NURSING CARE MANAGEMENT 103

CARE OF CLIENTS WITH PROBLEMS IN OXYGENATION, FLUID AND

ELECTROLYTE BALANCE, NUTRITION AND METABOLISM AND
ENDCORINE

ACUTE MYOCARDIAL
INFARCTION
A CASE STUDY presented to the Faculty of the College of Nursing and Allied
Health in partial fulfillment of the requirements in NCM 103

AY 2016 2017

TABLE OF CONTENTS
I.

INTRODUCTION..
Overview of the Disease....
Statistical Data...
Scope and Limitation.
Background of Study..

II.

PATIENTS PROFILE..

III.

PATIENTS HISTORY.
Present Health History...
Past Health History
Family History...
Developmental History......
Socioeconomics.....
Psychological.........
Socio-cultural.....
Spiritual......
Nutrition.....
Elimination.........
Exercise......
Hygiene......
Sleep and rest.

IV.

PHYSICAL ASSESSMENT.

V.

ANATOMY AND PHYSIOLOGY..

VI.

PATHOPHYSIOLOGY...

VII.

DIAGNOSTIC PROCEDURE

VIII. MEDICAL MANAGEMENT..

IX.

NURSING MANAGEMENT...

X.

DRUG STUDY..

XI.

NURSING CARE PLAN.

XII.

RECOMMENDATION...

XIII. SUMMARY OF DISCHARGE..

Medications.
Environment
Treatment
Health Teaching..
Out-Patient..
Diet......
Spiritualization
Bibliography....

I.

Introduction

A. Description of Health Condition

(Overview of the Case)
Acute Myocardial Infarction
MI refers to the process by which areas of myocardial cells in the heart are
permanently destroyed. Like unstable angina, MI is usually caused by reduced blood ow
in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or
thrombus. (Hinkle, J. & Cheever, K. 2014)

A myocardial infarction (MI), or

heart attack, results in the death of heart
muscle. The affected myocardial cells in

the

heart are permanently destroyed. An MI

occurs from a partial or complete
blockage of a coronary artery, which
decreases the blood supply to the cells

of

the heart supplied by the blocked coronary artery. The extent of the cardiac damage varies
depending on the location and amount of blockage in the coronary artery. This is a
potentially devastating condition. The ability of the heart to contract, relax, and propel
blood throughout the body requires healthy cardiac muscle. Resulting depends on speed
and effectiveness of treatment.
Myocardial infarction is identied by type. Non ST-segment elevation
myocardial infarction (NSTEMI) is also known as a nonQ-wave MI. An ST-segment
elevation myocardial infarction (STEMI) is also known as a Q-wave MI and is the
deadliest type because usually it is caused by a complete blockage of the artery. With
timely reperfusion, cell death may not occur, which reduces the permanent damage
(reected by a Q-wave appearance). (Williams, L. & Hopper, P. 2011)
Myocardial infarction occurs when complete obstruction of a coronary artery
interrupts blood supply to an area of myocardium. Affected tissue becomes ischemic and
eventually dies (infarcts) if the blood supply is not restored. The necrotic area is bordered
by an area of injured or damaged tissue, which is in turn surrounded by an area of
ischemic tissue.

As myocardial cells die, they lyse and release various cardiac isoenzymes into the
circulation. Elevated serum levels of creatinine kinase (CK) and cardiac-specific
troponins are specific indicators of myocardial infarction. (LeMone, P., Burke, K. &
Bauldoff, G. 2011.)
Clinical Manifestations

Chest pain that occurs suddenly and continues despite rest and medication is the
presenting symptom in most patients with an MI.
They may have cool, pale, and moist skin.
Their heart rate and respiratory rate may be faster than normal.
(Hinkle, J. & Cheever, K. 2014)
When listening to lung sounds, crackles or wheezing may be heard.
The pulse may be rapid or irregular, and an extra heart sound (referred to as S3 or
S4) may be present.
(Williams, L. & Hopper, P. 2011)

Risk Factors

Age: 65 or older

B. Statistical Data
Each year in the United States, 785,000 people have acute MIs and many
of these people die as a result (Roger et al., 2011). Many of those who die never
reach a hospital.

C. Scope and Limitation

The first group of BSN III-A had their hospital exposure last November 3,
2016 at 6-3 shift at Laguna Medical Center Emergency Room under the
supervision of their Clinical Instructor, Mrs. Ma. Janice M. Bernardo; plus, the
consent from the patient. They found a suitable case to present on their final case
study. The scope of their duty on that specific day range from basic nursing
procedures including nurse-patient interaction; vital signs taking, recording and
monitoring; regulating and monitoring IV fluids; brief physical assessment and
history taking; bed making; patient teaching; and learning a lot during their
clinical duty. They werent allowed to administer medications, document on the
patients chart, and perform other procedures but they are permitted to observe
and participate on procedures done by the staff on duty.

D. Background of Study
This case was chosen by the group because it is timely with their present
discussion on Nursing Care Management 103 (NCM103) Care of Clients with
Problems on Oxygenation, Fluid and Electrolyte Balance, Nutrition and Metabolism,
and Endocrine allowing the students to identify with it. Moreover, they want to
deepen their knowledge about this Cardiovascular Disorder, master the different and
appropriate medical management, nursing management, and all particulars associated
with it.

II.
Hospital Number:

Patients Profile

Case Number:
Patients Name:

Sex:

Male

Age:

52

Birthdate:
Birthplace:
Permanent Address:

Labuin, Pila, Laguna

Nationality:

Filipino

Religion:

Catholic

Civil Status:

Married

Occupation:
Educational Attainment:
Family Income:
Number of Children:
Allergies:

Clinical/Admitting Data
Admission Date:

November 2, 2016

Admission Time:

8:00 AM

Admitting Physician:

Dra. Buan

Admitting Clerk:
Admission Diagnosis:
Principal Diagnosis:

AMI, HCVD

III. Patients History

A. Present Health History
On November 2, 2016, the patient was admitted to Laguna Medical Center
Emergency Department due to complaints of on and off severe chest pain and difficulty
of breathing, which began 5 days straight prior to admission. His initial physical
assessment upon admission are: blood pressure of 160/90 mmHg; cardiac rate of 86 beats
per minute; and adventitious breath sounds. The physicians impression was Acute
Myocardial Infarction and Hypertensive Cardiovascular Disease and ordered medications
for chest pain and hypertension and other conservative emergency measures.

B. Past Health History

The patient is a smoker and drinks alcohol occasionally. He started to have high
blood pressure when he was 30 years old. He has never been hospitalized before and does
not experienced any uncommon illnesses or diseases in the past. He is the only one who
is hypertensive in their family and was not aware on why he has experienced chest pain
and difficulty of breathing. Whenever he feels those symptoms he ignores it as he thought
hes simply tired and overworked and never considered taking any medications.
However, when the symptoms persist, he consulted on a nearby local health unit and was
given salbutamol nebulizer.

C. Family History

D. Developmental History

E. Socioeconomics
According to the patient, he works at the water station as a delivery boy near their
house, while his wife stays at home. He told us that he is the only provider in their family.
Their income is 150 php 200 php a day as estimated by our patients partner. According
to them, the income is insufficient because of expenses other than food.

F. Psychological
During interaction with the patient, it was observed that he was not able to
interact properly due to breathing difficulty.

G. Socio-cultural
As stated by the patient, whenever he feels dizziness and difficulty of breathing he
just takes a rest. But if it doesnt subside he goes to the local health unit in their barangay
and gives him a salbutamol via nebulization. The patient does not seek health care from
different sources such as the herbalists as he does not approved of it, but only from the
formal health sector.

H. Spiritual
Our patient is Roman Catholic. According to him, he is not active in attending
church even his wife. Though they are not regular Church attendees, they regard God as
eternal being who created and preserves all things.

I. Nutrition

J. Elimination

K. Exercise
Our patient is the one who provides the needs for his family, he works as a
delivery boy in a water station near their house then it serves as his daily exercise.

L. Hygiene

Before Hospitalization

During Hospitalization

Our patient takes a bath 4

Our patient or his wife is

5 times a week with

the one cleansing his

soap and shampoo,

body with towel, soap

including brushing his

and water and he brushes

teeth.

his teeth and washes his

After Hospitalization

hand regularly.

M.Sleep & Rest

Before Hospitalization

During Hospitalization

According to the patient,

During hospitalization, the

his constant sleep pattern

patient had a hard time

is sleeping at 9 in the

taking a rest during the day

evening then waking up at

and sleeping at night. He

After Hospitalization

5 o clock in the morning.

has difficulty in resting and

The duration of his sleep

sleeping due to the noise,

is 8 hours straight each

noxious odor and warm

night. Then during the

temperature of the

day, he is awake to go to

environment. He reports of

work.

having waking periods in

between his sleep at night
due to instances of
difficulty of breathing. He
estimated the length of
sleep and rest about
5hours.

IV. Physical Assessment

AREA
NEUROLOGIC

FINDINGS
Patient is alert.

Level of

Glasgow Coma

Consciousness
Cranial Nerve I

Score (GCS):
Can identify familiar

Olfactory
Cranial Nerve II

odors
Clear vision

Optic
Cranial Nerve III

INTERPRETATION

NORMAL
NORMAL

Oculomotor
Cranial Nerve IV

Can move eyes

Trochlear
Cranial Nerve V

downward
Can feel sensation in

NORMAL

Trigeminal

different parts of the

NORMAL

Cranial Nerve VI

face
Can follow direction

Abducens

of gaze, can move

NORMAL

eyes laterally or side

Cranial Nerve VII

to side
Patient can smile,

Facial

raise his eyebrows,

and puff his cheeks.
Can differentiate
between sweet and

Cranial Nerve VIII

salty taste.
Both ears can clearly

NORMAL

IMPLICATION

Auditory/Acoustic
Cranial Nerve IX

hear snap of a finger.

Able to swallow and

NORMAL

Glossopharyngeal
Cranial Nerve X

say AH.
Intact gag reflex.

NORMAL

Vagus
Cranial Nerve XI

NORMAL

Accessory
Cranial Nerve XII

Able to stick tongue

Hypoglossal

out and move it side

NORMAL

to side.

INTERPETATION

AREA
INTEGUMENTA

METHOD
Inspection

FINDINGS
With few

RY

and Palpation

and small

healing of wound or

light to deep

lesion that represents

brown

replacement by

secondary

connective tissue.

skin lesions

Young scars are red

(Scars) on

or purple, whereas

both lower

mature scars are

legs.

white or glistening.

Skin

Abnormal

IMPLICATION
Skin mark left after

Reference:
Weber J., & Kelly J.,
Health Assessment in
Nursing. 2013. Pg.

266

Normal

Skin color is
light brown,
generally
uniform
except in
areas
exposed to
the sun. Has
an equally
warm
temperature
on both arms
and legs.
With good
skin turgor
Hair
Nails

Inspection
Fingernails

Abnormal

Indication of bad

and toenails

hygiene

are

(Reference: Livestrong
(2016))

soiled/dirty
HEAD
Skull and Face
Eyes and Vision

Inspection

Eyebrows

Normal

have evenly
distributed
hair,
symmetricall
y aligned.
No
discoloration
of eyelids &
lids close
symmetricall
Ears and Hearing

Inspection

y.
Color of ears

and palpation

are same as
facial skin
(light
brown).
Symmetrical
ears and
equal in size
aligned on
the outer

Normal

canthus of
Nose and Sinuses

Inspection

the eye.
Nose is

and palpation

midline,

Normal

symmetric
and straight
on the face
without
swelling,
bleeding or
lesions.
Mouth and

Inspection

Oropharynx
NECK

Inspection

Symmetrical

Neck Muscles

and palpation

with head in
central
position.
Symmetrical
movement
of neck
muscles.
Movement
through full
range of
motion

Normal

without
complaint of
discomfort.
Lymph Nodes
Trachea and
Thyroid Gland
Chest
Lungs
Cardiovascular
system

Palpation
Palpation
Inspection
Palpation and
auscultation

AREA

METHOD

Abdomen

Inspection,

FINDINGS

INTERPRETATION

IMPLICATION

auscultation,
percussion and
palpation

Genitals

Inspection

Rectum/
Anus

Inspection

Musculoskeletal
AREA
Left Upper

FINDINGS
No evident masses,

Extremity

lesions, foreign
bodies or other

INTERPRETATION
Good

IMPLICATION

abnormalities. No
apparent muscle
wasting contraction.
Range of motion and
tone are within
normal limits.
Strength is 4/5 means
muscle is functioning
Right Upper

normally.
No evident masses,

Extremity

lesions, foreign

Good

bodies or other
abnormalities. No
apparent muscle
wasting contraction.
Range of motion and
tone are within
normal limits.
Strength is 4/5 means
muscle is functioning
Right Lower

normally.
No evident masses,

Extremity

lesions, foreign
bodies or other

Good

abnormalities. No
apparent muscle
wasting contraction.
Range of motion and
tone are within
normal limits.
Strength is 4/5 means
muscle is functioning
Left Lower

normally.
No evident masses,

Extremity

lesions, foreign

Good

bodies or other
abnormalities. No
apparent muscle
wasting contraction.
Range of motion and
tone are within
normal limits.
Strength is 4/5 means
muscle is functioning
normally.

V.

Anatomy and Physiology

The heart is a hollow, muscular organ located in the center of the thorax, where it occupies the
space between the lungs (mediastinum) and rests on the diaphragm. It weighs approximately 300
g (10.6 oz), although heart weight and size are influenced by
age, gender, body weight, extent of physical exercise and conditioning and heart disease. The
heart pumps blood to the tissues, supplying them with oxygen and other nutrients. The pumping
action of the heart is accomplished by the rhythmic contraction and relaxation of its muscular
wall. During systole (contraction of the muscle) the chambers of the heart become smaller as the
blood is ejected. During diastole (relaxation of the muscle), the heart chambers fill with blood in
preparation for the subsequent ejection. A normal resting adult heart beats approximately 60 to
80 times per minute. Each ventricle ejects approximately 70 mL of blood per beat and has an
output of approximately 5 L per minute.

The heart is composed of three layers. The inner layer, or endocardium, consists of endothelial
tissue and lines the inside of the heart and valves. The middle layer, or myocardium, is made up
of muscle fibers and is responsible for the pumping action. The exterior layer of the heart is
called the epicardium. The heart is encased in thin, fibrous sac called the pericardium, which is
composed of two layers. Adhering to the epicardium is the visceral pericardium. Enveloping the
visceral pericardium is the parietal pericardium, a tough fibrous tissue that attaches to the great
vessels, diaphragm, sternum, and vertebral column and supports the heart in the mediastinum.
The space between these two layers (pericardial space) is filled with about 30 mL of fluid, which
lubricates the surface of the heart and reduces friction during systole.
Heart Chambers
The four chambers of the heart constitute the right- and left sided pumping systems. The
right side of the heart, made up of the right atrium and right ventricle, distributes venous blood
(deoxygenated blood) to the lungs via the pulmonary artery (pulmonary circulation) for
oxygenation. The right atrium receives blood returning from the superior vena cava (head, neck,
and upper extremities), inferior vena cava (trunk and lower extremities) and coronary sinus
(coronary circulation). The left side of the heart composed of the left atrium and left ventricle
distributes oxygenated blood to the remainder of the body via the aorta (systemic circulation).
The left atrium receives oxygenated blood from the pulmonary circulation via the pulmonary
veins. The varying thicknesses of the atrial and ventricular walls relate to the workload required
by each chamber. The atria are thin-walled because blood returning to these chambers generates
low pressures. In contrast, the ventricular walls are thicker because they generate greater
pressures during systole. The right ventricle contracts against low pulmonary vascular pressure
and has thinner walls than the left ventricle. The left ventricle, with walls two-and-a-half times

more muscular than those of the right ventricle, contracts against high systemic pressure.
Because the heart lies in a rotated position within the chest cavity, the right ventricle lies
anteriorly (just beneath the sternum) and the left ventricle is situated posteriorly. The left
ventricle is responsible for the apex beat or the point of maximum impulse (PMI), which is
normally palpable in the left midclavicular line of the chest wall at the fifth intercostal space.

Heart Valves
The four valves in the heart permit blood to flow in only one direction. The valves, which
are composed of thin leaflets of fibrous tissue, open and close in response to the movement of
blood and pressure changes within the chambers. There are two types of valves: atrioventricular
and semilunar.

Atrioventricular valve
The valves that separate the atria from the ventricles are termed atrioventricular valves.
The tricuspid valve, so named because it is composed of three cusps or leaflets, separates the
right atrium from the right ventricle. The mitral, or bicuspid (two cusps) valve, lies between the
left atrium and the left ventricle. Normally, when the ventricles contract, ventricular pressure
rises, closing the atrioventricular valve leaflets. Two additional structures, the papillary muscles
and the chordae tendineae, maintain valve closure. The papillary muscles, located on the sides of
the ventricular walls, are connected to the valve leaflets by thin fibrous bands called chordae
tendineae. During systole, contraction of the papillary muscles causes the chordae tendineae to
become taut, keeping the valve leaflets approximated and closed.

Semilunar valve
The two semilunar valves are composed of three half-moon-like leaflets. The valve
between the right ventricle and the pulmonary artery is called the pulmonic valve; the valve
between the left ventricle and the aorta is called the aortic valve.

Coronary Arteries
The left and right coronary arteries and their branches supply arterial blood to the heart.
These arteries originate from the aorta just above the aortic valve leaflets. The heart has large
metabolic requirements, extracting approximately 70% to 80% of the oxygen delivered (other
organs consume, on average, 25%). Unlike other arteries, the coronary arteries are perfused
during diastole. An increase in heart rate shortens diastole and can decrease myocardial
perfusion. Patients, particularly those with coronary artery disease (CAD), can develop
myocardial ischemia (inadequate oxygen supply) when the heart rate accelerates. The left
coronary artery has three branches. The artery from the point of origin to the first major branch is
called the left main coronary artery. Two bifurcations arise off the left main coronary artery.
These are the left anterior descending artery, which courses down the anterior wall of the heart,
and the circumflex artery, which circles around to the lateral left wall of the heart. The right side
of the heart is supplied by the right coronary artery, which progresses around to the bottom or
inferior wall of the heart. The posterior wall of the heart receives its blood supply by an
additional branch from the right coronary artery called the posterior descending artery.
Superficial to the coronary arteries are the coronary veins. Venous blood from these veins returns
to the heart primarily through the coronary sinus, which is located posteriorly in the right atrium.

Cardiac Muscle
The myocardium is composed of specialized muscle tissue. Microscopically, myocardial
muscle resembles striated (skeletal) muscle, which is under conscious control. Functionally,
however, myocardial muscle resembles smooth muscle because its contraction is involuntary.
The myocardial muscle fibers are arranged in an interconnected manner (called a syncytium) that
allows for coordinated myocardial contraction and relaxation. The sequential pattern of
contraction and relaxation of individual muscle fibers ensures the rhythmic behavior of the
myocardium as a whole and enables it to function as an effective pump.

FUNCTION OF THE HEART: Conduction system

The specialized heart cells of the cardiac conduction system methodically generate and
coordinate the transmission of electrical impulses to the myocardial cells. The result is sequential
atrioventricular contraction, which provides for the most effective flow of blood, thereby
optimizing cardiac output. Three physiologic characteristics of the cardiac conduction cells
account for this coordination: Automaticity: ability to initiate an electrical impulse. Excitability:
ability to respond to an electrical impulse. Conductivity: ability to transmit an electrical impulse
from one cell to another.
The sinoatrial (SA) node, referred to as the primary pacemaker of the heart, is located at the
junction of the superior vena cava and the right atrium (Fig. 26-3). The SA node in a normal
resting heart has an inherent firing rate of 60 to 100 impulses per minute, but the rate can change
in response to the metabolic demands of the body. The electrical impulses initiated by the SA
node are conducted along the myocardial cells of the atria via specialized tracts called internodal
pathways. The impulses cause electrical stimulation and subsequent contraction of the atria. The

impulses are then conducted to the atrioventricular (AV) node. The AV node (located in the right
atrial wall near the tricuspid valve) consists of another group of specialized muscle cells similar
to those of the SA node. The AV node coordinates the incoming electrical impulses from the atria
and, after a slight delay (allowing the atria time to contract and complete ventricular filling),
relays the impulse to the ventricles. This impulse is then conducted through a bundle of
specialized conduction cells (bundle of His) that travel in the septum separating the left and right
ventricles. The bundle of His divides into the right bundle branch (conducting impulses to the
right ventricle) and the left bundle branch (conducting impulses to the left ventricle). To transmit
impulses to the largest chamber of the heart, the left bundle branch bifurcates into the left
anterior and left posterior bundle branches. Impulses travel through the bundle branches to reach
the terminal point in the conduction system, called the Purkinje fibers. This is the point at which
the myocardial cells are stimulated, causing ventricular contraction. The heart rate is determined
by the myocardial cells with the fastest inherent firing rate. Under normal circumstances, the SA
node has the highest inherent rate, the AV node has the second highest inherent rate (40 to 60
impulses per minute), and the ventricular pacemaker sites have the lowest inherent rate (30 to 40
impulses per minute). If the SA node malfunctions, the AV node generally takes over the
pacemaker function of the heart at its inherently lower rate. Should both the SA and the AV
nodes fail in their pacemaker function, a pacemaker site in the ventricle will fire at its inherent
bradycardic rate of 30 to 40 impulses per minute.

Physiology of Cardiac Conduction

Cardiac electrical activity is the result of the movement of ions (charged particles such as
sodium, potassium, and calcium) across the cell membrane. The electrical changes recorded
within a single cell result in what is known as the cardiac action potential.
In the resting state, cardiac muscle cells are polarized, which means an electrical difference
exists between the negatively charged inside and the positively charged outside of the cell
membrane. As soon as an electrical impulse is initiated, cell membrane permeability changes and
sodium moves rapidly into the cell, while potassium exits the cell. This ionic exchange begins
depolarization (electrical activation of the cell), converting the internal charge of the cell to a
positive one. Contraction of the myocardium follows depolarization. The interaction between
changes in membrane voltage and muscle contraction is called electromechanical coupling. As
one cardiac muscle cell is depolarized, it acts as a stimulus to its neighboring cell, causing it to
depolarize. Sufficient depolarization of a single specialized conduction system cell results in
depolarization and contraction of the entire myocardium. Repolarization (return of the cell to its
resting state) occurs as the cell returns to its baseline or resting state; this corresponds to
relaxation of myocardial muscle. After the rapid influx of sodium into the cell during
depolarization, the permeability of the cell membrane to calcium is changed. Calcium enters the
cell and is released from intracellular calcium stores. The increase in calcium, which occurs
during the plateau phase of repolarization, is much slower than that of sodium and continues for
a longer period. Cardiac muscle, unlike skeletal or smooth muscle, has a prolonged refractory
period during which it cannot be restimulated to contract. There are two phases of the refractory
period, referred to as the absolute refractory period and the relative refractory period.
The absolute refractory period is the time during which the heart cannot be restimulated to
contract regardless of the strength of the electrical stimulus. This period corresponds with

depolarization and the early part of repolarization. During the latter part of repolarization,
however, if the electrical stimulus is stronger than normal, the myocardium can be stimulated to
contract. This short period at the end of repolarization is called the relative refractory period.
Refractoriness protects the heart from sustained contraction (tetany), which would result in
sudden cardiac death. Normal electromechanical coupling and contraction of the heart depend on
the composition of the interstitial fluid surrounding the heart muscle cells. In turn, the
composition of this fluid is influenced by the composition of the blood. A change in serum
calcium concentration may alter the contraction of the heart muscle fibers. A change in serum
potassium concentration is also important, because potassium affects the normal electrical
voltage of the cell.

Cardiac Hemodynamics
An important determinant of blood flow in the cardiovascular system is the principle that
fluid flows from a region of higher pressure to one of lower pressure. The pressures responsible
for blood flow in the normal circulation are generated during systole and diastole.

CARDIAC CYCLE
Beginning with systole, the pressure inside the ventricles rapidly rises, forcing the
atrioventricular valves to close. As a result, blood ceases to flow from the atria into the ventricles
and regurgitation (backflow) of blood into the atria is prevented. The rapid rise of pressure inside
the right and left ventricles forces the pulmonic and aortic valves to open, and blood is ejected
into the pulmonary artery and aorta, respectively. The exit of blood is at first rapid; then, as the
pressure in each ventricle and its corresponding artery equalizes, the flow of blood gradually

decreases. At the end of systole, pressure within the right and left ventricles rapidly decreases.
This lowers pulmonary artery and aortic pressure, causing closure of the semilunar valves. These
events mark the onset of diastole. During diastole, when the ventricles are relaxed and the
atrioventricular valves are open, blood returning from the veins flows into the atria and then into
the ventricles. Toward the end of this diastolic period, the atrial muscles contract in response to
an electrical impulse initiated by the SA node (atrial systole). The resultant contraction raises the
pressure inside the atria, ejecting blood into the ventricles. Atrial systole augments ventricular
blood volume by 15% to 25% and is sometimes referred to as the atrial kick. At this point,
ventricular systole begins in response to propagation of the electrical impulse that began in the
SA node some milliseconds previously. The following section reviews the chamber pressures
generated during systole and diastole.

Chamber Pressures.
In the right side of the heart, the pressure generated during ventricular systole (15 to 25
mm Hg) exceeds the pulmonary artery diastolic pressure (8 to 15 mm Hg), and blood is ejected
into the pulmonary circulation. During diastole, venous blood flows into the atrium because
pressure in the superior and inferior vena cava (8 to 10 mm Hg) is higher than that in the atrium.
Blood flows through the open tricuspid valve and into the right ventricle until the two right
chamber pressures equalize (0 to 8 mm Hg). In the left side of the heart, similar events occur,
although higher pressures are generated. As pressure mounts in the left ventricle during systole
(110 to 130 mm Hg) resting aortic pressure (80 mm Hg) is exceeded and blood is ejected into the
aorta. During left ventricular ejection, the resultant aortic pressure (110 to 130 mm Hg) forces
blood progressively through the arteries. Forward blood flow into the aorta ceases as the

ventricle relaxes and pressure drops. During diastole, oxygenated blood returning from the
pulmonary circulation via the four pulmonary veins flows into the atrium, where pressure
remains low. Blood readily flows into the left ventricle because ventricular pressure is also low.
At the end of diastole, pressure in the atrium and ventricle equilibrates (4 to 12 mm Hg). Figure
26-5 depicts the systolic and diastolic pressures in the four chambers of the heart.

Pressure Measurement.
Chamber pressures are measured with the use of special monitoring catheters and
equipment. This technique is called hemodynamic monitoring. Nurses caring for critically ill
patients must have a sophisticated working knowledge of normal chamber pressures and the
hemodynamic changes that occur during serious illnesses. The data obtained from hemodynamic
monitoring assist with the diagnosis and management of pathophysiologic conditions affecting
critically ill patients. Hemodynamic monitoring is covered in more detail at the end of this
chapter.

Cardiac output is the amount of blood pumped by each ventricle during a given period. The
cardiac output in a resting adult is about 5 L per minute but varies greatly depending on the
metabolic needs of the body. Cardiac output is computed by multiplying the stroke volume by
the heart rate. Stroke volume is the amount of blood ejected per heartbeat. The average resting
stroke volume is about 70 mL, and the heart rate is 60 to 80 beats per minute (bpm). Cardiac
output can be affected by changes in either stroke volume or heart rate.
CONTROL OF HEART RATE

Cardiac output must be responsive to changes in the metabolic demands of the tissues.
For example, during exercise the total cardiac output may increase fourfold, to 20 L per minute.
This increase is normally accomplished by approximate doubling of both the heart rate and the
stroke volume. Changes in heart rate are accomplished by reflex controls mediated by the
autonomic nervous system, including its sympathetic and parasympathetic divisions. The
parasympathetic impulses, which travel to the heart through the vagus nerve, can slow the
cardiac rate, whereas sympathetic impulses increase it. These effects on heart rate result from
action on the SA node, to either decrease or increase its inherent rate. The balance between these
two reflex control systems normally determines the heart rate. The heart rate is stimulated also
by an increased level of circulating catecholamines (secreted by the adrenal gland) and by excess
thyroid hormone, which produces a catecholamine-like effect. Heart rate is also affected by
central nervous system and baroreceptor activity. Baroreceptors are specialized nerve cells
located in the aortic arch and in both right and left internal carotid arteries (at the point of
bifurcation from the common carotid arteries).
The baroreceptors are sensitive to changes in blood pressure (BP). During elevations in BP
(hypertension), these cells increase their rate of discharge, transmitting impulses to the medulla.
This initiates parasympathetic activity and inhibits sympathetic response, lowering the heart rate
and the BP. The opposite is true during hypotension (low BP). Hypotension results in less
baroreceptor stimulation, which prompts a decrease in parasympathetic inhibitory activity in the
SA node, allowing for enhanced sympathetic activity. The resultant vasoconstriction and
increased heart rate elevate the BP.

CONTROL OF STROKE VOLUME

Stroke volume is primarily determined by three factors: preload, afterload, and

contractility. Preload is the term used to describe the degree of stretch of the cardiac muscle
fibers at the end of diastole. The end of diastole is the period when filling volume in the
ventricles is the highest and the degree of stretch on the muscle fibers is the greatest. The volume
of blood within the ventricle at the end of diastole determines preload. Preload has a direct effect
on stroke volume. As the volume of blood returning to the heart increases, muscle fiber stretch
also increases (increased preload), resulting in stronger contraction and a greater stroke volume.
This relationship, called the Frank-Starling law of the heart (or sometimes the Starling law of the
heart), is maintained until the physiologic limit of the muscle is reached.
The Frank-Starling law is based on the fact that, within limits, the greater the initial length or
stretch of the cardiac muscle cells (sarcomeres), the greater the degree of shortening that occurs.
This result is caused by increased interaction between the thick and thin filaments within the
cardiac muscle cells. Preload is decreased by a reduction in the volume of blood returning to the
ventricles. Diuresis, venodilating agents (eg, nitrates), and loss of blood or body fluids from
excessive diaphoresis, vomiting, or diarrhea reduce preload. Preload is increased by increasing
the return of circulating blood volume to the ventricles. Controlling the loss of blood or body
fluids and replacing fluids (ie, blood transfusions and intravenous fluid administration) are
examples of ways to increase preload. The second determinant of stroke volume is afterload, the
amount of resistance to ejection of blood from the ventricle. The resistance of the systemic BP to
left ventricular ejection is called systemic vascular resistance. The resistance of the pulmonary
BP to right ventricular ejection is called pulmonary vascular resistance.

VI. Pathophysiology

VII. Diagnostic Procedure

DATE: 11/03/2016

LABORATORY
TEST

NORMAL
VALUES

RESULT

INTEPRETATION

Na (mEq/L)

135 148

134

DECREASE

Dont leave the patient unattended,

Raise side rails of the bed.

K (mEq/L)

3.5 5.4

3.1

DECREASE

Advise patient to rest. Assist patient.

RBS (mg/dL)

79 - 140

172

INCREASE

BUN (mg/dL)

9 20

41

INCREASE

Creatinine(mg/dL) 0.66 1.2

2.6

INCREASE

CK MB

25

INCREASE

POSITIVE

Troponin T

0 - 16

IMPLICATION

NURSING RESPONSIBILITY

Blood becomes
viscous.
Monitor patients input and urine
output.
Indication that you
have a heart
problem
Indication that
Patient may have
heart attack

Notify physician

Monitor patients Vital signs

especially the BP and Heart rate.

VIII. Medical Management

IX.

Doctors Order
Monitor V/S Q4

X.

Remarks

XI.

Take vital signs and compare

initial findings with clients data
to determine if there is any
progress to the clients
condition.

XII.

(Reference:Kozier&Erbs,
Fundamentals of Nursing 8th Edition
Volume 2 by Berman, Synder, Kozier,
Erb, Chapter 37, page 958)

I/O Q Shift & Record

XIII.

By monitoring the amount of

fluids a client takes in and
comparing this to the amount of
fluid a client puts out. The
healthcare team gain valuable
insight to the clients general
health as well as monitors
specific disease conditions.

XIV.

Purpose:

XV.

-helps evaluate clients fluid and

electrolyte balance

XVI. -suggests various diagnosis

XVII. -influence the choice fluid

therapy
XVIII. -document the clients ability to
tolerate oral fluids
XIX. -recognize significant fluid
losses
XX.

(Reference: Nursing Review By Ozlek,

retrieved from
nursingreviewbyozlek.blogspot.com)

O2 support via NC x 3L/min

XXI. Oxygen Therapy is for clients

whose gas exchanges is
impaired. Cannula is used to
deliver a relatively low
concentration of oxygen when
only minimal O2 support is
required.
XXII. (Reference: Kozier & Erbs,
Fundamentals of Nursing 8th Edition
Volume 2 by Berman, Synder, Kozier,
Erb, page 1375 & 1376)

D5LR 500 cc X 10 cc/hr only

XXIII. D5LR is a hypertonic solution

which draw fluid out of the
intracellular and interstitial
compartment, expanding
vascular volume. Expands
plasma volume.

XXIV.

LSLF diet in small amount

Diagnostic tests

Lab CBC

(Reference: Kozier&Erbs,
Fundamentals of Nursing 8th Edition
Volume 2 by Berman, Synder, Kozier,
Erb, Pg. 1455)

XXV.
XXVI. The CBC is a basic screening
test and one of the most
frequently ordered blood tests.
XXVII.

(Reference: Kozier & Erbs,

Fundamentals of Nursing 8th Edition
Volume 2 by Berman, Synder, Kozier,
Erb, Pg. 799)

BUN, Creatinine
RBS
12 lead ECG
CXR PA
Urinalysis

XXXIII.

XXVIII.
XXIX.
XXX.
XXXI.
XXXII.

XXXIV.

Nursing Management

XXXV. Nursing Management

Review diagnostic studies,

XXXVI. Rationale
To immediately report heavy bleeding

including/not limited to: chest

or signs and symptoms of shock to the

radiograph, cardiac stress testing,

physician or registered nurse.

ECG, echocardiogram, cardiac output

and ventricular ejection studies, and

heart scan or catheterization.

Evaluate client reports and evidence

To assess for signs of poor ventricular

of extreme fatigue, intolerance for

function and/or impending cardiac

activity, sudden or progressive weight

failure.

gain, swelling of extremities, and

progressive shortness of breath

Determine vital signs/hemodynamic

Provides baseline for comparison to

parameters including cognitive status.

follow trends and evaluate response to

Note vital sign response to activity or

interventions.

procedures and time required to return

to baseline.
Review signs of impending

Early detection of changes in these

failure/shock, noting decreased

parameters promotes timely

cognition and unstable or subnormal

intervention to limit degree of cardiac

blood pressure or hemodynamic

dysfunction.

parameters; tachypnea; labored

respirations; changes in breath sounds

(cackles, wheezing); distant or altered

heart sounds (murmurs,
dysrhythmias); neck vein and
peripheral edema; and reduced urinary

output.
Keep client on bed or chair rest in
position of comfort.

Administer high-flow oxygen via

mask or ventilator, as in dictated

Monitor vital signs frequently

Monitor cardiac rhythm continuously

Decreases oxygen consumption and

risk of decompensation.
XXXVII.
To increase oxygen available for
cardiac function/ tissue perfusion
XXXVIII.
To note response to activities and

interventions
To note effectiveness of medications
and/or assistive devices, such as

Administer blood or fluid

replacement, antibiotics, diuretics,

implanted pacemaker or defibrillator

To determine therapeutic, adverse, or
toxic effects of therapy.

inotropic drugs, antidysrhythmics,

steroids, vasopressors, and/or dilators,

as indicated. Evaluate response.

Restrict or administer fluids (IV/PO),

To maximize cardiac output.

To allow for timely alterations in

as indicated. Provide adequate

fluid/free water, depending client

needs.
Assess urine output hourly or
periodically; weigh daily, noting total

therapeutic regimen.

fluid balance.

Monitor rate of IV drugs closely, using

To prevent bolus or overdose.

infusion pumps, as appropriate.

Schedule activities and assessments.

To maximize rest periods.

Assist with or perform self-care

To maximize cardiac output.

activities for client.

Avoid the use of restraints whenever

May increase agitation and increase

possible if client is confused.

Use sedation and analgesics, as

the cardiac workload.

To achieve desired effect without

indicated, with caution.

compromising hemodynamic

Alter environment/bed linens and

readings.
To maintain body temperature in near-

administer antipyretics or cooling

measures, as indicated.
Instruct client to avoid/limit activities

normal range.

that may stimulate a Valsalva

response.
Encourage client to breath in/out

Which can cause changes in cardiac

pressure and/or impede blood flow.

To minimize causative factors.

Honesty can be reassuring when so

during activities that increase risk of

Valsalva effect; administer stool

softeners when indicated.

Provide psychological support.
Maintain calm attitude, but admit

much activity and worry are

concerns if questioned by the client.

Provide information about testing

apparent to the client.

To minimize/correct causative factors,

procedures and client participation.

maximize cardiac output.

Assist with special procedures, as

To minimize/correct causative factors,

indicated.
Explain dietary or fluid restrictions, as

maximize cardiac output.

To minimize/correct causative factors,

indicated.
Provide for adequate rest, positioning

maximize cardiac output.

To promote venous return.

client for maximum comfort.

Administer analgesics, as appropriate.

To promote comfort/rest.

Encourage relaxation techniques.

To reduce anxiety and conserve

Elevate legs when in sitting position;

energy.
To enhance venous return.

apply sequential compression devices

XXXIX.

(SCDs), if indicated.
Use a tilt table or other circulatory

XL.

support bed, as needed.

Give skin care and assist with frequent

To prevent orthostatic hypotension.

To avoid development of pressure

position changes.
Elevate edematous extremities and

sores.
To promote venous return.

avoid restrictive clothing.

Provide for diet restrictions, as

To maintain adequate nutrition and

indicated.
Note reports of anorexia or nausea and

fluid balance.
To maintain adequate nutrition and

withhold oral intake, as indicated.

Provide fluids and electrolytes, as

fluid balance.
To maintain adequate nutrition and

indicated.
Monitor intake/output and calculate

fluid balance.
To maintain fluid balance.

24-hour fluid balance.

Note individual risk factors present

To promote wellness.

and specify interventions for reduction

of identified factors.

Review specifics of drug regimen,

To promote wellness.

diet, exercise/activity plan.

Discuss significant signs/symptoms

Which may be signs of drug toxicity

that require reporting to healthcare

and/or electrolyte loss, especially

provider.
Emphasize importance of regular

potassium.
Which may indicate deteriorating

medical follow-up care. Review

cardiac function, heart failure.

danger signs requiring immediate

physician notification.
Encourage changing positions slowly,

dangling legs before standing.

Give information about positive signs

To reduce risk for orthostatic

hypotension.
To provide encouragement.

signs/circulation.
Encourage using relaxation techniques

To promote wellness.

and quiet activities.

Identify resources for weight

To provide support for change.

of improvement, such as decreased

edema, improved vital

reduction, cessation of smoking, and

so forth.

XLI.
XLII.
XLIII.

XLIV. Drug Study

XLV. N
a
m
e
o
f
D
r
u
g

XLVI. D
os
a
ge
/F
re
q
u
e
n
cy

XLVII. A
ctio
n/Cl
assif
icati
on

XLVIII. Mo
de of
Action

XLIX. Indicatio
n/Contra
indicatio
n

L.

Side
Effect
s

LI.

Nursing
Responsi
bility

LII.

LIII.

E
n
o
x
a
p
a
r
i
n
s
o
d
i
u
m
(
L
o
v
e
n
o
x
)

LIV.

D
os
a
ge
:
0.
4c
c
LV.
F
re
q
u
e
n
cy
:
LVI. Q
1
2
LVII. R
o
ut
e:
S
Q

LVIII. Che
mic
al
clas
s:
Low
mol
ecul
arweig
ht
hepa
rin
The
rape
utic
clas
s:
Anti
thro
mbo
tic
LIX. Pre
gna
ncy
cate
gory
:B

LX.

Potenti
ates the
action
of
antithro
mbin
III, a
coagula
tion
inhibito
r. By
binding
with
antithro
mbin
III,
enoxap
arin
rapidly
binds
with
and
inactiva
tes
clotting
factors
(primar
ily
thrombi
n and
factor

LXI.

Indicatio
n: To
prevent
ischemic
complica
tions of
unstable
angina.
To treat
acute STsegment
elevation
MI
(STEMI)
LXII. Contrain
dication:
Active
major
bleeding;
hypersen
sitivity to
benzyl
alcohol
(if only
the
multidos
e vial is
available
),
enoxapar
in,

LXIV. CNS:
Confu
sion,
epidur
al or
spinal
hemat
oma,
fever,
paraly
sis,
stroke
LXV. CV:
Atrial
fibrilla
tion,
conges
tive
heart
failure
,
hyperli
pidemi
a,
periph
eral
edema
LXVI. EENT
:
Epista
xis

Use cautiously in
those with
uncontrolled
hypertension.
Expect to give
drug with aspirin
to patient with
unstable angina
Watch closely for
bleeding. Notify
prescriber
immediately if
platelet count
falls below
100,000/mm3.
Expect to stop
drug and start
treatment if
patient has a
thromboembolic
event, such as a
stroke.
Test stool for
occult blood, as
ordered.
Check serum
potassium level
for elevation.
LXX. PATIEN
T

Xa).Wi
thout
thrombi
n,
fibrino
gen
cant
convert
to
fibrin
and
clots
cant
form

heparin
(includin
g lowmolecula
r-weight
heparins)
,or pork
products;
thromboc
ytopenia
and
positive
antiplatel
et
antibody
test while
taking
low
molecula
r-weight
heparin
LXIII.

LXVII. GI
:
Blood
y
stools,
diarrhe
a,
elevate
d liver
functio
n test
results
,
hemat
emesis
,
melen
a,
nausea
,
vomiti
ng
LXVIII. G
U:
Hemat
uria,
menstr
ual
irregul
arities
HEM

TEACHI
NG
Advise patient to
notify prescriber
about adverse
reactions,
especially
bleeding.
Instruct patient to
seek immediate
help for evidence
of
thromboembolis
m, such as
neurologic
changes and
severe shortness
of breath.

E:
Anemi
a,
hemor
rhage,
throm
bocyto
penia
RESP
:
Dyspn
ea,
pneum
onia,
pulmo
nary
edema
or
emboli
sm
SKIN:
Cutane
ous
vasculi
tis,
ecchy
mosis,
persist
ent
bleedi
ng or

oozing
from
mucou
s
membr
anes
or
surgic
al
wound
s,
pruritu
s, skin
necros
is at
injecti
on site
or
distant
from
injecti
on
site,
urticar
ia,
vesicul
obullo
us rash
Other
:Anap
hylaxi

s;
LXIX. hyperk
alemia
;
injecti
on site
erythe
ma,
hemat
oma,
irritati
on,
and
pain

LXXI.
LXXII.
LXXIII.

LXXIV.
Name

LXXV.D
os
a
ge
/F
re
q
u
e
n
cy

LXXVI. A
ction
/Clas
sifica
tion

LXXVII. Mo
de of
Action

LXXVIII. Indic
ation/Co
ntraindi
cation

LXXIX. Si
de
Effect
s

LXXX. Nursi
ng
Responsi
bility

LXXXI.
Losart

LXXXII.
Dosage:
1
0
0
m
g
ta
b
LXXXIII.
Frequen
cy
:
O
D
LXXXIV.
Route:
P
O
LXXXV.

LXXXVI. C
hemi
cal
class:
Angi
otens
in II
recep
tor
antag
onist
Ther
apeu
tic
class:
Antih
ypert
ensiv
e
LXXXVII.
Pregnancy
categ
ory:
C
(first
trime
ster),
D
(later
trime
sters)

LXXXVIII.
Blocks binding
of
angiote
nsin II
to
recepto
r sites
in
many
tissues,
includi
ng
vascula
r
smooth
muscle
and
adrenal
glands.
Angiot
ensin II
is a
potent
vasoco
nstricto
r that
also
stimula
tes the
adrenal

LXXXIX. Indic
ation: To
manage
hypertens
ion, To
reduce
stroke
risk in
patients
with
hypertens
ion
XC. Contrain
dication:
Hypersen
sitivity to
losartan
or its
compone
nts
XCI.

XCII. CNS:
Dizzin
ess,
fatigue
,
headac
he,
insom
nia,
malais
e
XCIII. CV:
Hypot
ension
XCIV. EENT
:
Nasal
conges
tion
XCV. GI:
Diarrh
ea,
indige
stion,
nausea
,
vomiti
ng
XCVI. HEM
E:
Throm

In some patients,
losartan is more
effective when
given in two
divided doses
daily; it may be
used with other
antihypertensive.
Monitor blood
pressure and
renal function
studies to
evaluate drug
effectiveness.
Periodically
monitor patients
serum potassium
level, as
appropriate, to
detect
hyperkalemia.
Monitor patient
for muscle pain;
rarely,
rhabdomyolysis
develops in
patients taking
other angiotensin
II receptor
blockers.

cortex
to
secrete
aldoster
one.
The
inhibiti
ng
effects
of
angiote
nsin II
reduce
blood
pressur
e.

bocyto
C.
PATIEN
penia
T
XCVII. M
TEACHI
S:
NG:
Back
Instruct patient to
pain,
avoid potassium
leg
containing salt
pain,
substitutes
muscle
because that may
spasm
increase risk of
s
hyperkalemia.
XCVIII. R
CI.
ESP:
Cough
, upper
respira
tory
tract
infecti
on
XCIX. SKIN:
Erythr
oderm
a
Other
:
Angio
edema
,
hyperk
alemia

,
hypon
atremi
a

CII.
CIII.
CIV.

CV.
Name

CVI. D
os
a
ge
/F
re
q
u
e
n
cy

CVII. Actio
n/Cla
ssific
ation

CVIII. Mode
of
Action

CIX. Indicatio
n/Contra
indicatio
n

CX.

Side
Effect
s

CXI. Nursing
Responsi
bility

CXII.
Capto

CXIII. D
os
a
ge
:
2
5
m
g
ta
b
CXIV. F
re
q
u
e
n
cy
:
O
D
CXV. R
o
ut
e:
P
O
CXVI.

CXVII. C
hemi
cal
class:
ACE
inhibi
tor
Ther
apeu
tic
class:
Antih
ypert
ensiv
e
CXVIII. P
regn
ancy
categ
ory:
C
(first
trime
ster),
D
(later
trime
sters)

CXIX. By
inhibiti
ng
angiote
nsinconvert
ing
enzyme
,
captopr
il:
prevents
conversion of
angiotensin I
to angiotensin
II, a potent
vasoconstrictor
that also
stimulates the
adrenal cortex
to secrete
aldosterone.
Inhibiting
aldosterone
increases
sodium and
water
excretion,
reducing blood
pressure.
may inhibit

CXX. Indicatio
n: To
control
hypertens
ion,
CXXI. Contrain
dication:
CXXII. Hype
rsensitivi
ty to
captopril,
other
ACE
inhibitors
, or their
compone
nts

CXXIII. C
Closely monitor
NS:
patients blood
Fever
pressure,
CXXIV. C
especially when
V:
therapy starts and
Chest
dosage increases.
pain,
Monitor renal
hypote
function tests for
nsion,
signs of
orthost
nephrotic
atic
syndrome, such
hypote
as proteinuria
nsion,
and increased
palpita
BUN and serum
tions,
creatinine levels.
tachyc
Also watch for
ardia
such renal
CXXV. EE
evidence as
NT:
oliguria,
Loss
polyuria, and
of
urinary
taste
frequency.
CXXVI. G
CXXVII. PATI
U:
ENT
Dysuri
TEACHI
a,
NG:
impote Instruct patient to
nce,
take captopril 1
nephro
hour before
tic
meals.
syndro

renal and
vascular
production of
angiotensin II.
decreases
serum
angiotensin II
level and
increases renin
activity. This
decreases
aldosterone
secretion,
slightly
increasing
serum
potassium
level and fluid
loss.
decreases
vascular tone
and blood
pressure.

me,
nocturi
a,
oliguri
a,
polyur
ia,
protein
uria,
urinar
y
freque
ncy
HEM
E:
Eosino
philia
MS:
Arthra
lgia
RESP
:
Cough
SKIN:
Photos
ensitiv
ity,
pruritu
s, rash
Other
:

Tell patient to
rise slowly from
sitting or lying to
minimize
orthostatic
hypotension.
Warn patient not
to stop drug
abruptly.
Urge patient not
to use salt
substitutes that
contain
potassium and to
consult
prescriber before
increasing
potassium intake
to avoid
increasing risk of
hyperkalemia.
Urge patient to
tell prescriber
about signs and
symptoms of
infection, such as
sore throat or
fever

Angio
edema
,
hyperk
alemia
,
hypon
atremi
a,
positiv
e ANA
titer

CXXVIII.
CXXIX.
CXXX.

CXXXI.
Name

CXXXII.
Dosage/F
re
q
u
e
n
cy

CXXXIII. A
ction
/Clas
sifica
tion

CXXXIV. Mo
de of
Action

CXXXV. Indic
ation/Co
ntraindi
cation

CXXXVI. Si
de
Effect
s

CXXXVII.
Nursing
Responsi
bility

CXXXVIII. CXXXIX.
Clonid
Dosage:
7
5
m
g
ta
b
CXL. F
re
q
u
e
n
cy
:
pr
n

1
6
0/
9
0
CXLI. R
o
ut
e:
S
L
CXLII.

CXLIII. C
hemi
cal
class:
Imida
zolin
e
deriv
ative
Ther
apeu
tic
class:
Anal
gesic,
antih
ypert
ensiv
e
CXLIV. P
regn
ancy
categ
ory:
C

CXLV. Stimula
tes
periphe
ral
alphaadrener
gic
recepto
rs in
the
CNS to
produc
e
transien
t
vasoco
nstricti
on and
then
stimula
tes
central
alphaadrener
gic
recepto
rs in
the
brain
stem to
reduce

CXLVI. Indic
ation: To
manage
hypertens
ion,
CXLVII. Cont
raindicat
ion:
CXLVIII. Antic
oagulant
therapy
(epidural
infusion);
bleeding
diathesis;
hypersen
sitivity to
clonidine
or its
compone
nts,
including
adhesive
used in
transder
mal
patch;
injection
site
infection
(epidural

CXLIX. C
NS:
Agitati
on,
delusi
onal
percep
tion,
depres
sion,
dizzin
ess,
drowsi
ness,
fatigue
,
headac
he,
malais
e,
nervou
sness,
parest
hesia,
sedatio
n,
syncop
e,
weakn
ess
CL. CV:

Use clonidine
cautiously in
elderly patients,
who may be
more sensitive to
its hypotensive
effect.
Monitor blood
pressure and
heart rate often
during clonidine
therapy.
Be aware that
stopping drug
abruptly can
elevate serum
catecholamine
levels and cause
such withdrawal
symptoms as
nervousness,
agitation,
headache,
confusion,
tremor, and
rebound
hypertension.
Expect
hypertension to
return within 48

periphe
ral
vascula
r
resistan
ce,
heart
rate,
and
systolic
and
diastoli
c blood
pressur
e. May
produc
e
analges
ia by
prevent
ing
transmi
ssion of
pain
signals
to the
brain at
presyna
ptic and
post
junctio

infusion)

Arrhyt
hmias,
chest
pain,
conges
tive
heart
failure
, highdegree
AV
block,
orthost
atic
hypote
nsion,
Rayna
uds
pheno
menon
EENT
:
Acco
mmod
ation
disord
er,
blurre
d
vision,
burnin

hours after drug

is discontinued.
CLVI.
PATI
ENT
TEACHING
Advise patient to
take drug exactly
as prescribed and
not to stop
abruptly because
withdrawal
symptoms and
severe
hypertension
may occur.
Instruct patient to
consult
prescriber if dry
mouth or
drowsiness
becomes a
problem during
oral clonidine
therapy. To
minimize these
effects,
prescriber may
suggest taking
most of dosage at
bedtime.

nal
alpha2adrenor
eceptor
s in the
spinal
cord.
With
epidura
l
adminis
tration,
clonidi
ne
produc
es
analges
ia in
body
areas
innerva
ted by
the
spinal
cord
segmen
ts in
which
the
drug
concent

g eyes,
decrea
sed
lacrim
ation,
dry
eyes
and
mouth,
salivar
y
gland
pain
CLI. GI:
Consti
pation,
hepatit
is,
mildly
elevate
d liver
functio
n test
results
,
nausea
,
vomiti
ng
CLII. GU:
Decrea

rates.

sed
libido,
erectil
e
dysfun
ction,
nocturi
a
CLIII. HEM
E:
Throm
bocyto
penia
CLIV. SKIN:
Angio
neuroti
c
edema
,
pruritu
s, rash,
urticar
ia
CLV. Other
:
Weigh
t gain,
withdr
awal
sympt
oms

CLVII.
CLVIII.
CLIX.
Name

CLX. D
os
a
ge
/F
re
q
u
e
n
cy

CLXI. Actio
n/Cla
ssific
ation

CLXII. Mo
de of
Action

CLXIII. Indic
ation/Co
ntraindi
cation

CLXIV. Si
de
Effect
s

CLXV.Nursing
Responsi
bility

CLXVI.
Carve

CLXVII.
Dosage:
6.
2
5
m
g
ta
b
CLXVIII.
Frequen
cy
:
B
I
D
CLXIX.
Route:
P
O
CLXX.

CLXXI. C
hemi
cal
class:
Nons
electi
ve
betaadren
ergic
block
er
with
alpha
1adren
ergic
block
ing
activi
ty
Ther
apeu
tic
class:
Antih
ypert
ensiv
e,
heart
failur

CLXXII. Red
uces
cardiac
output
and
tachyca
rdia,
causes
vasodil
ation,
and
decreas
es
periphe
ral
vascula
r
resistan
ce,
which
reduces
blood
pressur
e and
cardiac
worklo
ad.
When
given
for at
least 4

CLXXIII. Indic
ation: To
control
hypertens
ion,
CLXXIV. Cont
raindicat
ion:
CLXXV. Asth
ma or
related
bronchos
pastic
condition
s;
cardioge
nic
shock;
decompe
nsated
heart
failure
that
requires
I.V.
inotropic
s; history
of
serious
hypersen
sitivity

CLXXVI. C
Monitor patients
NS:
blood glucose
Asthen
level, as ordered,
ia,
during carvedilol
depres
therapy because
sion,
drug may alter
dizzin
blood glucose
ess,
level.
fatigue
If patient has
, fever,
heart failure,
headac
expect to also
he,
give digoxin,
hypest
a diuretic,
hesia,
and an ACE
hypoto
inhibitor.
nia,
PATIENT
insom
TEACHING
nia,
:
light Instruct
headed
patient
ness,
prescribed
malais
extended
e,
release
parest
capsules to
hesia,
swallow them
somno
whole. If
lence,
swallowing
stroke,
capsules is
syncop
difficult, tell
e,
patient he
vertigo
may open

e
treat
ment
adjun
ct
Preg
nanc
y
categ
ory:
C

weeks,
carvedi
lol
reduces
plasma
renin
activity.

reactions,
such as
anaphyla
xis,
angioede
ma, or
StevensJohnson
syndrom
e;
hypersen
sitivity to
carvedilo
l or its
compone
nts;
secondor thirddegree
AV
block,
severe
bradycar
dia or
hepatic
impairme
nt, or
sick
sinus
syndrom
e unless

CLXXVII.
CV:
Angin
a,AV
block,
bradyc
ardia,
edema
, heart
failure
,
hypert
ension
,
hypert
riglyce
ridemi
a,
orthost
atic
hypote
nsion,
palpita
tions,
periph
eral
vascul
ar
disord
er
CLXXVIII.

capsule and
sprinkle
beads on a
spoonful of
cold
applesauce
and then eat
the
applesauce
immediately
without
chewing.
Warn patient
that drug may
cause
orthostatic
hypotension,
lightheadedness,
and dizziness;
advise him to
take
precautions.
Tell patient
with heart
failure to
notify
prescriber if
he gains 5 lb
or more in 2
days or if

pacemak
er is in
place

EENT:
Blurre
d
vision,
dry
eyes,
period
ontitis,
pharyn
gitis,
rhinitis
CLXXIX. E
NDO:
Hyper
glyce
mia,
hypogl
ycemi
a GI:
Abdo
minal
pain,
diarrhe
a,
elevate
d liver
functio
n test
results
,
melen

shortness of
breath
increases,
which may
signal
worsening
heart failure.
Stress the
need to seek
emergency
care if patient
develops
hives or
swelling of
the face, lips,
tongue, or
throat that
causes
trouble
swallowing
or breathing.

a,
nausea
,
vomiti
ng
CLXXX. G
U:
Album
inuria,
hemat
uria,
elevate
d
BUN
and
creatin
ine
levels,
impote
nce,
renal
insuffi
ciency,
UTI
CLXXXI. H
EME:
Aplast
ic
anemi
a,
decrea

sed
PT,
throm
bocyto
penia,
unusua
l
bleedi
ng or
bruisin
g
CLXXXII.
MS:
Arthra
lgia,
arthriti
s, back
pain,
muscle
cramp
s
CLXXXIII.
RESP:
Dyspn
ea,
increas
ed
cough
CLXXXIV.
SKIN:
Jaundi

ce,
pruritu
s,
purpur
a,
urtica
ria
Other
:
Anaph
ylaxis,
angioe
dema,
fluid
overlo
ad,
gout,
hyperk
alemia
,
hyperu
ricemi
a,
hypon
atremi
a,
hypov
olemia
, viral
infecti
on,

weight
gain or
loss

CLXXXV.
CLXXXVI.
CLXXXVII.

CLXXXVIII.CLXXXIX.
Name
Dosage/F
re
q
u
e
n
cy

CXC. Actio
n/Cla
ssific
ation

CXCI. Mode
of
Action

CXCII. Indic
ation/Co
ntraindi
cation

CXCIII. Si
de
Effect
s

CXCIV. Nursi
ng
Responsi
bility

CXCV.
Clopid

CXCVI.
Dosage:
7
5
m
g
ta
b
CXCVII.
Frequen
cy
:
O
D
CXCVIII.
Route:
P
O
CXCIX.

CC.

Che
mical
class:
Thien
opyri
dine
deriv
ative
Ther
apeu
tic
class:
Platel
et
aggre
gatio
n
inhibi
tor
Preg
nanc
y
categ
ory:
B

CCI.

Binds
to
adenosi
ne
diphosp
hate
(ADP)
recepto
rs on
the
surface
of
activate
d
platelet
s. This
action
blocks
ADP,
which
deactiv
ates
nearby
glycopr
otein
IIb/IIIa
recepto
rs and
prevent
s
fibrino

CCII. Indicatio
n: To
reduce
atheroscl
erotic
events,
such as
stroke
and MI,
in
patients
with
atheroscl
erosis
documen
ted by
recent
stroke,
MI.
CCIII. Contrain
dication:
Active
pathologi
cal
bleeding,
including
peptic
ulcer and
intracrani
al
hemorrha

CCV. CNS:
Confu
sion,
depres
sion,
dizzin
ess,
fatigue
,
halluci
nation
s,
headac
he
CCVI. CV:
Chest
pain,
edema
,
hyperc
holeste
rolemi
a,
hypert
ension
,
hypote
nsion,
vasculi
tis
EENT

In patient with
acute coronary
syndrome, expect
to give aspirin
with clopidogrel.
Obtain blood cell
count, as ordered,
whenever signs
and symptoms
suggest a
hematologic
problem.
Monitor patient
who takes aspirin
closely because
risk of bleeding
is increased.
PATIENT
TEACHING
Discourage use
of NSAIDs,
including OTC
preparations,
during
clopidogrel
therapy because
of potential for
bleeding.
Caution patient
that bleeding

gen
from
attachin
g to
recepto
rs.
Withou
t
fibrino
gen,
platelet
s cant
aggrega
te and
form
thrombi
.

ge;
hypersen
sitivity to
clopidogr
el or its
compone
nts
CCIV.

:
Altere
d
taste;
conjun
ctival,
ocular,
or
retinal
bleedi
ng;
epistax
is;
rhinitis
; taste
disord
ers
CCVII. GI
:
Abdo
minal
pain;
acute
liver
failure
;
colitis;
diarrhe
a;
duode
nal,

may continue
longer than
usual. Instruct
him to report
unusual bleeding
or bruising.

gastric
, or
peptic
ulcer;
elevate
d liver
functio
n test
results
;
gastriti
s;
indige
stion;
nausea
;
noninf
ectious
hepatit
is;
pancre
atitis
GU:
Elevat
ed
serum
creatin
ine
level,
glomer
ulopat

hy,
UTI
CCVIII. H
EME:
Agran
ulocyt
osis,ap
lastic
anemi
a,
neutro
penia,
pancyt
openia
,
prolon
ged
bleedi
ng
time,
throm
bocyto
penic
purpur
a,
throm
botic
throm
bocyto
penic
purpur

a,
unusua
l
bleedi
ng or
bruisin
g
CCIX. MS:
Arthra
lgia,
back
pain,
myalgi
a
CCX. RESP
:
Bronc
hitis,
bronch
ospas
m,
cough,
dyspne
a,
intersti
tial
pneum
onitis,
upper
respira
tory

tract
infecti
on
CCXI. SKIN:
Erythe
ma
multif
orme,
lichen
planus
,
pruritu
s,
purpur
a,
rash,
Steven
sJohnso
n
syndro
me,
toxic
epider
mal
necrol
ysis
Other
:
Anaph
ylaxis,

angioe
dema,
flulike
sympt
oms,
serum
sickne
ss

CCXII.
CCXIII.
CCXIV.

CCXV.
Name

CCXVI.
Dosage/F
re
q
u
e
n
cy

CCXVII. A
ction
/Clas
sifica
tion

CCXVIII. Mo
de of
Action

CCXIX. Indic
ation/Co
ntraindi
cation

CCXX. Si
de
Effect
s

CCXXI. Nursi
ng
Responsi
bility

CCXXII.
Aspiri
CCXXIII.
aspirin

CCXXIV.
Dosage:
8
0
m
g
ta
b
CCXXV.
Frequen
cy
:
O
D
CCXXVI.
Route:
P
O
CCXXVII.

CCXXVIII.
Chemical
class:
Salic
ylate
Ther
apeu
tic
class:
Antiinfla
mmat
ory,
antipl
atelet
,
antip
yretic
,
nono
pioid
analg
esic
Preg
nanc
y
categ
ory:
D

CCXXIX. Blo
cks the
activity
of
cycloox
ygenas
e, the
enzyme
needed
for
prostag
landin
synthes
is.
Prostag
landins,
importa
nt
mediat
ors in
the
inflam
matory
respons
e, cause
local
vasodil
ation
with
swellin
g and

CCXXX. Indic
ation: To
reduce
the
severity
of MI,
CCXXXI. Cont
raindicat
ion:
CCXXXII.Aller
gy to
tartrazine
dye,
asthma,
bleeding
problems
(such as
hemophil
ia),
hypersen
sitivity to
aspirin or
its
compone
nts,
peptic
ulcer
disease

CCXXXIII.

CNS:
Confu
sion,
CNS
depres
sion
EENT
:
Hearin
g loss,
tinnitu
s
CCXXXIV.
GI: Diarrhea,
GI
bleedi

ng,
heartb
urn,
hepato
toxicit
y,
nausea
,
stomac
h pain,
vomiti
ng
HEM

E:

Dont crush
timed-release or
controlled release
aspirin tablets
unless directed.
Ask about
tinnitus. This
reaction usually
occurs when
blood aspirin
level reaches or
exceeds
maximum for
therapeutic
effect. PATIENT
TEACHING:
Advise adult
patient taking
low-dose aspirin
not to also take
ibuprofen
because it may
reduce the
cardio
protective and
stroke
preventive
effects of
aspirin.
Instruct patient

pain.
With
blockin
g of
cycloox
ygenas
e and
inhibiti
on of
prostag
landins,
inflam
matory
sympto
ms
subside
. Pain is
also
relieve
d
because
prostag
landins
play a
role in
pain
transmi
ssion
from
the
periphe

Decrea
sed
blood
iron
level,
leukop
enia,
prolon
ged
bleedi
ng
time,
shorte
ned
life
span
of
RBCs,
throm
bocyto
penia
CCXXXV.SK
IN:
Ecchy
mosis,
rash,
urticar
ia
Other
:
Angio

to take aspirin
with food or
after meals
because it may
cause GI upset
if taken on an
empty stomach.
CCXXXVI.

ry to
the
spinal
cord.
Aspirin
inhibits
platelet
aggrega
tion by
interfer
ing
with
product
ion of
thromb
oxane
A2, a
substan
ce that
stimula
tes
platelet
aggrega
tion.
Aspirin
acts on
the heat
regulati
ng
center
in the

edema
,
Reyes
syndro
me,
salicyl
ism
(dizzin
ess,
tinnitu
s,
difficu
lty
hearin
g,
vomiti
ng,
diarrhe
a,
confus
ion,
CNS
depres
sion,
diapho
resis,
headac
he,
hyperv
entilati
on,

hypoth
alamus
and
causes
periphe
ral
vasodil
ation,
diaphor
esis,
and
heat
loss.

CCXXXVII.
CCXXXVIII.
CCXXXIX.

and
lassitu
de)
with
regular
use of
large
doses

CCXL.
Name

CCXLI.
Dosage/F
re
q
u
e
n
cy

CCXLII. A
ction
/Clas
sifica
tion

CCXLIII. Mo
de of
Action

CCXLIV. Indic
ation/Co
ntraindi
cation

CCXLV. Si
de
Effect
s

CCXLVI. Nursi
ng
Responsi
bility

CCXLVII.
Cefuro

CCXLVIII.
Dosage:
7
5
0
m
g
CCXLIX.
Frequen
cy
:
q
8
x
3
d
os
es
CCL. R
o
ut
e:
I
V
CCLI.

CCLII. C
hemi
cal
class:
Seco
ndgener
ation
cepha
lospo
rin,
7amin
ocep
halos
poran
ic
acid
Ther
apeu
tic
class:
Antib
iotic
Preg
nanc
y
categ
ory:
B

CCLIII. Inte
rferes
with
bacteria
l cell
wall
synthes
is by
inhibiti
ng the
final
step in
the
crosslin
king of
peptido
glycan
strands.
Peptido
glycan
makes
the cell
membr
ane
rigid
and
protecti
ve.
Withou
t it,
bacteria

CCLIV. Indic
ation:
CCLV.Contrain
dication:
CCLVI. Hype
rsensitivi
ty to
cephalos
porins or
their
compone
nts

CCLVII. C
NS:
Chills,
fever,
headac
he,
seizure
s
CCLVIII. C
V:
Edema
EENT
:
Hearin
g loss,
oral
candid
iasis
CCLIX. GI
:
Abdo
minal
cramp
s,
diarrhe
a,
elevate
d liver
functio
n test
results

Give I.V. injection

over 3 to 5
minutes through
tubing of a
flowing
compatible I.V.
fluid.
Monitor I.V. site
for extravasation
and phlebitis.
Monitor BUN and
serum creatinine
levels and fluid
intake and output
to detect signs of
nephrotoxicity.
Monitor patients
with renal
impairment
closely because
they may have
greater toxic
reactions to
cefuroxime.
Monitor patient
for allergic
reactions
continuing up to a
few days after
therapy starts.

l cells
rupture
and die.

,
hepati
c
failure
,
hepato
megal
y,
nausea
,
pseudo
membr
anous
colitis,
vomiti
ng
CCLX. G
U:
Elevat
ed
BUN
level,
nephro
toxicit
y,
renal
failure
,
vagina
l
candid

CCLXII. PATI
ENT
TEACHING.
Urge patient to
report watery,
bloody stools to
prescriber
immediately, even
up to 2 months
after drug therapy
has ended.

iasis
HEM
E:
Eosino
philia,
hemol
ytic
anemi
a,
hypopr
othro
mbine
mia,
neutro
penia,
throm
bocyto
penia,
unusua
l
bleedi
ng
CCLXI. M
S:
Arthra
lgia
RESP
:
Dyspn
ea
SKIN:

Ecchy
mosis,
erythe
ma,
erythe
ma
multif
orme,
pruritu
s, rash,
Steven
sJohnso
n
syndro
me
Other
:
Anaph
ylaxis;
injecti
on site
edema
, pain,
and
rednes
s;
superi
nfectio
n

CCLXIII.

CCLXIV.
CCLXV.
CCLXVI.

Nursing Care Plan

CCLXVII.
CCLXVIII.

Recommendation

CCLXIX.
A. Medications
B. Environment
C. Treatment
D. Health Teaching
E. Out-Patient
F. Diet
G. Spiritualization
CCLXX.

Summary of Discharge

CCLXXI.

Bibliography

CCLXXII. Hinkle, J. & Cheever, K. 2014. Brunner and Suddarths Textbook of MedicalSurgical

Nursing 13th Edition. Philippines: Lippincott Williams & Wilkins. Pg.

741-742
CCLXXIII.

Williams, L. & Hopper, P. 2011. Understanding Medical-Surgical

Nursing. United States of America: F. A. Davis Company. Pg. 468

CCLXXIV.

LeMone, P., Burke, K. & Bauldoff, G. 2011. Medical-Surgical Nursing:

Critical Thinking in

Patient Care. United States of America: Pearson

Education, Inc. Pg. 702

CCLXXV. Bartlett & Jones. (2015) 2015 Nurses Drug Handbook Fourteenth Edition, United
States of
CCLXXVI.
CCLXXVII.

America: Jones & Bartlett Learning, LLC, an Ascend Learning Company

Nurseslabs. (2016) D5LRS (Lactated Ringers Solution). Retrieved from

CCLXXVIII. http://nurseslabs.com/d5lrs-iv-fluid-study/
CCLXXIX.