Creatine phosphokinase (CPK), also called creatine kinase (CK), catalyzes the reversible exchange of phosphate between creatine and adenotriphosphate (ATP). Important in intracellular storage and release of energy, CPK exists almost exclusively in skeletal muscle, heart muscle, and, to a lesser extent, brain. No CPK is found in the liver. Anything that damages skeletal or cardiac muscle elevates serum CPK levels. Brain injury affects serum CPK levels much less, probably because relatively little enzyme crosses the blood-brain barrier.

Spectacular CPK elevations occur in the early phases of muscular dystrophy, but CPK elevation diminishes as the disease progresses and muscle mass decreases. Levels of CPK may be normal to low in late, severe cases. Additional causes of elevated CPK, and the magnitude of those elevations, are listed in Table 5-20.

The CPK molecule consists of two parts, which may be identical or dissimilar. These two constituent chains are called M (muscle) and B (brain). Three diagnostically significant isoenzymes have been identified in relation to the two main components of CPK. Brain CPK (CPK-BB, CPK₁) is almost entirely BB, cardiac CPK (CPK-MB, CPK₂) contains 60 percent MM and 40 percent MB, and skeletal muscle CPK (CPK-MM, CPK₃) contains about 90 percent MM and 10 percent MB. The isoenzyme normally present in serum is almost entirely MM, and only CPK-MM (CPK₃) rises when skeletal muscle is damaged. In contrast, serum CPK-MB (CPK₂) rises only when heart muscle is damaged.

Drugs that may produce elevated CPK levels include anticoagulants, morphine, alcohol, salicylates in high doses, amphotericin-B, clofibrate, and certain anesthetics. Any medication administered intramuscularly (IM) also elevates CPK. In addition to late muscular dystrophy, decreased levels are seen in early pregnancy.

Myoglobin is an oxygen-carrying protein normally found in cardiac and skeletal muscle. In acute myocardial infarction (AMI), myoglobin levels rise within 1 hour. Although myoglobin alone is not particularly sensitive to cardiac damage, in conjunction with CPK-MB it has a diagnostic capability approaching 100 percent in correctly identifying AMI.²⁹ See Table 5-21.

• Vigorous exercise, deep intramuscular (IM) injections, delirium tremens, and surgical procedures in which muscle is transected or compressed may produce elevated levels.
• Drugs that may produce elevated CPK levels include anticoagulants, morphine, alcohol, salicylates in high doses, amphotericin-B, clofibrate, and certain anesthetics.
• Early pregnancy may produce decreased levels.

• Signs and symptoms of acute myocardial infarction:
  • Acute myocardial infarction releases CPK into the serum within the first 48 hours, and values return to normal in about 3 days.
  • CPK levels rise before aspartate aminotransferase and lactic dehydrogenase levels rise.
  • The isoenzyme CPK-MB (CPK₂) rises only when the heart muscle is damaged; it appears in the first 6 to 24 hours and is usually gone in 72 hours.
  • Both total CPK and MB fraction may rise in severe angina or extensive reversible ischemic damage.³⁰
  • Recurrent elevation of CPK suggests reinfarction or extension of ischemic damage.
  • An elevated CPK level helps to differentiate myocardial infarction from CHF and conditions associated with liver damage.
• Family history of Duchenne's muscular dystrophy:
  • Spectacular CPK elevations occur in the early phases of muscular dystrophy, even before clinical signs or symptoms appear.
  • CPK elevation diminishes as the disease progresses and muscle mass decreases.
• Signs and symptoms of other disorders associated with elevated CPK levels (see Table 5-20)

Nursing Care Before the Procedure

Client preparation is the same as that for any test involving the collection of a peripheral blood sample (see Appendix I).

• It is recommended that any drugs that may alter test results be withheld for 12 to 24 hours before the test, although this practice should be confirmed with the person ordering the study.
• Vigorous exercise and IM injections also should be avoided for 24 hours before the test.

A venipuncture is performed and the sample collected in a red-topped tube. The sample should be handled gently to avoid hemolysis and transported promptly to the laboratory.

Nursing Care After the Procedure

Care and assessment after the procedure are the same as those for any study involving the collection of a peripheral blood sample.

• Resume any drugs withheld before the test, as well as usual activities.
• Abnormal values: Note and report increased levels of CPK, CPK-MB, lactic dehydrogenase (in relation to myocardial infarction), and CPK-MM (in relation to muscular dystrophy). Monitor vital signs. Monitor ECG for dysrhythmias. Monitor for fluid overload (distended neck veins, dyspnea, crackles on auscultation). Repeat ordered CPK and lactic dehydrogenase enzyme and isoenzyme tests.