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CARDIOVA SC ULAR DIS ORDE R

CORONARY ARTERY DISEASE (CAD)
ANGINA
UNCOMPLICATED MYOCARDIAL INFARCTION (MI)

CORO NAR Y ART ERY DIS EA SE ( CA D)

Results from narrowing of coronary arteries over time from atherosclerosis
(hardening of arteries)
Primary effect – loss of oxygen and nutrients to myocardial tissue because of
diminished blood flow

PA THO PH YS IOL OG Y
Fatty fibrous plaques progressively narrow coronary artery lumina reducing
the volume of blood that flows through them leading to myocardial ischemia
Vascular changes that keep diseased vessel from dilating → this causes altered
oxygen supply & demand which threatens myocardium beyond the lesion →
myocardial ischemia within 10 seconds of occlusion
Transient ischemia – reversible changes at cellular & tissue levels depressing
myocardial function
Hypoxia, reduced energy to heart & acidosis rapidly impairs left ventricular
function
Strength of contraction to affected area reduced (fibers shortening
inadequately) → resulting in less force and velocity
Wall motion is abnormal – less blood ejected from heart with each contraction
RESTORING B LO OD FLOW THROUGH CORONARY ARTERIES
RESTOR ES AEROBIC METAB OLISM AND CONTRACTILITY

Ris k F act or s
Refer to Table 33-2, pg. 802
Un modifiable
Age
Gender (men> women until 60 yr of age)

Race (African Americans < Whites)

Genetic predisposition & family history of heart disease

Mo difia bl e Ma jo r Ri sk Fa cto rs
Modifiable
Major

Cigarette smoking
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Hypertension
Elevated lipid level
Obesity
Physical inactivity
Contributing

Hyperglycemia (DM)
Stressful lifestyle (aggressive, hostility, Type A coronary prone)
Use of oral contraceptives
Infection (gingivitis)

Geography - industrialized regions

Si gn s & S ympt oms

Angina (classic sign)
Burning,squeezing or tightness in chest, radiates to left arm, neck, jaw or
shoulder blade
Nausea & Vomiting – results from reflex stimulation of vomiting centers by
pain
Cool extremities & pallor – sympathetic stimulation
Diaphoresis – sympathetic stimulation
Xanthelasma – result from hyperlipidemia
Women, Blacks, & Hispanics

Atyp ical p re se ntati on

May experience no chest discomfort
Dyspnea
Fatigue
Diabetics
Central neuropathies – no chest pain
Only see sympathetic stimulation (cool extremities, diaphoresis, N & V)

Sta bl e An gi na
Refers to chest pain occurring intermittently over a long time with the same
pattern of onset, duration, and intensity of symptoms; pain is predictable in
frequency & duration
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Relieved by rest or cessation of activity and nitroglycerin

Un stab le A ng in a
Progressive or perinfarction angina
Unpredictable (change in pattern)
Occurs during minimal or no exercise or exertion, during sleep, or
at rest
Ass. With deterioration of once stable atherosclerotic plaque;
rupture

Pri nzme tal ’s or V aria nt An gin a

Occurs at rest; not related to physical exercise or emotional stress
Pain caused by spasm of coronary artery
Symptoms – pain & marked ST segment elevation on ECG
Rare form of angina, may occur in absence of CAD
Triggered by smoking

Ab no rmal Lab Fin din gs

Lipid levels – may be elevated indicating atherosclerotic involvement
Cardiac enzymes
C-reactive protein (CRP) - marker for inflammation

Tes t to Help Di ag no si s C AD
ECG – Measures heart’s electrical activity; may show parts of heart muscle
damage
 Exercise or pharmacological stress test
Echocardiography
Coronary angiogram – shows any blockages &/or narrowing
CXR – detect heart enlargement, cardiac calcification & pulmonary congestion
Nuclear imaging
PET scan- Positron Emission Tomography

Dec rea si ng Ri sk Fa cto rs fo r CAD

Refer to Table 33-3, pg. 805
Lifestyle changes, include reducing saturated fat and cholesterol in the diet
Other therapies - Omega-3 polyunsaturated fatty acids (derived from fish oil)
and flax seed oil, olive oil (recently approved by FDA)
Refer to natural lipid-lowering agents, pg. 809
American Heart Association Diet
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Use AHA Step I or II diet pg. 807



Limit total fat intake to 25% to 35% total calories each day

Calories should come from carbohydrates such as bread, cereal, rice and
grains. 15% from proteins, meat, fish eggs, or beans
Exercise
Weight control
Don’t smoke
Limit alcohol intake
Eat 20 to 30 grams of soluble fiber every day

Tr eatme nt fo r A ng in a
Nitrates – Dilate peripheral blood vessels, coronary arteries & collateral
vessels No Viagra- Causes Blindness if used together
Nitroglyce rin (sublingual, IV, spray, ointment, transdermal controlled-

release)
Isosorbide dinitrate (SL or oral)

Isosorbide monotrate (oral)

Beta- Adrenergic blocking agent s ; direct decrease in myocardial

contractility, HR, SVR, & BP; reduce myocardial O2 demand (e.g. Tenormin,
Lopressor, Inderal).
Calcium Chan nel blocking agen ts – depresses SA node rate of discharge
& conduction through AV node (negative inotropic effect); systemic vasodilation
with decrease SVR and decrease myocardial contraction (e.g. Norvasc,
Cardizem, Isoptin, Procardia).
Do not drink grapefruit jucie
Antiplatelet & A nticoagulant first line pharmacologic intervention: ( e.g.
Aspirin, intolerance of ASA (use ticLid, plavix), Heparin, Lovenox, fragmin
Plavix- very important- stops platelets from clumping makes blood flow
smoother
Lovenox- low molecular heparin
Heparin infusion -

DRU G THERA PI ES
Antilipedemic drugs – reduce serum cholesterol or triglyceride
Niacin (Nicotinic Acid, Vit B3)
Lowers LDL and triglycerides & raises HDL
Cause itching and flushed face. Take an aspirin 30 mins before taking niacin
Bile acid sequetrants (colestipol, cholestyraine) -
Bind cholesterol in the bowels and get rid of it in the stool; used to lower
LDL and raise HDL
 May cause diarrhea and gas
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Statins(HMG CoA reductase inhibitors (lovastatin [Mevacor], pravastatin

[Pravachol], fluvastatin [ Lescol], simvistatin [Zocar], atorvastatin [Lipotor]
Lower LDL and triglyceride levels and in some patients can raise HDL
Diarrhea, nausea, vomiting & leg cramps. Require liver function studies
(work in liver)
Anti-hypertensive meds – control BP
Estrogen replacement therapy – reduce risk CAD in post menopausal women

Gemfibrozil (Lopid)
Lowers TG, minimal or no effect on chol.
Used to treat hypertriglyceridemia to prevent pancreatitis
Major S. E.: GI complaints, myopathy, HA, dizziness, fatigue, blurred vision
Monitor fasting lipid profile, liver enzymes, FBS
Don’t use with statins, this might damage muscle and cause gall stones

Tr ea tm en t
Coronary artery bypass graft (CABG)
Surgery to restore blood flow by bypassing an occluded artery using another
vessel –Internal mammary artery (chest); Saphenous Vein (from leg)
Fig 33-18, pg 822
“Key-hole” – minimally invasive surgery
Precutaneous transluminal coronary Angioplasty (PTCA) or angioplasty –
minimally invasive tx to open blocked arteries; with or without stent
placement – hold artery open
Drug-eluting stent placement (Taxus) - holds a reopened artery open &
minimize the risk of restenosis

PTC A
Nur si ng Diag no si s an d Clie nt G oal s, A ng in a
Nur sing Diagnosi s
Acute Pain
Ineffective myocardial tissue perfusion
Anxiety R/T fear of death
Activity intolerance
Knowledge deficit about disease and methods to avoid complications
Noncompliance, ineffective management of therapeutic regimen R/T failure to accept
necessary lifestyle changes
Cli ent goals (outcom es )
Painrelief & absence of return of pain
Reduction of anxiety
Awareness of underlying nature of disorder
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Understanding Rx care
Adherence to self care program
Modify risk factors
Absence of complications

Nur si ng Man ag eme nt CA D

Identify persons at risk for CAD
Obtain personal and family hx
Environmental factors – eating habits, type of diet, level of exercise
Psychosocial hx – smoking habits, alcohol ingestion, type A behavior, recent life-
stressing events, sleeping habits, presence of anxiety or depression
Identify pt attitude & benefits of health & illness
Educational background
Once high risk person identified – preventive measures taken –
modifiable risk factors

ASSE SSME NT , AN GI NA & MI

•Gather info about symptoms & activities, those that precede and precipitate
attack
•Refer Table 33-15, pg 825
•See Table 28-4 pg 723, ask questions using the PQRST format- handout

Nur si ng Man ag eme nt

If nurse present during an angina attack, do this
Administer oxygen
Assess Vital Signs
12-lead EKG
Nitrate followed by narcotic analgesic if needed; prompt pain relief
Physical assess of chest
Position pt comfortably

PT & FAM ILY TEACH IN G

Reassure long, productive life is possible
Teaching tools – one-to-one on daily care, pamphlets, films at beside, heart
model, written info
Assist to identify factors that precipitate angina & instructions on how to avoid
Help to identify risk factors
Teach about diet low in Na & saturated fats maintaining ideal body weight;
exercise program
Counseling R/T threat to identity & self esteem
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Myoca rdia l Inf ar cti on (Hear t At tac k)

Reduced blood flow through one of coronary arteries results I
myocardial ischemia and necrosis
Mortality high if treatment is delayed
Occlusion stem from atherosclerosis, thrombosis, platelet aggregation or
coronary artery stenosis or spasm
Prolonged ischemia longer than 20 minutes – irreversible cell damage
and muscle death – site depends on vessel involved

Myo card ial Infa rc tio n Pa thop hy siol ogy

Site of occlusion depends on vessel involved
Circumflex branch left coronary artery – lateral wall infarction
Anterior descending branch left coronary artery – anterior wall infarction
Right coronary artery or its branches – True posterior or inferior wall
infarction; also right ventricular infarction and cause right sided heart failure
Central area of necrosis or infarction surrounded by area potentially viable
hypoxic injury – recover if revascularization occurs (circulation restored in 6
hours)
Change s that occur in MI
Cardiac enzymes and proteins released by infarcted myocardial cells – used

in diagnosis of MI
In 24 hours infarcted muscle becomes edematous and cyanotic

Next several days leukocytes infiltrate the necrotic area & begin to remove

dead cell thinning ventricular wall

Cau se s (Pre di spo sin g Ri sk Fa cto rs )

Family Hx of MI
Gender (men, postmenopausal women more susceptible)
Hypertension
Smoking
Elevated triglycerides, cholesterol, & LDL
Obesity
Excess intake of saturated fats
Sedentary lifestyle
Aging
Stress or type A personality
Drug use (cocaine & amphetamines)

Sig ns & S ymp to ms - M I

Hallmark – severe. Immobilizing CP unrelieved by rest or nitrate
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CP not evident in all patients ( may present with weakness, indigestion SOB)
Nausea & Vomiting (reflex stimulation of vomiting center by severe pain)
CNS stimulation – increased catecholamines (norepinephrine and epinephrine
released ) result in diaphoresis and vasoconstriction pf peripheral blood vessels;
skin ashen, clammy & cool (“cold sweat”)
Fever – day after MI – inflammatory response
Changes in vital signs
Jugular vein distention reflects ventricular dysfunction and pulmonary
congestion
S3 & S4 heart sounds – ventricular dysfunction
Loud murmur in apex
Reduced urine output – reduced renal perfusion and increased aldosterone and
antidiuretic hormone

Diag no si s – MI
Serial measurement of cardiac markers (Q 8 hrs X’s 3) – show characteristic
rise and fall
Creatine kinase (CK) – rises within 4-6 hrs of MI (maybe skeletal, brain, or
heart)
CK-MB- starts to rise within 10-30 mins; rises within 4-6 hrs after acute
MI & peaks in 24 hours
Indication of MI - > 7.5 ng/ml
Troponin – starts & peaks same as CK-MB and remains elevated up to 3
weeks
Troponin I highly specific to cardiac tissue
WBC – elevated
Increased FBS – release of catecholamines
C-reactive protein & Erythrocyte sedimentation rate from inflammation
Myoglobin – helps determine MI

Diag no si s
ECG - in specific leads T-wave inversion (ischemia), ST segment
elevation (injured cardiac tissue), & abnormal Q wave - 12 lead
ECHO – show ventricular wall motion abnormalities
CXR show left-sided heart failure or cardiomegaly form ventricular
dilation
Nuclear imaging scanning
Cardiac catheterization - info about which coronary artery is blocked
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DR UG THE RAP Y FOR MI

Morphine sulfate (MSO4) is given for acute chest pain relief b/c it reduces
anxiety and fear and decreases the cardiac workload by lowering myocardial
oxygen consumption
IV nitroglycerin (Tridil) may be used in the initial therapeutic tx
Antiarrhythmic drugs – arrhythmias are the most common complication after
an MI
Positive Inotropic drugs – that increase the heart’s contractility may be used in
patient with acute MI (e.g. Dobutrex, digitalis, amrinone (Inocor).
Beta-Adrenergic blockers – used in acute phase of the MI and during a 1 year
follow-up regimen, can decrease morbidity (Drug choice and dose depend on the
MD)
Calcium Channel blockers – may be used in the TX of MI where the pt also
underwent PTCA to restore perfusion

DRU G THERA PY
Angiotensin – converting enzyme (ACE) inhibitors – may be used
following MIs – help prevent ventricular remodeling and prevent or slow the
progression of heart failure (e.g. captopril (Capoten) and enalapril (Vasotec)
Stool softe ners – After an MI the pt is predisposed to constipation as result
of bed rest and narcotic administration. Given to facilitate and promote comfort
of bowel evacuation; prevents straining and resultant vagal stimulation from the
Valsalva’s maneuver
Fibrinolytics (streptokinase, t-PA, reteplase (Retavase) given to dissolve or
lyses the thrombus Chart 28-7, pg 727; Not used after major surgery or
hemorrhagic stroke
Major complication - _Bleeding__
IV Heparin – pt’s who have received fibrinolytic therapy to increase chances
of patency in affected coronary artery
Monitor Partial Prothrombin time (PTT) – 1-2 times normal
Complication - bleeding

- 60-80
- If less than 60 - another dose of heparin
- If more than 80- Decrease heparin

Nut riti on al Th er apy

Diet is restricted in saturated fats and cholesterol and sodium to prevent fluid
retention. The patient may have a clear liquid diet the first day is there is
nausea
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Treatm en t
Assessment of pt in emergency department within 10 minutes of symptoms
onset
“Ti me is muscle” refl ect urge nc y of app ropr ia te trea tme nt
Oxygen – 2-3 LMP/NC – increase blood oxygenation
Nitroglycerin SL or IV to relieve chest pain (parameters – BP systolic less
than 90 mm Hg or heart rate less than 50 or greater than 100)
Morphine or meperidine – analgesia – pain sympathetic nervous system,
leading to in increase in heart rate & vasoconstriction
Aspirin Q day indefinitely – inhibit platelet aggregation
Continuous cardiac monitoring – detect arrhythmias and ischemia
IV fibrinolytic therapy – beneficial within 3 hours after symptoms start
IV heparin – Patients who have received fibrinolytic therapy to increase
chances of patency in affected coronary artery (Monitor PTT – 1-2 times
normal)
PTCA
Glycoprotein IIb/IIIa receptor blocking agents – strongly inhibit platelet
aggregation
Limit physical activity for first 12 hours to reduce cardiac workload; limiting
area of necrosis
Be prepared to administer ACLS
Atropine, epinephrine, amiodarone, defibrillator, pacing)
Risk modification program
Lipid lowering agents

CABG
CABG procedure – main surgical tx for CAD to produce new pathway
beyond the occluded coronary artery
AIM – area distal to obstruction continue to receive blood flow
Uses blood vessels to go around (bypass) clogged coronary heart
arteries
Internal mammary artery (chest)
Saphenous Vein (from leg)
Fig 33-18, pg 822

Ca rd ia c R eh ab Ph as es
oRefer to Table 33-16, pg. 829
oPlan individualized care (by phases)
Phase I – predominately during admission to the hospital. Low-level
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activities & initial education for pt & family

Phase 2 – pt discharged. Lasts 4-6 weeks or up to 6 months.
Supervised exercise training I individualized based on results
of exercise stress test
Phase 3 – Maintain CV stability & long-term conditioning. Pt usually
self-directed during this phase & no supervised
program required
Phase 4 – time of recovery and maintenance – involve community
rehab program

Phy sic al Acti vity

Refer to Table 33-20, pg 832

Ph ysical exercise
Gradual increase in activity level
Watch symptoms rather than HR
Resump tion of sexual activ ity
Refer to Table 33-21, pg. 832
Resume after 1st phase of recovery and being discharged from hospital
Inability to perform sex is common
Discuss feeling in this area
May need prophylactic nitroglycerin
Avoid heavy meal before sex (wait 1-3 hours after eating a full meal – allow
digestion)
Avoid anal intercourse

As se ss me nt, MI
Assess level of consciousness
Evaluate chest pain
Assess heart rate and rhythm; dysrhythmias may indicate not enough oxygen
to the myocardium
Assess heart sounds; S3 can be an early sign of impending left ventricular
failure
Measure blood pressure to determine response to pain and TX; note pulse
pressure which may narrow after MI
Assess peripheral pulses, rate, rhythm and volume
Evaluate skin color and temperature
Auscultate lung fields at frequent intervals
Assess bowel motility
Observe urinary output and check for edema
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NUR SI NG DIA GN OSE S & C LIE NT G OAL S – MI

•Acute pain
•Decreased myocardial perfusion R/T reduced coronary blood flow
•Potential impaired gas exchange R/T fluid overload
•Risk for ineffective peripheral tissue perfusion R/T decreased cardiac output
•Anxiety R/T fear of death
•Knowledge deficit about MI, self-care

Relief
of symptoms of ischemia (chest pain, ST segment changes)
Absence of respiratory difficulties
Adequate tissue perfusion
Reduced anxiety
Adherence to self-care program
Prevention or early recognition of complications

Nur si ng Int er ve nti on s

Top priority – pain relief, once airway, pain relief breathing and circulation
have been stabilized
Administer oxygen and other medications as directed
Monitor at least every hour for indications of decreased cardiac output–
sustained HR>20 BPM over baseline, lowered BP, decreased urine output
Monitor cardiac rhythm, continuous ECG for premature ventricular contractions
(PVCs) (the most common dysrhythmia), or ventricular tachycardia (VT) which
precede ventricular fibrillation (lethal arrhythmia)
Monitor lung sounds fro crackles, wheezes, consolidation
Maintain patent IV line
Maintain restful environment
Bedrest first few days – severe MI
Rest in chair 12-24 hours after event – uncomplicated MI
Give brief explanations for all procedures, tests, and equipment and encourage
verbalization of feelings & relieve anxiety
Morphine given PRN (rate on pain scale 1-10)
Frequent VS, I & O (Q 4-8 hrs)
Anxiety
Table 33-17 emotional behavioral responses
Denial, Anger, Anxiety & fear, dependency, depression, realistic acceptance
Patient teaching starts on admit (CCU), assess learning needs

Hom e c are reg ard in g cli ent edu cati on

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Short and long- acting nitrates, how to administer and store them
Sublingual nitrates – take SL NTG at pain onset, then x2 at five-minute
intervals, if pain persists, call for assistance and transport to ER
Store in dry, dark bottle and obtain new bottle every 6 months, shelf life is 3
to 6 months once bottle is opened; a tingling under the tongue indicates
potency of med
Transdermal nitrates – rotate sites in non-hairy areas above the knees or
elbows and wash site after patch removed

Pa tie nt Ed ucati on
How to increase activity level slowly
How to weigh daily
Diet changes – low fat, low cholesterol, moderate to low salt
When sexual activity can resumed
Evaluate for medication effectiveness
How to take radial pulse daily, best before getting out of bed
What adverse reactions would require medical assistance, such as persistent
anorexia, N/V, or change in vision