(*) LABORATORY AND DIAGNOSTIC TESTS

Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
Chemistry:
Cholesterol < Screening tool for atherosclerotic coronary disease. Elevated levels are
found with type II family hypercholesterolemia, hyperlipoproteinemia,
hepatocellular disease, biliary cirrhosis, cholestasis, nephrotic syndrome,
glomerulonephritis, chronic renal failure, hypothyroidism, DM, alcoholism,
obesity, and a diet high in cholesterol and fats. Decreased levels are found
in alpha-hypoprotein deficiency, hepatocellular disease, malignant liver
neoplasm, hyperthyroidism, malabsorption syndrome, malnutrition,
megaloblastic anemia, severe burns, and COPD.
HDL M > mmol/L Collects cholesterol from the body’s tissues (and vascular endothelium) and
W> brings it back to the liver.
“Good cholesterol”
LDL < mg/dl Carry cholesterol from the liver to cells of the body
“Bad cholesterol”
VLDL mg/dl Carry newly synthesized triacylglycerol from the liver to adipose tissue
Triglycerides (M) Evaluates for atherosclerosis and the body‘s ability to metabolize fats.
(F) Elevated levels are found with hyperlipoproteinemia, liver disease, and
alcoholism, nephritic syndrome and renal disease, hypothyroidism, DM,
pancreatitis, MI, and gout. Decreased levels are found with congenital
alpha-bta lipoproteinemia, malnutrition, and hyperthyroidism.
Glucose FBG Measures BGL, the most important carbohydrate in body metabolism.
> in DM (x2) Primary source of energy in most cells. Elevated levels are found with DM,
hyperthyroidism, Cushing’s disease, pancreatitis, pregnancy, severe liver
OGTT
disease, shock, trauma, and drugs such as glucagon, adrenal corticosteroids,
 < oral contraceptives, and some diuretics. Decreased levels are found with
baseline Addison’s disease, insulinoma, hypopituitarism, insulin-producing tumors,
 < 30-60 acute alcohol ingestion, myxedema, and drugs such as insulin, salicylates,
min sulfonamides and MAO inhibitors.
 < 120
min
 > 120
min in DM
Hemoglobin A1C (N) % Measures the amount of glycosylated hemoglobin as a percentage of the
Diabetic control total hemoglobin.
< % good
% fair As RBCs circulate they combine with HbA1 with some of the glucose in
the blood stream to form glycohemoglobin. The amount of GhB depends
> % poor
on the amount of glucose available in the blood stream over the RBCs 120
day lifespan

Prior to 2010, A1C was only used in monitoring BGL, but in 2010 the ADA
recommended the use of A1C in diagnosis of DM. An advantage is that
fasting is not necessary, and less day-to-day alterations in BGL during
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
periods of stress and illness don’t affect results.
BUN Measures the nitrogen fraction of urea, the chief end product of protein
metabolism. Elevated levels are associated with CHF, shock, hypovolemia,
renal disease, infection, MI, DM, excessive protein ingestion, neoplasms,
Addison’s, pancreatitis, tissue necrosis, GI bleed, hyperalimentation, drugs:
allupurinol, aminoglycosides, cephalosporins, chloral hydrate, neoplastic
drugs, ASA, thiazide diuretics, MSO4, codeine, propranolol, nephrotoxic
drugs, long-term steroids. Decreased levels are found with hemodialysis,
inadequate protein intake, severe liver disease, water intoxification,
malabsorption syndrome, amyloidosis, pregnancy, acromegaly, drugs:
chloramphenicol, streptomycin, IV dextrose.
Creatinine Creatinine is a catabolic byproduct of muscle energy metabolism and is
excreted by the kidney. It is not dramatically affected by fluid balance,
nutritional status, or liver function, as is the BUN. Creatinine is dependent
on muscle mass. Creatinine clearance = GFR, and is defined as the
measurement of the rate at which the kidneys are able to clean the
creatinine from the blood. Decreased creatinine clearance is found with
disorders of kidney function, shock, hemorrhage, CHF, and liver failure.
Increased creatinine is found with high CO, pregnancy, burns, and carbon
monoxide poisoning. Increased serum creatinine is found with
glomeronephritis, pyelonephritis, acute tubular necrosis, and urinary
obstruction. Increased urine creatinine is found with acromegaly,
gigantism, DM, and hypothyroidism. Decreased urine creatinine is found
with hyperthyroidism, anemia, muscular dystrophy, polymyositis,
neurogenic atrophy, inflammatory muscle disease, advanced renal disease,
and leukemia.
Calcium (Ca++) The most abundant mineral in the body, of which over 90% is stored in the
skeleton and the teeth. Essential for intra and extracellular fluid exchange,
blood clotting, maintaining a regular heartbeat, excitation of the skeletal
muscles, conduction of neuromuscular impulses, and bone formation.
Elevated levels are found with hyperparathyroidism, metastatic cancer,
multiple myeloma, vitamin D intoxification, overuse of calcium antacids,
polycythemia vera, Paget’s disease, dehydration, acidosis, and milk-alkali
syndrome. Decreased levels are found in hypoparathyroidism, vitamin D
deficiency, alcoholism, massive blood transfusions, acute pancreatitis,
malnutrition, renal tubular disease, and alkalosis. Clinical manifestations:
tetany, cardiac arrhythmia, carpopedal spasms.
Phosphorous The amount of phosphorous in the bone and skeletal muscle is controlled
by parathyroid hormone and calcium metabolism. An inverse relation
exists b/t calcium and phosphorus. Elevated levels are found with
hypocalcemia, acute or chronic renal failure, increased tubular reabsorption
(hypoparathyroidism, Addison’s, sickle cell anemia), increased cellular
release of phosphate (neoplasms, excessive tissue breakdown), bone disease
(healing fractures, Paget’s), increased phosphate load (hemolysis of blood,
massive transfusion), magnesium deficiency, and childhood. Decreased
levels are found with renal or intestinal loss, renal tubular defects,
administration of diuretics, primary hyperparathyroidism, hypokalemia,
hypomagnesemia, dialysis, acute gout, primary hypophosphatemia,
idiopathic hypercalciuria, decreased intestinal absorption (malabsorption,
vit D deficiency, malnutrition, vomiting, diarrhea, antacid abuse) and
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
intracellular shift of phosphate (alcoholism, DM, acidosis, TPN, respiratory
alkalosis, salicylate poisoning, Cushing’s syndrome, prolonged
hypothermia, administration of anabolic steroids, androgens, epinephrine,
glucagon, insulin)
Sodium (Na+) The major cation of the extracellular fluid. Sodium functions by
maintaining osmotic pressures, acid-base balance, and transmitting nerve
impulses. Sodium is vital for life, and when levels are increased or
decreased, there can be serious consequences. Clinical manifestations:
impaired LO and convulsions. Elevated levels are found in Cushing’s
disease, CHF, dehydration, diaphoresis, diarrhea, DI, hypovolemia,
ostomies, toxemia, vomiting, and hyperaldosteronism. Decreased levels are
found with adrenal insufficiency, Addison’s disease, bowel obstruction,
burns, hypotension, cerebral palsy, CRF, myxedema, malnutrition, and
cirrhosis.
Chloride (Cl-) The major extracellular anion and exists mainly in combination as sodium
chloride or hydrochloric acid. In combination with sodium, maintains
osmolality and water balance and is instrumental in maintaining acid-base
balance. Decreased levels are found with loss of gastric contents due to
vomiting or suction, prolonged diarrhea, excessive use of K+ wasting
diuretics, excessive sweating such as from fever or heat exhaustion,
diabetic ketoacidosis, Addison’s disease, acute infection, and prolonged
infusion of IV dextrose solutions causing a dilutional effect. Clinical
manifestations of hypochloremia are hyperirritability, tenany, or muscular
excitability; slowed respirations, and hypotension secondary to fluid loss.
Elevated levels are found with losses of bicarbonate from the lower GI
tract in diarrhea, renal tubular acidosis, mineralocorticoid deficiency,
hyperparaphyroidism, and excess administration of amino acids during
hyperalimentation. Clinical manifestations of hyperchloremia are
weakness, lethargy, unconsciousness (a late sign) and Kussmaul
respirations.
Potassium (K+) The majority of K+ is found within cells where it has a major influence on
the conduction of electrical impulses in cardiac and skeletal muscle.
Extremes of this electrolyte potentially can be very severe and can be life
threatening to the client. Elevated levels are associated with acidosis,
insulin deficiency, causes of cell destruction (trauma, necrosis, burns),
acute or chronic renal failure, drugs: K+ supplements, amphotericin B,
heparin, isoniazid. Decreased levels are associated with alkalosis, insulin
excess, GI loss (through vomiting, diarrhea, fistula, or NG suction),
excessive diuresis, drugs: furosemide, thiazide diuretics, cortisone, lithium,
kayexalate, insulin.
CO2 (serum) (N) 23-30 Measures the CO2 in the blood. Helps in evaluating pH status of the
patient and to assist in evaluation of electrolytes. It is a rough guide to acid-
base balance.

Indirect measure of HCO3-anion, a major player in acid-base balance.

Do not confused with PCO2

Albumin The smallest protein and the major protein found in the blood. The protein,
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
although small, is too large to filter through the renal glomeruli. The
presence of albumin in the urine, therefore, is an indicator of renal disease.
Elevated levels are found in nephritis, glomerulonephritis, polycystic
kidneys, kidney tumors, and pyelonephritis. Albumin is a very sensitive
indicator of beginning nephropathy for people with DM. Nonrenal
transient causes of proteinuria are strenuous exercise, fever, CHF, stress,
trauma, and seizures. Decreased levels are found with malnutrition due to
lack of amino acids, pregnancy where levels progressively decrease until
delivery, liver disease because the liver is the site of albumin synthesis,
protein-loosing enteropathies and nephropathies, third space losses, over
hydration, increased capillary permeability, inflammatory diseases and
familial idiopathic dysproteinemia.
Bilirubin Total: Produced by the liver, spleen and bone marrow. It is also the byproduct of
Direct: hemoglobin metabolism. Direct bilirubin is excreted by the GI tract;
indirect bilirubin normally circulates in the blood stream. Can be measured
Indirect:
by urine and serum samples. Note: there is not direct lab test for indirect
bilirubin, but rather it is determined by subtracting the direct from the total.
BLOOD: Elevated total, direct, and indirect bilirubin levels are found
with alcoholism, biliary obstruction, or calculi, anemia, hepatitis, malaria,
MI, pancreatitis, cirrhosis, Gilbert’s disease, pulmonary embolism, and
mononucleosis, and sickle cell anemia. Decreased total, direct, and
indirect bilirubin levels are not clinically significant. URINE: Elevated
levels are found with cirrhosis, hepatitis, mononucleosis, and
hyperthyroidism.
CK (CPK) CK CPK is the enzyme contained in the heart muscle, skeletal muscle and the
 MM brain. When heart muscle is damaged, such as in a MI, CPK is released
into the blood. The CPK is composed of 3 isoenzymes CPK-BB (brain),
 BB CPK-MB (cardiac) and CPK-MM (muscle). Total CPK levels are
 MB elevated with myopathy due to alcoholism, electrical cardioversion or
defibrillation, cardiac catheterization, stroke, and surgery. CPK-MB is
elevated with MI, cardiac surgery, myocarditis, and Rye’s syndrome. CPK-
BB is elevated with stroke, seizure, pulmonary infarction, and intestinal
ischemia. CPK-MM is elevated with muscular dystrophy and skeletal
muscle injury.
Troponin T< ng/ml Performed on patients with chest pain to determine if the pain is caused by
I< ng/ml cardiac ischemia. It is a specific indicator of cardiac muscle injury. It is
helpful in predicting the possibility of future cardiac events.

Troponins are proteins that exist in skeletal and cardiac muscle. Cardiac
specific troponins (T&I) are specific for cardiac injury, nearly always
normal in noncardiac muscle diseases, elevate sooner and remain elevated
longer than CK-MB. Elevate 3 hours after injury remain elevated for 7-14
days Troponins are drawn to evaluate unstable angina, reperfusion, estimate
MI size, detect periooperative MI, severity of pulmonary emboli
Myoglobin (N) < mcg/L Used in early detection of suspected acute MI. Myoglobin is a oxygen-
binding protein found in cardiac and skeletal muscle. Increased levels
indicate cardiac muscle injury or death within 3 hours. More sensitive than
CK-MB but not as specific. Trauma, inflammation, or ischemic changes to
noncardiac skeletal muscle can also elevate myglobin
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
D-dimer (N) < mcg/ml Identifies intravascular clotting. D-dimer assesses both thrombin and
plasmin activity. As plasmin acts on the fibrin clot, degradation products
and d-dimer is produced. Normal plasma does not have fragment d-dimer.
Used to diagnose DIC. High levels can also indicate DVT, pulmonary
emboli, SSA, thrombosis of malignancy. D-dimer can be used to determine
duration of anticoagulation therapy in patients with DVT
CRP (N) < mg/dl An acute-phase reactive protein used to indicate an inflammatory illness,
C-Reactive Protein Cardiac risk: bacterial infections, and is believed to be of value in predicting coronary
events. It will elevate with tissue necrosis. Elevated values indicate
 Low < presence of, but not cause of, disease. With MI, CRP correlates with peak
 Average levels of the CK-MB, but 18-72 hours later. Levels do not elevate with
 High > angina.

Atheromatous plaques in diseased arteries contain inflammatory cells.

CBC:
RBC The calculation of the RBCs per cubic millimeter. The RBC (erthyrocyte) is
the major carrier of hemoglobin and thus carrier of oxygen to cells and
carbon dioxide to the lungs for excretion. The average RBC has a life of
120 days and must be constantly replaced by new erythrocytes made by
bone marrow. Alterations to normal levels can be caused by blood loss,
destruction of RBCs, failure of the bone marrow to make new RBCs, and
suppression of erythropoiesis by other diseases such as renal disease.
Elevated levels are found with burns, chronic hypoxia, COPD,
dehydration, high altitude, polycythemia vera, pulmonary fibrosis, sickle
cell disease, thalassemia. Decreased levels are found with bone marrow
suppression, chemotherapy, chronic inflammation or infection, hemolytic
anemia, hemorrhage, Hodgkin’s disease, leukemia, multiple myeloma,
hemodilation, systemic lupus erythematosus and vit B6 B12 or folic acid
deficiency.
Hematocrit % of RBC mass to original blood volume. Losing blood from whatever
cause will causes hematocrit levels to decrease. Monitors blood loss,
diagnoses suspected anemia and monitors treatment of anemia.
Hemoglobin and hematocrit are often obtained together to evaluate a wide
variety of hematological disorders. Severe increased levels could indicate
life-threatening crises such as hemoconcentration (evidenced by decreased
pulse pressure, tachycardia, thirst, and weakness) or a polycythemia
overtransfusion (with symptoms of extremity pain or redness, facial
flushing, irritability). Severely decreased levels could also indicate life-
threatening crises such as hemodilution or blood loss (could exhibit clinical
manifestations of hemorrhagic shock).
Hemoglobin The main intracellular protein of erthyrocytes, it is the oxygen carrying
compound contained in RBCs. See hematocrit.
WBC: The body fights infection by using WBCs, or leukocytes. They encapsulate
organisms and destroy them. WBCs >10,000 cell/mm3 may indicate
leukemia, trauma, or tissue injury, infection from mot bacteria, or death of
tissue (as with burns, MI, or gangrene). WBCs <5,000 cell/mm3 may
indicate bone marrow depression, viral infections, bone marrow disorders
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
(pernicious anemia, aplastic anemia), and iron deficiency anemia.
Neutrophils: Increased in burns, crushing injuries, diabetic acidosis, and infections;
decreased in bone marrow failure following antineoplastic chemotherapy or
radiation therapy or in agranulocytosis, dietary deficiencies, and
autoimmune diseases.
Platelet count Measures the number of platelet cells. Platelets are essential for
coagulation, hematasis, and clot formation. Platelets initiate the process of
hemostasis by aggregating quickly at the site of a damaged blood vessel
and adhere to the endothelium formation a platelet cot to plug the opening.
A high platelet count reflects the potential for serious clinical concerns. A
platelet count below 30,000 places the client at a high risk for bleeding
and a level above 1,000,000 indicates a high risk for thrombosis. Elevated
levels are found with living in high altitudes, exercising extensively over
several months or living in chronically cold environments, anemias (post
hemorrhagic, iron deficiency), carcinomatosis, chronic heart disease,
cirrhosis, leukemia (chronic), pancreatitis (chronic), polycythemia vera,
post surgery, chlild birth, trauma and hemorrhage, spleenectomy, and TB.
Decreased plate counts are found with anemias (aplitic, pernicious),
antibody/ HLA antigen reactions, bone marrow malignancies, burns
(severe), chronic cor pulmonale, disseminated intravascular coagulation,
infections (Rocky Mountain spotted fever, meningococcemia, idiopathic
thrombocytopenia purpura), hemolytic disease of the newborn, leukemias
(acute), lymphomas, and spleenomegaly (in liver disease).
Coagulation tests: Identify drugs that this patient is on that might affect these levels.
aPTT (N) 25-35 sec Indicator of the effectiveness of anticoagulant therapy and a screening test
(T) 46-70 for bleeding tendencies and identifies deficiencies in most of the intrinsic
and final common clotting pathways. Often ordered with APTT b/c if both
(C) >70
are prolonged, the pathology is the final common clotting pathway (factors
I, II, V, X), while if only the APTT is prolonged the abnormality is related
to the extrinsic pathway (factors VIII, IX, X, XI, XII). Actual process of
testing PTT involves determining the length of time it takes for a fibrin clot
to form. The APTT involves the addition of an activator that speeds up the
clotting time and results in a narrower range of normal. APTT is usually
the test of choice when monitoring effectiveness of Heparin.
PTT (N) See above
(T)
(C)

PT/ INR PT (N) 11-12.5 The coagulation test that measures the time it take to form a firm fibrin clot
(N) INR 0.75- after thromboplastin (factor III) and calcium are added to the serum sample.
1.25 PT evaluates the extrinsic pathway of coagulation, specifically the
activation of factor X by prothrombin, factor III, and calcium. Prothrombin
(T) INR= 2-3
is a vit K dependent protein produced by the liver. The PT is also
expressed in terms of INR using standard thromboplastin reagents. Using
both the PT and INR, the clinician can make decisions regarding the
appropriate dosage of warfarin/ coumadin for oral coagulation therapy.
However, INR is not accurate in clients with liver disease. Differentiates
b/t clients with factor V, VII, and X deficiencies, which alter the PT, and
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
those with hemophilia A and B, which do not alter the PT. Elevated levels
are found in liver disease, severe bone marrow depression, collagen
disease, cancer, DIC, chronic pancreatitis, and toxic shock syndrome.
Decreased levels are found in pulmonary embolus, thrombophlebitis, MI,
and multiple myeloma.
Indication Preferred INR
DVT prophylaxis 1.5-3
Orthopedic surgery 2-3
DVT 2-3
Atrial Fibrillation 2-3
Pulmonary Emboli 2.5-3.5
Prosthetic Valve prophylaxis 3-4
Activated Clotting (N) 70-120 Measures the effect of heparin as an anticoagulant during cardiac
Time (ACT) seconds angioplasty, hemodialysis, and cardiopulmonary bypass surgery. Measures
(T) 150-210 sec the time for whole blood to clot after the addition of particulate activators.
Also helps determine appropriate dose of protamine sulfate to reverse effect
of heparin
Anti-factor Xa
Drug therapeutic
levels:
Digoxin
Theophyllin
Dilantin

Peak and Trough levels:

Urinalysis: Excessive concentration of bases in the body fluids leads to alkalosis.

Color
Clarity
Specific gravity
pH
leukocyte esterase
protein
glucose
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient
ketone
bile
blood
nitrate
WBC
RBC
Epithelial cells
Bacteria
urolbilinogen

Misc labs
Serum osmolality

Urine osmolality

Respiratory/
metabolic: ABGs

pH
CO2 (resp)
HCO3 (metabolic)
PO2 =
O2 sat =
O2 content =
_______% arterial
_______% venous

Imaging Studies
 Normal values
Test Interpretation/Analysis **
Critical Values
If abnormal, describe possible reasons for this patient