Page 135 - Cardiac Nursing

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A A A A Atherosclerosis, Inflammation, and Acute
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C C C Coronary Syndrome
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Bradley E. Aouizerat / Polly E. Gardner /
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Gaylene Altman
Acute coronary syndrome encompasses the lcliiniic lal entities of my- chest pain that may lead to myyocardial infarction or preinnfarct t
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oc ocardial ischemia and myyocardial infarction. The diagnosis of f an angina,, cann developp in some patients withh unst bablle angina. 3,8,9
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acute coronary syndrome is based on history, risk factors, diag- The coronary arteries supply blood flow to meet the specific
nostic laboratory tests, functional studies, and, to a lesser extent, demands of the myocardium under varying workloads such as
the electrocardiogram (ECG). This chapter focuses primarily on stress, sleep, or exercise. If oxygen needs are not met, then normal
the incidence, mechanisms, causes, and pathophysiology, includ- coronary arteries dilate to increase delivery of oxygenated blood to
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ing the cellular and metabolic changes of myocardial ischemia and the myocardium. Various pathologic states can affect the en-
infarction. Hemodynamic mechanisms affecting the balance of dothelium of the epicardial arteries impairing and impacting the
oxygen supply and demand are addressed. The role of inflamma- normal vasomotor response of vasodilatation when myocardial
tion in myocardial ischemia and myocardial infarction is also ad- demand increases. Atherosclerotic plaques (discussed later in this
dressed. Clinical manifestations are briefly discussed and are fully chapter) are the primary cause of endothelial injury and dysfunc-
detailed in Chapter 22. tion, interfering with normal vasomotor response causing a para-
doxical response of vasoconstriction. 10–15
The heart is an aerobic organ that relies on oxidation of sub-
INTRODUCTION strates for maximal efficiency. The myocardium has a small mar-
gin of oxygen debt to maintain normal function. Myocardial oxy-

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Many factors affect the pathophysiologic events that lead to is- gen consumption (MVO 2 ) is a measure of the heart’s total
chemia, infarction, and injury of myocardial muscle. Injury to the metabolism and is used to determine myocardial oxygen con-
myocardium can range from reversible to permanent damage of sumption. 16 Factors that determine myocardial oxygen consump-
cellular components in localized tissue. Ischemia occurs from a tion are heart rate, contractility, systolic wall tension, and meta-
transient imbalance of blood supply to an area of tissue, with the bolic and vasomotor regulations of coronary blood flow. 4,16
chief result being tissue hypoxia. Ischemia can be a sudden event Heart rate has a linear relationship with myocardial oxygen con-
or a gradual occurrence from a partial or totally occluded coronary sumption. The faster the heart rate, the greater the myocardial oxy-
vessel or vessels. The burden of the ischemic event depends on the gen consumption. Myocardial contractility is influenced by differ-
sensitivity of the tissue to hypoxia, the degree and duration of is- ent stimuli. Positive inotropes such as epinephrine or dobutamine
chemia, and the ability of the tissue to regenerate when conditions augment the contractile forces of the myocardium, increasing my-
improve. 1,2 ocardial oxygen consumption. Researchers believe the increase in

Myocardial ischemia is a condition that results from diminished MVO 2 may result from enhanced excitation–contraction coupling
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oxygen supply coupled with inadequate removal of metabolites be- or more rapid uptake of calcium by the sarcoplasmic reticulum. 5,16
cause of reduced perfusion to the heart muscle. 3,4 Pure anoxia or Evans and Matsuoka, who concluded that a relationship exists
hypoxia, without metabolic clearance, can occur in patients with between myocardial tension during systole and metabolism of
congenital heart disease, severe anemia, asphyxiation, carbon contractile tissue, described myocardial systolic wall tension in
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monoxide poisoning, or cor pulmonale. Myocardial ischemia can 1915 (as cited in Braunwald, 2000). 16 For every heart beat there
occur as a result of reduced oxygen and nutrient supply or increased is a generated ventricular tension or pressure, as measured in the
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metabolic demand to meet tissue demands (Fig. 5-1). In the pres- area under the left ventricular curve. See Chapter 1 for discussion
ence of coronary artery occlusion, an increase in oxygen demand re- of the Starling mechanism. Increases in myocardial tension or
quirements from exercise or emotional stress can cause a transitory pressure increase myocardial oxygen consumption.
imbalance known as demand ischemia. Angina pectoris is a condi- Low blood pressure causing decreased blood return can lead to
tion characterized by chest pain or discomfort, which results from imbalances of oxygen supply and demand. Examples are hypotension
myocardial ischemia. Patients with chronic stable angina experience or hypovolemia. Increased oxygen demand is caused by conditions
this demand ischemia when they exert themselves yet obtain relief such as hyperthyroidism, anemia, or hyperviscosity of the blood.
with rest. An abrupt or acute reduction in blood flow to my-
ocardium is termed supply ischemia. This abrupt imbalance is caused
by an increase in coronary vascular tone, such as coronary va- MECHANISMS THAT REGULATE
sospasm, or by a marked reduction or cessation of blood flow CORONARY BLOOD FLOW
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caused by thrombi or platelet aggregation. Supply ischemia is seen in
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patients with unstable angina or myocardial infarction. Unstable Mechanisms that determine coronary blood flow can be divided
angina is not relieved with rest. Crescendo angina, a worsening into mechanical factors and metabolic mediators. Mechanical
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