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Lecture 7

NURS 4526 Lecture Notes - Lecture 7: Coronary Artery Disease, Isosorbide Dinitrate, Unstable Angina


Department
Nursing
Course Code
NURS 4526
Professor
Ruth Robbio
Lecture
7

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Acute Coronary Syndrome: Notes for Students
1
Chronic Stable Angina
Reversible (temporary) myocardial ischemia = angina (chest pain);
intermittent chest pain
O2 demand > O2 supply
Primary reason for insufficient blood flow is narrowing of coronary arteries
by atherosclerosis
For ischemia to occur, the artery is usually 75% or more stenosed
Pain usually lasts 3 to 5 minutes
Subsides when the precipitating factor is relieved
Pain at rest is unusual
ECG reveals ST segment depression
Precipitating factors
Physical exertion
Temperature extremes
Strong emotions
Heavy meal
Tobacco use
Sexual activity
Circadian rhythm: early morning after waking
Drug therapy
Decrease O2 demand and/or increase O2 supply
Short-acting nitrates: Sublingual nitro
Long-acting nitrates: isosorbide dinitrate (Isordil)
β-adrenergic blockers
Calcium channel blockers if β-adrenergic blockers are poorly
tolerated, contraindicated, or do not control anginal symptoms
Angiotensin-converting enzyme inhibitors
Diagnostic Studies
Health history/physical examination
Laboratory studies
12-lead ECG
Chest x-ray
Echocardiogram
Exercise stress test
ACS
When ischemia is prolonged and not immediately reversible, acute coronary
syndrome (ACS) develops
Unstable angina (UA)
NonST-segment-elevation myocardial infarction (NSTEMI)
ST-segment-elevation (STEMI)
Deterioration of a once stable plaque that stimulates platelet aggregation
and local vasoconstriction with thrombus formation
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Acute Coronary Syndrome: Notes for Students
2
Result
Partial occlusion of coronary artery: UA or NSTEMI
Total occlusion of coronary artery: STEMI
Unstable angina
Unpredictable and represents medical emergency
Myocardial infarction
Result of sustained ischemia (>20 minutes), causing irreversible
myocardial cell death (necrosis)
Necrosis of entire thickness of myocardium takes 4 to 6 hours
The degree of altered function depends on the area of the heart
involved and the size of the infarct
Contractile function of the heart is disrupted in areas of
myocardial necrosis
Most MIs involve the left ventricle (LV)
Clinical Manifestations
Pain
Total occlusion  anaerobic metabolism and lactic acid
accumulation  severe, immobilizing chest pain not relieved by
rest, position change, or nitrate administration
Described as heaviness, constriction, tightness, burning, pressure,
or crushing
Common locations: substernal, retrosternal, or epigastric areas;
pain may radiate
Sympathetic nervous system stimulation from catecholamines
released from ischemic myocardial cells results in
Release of glycogen
Diaphoresis
Vasoconstriction of peripheral blood vessels
Skin: ashen, clammy, and/or cool to touch
Cardiovascular
Initially,  HR and BP, then  BP (secondary to  in CO)
Crackles
Jugular venous distension, hepatic engorgement & peripheral
edema
Abnormal heart sounds
S3 or S 4
Holosystolic murmur
Nausea and vomiting
Can result from reflex stimulation of the vomiting centre by the
severe pain
Fever
Increased during first 24 hours and may persist for up to 1 week
Systemic manifestation of the inflammatory process caused by cell
death
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