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126 PA R T I I / Physiologic and Pathologic Responses
Clinical Manifestations of 5. Feigl, E. O. (1989). Coronary autoregulation. Journal of Hypertension
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Myocardial Infarction 6. Opie, L. H. (1989). Reperfusion injury and its pharmacologic modifi-
cation. Circulation, 80, 1049–1062.
Acute myocardial infarction or acute coronary syndrome may 7. Hackam, D. G., & Anand, S. S. (2003). Emerging risk factors for ath-
present with a sudden onset of severe chest, jaw, back, or arm pain erosclerotic vascular disease: A critical review of the evidence. Journal of
or pressure. The pain is described as heavy, crushing, and like a the American Medical Association, 290, 932–940.
tight squeeze or elephant on the chest. Sometimes the pain will ra- 8. Braunwald, E., & Kloner, R. A. (1985). Myocardial reperfusion: A double-
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edged sword? Journal of Clinical Investigations, 76, 1713–1719.
diate to the shoulder, neck, and jaw and may be associated with 9. Cohen, M. V. (1978). The functional value of coronary collaterals in
symptoms of fatigue, lightheadedness, nausea, shortness of breath, myocardial ischemia and therapeutic approach to enhance collateral
or diaphoresis. At least 40% to 50% of individuals do not experi- flow. American Heart Journal, 95, 396–404.
ence pain, especially in diabetic individuals or older adults. 25,54 10. Corti, R., Fuster, V., & Badimon, J. J. (2003). Pathogenetic concepts of
Some patients may have unrelenting gastric distress. Peripheral acute coronary syndromes. Journal of the American College of Cardiology,
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vasoconstriction may cause cool, clammy skin. Sometimes a low- 11. Davies, M. J., & Thomas, A. (1984). Thrombosis and acute coronary-
grade fever may result from the inflammatory response within the artery lesions in sudden cardiac ischemic death. New England Journal of
myocardium. Medicine, 310, 1137–1140.
The extent of complications after a myocardial infarction de- 12. Falk, E., Shah, P. K., & Fuster, V. (1995). Coronary plaque disruption.
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pends on the location and extent of necrosis and ischemia, the 13. Houston, D. S., Shepherd, J. T., & Vanhoutte, P. M. (1986). Aggregat-
physiologic status of the patient before the event, and timing and ing human platelets cause direct contraction and endothelium-depend-
availability of therapeutic interventions. Myocardial infarction ent relaxation of isolated canine coronary arteries. Role of serotonin,
can occur in the various regions of the heart muscle. An ECG is thromboxane A2, and adenine nucleotides. Journal of Clinical Investiga-
tions, 78, 539–544.
used in the diagnosis to localize the affected area. The zone of in- 14. Kullo, I. J., & Ding, K. (2007). Mechanisms of disease: The genetic ba-
farction and necrosis is surrounded the zone of hypoxia, which is sis of coronary heart disease. Nature Clinical Practice Cardiovascular
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silent and is not reflected on the ECG. Transmural infarctions re- 15. Lee, R. T., & Libby, P. (1997). The unstable atheroma. Arteriosclerosis,
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flect as a Q wave on the ECG in the region of infarction. Non- Thrombosis, and Vascular Biology, 17, 1859–1867.
transmural or non-Q (zone of hypoxia) wave infarctions do not 16. Braunwald, E. (2000). 50th anniversary historical article. Myocardial
oxygen consumption: the quest for its determinants and some clinical
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are reflected as ST-segment depression or T-wave inversions, or as 17. Mombouli, J. V., & Vanhoutte, P. M. (1999). Endothelial dysfunction:
nonspecific ST-T wave changes. See Chapter 18 for electrocardio- From physiology to therapy. Journal of Molecular and Cellular Cardiol-
graphic examples of myocardial infarction. ogy, 31, 61–74.
18. Gibson, C. M., Dotani, M. I., Murphy, S. A., et al. (2002). Correlates
of coronary blood flow before and after percutaneous coronary inter-
vention and their relationship to angiographic and clinical outcomes in
IMPLICATIONS FOR NURSES the RESTORE trial. Randomized Efficacy Study of Tirofiban for Out-
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comes and REstenosis. American Heart Journal, 144, 130–135.
19. Gorlin, R. (1982). Role of coronary vasospasm in the pathogenesis of
Acute coronary syndrome addresses both myocardial ischemia and myocardial ischemia and angina pectoris. American Heart Journal, 103,
myocardial infarction. Myocardial ischemia is a condition that re- 598–603.
sults from reduced supply of oxygen and nutrients to the my- 20. Lee, S. H., Wolf, P. L., Escudero R., et al. (2000). Early expression of an-
ocardium or increased demand of the myocardium for oxygen and giogenesis factors in acute myocardial ischemia and infarction. New Eng-
land Journal of Medicine, 342, 626–633.
nutrients. Myocardial infarction is a condition that results from an 21. Libby, P. (1995). Molecular bases of the acute coronary syndromes. Cir-
interruption in the normal coronary blood flow to the myocardium. culation, 91, 2844–2850.
Changes occur within seconds in the myocardium if ischemia 22. Libby, P. (2000). Changing concepts of atherogenesis. Journal of Inter-
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persists, including shifting from aerobic metabolism to anaerobic nal Medicine, 247, 349–358.
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metabolism through the glycolic pathway. Cell death occurs after 23. Raines, E. W., Dower, S. K., & Ross, R. (1989). Interleukin-1 mitogenic
20 minutes if coronary blood flow is not restored. Nurses play a activity for fibroblasts and smooth muscle cells is due to PDGF-AA.
Science, 243, 393–396.
very important role in identifying patients through careful history 24. Ross, R., Wight, T. N., Strandness, E., et al. (1984). Human atheroscle-
taking and identifying early signs and symptoms of ischemia. Early rosis. I. Cell constitution and characteristics of advanced lesions of the
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intervention of establishing and restoring coronary blood flow will superficial femoral artery. American Journal of Pathology, 114, 79–93.
salvage myocardium and save the patient short-term and long-term 25. Fuster, V., Badimon, L., Badimon, J. J., et al. (1992). The pathogenesis
of coronary artery disease and the acute coronary syndromes (2). New
postinfarction complications. Nurses can help patients identify risk England Journal of Medicine, 326, 310–318.
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factors that can be modified and promote positive outcomes and re- 26. Ross, R. (1999). Atherosclerosis—an inflammatory disease. New England
sponses to lead healthy and productive lives. Journal of Medicine, 340, 115–126.
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plaque caps are locally weakened when macrophages density is increased.
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