What happens when we have
a lot of
or an excess potassium,
also known as hyperkalemia.
Hyperkalemia can reflect the removal of infusions,
cellular breakdown such as tumor lysis or Rhabdo,
which is actually very, very important
and in this specific incidence in hyperkalemia,
trans-cellular shifting is associated with acidemia.
There may be impaired renal excretion
also contributing to hyperkalemia.
What are some clinical consequences?
Classically, EKG changes.
Please commit this to memory.
EKG changes associated with hyperkalemia include
shortened QT intervals,
and potentially, can progress
to ventricular fibrillation.
There are priorities in the
management of hyperkalemia.
Because of the extensive and severe
consequences of hyperkalemia on the heart,
the first step is to stabilize the myocardium.
Then redistribute the potassium.
And if necessary,
excrete the excess.
Let's discuss the individual actions
of how we can manage hyperkalemia.
First, calcium gluconate.
Calcium gluconate contributes to
membrane stabilization of the myocardium,
induced by hyperkalemia.
Next, use of bicarb.
Recall that acidemia causes
trans-cellular shifting of intracellular potassium
into the extracellular space.
Bicarb increases the pH
and drives the trans-cellular shifting
in the reverse process.
This also releases hydrogen from the cell
in exchange for potassium.
Insulin is important.
It also –
because it potentially is a
sodium potassium ATPase,
allowing the maintenance of the
normal trans-cellular gradient
of mostly intracellular potassium
and extracellular sodium.
If all those mechanisms don't work,
we can institute dialysis
or use binders and exchangers.
An example of a binder
and exchanger is [indiscernible 2:19].
Let's move on to a discussion of hypokalemia
when the potassium is too low.
This can also be equally dangerous.
Hypokalemia may be a reflection of
changes to the true inadequate intake
or again trans-cellular shifting,
except in this situation
it’s due to alkalemia.
Lasix or loop diuretics often cause hypokalemia.
And overall weakness and
overall muscle dysfunction
can also cause hypokalemia.
What are the EKG changes?
I also recommend you
commit this to memory.
Prolonged QT intervals.
Depressed T waves,
which is different than hyperkalemia
where we see PT waves.
And ultimately, it can cause torsades
if coupled with hypomagnesium.
How do we fix hypokalemia?
Well, it’s simple.
Now, an important clinical pearl.
Sometimes, on the wards,
you continue repleting the potassium
and yet your plasma potassium levels
never actually come up.
Part of the reason this is happening
is because as you’re repleting the plasma potassium
it is actually shifting intracellularly.
This suggests to you that
there's been far more depletion of potassium
than you first recognized.
This is an incredibly high yield slide.
Let’s spend a little time here.
Electrolyte disturbances, again,
are not only important
for physiologic daily function,
but incredibly high yield test topics.
the manifestations is one that
do not correct too quickly
because if one corrects more than 12 meq/L
in 24-hour period,
it can lead to osmotic demyelination syndrome.
It was formerly known as CPM.
or symptom of inappropriate
antidiuretic hormone secretion
the treatment is demeclocycline
to make the collecting tubules less
responsive to antidiuretic hormone.
your deep tendon reflexes.
Remember those OB patients.
OB patients oftentimes get
infusions of magnesium.
Now, one of the signs that
they have too much magnesium
is decreased deep tendon reflexes.
Hypocalcemia causes prolonged QT intervals
and numbness around the mouth,
potentially Tetany if extreme.
Hypocalcemia is an important concept
discussed in the parathyroid lectures.
And lastly, hypercalcemia.
Hypercalcemia associated with hyperparathyroidism
is associated with bony pain,
and neurological disturbances.
This slide should be committed to memory
to help you answer standardized examination questions.
Thank you very much for joining me
on this discussion of fluids and electrolytes.