Page 148 - Cardiac Nursing

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124 PA R T I I / Physiologic and Pathologic Responses
The electrocardiographic findings with myocardial ischemia or depression. 174,248,249 In addition, patients qualify under the
result from cellular changes. These changes may be reflected as definition of myocardial infarction if they have any pathological
ST-segment depression or T-wave inversion. Two conditions, findings of myocardial necrosis.
Prinzmetal angina resulting from coronary artery spasm and peri-
carditis, are associated with ST-segment elevation. Refer to Chap- Cellular Mechanisms and Events
ter 15 for electrocardiographic examples of ischemic changes.
Caused by Myocardial Infarction
Clinical Manifestations of Prolonged ischemia of more than 30 minutes will cause irre-
Myocardial Ischemia versible cellular damage of the myocardium and is termed my-
ocardial infarction. 3,41 Sudden occlusion of a coronary artery
Angina pectoris is the clinical description of chest pain or pressure leads to an ischemic zone with potentially viable tissue that sur-
that results from myocardial ischemia. Some patients describe a sen- rounds this zone. The size of this ischemic zone and the degree of
sation of heaviness, tightness, or pressure to severe, clutching, grip- blood flow within the area depends on the anatomy of the coro-
like pain. The pain or discomfort may be localized or radiate to the nary circulation and the area of occlusion within the blood vessel.
shoulder, neck, jaw, or right or left arms. Associated symptoms in- Collateral vessels, which form anastomoses or connections be-
clude lightheadedness, dyspnea, diaphoresis, and fatigue. Anginal tween major coronary branches, develop in some patients with
9
pain is probably caused by extracellular accumulation of substances long-standing atherosclerosis. When a coronary branch is oc-
in the area of ischemia. 53 These substances include adenosine, cluded, pressure changes occur in neighboring arteries that cause
potassium, lactic acid, and bradykinin. Abnormal stretching of the rapid recruitment of these collateral vessels to minimize this in-
myocardium irritates afferent nerve fibers of the heart. Afferent farct zone. Ischemia is a major stimulus for angiogenesis, the
nerve fibers that enter the spinal column from levels C3 to T4 ac- growth of new capillaries. 20 This revascularization occurs mainly
count for the variety of locations and radiation patterns. 247 by sprouting or intussusception. Many cytokines stimulate en-
There are three types of angina, including stable angina, unsta- dothelial and smooth muscle cell proliferation with the migration
ble angina, and Prinzmetal angina. 236 Stable angina is a condition or recruitment of activated monocytes. 12 Once coronary blood
in which there is chronic stable stenosis of one or more coronary ar- flow is interrupted and the delivery of nutrients to the my-
teries that are inefficient in supplying oxygenated during exertional ocardium is blocked, the area of myocardium becomes depressed
or emotional stress. When the patient rests, the anginal pain re- and hypokinetic. Gradually irreversible cardiac myocyte death oc-
solves. Unstable angina is a condition characterized by pain that is curs within the ischemic zone, leading to necrosis. The endocar-
not relieved with rest. This pain often indicates that there is an acute dial region is the first area of tissue that dies, followed by the mid-
thrombosis of a coronary artery. Prinzmetal angina is a condition myocardium or subendocardium. If the ischemia persists, then
caused by vasospasm of one or more coronary arteries. It can occur eventually the infarct will be transmural, the full thickness of the
at night during sleep and has a cyclical pattern to its occurrence. myocardium. Loss of functional myocardium results in reduced
This condition may result from overstimulation of the sympathetic left ventricular function affecting the patient’s quality of life and
nervous system, increased flux of calcium in arterial smooth muscle morbidity and mortality. 250
cells, or impaired function of thromboxane or prostaglandins. 13,20 The development of infarction is a cascade of events including
the migration and infiltration of leukocytes, release of metabolic
mediators, cytokines, growth factors, and activation of coagula-
INCIDENCE OF MYOCARDIAL tion and complement systems. Cellular edema and inflammatory
INFARCTION response ensue. 22 Myocardial necrosis activates the complement
system, releases free radicals, triggers a cytokine cascade and
Acute myocardial infarction is the leading cause of morbidity and chemokine upregulation, releasing IL-8, C5a, proteolytic en-
mortality of women and men in the United States. There are 1.3 zymes, and adhesion molecules. 23 Monocyte chemoattractant
million reports of patients who experience nonfatal myocardial in- protein-1 may regulate mononuclear cell recruitment with accu-
farctions each year. For every 100,000 people, there are at least mulation of monocyte-derived macrophages, mast cells, growth
600 people who experience a coronary event. 8 factors, and fibroblasts. 22 Endothelin-1, IL-1 , and TNF are a
Approximately 500,000 to 700,000 deaths occur from coro- few of the inflammatory factors elevated with ischemia. 251
nary artery disease per year in the United States. More than half The cascade of inflammatory events along with angiogenesis
these deaths occur in the field or prehospital setting because of de- and matrix metalloproteases may regulate extracellular matrix
lay and access to medical treatment. Ten percent of patients die deposition and mediate ventricular remodeling. 15,20,252,253 The
within the hospital setting. Another 10% of patients die within the inflammatory mediators lead to recruitment of blood-derived
first year after infarct. 228 Myocardial infarction usually occurs in primitive stem cells, which differentiate into endothelial cells and
patients older than 45 years. Certain subpopulations of patients are lead to some myocardial regeneration. 254 Certain metallopro-
at risk for myocardial ischemia and infarction, including insulin- teases are elevated in the blood of patients prone to rupture of ath-
dependent diabetic patients, cocaine and amphetamine users, and erosclerotic plaques. 255
patients with hypercholesterolemia or a positive family history of In addition, the myocardial cells release catecholamines, plac-
early-onset (45 years old or younger) coronary artery disease. ing the patient at risk for atrial and ventricular arrhythmias and
The American College of Cardiology criteria for myocardial heart failure. Catecholamines mediate the release of glycogen and
infarction are a typical rise and gradual fall of troponin or a rapid glucose from the body’s cell storage. Within 1 hour after a my-
rise and fall of creatine kinase-MB, with at least one of the fol- ocardial infarction, there is a rise in levels of free fatty acids and
lowing: symptoms of ischemia, development of pathological Q- glycerol. 256 Norepinephrine stimulates liver and skeletal muscle
waves on the ECG, electrocardiographic changes of ST elevation cells, elevating blood glucose levels and suppressing insulin