One of the most common lab tests ordered for your patients is the BMP, otherwise known as the basic metabolic panel. This lab test looks at eight different components which provide a wealth of information about your patient’s condition. The components of the BMP are sodium, potassium, calcium, chloride, carbon dioxide, glucose, BUN and creatinine. Let’s take a look at each of these. 


Sodium is the most abundant extracellular cation (positively charged ion) and the biggest contributor to serum osmolality. The body maintains sodium balance through a variety of mechanisms:

  • Antidiuretic hormone (ADH) controls the reabsorption of water, which affects serum sodium levels
  • Aldosterone causes the body to hold on to sodium by decreasing renal excretion
  • Natriuretic hormone causes the kidneys to excrete more sodium

Sodium is very closely tied to water balance in the body. For example, if an individual is dehydrated (and fluid volume is low), then sodium levels increase due to being more concentrated. In this case, the kidneys would work to compensate by holding on to water. In a patient with hypervolemia, sodium levels are decreased due to dilution. In this case, the kidneys work to maintain balance by excreting water and holding on to sodium.

Both hypo and hypernatremia can occur in the clinical setting, but hyponatremia is far more common. It’s also important to note that the etiology of sodium abnormalities is often due to fluid imbalances rather than too much or too little sodium intake. However, a patient who receives a large amount of sodium in their IV fluids can certainly develop hypernatremia as a result.

When it comes to hyponatremia, the patient is at risk for significant neurological complications due to cerebral edema. Signs and symptoms of hyponatremia can range from confusion and lethargy to seizures and coma.

In general, the sodium level will be of great importance in patients who have fluid imbalances, renal dysfunction, and changes in level of consciousness.

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Potassium is the major cation inside the cell and even small changes in the serum level can have a significant effect on your patient. It’s important to understand that while the kidneys excrete potassium, they do not reabsorb potassium. If the patient doesn’t get enough potassium through their IV fluids, PO supplementation or their diet, potassium levels can decrease rapidly.

Potassium levels are regulated in the body through a few mechanisms:

  • As sodium is reabsorbed, potassium levels decrease
  • Aldosterone increases renal losses of potassium
  • Acidotic states tend to increase serum potassium levels by shifting potassium out of the cell while alkalotic states tend to decrease serum potassium levels by shifting potassium into the cell.

Hyperkalemia and hypokalemia are common imbalances, and both can cause serious cardiac dysrhythmias. The classic sign of hyperkalemia on the ECG is a tall, peaked T-wave and hypokalemia often causes frequent PVCs. 

Hypokalemia can occur for a wide range of reasons including diarrhea/vomiting, Cushing’s syndrome, and insulin administration (remember that insulin unlocks the cell to let glucose enter and potassium comes along for the ride). If you have a patient with hypokalemia who is also taking digoxin, they will be at very high risk for significant cardiac arrhythmias.

Hyperkalemia can also occur for a number of reasons including renal failure, dehydration, crush injury, cellular necrosis, and administration of hemolyzed blood products. 

And, your most common reason for watching potassium levels closely will be because your patient is taking a diuretic: 

  • Loop diuretics (ex: furosemide) cause hypokalemia
  • Potassium-sparing diuretics (ex: spironolactone) can cause hyperkalemia, especially if the patient is receiving potassium supplementation


Though calcium is not very abundant in the serum (most of it is located in the bone), it has a very important role in nerve impulse transmission, cardiac and skeletal muscle contraction, blood pressure regulation and the formation of blood clots.

A key concept to understand about calcium is the concept of bound vs free (or ionized) calcium. Some of the serum calcium is bound to proteins and is not biologically active, while the other form is biologically active. This is called the free or ionized calcium. This is important to understand because when your patient has a low albumin level, the calcium level on the serum lab test will be falsely low because it is measuring both forms of calcium and does not accurately represent the biologically active or ionized calcium level. In this situation, it’s important to calculate the serum ionized calcium level to get a better understanding of the patient’s true calcium balance. You can use an online calculator to do this, or you can obtain an ionized calcium from the ABG.

The most common causes of hypercalcemia are hyperparathyroidism and cancer. Hypocalcemia can occur for a variety of reasons, including large-volume fluid resuscitation (due to hemodilution) and in massive blood transfusions. Recall that banked blood has citrate added to it to prevent it from coagulating. This citrate binds with calcium leading to hypocalcemia, which explains why your patient may require calcium replacement after receiving blood products. Other causes for hypocalcemia include hypoparathyroidism, renal failure, acute pancreatitis, rhabdomyolysis and intestinal malabsorption.

There are many signs and symptoms of calcium imbalance and some of the most significant are cardiac related. Hypercalcemia can cause bradycardia and cardiac arrest, while hypocalcemia can cause heart blocks, ventricular fibrillation and torsades de pointes. It’s also important to know that hypocalcemia can cause laryngospasm with stridor that can lead to respiratory arrest.


Chloride is the most abundant extracellular anion (negatively charged ion). It plays an important role in maintaining acid-base balance and works with sodium to maintain osmotic pressure and water balance. 

While hyperchloremia is not very common, it can occur with a variety of conditions including dehydration, hypernatremia, diabetic ketoacidosis, and with large volumes of sodium chloride. When chloride levels are elevated, the kidneys excrete bicarbonate as a compensatory mechanism, which leads to a specific type of acidosis called hyperchloremic acidosis.

Hypochloremia can occur due to things like fluid volume overload, CHF, excessive gastric suction, vomiting, SIADH, Addison’s disease and diuretic use.


On the BMP, carbon dioxide is an indirect measure of bicarbonate, which tells us about acid-base balance. Don’t confuse this with PaCO2, which is a direct measure of carbon dioxide and obtainable from the ABG.

Elevated CO2 levels are associated with metabolic alkalosis and severe vomiting/diarrhea, while decreased levels are associated with metabolic acidosis, renal failure and diabetic ketoacidosis (among others!).


Serum glucose is pretty straightforward as it simply reflects the glucose level in the blood. A serum glucose is helpful in the clinical setting to catch hyper or hypoglycemia when the patient isn’t undergoing routine fingerstick testing, and is utilized when blood sugar levels fall outside the range of the glucometer. When the glucometer reads “low” or “high” a serum glucose can determine the exact value for more targeted treatment. 

In addition, fingerstick testing is not reliable on patients with poor perfusion (such as those in shock), so serum glucose testing will be utilized instead. 


The BUN (pronounced B-U-N) measures the level of urea nitrogen in the blood. Urea is formed in the liver as a byproduct of protein metabolism and transported to the kidneys for excretion, so it is an indicator of the health of both of these vital organs. However, you will most often be evaluating the BUN as it relates to renal function since renal impairment is far more common than liver disease. 

One thing to take into account is the ratio of BUN to creatinine. When BUN rises more significantly than creatinine, this is called a high BUN:Cr ratio and can be due to reduced blood flow to the kidneys such as in dehydration and heart failure. Other reasons for a high BUN are renal insufficiency or renal disease, a high protein diet, Addison’s disease and GI bleeding. Note that an elevated BUN is an expected finding in your patient who is on dialysis.


Creatinine is a waste product of creatine phosphate, which is used in the contraction of skeletal muscle. It is excreted by the kidneys, making it an excellent indicator of kidney function. Unlike BUN (which can be elevated for a variety of reasons), creatinine is essentially elevated in renal dysfunction and dehydration. When creatinine levels increase twofold, this is indicative of a 50% reduction in GFR.

Many medications can cause renal damage, causing creatinine to increase. Common examples are cephalosporins, aminoglycosides and chronic use of loop diuretics. Additionally, many medications rely on adequate renal function for excretion and dosing will be reduced in patients with renal impairment – examples include lithium, enoxaparin and allopurinol. 

While an elevated creatinine level is an expected finding in your dialysis patients, you’ll be watching creatinine levels very closely in patients with acute kidney injury, including those with sepsis. It’s also important to know the patient’s creatinine level before administering furosemide as it can further cause renal damage.


You can review the components of the BMP again while you’re on the go in episode 303 of the Straight A Nursing podcast. Tune in wherever you get your podcast fix, or straight from the website here.


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