PAPERS ABOUT

ARITMIA

ARRANGED BY :
GROUP 6

1. RIZKY AMRIN S (NIM 21117102)

2. SHELI SULISTIA NINGSIH (NIM 21117106)
3. SRI WAHYUNI (NIM 21117114)
4. SUSANTI (NIM 21117115)
5. TIARA AMELIA (NIM21117120)
6. TINNE AGUSTIEN H (NIM 21117122)
7. TUTI DWI SOPIYATI (NIM 21117125)
8. WINDAH ANISYAH (NIM 21117134)

HIGH SCHOOL OF HEALTH SCIENCE MUHAMMADIYAH

PALEMBANG NURSING STUDY PROGRAM

CLASS 2C SEMESTER 3

YEAR 2018/2019
 FOREWORD

We thank you for the presence of Allah SWT who has given His blessings so that we can
complete a paper entitled "Arrhythmia" well. We compile this paper to complete the task
of medical surgical nursing courses (KMB).

In the preparation of this paper there were not a few difficulties we encountered. But
thanks to the guidance and assistance from various parties, this paper can be resolved
properly. On this occasion we would like to express our deepest gratitude to the lecturers
of this course.

We hope for constructive criticism and suggestions for the sake of further development.
Finally the author still hopes that this paper will be useful for all of us.

Compiler,

Palembang, September 26, 2018

 CHAPTER I

PRELIMINARY

A. BACKGROUND

Health problems that affect the cardiovascular system that require nursing care can be
experienced by people at various ages. The cardiovascular system includes the heart,
circulation or blood circulation and blood condition which is a very important part of the
body because it is an arrangement that delivers oxygen and nutrients throughout the body.

If one of these organs experiences an gangue, especially the heart, it will disrupt all body
systems. Arrhythmia is one of the disorders of the cardiovascular system. Arrhythmia is
irregular jangtung rhythm. Arrhythmia is caused due to disruption of the mechanism of
impulse formation and conduction. This includes the disturbance of the nervous system.
Changes are characterized by beats or rhythms which are retention in treatment.

B. PROBLEM FORMULATION

1. What is the definition of arrhythmia?

2. What are the etiologies of arrhythmias?

3. How are arrhythmias?

4. What is the pathophysiology of arrhythmias?

5. What are the signs and symptoms of arrhythmia?

6. What are the complications that arise in arrhythmia patients?

7. How do you use arrhythmia support?

8. What is medical management in arrhythmia patients?

9. What are the assessment and intervention measures for arrhythmia patients?
AIM

General purpose:

The purpose in making this paper in general is to help students learn about arrhythmias
and arrhythmia nursing care

Special purpose:

1. Knowing the definition of arrhythmia

2. Knowing the etiology of arrhythmias

3. Knowing the effects of arrhythmias

4. Knowing the pathophysiology of arrhythmias

5. Knowing the signs and symptoms of arrhythmias

6. Knowing arrhythmia complications

7. Study supporting diagnoses

8. Study medical and nursing management

9. Studying intervention assessment approaches

CHAPTER II

THEORETICAL BASIS

A. DEFINITION

Heart rhythm disturbances or arrhythmias are complications that often occur in

myocardial infarction. Arthritis or dysrhythmias are changes in the frequency and rhythm
of the heart caused by abnormal or automatic electrolyte conduction (Doenges, 1999).

Arrhythmia arises due to electrophysiological changes in myocardial cells. This

electrophysiological change manifests as a change in the shape of the action potential,
namely a graphical record of cell electrical activity (Price, 1994).

Heart rhythm disturbances are not only limited to heart rate irregularities but also include
pulse speed and conduction disorders (Hanafi, 1996).

B. ETIOLOGY

The most common causes of ventricular arrhythmias are myocardial disease (ischemia
and infarction), which is accompanied by changes in electrolyte balance, metabolic
disorders, drug toxicity and coronary vasospasm. Because the implus originates from the
ventricle, it is not through a normal conduction system but rather ventricular muscle
tissue. This gives rise to a wide QRS complex picture (<0.12 seconds)

The basic causes of an arrhythmia are often difficult to recognize but the following
arithmetic factors can be of concern:

1. Hypoxia: myocardium that lacks oxygen becomes irritable

2. skemia: myocardial infarction and angina trigger

3. Sympathetic stimulation: muscle tone buildup due to any cause (hyperthyroidism,

congestive heart failure, physical exercise etc.) can cause arrhythmias.

4. Drugs: the effects of digitalis drugs or even anti-arimia drugs themselves

5. Electrolyte disturbances: imbalance of potassium, calcium and magnesium

6. Bradycardia: a very slow heart frequency can predispose to arrhythmias

7. Stretch: ventricular hypertrophy

Two types of myocardial infarction complications that must be addressed are:

a. Electrical instability or arrhythmia

b. Mechanical dysfunction or heart pump failure

C. ANATOMY PHYSIOLOGY

The anatomy and physiology of the heart, the heart wall consists of three different layers,
namely:

1. The endocardium is a thin layer of endothelium, a unique epithelial tissue that lines the
inside of the entire circulatory system inside

2. Myocardium is the middle layer consisting of the heart muscle, forming part of the
heart wall.

3. Epicardium is a thin membrane on the outside that wraps the heart. when pulsating,
every room of the heart relaxes and is filled with blood (called diastole), then the heart
contracts and pumps blood out from the heart room (called disto) both atria relax and
contract simultaneously.

Heart electrical activity has 2 types of heart muscle:

a. 90% of heart muscle cells are contractile cells, which perform mechanical work, which
is pumping. these workers' cells in normal circumstances do not produce their own action
potential.

b. On the contrary, a small part of the remaining cells are authoritative cells, not
contracting, but self-exhaling triggers and delivers the action potential responsible for
contracting the workers' cells. heart cells that are capable of experiencing authorization
are found in the following location locations:

• Sinoatrium (SA) node, a small area specifically on the wall of the right atrium near the
superior vene cava hole.

• The antrioventicular (AV) node is a small bundle of heart muscle cells in the right
atrium near the septum, just above the atrial and ventricular junction.
D. PATHOPHYSIOLOGY

As already mentioned in the etiology, ventricular arrhythmias are generally caused by

ischemia or myocardial infarction. The location of the infarction affects the process of
arrhythmia. For example, if an anterior infarction occurs, then stenosis is usually in the
right coronary artery which also plays a role in bleeding the SA node so that the heart's
natural impulses are disrupted.

As a result of the death of these heart muscle cells, can cause disruption in cardiac
depolarization and repolarization, thus affecting the heart rhythm. With the release of
various intracellular enzymes and potassium ions and the accumulation of lactic acid, the
heart's electrical conductive pathways are disrupted. This can cause atrial or ventricular
depolarization and arrhythmia. Decreased myocardial contractility as a result Cell death
can also stimulate the activation of catecholamines which increase the excitability of the
sympathetic nervous system, resulting in an increase in heart frequency, increased oxygen
demand and vasoconstriction. In addition, ventricular myocardial irritability is also the
cause of ventricular arrhythmias, both VES <VT and VF.

E. SIGNS AND SYMPTOMS

Cardiac arrhythmias include many conditions,

The most common symptom of arrhythmias is abnormalities of the heartbeat, called

palpitations. this may be rare, frequent or continuous. some of these arrhythmias are
harmless (even though they disturb the patient) but many of the arrhythmias will be
problematic.

Some arrhythmias do not show symptoms and do not increase mortality. however, some
arrhythmias are signs and symptoms that cause problems, for example the risk of clotting
or blockage of blood in the heart and the high risk of insufficient blood distributed by the
heart, due to a weak heartbeat, others increase the risk of embolism and stroke, heart
failure and death. arrived at if the arrhythmia causes the heartbeat too quickly, too slow or
too weak to supply blood for the body's needs will cause lower blood pressure and cause
lightheadedness or dizziness or syncope (fainting).

F. COMPLOCATION

Certain arrhythmias can increase the risk of developing conditions such as:

• Stroke, when your heart is unable to pump blood effectively, which can cause blood to
slow down. This causes blood clots to form, if blood clots are carried away, can travel and
block the brain arteries, causing stroke, this can damage part of your brain or cause death,
for people who have atrial fibrillation, warfarin (coumadin) or etexlate (pradaxa ) can
help prevent blood clots that can cause a stroke.

• Heart failure . this can happen if your heart is pumping ineffective for a long time
due to bradycardia or tachycardia, such as atrial fibrillation. sometimes, controlling the
rate of arrhythmia that causes heart failure, can improve the function of your heart. (heart
failure: heart failure in the inability of the heart to pump efficiently and consistently,
causing excess fluid to collect in the legs and lungs).

• Without immediate medical treatment, ongoing ventricular tachycardia often worsens

into ventricular fibrillation

• Blood pressure drops dramatically, can damage vital organs, including the brain, which
is in dire need of blood supply

• In severe cases, the heart rhythm can become so chaotic that it causes sudden death.

G. SUPPORTING DIAGNOSIS

1. ECG: shows a pattern of ischemic injury and conduction disturbance states the type /
source of dysrhythmias and the effects of electrolyte imbalances and heart medications.

2. Holter monitor: ECG picture (24 hours) may be needed to determine where
dysrhythmias are caused by special symptoms if active patients (at home / work) can also
be used to evaluate pacemaker function / antidysrhythmic drug effects. evaluate
pacemaker function / antidysrhythmic drug effects.

3. Chest photo: can show support = suggestion of cardiac shadow with respect to
ventricular or valve dysfunction.

4. Allow imaging of myocardia: can show ischemic / myocardial damage that can affect
conduction normal or interfere with wall movement and pump ability.

5. Exercise stress tests: can be done to demonstrate exercises that cause dysrhythmias.

6. Electrolytes: Increased or decreased potassium, calcium and magnesium can cause

dysrhythmias.

7. Examination of drugs: Can state the toxicity of heart drugs, the presence of street drugs
or suspected drug interactions for example digitalis, quinidin.

8. Thyroid examination: an increase or decrease in serum thyroid levels can cause an

increase in dysrhythmias.

9. Sedimentation rate: It can also cause acute inflammatory processes such as

endocarditis as a precipitating factor for dysrhythmias.

10. GDA / pulse oximetry: Hypoxemia can cause / exacerbate dysrhythmias.

H. MEDICAL MANAGEMENT

1. Medical therapy Antiarrhythmic drugs are divided into 4 classes:

1. Anti arrhythmia

i. Class 1: sodium channel blocker

ii. Class 1 A, Quinidine is a drug used in maintenance therapy to prevent recurrence of

atrial fibrillation or flutter. Procainamide for extra ventricular systole atrial fibrillation
and arrhythmias that accompany anesthesia. Dysopiramide for acute and recurrent SVT

iii. Class 1 B, Lignocain for ventricular arrhythmias due to myocardial ischemia,

ventricular tachycardia. Mexiletine for entricular arrhythmias and VT

iv. Class 1 C, Flecainide for ectopic ventricles and tachycardia

2. Anti arrhythmia Class 2 (Beta adrenergic blockade) Atenolol, Metoprolol, Propanolol:
indications of cardiac arrhythmias, angina pectoris and hypertension

3. Anti arrhythmia class 3 (Prolong repolarisation) Amiodarone, VT indication, SVT

recurs

4. Grade 4 anti-arrhythmia (calcium channel blocker) Verapamil, an indication of

supraventricular arrhythmias

2. Mechanical therapy a. Cardioversion: involves using an electric current to stop

dysrhythmias that have a GRS complex, usually an elective procedure

b. Defibrillation: asynchronous cardioversion used in emergencies.

c. Cardioverter defibrillator implants: a tool for detecting and terminating life-threatening

episodes of ventricular tachycardia or in patients at risk of developing ventricular
fibrillation.

d. Pacemaker therapy: an electrical device capable of producing repeated electrical

stimuli to the heart muscle to control the frequency of the heart.
CHAPTER III

NURSING CARE

A. NURSING ASSESSMENT

Assessment

a. Disease history

- Family risk factors, for example: Heart disease, stroke, hypertension.

- History of previous IM (dysrhythmias), cardiomyopathy, GJK, heart disease,

hypertension.

- The use of digitalis, quinidin and other antiartitic drugs is likely to occur intoxication.

Psychosocial conditions.

b. Physical assessment

- Activity: general fatigue.

- Circulation: changes in BP (Hypertension or hypotension): pulse may be irregular, extra

sounds, pulses decrease, skin color and humidity change, for example: pale cyanosis,
sweating, edema, decreased urine output when cardiac output declines heavily.

- Ego Integrity: feeling nervous, feeling threatened, anxious, afraid, rejecting, angry,
restless, crying.

- Food / fluid: loss of appetite, anorexia, food intolerance, nausea vomiting, changes in
body weight and changes in skin moisture.

- Neurosensory: dizziness, throbbing, headache, disorvelation, confusion, lethargy,

pupillary changes.

- Pain / discomfort: mild to severe chest pain, can be lost or not with antianginal drugs,
anxiety.
- Respiratory: chronic peruvian disease, shortness of breath, coughing, changes in
respiratory rate / depth, additional breath sounds (krekels, rhonchi, wheezing) may
indicate respiratory complications such as left heart failure (pulmonary edema) or
pulmonary thromboembolytic phenomena, hemoptysis.

B. NURSING AND INTERVENTION DIAGNOSIS

a. A high risk of decreased cardiac output is associated with electrial conduction

disorders, decreased myocardial contractility.

Outcome / criteria results:

- Maintain / improve adequate cardiac output as evidenced by BP / pulse in the normal

range, adequate urine output, the pulse is felt the same, normal mental status.

- Indicates a decrease in frequency / no dysrhythmias.

- Participate in activities that reduce myocardial work.

Interventions:

- Auscultation of the apical pulse, frequency analysis, heart rhythm.

Rational: tachycardia (although at rest) usually occurs to compensate for the decrease in
ventricular contractility.

- Record heart sounds

Rational: S1 and S2 may be weak because of the decrease in pump work. Murmurs can
show valve incompetence / stenosis.

- Palpation of peripheral pulses

Rational: decreased cardiac output can show a decrease in radial, popliteal, dorsal, pedis
and posttibial pulse. The pulse may be rapidly lost or irregular for dipalpation and
alternan pulse.

- Monitor TD

Rational: in early, moderate or chronic blood pressure can increase, further CHF in the
body can no longer compensate and hypotension cannot be normal anymore.

- Assess the skin for pallor and cyanosis.

Rational: pale shows decreased peripheral perfusion secondary to inadequate cardiac
output, vasoconstriction and anemia.

- Provide supplemental oxygen with nasal cannula / mask and medication as indicated
(collaboration).

Rational: increase oxygen supply for myocardial needs to counteract the effects of
hypoxia / ischemia.

b. Activity intolerance is associated with an imbalance between oxygen supply, general

weakness, long bed rest / mobilization

Outcome / criteria results:

- The client will participate in the desired activity.

- Meet self-care.

- Achieving an increase in tolerance of activity that can be measured, as evidenced by

decreased weakness and fatigue.

Interventions:

- Check vital signs before and immediately after activity, especially if clients use
vasodilators, diuretics and beta blockers.

Rational: orthostatic hypotension can occur with due activity

Drug effects (vasodilation), fluid transfer (diuretic) or the effect of heart function.

- Record the cardiopulmonary response to activity, note tachycardia, dysrhythmia,

dipsnea, sweating and pale.

- Evaluation of increased activity intolerance.

Rational: decrease / inability of myocardium to

Increase volume volume during activity can

Causes increased fatigue and weakness.

- Evaluation of increased activity intolerance.

Rational: can show increased cardiac decompensation

Rather than excess activity.

- Implementation of cardiac rehabilitation / activity (collaborative) programs.

Rational: gradual increase in work avoidance activities

Heart / excessive oxygen consumption.

c. Excess fluid volume is associated with decreased glomerular phytation rate (decreased
cardiac output) / increased ADH product and sodium / water retention.

Outcome / criteria results:

- Demonstrating a steady volume of liquid with a balance of input and expenditure.

- Clean / clear breath sounds, vital signs in an acceptable range.

- Stable weight and no edema.

- Stating an understanding of individual fluid restrictions.

Interventions:

Monitor urine expenditure, record the number and color of the time when diuresis occurs.

Rational: urine expenditure may be small and concentrated because

Decreased perfusion occurs.

- Monitor / calculate the balance of income and expenditure for 24 hours.

Rational: diuretic therapy can be caused by fluid loss

Sudden / excessive (hypovolemia) despite edema /

Ascites still exists.

- Maintain sitting or bed rest with the semifowler position in the acute phase.

Rational: the position increases renal filtration and decreases ADH production so that
diuresis increases.

- Monitor TD and CVP (if available).

Rational: hypertension and increased CVP show excess fluid and can indicate an increase
in pulmonary congestion, heart failure.
- Assess bowel sounds, record complaints of anorexia, nausea, abdominal distention and
constipation.

Rational: visceral congestion (occurs in advanced CRF) can interfere with gastric /
intestinal function.

- Consul with nutritionists.

Rational: need to provide a diet that is acceptable to clients who meet calorie needs in
sodium restriction.

CHAPTER IV

COVER

A. CONCLUSION

Arrhythmias or dysrhythmias are changes in the frequency and rhythm of the heart
caused by abnormal or automatic electrolyte conduction (Doenges, 1999).

Arrhythmia arises due to electrophysiological changes in myocardial cells. This

electrophysiological change manifests as a change in the shape of the action potential,
namely a graphical record of cell electrical activity (Price, 1994).

The most common causes of ventricular arrhythmias are myocardial disease (ischemia
and infarction), which is accompanied by changes in electrolyte balance, metabolic
disorders, drug toxicity and coronary vasospasm. Because the implus originates from the
ventricle, it is not through a normal conduction system but rather ventricular muscle
tissue.

1. Medical therapy

1) Anti-arrhythmic drugs divided into 4 classes, namely:

a. Anti arrhythmia

b. Class 1: sodium channel blocker

i. Class 1 A, Quinidine is a drug used in maintenance therapy to prevent recurrence of

atrial fibrillation or flutter. Procainamide for extra ventricular systole atrial fibrillation
and arrhythmias that accompany anesthesia. Dysopiramide for acute and recurrent SVT

ii. Class 1 B, Lignocain for ventricular arrhythmias due to myocardial ischemia,

ventricular tachycardia. Mexiletine for entricular arrhythmias and VT

iii. Class 1 C, Flecainide for ectopic ventricles and tachycardia

c. Anti arrhythmia Class 2 (Beta adrenergic blockade) Atenolol, Metoprolol, Propanolol:

indications of cardiac arrhythmias, angina pectoris and hypertension

d. Anti arrhythmia class 3 (Prolong repolarisation) Amiodarone, VT indication, SVT

recurs

e. Grade 4 anti-arrhythmia (calcium channel blocker) Verapamil, an indication of

supraventricular arrhythmias.

2. Mechanical therapy

a. Cardioversion
b. Defibrillation

c. Cardioverter defibrillator implantable

d. Pacemaker therapy

C. SUGGESTIONS

With the preparation of this paper, it is hoped that all readers will be able to know and
understand the problem of arrhythmia. If you want to add insight and want to know more,
then we hope to be able to read scientific books related to arrhythmia.

BIBLIOGRAPHY
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Price, Sylvia Anderson. Patofisiologi : konsep klinis proses-proses penyakit. Alih bahasa Peter
Anugrah. Editor Caroline Wijaya. Ed. 4. Jakarta : EGC ; 1994.
Santoso Karo karo. Buku Ajar Kardiologi. Jakarta : Balai Penerbit FKUI ; 1996
Smeltzer Suzanne C. Buku Ajar Keperawatan Medikal Bedah Brunner & Suddarth. Alih
bahasa Agung Waluyo, dkk. Editor Monica Ester, dkk. Ed. 8. Jakarta : EGC; 2001.
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