of the repolarization time. This is thought to be the mechanism responsible for some of the early electrocardiographic manifestations of hyperkalemia, such as ST-T segment depression, peaked T waves, and Q-T interval shortening
from: www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/
Can you explain clearly on the point why hyperkalimia can make depolarization late than normal?
Thanks, this is a tricky subject :)
Anete Libeka Glad the video helped
+MEDCRAMvideos thanks man could u explain why hyponatremia,hypoglycemia and metabolic acidosis occur in adrenal failure
all hydroelectrolytes disorders basically
Great explanation 👌🏽
Glad it was helpful!
I think der r some errors here..
Firstly..tendency to depolarise increases initially bcz K conc outside the cell becomes high nd hence its difficult fr K to leave the cell nd hence the polarity inside bcmz more postve nd towrds the threshold potential..bt then free flow of Na should happen and it wont happen bcz f increased postve charge inside the cell..this will actually delay the depolarisation.Now during the repolarisation, initially der s a plateau phase where K efflux and Ca influx happens simultaneously..but since K does not leave as easily as expected bcz f reduced gradient,there will be prolongation in the repolarisation which is evident from the delayed or wide QRS..Eventually leading to absent atrial depolarisation and sine wave pattern nd ventricle fires at its own rate and produce ventricular fibrilations nd cardiac arrest @ d end evidenced by asystole in ECG
Great Lecture !!! Thank you
Other than Angiotensin II and adrenocorticotropic hormone, what else triggers the adrenal gland to secrete mineralocorticoids? I didn't even think adrenocorticotropic hormone did this, I thought it only stimulated the release of cortisol. Please explain thank you
Dude, you sound EXACTLY like Sal Khan...unless you narrate the MCAT videos on Khan Academy?
Why there is a hyperpolarization due to inactivated sodium channels, thanks
@miranda ti please did you get a reply, I'm stucked here too
thank you , I suggest to have a lecture on action potential and anti arrythmics , thanks again .
+رصاصة الرحمة Thank you for the topic suggestion
Thanks that's what i was looking for 😊😊
:)
Thanks for Good Explanation :) So with Hyperkalemia will become more Depolarized at RMP?
Thanks a lot a great explanation
Is cushing disease causes hypokalemia or hyperkalemia ?
Adrenal failure is Addison disease not Cushing sir
What about a burning left arm ? Going to the doctors soon but I’ve had this for about 3 weeks while on keto . I think it’s from high potassium
Sooooo helpful!! Thank you 😊
Thank you for the video, very informative
Amazing videos!! Can you touch on some of the other electrolytes. Na+, calcium, magnesium etc. That would be very helpful.
See the whole series at www.medcram.com along with other top quality videos including reviews in pulmonary, cardiology, infectious disease, and hematology!
You also get an absent p wave right?
Adrenal failure is known as Addisons Diseases, not Cushing’s syndrome.
it is said that hyperkalaemia is often associated with metabolic acidosis.... yet the only cause in which acidosis and hyperkalaemia occur is addison's disease.
other causes of metabolic acidosis ( DKA, acetazolamide, diarrhea, and renal tubular acidosis are associated with hypokalaemia.
would you like to explain that please??
+Nada Dwiddar this is because acidosis itself causes hyperkalemia. Protons in the serum go into the cell in exchange for potassium which comes out of the cell causing hyperkalemia.
Great lecture but I have a pressing question, can you please tell me the name of the song that is at the end. :)
excellent video
Do you have a video on hypokalemia too?
+miranda ti Not yet...
is there any of hypokalemia?
Thanks
Hyperkalemia simplified!!
Is 3.47 level is dangerous what to do on this level.
No thats normal
But why Does acidosis cause hyperkalemia ? This remains my question :p Maybe you can clarify for us sir ?
pulmonary embolism
Thank you so much 😭
why a grain of salt if hemolysis occurs?
Thank you T_T
can u expalin the relationship between k level and acid base balance..... very confusing
+Nada Dwiddar yes as the blood pH goes down this causes protons in the blood to go into the cells. Potassium then comes out of the cells to balance it and this causes hyperkalemia. The opposite occurs when the blood pH goes up.
MedCram - Medical Lectures Explained CLEARLY thank you very much..... 😊😊
Dialysis patients should never use salt substitute.
Very informative! Thank you so much! 😃😃 27/2/2019
my dad had hyperkalemia and doctors placed a pacemaker in his neck
Not so helpful.... 6/10...only
a very informative topics
I’m 24 but suffering hyperkalemia rn 🥺
Tall tented t wave.. hyperkalemia..
WAY too scientific for most viewers to understand... this sounds like a doctoral dissertation!!
🥰
Can you do a lecture on hypokalemia?