Cardiac Enzymes: Normal Creatine Kinase: 1 to 130U/L
These are enzymes that are found in heart tissue that are released and serve as catalysts for the heart’s
various biochemical reactions. They will appear in serum as a result of myocardial injury (usually
ischemia). Initial panel includes serum lactate dehydrogenase (LDH), serum glutamicoxaloacetic
transaminase (SGOT), and creatine kinase (CK). Key cardiac enzymes are Troponin and Creatine
Phosphokinase (CPK).
Troponin: Normal Troponin: <0.1 ng/mL to 3.1 ng/mL
It has become the standard of care for diagnosis myocardial injury (MI). These are cardiac regulatory
proteins that are involved in calcium-mediated interaction of actin and myosin in cardiac muscle.
Controls how the heart muscle will respond to the signal received to contract and regulates force that it
will contract. Cardiac troponins begin to rise 2 to 3 hours after an acute MI, peak by 14 to 20 hours, and
return to baseline within 5 to 10 days. It is considered the most accurate cardiac enzyme test in the
diagnosis of a MI.
Brain Natriuretic Peptide (BNP): Values: Elevated in mild heart failure; 600 to 900 pg/mL in moderate
heart failure; >900 pg/mL in severe heart failure
BNP is a natriuretic hormone that increases discharge of sodium through urine, and decreases systemic
vascular resistance and central venous pressure. These actions lead to a decrease in cardiac output and
in blood volume. It helps differentiate between dyspnea due to heart failure from pulmonary disease.
They are elevated in both systolic and diastolic heart failure. It is a useful guide to therapy in and
prognostication of heart failure, acute coronary syndrome and stable angina. Levels tend to be higher in
people with renal failure and older people and lower in obese and in women. According to the textbook
it is elevated in mild heart failure: 600 to 900 pg/mL in moderate heart failure and > 900 pg/mL in
severe heart failure.
C-Reactive Protein (CRP): Normal: <8 mg/L
CRP is a non-specific marker of acute inflammation produced by liver and adipocytes. Levels are
elevated in infection and several long-term diseases, including cancer, rheumatologic disease such as
lupus, rheumatoid arthritis and giant cell arteritis, inflammatory bowel disease and osteomyelitis.
Elevations from baseline within normal range as well as above normal are predictive of risk for MI,
stroke, peripheral vascular disease and sudden cardiac death.
Procalcitonin:
Procalcitonin maybe a more useful marker for distinguishing bacterial infections from aseptic
inflammation than CRP. Precursor protein of calcitonin. Helps to distinguish inflammation caused
secondary to bacterial or fungal infection from viral or other aseptic inflammatory conditions. Low levels
represent low risk of sepsis and may be due to viral infection. High levels high probability of sepsis that
is bacterial cause.
Hemoglobin and Hematocrit-Normal hemoglobin levels for men is 13.5 to 15.5 g/dL and for women is 12.5to 14.5 g/dL.
Normal hematocrit for men is 42% to 52% and for women is 37% to 48%. It is a proportion of whole
blood that is composed of RBCs (hemoglobin carrying cell).
Hemoglobin is an iron-containing globular protein consisting of 2 pairs of polypeptides. Its primary
function is transporting oxygen from the lungs to tissues. A high level can be due to: chronic hypoxia;
hematologic disease (i.e., polycythemia vera); dehydration; or hemoconcentration.
Abnormal hemoglobin and hematocrit levels from iron in ferric form of methemoglobinemia,
abnormalities in polypeptide chain such as hemoglobinopathies such as thalassemias and sickle cell
disease.
Decreased hemoglobin production can be caused by bone marrow problems such as aplastic anemia,
myelosuppressive drugs, idiosyncratic reaction to drugs, or infiltration of bone marrow by other cells.
Other decreased production problems can be caused by deficiencies in iron, vitamin B12 cofactors and
erthropoitin. Other causes are malignancy, chronic disease, hypothyroidism and hypopituitarism.
Another cause for low hemoglobin and hematocrit levels can be increased loss or breakdown of red
blood cells (RBCs): the fault of RBCs from membrane defects, enzymatic deficiencies, or hemoglobin
disorders; acquired causes of hemolysis such as drugs, toxins, or infections; hypersplenism; or bleeding.
Blood Urea NitrogenNormal blood urea nitrogen (BUN) is 7 to 21 mg/dL. It is the most common nonprotein nitrogenous
compound in the blood and used to assess renal function in adult. It is indicative of the body’s ability to
clear nitrogenous wastes in the form of urea (breakdown product of amino acids) in urine. It reflects
protein intake and metabolism as well as glomerular and proximal tubule function in the kidney.
An increased BUN can be caused by gastrointestinal protein absorption from dietary factors or heme in
bowels (i.e., gastrointestinal bleeding).
A decreased can be from decreases in protein intake or liver impairment.
Magnesium-Normal magnesium level is 0.7 to 1.1 mmol/L (1.8 to 3.0 mg/mL). It is the other major cation besides
Calcium. It helps maintain membrane potentials at cellular level and maintains potassium hemostasis.
1% to 2% of magnesium is in the serum.
Hypomagnesaemia (low magnesium) is associated with hyponatremia, hypocalcemia and
hypophosphatemia. Symptoms include: tremulousness; hyperreflexia; ataxia; convulsions; and death
and dysphagia. An EKG will reveal a rapid polymorphic ventricular tachycardia (torsades de pointes). It
can cause atria or ventricle dysrhythmias. It is due to absorption problems from malnutrition per se or
due to alcoholism, diarrhea, intravenous alimentation, or intestinal bypass surgery. Psychological
problems: bulimia; laxative abuse; and aggressive weight reduction. Another cause of absorption
problems are short bowel syndrome or malignancies, especially in bowel. It can be due to excessive loss
in urine from: use and abuse of diuretics; postobstructive diuresis; acute tubular necrosis;
hypercalcemia; or hereditary renal magnesium wasting. Then there are miscellaneous causes such as:
association with hyperaldosteronism, diabetic ketoacidosis, and excessive lactation; exchange
transfusions; or acute intermittent porphyria.
Hypermagnesemia (high magnesium) is uncommon but symptoms include: hyporeflexia; muscle
weakness; hypotension; bradycardia; coma; and death. Causes of hypermagnesemia are renal failure
and abuse of magnesium-based laxatives. It can be induced to treat eclampsia.
Lactate-Normal lactate value is less than 2 mmol/L. Anion of lactic acid most commonly formed in ischemic cells
due to a consequence of anaerobic glycolysis and the use of pyruvate for generation It is used to
indicate severity of shock and provides rough idea of tissue perfusion, oxygen delivery and oxygen use.
A high lactate level is associated with increased mortality in a patient in shock and bowel ischemia. A
low lactate level can be due to anaerobic metabolism or reduced degradation of lactate due to the liver.
Glucose-Normal glucose level is 70 to 110 mg/dL. Glucose is influenced by nutritional, liver, hormonal, and
pancreatic factors. Glucagon and adrenal steroid increase glucose via liver breakdown of stored
glycogen. Insulin is produced by islet cells in pancreas and critical for transfer of glucose into cells.
There are two types of diabetes which is high glucose levels (hyperglycemia).
Type I diabetes: is from a pancreatic injury or islet cell dysfunction. It impairs insulin production and
results in serum hyperglycemia.
Severe hyperglycemia will cause diabetic ketoacidosis and if untreated or high enough hyperosmolar
state with coma.
Type 2 diabetes is from cellular resistance to insulin. It can produce hyperglycemia and deranged
glucose metabolism.
Hypoglycemia (low glucose) can be due to: insulin-secreting tumors; exogenous insulin overdoses;
severe liver injury due to depletion or failure to metabolize liver glycogen. It can cause severe--coma
and death.
PT: It is used to evaluate ability of blood to clot—how likely is the patient to have a bleeding or clotting
problem during or after surgery. It evaluates extrinsic pathway, which includes tissue factor, factor VII,
and coagulation factors in common pathway (prothrombin, V, X, and Fibrinogen). It is often used to
monitor anticoagulation in patients using Coumadin, which acts on these factors.
aPTT: It is used to assess intrinsic clotting pathway and to evaluate if heparin therapy is effective, and to
detect presence of clotting disorder. Extended times can be due to anticoagulation therapy, lupus, liver
problems, hematologic disorders, toxins or drugs, or disseminated intravascular coagulation associated
with multiorgan failure syndrome.
Some invasive procedures you may not want blood to clot as quickly as normal and other times some
patients may not clot fast enough, either way you would want to be aware of these issues so you could
address them before surgery and avoid complications during surgery and after.