Focus on Coronary Artery Disease and Acute Coronary Syndrome

Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Focus onCoronary Artery Disease and

Acute Coronary Syndrome(Relates to Chapter 34, “Nursing Management:

Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook)


A type of blood vessel disorder that is included in the general category of atherosclerosisBegins as soft deposits of fat that harden with age

Referred to as “hardening of arteries”

Coronary Artery Disease and Acute Coronary Syndrome


Cardiovascular diseases are the major cause of death in the United States

Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general

Coronary Artery Disease and Acute Coronary Syndrome (Cont’d)


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

Coronary Artery Disease Etiology and Pathophysiology


Risk factors can be categorized asNonmodifiable risk factors• Age • Gender• Ethnicity• Family history• Genetic predisposition

Risk Factors for CAD


Risk factors can be categorized asModifiable risk factors• Elevated serum lipids• Hypertension• Tobacco use• Physical inactivity

Risk Factors for CAD (Cont’d)

• Obesity• Diabetes• Metabolic syndrome• Psychologic states


Identification of people at high riskHealth history, including use of prescription/nonprescription medications

Presence of cardiovascular symptoms• Examples???

Environmental patterns: diet, activity

Values and beliefs about health and illness• Why is this important?

Risk Factors for CADHealth Promotion


Health-promoting behaviorsPhysical fitness• 30 minutes >5 days/week• Regular physical activity contributes to: Weight reduction Reduction of >10% in systolic BP In some men more than women, an

increase in HDL cholesterol

Risk Factors for CADHealth Promotion (Cont’d)


Health-promoting behaviorsNutritional therapy• ↓saturated fats• ↓cholesterol• ↑monounsaturated fats

Nuts, olive oil• ↑omega-3 fatty acids• ↑fruit and whole grains



Health-promoting behaviorsCholesterol-lowering drug therapy• Drugs that restrict lipoprotein production: Statins, niacin• Drugs that increase lipoprotein removal: Bile acid sequestrants• Drugs that decrease cholesterol absorption: Ezetimibe (Zetia)



StatinsSerious side effects• Liver damage• Myopathy• Rhabdomyolysis

Cholesterol-lowering drug therapy


Nicotinic acid (niacin)Flushing• Administer ASA 30-60 prior

GI disturbances• N/V/D



Bile acid sequestrantsGI disturbances• Bloating• Constipation• Dyspepsia

May interfere with absorption of other medications• Separate administration times



Health-promoting behaviorsAntiplatelet therapy • Aspirin

Inhibits activity of thromboxane A2 Suppresses platelet aggregation

• Clopidogrel (Plavix)



Strategies to reduce risk factors are effective but often underprescribed

Necessary to modify guidelines for physical activity

Two points when elderly may consider lifestyle change(s)When hospitalized When symptoms result from CAD and not normal aging

Gerontologic Considerations


Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms

Clinical Manifestations of CAD Chronic Stable Angina (Cont’d)


Etiology and pathophysiologyReversible (temporary) myocardial ischemia = angina (chest pain)• O2 demand > O2 supply

Clinical Manifestations of CAD Chronic Stable Angina


Etiology and pathophysiologyPrimary 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 minutesSubsides when the precipitating factor is relieved

Pain at rest is unusualECG reveals ST segment depression



Silent ischemiaUp to 80% of patients with myocardial ischemia are asymptomatic

Associated with diabetes mellitus and hypertension

Confirmed by ECG changes

Chronic Stable Angina Types of Angina


Prinzmetal’s (variant) anginaOccurs at rest usually in response to spasm of major coronary artery

Seen in patients with a history of migraine headaches and Raynaud’s phenomenon

Spasm may occur in the absence of CAD

Chronic Stable AnginaTypes of Angina (Cont’d)


Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supplyShort-acting nitrates: Sublingual

Long-acting nitrates• Nitroglycerin ointment• Transdermal controlled-release nitroglycerin

Chronic Stable Angina Nursing and Collaborative Management


Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supplyβ-Adrenergic blockersCalcium channel blockers• If β-adrenergic blockers are poorly tolerated, contraindicated, or do not control anginal symptoms• Used to manage Prinzmetal’s angina

Angiotensin-converting enzyme inhibitors

Chronic Stable Angina Nursing and Collaborative Management (Cont’d)


Diagnostic studiesHealth history/physical examination

Laboratory studies12-lead ECGChest x-rayEchocardiogram Exercise stress test

Chronic Stable AnginaNursing and Collaborative Management (Cont’d)


Diagnostic studiesCardiac catheterization • Diagnostic• Coronary revascularization: Percutaneous coronary intervention Balloon angioplasty Stent

Chronic Stable AnginaNursing and Collaborative Management (Cont’d)


Placement of aCoronary Artery Stent

Fig. 34-9


Pre- and Post-PCIwith Stent Placement

Fig. 34-10


When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops

ACS encompasses:Unstable angina (UA)Non–ST-segment-elevation myocardial infarction (NSTEMI)

ST-segment-elevation myocardial infraction (STEMI)

Acute Coronary Syndrome


Relationship Between CAD, Chronic Stable Angina, and ACS

Fig. 34-11


Unstable anginaNew in onsetOccurs at restHas a worsening pattern

UA is unpredictable and represents a medical emergency

Clinical Manifestations of ACS Unstable Angina


Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis)

Necrosis of entire thickness of myocardium takes 4 to 6 hours

Clinical Manifestations of ACS Myocardial Infarction (MI)


Acute Myocardial Infarction

Fig. 34-13


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 of ACS Myocardial Infarction


Pain Total occlusion → anaerobic metabolism and lactic acid accumulation → severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration

Clinical Manifestations of ACS Myocardial Infarction


Pain Described as heaviness, constriction, tightness, burning, pressure, or crushing

Common locations: substernal, retrosternal, or epigastric areas; pain may radiate

Clinical Manifestations of ACS Myocardial Infarction (Cont’d)

Possible Location of Chest Pain

Fig. 34-7


Sympathetic nervous system stimulation results in Release of glycogenDiaphoresisVasoconstriction of peripheral blood vessels

Skin: ashen, clammy, and/or cool to touch



CardiovascularInitially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO)

Crackles Jugular venous distentionAbnormal heart sounds• S3 or S4

• New murmur



Nausea and vomitingCan result from reflex stimulation of the vomiting center by the severe pain

FeverSystemic manifestation of the inflammatory process caused by cell death



DysrhythmiasMost common complicationPresent in 80% of MI patientsMost common cause of death in the prehospital period

Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock

Complications of Myocardial Infarction


Heart failureA complication that occurs when the pumping power of the heart has diminished

Complications of Myocardial Infarction (Cont’d)


Cardiogenic shockOccurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure

Requires aggressive management



Papillary muscle dysfunctionCauses mitral valve regurgitation

Condition aggravates an already compromised LV

Ventricular aneurysmResults when the infarcted myocardial wall becomes thinned and bulges out during contraction



Acute pericarditisAn inflammation of visceral and/or parietal pericardium

May result in cardiac compression, ↓ LV filling and emptying, heart failure

Pericardial friction rub may be heard on auscultation

Chest pain different from MI pain • Worse when recumbent• Improves when leaning forward



Acute pericarditis


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 angiographyOthers: Exercise stress testing, echocardiogram

Diagnostic Studies Unstable Angina and Myocardial Infarction


Emergency managementInitial interventions• ECG• MONA

Ongoing monitoringEmergent PCI Treatment of choice for confirmed MI

Balloon angioplasty + drug-eluting stent(s)

Ambulatory 24 hours after the procedure

Collaborative CareAcute Coronary Syndrome


Fibrinolytic therapyIndications and contraindications• Read these on your own

Marker of reperfusion: Return of ST segment to baseline

Rescue PCI if thrombolysis failsMajor complication: Bleeding

Collaborative CareAcute Coronary Syndrome (Cont’d)


Drug therapyIV nitroglycerinMorphine sulfateβ-adrenergic blockersAngiotensin-converting enzyme inhibitors

Antidysrhythmia drugsCholesterol-lowering drugsStool softeners



Nutritional therapy Progress diet to • Low-salt• Low-saturated fat• Low-cholesterol



Coronary surgical revascularization Fail medical managementPresence of left main coronary artery or three-vessel disease

Not a candidate for PCI (e.g., lesions are long or difficult to access)

Failed PCI with ongoing chest pain



Coronary surgical revascularization Coronary artery bypass graft (CABG) surgery• Requires cardiopulmonary bypass• Uses arteries and veins for grafts



CABG Surgery

Fig. 34-16


Nursing AssessmentSubjective Data• Health history• Functional health patterns

Objective Data

Nursing ManagementChronic Stable Angina and ACS


Nursing DiagnosesAcute painIneffective tissue perfusion (cardiac)

AnxietyActivity intolerance

Nursing Management Chronic Stable Angina and ACS (Cont’d)


Planning: Overall goalsRelief of painPreservation of myocardiumImmediate and appropriate treatment

Effective coping with illness-associated anxiety

Participation in a rehabilitation plan

Reduction of risk factors

Nursing Management Chronic Stable Angina and ACS (Cont’d)


Health Promotion• Therapeutic lifestyle changes to reduce cardiac risk factors

Nursing ManagementChronic Stable Angina


Acute Interventions for anginal attackWhat should the patient do at home?

What are your initial interventions?

Nursing ManagementChronic Stable Angina (Cont’d)


Acute Intervention• Pain: Nitroglycerin, morphine, oxygen• Continuous monitoring

ECG VS, pulse oximetry Heart and lung sounds

• Rest and comfort Balance rest and activity Begin cardiac rehabilitation

Nursing ManagementACS


Ambulatory and Home CareStart discharge planning upon admission

Patient teaching Physical exerciseResumption of sexual activity• Emotional readiness of patient and partner• Physical expenditure

Nursing ManagementACS (Cont’d)


EvaluationRelief of painPreservation of myocardiumImmediate and appropriate treatment

Effective coping with illness-associated anxiety

Participation in a rehabilitation plan

Reduction of risk factors

Nursing ManagementACS (Cont’d)


Unexpected death from cardiac causesMost deaths occur outside of hospital

CAD accounts for about 80% of all SCDs

Sudden Cardiac Death (SCD)


Primary risk factorsLeft ventricular dysfunction (EF 30%)

Ventricular dysrhythmias after MI

Sudden Cardiac DeathEtiology and Pathophysiology (Cont’d)


Case Study


Case Study

58-year-old male is admitted for an elective knee replacement

During admission history, it is noted that he is taking hypertension medication


Case Study (Cont’d)

When asked, he states that he does not know what his blood pressure usually is

His BMI is 40 kg/m2

His fasting glucose level is elevated



His job is very physical (he is a bricklayer)It has become more difficult due to his “bad knees”

He is worried he will be fired



Outside of work, he does not participate in any physical activity

He does not smoke

He has not had a check-up with his physician in several years


Discussion Questions

1.What are his nonmodifiable risk factors for CAD?

2.What are his modifiable risk factors for CAD?


Discussion Questions (Cont’d)3.What teaching should you

do with him about his risk for developing CAD?

Documents

Focus on Coronary Artery Disease and Acute Coronary Syndrome