Since this video was published in 2013, 2 newer drugs for hyperkalemia have been approved and entered common practice: patiromer (a.k.a. Veltassa) and sodium zirconium cyclosilicate (a.k.a. Lokelma), which have less risk of side effects as compared to kayexalate.
Is rum potassium a good indicator of hyperkalemia? I take beta blockers due to Long QT and have noticed that my sodium is chronically low (around 133 to 135) and potassium is chronically high now (around 5.0 to 5.3). I see these readings are not far enough out of reference range to trigger noticeable ECG signs but I have had a First Degree AV Block and then my first ever Afib episode. Is it possible that the serum levels fluctuate daily and may slip in and out of dangerous levels?
Thanks Dr.Strong for the exciting easy to understand videos. In regards to Cation exchangers, what are your comments about the novel agents (like patiromer) ?
I can't offer specific, individualized medical advice here, and I recommend you speak to your own physicians about your health concerns. However, I will say that since this video was published in 2013, two newer drugs for hyperkalemia have entered common practice: patiromer (a.k.a. Veltassa) and sodium zirconium cyclosilicate (a.k.a. Lokelma), which have less risk of side effects as compared to kayexalate. But these may not yet be available in all locations throughout the world.
Dr. Strong, can you explain about TTKG? Should I learn about it? Is it practical? It can be found all over classic textbooks such as Harrison and Cecil
The etiology of potassium disorders is usually evident from the history, and is less often a diagnostic mystery than hyponatremia or even calcium disorders. The TTKG is rarely used in practice, and learning about it is low yield.
I'm sorry but I can't offer specific, individualized medical advice on here. I recommend speaking with your physician. (However, I will point out that this comment is on the video for hyperkalemia - which means potassium that is too high, not too low)
Normally, there is high conc. of K+ inside the cell. In (metabolic) acidosis, H+ conc in blood is increased. Then to maintain the ionic balance, these cations get exchanged. H+ moves in and K+ comes out of the cell. Leading to increased conc of K+ in blood, i.e. hyperkalemia. Hope this helps. :)
Always in hyperkalemia, since the choice and urgency of interventions is as dependent on the presence/absence of EKG changes as it is on the absolute potassium concentration. With hypokalemia, I arbitrarily ask housestaff to check an EKG if it's less than 3.0 mEq/L, but there is no rationale for this specific cutoff.
Dear Professor Strong, Thank you very much for your great lectures. However, as a European medical doctor I am taken aback when you denote those sentenced to death as "patients" (4:54).
+georg reining I must not have listened to the complete recording after making it. When I talk about hyperkalemia in person, that line comes across way more sarcastically than it does here! I'm actually really annoyed with myself that it sounds straight in the recording - and now am wondering about reposting the video. I try to keep politics completely out of the comments section on the channel, but I'll make an exception to state that I find capital punishment to be an abomination with which no doctor should ever assist. Thanks for pointing this out.
Warning! In individual patients, the serum potassium level may not correlate closely with the ECG changes as Dr Strong has pointed out and patients with relatively normal ECGs may still experience sudden hyperkalaemic cardiac arrest!!!!!(LITFL)
Allibaby78 Thanks for emphasizing this Allibaby! Bottom line: Risk of arrest from hyperkalemia is a complex and incompletely understood combination of absolute serum potassium level, presence and severity of EKG changes, and rapidity with which the hyperkalemia develops. An abrupt increase in potassium from something like inadvertent (or intentional) IV potassium bolus, rhabdomyolysis, or tumor lysis syndrome, could certainly result in arrest before changes show up on EKG. In general, rapidly acting therapies (e.g. calcium, insulin, beta agonists) are indicated when either EKG changes are present, or the K is unusually high (>6.5-7) irrespective of EKG changes. Some also use an unusually rapid increase in K as a reason to give rapidly acting therapies (even if there are no EKG changes and the K is
I imagine that rebound hyperkalemia could possibly occur after diuretics or kayexalate, but the only time I've actually seen it is after hemodialysis. Rebound would also be expected in a patient with severe hyperkalemia was treated only with therapies that lead to a transmembrane shift (e.g. insulin, beta agonists), since that effect wears off after a few hours, which is why those therapies should only be considered temporzing measures.
Since this video was published in 2013, 2 newer drugs for hyperkalemia have been approved and entered common practice: patiromer (a.k.a. Veltassa) and sodium zirconium cyclosilicate (a.k.a. Lokelma), which have less risk of side effects as compared to kayexalate.
The best. Period.
Love your lectures. You are the best teacher.
Thank you Dr Strong for a great video - please explained exactly - mechanism of action - how calcium gluconate stablizes the membranes - G
Thank you Dr Strong , I watch this for second time. Best lecture.
Extremely good and practically useful
As always: very clear and nicely put
Is rum potassium a good indicator of hyperkalemia? I take beta blockers due to Long QT and have noticed that my sodium is chronically low (around 133 to 135) and potassium is chronically high now (around 5.0 to 5.3). I see these readings are not far enough out of reference range to trigger noticeable ECG signs but I have had a First Degree AV Block and then my first ever Afib episode. Is it possible that the serum levels fluctuate daily and may slip in and out of dangerous levels?
I'm very sorry, but I can't answer personal health questions here. I recommend speaking with your cardiologist or primary care doctor.
Thank you so much 🙏🏻🙌🏻
vieos r simplified esy to understand......thank u Dr. eric
Thanks Dr.Strong for the exciting easy to understand videos. In regards to Cation exchangers, what are your comments about the novel agents (like patiromer) ?
Your video is very useful. Thanks a lot!
Another great video! Thanks
The patient that developed hyperkalemia on penicillin G K,was resuscitated, and electrocardiographic changes reversed by calcium chloride.
Great video series! Thank you!
Sir pleas answer me what is the best medicine to take for hyperkalemia? I need it very much
I can't offer specific, individualized medical advice here, and I recommend you speak to your own physicians about your health concerns. However, I will say that since this video was published in 2013, two newer drugs for hyperkalemia have entered common practice: patiromer (a.k.a. Veltassa) and sodium zirconium cyclosilicate (a.k.a. Lokelma), which have less risk of side effects as compared to kayexalate. But these may not yet be available in all locations throughout the world.
thank you for sharing!
Dr. Strong, can you explain about TTKG? Should I learn about it? Is it practical? It can be found all over classic textbooks such as Harrison and Cecil
The etiology of potassium disorders is usually evident from the history, and is less often a diagnostic mystery than hyponatremia or even calcium disorders. The TTKG is rarely used in practice, and learning about it is low yield.
@@StrongMed Thanks for your swift respons
Hello doc, my hand is light and my potassium is 3.30 if my potassium is low, is it light to control? and my hand is cramping😊
I'm sorry but I can't offer specific, individualized medical advice on here. I recommend speaking with your physician. (However, I will point out that this comment is on the video for hyperkalemia - which means potassium that is too high, not too low)
Can you plz explain about covid strain and various vaccine
Thank you for showing ecg examples of the different degrees of hyperkalemia.
RqrqrqqqrllralekriirtkFidkelrllrkfKFKFGKFKKF
FKFLFLFLFKFLFKFFK
FKFL
ÑKKFKFKFKFFFLLFFFFEErrrkrkeklrkr
FkkffLNFLRooffoflflfffiw
Kekek
Ke
Kelekellelekekelekekekememmeaemaeameaaemnaennaenmenaemenraaamraaaj
Eaaaaeaaeeaaaee
Raaa
Rar
Ai
Rkkfkrk
FFrr
Dr why does acidosis cause hyperkalemia i dont understand ? Can you clarify for us ?
Normally, there is high conc. of K+ inside the cell. In (metabolic) acidosis, H+ conc in blood is increased. Then to maintain the ionic balance, these cations get exchanged. H+ moves in and K+ comes out of the cell. Leading to increased conc of K+ in blood, i.e. hyperkalemia.
Hope this helps. :)
In order to compensate acidosis , excess H ion moves into cell and k out cell, that’s how acidosis causing hyperkalemia
You didn't mention calcium resonium use
Sorry, calcium resonium is not available in my home country (USA).
Sound is too low sir!!
When to do EKG in hypo and hyperkalemia?
Always in hyperkalemia, since the choice and urgency of interventions is as dependent on the presence/absence of EKG changes as it is on the absolute potassium concentration.
With hypokalemia, I arbitrarily ask housestaff to check an EKG if it's less than 3.0 mEq/L, but there is no rationale for this specific cutoff.
Strong Medicine ❤️
Dear Professor Strong,
Thank you very much for your great lectures.
However, as a European medical doctor I am taken aback when you denote those sentenced to death as "patients" (4:54).
+georg reining I must not have listened to the complete recording after making it. When I talk about hyperkalemia in person, that line comes across way more sarcastically than it does here! I'm actually really annoyed with myself that it sounds straight in the recording - and now am wondering about reposting the video. I try to keep politics completely out of the comments section on the channel, but I'll make an exception to state that I find capital punishment to be an abomination with which no doctor should ever assist. Thanks for pointing this out.
Serum potassium > 5.5 mEq/L is associated with repolarisation abnormalities=tall peaked T-waves
Warning! In individual patients, the serum potassium level may not correlate closely with the ECG changes as Dr Strong has pointed out and patients with relatively normal ECGs may still experience sudden hyperkalaemic cardiac arrest!!!!!(LITFL)
Allibaby78 Thanks for emphasizing this Allibaby! Bottom line: Risk of arrest from hyperkalemia is a complex and incompletely understood combination of absolute serum potassium level, presence and severity of EKG changes, and rapidity with which the hyperkalemia develops. An abrupt increase in potassium from something like inadvertent (or intentional) IV potassium bolus, rhabdomyolysis, or tumor lysis syndrome, could certainly result in arrest before changes show up on EKG. In general, rapidly acting therapies (e.g. calcium, insulin, beta agonists) are indicated when either EKG changes are present, or the K is unusually high (>6.5-7) irrespective of EKG changes. Some also use an unusually rapid increase in K as a reason to give rapidly acting therapies (even if there are no EKG changes and the K is
U r my god
Excellent video!
At the very end, you mention rebound hyperkalemia. Is it only seen after hemodialysis? Where else is it seen?
I imagine that rebound hyperkalemia could possibly occur after diuretics or kayexalate, but the only time I've actually seen it is after hemodialysis. Rebound would also be expected in a patient with severe hyperkalemia was treated only with therapies that lead to a transmembrane shift (e.g. insulin, beta agonists), since that effect wears off after a few hours, which is why those therapies should only be considered temporzing measures.
Great lecture Eric i am using your material for USMLE step 3
one more to clear,,,sine waves look like VT...how to differentiate.....
The short answer is that there isn't any reliable way to differentiate the "sine wave" rhythm from VT on EKG. Although, an unusually slow (i.e.
good