If you’re a nursing student (or about to be) there’s one thing that comes up over and over and over…electrolytes. Having an understanding of how electrolytes work, why they’re important, and what to do when they’re off-kilter is a huge part of your job. In this guide, we’ll take a quick look at some electrolyte pearls of wisdom.


You probably already know that calcium is THE major building block of teeth and bones, but even more importantly…it’s a key player in cardiac muscle depolarization and is crucial for nerve impulse transmission. It is also important to note that calcium is a pretty patent vasoconstrictor, so if your patient is hypotensive AND has hypocalcemia, then correcting the calcium level could help their blood pressure.

Calcium is found in two forms…bound and unbound. It is the unbound or “free calcium” we care most about when measuring it (also called “ionized calcium”). If you don’t have an ionized calcium level, you can calculate a corrected calcium level with the formula:

serum Ca = 0.8(4.0-serum albumin)

Hypercalcemia (serum calcium > 11mg/dL or ionized Ca > 5mEq/L) is a cause for concern because it can cause cardiac arrhythmias (bradycardia and a short QT interval…read this for more about the QT). At serum levels above 12 mg/dL you can have cardiac arrest…so keep an eye on those levels! Your patient with hypercalcemia will show the following symptoms:

  • nausea/vomiting
  • weakness
  • blurred vision
  • constipation or ileus
  • decreased deep tendon reflexes

Hypercalcemia is typically caused by cancers, end-stage renal disease, prolonged use of aluminum-containing antacids, adrenal insufficiency and osteoporosis. Because of calcium’s inverse relationship with phosphorus, you’ll also see hypercalcemia when hypophosphatemia is present.

So…what are you going to do about it? First of all, treat the underlying cause! While you’re at it, get your patient on telemetry monitoring and run an 12-lead EKG to keep an eye on cardiac function. Get the patient on some fluids and possibly a diuretic to increase renal excretion. If you gotta give other drugs, you can give Iv phosphate (makes sense, yes?) or calcitonin if the hypercalcemia is severe.

Hypocalcemia (serum calcium < 8.5 mg/dL or ionized < 4.5 mEq/L) can also cause cardiac arrhythmias, and that’s what we care most about. With hypocalcemia, you can see heart blocks, V-fib and torsades de pointes.

You’ll usually see hypocalcemia caused by renal disease, parathyroidectomy or hypoparathyroidism and in cases of multiple blood transfusions containing citrate (which binds to calcium).

To correct hypocalcemia, you’re going to first address the underlying cause if you can. You want to supplement with IV calcium gluconate and give it slowly (over 10-15 minutes…otherwise your BP will go dangerously high). Also monitor your patient for cardiac arrhythmias, laryngospasm and stridor. If the levels aren’t scary low, then you can correct with PO supplements along with Vitamin D (Vitamin D deficiency can set your pt up for hypocalcemia as well).



The main reason we care about magnesium is because of its key role in cardiac electrophysiology. Sure, it does other stuff…but mostly we care about the ol’ ticker so that’s why we follow it closely.

Hypermagnesemia occurs at levels > 3.0 mg/dL and it makes us nervous because it can lead to cardiac arrhythmias (namely bradycardia). Because elevated mag levels can cause decreased deep tendon reflexes and weakness, we also want to watch for depressed respiratory function. I had a patient with a mag level of 7 (she had been on a Mag gtt for pre-eclampsia and by the time she got to our hospital her Mag level hadn’t been checked in a while…she was OUT).

Common causes of elevated Mag levels are renal impairment and chronic use of magnesium-containing laxatives (like Milk of Magnesia or Mylanta).

To treat your patient with hypermagnesemia you’re going to first address the underlying cause. Calcium gluconate may be warranted if levels are dangerously high. In addition, get your patient on a cardiac monitor (of course!) and monitor for sedation/respiratory depression. You can also encourage renal excretion or dialysis if the kidneys aren’t functioning well.

Hypomagnesemia occurs at levels < 1.8 mg/dL. Because of magnesium’s role in cardiac electrophysiology, we know that hypomagnesemia can cause a prolonged QT interval, a wide QRS, ST depression and T-wave inversion…along with that prolonged QT comes the other biggie…torsades de pointes (a weird form of V-tach that can be corrected by giving IV magnesium).

Your patient can have low mag levels due to excessive GI drainage, alcohol withdrawal, hypothyroidism and a bunch of different drugs (including corticosteroids).

As always, the first thing you want to do in regards to treatment is to identify what’s causing it and fix it. You can also replace via IV infusion (2g over 2 hrs). If it’s super low, monitor the EKG and keep an eye out for arrhythmias! If your pt is on digitalis, watch for signs of toxicity as this can occur when mag is low.


Chloride is what I like to think of as the forgotten electrolyte…poor little ol’ chloride! Let’s check out some important functions of this often-overlooked electrolyte. It is THE most abundant extracellular anion and will combine with cations to form sodium chloride, potassium chloride and calcium chloride…pretty cool, huh?

The thing we love the most about chloride is its ability to help maintain osmotic pressure and thereby maintain fluid balance in the body. It’s also a key player in acid-base balance AND it helps maintain electroneutrality. You may hear people talk about the “chloride shift”…this is a way to maintain pH and it occurs because acidosis causes bicarbonate to be released into the plasma in exchange for chloride…the chloride is “shifted” into the cell. This works because both bicarb and chloride are negatively charged, so switching the two doesn’t affect electroneutrality. I told you chloride was cool.

Hyperchloremia (Cl > 110 mEq/L and SCARY levels > 115) causes metabolic acidosis, peripheral vasodilation and hypotension. Your patient will have decreased cardiac output and tachypnea in an effort to compensate. You may see Kussmaul’s respirations as the body tries to blow off the CO2. 

It has many causes including overdose (salicylate, methanol, ethylene glycol), hypernatremia, intake of Kayexalate (causes K to be excrete and Cl to be absorbed in the GI tract), DKA and dehydration.

Like with all other electrolyte imbalances,  your first course of action is to identify and treat the cause. You’ll also want to give IV fluids that DO NOT contain chloride, possibly give sodium bicarbonate to correct acidosis and monitor the pt for hypotension and respiratory compromise.

Hypochloremia (Cl < 95 mEq/L and REALLY BAD if < 80) is a cause for concern because it can cause hypoventilation and convulsions.

Hypochloremia can be caused by excessive GI losses of chloride (vomiting, suctioning, diarrhea), dehydration due to excessive sweating or in patients with cystic fibrosis, use of loop diuretics and fluid overload.

After you’ve identified and treated the cause, you’re going to replace PO or IV, monitor neuro status and check some labs (chloride, bicarbonate, sodium, potassium, ABG).


Potassium is probably THE electrolyte whose value you will always know…that’s because we keep a super close eye on this guy. Why? Because of potassium’s HUGE role in cardiac conduction. It also plays a role in smooth and skeletal muscle but we really really care about the heart. A lot.

Hyperkalemia is present at levels > 5.0 (ish) and is CRITICAL when it gets above 6.4. You will see tall, spiked T waves on the cardiac monitor and probably also a prolonged QTc. Your patient may complain of muscle cramping, diarrhea, confusion, nausea and numbness/tingling of the face, hands and feet. At critical levels your patient is at HUGE risk for cardiac arrest, so you gotta fix this STAT!

But first…what causes hyperkalemia? Usually it’s caused by renal failure, but it can also be due to trauma, burns, ischemic tissue and chemotherapy…all of which cause the lysis of cells and the release of K into the bloodstream. Other causes include DKA and the use of potassium-sparing diuretics.

To treat your patient, you want to make sure they are on the cardiac monitor. If levels are critically high, then you’re going to give a bunch of drugs…kayexalate (will make them poop…a lot), insulin + glucose (to move K back into the cell), calcium (it doesn’t decrease K, but it protects the heart) and albuterol (also causes a potassium shift).

Hypokalemia occurs at levels < 3.5 and we get REALLY worried when it’s < 2.5. When K is low, your patient may feel weak, have an upset stomach, be confused and have decreased deep tendon reflexes. The ECG will show ST depression, flat/inverted T-waves, an enlarged Q wave on top of the T-wave that makes the QT interval look really long (though it’s not).

The most common cause of hypokalemia is excessive diuresis. It can also be caused by excessive GI output, alcoholism or shifts of potassium that occur in metabolic alkalosis and during insulin administration.

If your patient’s levels are low, the only thing to really do is replace PO or IV. If giving PO, give with food as the pills can cause GI upset. If giving IV, give slowly (10 mEq per hour if not on cardiac monitor…20 mEq per hour if continuously monitored). Simple!



Who doesn’t love sodium? Especially on the rim of a margarita glass or sprinkled over some fresh-from-the-fryer tortilla chips. Yum! In the body, sodium is super important because it plays a huge role in neuromuscular function, osmolality and acid-base balance. Good stuff!

Hypernatremia (Na > 147 and/or a serum osmolality > 300 mOsm) can cause twitching, seizures, agitation, coma, muscle weakness and lethargy. Your patient will also show signs of dehydration such as tachycardia, flushing, poor skin turgor and a low-grade fever.

It is usually caused by an increase in sodium intake when renal insufficiency is present OR large water losses such as with diabetes insipidus. It is also pretty common in hypoaldosteronism and Cushing’s syndrome.

The most common way to treat hypernatremia is to dilute it with free water (not NaCl!) or hypotonic solutions if giving IV (0.45% NaCl or D5W). If it’s due to diabetes insidious or Cushing’s, treat the underlying cause. You got this!

Hyponatremia (Na < 135 with PANIC levels when < 110) is of concern because of its affect on neuro status, but it can cause other problems as well such as muscle spasms, diarrhea, vomiting and diminished deep tendon reflexes.

Recall that sodium plays a role in osmolality…basically water follows salt. As the sodium levels in the serum decrease, the water is going to move INTO the cell in order to try to equalize the osmotic gradient. This becomes concerning when we’re talking about brain cells…when brain cells swell very very bad things happen. For more on this, read our post on hyponatremia!

To treat hyponatremia, you’ll (say it with me now) identify and treat the underlying cause. If the hyponatremia is mild, the treatment is basically just fluid restriction and increase of sodium intake. If it’s severe,  you’ll need to correct it with hypertonic saline, which must be given VERY slowly to gradually correct the sodium levels (doing so too quickly can cause “locked in syndrome.”)


Phosphorus is the main anion in the CSF and THE MAIN component of ATP… the ATP situation is why we care so much about it, but we also care about it in relation to calcium. When calcium levels are up, phos is down and vice versa. So in a way, we care about phos for the same reasons we care about calcium. The body is a mysterious wonder! In fact, NCLEX questions will often ask about hyperphosphatemia when they are REALLY asking about hypocalcemia…tricky tricksters!

Hyperphosphatemia (>4.5) manifests as signs of hypocalcemia…twitching, tingling, irritability, muscle cramps, and numbness. It’s usually due to renal failure, but can also be caused by Vitamin D toxicity, increased cell lysis and hypoparathyroidism.

In addition to treating the underlying cause and the accompanying hypocalcemia, you might give oral meds that bind phosphorus or diuretics. You can also give insulin + glucose to move phos into the cell. If it’s severe…dialysis, baby!

Hypophosphatemia (< 3.0) can cause paresthesia that looks like Guillain-Barre syndrome…scary! If ATP isn’t functioning well, do you think your body has any “oomph”? Nope! You’ll also see hypotension, myocardial depression, hemolytic anemia respiratory depression.

Low phos levels are caused by decreased intake (alcoholism and eating disorders), diuresis, DKA, hyperparathyroidism and chronic diarrhea (among others, but these are the more common ones).

To treat hypophosphatemia, you’ll tackle the underlying cause (of course!).  If it’s mild, simply increasing PO intake is usually all it takes (K-Phos or Neutra Phos tablets). If it’s severe, then you’re going to replace via IV…the bad news is that phos is not compatible with ANYTHING, so you’ll need a dedicated line.


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If you’d like to learn MORE about electrolytes, I highly recommend this book. (#ad)

And…if you’d like a handy resource sheet to carry with your in your clinical binder, turn into a T-shirt or put under your pillow at night, I’ve got some right here…they include all the information covered in this post and SO MUCH more!

I hope this helps you understand the role of electrolytes…it’s information every nurse uses every single day. Learn it, live it, love it!