Hypernatremia & Hyponatremia
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[MUSIC PLAYING]
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Welcome to MedSimu Nursing Podcast.
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Today, we're doing a deep dive into two really critical
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electrolyte imbalances.
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Isn't it?
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Fluid balance, nerves, muscles, getting these imbalancing
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right is key for patient care, not just the exam.
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Exactly.
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So we'll unpack what they are, what causes them,
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how your patients might present,
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and crucially, what we do as nurses.
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- Sounds good.
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Where should we start?
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Hyponutremia.
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- Yeah, let's start there.
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So hyponutremia, that's when the serum sodium
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drops below 135 millikeal, right?
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- That's the number.
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And you know, you can't really talk about sodium
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without talking about water.
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They're intrinsically linked.
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- Definitely.
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How does that fluid volume part
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play into causing hyponutremia?
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- Well, think about it.
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Sodium's the main salute outside our cells.
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So if you mess with the water balance,
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you mess with the sodium concentration,
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like if you lose fluids but replace them only
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with plain water or hypotonic fluids,
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you dilute the sodium that's left.
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- Okay, so dilution is one way.
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- Right, or conversely, you could be
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in a state of fluid overload.
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Just too much water overall,
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which again dilutes the sodium.
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And we also have to remember ADH antidiuretic hormone.
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- The hormone from the pituitary.
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- Exactly.
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It tells the kidneys how much water to hang onto.
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So if ADH is out of whack, like in SIADH,
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you hold on to too much water and boom, diluted sodium,
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it really highlights how fluid status is critical context.
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- That makes a lot of sense.
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So let's break down the main culprits.
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What causes that sodium to drop?
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- Okay, we can kind of group them.
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First, there's increased sodium excretion,
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losing too much sodium.
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- Like how?
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- Well, think excessive sweating diaphoresis.
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Also, certain diuretics make the kidneys dump sodium,
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vomiting, diarrhea, wound drainage,
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especially GI drainage, those are big ones,
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and kidney disease itself,
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where conditions where you have
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decreased aldosterone secretion.
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Remember, aldosterone helps retain sodium.
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- Right, so if aldosterone's low, you lose sodium.
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Got it, what's the second category?
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- Second is simply inadequate sodium intake.
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This isn't usually the sole cause, but it contributes,
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especially in patients who are NPO nothing by mouth
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for a while, or on really strict low-salt diets.
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- Okay, and the third, you mentioned dilution earlier?
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Yes, the third is dilution of serum sodium.
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This is a big category.
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Excessive intake of hypertonic fluids
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like drinking tons of water or getting hypertonic IVs.
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Even hypotonic irrigation fluids can be absorbed.
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- Wow, okay.
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- Then there's renal failure, fresh water drowning
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where the body absorbs hypertonic water.
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SIADH, which we mentioned syndrome of inappropriate ADH,
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even hyperglycemia, high blood sugar
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and congestive heart failure can lead to relative dilution.
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- That's quite a list of potential causes.
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So when you're assessing your patient,
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what signs and symptoms should make you think,
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"Hmm, maybe this is hyponetremia."
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- It really depends on their fluid status, which is key.
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Let's start with cardiovascular.
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If they're normal volumic, normal fluid volume,
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you might see a rapid pulse, but blood pressure might be okay.
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- And if they're low on fluid, hypovolemic.
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- Then you'd expect more like a thready, weak, rapid pulse,
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definitely hypotension, and maybe flat neck veins,
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signs of dehydration, basically.
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- Okay, and if they're overloaded, hypervolemic.
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- Then you might see a rapid bounding pulse
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and blood pressure could be normal or even high,
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plus potentially signs of fluid overload elsewhere.
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- Right, what about other systems, respiratory?
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- Respirations might become shallow and ineffective,
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but that's usually a later sign due to muscle weakness.
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If they are hypervolemic though,
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you might hear crackles, pulmonary edema.
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- Okay, and neuromuscular.
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- Generalized muscle weakness is pretty common,
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especially in the arms and legs.
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You might find diminished deep tendon reflexes.
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Early on, you might notice muscle twitching,
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but later that progresses to just weakness.
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- And the brain, CNS effects.
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- Oh, definitely.
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Headache is common, you might see personality changes,
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confusion, it can progress to seizures,
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and even coma in severe cases.
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It's a major concern.
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- Sounds like it.
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What about GI?
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- You might see increased GI motility,
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hyperactive bowel sounds, maybe nausea,
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cramping, diarrhea.
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- And renal.
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What are we looking for in terms of urine?
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Output can vary, could be up or down,
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depending on the cause,
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but a key lab finding is often
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decreased urine specific gravity.
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The urine is dilute because the body's trying
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to get rid of excess water
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or can't concentrate urine properly.
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- And skin.
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- Often dry mucous membranes.
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- So a wide range of signs.
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Once I suspect or confirm hypernatremio,
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what are the nursing priorities?
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What do we do?
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- First and foremost, ongoing monitoring is crucial.
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Keep a close eye on all those systems.
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cardiovascular, respiratory, neuromuscular,
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cerebral, renal, GI, constant reassessment.
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- Makes sense.
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What about specific treatments?
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- Well, if it's hyponatremia with a fluid deficit,
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hypervolemia, then we'll likely be giving IV sodium chloride
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infusions to replace both sodium and volume.
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- Okay, and if it's fluid excess?
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- If it's hypervolemic hyponatremia,
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then maybe osmotic diuretics will be ordered
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to help pull off that excess water,
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while being careful not to worsen
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the sodium level too quickly.
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- What about for SIADH?
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For SIADH, specific medications that block ADH action
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might be used alongside fluid restriction usually.
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And patient education.
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Big role there.
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If appropriate for the cause, educating the patient
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on increasing oral sodium intake.
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It helps to give examples of high sodium foods.
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Like what?
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Things like bacon, butter, canned foods, cheese, hot dogs,
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ketchup, lunch meats, milk, mustard, lots of processed
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foods, snack foods, soy sauce, table salt, even many breads.
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just making them aware.
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- That's a good practical list.
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Any other really critical points for intervention?
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- Yes, a really important one, lithium.
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If your patient is on lithium, hyponatremia
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is a major risk factor for lithium toxicity
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because the kidneys might retain more lithium
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when sodium is low.
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- Ah, so they're reabsorbing lithium along with sodium?
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- Kind of, yes.
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So you need very close monitoring of lithium levels
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in that situation, it's critical.
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- Final point, okay, that covers hyponatremia well.
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Let's switch gears now and talk about the opposite.
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Hypernatremia, what's the definition there?
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- Hypernatremia is when the serum sodium level
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goes above 145 milliQL.
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- Okay, and what pushes the sodium level that high?
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What are the common causes?
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- Again, we can group them.
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First, decreased sodium excretion.
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The body is holding onto too much sodium.
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- What causes that?
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- This can happen with corticosteroid use,
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conditions like Cushing syndrome,
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where you have excess corticosteroids naturally,
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renal failure sometimes,
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and hyperadosteronism, too much aldosterone,
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telling the kidneys to keep sodium.
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- Okay, so holding on to too much sodium, what else?
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- Second, increased sodium intake.
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Pretty straightforward, either eating way too much salt
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or getting excessive amounts of sodium containing IV fluids.
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Third is decreased water intake.
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This is a big risk for patients who are NPO
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or maybe unconscious or unable to access water
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for some reason, they become dehydrated
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and the sodium gets concentrated.
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- That makes sense.
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- And fourth is increased water loss,
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losing more water than sodium.
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This happens with things like a high metabolic rate,
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fever, hyperventilation, infections,
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excessive sweating again, really watery diarrhea,
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and a condition called diabetes insipidus.
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- Diabetes insipidus, that's related to ADH too, right?
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But the opposite of SIAD.
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- Exactly, with diabetes insipidus,
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you have a deficiency of ADH
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or the kidneys don't respond to it,
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so you lose massive amounts of dilute urine,
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just pure water loss, essentially,
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leaving sodium behind and concentrated.
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- So again, it's about that balance
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between sodium and water.
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- Got it.
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Now, assessment for hypernatremia.
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What are we looking for?
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Cardiovascular signs.
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- Like with hyponatremia, the heart rate in BP
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often reflect the fluid volume status.
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You might see a rapid pulse
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if they're normovolemic or hypovolemic.
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If they happen to be hypervolemic with high sodium,
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maybe a rapid bounding pulse.
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- Any specific respiratory signs?
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not usually directly linked to the high sodium itself.
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- Okay, neuromuscular?
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- Early on you might see muscle twitching,
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maybe irregular contractions,
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but as it worsens it typically progresses
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to skeletal muscle weakness
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and diminished or even absent deep tendon reflexes.
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- And the CNS, you said that was key in hyponatremia too?
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- Absolutely critical in hyponatremia as well.
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Altered cerebral function is really the hallmark.
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What you see might depend a bit on fluid status again.
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- How so?
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In patients who are normovolemic or hypovolemic,
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you might see more agitation, confusion, maybe seizures.
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If they're hypervolemic, it might present more as lethargy,
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stupor, or even coma.
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But across the board, a major symptom is extreme thirst.
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Ah, that makes sense.
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The body is screaming for water.
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Precisely.
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So GI-wise, that extreme thirst is the main thing.
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Renal signs.
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Urine.
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Again, output can vary depending on the cause.
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Like in DI, output is huge.
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But often, if the cause is dehydration,
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the kidneys try to compensate.
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So you'll see increased urine specific gravity,
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very concentrated urine as the body
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desperately tries to hold onto water.
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- And skin and mucous membranes.
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- You'd expect to see dry, maybe flushed skin.
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Dry, sticky tongue and mucous membranes are classic signs.
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Edema might be present or absent
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depending on the overall fluid situation.
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- Okay, so we recognize the signs.
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What are the nursing interventions for hypernatremia?
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- Again, vigilant monitoring is paramount.
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Cardiovascular, respiratory, neuromuscular,
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cerebral, renal, integumentary, track everything closely.
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- And specific treatments.
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- If the cause is primarily fluid loss,
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then fluid replacement is key.
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Usually with IV fluids, often hypotonic
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or isotonic solutions, given carefully
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to avoid lowering the sodium too quickly.
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- Right, correcting too fast can be dangerous
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for the brain too, can't it?
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- Absolutely, slow controlled correction is essential.
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Now, if the problem is impaired sodium excretion
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by the kidneys, then diuretics that promote sodium loss
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might be ordered like loop diuretics.
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- Okay, what about intake restrictions?
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- Yes, restricting sodium intake is usually necessary.
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We'd educate the patient again
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about those high sodium foods to avoid.
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And sometimes, depending on the situation and fluid status,
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fluid intake might also be restricted,
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though often fluid replacement is needed.
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- Anything else critical to monitor?
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- Definitely monitor potassium levels.
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Correcting sodium and fluid imbalances
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can cause shifts in potassium,
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and potassium imbalances, as you know,
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can lead to dangerous cardiac arrhythmias.
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So keep a close eye on the potassium too.
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- So it sounds like similar to hyponutremia,
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it's about careful monitoring,
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identifying the root cause, too much sodium in,
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not enough sodium out, or too little water,
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and tailoring the intervention,
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whether it's fluids, diuretics, or restrictions.
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- You've got it.
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It's all about restoring that balance safely
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and effectively based on the underlying problem.
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- All right, great.
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Let's do a quick one minute wrap up for everyone tuning in,
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especially those studying for the NCLEX.
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we've just tackled two major electrolyte imbalances.
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Hyponatremia, which is sodium below 135,
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and hyponatremia, sodium above 145.
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We emphasize how closely tied sodium is to fluid balance
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and how imbalances can stem from issues
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with sodium excretion, sodium intake,
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or very commonly, water balance.
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Either too much water diluting the sodium
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or too little water concentrating it.
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We walk through the key causes for each,
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like diuretics, GI losses, SIADH for hyponatremia,
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and things like dehydration, diabetes, and sepetis,
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or excess sodium intake for hyponatremia.
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- Don't forget the assessment findings.
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- Absolutely.
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We cover the assessment findings
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remembering that neuro changes are significant in both,
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but also looking at cardiovascular signs,
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which depend heavily on fluid status,
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plus neuromuscular GI, renal, and skin changes.
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Thirst is a big one for hyponatremia.
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- Mary, too.
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And finally, nursing interventions.
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Always start with close monitoring of all systems.
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For hyponutremia, interventions might involve
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sodium replacement if needed, fluid restriction
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or diuretics if overloaded, and specific meds for SIADH.
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For hyponutremia, it's often about careful fluid replacement,
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diuretics to help excrete sodium if needed,
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and sodium restriction.
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And in both cases, watching electrolytes like potassium
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is vital.
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And that patient education piece is always important too.
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Definitely.
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So mastering these concepts, causes, assessment, interventions, is fundamental not just for
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the exam, but for safe patient care every day.
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Couldn't agree more.
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Keep reviewing these, understand the why behind the signs and treatments.
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While that wraps up our deep dive on sodium imbalances for today, we hope this has helped
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clarify these crucial topics for you.
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Keep up the great work with your studies.
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And be sure to join us next time on MedSimu Nursing Podcast as we continue unpacking essential
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knowledge for your nursing journey.
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(upbeat music)
