Nursing Care Plan Angina Coronary Artery Disease Acute Coronary Syndrome


I. Pathophysiology
a. The disorder is characterized by a narrowing of coronary
arteries due to atherosclerosis, spasm or, rarely, embolism.
b. Atherosclerotic changes in coronary arteries results in damage
to the inner layers of the coronary arteries with stiffening
of vessels and diminished dilatory response.
c. Accumulation of fatty deposits and lipids, along with
development of fibrous plaques over the damaged areas in
the vessels, causes narrowing of the arteries, thus reducing
the size of the vessel’s lumen and impeding blood flow to
the myocardial tissues.
d. Decreased delivery of oxygen and nutrients to the tissues
causes transient myocardial ischemia and pain.
e. Hard plaque causes hardened arteries, whereas soft plaque
can cause formation of blood clots.
II. Types
a. Stable
i. Most common type, precipitated by physical exertion,
emotional stress, exposure to hot or cold temperatures,
heavy meals, and smoking
ii. Occurs in a regular pattern, usually lasts 5 minutes or
less, and is easily relieved by medications
b. Unstable
i. May be new onset of pain with exertion or at rest, or
recent acceleration in severity of pain
ii. Occurs in no regular pattern, usually lasts longer (30 minutes),
not generally relieved with rest or medications
iii. Sometimes grouped with myocardial infarction (MI)
under the diagnosis of acute coronary syndrome (ACS)
c. Variant (Prinzmetal’s)
i. Rare, usually occurs at rest—midnight to early morning
ii. Pain possibly severe
iii. Electrocardiogram (ECG) changes due to coronary
artery spasm
III. Classification
a. New York Heart Association Classification (9th edition
update, 1994) quantifies the functional limitation imposed
by patients’ symptoms:
i. Class I—no limitation of ordinary physical activity
ii. Class II—slight limitation of ordinary physical activity
b. Prevalence: leading cause of death in Caucasians, African
Americans, Hispanics, and American Indians for both males
and females
iii. Class III—moderate limitation of activity; comfortable
at rest, but less than ordinary activities cause symptoms
iv. Class IV—unable to perform any physical activity
without discomfort, therefore severe limitation and may
be symptomatic even at rest
i. Class 1—no angina with usual physical activities such
as walking, climbing stairs; occurs with strenuous,
rapid, or prolonged exertion at work or recreation
ii. Class 2—slight limitation of ordinary activity with
angina occurring with moderate exertion such as walking
or climbing stairs rapidly, walking uphill, activity
after meals, activity in cold or wind, during emotional
stress, or during the few hours after awakening
iii. Class 3—marked limitations of ordinary physical
activity with angina occurring during mild exertion,
such as walking one to two level blocks or climbing one
flight of stairs at a normal pace
iv. Class 4—angina at any level of physical exertion; may
be present even at rest
IV. Etiology
a. Increased cardiac workload: exertion, hypertension, aortic
stenosis or regurgitation, hypertrophic cardiomyopathy
b. Decreased O2 supply: severe anemia, hypoxia
c. Risk factors: being overweight and obese, smoking, sedentary
lifestyle, diabetes, family history of early heart disease,
metabolic syndrome (fasting hyperglycemia and insulin
resistance, hypertension, central obesity, decreased highdensity
lipoprotein [HDL] and elevated low-density
lipoprotein [LDL] cholesterol, elevated triglycerides)
V. Statistics (National Heart, Lung and Blood Institute
[NHLBI], 2007; Centers for Disease Control and Prevention
[CDC], 2007b)
b. Canadian Cardiovascular Society Functional Classification
(CCSC) System of unstable angina aids in determining the
risk of adverse outcomes and level of treatment needs:
c. Mortality: There were 872,000 deaths from cardiovascular
disease in 2004; accounts for approximately
36% of total deaths.
d. Cost: An estimated $432 billion was spent in 2007.

Care Setting
Clients judged to be at intermediate or high risk for MI are
often hospitalized for further evaluation and therapeutic

Nursing Priorities
1. Relieve or control pain.
2. Prevent or minimize development of myocardial complications.
3. Provide information about disease process, prognosis,
and treatment.
4. Support client or significant other (SO) in initiating
necessary lifestyle or behavioral changes.

Discharge Goals
1. Desired activity level achieved, with return to activity
baseline, and self-care needs met with minimal or no
2. Remains free of complications.
3. Disease process, prognosis, and therapeutic regimen
4. Participates in treatment program and behavioral
5. Plan in place to meet needs after discharge.


May be related to
Increased cardiac workload and oxygen consumption
Decreased myocardial blood flow, tissue ischemia
Possibly evidenced by
Reports of pain varying in frequency, duration, and intensity, especially as condition worsens
Narrowed focus
Distraction behaviors, such as moaning, crying, pacing, or restlessness
Autonomic responses, such as diaphoresis, BP and pulse rate changes, pupillary dilation, increased or decreased respiratory rate
Desired Outcomes/Evaluation Criteria—Client Will
Pain Level
Report anginal episodes decreased in frequency, duration, and severity.
Demonstrate relief of pain as evidenced by stable vital signs and absence of muscle tension and restlessness.

Pain Management
Instruct client to notify nurse immediately when chest pain
Assess and document client response and effects of
Identify precipitating event, if any; identify frequency, duration,
intensity, and location of pain.
Observe for associated symptoms, such as dyspnea, nausea,
vomiting, dizziness, palpitations, and desire to urinate.
Evaluate reports of pain in jaw, neck, shoulder, arm, or hand
(typically on left side).
Place client at complete rest during anginal episodes.
Elevate head of bed if client is short of breath.
Monitor heart rate and rhythm.
Monitor vital signs every 5 minutes during initial anginal
Stay with client who is experiencing pain or appears anxious.
Maintain quiet, comfortable environment; restrict visitors as
Provide light meals. Have client rest for 1 hour after meals.
Provide supplemental oxygen, as indicated.
Administer anti-anginal medication(s) promptly, as indicated,
for example:
Nitrates: NTG sublingual (Nitrostat, NitroQuick); extended
release tablets and capsules, such as Nitrong and
Nitrogard SR; metered-dose spray (Nitrolingual); transdermal
patch (Minitran, Nitrodisc); transdermal ointment
(Nitrol, Nitro-Bid); isosorbide (Isordil, Imdur)
Beta blockers, such as atenolol (Tenormin), carteolol
(Cartrol), labetalol (Normodyne), nadolol (Corgard),
metroprolol (Tropol XL), and propranolol (Inderal)
Calcium channel blockers, such as bepridil (Vascor),
amlodipine (Norvasc), nicardipine (Cardene), nifedipine
(Procardia), felodipine (Plendil), isradipine (DynaCirc),
and diltiazem (Cardizem)
Analgesics, such as acetaminophen (Tylenol)
Morphine sulfate (MS)
Monitor serial ECG changes.

Pain and decreased cardiac output may stimulate the sympathetic
nervous system to release excessive amounts of
norepinephrine, which increases platelet aggregation, and
release of thromboxane A2. This potent vasoconstrictor
causes coronary artery spasm, which can precipitate,
complicate, and prolong an anginal attack. Unbearable
pain may cause vasovagal response, thus decreasing BP
and heart rate.
Provides information about disease progression. Aids in
evaluating effectiveness of interventions and may indicate
need for change in therapeutic regimen.
Helps differentiate chest pain and aids in evaluating possible
progression to unstable angina. Stable angina usually lasts
3 to 15 minutes and is often relieved by rest and sublingual
nitroglycerin (NTG); unstable angina is more intense,
occurs unpredictably, may last longer, and is not usually
relieved by NTG or rest.
Decreased cardiac output, which may occur during ischemic
myocardial episode, stimulates sympathetic or parasympathetic
nervous system, causing a variety of vague
sensations that client may not identify as related to
anginal episode.
Cardiac pain may radiate; for example, pain is often referred
to more superficial sites served by the same spinal cord
nerve level.
Reduces myocardial oxygen demand to minimize risk of
tissue injury and necrosis.
Facilitates gas exchange to decrease hypoxia and resultant
shortness of breath.
Clients with unstable angina have an increased risk of acute
life-threatening dysrhythmias, which occur in response to
ischemic changes and stress.
BP may initially rise because of sympathetic stimulation and
then fall if cardiac output is compromised. Tachycardia also
develops in response to sympathetic stimulation and may
be sustained as a compensatory response if cardiac output
Anxiety releases catecholamines, which increase myocardial
workload and can escalate or prolong ischemic pain.
Presence of nurse can reduce feelings of fear and
Mental or emotional stress increases myocardial workload.
Decreases myocardial workload associated with work of
digestion, reducing risk of anginal attack.
Increases oxygen available for myocardial uptake and reversal
of ischemia.
NTG has been the standard for treating and preventing
anginal pain for more than 100 years. Today, it is available
in many forms and is still the cornerstone of anti-anginal
therapy. Rapid vasodilator effect lasts 10 to 30 minutes
and can be used prophylactically to prevent, as well as
abort, anginal attacks. Long-acting preparations are used
to prevent recurrences by reducing coronary vasospasms
and reducing cardiac workload. May cause headache,
dizziness, and light-headedness—symptoms that usually
pass quickly. If headache is intolerable, alteration of dose
or discontinuation of drug may be necessary. Note: Isordil
may be more effective for clients with variant form of
Reduce angina by reducing the heart’s workload. (Refer to
ND: risk for decreased Cardiac Output following.) Note:
Often, these drugs alone are sufficient to relieve angina in
less severe conditions.
Produce relaxation of coronary vascular smooth muscle,
dilate coronary arteries, and decrease peripheral vascular
Usually sufficient analgesia for relief of headache caused by
dilation of cerebral vessels in response to nitrates.
Potent opioid analgesic may be used in acute onset because
of its beneficial effects. Such effects include peripheral
vasodilatation and reduced myocardial workload; sedation,
which produces relaxation; and interrupted flow of vasoconstricting
catecholamines, thereby effectively relieving
severe chest pain. MS is given intravenously (IV) for rapid
action and because decreased cardiac output compromises
peripheral tissue absorption.
Ischemia during anginal attack may cause transient
ST-segment depression or elevation and T-wave inversion.
Serial tracings verify ischemic changes, which may
disappear when client is pain free. They also provide a
baseline against which to compare later pattern changes.

a. Morbidity: There are an estimated 79.4 million Americans
with some form of cardiovascular disease.
i. Coronary artery disease (CAD) accounting for 15.8 million;
angina, approximately 9 million
ii. 400,000 new cases annually, most are over age 65