CORONARY HEART DISEASE

Arranged by :

Group 3

1. Selvi Suci Hayati (21117104)

2. Suwindry (21117116)

3. Shinta Prima D (21117110)

4. Weni Dwi Cahyani (21117130)

5. Tuti Alamiah (21117126)

6. Winda Claudya (21117133)

7. Yola Alfina (21117138)

Lecturer : Sukron,MNS

NURSING SCIENCE STUDY PROGRAM

STIKes MUHAMMADIYAH PALEMBANG

2018/2019

FOREWORD
 We thank God for the presence of Allah SWT for His abundance of grace and

grace, so that I can complete the writing of the paper "Coronary Heart Disease" to

complete the task of learning the surgical medical nursing courses I stikes

muhammadiyah palembang. We have made every effort to write this paper in the

hope that it will benefit the reader. Building criticism and suggestions are needed

to improve this paper. Finally, we would like to thank and hope that God will give

reward in kind to those who have provided assistance, and make this a worship.

Amen ya, Rabb.

Palembang, September 22, 2018

Author,

ii
 TABLE OF CONTENTS

Foreward ........................................................................................................ ii

Table of content ............................................................................................... iii

CHAPTER I INTRODUCTION

A. Background ......................................................................................... 1

B. Problem formation ............................................................................... 2

C. Purpose ................................................................................................ 2

CHAPTER II DISCUSSION

A. Definition of heart failure .................................................................... 4

B. Etiology of Heart Failure .................................................................... 4

C. Anatomy of Physiology of Heart Failure ............................................ 6

D. Pathophysiology of Heart Failure ....................................................... 8

E. Signs and Symptoms ........................................................................... 9

F. Complications of Heart Failure ........................................................... 10

G. Management of therapy ....................................................................... 13

H. Nursing Care ....................................................................................... 18

CHAPTER III CLOSING

A. Conclusion .......................................................................................... 29

B. Suggestions .......................................................................................... 30

BIBLIOGRAFY ............................................................................................ 31

iii
 CHAPTER I

PRELIMINARY

A. Background

Coronary heart disease is the main case of the cause of death and

pain in humans. Although precautions have been taken, such as dietary

regulation, cholesterol reduction and weight management, diabetes and

hypertension, coronary heart disease remains a major health problem.

The main problem in coronary heart disease is coronary atherosclerosis.

Is a progressive disease that occurs gradually, namely thickening of the

coronary artery wall. Coronary atherosclerosis is considered a passive

process because most of it is produced by cholesterol in the arterial wall

(Yuet Wai Kan, 2000).

Coronary heart disease is the number one killer in developed

countries and can also occur in developing countries. The duina health

organization (WHO) has stated the fact that coronary heart disease

(CHD) is a modern epidemic and cannot be avoided by aging factors. It

is estimated that if the incidence of CHD reaches zero it can increase life

expectancy of 3 to 9% (Shivaramakrishna. 2010).

The description of the case above shows the importance of this disease

that has not received attention about the magnitude of a person's risk,

disability, loss of work, and at the time of admission. In the decades since

the last clinical conference by the New York Heart Association or the

New York health association, this subject, from a number of workshops,

1
 has produced important new information about this disease, prevention

and control methods. This is stated in the amount of clinically clear

changes in CHD and the number of factors that may be relevant, the large

number of patients participating, the group that will be included in all

cases of CHD arising in the general population with clear characteristics.

B. Problem Formulation

The problem formulation of the preparation of this paper is:

1. Definition of coronary heart disease (CHD)

2. Etiology of coronary heart disease (CHD)

3. Pathophysiology (CHD)

4. Signs and Symptoms of coronary heart disease (pjk)

5. Complications of coronary heart disease (CHD)

6. Anatomy of the coronary heart disease (CHD)

7. Supporting diagnosis

8. Medical management

9. Askep for coronary disease

C. Purpose

1. To find out the definition of coronary heart disease (CHD)

2. To find out the etiology of coronary heart disease (CHD)

3. To find out Pathophysiology (CHD)

2
4. To find out the signs and symptoms of coronary heart disease

(pjk)

5. To find out the complications of coronary heart disease (CHD)

6. To find out the anatomy of the coronary heart disease (CHD)

7. To find out supporting diagnoses

8. To find out medical management

9. To find out Askep for coronary heart disease

3
 CHAPTER II

DISCUSSION

A. Definition of Coronary Heart Disease

American heart assuciation (AHA), defining coronary heart disease is

a general term for accumulating plaque in the heart arteries that can cause

a heart attack, this buildup of plaque in the coronary arteries is called

atherosclerosis (AHA, 2012 p. 14).

Coronary heart disease (CHD) is a condition where coronary artery

plaque builds up. This causes the coronary arteries to narrow or become

blocked. Coronary arteries are arteries that supply the blood of the heart

muscle by carrying a lot of oxygen. There are several factors that trigger

this disease, namely lifestyle, genetic factors, age, and illness and others.

(norhasimah, 2010: p. 48).

B. Etiology of Coronary Heart Disease

Etiology of Coronary Heart Disease is the narrowing, blockage, or

abnormalities of coronary arteries. The narrowing or blockage of blood

vessels can stop blood flow to the heart muscle which is often

characterized by pain. In severe conditions, the heart's ability to pump

blood can be lost.(7) This can damage the heart rhythm control system

and end in death. (Hermawatirisa, 2014: p. 2).

4
 The narrowing and blockage of the coronary arteries is caused by

cholesterol and triglyceride fats which are getting more and more and

accumulate below the innermost layer of endothelium from the walls of

arteries. This can cause blood flow to the heart muscle to decrease or

stop, thus disrupting the work of the heart as a blood pumper. The

dominant effect of the coronary heart is the luster of oxygen and nutrients

to the heart because blood flow to the heart decreases. The formation of

fat plaques in the arteries affects the formation of clots of blood flow

which will encourage a heart attack. The process of plaque formation

which causes a shift in the arteries is called arteriosclerosis.

(Hermawatirisa, 2014: p. 2).

Initially heart disease was monopolized by parents. However, at this

time there is a tendency for this disease to be suffered by patients under

40 years of age. This is usually the case because of a shift in lifestyle,

environmental conditions and the profession of the community that raises

the 'trend' of new 'degenerative' diseases. A number of lifestyle behaviors

encountered in urban communities include eating ready-to-eat foods that

contain high levels of saturated fat, smoking habits, alcoholic beverages,

excessive work, lack of exercise, and stress. (Hemawatirisa, 2014: p.

2).(8)

5
C. Anatomy of Physiology of Coronary Heart Disease

Unlike the other muscles in the body that rest more, the heart muscle

never stops beating. The coronary arteries distribute blood to meet oxygen

and nutrition needs of the heart muscle. So, the coronary arteries are very

vita to keep the heart can continue to work normally. There are 2 main

coronary arteries that come out of the aorta, namely the left coronary

artery and right coronary artery. Blockage of blood flow to coronary

vessels will result in myocardial death, which is the basis of the

pathogenesis of acute myocardial infarction.

1. Left main (LM) coronary artery

The main left coronary artery, better known as left main (LM),

exits the left aortic sinus and then immediately divides into the

anterior descending (LAD) and left cirumflex (LCX) lerft arteries. The

LM artery runs between the right ventricle outflow tract which is

located in front of it, and the left atrium is located behind it and then

branched into the LAD artery and LCX artery.

2. Artery left descending anteriol (LAD)

The LAD artery runs in the front interventricular trench to the

heart apex. This artery supplies the front of the septum through the

septal branches and the left ventricular front through diagonal

branches, most of the left ventricle and also the antrio-ventricular

beam. Diagonal branches come out of the LAD artery and run

6
 sideways supplying the lateral antero wall of the left ventricle,

diagonal branches can be more than one

3. Arteri left circumflex (LCX)

LCX arteries run in the left atrioventricular trench between the left

and left ventricles and supply the left ventricular sidewall through

more than one marginal obtuse branches (M1, M2, etc.). LCX arteries

generally end up as marginal obtuse branches.

4. Right coronary arterty (RCA)

The right coronary artery exits from the right aortic sinus and

travels in the right atrioventricular trench between the right atrium and

right ventricle to the lower part of the septum. The first branch of

RCA is the small conus branch that supplies the outflow of the right

ventricle.

5. Coronary vein

Most venous blood is channeled through veins that run side by

side with coronary arteries. The cardiac vein empties into the coronary

sinus which is a large vein that ends in the right atrium. a small

portion of blood from the coronary circulation comes directly from the

heart muscle through small veins and is channeled directly into four

heart chambers.

6. Coronary sinus

Walk right in the atrioventricular trench. It ends at the back

wall of the right atrium, between the base of the inferior vena cava

7
 and atrioventricular cleft and receives moderate and small cardiac

venous blood.

D. Pathophysiology of Coronary Heart Disease

The phase of coronary heart disease can be known based on the

relationship between clinical symptoms and endothelium pathology that

can be seen by angioscopy. At the beginning of the disease there will be a

layer of fat on the surface of blood vessels. If the lesion widens it will

cause partial obstruction by a slippery surface plaque. If the plaque

increases, the coronary flow will decrease and cause stable angina. Some

plaques will ulcerate and cause platelet collections at the site. The platelet

collection will result in periodic removal of the coronary vasoconstrictor

from the bloodstream and cause accelerated angina, the intermediate form

of stable angina to unstable angina. If the loose embolism is large enough

to cause sudden death.

Sticking platelets can form small thrombus. If the thrombus is large

enough and causes total obstruction it will become a myocardial infarction.

After an infarction occurs, the thrombus will lysis by an endogenous

process. Endothelial ulceration heals within a few weeks. The healing

process is sometimes not entirely perfect, often the remaining thrombus

forms a blockage in the blood vessels resulting in stable angina. The

plaque can rupture again, and so on

8
 So the precipitating mechanism that changes the status of a patient

with stable clinical symptoms such as acute myocardial infarction is

closely related to the pathogenesis of atherosclerosis, platelet aggregation,

intra-coronary thrombosis and coronary vasospasm. So for people with

coronary disease with impaired coronary blood flow, the main treatment is

revascularization and reperfusion, both mechanically and medically.

E. Signs and Symptoms

1. Chest pain (Angina).

You may feel pressure or tightness in the chest, as if someone

is standing on your chest. Pain, called angina, is usually triggered by

physical or emotional distress. It usually disappears within minutes

after stopping activities that cause pressure. In some people, especially

women, this pain may be brief or sharp and feels on the abdomen,

back, or arms.

2. Shortness of breath.

If the heart cannot pump enough blood to meet your body's

needs, you can experience shortness of breath or extreme fatigue

without effort.

3. Heart attack.

If the coronary arteries become completely blocked, you may

experience a heart attack. The classic symptoms of a heart attack

9
 include stifling pressure and pain in the shoulder or arm, sometimes

with shortness of breath and sweating. Women may experience less

typical signs of a heart attack than men, including nausea and back or

jaw pain. Sometimes a heart attack occurs without any clear signs or

symptoms.

F. Complications of coronary heart disease

1. Congestive heart failure

Congestive heart failure is a circulation of myocardial

dysfunction. The place of congestion depends on the ventricles

involved. Left ventricular dysfunction or left heart failure, causing

congestion in the pulmonary vein, while right ventricular dysfunction

or right heart failure results in systemic venous congestion. Failure of

both ventricles is called ventricular failure. Left heart failure is the

most common complication after myocardial infarction.

Myocardial infusion interferes with myocardial function

because it causes a decrease in the strength of contraction, causing

abnormalities in wall movement and changing the power of the heart

chamber. with the reduced ability of the left ventricle to empty itself,

large volumes of volume of the vent volume are reduced so that the

remaining ventricular volume increases. This causes an increase in the

left heart. This pressure increase is channeled back to the pulmonary

vein. If the hydrostatic pressure in the pulmonary capillary exceeds

10
 the vascular oncotic pressure, there is a process of transudation into

the interstitial space. If this pressure is still increasing again there is

pulmonary edema due to permeation of fluid into the alveoli.

2. Cardiogenic shock

Cardiogenic shock is a complex clinical syndrome in which

the heart is unable to maintain adequate to meet the metabolic needs

of the body which is characterized by decreased consciousness to

coma

Cardiogenic shock is caused by coronary disease and IMA which

can weaken the heart muscle so that the heart is unable to pump blood

and can eventually reduce consciousness and even tightness.

Cardiogenic shock can be prevented by limiting activity so that

increased metabolism and oxygen demand can be prevented.

3. Arrhythmia

Arrhythmias are abnormal heart rhythms originating from SA

nodes and AV nodes and HIS files and purkinye systems. To find out

this arrhythmia only by ECG examination. Actually this arrhythmia is

not dangerous but in some cases it can indicate a dangerous disease.

proper examination and diagnosis can prevent arrhythmias from

getting worse.

4. Heart attack

If cholesterol plaque and blood clots have blocked blood

vessels, a heart attack can occur. Lack of blood flow to the heart

11
 can damage the heart muscle. The amount of damage depends on

how quickly you get treatment or medical help

5. Other arterial diseases

The process that causes cholesterol plaques to accumulate in

the coronary arteries will affect all the arteries in the body.

Atherosclerotic plaques in the carotid arteries in the neck, which

supply blood to the brain can cause strokes

Plaques in other places can inhibit blood flow in the arteries

that supply blood to the legs, arms, or vital organs, or they can cause

interference in the aorta, which is greater in the body.

6. Pericarditis

Symptoms of pericarditis include recurrent chest pain, usually

typical of sharp and associated posture and breathing.

7. Investigation (diagnosis)

Diagnosis for coronary heart disease can be done by physical

examination, history taking. Cardiac ultrasound examination can be

done by echocardiography. The echocardiography system can display,

analyze and capture the heart in full in one heartbeat. Technological

development has created a new tool, namely Computed tomography

(CT) which has long played an important role in detecting diseases for

years. The development of technology, so as to create a new

generation with CT scanners that can perform coronary CT

12
 angiography (CTA) by reducing radiation doses on routine clinical

examinations.

In addition to CT can also use in vitro tests in the laboratory,

through the use of new biomarkers, especially in emergency care can

influence and support clinical decisions. In heart failure the use of

natriuretic circulating peptide B (BNP) is very relevant, because this

level of biomarker is a good indicator of the extent to which heart

function is impaired. BNP is used both for initial diagnosis and for

therapeutic monitoring. In some patients, heart attack is a direct cause

of cardiac insufficiency, so the rapid detection of myocardial

infarction is very important in preventing further myocardial damage

and subsequent heart failure. (Ekinci, 2010)

G. Management of therapy

Therapy is based on knowledge of the mechanism, clinical

manifestations, natural and pathological travel both from the cellular,

anatomical and physiological aspects of CHD cases. In principle,

therapy is intended to treat angina pain quickly, intensively and

prevent continued ischemia and the occurrence of acute myocardial

infarction or sudden death. Guidelines for Management of

Cardiovascular Disease in Indonesia in 2009.

The recommended drugs for CHD sufferers are:

a. Nitrate group

13
 The mechanism of action of vasodilatory nitrate group,

decreases diastolic filling, decreases intracardiac pressure and

increases subendocardial perfusion. Short-acting nitrates sublingual

use for prophylaxis, long working nitrates, oral or transdermal use to

maintain nitrate-free periods. Short-term nitrate work is given to

each patient to be used if there is chest pain. Nitrate doses given 5

mg sublingual can be repeated three times a day (Anonim, 2009).

b. Β blocker (beta blocker)

There is evidence that administration of beta blockers in

angina patients who have previously experienced a myocardial

infarction, or heart failure has an advantage in prognosis. Based on

these data beta blockers are the first-line drug therapy for angina in

patients without contraindications (Anonim, 2009). Beta blockers

can cause side effects such as indigestion, nightmares, fatigue,

depression, AV block allergic reactions, and bronchospasm. Beta

blockers can aggravate glucose tolerance in diabetic patients also

interfere with the metabolic and autonomic response to

hypoglycemia (Anonim, 2000). The dose of beta blockers varies

widely for propanolol 120-480 / day or 3 times a day 10-40mg and

for bisoprolol 1x daily 10-40mg.

c. Calcium antagonists

The mechanism of action of calcium antagonists as coronary

and systemic vasodilation by inhibiting calcium entry through L-type

14
 canals. Verapamil and diltiazem also reduce myocardial contractility,

heart frequency and AV node conduction. Calcium dyhidropyridin

antagonists (eg, nifedippin, amlodipine, and felodipine) are more

selective in blood vessels (Anonim, 2009). Conventional

administration of nifedipine increases the risk of heart infarction or

recurrent angina 16%. Explanation of why the use of nifedipine

monotherapy can increase mortality because this drug causes reflex

tachycardia and increases myocardial oxygen demand (Anonimª,

2006). The dose for the calcium antagonist is nifedipine dose 3x5-

10mg, diltiazem dose 3x30-60mg and verapamil dose 3x 40-80mg.

d. Antiplatelet drugs

Antiplatelet therapy is given to prevent coronary thrombosis

because the benefits are greater than the risk. Low-dose aspirin (75-

150mg) is the drug of choice in most cases. Clopidogrel may be

considered as an alternative in patients who are allergic to aspirin, or

as post-insertion cent, or after acute coronary syndrome. In patients

with a history of gastrointestinal bleeding aspirin combined with

proton pump inhibition is better than clopidogrel. For Clopidogrel at

a dose of 75 mg once a day (Anonymous, 2009) Aspirin works by

suppressing the formation of thromboxane A2 by inhibiting

cyclooxygenase in platelets (platelets) through irreversible

acetylation. This event inhibits platelet aggregation through this

15
 pathway. Some of the benefits can occur because the anti-

inflammatory ability can reduce plaque rupture (Anonimª, 2006).

e. Inhibitor of Angiotensin Conversion Enzyme (ACE-I)

ACE-I is a drug that has been widely recognized as an

antihypertensive drug, heart failure, and left ventricular dysfunction.

In addition, in two large randomized controlled studies of ramipril

and perindopril a decrease in cardiovascular morbidity and mortality

in patients with stable coronary heart disease without heart failure.

ACE-I is an indication in patients with stable angina pectoris

accompanied by comorbidities such as hypertension, DM, heart

failure, asymptomatic left ventricular dysfunction, and post

myocardial infarction. In angina patients without accompanying the

accompanying disease ACE-I needs to be taken into account the

benefits and risks (Anonim, 2009). Dosage for the use of ACE-I

drugs for captopril 6.25-12.5 mg three times a day. For ramipril the

initial dose is 2.5 mg twice a day with a further 5 mg dose twice a

day, lisinopril doses 2.5-10 mg once daily (Lacy et al, 2008).

f. Bloker Receptor Antagonists

The mechanism by preventing the effects of angiotensin II,

these compounds relax smooth muscle thus encouraging

vasodilation, increasing the excretion of salt and water in the

kidneys, decreasing plasma volume, and reducing cell hypertrophy.

16
 Angiotensin II receptor antagonists theoretically also overcome

some ACEI weaknesses (Oates and Brown, 2007). Blocker receptor

antagonists are given if the patient is intolerant with ACE-I

(Anonim, 2009). The dose for valsartan is 40 mg twice a day with

an advanced dose of 80-160 mg, maximum dose of 320 mg (Lacy

et al, 2008).

g. Anti cholesterol

Statins reduce the risk of atherosclerosis complications by 30%

in stable angina patients. Some studies also show the benefits of

statins on various cholesterol levels before therapy, even in patients

with normal cholesterol levels. Statin therapy should always be

considered in patients with stable coronary heart disease and stable

angina. The target dose of statin therapy to reduce cardiovascular

morbidity and mortality should be based on clinical studies that have

recommended a dose of statin is simvastatin 40 mg / day, pravastatin

40 mg / day, and atorvastin 10 mg / day. If the dose above the total

cholesterol and LDL levels do not reach the target, then the dose can

be increased according to the patient's tolerance until it reaches the

target (Anonim, 2009). Statins can also improve endothelial

function, stabilize plaque, reduce thrombus formation, are anti-

inflammatory, and reduce lipid oxidation. Statins should be

continued to benefit from long-term survival (Anonimª, 2006).

Contraindications to patients with active liver disease, in pregnancy

17
 and lactation. Reversible side effects of miosis are rare but rare side

effects. Statins also cause headaches, changes in the value of kidney

function and gastrointestinal effects (Anonim, 2000).

H. Nursing Care

Nursing Study

a. Activity and rest

Weakness, fatigue, inability to sleep (may get Tachycardia and

dyspnea during rest or during activities).

b. Circulation

 Have a history of IMA, coronary heart disease, CHF, high

blood pressure, diabetes mellitus.

 Blood pressure may be normal or increased, the pulse may be

normal or delayed capilary refill time, dysrhythmia.

 Heart sounds, additional S3 or S4 heart sounds may reflect the

occurrence of heart / ventricular failure of losing contractility.

 Murmur if there is a result of a valve insufficiency or a

dysfunctional papillary muscle.

 Heart rate may increase or decrease (tachy or bradi cardia).

Heart rhythm may be irregular or normal.

 Edema: Jugular vein distension, odema anasarka, crackles may

also occur with heart failure.

 Skin color may be pale both on the lips and on the nails.

18
c. Elimination

Bowel sounds may increase or also normal.

d. Nutrition

Nausea, loss of appetite, decreased skin turgor, heavy sweating,

vomiting and weight changes.

e. Individual hygiene

Dyspnea or chest or chest pain palpitates during activity.

f. Neoru sensory

Great headache, Changes mentation.

g. Comfort

 The onset of sudden chest pain that does not disappear with

rest or with nitroglycerin.

 The location of substerbnal front chest pain which may spread

to the arms, jaw and face.

 Pain characteristics can be said to be a pain that has been

experienced. As a result of the pain, it may get a grinning face,

changes in pustur body, crying, decreased eye contact, changes

in heart rhythm, ECG, blood pressure, respiration and skin

color and level of consciousness.

h. Respiration

Dispnea with or without activity, productive cough, history of

smokers with chronic respiratory disease. On examination it may get

19
 an increase in respiration, pale or cyanosis, breath sounds of crakcles

or wheezes or vesicles. Clear sputum or also pink / pink tinged.

i. Social interaction

Stress, difficulty in adapting to stressors, uncontrolled emotions.

j. Knowledge

History in the family is suffering from heart disease, diabetes,

stroke, hypertension, smokers.

1. Diagnose nursing

Pain is related to the accumulation of myocardial ischemia. Safety

disorders: Anxiety b.d lack of knowledge about disease.Cardiac output

decreases b.d Changes in myocardial contractility or inotropic changes,

changes in frequency, rhythm, cardiac conduction, structural changes. (eg

valvular abnormalities, ventricular aneurysms).

2. Interventions

NO Nursing Purpose Intervention Rational

diagnoses

1 Related pain After performing 1. review 1. The data can

With nursing actions documentation help determine

accumulation of for 1 x 24 hours and report: the causes and

lactic acid the patient does a. patient's effects of chest

ischemia not experience complaints about pain and is a

myocardium pain with pain: chest pain baseline for

20
- The patient include location, comparing post-

does not radiation duration treatment

complain of of pain and symptoms:

chest pain factors that affect a. therapy there

- The patient pain are various

looks calm and b. the effect of conditions

can rest chest pain on related to chest

cardiovascular search there are

- TTV is within hemodynamic typical clinical

normal limits perfusion of the findings in

heart, brain, ischemic chest

- Blood pressure: kidneys. pain

110-120 / 60-80 b. Mycard

mm Hg 2. ECG infarction

monitoring decreases

- RR: 16 -20 X / 3. TTV cardiac

minute monitoring contractility and

4. Give O2 ventricular

- HR: 60 -100X. according to the compliance and

minute condition of the can cause

patient dysrhythmias

- T: 36,5-37,5 c 5. give the (decreased

semifowler cardiac output)

21
Good urine position. resulting in

output is 1-2 cc / 6. Encourage the decreased blood

kg bw / hour patient to bedrest pressure and

completely tissue percussion

during chest pain. heart frequency

can increase as a

7. give a quiet compensatory

environment mechanism to

slow activities maintain cardiac

and comfortable output.

actions. 2. knowing of

8. give therapy changes in ECG

according to the picture and the

program presence of AMI

complications.

3. an increase in

TD HR, RR,

indicating pain

that is very felt

by the patient.

4. O2 therapy

can increase O2

supply to the

22
 heart

5. helps

maximize lung

compliance.

6. reduce

consumption of

O2.

7. decreases

external stimuli.

8. for the healing

process of the

patient.

2 Safety After nursing provide an By knowing risk

disorders: action for 2 x 24 explanation of factors, patients

Anxiety b.d hours the patient the risk factors and families can

lack of shows: for CAD: prevent and

knowledge - Patients or smoking, high modify a

about disease families are calm cholesterol diet, healthier

- Patients and diabetes, lifestyle.

families can find hypertension, 2. patients will

out and mention stress. be appreciated.

again about the 2. give emotional 3. By knowing

diseases that support: warm the procedure the

23
patients suffer attitude and patient and

from how to empathy family will

prevent and treat 3. explain each participate in

them. procedure that taking action

will be carried besides that it

out on the patient can also reduce

and family. the patient's

4. provide an anxiety level.

explanation of

patient care at 4. increase

home: patient

-The influence of knowledge

CAD and family so the

-Healing process family can

-Types of anticipate a

treatment repeat attack.

-The influence of 5. to know and

drugs evaluate the

-Limiting diet: success rate of

low cholesterol the intervention

3 / week that has been

exercise: jogging, done.

aerobics

24
 -stop smoking

-manajement

stress

- when the

chapter does not

push

5. review anxiety

levels

3 Cardiac output After nursing 1. Auscultation Tachycardia

decreases b.d action, the client of the apical usually occurs to

Changes in showed a pulse, assess compensate for

myocardial decrease in frequency, heart the decrease in

contractility or cardiac output. rhythm. cardiac

inotropic 2. Record the contractility.

changes, Result Criteria: heart sound. 2. S1 and S2

changes in - The frequency 3. Palpate are weak,

frequency, of the heart peripheral pulse. because of the

rhythm, cardiac increases 4. Monitor blood decrease in

conduction, pressure. pump S3 work

structural - Stable 5. Monitor urine as the flow into

changes. (eg hemodynamic output, record the foyer which

valvular status decreased output, is distention. S4

abnormalities, and concentration shows valve

25
ventricular - Adequate urine or concentration incopetence or

aneurysms) output of urine. stenosis.

6. Assess 3. To find out

- There is no changes in the function of

dispnu sensory the heart pump

examples: which is strongly

- Akral Warm lethargy, influenced by

confusion, CO and heart

disorientation, filling.

anxiety and

depression. 4. To find out

7. Give a semi the function of

recumbent (semi- the heart pump

fowler) break to which is strongly

the bed. influenced by

8. Collaborate CO and heart

with doctors for filling.

therapy, oxygen,

heart 5. With a

medications, decrease in CO

diuretic drugs affects the blood

and fluids. supply to the

kidneys which

26
 also affects the

release of

aldosterone

hormones that

function in the

process of

urinary

discharge.

6. Shows

inadequate

cerebral

perfusion

secondary to

decreased

cardiac output.

7. Improves

insufficiency of

heart

contractions and

decreases

oxygen demand

and decreases

venous return.

27
 8. Helps in

chemical

processes in the

body

28
 CHAPTER III

COVER

A. Conclusion

Coronary heart disease is the main case of the cause of death and pain

in humans. Although precautions have been taken, such as dietary

regulation, cholesterol reduction and weight management, diabetes and

hypertension, coronary heart disease remains a major health problem.

The main problem in coronary heart disease is coronary atherosclerosis.

Coronary heart disease (CHD) is a condition where coronary artery

plaque builds up. This causes the coronary arteries to narrow or become

blocked. Coronary arteries are arteries that supply the blood of the heart

muscle by carrying a lot of oxygen. There are several factors that trigger

this disease, namely lifestyle, genetic factors, age, and illness and others.

(norhasimah, 2010: p. 48).

B. Suggestions

1. A balanced lifestyle and avoid the risk of stress.

2. Eating fibrous foods, do not overeat and control cholesterol,

control blood pressure and blood sugar, and control health

regularly.

29
3. Stop smoking, because smoking causes the elasticity of the blood

vessels to decrease, thereby increasing the shift in arterial blood

vessels that triggers a stroke.

4. Regular exercise, adequate rest.

30
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AHA, 2012 hal:14

Norhasimah, 2010: hal:48

hermawatirisa,2014: hal 2

Lacy et al,2008

Carpenito J.L 1998. Buku.Saku Diagnosa Keperawatan

Doegoes, Marylin E. 2000. Rencana Asuhan Dan Dokumentasi Keperawatan.

Edisi 3 EGC. Jakarta

Kaplan, Norman M. 19961. Pencegahan Penyakit Jantung Koroner. EGC

Jakarta

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