Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 12

Complete Metabolic Panel

The Basic Metabolic Panel (BMP) include the common chemistries ordered when screening for or monitoring disease.
The Complete Metabolic Panel (CMP) is a broad screening tool to evaluate organ function.

Results include:

 Sodium (Na⁺)
 Potassium (K⁺)
 Chloride (Cl⁻)
 Bicarbonate (CO₂⁻)
 Glucose
 Blood Urea Nitrogen (BUN)
 Creatinine
 Calcium
 Total protein
 Albumin
 Alkaline Phosphatase (Alk Phos)
 Alanine amino transferase (ALT)
 Aspartate amino transferase (AST)
 Bilirubin

Cations
Sodium (136-145 mEq/L)

Sodium is the major cation in the extracellular space. The sodium content in the blood is a result of a balance
between dietary sodium intake and renal excretion. Water and sodium are closely interrelated. Critical values are
<120 or >160 mEq/L.

Hypernatremia (>145 mEq/L):

 These patients are usually dry


 Dry mucous membranes, thirst, agitation, restlessness, hyperreflexia, mania, and convulsions
 Most common in patients with
o An impaired thirst mechanism (common after strokes)
o An inability to replace water depleted through normal insensible losses (skin and respiration)
o Renal and GI losses

Hyponatreima (<136 mEq/L)

 Check serum osmols ====lab you order


o Na⁺ is the main osmol in the blood. Therefore, if the Na⁺ is truly low, you would expect the serum
osmolality to be low as well.
 Urine osmolality
 Helps differentiate between conditions associated with impaired free water
excretion and primary polydipsia. A urine osmolality >100mOsm/kg indicates
impaired ability of the kidneys to dilute the urine
 Serum osmolality
 Readily differentiates between true hyponatremia and pseudohyponatremia
 Urinary sodium concentration
 Helps differentiate between hyponatremia secondary to hypovolemia
(<25mEq/L) and SIADH (>25mEq/L)
 If a patient’s serum osmolality is high
o You must assume that another osmol in the blood is elevated, thus misleadingly lowering their
sodium result.
o This is called pseudohyponatremia.
o The most common cause is an elevated glucose level.
o Other causes include increased lipids, methanol, ethylene glycol, isopropyl alcohol, and ethanol.
 If a patient’s serum osmolality level is low
o You must determine their volume status (“HOPE Foley” and “FUN BUN”)
 History of vomiting, diarrhea, or alcohol intake
 Orthostatic vital signs (lying, sitting, standing)
 Physical Examination, is the patient dry? Check mucous membranes, axillae, groin.
 Foley catheter to monitor I’s & O’s
 FeNa⁺ (fractional excretion of sodium) result <1% in dehydration
 Urine specific gravity
 Na⁺, is it elevated?
 BUN, is the BUN/creatinine ration >20?

A guy in the Navy boards his ship and crosses the sea, docking in a port of ill repute. He disembarks, visits a brothel
and then re-boards his ship to set sail. The CDC had heard of the sailor’s risky behavior and became concerned about
foreign STD’s being brought back to the United States. They were on the U.S. dock for the sailor to come home. Prior
to the sailor disembarking, the CDC could be heard yelling, “Hey ‘EU’ on the ‘SHIP’, you need a VD Dart’!”

Euvolemic Hypovolemic Hypervolemic


S – SIADH V – vomiting C – Congestive heart failure
H – Hypothyroid D – diarrhea N – Nephrotic syndrome
I – Inappropriately giving a child D – diuretics C – Cirrhosis
too much water
P – Primary polydipsia A – Addison’s disease
R – Renal tubular acidosis
T – Third spacing fluid

EU on the SHIP represents conditions in which hyponatremia is present in a hypo-osmolar, euvolemic state.

Na⁺ is decreased.

Serum osmols are decreased.

Volume status is normal.

 Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH, actually inappropriately high ADH)


o This is a disorder in which continued ADH secretion occurs in spite of low serum osmolality
o Oversecretion of ADH stimulates the kidney to reabsorb free water
o It can be seen in patients with pulmonary disease, lung CA, or Tuberculosis. Certain lung tumors
can secrete ADH, thus maintaining a patient’s normal volume status while decreasing serum Na⁺
levels.
 Hypothyroidism
o Check a TSH level (thyroid stimulating hormone)
 Inappropriately giving a child too much water
o It is sometimes common in lower socioeconomic status patients
o Formula is sometimes diluted with water in an attempt to make it last longer which can greatly
reduce the necessary electrolytes and osmols required by the child
 Primary polydipsia
o Seen in certain psychiatric conditions, endurance events, and ecstasy use
o When left with unrestricted access to water, a patient may drink gallons daily
o The body will urinate out the excess, thus causing their Na⁺ level to drop
o This can lead to seizures

VD DART represents conditions in which hyponatremia is present in a hypo-osmolar, hypovolemic state.

Na⁺ is decreased.

Serum osmols are decreased.

Volume status is decreased.

 Vomiting
 Diarrhea
 Diuretics
o Many diuretics work by inhibiting sodium reabsorption by the kidneys
 Addison’s Disease
o Acute adrenal insufficiency
o Sodium is not reabsorbed by the kidneys and is lost in the urine
o These patients need you to add cortisol
o Patients present with vague symptoms and the diagnosis can be difficult
 MAGIK (some causes of Addison’s disease)
 Meningitis (Neisseria meningitis)
 Adrenal hemorrhage (trauma or childbirth)
 Granulomatous disease (Sarcoidosis or Tuberculosis)
 Immunocompromised states (HIV or chronic steroid use)
 Ketoconazole use
 Renal tubular acidosis
o Caused by the inability of the kidneys to conserve bicarbonate and to adequately acidify the urine
o Can result from ingested toxins causing acute trauma to the kidneys
 Third spacing fluid
o Fluid leaks from the blood into the interstitium
o Can be seen in severe burns and pancreatitis

CDC represents CNC in the mnemonic. It represents conditions in which hyponatremia is present in a hypo-osmolar,
hypervolemic state.

Na⁺ is decreased.

Serum osmols are decreased.

Volume status is increased.


 Congestive heart failure (CHF)
 Nephrotic Syndrome
 Cirrhosis

Correcting sodium levels

 Sodium should never be corrected rapidly


 You cannot correct Na⁺ more than 12 mEq/L over a 24 hour period, should start at 4 to 6 mEq/L per day
o Doing so may cause pontine demyelination, a dangerous condition caused by rapid changes made
to brain fluids
o This can result in brain swelling and death
 Treatment truly depends on cause
o Hyponatremic and hypovolemic
 Treatment is usually IV fluids
o Hyponatremic and hypervolemic
 Treatment can either be fluid restriction or fluid reduction with diuretics

It is critically important to learn how to appropriately determine a patient’s volume status and the physical signs of
hypovolemia and hypervolemia. If you suspect a patient is dehydrated and put them on IV fluids, but instead they
turn out to be hypervolemic, you will make the patient’s condition much worse.

Potassium (3.5-5.0 mEq/L)

Potassium is the major cation in the intracellular space. The major role of K⁺ is in regulating muscle and nerve
excitability. The cardiovascular system is of principle concern in K⁺ abnormalities. Abnormalities of K⁺ are usually
related to problems with insulin, aldosterone, acid-base balance, renal function, or GI and skin losses. Critical values
are <2.5 or >6.5 mEq/L.

Serum potassium concentration depends on many factors:

 Aldosterone: Increases renal losses of potassium.


 Sodium reabsorption: As sodium is reabsorbed, potassium is lost.
 Acid-base balance: Alkalotic states tend to lower serum potassium levels by causing a shift of potassium
into the cell. Acidotic states tend to raise serum potassium levels by reversing the shift.

Hyperkalemia (>5.0 mEq/L):

 #1 cause is lab error/hemolysis, repeat lab value


 Check a 12 lead EKG as elevated levels will adversely affect the heart.
o Flattened P waves
o Widened QRS complex
o Peaked T waves
 Treatment is a 3 step process
o Protect the heart if EKG changes are present
 Treat with calcium
 Calcium is cardio protective for 30-45 minutes
 1 amp of calcium chloride or calcium gluconate
o Shift potassium back into the cells
 Insulin and Glucose =====MC
 Sodium bicarbonate
 High dose Proventil
o Remove the potassium from the body
 Kayexalate (15 or 30 g)
 Loop diuretic
 Hemodialysis
 Symptoms include irritability, nausea, vomiting, intestinal colic, and diarrhea

Etiologies of hyperkalemia:

Apparent excess – extracellular shifting of K⁺

 Metabolic acidosis – to maintain physiologic pH during acidosis, hydrogen ions are driven from the blood
and into the cell; to maintain electrical neutrality, potassium is expelled from the cell into the blood

True excess

 Increased intake
o Endogenous
 Hemolysis
 Rhabdomyolysis
 Muscle crush injuries
 Burns
o Exogenous
 Salt substitutes
 Drugs (PCN, potassium supplementation)
 Decreased output
o Acute or chronic renal failure (most common)
o Drugs
 Potassium sparing diuretics (Spironolactone)
 ACE-inhibitors
 NSAIDs
 β₂ adrenergic antagonists
 Heparin
 Trimethoprim
o Deficiency of adrenal steroids
o Addison’s disease

Hypokalemia (<3.5 mEq/L):

 Check a 12 lead EKG


o Flattened T waves
o Prominent U waves
 Treatment
o Replace K+
 Symptoms include weakness, paralysis, hyporeflexia, ileus, cardiac arrhythmias

Etiologies of hypokalemia:

 Deficient dietary intake


 Burns
 Gastrointestinal disorders (diarrhea, vomiting)
 Diuretics – increase renal excretion of potassium
 Hyperaldosteronism
 Cushing syndrome – glucocorticosteroids have an “aldosterone-like” effect
 Renal tubular acidosis
 Licorice ingestion
 Metabolic Alkalosis – to maintain physiologic pH during alkalosis, hydrogen ions are driven out of the cell
and into the blood; to maintain electrical neutrality, potassium is driven into the cell from the blood
 Insulin administration
 Ascites – decreased renal blood flow from reduced intravascular volume that results in a collection of fluid
which stimulates aldosterone secretion
 Renal artery stenosis
 Cystic fibrosis – loss due to secretions and sweat

Anions
Chloride (98-106 mEq/L)

Chloride is the most abundant extracellular anion. The primary purpose is the maintain electrical neutrality, it
follows sodium. It helps to maintain extracellular osmolality. Critical values are <80 or >110 mEq/L.

Hyperchloremia:

 Symptoms include lethargy, weakness, deep breathing

Hypochloremia:

 Symptoms include hyperexcitability of the nervous system and muscles, shallow breathing, hypotension,
and tetany

Bicarbonate (23-30 mEq/L)

Bicarbonate is made in the kidneys. It is produced slowly, over a period of hours to days. Lab result is expressed as
“total carbon dioxide” (CO2). Increases with alkalosis; decreases with acidosis.

Anion Gap (normally <16)

 A calculated value helpful in diagnosing a metabolic acidosis


 Calculated using the following formula
o Sodium – (Chloride + Bicarbonate)
 Having an anion gap >16 equates to having a “funky” acid (lactic acid, ketoacid etc) in the body
 Acids not routinely produced in the body are not measured by electrolyte panels
 When these acids are present in the body they will produce an academia, thus a decrease in the serum
bicarbonate (as this buffer is consumed) and therefore an increase in the calculated anion gap

Metabolic Acidosis

 The body does not tolerate being in an acidotic state very well. It has two responses to the condition, one is
rapid and one is slow.
o Increase your respiratory rate – rapid response
 Kussmaul breathing – abnormally deep, very rapid sighing respirations
 An immediate respiratory response as an attempt to blow off CO2, thus raising in body
pH
o Kidney response – slow response
 Increase body’s bicarbonate
 Causes of metabolic acidosis
o K = Ketones (DKA or starvation)
o U = Uremia
o S = Sepsis
o S = Salicylates
o M = Methanol (other alcohols)
o A = Aldehydes and all other heavy chemicals (iron)
o L = Lactic acidosis
or
o M = Methanol
o U = Uremia
o D = Diabetes
o P = Paraldehyde
o I = Iron
o L = Lactate
o E = Ethanol, ethylene glycol
o S = Salicylates, starvation

Renal Functions

BUN (10-20 mg/dL)

BUN is an indirect and rough measurement of renal function and glomerular filtration rate. It is also a measurement
of liver function. It measures the amount of urea nitrogen in the blood.

 Urea is formed in the liver as the end product of protein metabolism and digestion
 The urea is deposited in the blood and transported to the kidneys for excretion
 When elevated – Azotemia (uremia)

Creatinine (0.5-1.2 mg/dL)

Creatinine is a catabolic product of creatine phosphate which is used in skeletal muscle contraction.

 For normal, healthy patients in a steady state, the rate of creatinine production equals secretion
 A rise in serum creatinine almost always indicates worsening renal function

CrCl

Specific measurement for kidney function. For renal adjustment for drug dosing, you use CrCl.

[(140 – Age) x wt]/(0.814 x Cr) for male. For female you multiple the total by 0.85

BUN/Creatinine Ratio

 Only matters when the values are elevated


 If the BUN or Creatinine values are abnormal, we must first determine the ratio in order to determine the
etiology

Prerenal (ratio >20)

 Decreased renal profusion


o Dehydration – most common
o Blood loss
o Shock
o CHF
 Increased protein breakdown
o GI bleed
o Crush injury
o Burns
o Fever
o Corticosteroids
o Tetracyclines
o Excessive amino acid or protein intake

Intrarenal (ratio <20)

 Renal disease
o Glomerulonephritis
o Pyelonephritis
o Acute tubular necrosis
 Renal failure
 Nephrotoxic drugs
 Severe hypertension
 Diabetes
 Polycystic kidney
 Chronic analgesic overuse

Postrenal (ratio >20)

 Ureteral obstruction from stones, tumor, or congenital anomalies


 Bladder outlet obstruction from prostatic hypertrophy (most common) or cancer
o Must do a DRE and place a Foley catheter
Calcium (9.0-10.5 mg/dL)

Calcium is necessary in many metabolic enzymatic pathways. It is vital for muscle contractility, cardiac function,
neural transmission, and blood clotting. Critical values are <6 or >13 mg/dL.

Corrected Ca = Ca + 0.8[(4.0 - serum albumin)]

Where normal albumin value is 4.0 or 4.4

 Used to evaluate parathyroid function and calcium metabolism


 One half exists in the blood in its free (ionized) form
 One half exists in its protein-bound form (mostly with albumin)

Hypercalcemia

 Symptoms include anorexia, nausea, vomiting, somnolence, and coma


 Hyperparathyroidism – most common
 Metastatic tumor to bone
 Paget disease
 Hypervitaminosis D
 Lymphoma
 Sardoidosis

Hypocalcemia

 Hypoparathyroidism
 Renal failure
 Rickets
 Malabsorption
 Hypovitaminosis D

Total protein (6.4-8.3 mg/dL)

Proteins are the most significant component contributing to the osmotic pressure within the vascular space. The
osmotic pressure acts to keep fluid within the vascular space, minimizing extravasation of fluid. Total serum protein
is a combination of prealbumin, albumin, and globulins.

Albumin (3.5-5 g/dL)

Albumin is a protein that is formed within the liver. This makes up about 60% of the total protein. The major
purpose is to maintain colloidal osmotic pressure. Albumin transports drugs, hormones, and enzymes.

Increased albumin levels

 Dehydration – as intravascular volume diminishes, albumin measurements increase

Decreased albumin levels

 Malnutrition – lack of amino acids available for building proteins and liver dysfunction
 Pregnancy
 Liver disease
 Protein losing enteropathies – large volumes of protein are lost from the intestines
 Third space losses – large amounts of albumin can be lost in the serum that weeps from open burns and
readily accumulates in the peritoneum with ascites

Alkaline Phosphatase (30-120 units/L)

Alk Phos is found in many tissues, the highest concentrations are found in the liver, biliary tract epithelium, and
bone. This is important for detecting liver and bone disorders.

Increased Alk Phos levels

 Primary cirrhosis
 Intrahepatic or extrahepatic biliary obstruction
 Primary or metastatic liver tumor – Alk phos is found in the liver and biliary epithelium and excreted into
the bile, obstruction can cause increased levels
 Pregnancy
 Metastatic tumor to the bone
 Hyperparathyroidism
 Paget disease
 Rheumatoid arthritis
 Elderly

Decreased Alk Phos levels

 Malnutrition
 Pernicious anemia
 Scurvy (vitamin C deficiency)

Alanine Aminotransferase (4-36 units/L)

ALT is used to identify hepatocellular diseases of the liver. ALT is found predominantly in the liver.

Aspartate Aminotransferase (0-35 units/L)

AST is found in heart muscle, liver cells, skeletal muscle, and to a lesser degree in the kidneys, pancreas, and RBCs.

 Tested in the cardiac enzyme series


 Aids in determining the timing and extent of acute myocardial infarction
o Rises within 6-10 hours
o Peaks at 12-48 hours
o Returns to normal in 3-4 days
 Diseases that affect the hepatocyte will cause elevated levels
o Acute hepatitis
o Acute extrahepatic obstruction – gallstone
o Hepatic cirrhosis
o Infectious mononucleosis
 Skeletal muscle diseases
o Skeletal muscle trauma
o Multiple traumas
o Severe, deep burns
 Other diseases
o Acute hemolytic anemia
o Acute pancreatitis
 Decreased levels are found in
o Acute renal disease
o Diabetic ketoacidosis
o Pregnancy
o Chronic renal dialysis
o

AST > ALT =Alcohol

ALT > AST = hepatitis

Bilirubin (0.3-1.0 mg/dL)

Bilirubin is a constituent of the bile, which is formed in the liver. Bilirubin metabolism begins with the breakdown of
RBCs in the reticuloendothelial system (mostly in the spleen). Total serum bilirubin level is the sum of the
conjugated (direct) and unconjugated (indirect) bilirubin. Critical values >12 mg/dL.

Indirect bilirubin

Hemoglobin is released from RBCs and broken down into heme and globin molecules. Heme is then catabolized to
form biliverdin, which is transformed to bilirubin. This form is called unconjugated (indirect) bilirubin.

Increased blood levels of indirect bilirubin

 Sickle cell anemia


 Hemolytic jaundice
 Hemolytic anemia
 Pernicious anemia
 Hepatitis
 Cirrhosis
 Sepsis
 Sjogren disease

Direct bilirubin

In the liver, indirect bilirubin is conjugated with a glucuronide molecule, resulting in conjugated (direct) bilirubin.
This is then excreted from the liver cells to the kidneys and into the intrahepatic canaliculi, which eventually lead to
the hepatic ducts, the common bile duct, and the bowel.

Increased blood and urine levels direct bilirubin

 Gallstones
 Extrahepatic duct obstruction
 Extensive liver metastasis

Hepatic increase indirect

Post hepatic increase direct


Some with hemolytic anemia will have increase indirect bilirubin, increase LDH and decrease hepatoglobin

You might also like