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with hyperkalemia hyper means over and
cal refers to potassium an email refers
to the blood so hyperkalemia means
higher than normal potassium levels in
the blood generally over five point five
militants per liter now total body
potassium can essentially be split into
two components intracellular and
extracellular potassium or potassium
inside and outside cells respectively
the extracellular component includes
both the intravascular space which is in
space within the blood and lymphatic
vessels and the interstitial space the
space between cells where you typically
find fibrous proteins and long chains of
carbohydrates which are called
glycosaminoglycans now the vast majority
around 98 percent of all the body's
potassium is intracellular or inside of
the cells in fact the concentration of
potassium inside the cells is about a
hundred and fifty mil equivalents per
liter whereas outside the cell it's only
about four point five militants per
liter
keep in mind that these potassium ions
carry a charge so the difference in
concentration also leads to a difference
in charge which establishes an overall
electrochemical gradient across the cell
membrane and this is called the internal
potassium balance this balance is
maintained by the sodium potassium pump
which pumps two potassium ions in for
every three sodium ions out as well as
potassium leak channels and inward
rectifier channels that are scattered
throughout the membrane this
concentration gradient is extremely
important for setting the resting
membrane potential of excitable cell
membranes which is needed for normal
contraction of smooth cardiac and
skeletal muscles also though in addition
to this internal potassium balance
there's also an external potassium
balance which refers to the potassium
you get externally through the diet
every day on a daily basis the amount of
potassium that typically gets taken in
usually ranges between 50 milli
equivalents per liter to 150 mil
equivalents per liter which is way
higher than the extracellular potassium
concentration of 4.5 militants per liter
so your body has to figure out a way to
excrete most of what it takes in this
external balancing act is largely taken
care of by the kidneys where access
potassium is secreted into a renal
tubules and excreted in the urine also
though a small amount of dietary
potassium is also lost via the
gastrointestinal tract and the sweat so
in order for there to be too much
potassium in the blood or hyperkalemia
there are two possibilities the first is
an external balance shift which is most
often caused by a decrease in potassium
excretion in the kidneys which raises
the level of potassium in the blood
the second is an internal balance shift
where potassium moves out of cells and
into the interstitial and blood
one potential cause of an internal
potassium balance shift is insulin
deficiency this is because after a meal
glucose increases in my blood and at the
same time insulin is released which
binds the cells and stimulates the
uptake of that glucose insulin also
increases the activity of the sodium
potassium pump which pulls potassium
into cells people with type 1 diabetes
don't make enough insulin so when they
eat a meal especially a meal with a lot
of potassium that potassium sits in the
blood instead of being taken into cells
and this causes hyperkalemia another
cause of an internal potassium balance
shift could be an acidosis which is when
the blood becomes too acidic in other
words there's a higher concentration of
hydrogen ions which means a lower blood
pH one way the body can increase the
blood pH is by moving hydrogen ions out
of the blood and into cells to
accomplish this cells use a complex
series of multiple ion channels
exchangers and pumps to exchange
hydrogen ions for potassium ions across
the cell membrane so in order to help
compensate for an acidosis hydrogen ions
enter cells and potassium ions leave the
cells and enter the blood which might
help with the acidosis but results in
hyperkalemia now this isn't always the
case for acidosis though for example in
respiratory acidosis potassium levels
aren't affected because co2 s lipid
soluble and freely moves into cells
without being exchanged for potassium
therefore no hyperkalemia
similarly when there's a metabolic
acidosis from excess organic acids like
lactic acid and keto acids protons can
enter cells with the organic anion
rather than having to get exchanged for
potassium ions
certain catecholamines can also shift
potassium out of cells and this is via
beta-2 adrenergic and alpha adrenergic
receptors on cell membranes
when activated beta-2 adrenergic
receptors stimulate the sodium potassium
pump which pulls potassium from the
blood into cells meanwhile alpha
adrenergic receptors cause a shift of
potassium out of cells via calcium
dependent potassium channels so that
said beta-2 adrenergic antagonists also
known as beta blockers
and alpha adrenergic agonists both
causes shift in potassium out of the
cells and into the blood another
important mechanism is hyper osmolarity
which is where there's an increased
extracellular osmolarity relative to the
intracellular space this osmotic
gradient pulls water out of cells
and into the extracellular space less
water in the cells increases the
intracellular potassium concentration
which increases potassium concentration
gradient and pushes more of it out of
the cell and into the interstitium and
blood cell lysis is yet another cause of
hyperkalemia since so much potassium
skepta within the cell when a large
number of cells die or lyse potassium is
released into the blood which causes
hyperkalemia examples of large scale
cell lysis are severe burns
rhabdomyolysis or breakdown of skeletal
muscle and tumor lysis as a result of
chemotherapy a final example of internal
potassium balance leading to
hyperkalemia is exercise during exercise
while the body and the body cells are
working harder more cellular ATP which
is the molecular unit of currency gets
consumed the depletion of ATP triggers
potassium channels on the membrane of
muscle cells to open up which allows
potassium to move down its
electrochemical gradient and out of the
cell usually this shift is small but if
combined with beta blockers or kidney
issues strenuous exercise can lead to
hyperkalemia
all right on to external potassium
balance shifts resulting in hyperkalemia
which has to do with potassium intake
and excretion that said simply taking in
too much potassium can lead to
hyperkalemia but this would typically be
from rapid excessive infusion of
potassium into the bloodstream like in
patients receiving intravenous fluids
and this would be considered an
iatrogenic cause which means that it
results from a medical treatment or
procedure most other cases though have
to do with the kidneys and their ability
to regulate what stays in the blood and
gets excreted into the urine the kidney
does this by the processes of filtration
reabsorption and secretion in the
nephron first off potassium is freely
filtered from the blood into the urine
at the glomerulus after that about 67
percent is reabsorbed in the proximal
convoluted tubules and an additional 20%
is reabsorbed in the thick ascending
limb and that leaves about thirteen
percent of the initial amount right and
at this point the distal tubules and
collecting ducts of the nephron can
either reabsorb or secrete potassium
depending on what the body needs
now reabsorption in this area is taken
care of by the Alpha intercalated cells
while secretion is controlled by the
principal cells typically four people on
a normal diet more potassium is secreted
than reabsorbed at this stage and it
could even be that all of the remaining
potassium is secreted out if it's simply
not needed now an important hormone that
helps regulate potassium reabsorption or
secretion in the kidneys is aldosterone
aldosterone
increases the number of sodium channels
and the number of potassium channels on
the lumen side of the principal cell as
well as sodium potassium pumps on the
basolateral side of the principal cells
this allows sodium to move from the two
Buhl into the cell and then get pumped
into the blood by the sodium potassium
pumps as the pumps collectively move
more sodium into the blood under the
influence of aldosterone more potassium
gets pumped into the cell which raises
the intracellular potassium
concentration having more intracellular
potassium and also having more potassium
channels promotes potassium secretion
all that being said in situations where
somebody's unable to produce enough
aldosterone or hypo aldosterone ism also
known as adrenal insufficiency then
there's less potassium secretion by the
principal cells and therefore more
potassium tert aend which leads to
hyperkalemia
along the same lines drugs that reduce
the effect of aldosterone can also cause
hyperkalemia and these are drugs like
reading inhibitors ACE inhibitors
angiotensin ii receptor antagonists
selective aldosterone blockers and
potassium sparing diuretics
now acute kidney injury can cause a low
glomerular filtration rate which is the
volume of blood filtered through the
kidneys over a period of time and this
can lead to oliguria and hyperkalemia in
these situations the nephron tries to
hold on to salt in water so by the time
the filtrates moved into the distal
tubules
there's very little of both sodium and
water remaining in the lumen having
little water in the lumen creates a
relatively high potassium concentration
in the lumen in addition to this because
less sodium is in the distal tubules
less if it moves through the luminal
sodium channel into the principal cell
and gets pumped over to the other side
by the basolateral sodium potassium pump
and this means less potassium gets into
the principal cell and this leads to
more potassium in the blood in
hyperkalemia
all right so there are all these ways to
develop hyperkalemia but what happens
when somebody has hyperkalemia well
remember that the concentrations of
potassium inside and outside the cells
is really super important for
maintaining the resting cell membrane
potential and ultimately for allowing a
cell to depolarize in a muscle to
contract and that includes all muscles
skeletal smooth and cardiac so with too
much potassium outside the cell the
membrane potential can become more
positive to the point of even causing
contraction initially this might cause
mild intestinal cramping but eventually
the resting membrane potential gets so
high that it's above the threshold
potential meaning that once the muscle
depolarizes and contracts it can't
repolarize to allow another contraction
in skeletal muscles this can cause
weakness in flaccid paralysis that
starts in the lower extremities and
ascends upward hyperkalemia though also
affects cardiac muscle contractions
which can lead to cardiac arrhythmias
and cardiac arrest
hyperkalemia is diagnosed based on the
presence of elevated potassium levels in
the blood generally over 5.5 millions
per liter it's also important to get an
electrocardiogram which typically shows
tall peaked t-waves with a narrow base
best seen in the precordillera is v1
through v6 as well as a shortened QT
interval an ST segment depression in
severe cases it can also cause a
prolonged PR interval a diminished or
absent P wave and a widened QRS complex
with severe hyperkalemia treatment might
be done by using calcium to stabilize
the myocardial cell membrane using
insulin glucose beta adrenergic agonists
and sodium bicarbonate to shift
potassium into the intracellular space
using resins that bind potassium to
promote potassium elimination in the
gastrointestinal tract using potassium
wasting diuretics to promote potassium
elimination in the kidneys and in severe
cases dialysis all right as a quick
recap hyperkalemia describes a high
concentration of potassium in the blood
which can be the result of shifts in
internal potassium balance where
potassium moves out of the body cells as
well as external potassium balance
problems having to do with the intake of
potassium and typically the kidneys
ability to regulate its excretion
either way the high potassium leads to
issues with muscle contractions which
can be issues with the smooth skeletal
or cardiac muscles
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