Hyperkalemia Explained Clearly – Fluid and Electrolyte Imbalances

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , /

welcome to another MedCram lecture
we’re going to talk about hyperkalemia hyperkalemia like anything else that
ends in e mia has to do with the blood and the K if you remember from the
periodic table has to do with potassium so we’re going to talk about high
potassium in the blood and that generally speaking is greater than 5.0
but of course the higher it goes the worse the symptoms can become so the
normal range for potassium is about 3.5 to 5.0 this is an extremely well
regulated system potassium has to be very well regulated in the blood and the
reason is is because the conduction system in the heart specifically and
also in the muscle depends heavily on potassium going through the membrane and
so the conductivity to potassium is very high so that if there is a problem with
the concentration of potassium outside the cell it’s really going to affect the
depolarization of those cells and so potassium abnormalities are really going
to hit the heart quite hard and cause arrhythmias and that’s why the body is
so keen on protecting the level of potassium so we’re going to talk about
the causes of hyperkalemia the manifestations of hyperkalemia and the
treatment of hyperkalemia okay so let’s talk about the causes the first cause is
excessive tissue release or transcellular
shifts okay so you can think about for instance diabetes remember what happens
in diabetes is there’s a lot of glucose around the cells so you’ve got a cell
here and you’ve got glucose outside the cell and that causes water to leave the
cell and for something to do something called Coronation shrinks basically and
when that happens the potassium concentration which is already high in
the cell is actually going to go up and this causes leakage of potassium outside
the cell and the fact in diabetes is insulin which especially in type 1
diabetics is rare and insulin is responsible for putting potassium back
inside the cell okay so that’s an important note is that insulin causes
potassium to shift back into the cell and in a patient with diabetes the
glucose is high that causes eventually potassium to leak outside the cell since
there’s no insulin it cannot be put back inside the cell another corollary to
this is something called HH or hypo Ren anemic hypo aldosterone ism okay so
that’s hypo renin the renin is the thing that this should be stimulating the
adrenal cortex to make aldosterone but as a fact that it doesn’t you get hypo
aldosterone now remember aldosterone works on the
distal convoluted tubules right about there and remember what it
does it causes potassium excretion and sodium reabsorption at the distal
convoluted tubules so if you don’t have enough aldosterone being
secreted from the zona glomerulosa of the adrenal cortex you’re going to get
an accumulation of potassium inside the serum the reason why I bring these up
together is this hypo Renick hypo aldosterone ism can be seen together
with diabetes so that’s just one cause of hyperkalemia
the next cause is kind of obvious and that’s just increased intake of
potassium so you got to kind of know what has potassium in it and some of the
things that have potassium in it our salt substitute so instead of having the
cation sodium that has the cation potassium the other thing that you can
see is the excessive intake in renal failure these people who are in renal
failure typically are the ones that are on salt substitutes in this potassium
cannot be cleared the other one that we kind of talked about if the zona
glomerulosa of the adrenal cortex is not secreting aldosterone is you will see
adrenal failure if it is a problem with the pituitary not stimulating the
adrenal cortex the aldosterone still is secreted in sufficient amounts that you
may not see hyperkalemia however if there is a direct attack on the adrenal
cortex where antibodies are destroying all three layers then your aldosterone
levels will be low and you will see hyperkalemia in addition to all of the
other things that you would see in adrenal failure for instance
hypoglycemia hyponatremia and metabolic acidosis the last thing that you would
see is of course in a potassium sparing diuretic so some examples of this would be
spironolactone or a miller ID incidentally other medications that
could also increase your potassium are things that can also affect shifting of
the cells or affect the other areas that we’ve already talked about the ones that
you should know about our ACE inhibitors so remember ace inhibitors inhibit a
switch is angiotensin converting enzyme which is in the lungs and that’s going
to affect the ability to make aldosterone the other thing that can do
this is beta blockers we’ll talk about treatment with beta agonists later but
beta blockers can affect shifting of potassium and actually caused it to go
out of the cell another cause is something that’s interesting and it’s
called pseudo hyperkalemia and it’s really based on the fact that all cells
in the body have high concentrations of potassium in it so where you see this is
if you have a patient with many cells that are drawn in a test tube so if you
have marked leukocytosis or thrombocytosis so they’ll be in
platelets as well and you get coagulation in the test tube that causes
these cells to lyse and release their potassium when you put this through the
laboratory equipment you’re going to see elevated potassium and they’ll sometimes
tell you if they see this and they’ll say hemolysis and if you get
hyperkalemia and they say by the way hemolysis was three plus then you may
have to take that with a grain of salt so to speak and maybe repeat the test
again to see and redraw the blood actually because if once there’s human
lysis you really need to get a new blood draw on that specimen okay let’s talk
about manifestations of hyperkalemia what would happen really has a lot to do
with the heart and the reason is is because the conductance of potassium in
the depolarization of cardiac conduction
cells is quite high such that potassium is always leaving the cells and so what
happens is you have a positive charge leaving the cell okay what’s that going
to do that’s going to generally make the inside of your cell negative and that’s
exactly what we see here down to close to negative 90 millivolts you’ve got
this negative the problem here is is that when you have an abundance of
potassium in the solution in the serum in other words when you have
hyperkalemia these potassium ions are not going to leave the cell as quickly
and so whereas you would have a very negatively charged cell it’s not going
to be so negatively charged you’re going to get something called depolarization so these cells are more excitable and as
a result of that not only is it depolarized but instead of having a nice
sharp up tick it’s going to come up more slowly and the repolarization is going
to be somewhat dampened okay as a result of that when you look at a nice QRS
complex instead of having a discrete P wave q r s t what you’re actually going
to see is the P wave is almost going to be non-existent the R wave is going to
sort of come up slightly you’re going to have this s depression and then this T
wave and it’s almost going to look sinusoidal and of course the higher the
potassium and the faster the potassium has gotten high the more quickly you’re
going to see this if somebody is camping out at five to six and they go up to
seven you’re not going to see those changes because the body has a chance to
adjust perhaps but if someone is living in the three s two fours and then jumps
up to seven you’re more likely to see that the first thing that you’ll see
with hyperkalemia is you’ll actually see peaked t-waves
okay that’s the first thing that you’ll see and then eventually you’ll just see
this thing go sinusoidal so it’ll just kind of go like this and you’ll just go
into cardiac arrest so what you should you know about manifestations you will
have depolarization due to low potassium conductance lower than normal and then
after that you’ll get hyper polarization due to inactivated sodium channels
you’ll have this reduced phase zero velocity okay and you’ll have decreased
membrane excitability and then you’ll get increased potassium conductance and
accelerated repolarization okay so what should you know what would they actually
test you on a test about hyperkalemia I think the thing that they would test you
on is number one no that peaked t-waves is the first sign that you’ll see number
two if it eventually gets high enough you’ll get this sinusoidal wave and
number three hyperkalemia in general is going to affect the heart and all of
this is an emergency now in the next video we’re going to
talk about the treatment of hyperkalemia and some of the reasons why this
treatment works you

55 thoughts on “Hyperkalemia Explained Clearly – Fluid and Electrolyte Imbalances

  1. I am a student and your videos help me. All your videos are so clear and interesting !! Thank you so much !!

  2. 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.

  3. 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?

  4. Great lecture but I have a pressing question, can you please tell me the name of the song that is at the end. 🙂

  5. See the whole series at www.medcram.com along with other top quality videos including reviews in pulmonary, cardiology, infectious disease, and hematology!

  6. 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?

  7. 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??

  8. 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.

  9. Amazing videos!! Can you touch on some of the other electrolytes. Na+, calcium, magnesium etc. That would be very helpful.

  10. 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

  11. 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.

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