Coronar Heart Diseases Hanan Sayed

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Medical Surgical Nursing Department (2nd year) Coronary Artery Disease

Coronary artery disease

Objectives:

Define the coronary artery diseases.

Identify the risk factors of coronary artery diseases.

Identify types of angina pectoris.

Describe the diagnostic procedures of angina pectoris.

Enumerate the medical management of angina pectoris.

Recognize the pharmacological mangments of angina pectoris.

Discuss the surgical management of angina pectoris.

Mention the nursing management of angina pectoris.

Define the myocardial infarction

Identify the clinical manifestation of myocardial infarction

Describe the diagnostic procedures of myocardial infarction.

Recognize the pharmacological mangments of myocardial

infarction

Discuss the complication of myocardial infarction

Mention the nursing management of myocardial infarction

Faculty of Nursing –Ain Shams University 39




Outlines:

•1 Definition of coronary artery diseases.

•2 Risk factors of coronary artery diseases.

•3 Angina pectoris:

1 Definition of angina.

2 Types of angina.

3 Diagnostic procedures of angina.

4 Medical management of angina.

5 Pharmacological managements of angina.

6 Surgical management.

7 Nursing Management of angina.

•1 Myocardial infarction:

Definition of myocardial infarction.

Clinical manifestations of myocardial infarction.

Diagnosis of myocardial infarction.

Pharmacological management of myocardial infarction.

Complications of myocardial infarction.

Nursing management of myocardial infarction.

Coronary Artery Disease

Definition of Coronary Artery Disease (CAD):

It is the term used to describe the effects of a reduction or complete

obstruction of the blood flow (and oxygen transport) through the coronary





arteries as a result of narrowing (atheosclerosis) and/or blood clot

(thrombus).

It has estimated that more than half of the deaths due to

cardiovascular disease are related to athreosclerotic pathology.

Risk Factors Leading to Coronary Artery Disease:

Risk factors can be categorized as unmodifiable and modifiable.

Unmodifiable risk factors are age, gender race and genetic inheritance.

Modifiable risk factors include elevated serum lipids, hypertension,

smoking, obesity, physical inactivity, and stress in daily living, although

control of diabetes is recommended.

A- Unmodifiable Major Risk factors:





Absolute risk of CAD increases with age in both men and women

as the result of progressive accumulation of coronary atherosclerosis with

aging.

• Men have a greater risk for developing coronary artery disease than

woman at earlier ages. During their reproductive years, women have a

much lower incidence of Coronary Heart Diseases (CHD) compared to

men of similar age. The reason for this difference is widely assumed to

the due to the protective effect of oestrogen.

• Oestrogen has well –documented effect on blood lipids and the

regulators of cardiovascular system, which should reduce risk.

• After the age of 65, the incidence in men and women equalizes.

• Black men have slightly lower CAD death rates (3.5%) compared

with white men. Black women have higher CAD death rates

(approximately twice the rate) than white women until age 74.

• Family history and hereditary: plays a role in how much cholesterol

your liver makes and how your body processes cholesterol. Some

people with high cholesterol levels have a genetic disorder called

familial hypercholesterolemia.

B- Modifiable Major Risk Factors:

1. Elevated Serum lipids:

Hypercholesterolemia is a relatively common condition that has

been associated with the development of atherosclerosis and





cardiovascular disease. An elevated serum lipid level is one of the most

formally established risk factors for CAD. More, the risk of CAD is

associated with serum cholesterol level of more than 200 m/g (5.2

mmol/L) or a fasting triglyceride level of more than 200 mg/dl

(1.7mmol/L).

2. Hypertension:

It is a major risk factor that is termed the “silent Killer” because it

has no specific symptoms and no early warning signs.The stress of

constantly elevated BP increases the rate of atherosclerotic development.

This related to the shearing stress, causing denuding injuries of the

endothelial lining. Atherosclerosis, in turn, causes narrowed, thickenedarterial walls and decreases the distensibility and elasticity of vessels.

3. Cigarette smoking:

It is a major risk factor for cardiovascular disease, includes

increases of plasma cholesterol. Triglycerides and fibrinogen, enhances

thromboxance production and platelet aggregation and decreases high – density lipoprotein (HDL)-cholesterol.

4. Physical Inactivity:

It is a major modifiable risk factor. Physical inactivity implies a

lack of adequate physical exercise on a regular basis. Physical active

people have increased HDL levels, and exercise enhances fibrinolytic

activity, thus reducing the risk of clot formation. It is also believed that

exercise encourages the development of collateral circulation.

5. Obesity:

It has joined cigarette smoking and elevated serum cholesterol as a

major modifiable risk factor for coronary heart disease (CHD). Obesity

increases risk for CAD indirectly through its associated with insulin

resistance, hyperlipidemia, “as obese persons are through to produce

increased level of LDL, which are strongly implicated in arteriosclerosis”

and hypertension.





C- Modifiable contributing risk factors:

1. Diabetes mellitus:

The incidence of CAD is greater among persons who have diabetes

even those with well-controlled blood glucose levels. The patient withdiabetes manifests CAD not only more but also at an earlier age.

Arterial wall exposure to abnormally high levels of circulating

insulin causes proliferation of smooth muscle cells inhibition of

glycolysis and synthesis of cholesterol, triglyceride and phospholipids.

2. Stress and behavior patterns:

Several behavior patterns have been correlated with CAD. Type A

behaviors include protectionism and a hard working, driving personality.

3. Psychological traits:

Depression, anxiety, and hostility have been demonstrated to be

associated with the risk of coronary artery disease and of adverse

outcomes after acute coronary events.

Angina Pectoris

The term angina comes from Latin word meaning to choke. Angina

pectoris literally translated as; pain (angina) in the chest (pectoris). Also

strangling of the chest and is a symptoms of myocardial ischemia.

Angina classically consists of reterosternal constricting

discomfort, which may radiate to arm, the throat, the jaw, the teeth, the

back or the epigastrium. It is usually a manifestation of CHD but any

situation which upsets the balance between myocardial oxygen supply

and demand may result in angina.





Myocardial oxygen demand is increased by exercise, emotional

stress, smoking tobacco, eating heavy meals, and exposure to cold

weather or extreme humidity. As long as coronary vasodilatation

increases blood supply, this extra demand can met.Coronary atherosclerosis or vasospasm, however, may prevent

adequate coronary vasodilatation, which may result in myocardial

ischaemia. Ischaemia is reversible, but if myocardial blood flow is not

increased or myocardial oxygen demands are not reduced, ischaemia can

progress to cell death.

Types of angina:

1. Stable angina:

Predictable and consistent pain that occurs on exertion and is

relieves by rest. It involves a fixed coronary artery lesion. Limiting the

oxygen supply at times of increased demand. Symptoms are therefore

typically provoked by an activity that increase myocardial oxygen

demand. The discomfort is usually relieves within 2-10 minutes by rest.

Classic associated symptoms are shortness of breath, sweating, palpitations and weakness. Symptoms tend to be worse in the morning,

coinciding with a peak in blood pressure, after heavy meals and in cold

weather. People with stable angina are at increased risk of AMI and

sudden death.

2. Unstable angina:

It can cause sudden death or result in myocardial infarction.Unstable angina usually results from the rupture of an atheromatous

plaque within the coronary circulation, which provides a stimulus for

platelet deposition and thrombosis. Characteristically, unstable angina

presents as: recent onset of experiencing angina symptoms (within the

past 4-6 weeks), a change in the symptoms experiences, i.e. the

discomfort has become more frequent, more easily triggered, more severe

or prolonged or less responsive to nitrate therapy, discomfort /pain and





associated symptoms occurring in the absence of physical or emotional

press and lasting more than 20 minutes.

3. Variant angina (Prinzmetal’s angina):

It is a less common of angina; it is characterized by episodes of

chest pain that occur at rest. This discomfort tends to be prolonged,

severe and not readily relieved by nitroglycerin. Variant angina is caused

by spasm of the coronary arteries and can be accompanied by transient

elevation of the segment.

4. Nocturnal angina:

It occurs only at night but not necessary when the person is in the

recumbent position or during sleep.

5. Angina decubitus:

It is chest pain that occurs only while the person is lying down andis usually relieved by standing or sitting.

6. Silent ischemia:

Approximately 70% of ischemic episodes in patients with CHD are

silent, making silent ischemia a more common occurrence than angina. In

addition, up to 30% of symptomatic myocardial infarctions are silent.

Diagnostic Procedures for Angina Pectoris:

Diagnosis:

When a patient has a history indicating CAD, the physician may

order several diagnostic studies after a detailed history and physical

examination, a chest X-ray is usually taken to look for cardiac





enlargement, cardiac calcification and pulmonary congestion laboratory

tests may be done to ascertain serum lipid and cardiac enzyme values.

Many clinicians now rely on the measurement of newly discovered

chemical risk factors to help guide management of patients at risk for CHD events. Theses measurement includes LDL particle size, HDL

subclass and anti-inflammatory markers.

Echocardiography (ECG): Changes are also helpful on making

diagnosis and remain a standard diagnostic test for patient with angina.

During the anginal episode, the electrocardiogram (ECG) may show

T-wave inversions and ST segment depressions in the

electrocardiograpgic leads associated with the anatomical region of

myocardial ischemia.

Stress echocardiograms may be used when a patient has an

abnormal baselines ECG. Another technique using an echocardiogram

can be used for the patient who is unable to exercise. In this patient, a

dobutamine stress echocardiogram can be performed.

Echocardiography is done during a stepwise infusion of doubutamine,

which causes a progressive increase in HR just as occurs with exercise,

that is the heart being exercises chemically.

Cardiac Catheterization and Coronary Angiography: There isaccumulating evidence that plaque catheterization can be used in clinical





practice. Cardiac catheterization is the most reliable as well as the most

invasive diagnostic procedure to evaluate chest pain.

Coronary Angiography: It gives a detailed study allows

visualization of the coronary arteries for obstruction and helps determine

the treatment and prognosis.

Intravascular ultrasound: It provides tomographic images of the

vessel wall including vessel size, plaque size, and plaque morphology.

During cardiac catheterization, a miniature ultrasound catheter is placed

beyond the target lesion site.

Positron emission tomography (PET):

It is a highly accurate, non – invasive test that can make images of the

blood flow inside the heart muscle, an indication of how well the

coronary arteries are working also useful in identifying and quantifying

ischemia and infarction.

Cardiac Computed topography and electron-beam computed

topography: The technique helps to measure coronary stenosis in patients who complain of atypical chest pain by using a high-speed

version of CT radiography to gauge calcium densities in the heart’s

arteries.

Magnetic resonance imaging: These techniques are used to study

atherosclerotic lesion morphology in human vessels. The technique has

the important advantage of being non invasive, not-dependant on

exercise and potentially useful to exclude the diagnosis of major

obstructive coronary artery disease.

Medical Management:

The objectives of medical management of angina are to decrease

the oxygen demands of the myocardium and to increase the oxygen

supply. Medically, these objectives are met through pharmacologic

therapy and control of risk factors.





vessels, causing a decrease in blood pressure and an increase in coronary

artery perfusion. Calcium channel blocker increase myocardial oxygen

supply by dilating the smooth muscle wall of the coronary arterioles; they

decrease myocardial oxygen demands by reducing systemic arterial

pressure and thus the workload of the left ventricle.

4. Antiplatelet and anticoagulant:

They are administered to prevent platelet aggregation, which

impedes blood flow. Aspirin and ticlopidine. Aspirin prevents platelet

aggregation and has been shown to reduce the incidence of MI and death

in patients with CAD.

5. Heparin:

It is prevents the formation of new blood clots. If the patient's

angina is considered to indicate a significant risk for a cardiac event.

6. Oxygen administration:

It is usually initiated at the onset of chest pain in an attempt to

increase the amount of oxygen delivered to the myocardium and to

decrease pain. Oxygen inhaled directly increases the amount of oxygen

in the blood.

7. Arginine-rich medical food:

When used as an adjunct to traditional therapy, improves vascular

function, exercise capacity and aspects of quality of life inpatients with

stable angina.

8. Vitamin E (a-tocopherol):

It is carried in LDL particles and is very effective in protecting

LDL from oxidation.

9. Vitamin C:

It is likely has no effect in preventing coronary heart diseases

according to epidemiologic and clinical intervention trials. Vitamin C,

one of the primary water-soluble

II. Surgical Management in Angina Pectoris:





Coronary revascularization:

Coronary revascularization procedures are usually undertaken to

relieve angina symptoms, although some patients may be referred for

prognostic reasons. Candidates for revascularization include those with

evidence of continuing extensive ischaemia or symptoms that persist

despite optimal medical therapy.

1. Percutaneous Transliuminal Coronary Angioplasty (PTCA):

It may be used to treat patients with recurrent chest pain that is

unresponsive to medical therapy, those with atheromas that occlude at

least 70% of the internal lumen of a major coronary artery.

2. Coronary artery bypass grafting surgeries (CABG):

It is still major intervention in the treatment of patients with

coronary heart disease. Current CABG is a surgical procedure in

which a blood vessel from another part of the body is grafted to the

occluded blood vessel so that blood can flow around the occlusion around

the occlusion.3. Atherectomy:

It is an invasive interventional procedure that involves the removal

of the atheroma, or plaque, from a coronary artery.

4. Transmyocardial Laser Revascularization (TMLR):

The C02 TMR therapy is a surgical procedure that relieves chest

pain in debilitated heart patients. A cardiac, surgeon utilizes the laser to

create approximately 20 to 40 channels to allow oxygen-rich blood to

reach prove deprived areas of the Patient's heart.

Nursing Care in The Acute Situation:

It is should be aimed toward minimizing of eliminating myocardial

ischemia and preventing progression to infarction.

Assessment:





Subjective and objective data should be obtained from the

patient. Patients with angina typically present with chest discomfort

described as heaviness, squeezing, choking, or smothering sensation. The

nurse uses the P, Q, R, S, T method of pain assessment when taking the

patient's history. The P, Q, , -S, T characteristics of chest pain due to

myocardial ischemia

Precipitating and palliative factors:

P → Precipitating

• Exercise. • Exercise after a large meal • Exertion

• Stress on anxiety. • Walking on a cold or windy day • Cold weather

• Fear • Anger R →Region and radiation

• Substernal with radiation to the neck, left arm or jaw, upper chest, epigastric,

left shoulder, intrascapular

P→ Palliative

• Stop exercise • Site down • Use sublingual nitroglycerin

Q→ Quality

• Heaviness • Tightness • Squeezing • Choking

• Suffocation • Vice-like

S→ Severity

• Pain rated on a scale of 1 to 10 with 10 being the worst pain ever experienced,

often rated as 5 or above.

• Pain can last longer than 30 minutes for unstable angina or myocardial

infarction

Nursing Diagnosis:

Based on the assessment data, major nursing diagnosis for the

patient may include the following: altered myocardial tissue perfusion

secondary to CAD, as evidenced by chest pain- (or equivalent

symptoms), 2) anxiety related to fear of death, -3) knowledge deficit

about the underlying disease and methods for avoiding complications, 4)

ineffective management of therapeutic regimen, 5) noncompliance,

related to failure to accept necessary lifestyle changes, 6) activity

intolerance related to myocardial ischemia.





Planning:

The major goals for the patient are to: prevent or minimize chest

pain, cope with the anginal pain and any other symptoms, reduce anxiety,

1. Nursing Intervention for Chest Pain:

When a patient sense chest pain, the nurse should direct the patient to:

Stop all activities and sit or rest in bed in a semi-Fowler’s position

to reduce the oxygen requirements of the ischemic myocardium.

Assesses the patient's pain, asking the standard (questions to

determine whether the pain is the same as the patient typically

describes.

Measuring vital signs and observing for signs of respiratory distress. If

the patient is in the hospital, a 12- lead ECG is usually obtained and

scrutinized for ST-segment and T-wave changes.

Nitroglycerin is administered sublingually and the patient’s response is

assessed.

• Oxygen is usually administered at 2 l/min by nasal cannula even

without evidence of respiratory distress.

2. Nursing Intervention for Reducing Anxiety:

Explain to the patient and family reasons for hospitalization, diagnostic

tests, and therapies administered.

Encourage the patient to verbalize fears and concerns regarding illness.

Answer the patient’s questions with concise explanations.

Administer medications to relieve patient anxiety as directed.

Teach relaxation techniques.

3. Nursing Intervention for Maintaining Cardiac Output:

The nurse should monitor carefully the patient’s response to drug

therapy.





• Take blood pressure and heart rate in a sitting and lying position on

initiation of long-term therapy provides baseline data to evaluate for

orthostatic hypotension that may occur with drug therapy.

4. Identify Suitable Activity Level to Prevent Angina Attacks:

Advise the patient on the following:

• Participate in a normal daily program of activities that do not produce

chest discomfort, shortness of breath, and undue fatigue.

• Begin regular exercise regimen as directed by health care provider.

• Avoid activities known to cause anginal pain-sudden exertion, walking

against the wind, extremes of temperature, high altitude emotionally

stressful situations; these may accelerate heart rate blood pressure, and

increase cardiac work..

• Refrain from engaging in physical activity for 2 hours after meals.

• Rest after each meal if possible.

• Do not undertake activities requiring heavy effort (e.g., carrying heavy

objects).• Try to avoid cold weather if possible, dress warmly and walk more

slowly. Wear scarf over nose and mouth when in cold air.

• Reduce weight , if necessary, to reduce cardiac load.

5. Instruct about appropriate Use of Medication and Side Effects:

•

Carry nitroglycerin at all times; nitroglycerin is volatile and isinactivated by heat, moisture, air, light, and time, keep nitroglycerin in

original dark glass container, tightly closed to prevent absorption of

drug by other pills or pillbox and nitroglycerin should cause a slight

burning or Stinging sensation under the tongue when it is potent.

• Place nitroglycerin under tongue at first sign of chest discomfort; stop

all effort or activity; sit, and take nitroglycerin tablet-relief should be

obtained in a few minutes, bite the tablet between front teeth and slip





under tongue to dissolve if quick action is desired, repeat dosage in a

few minutes for total of 3 tablets if relief is not obtained.

• Educating the patient and his /her family about diets that are low in

sodium and reduce in saturated fats may be appropriate.

• Maintaining ideal body weight is important.

• Patient may need to eat several meals in place of three moderates to

large meals each day.

Myocardial Infarction

Myocardial ischaemia results when coronary blood supply is

insufficient in providing the oxygen needed to maintain myocardial tissue

oxygen tension. This situation results in anaerobic respiration and is the

result f an imbalance between myocardial oxygen supply and demand. A

sudden or complete cessation of blood flow, as may result from a

thrombus, results in necrosis of myocardial tissue (myocardial infarction).





Critical restriction to blood flow occurs when the diameter of the lumen is

reduced by more than half.

Clinical Manifestations:

Chest pain is severe, diffuse steady substernal pain of a crushing

and squeezing nature; not relieved by rest or sublingual vasodilator

therapy, but requires narcotics; may radiate to the arms (commonly the

left), shoulders, neck, back, and/or jaw; continues for more than 15

minutes and may produce anxiety and fear, resulting in an increase in

heart rate, blood pressure and respiratory rate. Diaphoresis, cool clammy

skin, facial pallor. Hypertension or hypotension. Bradyeardia or

tachycardia. Premature ventricular and/or atrial beats, palpitations, severe

anxiety, dyspnea, disorientation, confusion, restlessness fainting, marked

weakness, nausea, vomiting, hiccups and a typical symptoms, epigastric

or abdominal.

Diagnosis:

• Elecrocardiographic changes with myocardial infarction: the 12-lead

ECG is central to the diagnosis of MI because patients with ST

segment elevation.

• Ambulatory Electrocardiography (holter Monitoring): is the

continuous ECG monitoring of a person going about normal activities.

• Laboratory test:

Creatine Kinase (CK):

Elevation of CK-MB offers a more definitive indication of

myocardial cell. For the patient with an MI, the CK-MB appears in

the serum in 6 to 12 hours, peaks between 12 and 28 hours and

returns to normal levels in about 72 and 96 hours.

Lactase dehydrogenase (LDH):





Peak LDH levels are reached in about 2 to 3 days and levels remain

elevated for 7 to 10 days.

• Echocardiogram:

Is a noninvasive ultrasound test involving the transmission of

high –frequency around waves into the heart?

• Cardiac Imaging:

• Radionmelide studies may be performed to identify areas, of,

Myocardium at risk as well as tissue necrosis. Technetium- 99m

sestamibi is a radioisotope that is taken up by myocardial tissue in

proportion to blood flow in the region and may be used to identify

areas of tissue viability.

Management of Myocardial Infarction:

The goal of medical management is to minimize myocardial

damage, preserve myocardial function, and prevent complications. These

goals are now achieved by reperfusion the area by emergency use of

PTCA or thrombolytic medications. Its efficiency decreasing with

increasing time between symptoms onset and treatment.

1. Thrombolytic Therapy:

If the patient is diagnosed with an MI, thrombolytic therapy may be

used to establish reperfusion if there are no contraindications for its use.

Thrombolytic therapy provides maximal benefit if given within the first 2

to 3 hours after the onset of symptoms. Significant benefit does occur if

given up to 6 hours after onset of symptoms, and some benefit has been

shown up to 12 hours.

2. Analgesic:

The analgesic of choice for acute MI remains morphine sulfate

administered in intravenous boluses. Not only does morphine reduce pain





and anxiety, but it also reduces preload, which in turn decreases the

workload of the heart, and relaxes bronchioles to enhance oxygenation.

3. Softeners and laxatives:

Softeners and laxatives because the valsalva maneuver decreases

coronary blood flow, straining at stool should be avoided in post –MI

patients.

4. Beta-blockers

They are effective agents for secondary prevention post myocardial

infarction (MI).

5. Primary angioplasty:

Early reperfusion of myocardial tissue is essential to preserve

myocardial function.

6. Emergent PTCA:

The patient in whom an acute MI is suspected may referred for an

immediate PTCA.

Complication of myocardial Infarction:

1. Arrhythmias:

The most common complications alter MI are arrhythmias, resent

in 80% of MI patients. Arrhythmias are caused by any condition that

affect the myocardial sensitivity to nerve impulses, such as ischemia,

electrolyte imbalances, and sympathetic nervous system stimulation

2. Right ventricular infarction:





Infarctions that primarily cause damage to the right ventricle (RV)

are often seen with large inferior, inferolateral, or inferoposterior MIS.

3. Ventricular aneurysms:

They are serious complications of transmural myocardial

infarction, leading to severe hemodynamic compromise (heart failure,

thromboembolism angina and arrhythmias). It results when the infarcted,

myocardial all becomes thinned and bulges out during contraction.

Surgery has been frequently indicated, and it improves symptoms and the

quality of life with a better survival. Hemodynamic compromise (heart

failure, thromboembolism angina and arrhythmias).

4. Pericarditis:

Acute pericarditis, an inflammation of the visceral or parietal

pericardium, or both, may result in cardiac compression, decreased

ventricular filling and emptying, and cardiac failure. It may occur 2 to 3

days after an acute MI as a common complication of the infarction.5. Congestive heart failure (CHF):

It is a complication that occurs when the pumping power of the

heart has diminished. In the patient with an acute MI it is common to see

some degree of LV dysfunction in the first 24 hours.

6. Pulmonary embolism:

It may be seen in the patient with MI who has had bouts of CHF or

has been extremely immobile because of prolonged bed rest.

7. Dressler's syndrome (post-MI syndrome):

It is characterized by pericarditis with effusion and fever that

develops 1 to 4 weeks after MI. It may also occur after open-heart

surgery. It is thought to be caused by an antigen-antibody reaction to the

necrotic myocardium.

8. Cardiogenic shock:





It occurs when inadequate oxygen and nutrients are supplied to the

tissues because of sever L.V failure. It occurs when there is loss of

function of at least 40% of the LV. because of infarction.

Nursing Management for Patient with Myocardial infarction:

The Management goal for the patient in the intensive care unit and

intermediate care unit continues to be maximizing cardiac output while

carefully minimizing cardiac workload.

Assessment:

Systematic assessment includes a careful history, particularly as it

relates to symptoms: chest pain, difficulty breathing (dyspnea),

palpitations, faintness (syncope), or sweating (diaphoresis). Each

symptom must be evaluated with regard to time, duration, and the factors

that precipitate the symptoms and relieve it. A precise and complete

physical assessment is critical to detect complications, and any change in

patient status is reported immediately.

Nursing Intervention:Reliving chest pain:

The accepted method for relieving chest pain associated with MI is

the intravenous administration of vasodilator and anticoagulant therapy.

• Nitroglycerin and heparin are the medications of choice,

respectively.

•

Thrombolytic therapy (e.g., streptokinase, anistreplase) is highlydesirable for patients who present to the health care facility

immediately and who qualify clinically (i.e., there is no major

contraindication to the medication).

• Vital sign are assessed frequently as long as the patient is

experiencing pain.

• Physical rest, in bed with the backrest elevated or in a cardiac chair,

will help decrease chest discomfort and dyspnea.





• Elevation of the head beneficial of the following reasons, better lung

expansion and gas exchange, drainage of the upper lung lobes

improves and venous return to the heart decreases (preload) which

reduces the work of the heart.

• Administer narcotics as prescribed (morphine or meperidine)

decreases sympathetic activity and reduces heart rate, respirations,

blood pressure, muscle tension, and anxiety.

• Promoting Adequate tissue perfusion,

Keeping the patient on bed or chair rest is

particularly helpful in reducing myocardial oxygen

consumption, (MV02).

Checking skin temperature and peripheral pulses,

frequently is important to ensure adequate tissue perfusionoxygen may be administered to enrich the supply of

circulation oxygen.

Improving respiratory function:

Encouraging the patient to breath

deeply and change position frequently helps keep fluid

from pooling in the lung bases.Reducing anxiety:

Developing a trusting

and caring relationship with the patient is critical in

reducing anxiety.

• Monitoring and managing

potential complications:





The nurse monitors the patient closely for changes in cardiac rate

and rhythm, heart sounds, blood pressure, chest pain, respiratory status,

urinary output, skin color and temperature, sensorium and laboratory

values.

• Maintain

i hemodynamic stability:

Mo

nitor BP every 2 hours or as directed-hypertension increases

after Load of the heart, elevating oxygen demand,

hypotension causes reduced coronary and tissue perfusion.

Monitor respirations and lung fields every 2 to 4 hours or as

prescribed by observing for dyspnea tachypnea frothy pink

sputum, orthopnea-may indicate left ventricular failure,

pulmonary embolus, pulmonary edema.

Ev

aluate heart rate and heart sounds every 2 to 4 hours or as

directed. Evaluate the major arterial pulses (weak pulse

and/or presence of pulse alternates indicates decreased

cardiac output; irregularity results from dysrhythmias).

Ta

ke body temperature every 4 hours or as directed (more

patients develop an increase in temperature within 24 to 48

hours due to tissue necrosis).

Ob

serve for presence of edema.

Mo

nitor skin color and temperature (cool, clammy skin and pallor associated with vasoconstriction secondary to

decreased cardiac output).

Be

alert to change in mental status, such as confusion,

restlessness, disorientation.

• Increasing activity tolerance:





Minimize environmental noise, provide a comfortable

environmental temperature, and avoid unnecessary interruptions

and procedures.

Promote restful diversional activities for patient (reading,

listening to music, drawing crosswords puzzles, crafts) and

encourage frequent position changes while in bed

• Teaching patients self-care , the most effective way to increase the

probability that the patient will comply with a self- care regimen

after discharge is to provide adequate education about the disease

process and to facilitate the patient's involvement in a cardiac

rehabilitation, program.

Coronar Heart Diseases Hanan Sayed

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