Diagnostic 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.
Laboratory 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 medications
· To assess the effects of medications (e.g., the effects of diuretics on serum potassium levels)
· To screen generally for abnormalities
Because 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.
Plasma 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 concentrations.
Because 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.
Myoglobin, 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.
Troponin 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.
Cholesterol, 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 (LDL + 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.
Cholesterol (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.
LDLs (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.
HDLs (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.
Triglycerides (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.
Sodium, 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.
Serum 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.
Magnesium 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.
Blood 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.
The 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).
The 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.
Partial 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 replacements.
The 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).
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