Page 275 - Cardiac Nursing

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C HAPTER 11 / Laboratory Tests Using Blood 251
evaluate the clinical signs and symptoms and other diagnostic depends on laboratory analysis of CK isoenzymes and may well
tests to ensure accurate diagnosis and treatment. be imperative in critically ill patients with multiple organ system
involvement.
Cardiac Enzymes Because of the wide range in baseline values among “healthy”
people, and various enzyme assay techniques, there are no uni-
Enzymes are protein substances that catalyze chemical reactions in form reference values for CK and CK isoenzymes. Consequently,
cells but do not themselves enter into the reaction. Substrates in the the practice of reporting the isoenzyme as a percentage of the to-
cells bind to the enzymes and form products. After the reaction, the tal CK, as well as in U/L has been encouraged.
enzyme molecule is free to undergo the same reaction with other
substrate molecules. Specific enzymes are responsible for nearly Creatine Kinase-BB. The brain fraction CK-BB (CK-1) is
every chemical reaction in the body. Some enzymes are present in seen infrequently in serum. Its rare appearance has been associated
almost all cells; others are specific to cells of certain organs. with brain trauma, cerebral contusions, and cerebrovascular acci-
dents. The presence of CK-BB in association with cancer has been
Creatine Kinase reported. Other causes of serum CK-BB activity include malignant
Creatine kinase is an enzyme specific to cells of the brain, my- hyperthermia, renal failure, and after central nervous system sur-
3
ocardium, and skeletal muscle, but also is found in minimal gery. With the significant improvement in diagnostic imaging
amounts in other tissues, such as smooth muscle. In these organ techniques, CK-BB is now rarely evaluated.
systems, the function of CK is primarily that of energy produc- Creatine Kinase-MM. CK-MM constitutes almost the en-
tion, where it serves as a catalyst in the phosphorylation of adeno- tire CK total in healthy people. Skeletal muscle injury or severe
sine diphosphate (ADP) to creatine and adenosine triphosphate muscle exertion is the most frequent source of high serum CK-
(ATP). In this manner, CK is responsible for the transfer of an MM (CK-3) levels. Specific examples include myopathy, vigorous
energy-rich bond to ADP. This reaction provides a rapid means of exercise, multiple intramuscular (IM) injections, electroconvulsive
forming ATP for contractile activity in muscle as well as for en- therapy, cardioversion, surgery, muscular dystrophy, convulsions,
ergy requirements in nonmuscle tissue. The reaction is reversible, and delirium tremens. Elevations in CK-MM fractions have also
and ATP can phosphorylate creatine to form creatine phosphate been noted in conditions producing less obvious effects on muscle,
and ADP during periods of rest. such as hypokalemia and hypothyroidism. 3
In an acute MI, inadequate oxygen delivery to the myocardium
causes cell injury. An acidic environment promotes the activity of Creatine Kinase-MB. Prior to the discovery of troponin,
lysosomal enzymes, which are responsible for cell membrane dam- CK-MB (CK-2) isoenzyme analysis had been an accepted means
age or destruction. CK is among the cellular enzymes that diffuse for diagnosis of an acute MI. Although troponin has superseded
from the damaged cell into the blood. CK is released after irre- CK-MB in the diagnosis of MI, most institutions continue to eval-
versible injury. The appearance of CK in the blood indicates uate CK, CK-MB, and troponin if MI is suspected.
cardiac, cerebral, or skeletal muscle necrosis or injury and follows When CK-MB is released from myocardial tissue, it has a bio-
a predictable rise and fall over a specified time (see Fig. 11-1). logic half-life in blood of hours-to-days. Total CK and CK-MB
Age, sex, race, physical activity, lean body mass, medications, rise within 2 to 8 hours after an acute MI. Peak levels are seen
and other unidentified factors are known to affect total CK. A pa- within 18 to 36 hours and are more than six times their normal
tient’s baseline CK level is related to his or her overall muscle value. If no additional myocyte necrosis occurs, levels return to
mass. Adults have lower values than children. Serum CK declines normal within 3 to 4 days. See Table 11-2 and Figure 11-1 for the
with age and older adults have very low values. CK values meas- typical appearance, peak, and disappearance of various biomark-
ured in women are lower than those of men; European Americans ers and enzymes.
have lower values than African Americans. Chronic exercise raises Elevated CK-MB levels have also been reported after myocar-
serum CK levels; however, there is a training effect, and well- dial damage from unstable angina, cardiac surgery, coronary an-
trained athletes have smaller increases in CK after physical exer- gioplasty, after defibrillation, in vigorous exercise, and after IM in-
tion. Medications that may increase CK include anticoagulants, jections, trauma, and surgery. Early and abnormally high increases
aspirin, furosemide, captopril, lidocaine, propranolol, and mor- in CK are sometimes seen after reperfusion by PCI or throm-
phine. In addition, high-intensity lipid-lowering therapy with bolytic agents. By 6 to 8 hours postangioplasty, 20% of patients
lipophilic statins (i.e., simvastatin or lovastatin) have been found have a mild increase in CK-MB. Elevations are occasionally seen
to increase CK. 33 Early and abnormally high increases in CK are in pericarditis, myocarditis, viral myositis, and sustained tach-
sometimes seen after reperfusion by PCI (Chapter 23) or throm- yarrhythmias. An increase in CK-MB may occur after cardiover-
bolytic agents. 2,3 sion, but that time course for increase is different for that of MI,
The importance of monitoring the concentration of serum with the mild increase of CK-MB peaking within 4 hours of car-
CK is related to its specificity in the organ in which it functions. dioversion.
Slightly different molecular forms (isoenzymes or isozymes) of CK Specimens for CK and CK-MB are collected on admission and
have different tissues of origin. The three CK isoenzymes are 8 to 12 hours later. CK and CK isoenzyme results should be eval-
combinations of the protein subunits, named for their primary uated along with troponin, myoglobin, ECG results, and clinical
sites of isolation—the muscle (M) and brain (B). CK-MM is the signs and symptoms for the detection of MI. Laboratory slips
predominant muscle isoenzyme, found in cardiac and skeletal should be marked with the date and time of any IM injections
muscle. It also can be detected in normal serum. The my- given to the patient in the prior 24 to 48 hours.
ocardium is primarily responsible for the CK-MB form. CK-BB Caution should be exercised in interpretation of CKs drawn in
is present in the brain, lung, stomach, prostate, and smooth mus- the emergency department. Only 25% to 40% of patients who are
cle of the gastrointestinal tract and bladder. Diagnostic precision having an MI have an abnormal CK at that point. An initial