This episode breaks down the 10 imbalances that show up again and again on the NCLEX: the six major electrolytes and the four acid–base disorders every nurse must master. You’ll learn the one classic sign that tells you an emergency is happening and the one lifesaving action that stabilizes the patient fast. We use real clinical reasoning—volume status, cardiac risks, neuromuscular changes, and the stabilizing-shift-remove sequence—to show you exactly how to think like a nurse when a number on the labs turns into a crisis at the bedside. From seizures in low sodium to peaked T-waves in high potassium, from Kussmaul respirations to metabolic alkalosis after days of vomiting, you’ll get a clear, simple, unforgettable system to save a life and crush your NCLEX questions with confidence.
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#Comprehensive Notes
##I. Overview
Focus: 6 electrolytes + 4 acid–base disorders
Goal: Know one classic sign + one lifesaving intervention for each
NCLEX weight: High (8–16 questions across categories)
Foundational rule: Always assess volume status first — dry vs overloaded guides almost every intervention
Classic sign: seizures (especially when levels plunge)
Why: water shifts into brain → swelling → seizure risk
Lifesaving action: 3% hypertonic saline, rapid bolus for active seizure
Additional pearls:
Chronic hyponatremia (e.g., “tea and toast” elderly patient): correct slowly to prevent osmotic demyelination syndrome
Limit correction to 6–8 points in 24 hours once stable
Classic sign: intense thirst + confusion
Why: brain cells shrink from dehydration
Lifesaving action: give free water (D5W IV, oral, or tube)
Rule: correct slowly to prevent cerebral edema
Classic sign: U-waves on ECG
Lifesaving action: potassium replacement
Safety rules:
Never exceed 10–20 per hour through a peripheral line
Oral preferred
Replace magnesium first—low magnesium prevents potassium correction
The most urgent electrolyte emergency
Classic sign: tall peaked T-waves → wide QRS → sine-wave → cardiac arrest
Three-step lifesaver sequence:
Stabilize: calcium gluconate protects myocardium
Shift: insulin + dextrose (or high-dose albuterol) moves potassium into cells
Remove: kayexalate, loop diuretics, or dialysis
Classic signs:
Chvostek sign (facial twitch with cheek tap)
Trousseau sign (carpal spasm with BP cuff)
Lifesaving action: slow IV calcium gluconate
Risk of fast push: bradycardia, severe hypotension
Often renal failure or magnesium infusions
Classic signs:
Profound hypotension
Loss of deep tendon reflexes (areflexia)
Lifesaving action:
Stop magnesium
Give calcium gluconate to counteract cardiac depression
pH + bicarbonate same direction → metabolic
pH + CO₂ opposite directions → respiratory
Treat the patient before the number
Volume status affects everything.
Cause: CO₂ retention from hypoventilation (opioids, COPD flare)
Signs: sleepiness, poor arousal
Lifesaving action: improve ventilation — stimulate, bilevel support, or intubate
Cause: hyperventilation (pain, anxiety, early sepsis, PE)
Signs: tingling around mouth and fingers, lightheaded
Lifesaving action: treat cause — calm anxiety, treat PE, manage pain
Classic sign: Kussmaul respirations (deep, rapid breathing)
DKA clue: fruity acetone breath
Mnemonic for causes: MUDPILES
Methanol
Uremia
DKA
Propylene glycol
Iron
Lactic acidosis
Ethylene glycol
Salicylates
Lifesaving action: treat underlying cause
DKA → insulin
Lactic acidosis → fix shock
Give bicarbonate only when pH < 7.1 and patient is crashing.
Cause: loss of stomach acid (vomiting, NG suction)
Often causes: secondary low potassium
Lifesaving action: normal saline + potassium
Chloride allows kidneys to excrete excess bicarbonate
Potassium replaces losses
Consider acetazolamide in severe cases.
pH high + bicarbonate high → metabolic alkalosis
Interventions: normal saline + potassium; consider acetazolamide
pH extremely low + bicarbonate low → metabolic acidosis
First action: start regular insulin infusion
pH low + CO₂ high + bicarbonate high → partially compensated respiratory acidosis
Welcome back to Think Like a Nurse. This is the conversation where we help you, the learner, really master some of the most complex topics in clinical practice.
And today we are diving deep, I mean really deep into the labs that can make or break a patient's stability. We're talking fluid, electrolyte, and acid base imbalances.
Yeah, if you're prepping for your boards or you're working in critical care, this is just it's non-negotiable stuff.
It's so high yield. You can expect what, maybe eight to 16 questions on these topics in a big exam. So, our mission today is simple.
We want to give you a kind of clinical cheat sheet. The one classic sign and the one lifesaver action for the six electrolytes and four acidbased disorders you have to know.
Exactly. We want you to feel confident, not overwhelmed. And before we jump in, quick acknowledgement. This review was created by Brooke Wallace. She's a 20-year ICU nurse, organ transplant coordinator, clinical instructor, and my published author.
Her whole thing is taking these tough nursing topics and just making them easier.
And if you want more or like comprehensive notes on everything we talk about today. You can find it all at think like a nurse.org.
Okay, let's do this. Where are we starting?
Sodium has to be sodium. It's the brain's electrolyte. When sodium goes wrong, the brain is what takes the hit,
right? So, let's start with low sodium, hyponetriia, sodium less than 135. What's that one sign that should make the hair on your arms stand up?
Seizures. Especially when that sodium just plummets, say below 120. Okay.
Yeah. When sodium is low, water rushes out of the vascular space and into the brain cells. It causes them to swell. And if that swelling is bad enough, your patient will seize. That is the emergency.
So, if your patient is actively seizing, a simple water restriction isn't going to cut it. We need something immediate, something powerful to pull that fluid out. What's the lifesaver action?
You're reaching for 3% hypertonic saline. And this is a huge high alert medication.
A very high alert med.
Exactly. The dose is usually 100 milliliters, and you give it fast. over just 10 to 20 minutes. The goal is just rapid stabilization. If the seizure continues, you can even repeat that dose up to three times.
I think that's where a lot of new nurses get nervous. You're giving this fluid that's designed to be so aggressive. What's the big risk?
Well, there are two things. Volume overload for one, but the really critical thing you worry about is correcting chronic hyponetriia too quickly.
Ah, okay. Let's talk about that classic patient scenario, the one you always see on exams, the tea and to patient.
Oh yeah. This is the elderly person, right? Often living alone, maybe not feeling well. So they're just drinking weak tea, maybe broth,
basically free water.
Exactly. Free water, zero salt. And then you add a common medication, maybe a thioide diuretic, and they show up in the ER confused, lethargic, with a sodium of like 118.
It's this weird combination of dehydration and water intoxication.
It is. And that patient is the reason we have this huge clinical pearl for chronic cases. If you correct it, too aggressively.
Yeah.
What's the catastrophe we're trying to prevent?
Osmotic demiination syndrome.
ODS. It's irreversible brain damage. It's terrifying. So, the rule is strict. Once they're stable, you restrict free water and you correct very slowly. No more than 6 to 8 mill equivalents per liter in a full 24 hours.
Okay, let's flip it. Hyperetreia, sodium above 145. This is usually true dehydration, right? A lack of water.
Yeah. And the signature sign here is confusion with just intense thirst. That is If the patient can even tell you they're thirsty, the brain cells are literally shrinking and that causes this really severe confusion.
And since the problem is a lack of water, the lifesaver action is pretty simple. Conceptually at least
we give free water usually is D5W introvenously that just metabolizes down to water or you know plain water by mouth or feeding tube. But again, slow is the name of the game. No more than 10 to 12 mil equivalents in 24 hours. Too fast and you can cause cerebral edema.
All right, switching gears. Let's talk potassium. the electrical giant.
All about the heart and muscles.
So, hypocalemia, low potassium, under 3.5. What's the ECG change that alerts us to danger?
You'll see flat or inverted T- waves. But the real giveaway, the thing to memorize is the prominent Uwave. It's this little bump right after the T-wave. If you see U waves, you have to think low potassium.
And the lifesaver is replacement, of course. But the speed is everything, right? Especially IV.
How fast is too fast?
Never ever exceed 10 to 20 mill equivalents per hour through a peripheral line. If you go faster, it is excruciating. It's a chemical flabitis just burns the vein. We always prefer to replace it by mouth if we can. Much safer.
I've seen students try to chase a low potassium for hours and the number barely moves. What's the one thing we always forget?
Ah, yes. You have to check and correct low magnesium first. Always.
Why is that?
If magnesium is low, the cell walls get leaky. They just can't hold on to the potassium you're trying to give them. It's like filling a bathtub with the drain wide open. You fix the mag and suddenly the potassium replacement starts working.
Magnesium is the gatekeeper. That makes perfect sense. Okay, now for the really scary one. Hyperc calmia.
Potassium above 5.5. And it's a true emergency above 6.5 or with any ECG changes at all.
And the classic ECG changes. It's terrifying.
Tall peaked T- waves. They look like these narrow sharp tents. And when you see those, you have not minutes because they progress to a wide QRS and then to that deadly sine wave pattern
which is basically cardiac arrest.
Imminent cardiac arrest. Yes.
So this requires the most critical three-step sequence. It's stabilize, shift, and remove.
Yeah.
What is the very first thing we give to protect the heart?
Calcium gluconate. Step one is always stabilize the cardiac membrane. It doesn't actually lower the potassium level, but it makes the heart muscle less irritable. It buys you time. It is the immediate lifesaver.
Okay. Heart stable. Step two is shifting that potassium out of the blood and into the cells. What do we use for that?
The go-to is regular insulin with dextrose. Insulin literally forces potassium into the cells. You can also use highdosese albuterol nebulizers which also helps shift potassium.
And finally, step three, we have to get it out of the body for good,
right? Removal options. You've got kioxilate, which works through the gut, loop diuretics like fioamide if the kidneys are working, or the most definitive way is dialysis.
So that's sequence. Calcium stabilizes, insulin shifts, and then removal.
Non-negotiable. You have to know it.
Okay, let's move on to calcium and magnesium. The taps and the reflexes.
Good way to put it.
Let's start with hypocalcemia. Low calcium makes everything twitchy. What are those two famous neurologic signs?
The chvastic sign. That's when you tap on the cheek over the facial nerve and you see the lip or nose twitch.
Okay. And the other one,
the truso sign. You inflate a blood pressure cuff and the patient's hand and forearm spasm. inward. It's called carpedal spasm.
If you see either of those, what's the intervention?
Calcium gluconate given slowly introvenously and I mean slowly. If you push it too fast, you can cause brady cardia and really bad hypotension.
Now, hypermagnesmia much rarer but deadly.
Yeah, you usually see it in kidney failure patients or maybe with magnesium sulfate infusions and L & D instead of twitchy. High magnesium makes everything profoundly relaxed. Too relaxed.
What are The two classic dangerous signs of that.
One, your blood pressure will be in the basement because magnesium is a potent vasoddilator. And two, you lose your deep tendon reflexes. The patient becomes a reflexic.
If you see that, what's the lifesaver?
Stop the mag immediately. And just like with hypercalemia, the antidote for the cardiac effects is calcium gluconate. It directly antagonizes the magnesium.
Great. That covers electrolytes. Let's tackle the four acid based disorders. This is what tricks up so many students.
It does. So, We need a quick trick right off the bat.
Okay, give it to us.
It's all about direction. If the pH and the bicarb move in the same direction, so they're both high or both low, it's metabolic. If the pH and the CO2 move in opposite directions, one high, one low, it's respiratory.
That one rule really does unlock most of it. But what's the big clinical principle here?
Treat the patient, not the number. And always, always look at their fluid volume status first. Are they dry? Are they overloaded? That context changes everything.
Perfect. So let's start with respiratory acid. osis, low pH, high CO2.
The cause is simple. CO2 retention. The patient is not breathing enough. They're hypoventilating. Think of a severe COPD flare up or an opioid overdose.
And the patient looks
sleepy, hard to arouse. They're just drowning in CO2. So, the lifesaver action is you have to improve ventilation,
wake them up, get them to breathe, maybe put them on by
or if they're really crashing, you have to intubate them. You have to take over and blow off that CO2.
Okay. Opposite problem, respiratory alkalossis. High pH, low CO2.
Now, they're hyperventilating, breathing too fast. This can be from anxiety, pain, a PE, even early sepsis,
and they feel
lightaded. They often complain of tingling around their mouth and fingers. That's from the electrolyte shifts. So, the lifesaver is to calm them down, treat the underlying cause. If it's PE, you treat the PE.
Got it. On to metabolic acidosis. Low pH, low by carb.
The classic sign here is the body trying to compensate. You'll see that deep, rapid cousal breathing. And in Ka you get that fruity acetone smell on their breath
and this is where that famous pneummonic comes in right for the causes muddy piles
muddy piles is essential it's methanol uremia DKA propyline glycol is zeta iron lactic acidosis ethylene glycol and salicellates basically all the things that can generate a ton of acid in the body
and the lifesaver action isn't just one thing is it
no it's about treating the root cause if it's DKA you give insulin if it's lactic acidosis from shock, you fix the shock. We only give bicarbonate if the pH is like below 7.1 and the patient is circling the drain.
Okay, last one. Metabolic alkalossis, high pH, high bicarb.
This is almost always caused by losing a ton of stomach acid. Think prolonged severe vomiting or continuous NG suction.
And it often causes a secondary hypocalemia.
It does. So the lifesaver action here feels a little counterintuitive.
We need to replace volume, but with what specifically?
Normal saline with potassium chloride. The saline, the sodium chloride is the magic cure. Giving that chloride allows the kidneys to finally excrete all that excess by carb. And of course, you replace the potassium they've lost.
That was an amazing high yield review. Let's try to apply this with a few practice scenarios. Put it to the test.
Let's do it. Scenario one. A client has been vomiting severely for 3 days. Their labs are pH 7.52, CO2 48, by 38, and potassium 2.9. What are the right interventions?
Okay. High PH, high by carb. That's screaming metabolic alkyossis.
Mhm. and that potassium is critically low.
So the answers have to be administering normal saline with a good dose of potassium chloride. For a case of the severe, you might even see an order for acettoolomide, which helps the kidneys dump by carb. But the key is saline and potassium.
Perfect. Scenario two, a priority question. A patient with severe DKA arrives. PH is 7.11, CO2 is 24, by carb is 10. What does the nurse do first?
This is severe metabolic acidosis. And the question is about the absolute first priority.
Exactly. While they definitely need fluids. The number one thing is to stop the acid factory.
So that means starting the regular insulin IV infusion. The insulin is what stops the ketone production. That's the root cause. Everything else follows, but insulin is first.
Great. Last question. A chronic COPD patient has these labs. PH 7.32, CO268, by carb 34. How do we interpret this?
Let's use the trick. The pH is low, so it's an acidosis. The CO2 is skyhigh. So the primary problem is respiratory acidosis.
Well, look at that by carb. It's also really high,
right? That tells you the kidneys are working overtime trying to compensate by holding on to base. But since the pH is still acidic below 7.35, the body hasn't won yet.
So, it's partially compensated respiratory acidosis. Exactly.
That really covers the 10 imbalances you have to know. Let's just do a super quick recap of those essential lifesaver rules.
Okay. Three things to burn into your brain. For high potassium, calcium gluconate stabilizes the heart. Insulin shifts potassium into the cells. And kiox gets it out of the body. If you know that sequence, you can save a life.
Perfect. Before we wrap up, we want to leave you with one final thought to connect all of this back to the bedside.
We kept saying volume status is crucial. So, think about this. In hyperetreia, your patient is dry and needs free water. In metabolic alkalossis from vomiting, your patient is also dry, but they need saline.
So, the thought is how does constantly assessing skin trigger, orthostatics, and urine output let you anticipate these problems before they even become critical.
Exactly. Your assessment of volume status dictates your entire approach. It's the foundation for all of this.
That really is the essence of thinking like a nurse. Thank you so much for joining us for this conversation. We invite you to check in for more conversations each week. And you can find all the notes for this session at think likeyounseurse.org.