tests and procedures are used to confirm the data ob-tained by history and
physical assessment. Some tests are easy to interpret, but others must be
interpreted by expert clinicians. All tests should be explained to the patient.
Some necessitate special preparation before they are performed and special
monitoring by the nurse after the procedure.
tests may be performed for the following reasons:
To assist in diagnosing an acute MI.
(Angina pectoris, chest pain resulting from an insufficient supply of blood to
the heart, cannot be confirmed by either blood or urine studies.)
To identify abnormalities in the
blood that affect the prog-nosis of a patient with a cardiac condition
To assess the degree of inflammation
To screen for risk factors
associated with atherosclerotic coronary artery disease
To determine baseline values before
performing therapeu-tic interventions
To monitor serum levels of
To assess the effects of medications
(e.g., the effects of diuretics on serum potassium levels)
To screen generally for
different laboratories use different equipment and dif-ferent methods of
measurements, normal test values may vary de-pending on the laboratory and the
health care institution.
cardiac enzyme analysis is part of a diagnostic profile that also includes the
health history, symptoms, and electrocardio-gram (ECG), associated with acute
MI. Enzymes are released from injured cells when the cell membranes rupture.
Most en-zymes are nonspecific in relation to the particular organ that has been
damaged. Certain isoenzymes, however, come only from myocardial cells and are released
when the cells are damaged, such as by sustained hypoxia resulting in
infarction or by trauma. The isoenzymes leak into the interstitial spaces of
the myocardium and are carried into the general circulation by the lymphatic
sys-tem and the coronary circulation, resulting in elevated serum en-zyme
different enzymes move into the blood at varying pe-riods after MI, enzyme
levels should be tested in relation to the time of onset of chest discomfort or
other symptoms. Creatine ki-nase (CK) and its isoenzyme CK-MB are the most
specific en-zymes analyzed in acute MI, and they are the first enzyme levels to
rise. Lactic dehydrogenase and its isoenzymes also are analyzed in patients who
have delayed seeking medical attention, because these blood levels rise and
peak in 2 to 3 days, much later than CK levels.
an early marker of MI, is a heme protein with a small molecular weight. This
allows it to be rapidly released from damaged myocardial tissue and accounts
for its early rise, within 1 to 3 hours after the onset of an acute MI.
Myoglobin peaks in 4 to 12 hours and returns to normal in 24 hours. Myoglobin
is not used alone to diagnose MI, because elevations can also occur in patients
with renal or musculoskeletal disease. However, neg-ative results are helpful
in ruling out an early diagnosis of MI.
I is measured in a laboratory test that has several ad-vantages over
traditional enzyme studies. Troponin I is a con-tractile protein found only in
cardiac muscle. After myocardial injury, elevated serum troponin I
concentrations can be detected within 3 to 4 hours; they peak in 4 to 24 hours
and remain ele-vated for 1 to 3 weeks. These early and prolonged elevations
make very early diagnosis of MI possible or allow for late diagnosis if the
patient has delayed seeking treatment.
triglycerides, and lipoproteins are measured to eval-uate a person’s risk for
developing atherosclerotic disease, espe-cially if there is a family history of
premature heart disease, or to diagnose a specific lipoprotein abnormality.
Cholesterol and triglycerides are transported in the blood by combining with
pro-tein molecules to form lipoproteins. The lipoproteins are referred to as
low-density lipoproteins (LDL) and high-density lipopro-teins (HDL). The risk
of CAD increases as the ratio of LDL to HDL or the ratio of total cholesterol
HDL) to HDL in-creases. Although cholesterol levels remain relatively constant
over 24 hours, the blood specimen for the lipid profile should be obtained
after a 12-hour fast.
(normal level, less than 200 mg/dL) is a lipid re-quired for hormone synthesis
and cell membrane formation. It is found in large quantities in brain and nerve
tissue. Two major sources of cholesterol are diet (animal products) and the
liver, where cholesterol is synthesized. Elevated cholesterol levels are known
to increase the risk for CAD. Factors that contribute to variations in
cholesterol levels include age, gender, diet, exercise patterns, genetics,
menopause, tobacco use, and stress levels.
(normal level, less than 130 mg/dL) are the primary transporters of cholesterol
and triglycerides into the cell. One harmful effect of LDL is the deposition of
these substances in the walls of arterial vessels. Elevated LDL levels are
associated with a greater incidence of CAD. In people with known CAD or
dia-betes, the primary goal for lipid management is reduction of LDL levels to
less than 100 mg/dL.
(normal range in men, 35 to 65 mg/dL; in women, 35 to 85 mg/dL) have a
protective action. They transport cholesterol away from the tissue and cells of
the arterial wall to the liver for excretion. Therefore, there is an inverse
relationship between HDL levels and risk for CAD. Factors that lower HDL levels
in-clude smoking, diabetes, obesity, and physical inactivity. In pa-tients with
CAD, a secondary goal of lipid management is the increase of HDL levels to more
than 40 mg/dL.
(normal range, 40 to 150 mg/dL), composed of free fatty acids and glycerol, are
stored in the adipose tissue and are a source of energy. Triglyceride levels
increase after meals and are affected by stress. Diabetes, alcohol use, and
obesity can ele-vate triglyceride levels. These levels have a direct
correlation with LDL and an inverse one with HDL.
potassium, and calcium are ions that are vital to cellular depolarization and
repolarization. In addition, the serum sodium concentration reflects relative
fluid balance. Generally, hypona-tremia (low sodium level) indicates fluid
excess, and hyperna-tremia (high sodium level) indicates fluid deficit.
potassium is affected by renal function and may be de-creased by diuretic
agents that are used to treat HF. A decrease in potassium causes cardiac
irritability and predisposes the patient receiving a digitalis preparation to
digitalis toxicity and dys-rhythmias. The effect of an elevated serum potassium
concentra-tion is myocardial depression and ventricular irritability. Both
hypokalemia and hyperkalemia can lead to ventricular fibrillation or cardiac
standstill. Calcium is necessary for blood coagulability and neuromuscular
activity. Hypocalcemia and hypercalcemia can cause dysrhythmias.
is integral to the absorption of calcium and the maintenance of potassium
stores. It is required in the metabolism of adenosine triphosphate, playing a
major role in protein syn-thesis, carbohydrate metabolism, and muscular
contraction. Ini-tial symptoms of hypermagnesemia are lethargy and decreased
neuromuscular activity. On the ECG, hypomagnesemia length-ens the QT interval,
predisposing the patient to life-threatening dysrhythmias.
urea nitrogen (BUN) is an end product of protein metab-olism and is excreted by
the kidneys. In the patient with cardiac disease, an elevated BUN level may
reflect reduced renal perfu-sion (from decreased cardiac output) or
intravascular fluid vol-ume deficit (from diuretic therapy or dehydration). The
cause of elevated BUN is determined from the serum creatinine: high BUN and
high creatinine reflect renal impairment, high BUN and normal creatinine
reflect intravascular fluid volume deficit.
serum glucose level is important to monitor, because many patients with cardiac
disease also have diabetes mellitus. In addition, the serum glucose level may
be mildly elevated in stressful situations, when mobilization of endogenous
epinephrine results in conversion of liver glycogen to glucose. Serum glucose
levels are drawn in a fasting state. Glycosylated hemoglobin is an im-portant
measure to monitor in people with diabetes, because it reflects the blood
glucose levels over 2 to 3 months. Hemoglobin A1C
is the common name for this test. The goal of diabetes man-agement is to
maintain the hemoglobin A1C below 7%
(normal range 4%–6%), reflecting consistent near-normal blood glucose levels.
This is particularly important for primary and secondary prevention of CVD
(Brundy et al., 2002; Smith et al., 2001).
formation of a thrombus is initiated by injury to a vessel wall or to the
tissue. These events activate the coagulation cascade, a complex series of
interactions among phospholipids, calcium, and various clotting factors that
converts prothrombin to throm-bin. The coagulation cascade has two pathways,
the intrinsic pathway and the extrinsic pathway. Coagulation studies are
rou-tinely performed before invasive procedures, such as cardiac catheterization,
electrophysiology testing, and coronary or car-diac surgery.
thromboplastin time (PTT) and activated partial thromboplastin time (aPTT)
measure the activity of the intrinsic pathway. The values of PTT and aPTT are
used to assess the ef-fects of heparin therapy. Patients receiving heparin have
their PTT or aPTT levels maintained at 1.5 to 2.5 times their baseline values
(reference range, 25 to 38 seconds). Prothrombin time (PT) measures the
extrinsic pathway activity and is used to mon-itor the effects of therapeutic
anticoagulation with warfarin (Coumadin). Laboratory results of PT also include
the Interna-tional Normalized Ratio
(INR). The INR provides a standardmethod for reporting PT levels,
eliminating the variation of PT results from laboratory to laboratory. The INR,
rather than the PT alone, is used to monitor patients receiving warfarin
therapy. The INR is maintained between 2.0 and 3.0 for patients with deep vein
thrombosis, pulmonary embolism, valvular heart dis-ease, or atrial fibrillation,
and between 2.5 and 3.5 for patients with mechanical prosthetic heart valve
complete blood cell count (CBC) identifies the total num-ber of white and red
blood cells, the platelet count, and the he-moglobin and hematocrit. The CBC is
carefully monitored in patients with CVD. White blood cell counts are monitored
in immunocompromised patients, including patients with trans-planted hearts,
and in situations where there is concern for infec-tion (eg, after invasive procedures
or surgery). The red blood cells carry hemoglobin, which transports oxygen to
the cells. The hematocrit is a measure of the relative proportion of red blood
cells and plasma. Low hemoglobin and hematocrit levels have se-rious
consequences for patients with CAD, such as more frequent angina episodes.
Platelets are the first line of protection against bleeding. Once activated by
blood vessel wall injury or rupture of atherosclerotic plaque, platelets
undergo chemical changes that form a thrombus. Patients are prescribed
medications to inhibit platelet function, including aspirin, clopidogrel
(Plavix), and intra-venous GP IIb/IIIa inhibitors (abciximab [ReoPro],
eptifibatide [Integrilin], tirofiban [Aggrastat]); therefore, it is essential
to mon-itor for thrombocytopenia (low platelet counts).