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Coronary Artery Disease 1

Pathophysiology and Nursing Considerations of Coronary Artery Disease

Lyra Sunshine Rider

Chico State University, Chico


Coronary Artery Disease

Coronary artery disease also known as atherosclerosis or ischemic heart disease is the most

prevalent cause of cardiovascular disease. (National Heart, Lung, and Blood Institute [NHLBI], 2011b).

In America, coronary artery disease (CAD) is the number one cause of death of both men and women

(NHLBI, 2011b). Atherosclerosis is believed to begin in childhood and is thought to progress more

rapidly as you age (NHLBI, 2011b). Atherosclerosis is the build up of lipids or fatty substances inside the

lining of the walls of the arterial blood vessels (Smeltzer, Bare, Hinkle, & Cheever, 2010). This abnormal

lipid accumulation narrows the vessels and impedes blood flow thus limiting oxygen delivery to the heart

and body (Smeltzer et al., 2010). This decrease in blood flow and oxygen delivery can result in angina

pectoris, myocardial ischemia or myocardial infarction . Coronary artery disease over time can also

weaken the heart muscle resulting in heart failure and arrythmias (NHLBI, 2011b).

Coronary Atherosclerosis Pathophysiology

Atherosclerosis begins when fatty streaks of lipids are deposited in the intima of the arterial wall

after a lesion is created (NHLBI, 2011b). Lesions of the intima of the arterial wall may occur from

damage caused by smoking, high cholesterol, high blood pressure, and diabetes. These lesions initiate an

inflammatory response which stimulates macrophages. Macrophages ingest and transport the lipids into

the arterial walls. These “foam cells” also release biochemicals that irritate and continue to damage the

vascular endothelium. This continuous inflammation of the vascular lining attracts platelets and can

initiate clotting inside the arterial lumen (Smeltzer et al., 2010).

The inflammation initiates smooth muscle cells to begin proliferating which forms a fibrous cap

over the initial lipid filled lesion. These fibrous caps are called atherosclerosis or plaques. Plaques

accumulate and begin to narrow the lumen of the vessel by protruding outward, obstructing flow through

the vessel which decreases blood and oxygen supply to the heart and body. Plaques are classified as stable

or unstable, contingent upon the thickness of the plaque and the degree of inflammation to the vessel.

Stable plaques are usually thick and have a fixed lipid pool that can withstand the pressure and stress of


blood flow and vessel contraction and dilation. Unstable plaques are considered vulnerable because they

have a thin cap and are affected by continued inflammation of the vessel (Smeltzer et al., 2010). If an

unstable plaque has an increase to the lipid core, it may rupture and seep into the outer layer of the plaque

becoming a site for platelets to adhere to the injury. Accumulation of platelets form a thrombus which

can increase the obstruction of blood flow to the heart or completely occlude blood flow (NHLBI,

2011b). The obstruction may result in angina pectoris, acute coronary syndrome, myocardial infarction,

and even death (Smeltzer et al., 2010).

Clinical Manifestations

Chest pain is the most common symptom of a plaque or a thrombus decreasing blood flow and

oxygen to the heart and is referred to as angina pectoris (Smeltzer et al., 2010). The heart signals the body

of the unmet myocardial oxygen demand. This often results in a squeezing or pressure felt in the chest

from the myocardial ischemia. Pain may radiate to the jaw, neck, back or shoulders and may also be

mistaken for indigestion (NHLBI, 2011b). If the ischemia lasts for an extended period of time or the

decrease in oxygen is large enough, permanent damage to myocardial cells may result. The damage to

myocardial cells begins scar tissue formation resulting in myocardial dysfunction such as decreased

cardiac output or heart failure. A substantial decrease in blood supply to the heart can also result in

sudden cardiac death (Smeltzer et al., 2010).

Patients may also present asymptomatic of chest pain during a coronary event, although the

“epidemiologic study of the people of Framingham, Massachusetts, showed that nearly 15% of men and

women who had coronary events, which included unstable angina, MIs, or sudden cardiac death events,

were totally asymptomatic prior to the coronary event.” (Smeltzer et al., 2010, p.757). Shortness of breath

is often reported as a symptom by older patients and patients with a history of diabetes or heart failure.

Atypical symptoms are generally experienced by women which may include nausea, weakness, and

dyspnea (Smeltzer et al., 2010).


Risk Factors and Patient Education

Risk factors that increase the probability for coronary artery disease are classified into two

categories, modifiable and non modifiable. Modifiable risk factors are those the patient can change by

making adjustments to their lifestyle or by using medications. Non modifiable risk factors are those a

patient has no control over. Some modifiable risk factors include: hyperlipidemia, cigarette use,

hypertension, diabetes mellitus, metabolic syndrome, obesity, diet and physical non activity. Non

modifiable risk factors include: family history of CAD, increasing age (men over 45, women over 55) and

race (higher incidence in African Americans). Patients with metabolic syndrome are also at high risk for

heart disease. Metabolic syndrome has the following risk factors: insulin resistance, central obesity,

dyslipidemia, blood pressure higher than 130/85 consistently, pro inflammatory state (high levels c-

reactive protein), and pro thrombotic state (Smeltzer et al., 2010).

The top four modifiable risk factors for CAD are tobacco use, diabetes mellitus, hypertension, and

cholesterol abnormalities. Nursing assessment of these risk factors and patient education on risk

modification are very important for improving health in patients suffering from CAD (Smeltzer et al.,

2010).

Cigarette cessation is highly encouraged to decrease the risk of developing CAD. Smoking

contributes to CAD by decreasing the amount of oxygen available to the heart and can also lower cardiac

output. Nicotinic acid in cigarette smoke causes constriction of the coronary vessels and increases heart

rate and blood pressure by stimulating the release of catecholamines which are associated with sudden

cardiac arrest. Cigarette smoking damages the vascular endothelium resulting in an increased number of

plaque and thrombus formations (Smeltzer et al., 2010).

Diabetes affects CAD development in various ways and has been known to accelerate heart

disease. Diabetes encourages dyslipidemia, this in turn increases platelet aggregation and thrombus

formation. Treatment and control of hyperglycemia can lead to improved endothelial function and patient

health by reducing the risk of developing plaques (Smeltzer et al., 2010).


The risk of a cardiovascular event increases in people with a blood pressure over 120/80.

Hypertension is a blood pressure that continually exceeds 140/90. Pressures at or above this high level

contribute to increased stiffness of the walls of the vessels (stenosis). Stenosis leads to increased

inflammation, vessel injury, and occlusion. The workload of the left ventricle is increased by

hypertension and this increase causes the heart to hypertrophy and may result in heart failure. Detection

and medical intervention is necessary to decrease this risk (Smeltzer et al., 2010).

In an effort to control cholesterol abnormalities all adults over 20 should have a fasting lipid panel

and then repeat after every 5 years, more often if there are abnormal results. The normal values for this

test are an LDL count less than 100 mg/dl ( less than 70 mg/dl in high risk patients), total cholesterol less

than 200 mg/dl, HDL cholesterol grater then 60 mg/dl, and triglyceride levels less than 150 mg/dl. It is

recommended that patients begin the Therapeutic Lifestyle Diet to help control their cholesterol levels.

This diet sets fat intake at 25-35% of calories, carbohydrates at 50-60% of intake, dietary fiber at 20-30 G

a day, protein at 15% of caloric intake and cholesterol less than 200 mg a day. Patients are encouraged to

increase their physical activity to 30 minutes of moderate exercise a day which increases LDL levels and

decreases triglyceride levels thus decreasing the risk of a coronary event. Lipid lowering medications can

also be prescribed to help the patient control cholesterol (Smeltzer et al., 2010).

Angina Pectoris

“Experts believe that nearly 7 million people in the United States suffer from angina. The

condition occurs equally among men and women.” (NHLBI, 2011a, p.1). Angina pectoris is the most

common symptom of coronary artery disease. (NHLBI, 2011a) Atherosclerotic narrowing of vessels is

the main cause of decreased blood flow to the heart resulting in an unmet oxygen demand. This usually

results during an increased myocardial demand for oxygen during exertion or emotional stress (Smeltzer

et al., 2010).

Pathophysiology

There are three main types of angina; stable, unstable, and refractory. Stable angina can be


relieved by rest or nitroglycerin intervention. It normally occurs on exertion and usually follows a

consistent and predictable pattern. Typical stable anginal episodes may be induced by the following:

physical exertion, exposure to cold, consuming a heavy meal, and emotional or physical stress. Unstable

angina is usually not relieved by rest or nitroglycerine. Symptoms continually increase in severity and

frequency and may occur while at rest. Intractable angina consists of severe incapacitating chest pain that

can be resistant to treatment (Smeltzer et al., 2010).

Physical symptoms of angina can vary from mild indigestion to severe symptoms such as a feeling

of impending doom. Common symptoms include pressure on the chest, vice like pain, pain deep in the

chest, radiating pain to the jaw or arm, and a strangling sensation. Diabetics may have mild or no pain

due to diabetic neuropathy. Women usually experience asymptomatic pain such as weakness or back

pain. Angina in the elderly also can present atypically due to diminished neurotransmitter responses

normal to the aging process. Many elderly people present only with dyspnea. This type of presentation is

an example of a “silent” CAD event. Other symptoms of angina include anxiety, weakness or numbness

of the upper extremities, diaphoresis, a pale complexion, dizziness, and nausea and vomiting (Smeltzer et

al., 2010).

Assessment and Diagnostics

Assessment of angina begins with a thorough patient history with an in depth focus on the

precipitating events that occurred before the episode. An ECG can show changes of the heart due to

ischemia. Lab tests such as a CRP and cardiac biomarkers can be run to rule out acute coronary

syndrome. A patient may also receive an exercise stress test or pharmacological stress test to help with

diagnosis (Smeltzer et al., 2010).

Medical and Pharmacologic Management

Medical management of angina includes both controlling risk factors and pharmacological

therapies. These are usually used in conjunction to decrease the myocardial demand and increase the

oxygen supply to the heart. As a last resort reperfusion procedures may be needed to restore blood flow to


the heart. These may include precutaneous transluminal coronary angioplasty (PTCA), Coronary artery

bypass graph (CABG), intracoronary stents, and atherectomy (Smeltzer et al., 2010).

Medications that may be prescribed to help control angina include: nitroglycerine, calcium

channel blockers, beta adrenergic blockers, antiplatelet medications and anticoagulants. Nitroglycerine is

a vasodilator which decreases pain and ischemia by decreasing myocardial oxygen demand. Calcium

channel blockers decrease the workload of the heart by slowing heart rate and decreasing the strength of

myocardial contractions. Beta blockers block beta adrenergic stimulation of the heart resulting in a

decrease in myocardial demand for oxygen. Anti platelet medications such as Aspirin and Plavix inhibit

platelet adhesion and thrombosis generation. Anticoagulants that may be prescribed include Heparin and

Fragmin which prevent the formation of new blood clots. Oxygen therapy may also be used to decrease

pain and increase the amount of oxygen available to the heart with target blood oxygen saturation being

above 93% (Smeltzer et al., 2010).

Nursing Process

Nursing assessment of angina includes a full patient history with an emphasis on the patient's

symptoms and activities before, during, and after the attack. Questions may include, “Can you rate the

pain?”, “When did the pain begin ?”, “What brings on the pain ?”, “What helps the pain go away ?”

(Smeltzer et al., 2010, p. 766). The nurse also needs to access the patient's risk factors for CAD to

determine an inclusive program of prevention, treatment, and patient education. Nursing diagnoses

pertaining to angina may include: “ineffective cardiac tissue perfusion secondary to CAD as evidenced by

chest pain or other prodromal symptoms.” “Death anxiety related to cardiac symptoms” and “ deficient

knowledge about the underlying disease and methods of avoiding complications” (Smeltzer et al., 2010,

p. 766). Potential complications that may develop are cardiogenic shock, acute coronary syndrome, MI,

dysrhythmias, heart failure, and cardiac death (Smeltzer et al., 2010). Nursing planning goals for angina

include the prevention of future episodes, reduction of anxiety, education regarding the condition and

prescribed treatment, compliance with home care, and absence of complications. Nursing interventions


would include treating angina, reducing anxiety, and preventing pain. Nursing treatment of angina

includes assessment of the current episode to see if the condition is worsening. Assessments may

include: directing the patient to stop all activity and to sit and rest to see if resting helps alleviate the pain

or by obtaining an EKG to assess ST segment and T wave changes. Nitroglycerine may also be

administered and the nurse needs to assess the patients response to interventions and monitor vital signs

continually. Oxygen administration of 2 liters by nasal cannula may also be needed by the patient if their

oxygen saturation is low or if their respiratory rate is increased. Expected patient outcomes after an

angina attack would include prompt resolution of pain, adherence to therapy program, and patient

demonstration of knowledge on how to prevent and recognize future attacks (Smeltzer et al., 2010).

Cultural Considerations

Special consideration during nursing assessments need to be give to patients of different cultural

backgrounds. “Native American healing practices vary greatly because there are more than five hundred

Native American Nations (commonly called tribes). There are many tribal differences, so it is not

surprising that healing rituals and beliefs vary a great deal” (American Cancer Society, 2008, p.9). In

Native American culture it is standard practice to utilize the services of shamanic healers or tribal elders

for healing (Department of Integrative Medicine [DIM], 2008). They believe health and disease is a direct

reflection of the patients balance with nature (DIM, 2008).

“A common Native American sense of spirituality includes a sense that each and every part of the

cosmos is imbued with spirit, not only people but everything including animals, plants, rocks, rivers, and

so on (Matheson, 1996).” Trust development with these patients is important for full disclosure of current

health practices (American Cancer Society, 2008). “Historically, outside society has sometimes

misinterpreted Native American culture and beliefs, which may increase this reluctance.” (American

Cancer Society, 2008, p.1).

Native American culture is steeped in ceremonial practice. Herbal remedies used in ceremonial

healing need to be identified due to possible interaction with medications (DIM, 2008). It is also


important to ascertain whether the patient has recently gone through a purification or cleansing ritual

which can alter fluid volume balance and electrolyte levels (American Cancer Society, 2008).

The patients spiritual needs must also be addressed (DIM, 2008). “Prayer is also an essential part

of all Native American healing techniques.” (American Cancer Society, 2008, p.1). A private room may

be necessary to allow the patient privacy for ceremonies and prayer with members from their tribe (DIM,

2008). The burning of herbs and chanting prayers to cleanse and purify the body are common practice

(American Cancer Society, 2008).

Discharge Planning

Before discharge it is the nurses job to educate the patient and family on the disease process, how

to identify complications, how to treat the symptoms when they develop, how to prevent recurrent

episodes of angina, and how to prevent further advancement of CAD by decreasing risk factors by

tangible lifestyle changes. It is imperative for the patient and their family to understand that any pain

unresolved after 15 minutes even after nitroglycerine administration needs to be treated and assessed in

the emergency room immediately (Smeltzer et al., 2010).

Acute Coronary Syndrome and Myocardial Infarction

Coronary artery disease also encompasses Acute coronary syndrome (ACS) (American Heart

Association [AHA], 2011). ACS includes both unstable angina and myocardial infarction (MI) both non-

ST-segment elevation MI and ST segment elevation MI (AHA, 2011). Acute coronary syndrome is an

emergent situation in which ischemia to the heart results in permanent damage and even death to

myocardial tissue (Smeltzer et al., 2010).

Pathophysiology

Unstable angina is usually a consequence from ischemia to the heart due to atherosclerotic

plaques, this may result in an MI if not treated promptly. In the occurrence of an MI there is a complete

occlusion of the blood flow to the heart. This lack of blood flow results in myocardial injury and death.

Additional causes of an MI include situations where an imbalance between myocardial oxygen supply


and demand exists such coronary artery vasospasm, decreased oxygen supply (attributed to anemia

decreased blood pressure or blood loss), and increased myocardial oxygen demand (increased hear rate,

cocaine use, or thyrotoxicosis) (Smeltzer et al., 2010).

The affected area can develop damage very quickly (in minutes) or can develop slowly (over

hours or days). Ischemia develops as the calls are deprived of oxygen and then progresses to cellular

damage and infarction of myocardial cells (Smeltzer et al., 2010). “The expression time is muscle reflects

the urgency of appropriate treatment to improve patient outcomes. Each year in the United States, nearly

1 million people have acute MI's, one fourth of these people die as a result (AHA 2007)” (Smeltzer et al.,

2010, p. 768).

MI's are subcategorized into two categories: non-ST-segment elevation MI (NSTEMI) and ST-

segment elevation MI (STEMI). Signs and symptoms of an MI include chest pain that continues despite

rest and medication, shortness of breath, chest pain, nausea, indigestion, and anxiety or sense of

“impending doom” (Smeltzer et al., 2010). Cool pale diaphoretic skin, dizziness, increased heart rate,

increased respiratory rate may also be present (AHA, 2011). An electrocardiogram is used to identify the

type and location of MI. Goals of medical intervention for an MI are to minimize and prevent damage to

the heart and to prevent additional complications (Smeltzer et al., 2010).

Assessment and Diagnostics

Acute Coronary Syndrome is usually diagnosed with a combination of diagnostic tests and a

physical exam. These tests usually include a 12 lead EKG and a serial cardiac biomarker lab test. An in

depth patient cardiac history is also completed which should include a description of the presenting signs

and symptoms, previous heart health history for self and immediate family, and the patient's risk factors

for heart disease. This combination of tests and physical examination help differentiate whether the

patient has unstable angina, a NSTEMI, or a STEMI (Smeltzer et al., 2010).

Diagnosis of unstable angina include the following assessment results. Clinical manifestations of

coronary ischemia are present but the EKG and cardiac biomarker lab tests show no evidence of a current


MI. STEMI diagnosis is contingent upon a 12 lead EKG displaying changes of two contiguous leads.

Significant damage to the myocardium is evidence of an MI. NSTEMI patients have elevated cardiac

biomarkers but no EKG findings showing MI (Smeltzer et al., 2010).

The 12 lead electrocardiogram (EKG) should be obtained within 10 minutes of the patient's arrival

to the hospital. Serial EKG's show changes in the recording of the heart rhythm such as T-wave inversion

due to myocardial ischemia that alters repolarization of cardiac cells. ST segment elevation (1 mm above

isometric line) which is a consequence of myocardial injury. The injured myocardial cells re-polarize

faster than normal cells causing the ST elevation. This elevation in two leads is a main diagnostic finding

of a MI. The development of abnormal Q waves resulting from the absence of depolarization current

from the infarcted myocardial tissue is also a main diagnostic finding of a MI. R wave height may also

decrease after a MI. An echocardiogram may be used for MI diagnosis in conjunction with the EKG. The

echocardiogram evaluates ventricular function and the hearts ejection fraction (Smeltzer et al., 2010).

Lab tests to help diagnose an acute MI include myoglobin and troponin cardiac biomarker panels.

Cardiac enzymes such as Creatinine kinase, myoglobin, and troponin are released into the blood upon

cellular cardiac injury and death. An elevated Creatinine Kinase MB is specific to damage to cardiac

cells and only increases when they are damaged thus being an indicator of acute MI (Smeltzer et al.,

2010). The level increases within a few hours of cardiac cellular damage and peaks within 24 hours of a

MI. Myoglobin which is found in both skeletal and heart muscle begins to increase within 1-3 hours of

injury and peaks at approximately 12 hours. Myoglobin level increase is not cardiac specific but the

absence of a level increase helps to rule out a MI. Troponin isomers I and T are specific for cardiac

muscle and are used to diagnose myocardial injury and MI. A Troponin level increase can be detected a

few hours after injury and can remain elevated for as long as 3 weeks (Smeltzer et al., 2010).

Medical and Pharmacologic Management

Medical management goals of acute coronary syndrome are to minimize myocardial damage,

preserve function, and prevent further complications. “These goals are facilitated by the use of guidelines


developed by the American College of Cardiology (ACC) and the AHA.” (Smeltzer et al., 2010, p.770).

Myocardial damage is reduced by re perfusing the area by PCI or thrombolytic therapy Reducing

myocardial demand and increasing the available oxygen supply via medications, as well as oxygen

therapy and bed rest can also lessen further damage to the myocardial cells (Smeltzer et al., 2010).

Pharmacologic therapy for a MI includes Aspirin, nitroglycerine, morphine, IV beta blockers, anti

platelet medication, angiotensin-converting enzyme inhibitors and non steroidal anti inflammatory drugs

(NSAIDS). Suspected MI patients are given an initial loading dose of a minimum of 162-325 mg dose of

Aspirin as an anti thrombolytic (Hennekens, C.H., Dyken, M.L., & Fuster, V., 2009). Morphine decreases

the workload of the heart by decreasing both preload and after load of the heart while reducing pain and

anxiety, thus making it the first choice in treatment of a MI. ACE inhibitors prevent the conversion of

angiotensin I to angiotensin II, resulting in a decrease in blood pressure and the excretion of sodium and

fluid from the kidneys thereby decreasing the workload and demand on the heart (Smeltzer et al., 2010).

Beta blockers such as Metoprolol and Atenolol are used to reduce the myocardial oxygen demand

by blocking the beta adrenergic stimulation of the heart which reduces heart rate by slowing the

conduction of electrical impulses through the heart. Blood pressure reduces as well as myocardial

contractility, helping balance the myocardial supply and demand of oxygen. Beta blockers help prevent

the recurrence of angina and MI by delaying the onset of ischemia (Smeltzer et al., 2010). New

recommendations for the safety of acute usage of beta blockers during an MI have been released.

(Kontos, M.C., Diercks, D.B., Ho, P.M., Wang, T.Y., Chen, A. Y., & Roe, M.T., 2011). In a recent study

from the American College of Cardiology it was found that the emergent use of Beta blockers in MI

patients showed an increase of in hospital complications versus a later use of beta blockers after 24 hours

after MI . The complications included an increase of cardiogenic shock in both STEMI and NSTEMI

patients (Kontos, M.C., Diercks, D.B., Ho, P.M., et al., 2011). “Risk factors for shock are common in

STEMI and NSTEMI patients treated with early BBs. Increasing numbers of risk factors were associated

with increased risk for shock or death in patients treated with BBs. These results are consistent with


current recommendations for avoiding early BB treatment for patients with acute MI.” (Kontos, M.C.,

Diercks, D.B., Ho, P.M., Wang, T.Y., Chen, A. Y., Roe, & M.T., 2011 p. 1).

The most used thrombolytic agent by hospitals is Alteplase (t-pa). Thrombolytics dissolve clot

blockages in coronary arteries therefore increasing perfusion and minimizing the area of infarcted tissue.

Thrombolytics have specific protocols that need to be followed for administration. Thrombolytic patients

should be assessed by a nurse for contraindications to thrombolytic therapy. Some contraindications

include active bleeding, recent surgery, head trauma, and pregnancy. Thrombolytic therapy needs to be

administered 3-6 hours after arrival at the hospital. Nursing considerations for patients on thrombolytic

therapy include minimizing the number of times a patient's skin is punctured, avoid intramuscular

injection, monitor for dysrhythmias and hypotension, check for signs and symptoms of bleeding

(Smeltzer et al., 2010).

Emergent treatment of a STEMI patient may be accomplished by Percutaneous coronary

intervention (PCI). PCI re-perfuses the ischemic myocardial tissue by opening the occluded artery. The

types of PCI vary and include percutaneous transluminal coronary angioplasty (PTCA), intracoronary

stent implantation, atherectomy, and brachytherapy. Patients should arrive to the cardiac catheter lab

within 60 minutes or less of arriving at the hospital for treatment (Smeltzer et al., 2010).

In PTCA a balloon tipped catheter is inserted into coronary vessels to re perfuse the heart by

reducing the blockage by either compressing the plaque or by breaking it apart. The body initiates an

inflammatory response (restenosis) after a PTCA procedure which causes vasoconstriction of the vessels

and may result in scaring and clot formation. A coronary artery stent may be placed after PTCA to keep

the artery open and provide structural support. Atherectomy is an invasive procedure that removes the

coronary plaque by grinding, cutting, or shaving and may be used in conjunction with PTCA.

Brachytherapy prevents vessel restenosis by gamma or beta radiation which inhibits smooth muscle cell

proliferation (Smeltzer et al., 2010).

ACS patients may undergo coronary artery revascularization procedures such as a coronary artery


bypass graft (CABG). During a CABG a blood vessel is grafted to an occluded artery so that blood can

flow beyond the occlusion and perfuse the heart. “For a patient to be considered for CABG, the coronary

arteries to be bypassed must have 70% occlusion (60% if in the main coronary artery).” (Smeltzer et al.,

2010, p.).Complications of a CABG may include MI, dysrhythmias, and hemorrhage (Smeltzer et al.,

2010).

Nursing Process

The nursing process for a patient with Acute coronary syndrome includes an in depth assessment

to determine the patients baseline condition which enables future analysis of any deviations from the

initial assessment. The assessment includes patient cardiac history of chest pain, dyspnea, palpitations,

diaphoresis, faintness, and palpitations. All symptoms need to be evaluated relating to onset, duration,

and resolution. A physical exam is also essential in determining a baseline of patient health. Two IV's are

usually placed for emergent medication administration (Smeltzer et al., 2010).

Nursing diagnosis for acute coronary syndrome includes consideration of clinical manifestations,

history, and diagnostic findings. Some potential nursing diagnoses may include “Ineffective cardiac tissue

perfusion related to reduced coronary blood flow”, “risk for imbalanced fluid volume” and “ death

anxiety related to cardiac event.” (Smeltzer et al., 2010, p.766). Some potential complications may

include acute pulmonary edema, cardiogenic shock, heart failure, dysrhythmias, and cardiac death


Planning and goals for the patient with acute coronary syndrome include the relief of pain,

prevention of myocardial damage, and reduced anxiety. Secondary goals include adherence to therapy

regimen, early recognition or absence of complications, and a decrease in risk factors contributing to

acute coronary syndrome (Smeltzer et al., 2010).

Nursing Interventions

Nursing interventions for acute coronary syndrome entail the following: relieve pain, improve

respiratory function, promote adequate tissue perfusion, reduce anxiety, and manage and identify


potential complications. The top priority for an ACS patient is to balance myocardial oxygen supply and

demand. This can be done through oxygen therapy by titrating the oxygen saturation between 96-100%

and administering the prescribed pharmacologic therapy. Vital signs should be assessed frequently along

with the patients pain rating. Bed rest and elevation of the head of the bed also help to decrease dyspnea.

Assessment of fluid volume status improves respiratory function by preventing overloading of the heart

and lungs. Frequent position changes should be encouraged to prevent pooling of fluid in the lungs


Tissue perfusion should be monitored by checking patients skin color, temperature, capillary refill,

and peripheral pule strength. Anxiety reduction and alleviation of fear are important nursing

interventions to reduce the sympathetic stress response, development of trust between nurse and patient

helps to facilitate this. Patient education, a restful environment, and relaxation techniques also help the

patient decrease fear and anxiety. Monitoring the patient carefully for changes in heart rate, rhythm, and

sound help to monitor for potential complications. The nurse also needs to assess respiratory status, pain,

urinary output, blood pressure, and lab values to determine the onset of complications (Smeltzer et al.,

2010).

Discharge

Preparing the ACS patient for discharge and self care at home includes assessing the patients

education needs. The level of understanding of the patient needs to be determined to ensure a successful

discharge. The patients understanding and educational needs should be assessed regarding ACS,

medication use, risk factors, identifying potential complications and when to seek help. Evaluation of the

ACS patient and expected patient outcomes include relief of angina, adequate tissue perfusion, decreased

anxiety, no complications, and patient adheres to self care regimen (Smeltzer et al., 2010).

A case manager or social worker may need to be involved in helping prepare the patient with

CAD for discharge. Arrangements can be made for financial assistance, home health or assisted living,

rehabilitation, dietary, transportation and counseling needs (Smeltzer et al., 2010).

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