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Unknown (00:01):
Hey friends and welcome
to nursing with Dr. Hobbick.
Today I am thinking aboutelectrolytes. Still thinking a
little bit about that fluidbalance. These two concepts are
pretty interwoven. And in alater episode I'll get into acid
base. Today I want to talk aboutelectrolytes and how they can be
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imbalanced. The first thing Iwant you to think about is
intake, absorption,distribution, and output.
Electrolytes can be imbalancedthrough intake if they're not
taking in enough or they'retaking in too much. Absorption
can affect your electrolytebalance by not absorbing
electrolytes appropriately, wecould end up with low levels
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distribution. This is big whenwe're talking about things like
potassium, calcium andmagnesium, especially potassium.
Because the levels of theseelectrolytes inside the cells in
the intracellular compartmentare much higher than they are in
the extracellular compartment.
Remember that when we're testingthe levels of these
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electrolytes, we're testing thelevels in the bloodstream in the
serum in the extracellularspace, the difference between
the levels is pretty dramatic.
Sodium is the most abundant canion in the extracellular
compartment. Potassium is themost abundant cat ion in the
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intracellular compartment. Andyou'll see the huge difference
when you look at the levels thatwe would see a normal level. Now
I want you to understand thatyou will see some variants in
reference ranges, don't let thatworry you too much. Just
memorize some set that you'reusing in your current program.
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And you'll get through justfine. So if I use reference
ranges that are different thanwhat you're used to, they
shouldn't be way off. If theyare Gosh, send me a message on
one of my platforms. You canfind me on Facebook, Instagram,
YouTube, Tik Tok, where else I'meverywhere, let's say potassium,
the normal range for potassiumis 3.5 to five. Now that's the
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serum level, the normal rangefor sodium is 135 to 145, you
may see 136 to 145, it doesn'tmatter that much. Obviously,
there's a huge differencebetween the number or the amount
rather of sodium then potassium,consider this if my patient has
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blunt force, trauma, or burns,or something that is going to
cause a lot of cells to burst,those cells will release all of
their intracellular contents,including their high
concentrations of these otherelectrolytes, that's going to
really mess up my balance ofelectrolytes in the bloodstream
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in the extra cellular space.
That would be a imbalance ofdistribution, we can have an
output. If there is too muchoutput or not enough output of
electrolytes that can also causeimbalance output, we normally
lose electrolytes through urine,feces a little bit through sweat
abnormally we could lose itthrough vomiting, wound
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drainage. Now we're talkingabout a lot of drainage not like
that little paper cut, we alsoneed to talk about other GI
losses gastric suction, if youput an end G tube into your
patient and it's to suction, youmight want to think about their
electrolyte balance. Just likeif they were vomiting, it's the
same thing. And if your patienthas diarrhea, they could be
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losing electrolytes. Thefunctions of the large intestine
are really to absorb water andelectrolytes. If we have
diarrhea, that stuff's movingthrough there so fast, he can't
do its job, we're going to losefluid. And electrolytes that
way, remember that fluid iswater with things dissolved in
it. In that case, we're losingboth electrolytes and water,
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let's just get an idea of plasmaversus intracellular
concentration. So I told youthat the plasma volumes for
potassium is 3.5 to five forsodium it's 135 or 136 to 145.
inside the cell, we have about14 mil equivalents per liter of
sodium only 14 When outside thecell we have 135 to 145. inside
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the cell, we have 140 Milletequivalents per liter of
potassium were outside the cellwe have 3.5 to five, you can see
that the concentrations of theseare very different on either
side. The reason for that has todo with how the body creates
energy, how the body createsnerve and muscle contraction.
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That's really what ourelectrolytes do for us besides
also contributing to osmolaritylike we talked about last week.
So we'll talk brieflyabout these different
electrolytes, sodium in sometextbooks is really described as
an osmolarity imbalance. Inother words, it's a
concentration issue in thebloodstream, the patient could
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have too much sodium or toolittle water, or they could have
a water excess or too littlesodium. If you need to go back
and refresh on some of theanatomy of the rest system ADH
hormone metric peptide, Irecommend the Khan Academy
videos they are fantastic onreview for pathophysiology.
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These are important concepts foryou to understand if you're
going to understand sodium andfluid balance despite potential
variations in diet, our kidneysreally manage our sodium pretty
well. Low serum sodium levelsare going to inhibit the
secretion of ADH and NP andtrigger the RAS system. This
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will increase sodium levels byincreasing the reabsorption of
sodium and enhancing the loss ofwater. If your patient has high
serum sodium that's going toinhibit aldosterone secretion
and stimulate secretion of ADHand NP. So these hormones and
the kidneys all together aregoing to maintain that water and
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sodium balance. I know that youall had an instructor who told
you if you take a cell and dropit into a hypotonic solution,
the cells gonna swell. Myinstructor said Hi, Bo, oh, you
can imagine me spreading my armsout as I exaggerate the cell
swelling. If a sodium imbalanceis a osmolality imbalance, that
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means that it's a concentrationimbalance. If my patient is
hyponatremia check, their bloodessentially becomes hypotonic.
What will happen to the cellslet's think about the brain,
that water is going to leave thebloodstream because there's too
much water and not enough saltin there. And it's going to go
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into the cells so the braincells could swell. Most of the
problems that we see related tohyponatremia are because of
reduced excitability of membranedepolarization and cellular
swelling. One of the most commoncauses of low sodium levels is
the overuse of diuretics. Wecould also experience a relative
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sodium deficit meaning too muchwater when actually because by
drinking too much water in avery short period of time,
Kidney Failure syndrome ofinappropriate antidiuretic
hormone secretion or si d hheart failure, a too much
hypotonic fluid administration.
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Anytime we add water, we couldbe diluting that blood one of
the most obvious things thatwe're going to see in a patient
with hyponatremia is thatcellular swelling which is going
to lead to altered mentalstatus, or changes in level of
consciousness. If you see yourpatient develop, sudden
worsening of confusion,especially if they're elderly or
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on diuretics, you could suspecta sodium problem, we'll see some
other changes, maybe generalmuscle weakness, because
neuromuscular changes will seean increase in intestinal
motility that will cause nausea,diarrhea, abdominal cramping and
hyperactive bowel sounds. Anycardiovascular changes that we
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see are typically related to thevolume rather than the
hyponatremia itself. If ourpatient has hyponatremia with
hypovolemia, we're gonna have arapid weak thready pulse, we
will have decreased bloodpressure and orthostatic
hypotension. Again, that isrelated to the hypovolemia more
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than hyponatremia. If ourpatient has hyponatremia that
occurs with hyperbole, Mia, wewill see full or bounding
pulses, maybe a normal or a highblood pressure, those symptoms
are going to be more related tothat volume than they are the
concentration of the sodiumitself. These are going to be
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treated by addressing both thesodium and the volume imbalance.
If the patient is hypovolemicand hyponatremia, you might
expect to give them andhypertonic IV solution like 3%
normal saline if the patient hashyponatremia that's accompanied
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by hyperkalemia. Thenmedications are going to be used
to get rid of water but notsodium. Next, let's talk about
hypernatremia. Too much sodium.
This can actually also occurwith a volume imbalance. But if
we have too much sodium we'regoing to have this condition
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called irritability.
The sodium is moving rapidlyacross cell membranes during
depolarization. And this makesexcitable tissues even more
easily excited. They overrespond to stimuli, water is
going to move into theextracellular compartment in
order to dilute that hyper azmolor hypertonic extracellular
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fluid. And so if we have highsodium levels, we can see
cellular dehydration. Rememberthat your anatomy and physiology
teacher told you if you drop thecell into a hypertonic solution,
it's going to shrink up. Alwaysthink about the Wicked Witch of
the West, right? She was eithera cell being dumped into a
hypertonic solution or she was aslug. I'm not sure which kidney
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failure is one of the mostcommon reasons you're going to
see high sodium levels. Ofcourse, if we administer too
much sodium containing IV fluid,we could see too much sodium in
the bloodstream. A patient whotakes in too much sodium,
corticosteroids and Cushingsyndrome, which are going to
cause similar problems. We'lladdress those in some other
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episodes and hyperaldosteronism.
If we have hypernatremia, as aresult of not having enough
water that causing us to havetoo concentrated a blood or too
much sodium. This might bebecause your patient is not
taking in anything by mouth.
Maybe they have a fever, a feveris going to increase those
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insensible losses of just waterhyperventilating, again, an
increase of water loss that'sinsensible, excessive diuresis
if they have watery diarrhea,and this is often something that
we'll see in dehydration,thinking about those brain cells
in this now hypertonic solution,they're going to shrivel up,
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they're going to becomedehydrated, we're going to have
altered cerebral function, thispatient will have mental status
changes, changes in cognitivefunction. This patient may have
a very short attention span beagitated or confused. If the
patient has overload also, theycould be lethargic or superest,
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or comatose. The most frequenttreatments are going to be 0.9%,
isotonic, or often called normalsaline. You might also see
dextrose 5% in 0.4, or 5% Sodiumchloride. This is often called
half normal saline. If thepatient's problem is excretion
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of sodium they may usemedications like furosemide, a
loop diuretic to facilitateexcretion of sodium through the
kidneys. Let's now talk aboutanother major player. Let's talk
about potassium. low potassium.
Minor changes can cause majorchanges in cell excitability and
can be life threatening becauseevery body system is affected by
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potassium. Some common reasonsthat we lose too much potassium
would be inappropriate orexcessive use of diuretics or
corticosteroids increasedsecretion of aldosterone,
Cushing syndrome, especiallydiarrhea, vomiting, wound
drainage, particularly gidrainage, prolonged nasal
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gastric suction, I mentionedthat earlier, it's the same as
that vomiting. If the patienthas kidney disease that impairs
the reabsorption of potassium,or being nothing by mouth,
meaning not taking in anythingin the mouth, we can also end up
with relative potassium deficitswith alkalosis hypokalemia can
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be associated with alkalosis. Ifthe patient has too much
insulin, insulin likes to takepotassium out of the bloodstream
and into the cell with glucose.
So if the patient has too muchinsulin, then it can cause that
potassium to go out of thebloodstream. It's the same way
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if you give the patient too muchinsulin IV, you can cause that
same thing to happen. If thepatient's on TPN, or total
parenteral nutrition, that'swhere they're getting all their
nutrition through an IV that cancause this. And if we give
patients IV therapy that has notvery much potassium in it, we're
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constantly losing potassium outof our kidneys. Normally, if we
don't replace it, then we canend up in this potassium
deficit. When we talk aboutpotassium, most of us are going
to think about the heart but wealso need to think about the
lungs, we can end up with thisrespiratory muscle weakness,
resulting in shallowrespirations that can actually
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result in respiratoryinsufficiency. So two big things
you want to monitor with yourpatients who are hypokalemic are
their respiratory rate andrhythm and depth and their
cardiovascular function withoutthat potassium
The GI tract slows down. Thiscan lead to hypoactive bowel
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sounds, nausea, vomitingconstipation, which can lead to
abdominal distension. We want tomonitor for that with our
patient auscultate their bowelsounds, and you can see ECG
changes like ST segmentdepression, flat or inverted T
waves. There's a hint inhyperkalemia, we'll see tall
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peaked T waves in hypokalemia,we'll see flat or inverted T
waves. And we might see someincrease in new waves. A star
point, older patients who aretaking digoxin are particularly
at risk for dysrhythmias. Toreplace potassium, we can give
it by mouth, we can give it IV,a couple more star points for
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you. Number one, potassiumshould never be mixed on the
floor, it should only be done bya pharmacist or registered
pharmacist, you should not havea dilution greater than one mil
equivalent of potassium per 10milliliters of solution. And it
should never be given IV push.
When we're giving potassium IVyou should use a pump. And you
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should never exceed therecommended rate of infusion is
somewhere around five to 10 milequivalents per hour, but should
never exceed 20 mil equivalentsper hour. Last star point for
this one, if your patient is notmaking urine. And I'm not
talking about urinary retention,I'm talking about a patient
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whose kidneys are not makingurine, you should reconsider
administering potassium, thatpatient may not have any way to
get extra potassium out of theirbody. And so we could cause them
to become hyperkalemic. highpotassium levels or hyperkalemia
are really going to affect yourheart. When we think about
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sodium we kind of think aboutthe brain and the swelling or
shrinking of brain cells. Whenwe think about potassium, we
often think about the heart,it's really sensitive to
increases in potassium. And thathyperkalemia is going to
interfere with conduction, whichcould lead to heart block or V
fib, which has been tricularfibrillation. Some common
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reasons that people end up withtoo much potassium would be over
ingestion. salt substitutes, ifyou look at the bottle may be
potassium. And that could be oneway that you end up with too
much potassium transfusion ofwhole blood or packed red blood
cells. This can be an issue ifthose cells burst or if they
have burst inside the bag, thenthey're going to release that
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potassium in the intracellularcompartment which is going to
raise Tassie and level kidneyfailure is going to be a big one
kidneys put out potassium. Ifthey're not working, they can't
put it out. And a patient who'staking potassium sparing
diuretics, the one that comes tomind is Spironolactone. These
encourage the kidneys to hold onto potassium, which can lead to
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high levels of potassium,especially if your patient
doesn't know that they shouldn'tbe eating salt substitutes with
that particular medication. Toomuch potassium can also be
caused by tissue damage, like Italked about earlier. Anything
that causes cells to break openand spill their contents
acidosis and hyperkalemia gotogether and uncontrolled
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diabetes. The reason is thepatient with uncontrolled
diabetes does not have thatinsulin to move the sugar and
the potassium into themselvesfrom the bloodstream. This is
going to be relatively rare inpeople who have normal kidney
function. The people who mayexperience high potassium levels
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are those who are going to betaking a potassium sparing
diuretic, or people who havecertain chronic illnesses. We
could see those tall peaked Twaves as far as cardiovascular
changes, we might see somechanges in our P or QRS complex,
this patient could end up withbradycardia or hypotension. We
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want to be monitoring that ECGto correct high potassium
levels, they're either going totry to use a medication that's
going to increase secretion, orthey're going to try to move
potassium from the extracellularto the intracellular space.
medications that excretepotassium would be those loop
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diuretics we talked aboutearlier. Or they might prescribe
a solution, an IV solution thatincludes glucose and insulin,
right? I mentioned that thatinsulin will take the glucose
and the potassium into thecells. But we want to make sure
that we don't take all of thesugar out of the bloodstream. So
we're going to give them alittle bit extra facilitate that
movement. We're going to talkabout calcium, low calcium can
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be caused by a couple of thingsyou'll want to think about the
thyroid particularlyThe parathyroid hypocalcemia and
hyperparathyroidism will gotogether. If the patient doesn't
take in enough calcium, or saythat they're lactose intolerant,
they may not take in enoughcalcium. We could have patients
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without absorption problems.
This would be someone withceliac disease or Crohn's
disease, if they don't take inenough vitamin D either through
diet or through sudden end stagekidney disease, diarrhea
sanatoria, which is fattystools, and wound drainage. But
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we can also have alkalosis, wecould have medications that bind
to calcium. If the calcium isbound to albumin, it's not free
to help with muscle and nerveconduction in the body. If we
have acute pancreatitis, orimmobility, we can end up with
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this symptoms for hypocalcemia.
A lot of these are going to beneuro muscular, so we might see
paraesthesia as a paraesthesiais a numbness or tingling
sensation. It usually starts inthe hands and feet and can
progress to the lips, nose andears. If it gets that far, we
could start to see neuromuscularoverstimulation, that can lead
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to tetany. Two tests that youcan do to look for this as
nurses. One is true SOS and oneis Fostex, you'll need to look
these up, it's going to bepretty visual, true SOS is where
I'm going to apply a bloodpressure cuff around the arm and
inflate it higher than thepatient's systolic pressure,
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this is going to cause a littlebit of a hypoxic condition. And
what we're going to see is thehand and fingers go into a spasm
in Palmer flexion. So they'regoing to the fingers are going
to come together, and a lot oftimes the hand will supinate a
little bit. Szostak sign iswhere you tap the face just
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below and in front of the earand this is going to trigger
facial twitching. A patient whohas chronic hypocalcemia can see
it in their bones, they're notgoing to have the bone density
that we would expect they mighthave unexplained bone pain,
something we'll focus on forthem is going to be injury
prevention. If they have thin,brittle bones, and we're going
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to replace calcium. It could bereplaced orally, or it could be
replaced IV depending on whatthe provider wants to do. High
levels of calcium orhypercalcemia can affect
excitable tissues. Those thatwe're going to see here are the
heart that skeletal musclenerves, intestinal smooth
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muscles, we're going to seedepending on the severity and
how fast the imbalance occurs,an increase in heart rate and
blood pressure, confusion,lethargy, maybe some decrease in
peristalsis, which will lead toconstipation, anorexia, nausea,
vomiting and abdominaldistension. Bowel sounds will be
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hypo active. Too much calciumcan be caused by too much intake
of calcium, too much intake ofvitamin D. We want to talk to
our patients about some over thecounter products that include
calcium like Tums, which arecalcium carbonate, kidney
failure. Again, if we can'texcrete these electrolytes they
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can end up too high and ourthiazide diuretics,
hyperparathyroidism andhypercalcemia go together.
malignancy, especially thebones, hyperthyroidism,
immobility can cause highcalcium levels use of
glucocorticoids and dehydration.
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The next major electrolyte todiscuss is magnesium. low
magnesium levels are typicallycaused by too much excretion of
magnesium often because of athiazide diuretic, or not enough
intake. Simple nursing does myvery favorite video on this
week, he does Magnum magnesium,the sheriff in town, I love the
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way that he does that, andallows you to remember that when
magnesium is around when there'smore magnesium, we're going to
have a decrease in a lot ofthings. And if we have low
magnesium, you know, the sharesout of town we're going to have
high wild and crazy stuffhappening. We can have
hypertension, we can have atrialor ventricular fibrillation,
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premature contractions of eitheratria or ventricles, increased
nerve impulse transmissionbecause normally magnesium
inhibits that. At the synapse,we'll see hyperactive deep
tendon reflexes, our patient canend up with too much magnesium
through intakemaybe an IV replacement of
magnesium or magnesiumcontaining antacids or
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laxatives, like milk ofmagnesia. Or once again, kidney
failure or decreased kidneyexcretion of magnesium. Now
we're going to have depressednerve impulse transmission, the
patient might be drowsy orlethargic, they could end up in
a coma, where patients going tohave absent deep tendon
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reflexes. And we need to thinkabout cardiac changes like
bradycardia, peripheralvasodilation, which is going to
lead to hypotension and we'regoing to want to monitor their
respiratory status because ifthe magnesium is decreasing
nerve impulses to the lungs,though it doesn't directly
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affect the lungs, it can causethe patient to have respiratory
insufficiency. Thank you forhanging out with me for an extra
long episode. I hope that thishelps you. I'm going to leave
you with just a couple of thingsto keep in mind. Sodium affects
the brain. Potassium affects theheart. Calcium affects the
musculoskeletal system, andmagnesium affects the nerves
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slash deep tendon reflexes.
That's all I've got for you fortoday. Reach out if you have
some topics you'd like to hearabout or to let me know that you
enjoy this podcast. Please leavea review. Hopefully it'll be a
good one. And I'll see you nexttime on nursing with Dr.
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Hobbick.