Focus on Coronary Artery Disease and Acute Coronary Syndrome

Focus onCoronary Artery Disease and

Acute Coronary Syndrome

Leading Causes of Death

2

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”

Coronary Artery Disease and Acute Coronary Syndrome

3

• Atherosclerosis (cont’d)

– Can occur in any artery in the body

– Atheromas (fatty deposits)

• Preference for the coronary arteries


4

• Atherosclerosis (cont’d)

– Terms to describe the disease process

• Arteriosclerotic heart disease

• Cardiovascular heart disease

• Coronary artery disease (CAD)


5

• 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

6

Pathogenesis of Atherosclerosis

7

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)

– Nonspecific marker of inflammation

– Increased in many patients with CAD– Chronic exposure to CRP associated with unstable

plaques and oxidation of LDL cholesterol


8

• Developmental stages: Fatty streaks– Earliest lesions– Characterized by lipid-filled smooth muscle cells– Potentially reversible


9

• Developmental stages: Fibrous plaque – Beginning of progressive changes in the arterial

wall– Lipoproteins 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


10

• 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


11

• Collateral circulation– Normally, some arterial anastomoses

(or connections) exist within the coronary circulation.


12

• Growth and extent of collateral circulation are attributed to two factors.– Inherited predisposition to develop new vessels

(angiogenesis)– Presence of chronic ischemia


13

• When occlusion of the coronary arteries occurs slowly over a long period, the chance that adequate collateral circulation will develop is greater.


14

Vessel Occlusion With Collateral Circulation

15

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.

• Nonmodifiable risk factors

• Age

• Gender

• Ethnicity

• Family history

• Genetic predisposition

Risk Factors for CAD

16

–Modifiable risk factors

• Elevated serum lipids

• Hypertension

• Tobacco use

• Physical inactivity


17

–Modifiable risk factors

• Obesity

• Diabetes

• Metabolic syndrome

• Psychologic states

• Homocysteine level


18

• Identification of people at high risk– Health history, including use of

prescription/nonprescription medications– Presence of cardiovascular symptoms– Environmental patterns: Diet, activity– Psychosocial history– Values and beliefs about health and illness

Risk Factors for CADHealth Promotion

19

• Health-promoting behaviors– Physical 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


20

• Health-promoting behaviors– Nutritional therapy

• Therapeutic lifestyle changes• Omega-3 fatty acids


21

• Health-promoting behaviors– Cholesterol-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)


22

• Health-promoting behaviors

– Antiplatelet therapy

• ASA

• Clopidogrel (Plavix)


23

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.

Question

24

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.”

Question

25

• 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 from

normal aging

Gerontologic Considerations

26

• Etiology and pathophysiology– Reversible (temporary) myocardial ischemia =

Angina (chest pain)

• O2 demand > O2 supply

Clinical Manifestations of CAD Chronic Stable Angina

27

• Etiology and pathophysiology– 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.


28

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


29

Location of Pain During Angina

30

Fig. 34-4. Location of pain during angina or myocardial infarction.

• Pain usually lasts 3 to 5 minutes.– Subsides when the precipitating factor is relieved– Pain at rest is unusual.– ECG reveals ST-segment depression and/or T-wave

inversion.


31

• Silent ischemia– Ischemia that occurs in the absence of any

subjective symptoms – Associated with diabetic neuropathy– Confirmed by ECG changes

Chronic Stable Angina Types of Angina

32

• Nocturnal angina– Occurs only at night but not necessarily during

sleep• Angina decubitus

– Chest pain that occurs only while lying down– Relieved by standing or sitting


33

• Prinzmetal’s (variant) angina– Occurs 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

34

• Prinzmetal’s (variant) angina– When spasm occurs

• Chest pain• Marked, transient ST-segment elevation

– May occur during REM sleep– May be relieved by moderate exercise or may

disappear spontaneously


35

• Microvascular angina– May occur in the absence of significant coronary

atherosclerosis or coronary spasm– Pain is related to myocardial ischemia associated

with abnormalities of the coronary microcirculation.• Coronary microvascular disease


36

• Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supply

– Short-acting nitrates: Sublingual

– Long-acting nitrates• Nitroglycerin (NTG) ointment• Transdermal controlled-release NTG

Chronic Stable Angina Nursing and Collaborative Management

37

• Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supply– 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

Chronic Stable Angina Nursing and Collaborative Management

38

• Diagnostic studies– Health history/physical examination– Laboratory studies– 12-lead ECG– Chest x-ray– Echocardiogram – Exercise stress test

Chronic Stable AnginaNursing and Collaborative Management

39

• Diagnostic studies– Cardiac catheterization/coronary angiography

• Diagnostic• Coronary revascularization: Percutaneous

coronary intervention (PCI)–Balloon angioplasty–Stent

Chronic Stable AnginaNursing and Collaborative Management

40

Placement of a Coronary Artery Stent

41

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.

Pre- and Post-PCI With Stent Placement

42

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.

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

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

(NSTEMI)– ST-segment-elevation MI (STEMI)

Acute Coronary Syndrome

43

Relationship Between CAD, Chronic Stable Angina, and ACS

44

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 NSTEMI– Total occlusion of coronary artery: STEMI

Acute Coronary Syndrome Etiology and Pathophysiology

Deterioration of once stable

plagueRupture Platelet

aggregation Thrombus

45

• Unstable angina– Change in usual pattern– New in onset– Occurs at rest– Has a worsening pattern

• UA is unpredictable and represents a medical emergency.

Clinical Manifestations of ACS Unstable Angina

46

• 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)

47

Myocardial Infarction From Occlusion

48

Fig. 34-9. Occlusion of the left anterior descending coronary artery, resulting in a myocardial infarction.

Acute Myocardial Infarction

49

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).

Full-Thickness MI

50

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 MIs involve the left ventricle (LV).

Clinical Manifestations of ACS Myocardial Infarction

51

• Pain – Total occlusion → Anaerobic metabolism and

lactic acid accumulation → Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration


52

• Pain – Described as heaviness, constriction, tightness,

burning, pressure, or crushing – Common locations: Substernal, retrosternal, or

epigastric areas; pain may radiate to neck, jaw, arms


53

• Stimulation of sympathetic nervous system results in – Release of glycogen– Diaphoresis– Vasoconstriction of peripheral blood vessels– Skin: Ashen, clammy, and/or cool to touch


54

• Cardiovascular– Initially, ↑ HR and BP, then ↓ BP (secondary to ↓

in CO) – Crackles Jugular venous distention– Abnormal heart sounds

• S3 or S4• New murmur


55

• Nausea and vomiting– Can result from reflex stimulation of the vomiting

center by severe pain• Fever

– Systemic manifestation of the inflammatory process caused by cell death


56

• 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.

Myocardial InfarctionHealing Process

57

• 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.


58

• By 6 weeks after MI, scar tissue has replaced necrotic tissue.– Area is said to be healed, but less compliant.

• Ventricular remodeling– Normal myocardium will hypertrophy and dilate in

an attempt to compensate for the infarcted muscle.


59

• 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

Complications of Myocardial Infarction

60

• Heart failure– A complication that occurs when the pumping

power of the heart has diminished


61

• Cardiogenic shock– Occurs when inadequate oxygen and nutrients are

supplied to the tissues because of severe LV failure– Requires aggressive management


62

• Papillary muscle dysfunction– Causes mitral valve regurgitation– Condition aggravates an already compromised LV.

• Ventricular aneurysm– Results when the infarcted myocardial wall

becomes thinned and bulges out during contraction


63

• Acute pericarditis– An 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


64

• Dressler syndrome– Characterized by pericarditis with effusion and

fever that develop 4 to 6 weeks after MI– Pericardial (chest) pain – Pericardial friction rub may be heard on

auscultation.– Arthralgia


65

• 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,

echocardiogram

Unstable Angina and MIDiagnostic Studies

66

Serum Cardiac Markers After MI

67

Fig. 34-12. Serum cardiac markers found in the blood after myocardial infarction. CK, Creatine kinase.

• Emergency management– Initial interventions Ongoing monitoring

• Emergent PCI – Treatment of choice for confirmed MI– Balloon angioplasty + Drug-eluting stent(s)

Collaborative CareAcute Coronary Syndrome

68

• Fibrinolytic therapy– Indications and contraindications– Best marker of reperfusion: Return of ST segment

to baseline– Rescue PCI if thrombolysis fails– Major complication: Bleeding


69

• Coronary surgical revascularization – Failed medical management– Presence 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– History of diabetes mellitus


70

• Coronary surgical revascularization – Coronary artery bypass graft (CABG) surgery

• Requires sternotomy and cardiopulmonary bypass (CPB)

• Uses arteries and veins for grafts – Minimally invasive direct coronary artery bypass

(MIDCAB)• Alternative to traditional CABG


71

CABG Surgery

72

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.

• Coronary surgical revascularization – 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


73

• Drug therapy– IV nitroglycerin– Morphine sulfate– β-Adrenergic blockers– Angiotensin-converting enzyme inhibitors– Antidysrhythmia drugs– Cholesterol-lowering drugs– Stool softeners


74

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

75

• Nutritional therapy – Initially NPO– Progress to

• Low salt• Low saturated fat• Low cholesterol


76

Types of Fat in Food

77

Fig. 34-3. Types of dietary fat.

• Nursing assessment

– Subjective data

• Health history

• Functional health patterns

– Objective data

Nursing ManagementChronic Stable Angina and ACS

78

• Nursing diagnoses

– Acute pain

– Risk for decreased cardiac tissue perfusion

– Anxiety

– Activity intolerance

Nursing Management Chronic Stable Angina and ACS

79

• Planning: Overall goals– Relief of pain– Preservation of myocardium– Immediate and appropriate treatment– Effective coping with illness-associated anxiety


80

• Planning: Overall goals (cont’d)– Participation in a rehabilitation plan– Reduction of risk factors– Health promotion

• Therapeutic lifestyle changes to reduce cardiac risk factors


81

• 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– Auscultation of heart sounds

Nursing ManagementChronic Stable Angina

82

• Ambulatory and home care– Patient teaching CAD and angina

• Precipitating factors for angina• Risk factor reduction• Medications

Nursing ManagementChronic Stable Angina

83

• 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

84

• Acute intervention– Anxiety– Emotional and behavioral reaction

• Maximize patient’s social support systems.

• Consider open visitation.


85

• Coronary revascularization CABG: ICU for first 24 to 36 hours– Pulmonary artery catheter for measuring CO,

other hemodynamic parameters– Intraarterial line for continuous BP monitoring– Pleural/mediastinal chest tubes for chest drainage


86

• CABG (cont’d) – Continuous ECG monitoring to detect

dysrhythmias (esp. atrial dysrhythmias)– Endotracheal tube/mechanical ventilation

• Extubation within 12 hours– Epicardial pacing wires for emergency pacing of

the heart– Urinary catheter to monitor urine output– NG tube for gastric decompression


87

• 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


88

• 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)


89

• Ambulatory and home care– Patient and caregiver teaching – Physical exercise– Resumption of sexual activity

• Emotional readiness of patient and partner

• Physical expenditure


90

• Evaluation– Relief of pain– Preservation of myocardium– Immediate and appropriate treatment– Effective coping with illness-associated anxiety– Participation in a rehabilitation plan– Reduction of risk factors


91

• Unexpected death from cardiac causes• Rapid CPR, defibrillation with AED, and early

advanced cardiac life support increase survival rates

Sudden Cardiac Death (SCD)

92

• 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)

Sudden Cardiac DeathEtiology and Pathophysiology

93

• Most SCDs caused by ventricular dysrhythmias (e.g., ventricular tachycardia)

• SCD occurs less commonly as a result of LV outflow obstruction (e.g., aortic stenosis).


94

• Primary risk factors

– Left ventricular dysfunction (EF 30%)

– Ventricular dysrhythmias following MI


95

• Diagnostic workup to rule out or confirm MI– Cardiac markers– ECG

• Cardiac catheterization• PCI or CABG

Sudden Cardiac Death Nursing and Collaborative Management

96

• 24-hour Holter monitoring• Exercise stress testing• Signal-averaged ECG• Electrophysiologic study (EPS)• Implantable cardioverter-defibrillator (ICD)


97

• Psychosocial adaptation– “Brush with death”– “Time bomb” mentality– Possible role changes

• Driving restrictions• Change in occupation


98

The most significant factor in long-term survival of a patient with sudden cardiac death is:

1. Absence of underlying heart disease.2. Rapid institution of emergency services and procedures.3. Performance of perfect technique in resuscitation procedures.4. Maintenance of 50% of normal cardiac output during

resuscitation efforts.

Question

99

Focus on Coronary Artery Disease and Acute Coronary Syndrome

Documents

Transcript of Focus on Coronary Artery Disease and Acute Coronary Syndrome