(Relates to Chapter 34, “Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
(Relates to Chapter 34, “Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook)
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eFig. 34-1. Leading causes of death for all men and women. CVD,
Cardiovascular disease.
Atherosclerosis: Type of blood vessel disorder
Begins as soft deposits of fat that harden with age
Referred to as “hardening of arteries”
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Can occur in any artery in the body
Atheromas (fatty deposits)
• Preference for the coronary arteries
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Terms to describe the disease process:
• Arteriosclerotic heart disease
• Cardiovascular heart disease
• Coronary artery disease (CAD)
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Atherosclerosis is the major cause of CAD.
Characterized by a focal deposit of cholesterol and lipid, primarily within the intimal wall of the artery
Endothelial lining altered as a result of inflammation and injury
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Fig. 34-1. Pathogenesis of atherosclerosis. A, Damaged endothelium. B, Diagram of fatty streak and
lipid core formation. C, Diagram of fibrous plaque. Raised plaques are visible: some are yellow, others
are white. D, Diagram of complicated lesion: thrombus is red, collagen is blue. Plaque is complicated by
red thrombus deposition.
+ C-reactive protein (CRP)
Non-specific marker of inflammation
Increased in many patients with CAD
Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol
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B. Developmental stages: Fatty streaks
Earliest lesionsCharacterized by lipid-filled smooth
muscle cellsPotentially reversible
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C. Developmental stages: Fibrous plaque
Beginning of progressive changes in the arterial wallLipoproteins transport cholesterol and other
lipids into the arterial intima. Fatty streak is covered by collagen, forming a
fibrous plaque that appears grayish or whitish.Result = Narrowing of vessel lumen
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D. Developmental stages: Complicated lesion
Continued inflammation can result in plaque instability, ulceration, and rupture.
Platelets accumulate and thrombus forms.
Increased narrowing or total occlusion of lumen
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Fig. 34-2. Vessel occlusion with collateral circulation. A, Open, functioning coronary artery.
B, Partial coronary artery closure with collateral circulation being established. C, Total
coronary artery occlusion with collateral circulation bypassing the occlusion to supply blood
to the myocardium.
Collateral circulation
Normally, some arterial anastomoses (or connections) exist within the coronary circulation.
Growth and extent of collateral circulation are attributed to two factors. Inherited predisposition to develop new vessels
(angiogenesis) Presence of slow chronic ischemia = Adequate
collateralsCopyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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• Age
• Gender
• Ethnicity
• Family history
• Genetic predisposition
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• Elevated serum lipids
• Hypertension
• Tobacco use
• Physical in-activity
• Obesity
• Diabetes
• Metabolic syndrome
• Psychologic states
• Homocysteine level
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Inc., an affiliate of Elsevier Inc.15
Identification of people at high risk:
Health history, including use of prescription/non-prescription medicationsPresence of cardiovascular symptomsEnvironmental patterns: Diet, activityPsychosocial historyValues and beliefs about health and illness
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Health-promoting behaviorsPhysical fitness• FITT formula: 30 minutes >5 days/week• Regular physical activity contributes to Weight reduction Reduction of >10% in systolic BP In some men more than women, increase in
HDL cholesterol
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Health-promoting behaviors
Nutritional therapy• Therapeutic lifestyle changes• Omega-3 fatty acids
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Cholesterol-lowering drug therapy:
• Restrict lipoprotein production: Statins, Niacin
• Increase lipoprotein removal: Bile acid sequestrants
• Decrease cholesterol absorption: Ezetimibe (Zetia)
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Antiplatelet therapy
• ASA
• Clopidogrel (Plavix)
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Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are:
1. Hypertension and cigarette smoking.2. Obesity and smokeless tobacco use. 3. Elevated serum lipids and diabetes mellitus.4. Physical inactivity and elevated homocysteine levels.
Audience Response Question
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The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective when the patient says,
1. “I should not eat any red meat such as beef, pork, or lamb.”
2. “I should have some type of fish at least 3 times a week.”3. “Most of my fat intake should be from olive oil or the oils
in nuts.”4. “If I reduce the fat in my diet to about 5% of my calories, I
will be much healthier.”
Audience Response Question
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Strategies under prescribed. Modify physical activity guidelines
Elderly may consider lifestyle change(s):When hospitalized When symptoms result from CAD and not
from normal aging
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Etiology and pathophysiology
Reversible (temporary) myocardial ischemia = Angina (chest pain)
• O2 demand > O2 supply
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Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis.
Referred pain in left shoulder and arm is from transmission of the pain message to the cardiac nerve roots.
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Intermittent chest pain that occurs over a long period with the samepattern of onset, duration, and intensity of symptoms
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Fig. 34-4. Location of pain during
angina or myocardial infarction.
Pain usually lasts 3 to 5 minutes.
Subsides when the precipitating factor is relievedPain at rest is unusual.ECG reveals ST-segment depression
and/or T-wave inversion.
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Silent ischemia
Nocturnal
Angina decubitus
Prinzmetal’s (variant) angina
Microvascular angina
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Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supply
Short-acting nitrates: Sublingual
Long-acting nitrates
• Nitroglycerin (NTG) ointment• Transdermal controlled-release NTG
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β-Adrenergic blockers
Calcium channel blockers
• If β-adrenergic blockers are poorly tolerated, contraindicated, or do not control angina
• Used to manage Prinzmetal’s angina
Angiotensin-converting enzyme inhibitors
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Diagnostic studies
Health history/physical examination
Laboratory studies
12-lead ECG
Chest x-ray
Echocardiogram
Exercise stress test
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Diagnostic studies
Cardiac catheterization/coronary angiography
• Diagnostic
• Coronary revascularization: Percutaneous coronary intervention (PCI)
Balloon angioplasty
StentCopyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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Fig. 34-6. Placement of a coronary artery stent. A, The stent is positioned at the site of the lesion.
B, The balloon is inflated, expanding the stent. The balloon is then deflated and removed. C,
The implanted stent is left in place.
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Fig. 34-7. A, A thrombotic occlusion of the right coronary artery is noted (arrows). B, Right
coronary artery is opened and blood flow restored following angioplasty and placement of a
4-mm stent.
Develop when ischemia is prolongedand is not immediately reversible
ACS encompasses: Unstable angina (UA)Non–ST-segment-elevation myocardial
infarction (NSTEMI)ST-segment-elevation MI (STEMI)
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Fig. 34-8. Relationships among coronary artery disease, chronic stable angina, and
acute coronary syndrome. Ml, Myocardial infarction.
Result Partial occlusion of coronary artery: UA or
NSTEMITotal occlusion of coronary artery: STEMI
Deterioration of once stable
plagueRupture
Platelet aggregation
Thrombus
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Change in usual patternNew in onsetOccurs at restHas a worsening pattern
Unpredictable and represents a medical emergency.
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Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis)
Necrosis of entire thickness of myocardium takes 4 to 6 hours.
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Fig. 34-9. Occlusion of the left anterior descending coronary artery,
resulting in a myocardial infarction.
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Fig. 34-10. Acute myocardial infarction in the posterolateral wall of the left ventricle. This is
demonstrated by the absence of staining in the areas of necrosis (white arrow). Note the
scarring from a previous anterior wall myocardial infarction (black arrow).
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Fig. 34-11. Myocardial infarction involving the full thickness
of the left ventricular wall.
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 MI’s involve the left ventricle (LV).Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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Pain
Total occlusion →Anaerobic metabolism and lactic acid accumulation → Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
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Pain
heaviness, constriction, tightness, burning, pressure, or crushing
Common locations: Substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms
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Stimulation of sympathetic nervous system results in :
Release of glycogenDiaphoresisVasoconstriction of peripheral blood
vesselsSkin: Ashen, clammy, and/or cool to touch
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Cardiovascular: Initially, ↑ HR and BP, then ↓ BP
(secondary to ↓ in CO) Crackles Jugular venous distentionAbnormal heart sounds• S3 or S4• New murmur
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Nausea and vomitingCan result from reflex stimulation of the
vomiting center by severe pain
FeverSystemic manifestation of the
inflammatory process caused by cell death
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Within 24 hours, leukocytes infiltrate the area of cell death.
Enzymes are released from the dead cardiac cells (important indicators of MI).
Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by second or third day.
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Development of collateral circulation improves areas of poor perfusion.
Necrotic zone identifiable by ECG changes and nuclear scanning
10 to 14 days after MI, scar tissue is still weak and vulnerable to stress.
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By 6 weeks after MI, scar tissue has replaced necrotic tissue.
Ventricular remodelingmyocardium hypertrophy and dilate to
compensate for the infarcted muscle.
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Dysrhythmias
Most common complication
Present in 80% of MI patients
Most common cause of death in the prehospital period
Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock
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Heart failure
A complication that occurs when the pumping power of the heart has diminished
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Cardiogenic shock
Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failureRequires aggressive management
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Papillary muscle dysfunctionCauses mitral valve regurgitationCondition aggravates an already
compromised LV.
Ventricular aneurysmResults when the infarcted myocardial
wall becomes thinned and bulges out during contraction
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Acute pericarditisAn inflammation of visceral and/or
parietal pericardiumMay result in cardiac compression, ↓ LV
filling and emptying, heart failurePericardial friction rub may be heard on
auscultation.Chest pain different from MI pain
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Dressler syndromeCharacterized by pericarditis with effusion
and fever that develop 4 to 6 weeks after MIPericardial (chest) pain Pericardial friction rub may be heard on
auscultation.Arthralgia
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Detailed health history and physical 12-lead ECG: Changes in QRS complex,
ST segment, and T wave can rule out or confirm UA or MI
Serum cardiac markers Coronary angiography Others: Exercise stress testing,
echocardiogramCopyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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Fig. 34-12. Serum cardiac markers found in the blood after myocardial
infarction. CK, Creatine kinase.
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Emergency management
Initial interventions Ongoing monitoring
1. Emergent PCI
Treatment of choice for confirmed MI
Balloon angioplasty + Drug-eluting stent(s)
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2. Fibrinolytic therapy
Indications and contraindications
Best marker of reperfusion: Return of ST segment to baseline
Rescue PCI if thrombolysis fails
Major complication: Bleeding
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3. Coronary Surgical Revascularization:
Coronary artery bypass graft (CABG) :• Requires sternotomy and cardiopulmonary
bypass (CPB)• Uses arteries and veins for grafts
Minimally invasive direct coronary artery bypass (MIDCAB)• Alternative to traditional CABG
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Off-pump coronary artery bypass
• Does not require CPB
Transmyocardial Laser Revascularization
• For patients with advanced CAD who are not surgical candidates or who have failed maximum medical therapy
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Fig. 34-13. Distal end of the left internal mammary artery is grafted below the area of blockage in the
left anterior descending artery. Proximal end of the saphenous vein is grafted to the aorta and the distal
end is grafted below the area of blockage in the right coronary artery.
Drug therapy IV nitroglycerinMorphine sulfateβ-Adrenergic blockersAngiotensin-converting enzyme inhibitorsAntidysrhythmia drugsCholesterol-lowering drugsStool softeners
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A patient is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscitation. When reviewing the health care provider’s admission orders, which of the following orders is it most important for the nurse to question?
1. Oxygen at 4 L/min per nasal cannula2. Morphine sulfate 2 mg IV every 10 minutes until the
pain is relieved3. Tissue plasminogen activator (t-PA) 100 mg IV infused
over 3 hours4. IV nitroglycerin at 5 mcg/minute and increase 5
mcg/minute every 3 to 5 minutes
Audience Response Question
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Nutritional therapy
Initially NPO
Progress to
• Low salt
• Low saturated fat
• Low cholesterol
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Fig. 34-3. Types of dietary fat.
Nursing assessment
Subjective data
• Health history
• Functional health patterns
Objective data
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Nursing diagnoses
Acute pain
Risk for decreased cardiac tissue perfusion
Anxiety
Activity intolerance
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Planning: Overall goals
Relief of pain
Preservation of myocardium
Immediate and appropriate treatment
Effective coping with illness-associated anxiety
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Planning: Overall goals (cont’d)
Participation in a rehabilitation plan
Reduction of risk factors
Health promotion
• Therapeutic lifestyle changes to reduce cardiac risk factors
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Acute interventions for anginal attack:
Administration of supplemental oxygen
Assess vital signs, pulse oximetry.
12-lead ECG
Prompt pain relief first with a nitrate followed by an opioid analgesic, if needed
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Ambulatory and home care:
Patient teaching CAD and angina
• Precipitating factors for angina
• Risk factor reduction
• Medications
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Acute intervention• Pain: Nitroglycerin, morphine, oxygen• Continuous monitoring ECG VS, pulse oximetryHeart and lung sounds
• Rest and comfort Balance rest and activity. Begin cardiac rehabilitation.
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Acute interventionAnxietyEmotional and behavioral reaction • Maximize patient’s social support
systems.• Consider open visitation.
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Coronary revascularization CABG: ICU for first 24 to 36 hoursPulmonary artery catheter for measuring
CO, other hemodynamic parameters Intraarterial line for continuous BP
monitoringPleural/mediastinal chest tubes for chest
drainage
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CABG (cont’d) Continuous ECG monitoring to detect
dysrhythmias (esp. atrial dysrhythmias)Endotracheal tube/mechanical ventilation• Extubation within 12 hoursEpicardial pacing wires for emergency
pacing of the heartUrinary catheter to monitor urine outputNG tube for gastric decompression
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CABG: Complications related to CPB
Bleeding and anemia from damage to RBCs and platelets
Fluid and electrolyte imbalances
Hypothermia as blood is cooled as it passes through the bypass machine
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CABG: Care is focused on :
Assessing the patient for bleeding (e.g., chest tube drainage, incision sites)
Monitoring fluid status
Replacing electrolytes PRN
Restoring temperature (e.g., warming blankets)
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Ambulatory and home care
Patient and caregiver teaching
Physical exercise
Resumption of sexual activity
• Emotional readiness of patient and partner
• Physical expenditure
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EvaluationRelief of painPreservation of myocardium Immediate and appropriate treatmentEffective coping with illness-associated
anxietyParticipation in a rehabilitation planReduction of risk factors
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Unexpected death from cardiac causes
Rapid CPR, defibrillation with AED, and early advanced cardiac life support increase survival rates
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Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow
Death usually within 1 hour of onset of acute symptoms (e.g., angina, palpitations)
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most caused by ventricular dysrhythmias (e.g., ventricular tachycardia)
less commonly as a result of LV outflow obstruction (e.g., aortic stenosis).
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Strongest predictor:
Left ventricular dysfunction (EF 30%)
Ventricular dysrhythmias following MI
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Diagnostic workup to rule out or confirm MICardiac markersECG
Cardiac catheterization PCI or CABG
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24-hour Holter monitoring Exercise stress testing Signal-averaged ECG Electrophysiologic study (EPS) Implantable cardioverter-defibrillator
(ICD)
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Psychosocial adaptation
“Brush with death”“Time bomb” mentalityPossible role changes• Driving restrictions• Change in occupation
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