(Relates to Chapter 34, “Nursing Management: Coronary ...

(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.


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”


3

Can occur in any artery in the body

Atheromas (fatty deposits)

• Preference for the coronary arteries


4

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


6


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)

Non-specific marker of inflammation

Increased in many patients with CAD

Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol


8

B. Developmental stages: Fatty streaks

Earliest lesionsCharacterized by lipid-filled smooth

muscle cellsPotentially reversible


9

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

Copyright © 2011, 2007 by

Mosby, Inc., an affiliate of

Elsevier Inc.

10

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

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.11


12

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.

13

• Age

• Gender

• Ethnicity

• Family history

• Genetic predisposition


14

• Elevated serum lipids

• Hypertension

• Tobacco use

• Physical in-activity

• Obesity

• Diabetes

• Metabolic syndrome

• Psychologic states

• Homocysteine level

Copyright © 2011, 2007 by Mosby,

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


16

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


17

Health-promoting behaviors

Nutritional therapy• Therapeutic lifestyle changes• Omega-3 fatty acids


18

Cholesterol-lowering drug therapy:

• Restrict lipoprotein production: Statins, Niacin

• Increase lipoprotein removal: Bile acid sequestrants

• Decrease cholesterol absorption: Ezetimibe (Zetia)


19

Antiplatelet therapy

• ASA

• Clopidogrel (Plavix)


20

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


21

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.”



22

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


23

Etiology and pathophysiology

Reversible (temporary) myocardial ischemia = Angina (chest pain)

• O2 demand > O2 supply


24

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.


25

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


26


27

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.


28

Silent ischemia

Nocturnal

Angina decubitus

Prinzmetal’s (variant) angina

Microvascular angina


29

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

Short-acting nitrates: Sublingual

Long-acting nitrates

• Nitroglycerin (NTG) ointment• Transdermal controlled-release NTG


30

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


31

Diagnostic studies

Health history/physical examination

Laboratory studies

12-lead ECG

Chest x-ray

Echocardiogram

Exercise stress test


32

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.

33


34

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.


35

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)


36


37

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


38

Change in usual patternNew in onsetOccurs at restHas a worsening pattern

Unpredictable and represents a medical emergency.


39

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

Necrosis of entire thickness of myocardium takes 4 to 6 hours.


40


41

Fig. 34-9. Occlusion of the left anterior descending coronary artery,

resulting in a myocardial infarction.


42

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).


43

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.

44

Pain

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


45

Pain

heaviness, constriction, tightness, burning, pressure, or crushing

Common locations: Substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms


46

Stimulation of sympathetic nervous system results in :

Release of glycogenDiaphoresisVasoconstriction of peripheral blood

vesselsSkin: Ashen, clammy, and/or cool to touch


47

Cardiovascular: Initially, ↑ HR and BP, then ↓ BP

(secondary to ↓ in CO) Crackles Jugular venous distentionAbnormal heart sounds• S3 or S4• New murmur


48

Nausea and vomitingCan result from reflex stimulation of the

vomiting center by severe pain

FeverSystemic manifestation of the

inflammatory process caused by cell death


49

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.


50

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.


51

By 6 weeks after MI, scar tissue has replaced necrotic tissue.

Ventricular remodelingmyocardium hypertrophy and dilate to

compensate for the infarcted muscle.


52

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


53

Heart failure

A complication that occurs when the pumping power of the heart has diminished


54

Cardiogenic shock

Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failureRequires aggressive management


55

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


56

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


57

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


58

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.

59


60

Fig. 34-12. Serum cardiac markers found in the blood after myocardial

infarction. CK, Creatine kinase.


61

Emergency management

Initial interventions Ongoing monitoring

1. Emergent PCI

Treatment of choice for confirmed MI

Balloon angioplasty + Drug-eluting stent(s)


62

2. Fibrinolytic therapy

Indications and contraindications

Best marker of reperfusion: Return of ST segment to baseline

Rescue PCI if thrombolysis fails

Major complication: Bleeding


63

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


64

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


65


66

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


67

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



68

Nutritional therapy

Initially NPO

Progress to

• Low salt

• Low saturated fat

• Low cholesterol


69


70

Fig. 34-3. Types of dietary fat.

Nursing assessment

Subjective data

• Health history

• Functional health patterns

Objective data


71

Nursing diagnoses

Acute pain

Risk for decreased cardiac tissue perfusion

Anxiety

Activity intolerance


72

Planning: Overall goals

Relief of pain

Preservation of myocardium

Immediate and appropriate treatment

Effective coping with illness-associated anxiety


73

Planning: Overall goals (cont’d)

Participation in a rehabilitation plan

Reduction of risk factors

Health promotion

• Therapeutic lifestyle changes to reduce cardiac risk factors


74

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 soundsCopyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

75

Ambulatory and home care:

Patient teaching CAD and angina

• Precipitating factors for angina

• Risk factor reduction

• Medications


76

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.


77

Acute interventionAnxietyEmotional and behavioral reaction • Maximize patient’s social support

systems.• Consider open visitation.


78

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


79

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


80

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


81

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)


82

Ambulatory and home care

Patient and caregiver teaching

Physical exercise

Resumption of sexual activity

• Emotional readiness of patient and partner

• Physical expenditure


83

EvaluationRelief of painPreservation of myocardium Immediate and appropriate treatmentEffective coping with illness-associated

anxietyParticipation in a rehabilitation planReduction of risk factors


84

Unexpected death from cardiac causes

Rapid CPR, defibrillation with AED, and early advanced cardiac life support increase survival rates


85

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)


86

most caused by ventricular dysrhythmias (e.g., ventricular tachycardia)

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


87

Strongest predictor:

Left ventricular dysfunction (EF 30%)

Ventricular dysrhythmias following MI


88

Diagnostic workup to rule out or confirm MICardiac markersECG

Cardiac catheterization PCI or CABG


89

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

(ICD)


90

Psychosocial adaptation

“Brush with death”“Time bomb” mentalityPossible role changes• Driving restrictions• Change in occupation


91

(Relates to Chapter 34, “Nursing Management: Coronary ...

Documents

Transcript of (Relates to Chapter 34, “Nursing Management: Coronary ...