A CASE STUDY ON AMANG RODRIGUEZ MEMORIAL HOSPITAL

RHEUMATIC HEART DISEASE

In Partial Fulfillment of the Academic Requirements
In Related Learning Experience,
Presented to the College of Nursing
SY 2010-2011



Submitted to:
VICTORIA BEDONIA, R.N. M.A.N
Clinical Instructor




Submitted by:
Balderosa, Jill Anne S.
Benitez, Mercedes F.
Bielza, Mary Grace S.
Boco, Carlito S.
Calitis, Reymin J.
Capada, Shiela Marie B.




Cascano, Jhonnylyn Ver S.
Cereza, Janice B.
Condino, Monalisa S.
Cruz, Geneva C.
David, Maria Socorro S.
De Dios, Mark Lester O.



GROUP 2

BSN3-1M
Pamantasan ng Lungsod ng Marikina
College of Nursing
Marikina City

TABLE OF CONTENTS
PAGE
GOALS AND OBJECTIVES ------------------------------------------------------------------- -- 1
INTRODUCTION --------------------------------------------------------------------------------- 2
PATIENTS PROFILE ----------------------------------------------------------------------------- 3
PHYSICAL ASSESSMENT -----------------------------------------------------------------------
PERSON GORDONS APPROACH ------------------------------------------------------------
COURSE IN THE WARD ------------------------------------------------------------------------
LABORATORIES ----------------------------------------------------------------------------------
ANATOMY AND PHYSIOLOGY ---------------------------------------------------------------
PATHOPHYSIOLOGY ---------------------------------------------------------------------------
PRIORITIZATION ---------------------------------------------------------------------------------
NUSRING CARE PLANS -------------------------------------------------------------------------
DRUG STUDY -------------------------------------------------------------------------------------
DISHARGE PLANNING -------------------------------------------------------------------------











GOALS AND OBJECTIVE
Goal
The purpose of the study is to let the student nurses gain more knowledge about the disease process of
rheumatic heart disease, ascites, pleural effusion, to know the causes, how it is acquired and prevented, and to render
proper nursing care through a systematic nursing process and examinations.
Obejctives:
To assess the patient condition / health status through interview, physical assessment, and interpretation of
laboratory findings.
To discuss the anatomy and physiology of the cardiovascular system and immune system.
To trace and discuss the pathophysiology of rheumatic heart disease and other complication.
To learn the indications of the different diagnostic exam and test done to the patient. Also, to identify the different
drugs administered to the patient and will be able to discuss their corresponding side effects, interventions of a
nurse to be considered and contraindications.
To formulate and apply nursing care plans utilizing the nursing process.
To learn new skills as well as sharpen the student nurses clinical skills required in the management of the patient
with rheumatic heart disease.
To be able to impart health teaching for the prevention of the recurrence of the disease to other family member.
To develop sense of unselfish love and empathy in rendering nursing care to the patient so that the student nurses
may be able to serve future patient with higher level of holistic understanding as well as individualized care.













INTRODUCTION
Rheumatic fever is a descending infection that develops as a consequence of a streptococcus throat infection
that has progressed and been left untreated. Rheumatic heart disease occurs as a consequence of rheumatic fever,
(autoimmune disease) which is an inflammatory condition affecting many of the bodys tissues including the heart, brain
and joints. It can affect anyone of any age or background but is more commonly seen in children.
Rheumatic fever typically follow streptococcal infection by about 2-3 weeks. Fever and migratory joint pain are
often initial manifestations. It has the potential of leading to rheumatic heart disease meaning that the valves of the
heart can become diseased by the disorder and may become so inflamed that they cannot close fully or open properly
due to stiffness. This can cause the blood in flow ineffectively through the valves and can also contribute to blood
leaking backwards through the valves resulting in an accumulation of fluids. These fluids can cause enlargement of the
heart and can lead to fluid buildup in the lungs and on the limbs causing swollen ankles. As the condition affects mainly
the valves of the heart, the symptoms are similar to those with other conditions of the valves and can include dizziness,
chest pain, shortness of breath, tiredness, tachycardia, irritability and on auscultation S
3
and/or heart murmurs may be
heard. For some there may be no symptoms initially, but they can develop over time and must be treated when
necessary.
The cause of rheumatic fever is still not entirely understood. It is known that rheumatic fever is always preceded
by an invasion of bacteria belonging to the group A beta hemolytic streptococcus family. Sooner or later, everybody has
a streptococcus infection, such as a streptococcus throat. Most of us get over it without any complications. But in 1 out
of every 100 children the strep infection produces rheumatic fever a few weeks later, even after the streptococcus
attack has long since subsided. There are several risk factors for streptococcal infection including environmental and
economical factor such as crowded living conditions, malnutrition, immunodeficiency, poor food handling, poor
sanitation and poor access to health care (lack of immunization).
The invasion of streptococcus sparks the production of protective agents called antibodies. For some reason, in
a kind of biological double cross, the antibodies attack not only the strep but also make war on the body's own tissues

the very tissues they are called upon to protect. Researchers are now suggesting the possible reason, although all the
evidence is not yet in. According to a widely held theory, the strep germ possesses constituents ( antigens ) that are
similar in structure to components of normal, healthy cartilage and connective tissuesfound abundantly in joints,
tendons and heart valvesin susceptible individuals. Failing to distinguish between them, the antibodies attack both.
The result: rheumatic fever involving joint and valve inflammation and, perhaps, permanent scarring.
Rheumatic heart disease (RHD) continues to be a common health problem in the developing world, causing
morbidity and mortality among both children with a median age of 10 years, although it also occurs in adults (20% of
cases). Although little longitudinal data are available, evidence suggests that there has been little if any decline in the
occurrence of RHD over the past few decades. Recent reports from the developing world have documented rheumatic
fever (RE) incidence rates as high as 206/100 000 and RHD prevalence rates as high as 18.6/1000. The high frequency of
RHD in the developing world necessitates aggressive prevention and control measures. The major interventions for
prevention and control include: (1) reduction of exposure to group A streptococci, (2) primary prophylaxis to prevent
initial episodes of RF, and (3) secondary prophylaxis to prevent recurrent episodes of RE. Because recurrent episodes of
RE cause increasingly severe cardiac complications, secondary prophylaxis is the most crucial feature of an effective RHD
programme.












PATIENTS PROFILE
A. Demographic data
Patient R is a 15 year old male born on April 9, 1995 at Quezon City. He is the third child among his five
siblings. He was admitted at Pedia ward ARMMC last September 15, 2010 with a chief complaint of difficulty
of breathing, edema and mild ascites and was diagnosed with Pleural Effusion left, Rheumatic Heart Disease
under the service of Dra. Pasala as his attending physician. He weighs 50 kgs and stands 1.56 meters. His vital
signs upon admission are BP 110/70 mmHg, CR 100 bpm, RR 36 bpm and have a temp of 36C.

B. History of past illness
Patient R was known to have on and off fever accompanied by sorethroat. It was
noticed to occur for at least 5 to 6 times per year since he was 5 years old. No consultations are done because
Paracetamol was noted to relieve the fever.

C. History of present illness
Present condition started 2 months PTA when patient was noticed to have on and off
Fever accomp[anied by abdominal pain, joint pain,swelling which is relieved by Paracetamol intake.
Consultation to a private Medical doctor and was diagnosed to have acute gastritis with sore throats.
Unrecalled medications were given.
1 month PTA, patient was noticed to have facial edema, DOB and easy fatigability. Parents prompted
to consult a private clinic and diagnosed to have RHD. He was then referred to Philippine Heart Center for
further management. Laboratories were requested and done. He was treated for RHD one week PTA. He was
then subsequently admitted in the institution due to progression of DOB and edema. Due to financial
constraints, patient was referred and transferred at ARMMC.

D. Environmental history
Patient R was living with his family. He is residing at Rodriguez Rizal. The place is somehow congested.
They are living in a bungalow type of house. The house is made up of wood and concrete. Electricity came
from Meralco and water is supplied by Maynilad.
E. Socio-cultural and economic factors
Patients family is in good terms with their neighborhood. He strives hard in school
believing he can finish his studies to further help his family. Being a Filipino family, patients family also
believes in herbolaryos but seldom consult them. Their family is being supported the father who is working as

construction worker and earns around Php5,000. The mother claimed to spend this earnings for food, school
needs, electrical and water bills, and some other family needs. No earnings was done for future
hospitalization and health maintenance.

F. Religious Factors
Patients family were all Roman Catholics. They usually go to church every Sunday
believing that God will help them in their everyday living.





















PHYSICAL ASSESSMENT
Assessment Normal Actual Remarks
Vital signs:
Temp:
RR:
PR:

BP:


36.5 37.5 C
15 20 cpm
60 90 bpm

120/80 mm Hg

36C
100
36

140/120



Increase RR due to
impaired gas exchanged
Due to aortic regurgitation
Weight:
Head:
Facial movements:
Hair:

Scalp:



Symmetrical
Fine and equally
distributed
Clean without dandruff
and thick lice

Symmetrical
Fine and equally
distributed with lice
with dandruff

Normal
Due to Unhygienic
practices
Due to Unhygienic
practices

Eyes:
Pupil:
Conjunctiva:
Sclera:
Visual Acuity:


PERLLA ( 3 7mm)
Pinkish
Anicteric
Grossly normal

PERRLA (4mm)
Pale
Anicteric
Grossly normal

Normal
tissue perfusion
Normal
Normal

Ear:
Gross Hearing:
External Canal:

gross hearing
no discharge

Grossly normal
Too many ear wax

Normal
Due to Unhygienic
practices
Nose:
Septum:
Gross Smell:
Sinuses:

Midline
Normal
(-) tenderness

Midline
Normal
(-) tenderness

Normal
Normal
Normal
Mouth:
Lips:
Mucosa:
Teeth:
Gums:
Tongue:

Pinkish
Pinkish
No carries (32 teeth)
Pinkish
Midline

Cyanotic
Pale
w/ caries (30 teeth)
pale
midline

Due to oxygenation
tissue perfusion
Unhygienic practices
tissue perfusion
Normal
Pharynx:
Uvula:
Tonsils:

Midline
Not inflamed

Midline
Not inflamed

Normal
Normal
Skin:
Gen. Color:
Texture:

Temp:

Turgor:
Wound/Dreesing/drains:


Pinkish
Smooth

Warm

Supple
No

dusky
Smooth

Cold clammy

Supple
no

Due to oxygenation
Normal

Due to response of SNS;
vasoconstriction
Normal
Normal
Abdomen:
Configuration:

Flat not tender

Distended abdomen

Due toaccumulation of



Bowel sounds:


5-20/min, tympanic upon
percussion



3/min,
fluid in the peritoneal
cavity
Due to stimulation of SNS
Cardiovascular:
Heart Sounds:

Peripheral Pulse:

Capillary Refill:
Orthostatic hypotension:

regular

Equal and strong

1-3 seconds
None

Murmur sound with S3

fast bounding pulse

4 secs.
Orthostatic hypotension

Due to regurgitation of
blood
Congestion of peripheral
tissue
Dec. tissue perfusion
Dec. cardiac output
Respiratory:
Breathing Pattern:

Shape of the chest:
Tactile fremitus:

Breath sound:

Regular, w/o cough

1:2
Symmetric

No adventitious sound
Difficulty of breathing

1:2
Dec. vibration to both
lungs
Diminished breath sound
Due to pulmonary
congestion
Normal
Accumulation of fluid in
the pleural space
Due to pulmonary
congestion and pleural
effusion
Back and Extremities:
ROM:
Spine:
Gait:
Muscle Tone:

full ROM
straight
Coordinated
Equally strong

Dec.ROM
Straight
Coordinated
Weak muscle

Due to joint pain
Normal
Normal
Due to fatigue and inc.
workload of the heart.














PERSON GORDONS APPROACH
Before Hospitalization During Hospitalization
Psychological:
Self Perception dati nakakatulong ako sa
gawaing bahay at nagaalaga sa
mga kapatid ko
madali na akong napapagod
kaya di na ako nakakatulong sa
kanila.
Description of self masigla ako dati ngayon hindi na
Body Image medyo payat ako dati tumaba ako dahil sa
pamamanas
Role Relationship Pattern:
Support System tatay ko ang sumusuporta sa
amin
siya pa rin ang sumusuporta
samin.
Family Function nakakatulong ako dati sa kanila pabigat na lang ako ngayon
Sufficiency of Income dati ngpakakasya nmin ang
suweldo ni tatay
din a kasya ung kinikita ni ni
tatay dahil lagi n akong nasa
ospital
Accessibility of health care and
nutritional resources
hindi kami ngpapacheck-up at
di kami umiinom ng kahit anong
vitamins dahil di n sapat ang
pera
lagi na akong nasa ospital
Cognitive Perceptual Pattern:
Hearing/visual Problem maayos naman ang paningin at
pandinig ko
maayos pa naman din ang
paningin at pandinig ko
Changes in memory matalas ang aking memorya at
nakakasagot pa nga ako sa
eskwela eh
wala naman ganung
pagbabago
Pain management dati tinutulog ko lang kapag
may sakit akong nararamdaman

Value Belief Pattern:
Things and personal values held
important
ang mahalaga sa akin ay ang
aking pag-aaral
ngayon ang mahalag sa akin ay
ang gumaling
Family and social values that
affect life
dati gusting gusto ko agad
makatapos ng pag-aaral para
makatulong sa pamilya ko
ngayon gusto lang ay gumaling
para di madagdagan ung gastos
Spirituality lagi kami nagdadasal ng sabay-
sabay tuwing gabi
di na namin nagagawa iyon
Religious practices that affect
hospitalization
lagi kaming nagsisimba tuwing
linggo
hindi n kami nakakapagsimba
tuwing lingo dahil inaasikaso nila
ako
Elimination:
Bowel movement pattern (time,
frequency and amount)
ngayon 2x akong dumudumi at
tuwing umaga at hapon
dati 1x ako dumudumi tuwing
umaga
Urinary Pattern (time, frequency,
amount and color)
Dati madalas akong umiihi at
marami un
ngayon konti lang ang naiihi ko
at din a madalas
Use of Aids (fluid, medication
and food)
Umiinom lang ako ng maraming
tubig
Furosemide as diuretics
Rest and Sleep Pattern: 6-8 hrs 3-5 hrs
Activities of Daily Living:
Feeding makaisa ako nakakain kailangan ko na ng katulong
Toileting makaisa ako dumumi kailanagan ko ng katulong

Bed Mobility kayang kaya ko naman dati kaya kong gumalaw kaya lang
nahihirapan ako
Gen. mobility nakakakilos naman ako pero di
ako masyadong nagpapagod
madali na akong napapagod
kahit sa konting kilos lang
Hygiene pag may pasok lang ako
naliligo
ngayon pinupunasan ako
Circadian Rhythms
Sleep Concerns madali lang ako nakakatuog
dati
nahihirapan na akong maktulog
dahil sa sakit
Nutrition:
Daily food intake (quality,
frequency, amount and quantity)
Magana naman ako kumain at
kahit ano nakakain ko.
ngayon wala na kong
masaydong gana






















COURSE IN THE WARD
On the day of admission, admitting impression was Pleural Effusion left, Rheumatic Heart Disease. He
has a chief complain of dyspnea. He was put on a DAT. Laboratories were requested. Venoclysis of PNSS was
started and IV meds (Pen G 1.2 M U Q6H, Captopril 25mg/tab tab BID, Furosemide 40mg/tab 1 tab BID,
Prednisone 20 mg/tab 1 tab TID after meals, Lanoxin 0.25mg/tab tab BID, INH 200 mg/tab 1 tab OD). Vital
signs are monitored Q1H. Intake and output were monitored every 4 hous. He was positioned on modified
high back rest. He was also hooked to oxygen inhalation via nasal cannula at 2-3 lpm.
On 2
nd
HD, Thoracentesis was also ordered which is not done.
On the 3rd HD, Furosemide was shifted to 40mg TIV Q12H. He was ordered for repeat CXR.
Thoracentecis was temporarily hold.
On the 4
th
HD, he was ordered to have PPD and sputum AFB tests.
On the 5th HD, IVF was maintained at same rate. Same day, IVf was shifted to heplock. Furosemide
was again increased to 40mg Q8H via heplock. CBC and APC was repeated.
On the 6
th
HD,patient complained of abdominal pain hence given Ranitidine 40 mg TIV. CXR result
revealed massive pleural effusion hence referred to Pulmo service. He was ordered for TPAG, Thoracentecis
was ordered. Furosemide was then again increased to 40 mg Q6H.
On 7
th
HD, Patient was seen by Cardiologist. Repeat serum K and Na was ordered. Albumin infusion
was ordered and Furosemide drip was started. Captopril was increased to 30mg tab BID. Pen G was shifted
to Cefuroxime 1.5 TIV Q8H. Repeat CXR is ordered after 48 hours (due 24 September 2010). Intake and
output were strictly monitored. Blood Pressure is 140/20 to which the doctor prescribed Dopamine drip.
Dyspneic episodes prompted physicians to bring patient to PICU at around 4pm.

On the 8
th
HD, at about 4 am patient expired with Final Diagnosis of Congestive Heart Failure 2
0
RHD,
Tricuspid and Aortic Regurgitation.

























LABORATORIES

Serology
(September 09, 2010)
Result Normal Values
C Reactive Protein CRP 33.7 H mg/dL 0.0 to 10.0 mg/dL
Anti Streptolysin O
Titer (ASO)
302.5 mg/dL (0.0-200.0)

Analysis: CRP is elevated during active inflammatory process. ASO titer is increased. This test is a test
for streptococcal antibodies. Streptococcus can be acquired by living in a crowded place where in close
contact to infected person is evident. It rises within 2 months of the onset and it is positive in most clients with
rheumatic heart disease.

HEMATOLOGY (September 08,2010)

Results
Normal Values
WBC 15.00 H 10 g/L
5.00-10.00
RBC 5.00 10-12 L
4:50-5.20
Hgb 125L g/L 140-170
Hct 0.39 L 0.42-0.51
platelet 351 10g/L 200-400
MCV 78 L 80-96
MCH 25.0 L 27.5-33.2
MCHC 320 L g/L 334-355
RDW 18.0 H % 12.6-14.6
ESR 19 mm/hr 0-10 mm/hr

Analysis: Supporting the serology result, WBC is increased contributing to the inflammatory process.
Erythrocyte sedimentation rate is elevated. It is the measurement of the rate at which RBCs settle out of
anticoagulated blood in an hour. It is usually elevated in infectious heart disorders. MCV, MCH, MCHC
determines relative volume, size, weight and the saturation of RBC.


























Analysis: This test is performed to assess the effects of cardiovascular diseases on renal function and the
existence of concurrent renal or systemic diseases like glumerulonephritis. In this result, there is the
presence or traces of blood. This may indicate malfunctioning of glomerulus and or inability of the kidney to
filter blood.







Urine Microscopy
(IU) (hpf) Normal values
RBC 21 17 3
WBC 4 1 28 5
Urinalysis
Actual Values Normal values
Physical Analysis
color

Straw

Yellow
transparency slightly cloudy Clear
specific gravity 1.010 1.015-1.025
Chemical Analysis
pH 5.0 4.6-8.0
protein Negative Negative
sugar Negative Negative
bilirubin Negative Negative
urobilinogen Negative Negative
blood Trace Negative
nitrites Negative Negative
leukocytes Negative Negative
Ketones Negative Negative

2D Echo
Binary Pressure Gradient Regurgitant fx
pulmonic valve .91 3
tricuspid valve .84 3 311
mitral valve 1.6 11
aortic valve 1.4 8 571

Analysis: The mitral valve is located between the left ventricle and left atrium. It is supported by the chorda
tendinae during ventricular systole to prevent valvular proplase into the atrium. The aortic valve lies between
the left ventricle and the aorta. These valves open during ventricular systole and they close during ventricular
diastole


X-RAY REPORT (September 08, 2010)

Chest AP
There is opacification of the right hemithorax spacing the upper lung with
obscuration of the right heart border bilateral hemidiaphragm, moderate to
massive pleural effusion suggest follow up check up.
True cardiac size is difficult to assess but appears enlarge.
Aorta is unremarkable
Left costophrenic sulcus is intact
No other remarkable finding


Analysis: Chest Xray suggest that the patient has pleural effusion. The test also suggests that the heart is
quite enlarge and could be possibly because of the congestion. The inability of the heart to pump normally
and allow normal flow of the blood is impaired and tries to accommodate those extra volumes of blood.









ANATOMY AND PHYSIOLOGY
LYMPHATIC SYSTEM
I. Body Defense System
A. Nonspecific defense system
- Mechanical barriers that cover body surfaces (skin and mucous membranes) and cells and chemicals that acts
to protect the body from invading pathogens.
- Responds immediately to protect the body from all foreign substances.
- Reduces the workload of the specific defense system by preventing entry and spread of microorganisms
throughout the body.
1. Surface body defense
- Bodys first line of defense against invasion of disease-causing microorganisms.
- Physical barriers:
Skin
Mucous membranes
- Chemical barriers:
Skin skin acidity (acid pH) inhibits bacterial growth and sebum are toxic to bacteria.
Stomach mucosa secretes HCl acid and protein-digesting enzymes.
Oral cavity saliva contains lysozyme that destroys bacteria.
Vagina highly acidic secretions that destroys bacteria.
2. Cells
1) Phagocytes
- confronts pathogens that make it through the mechanical barriers in nearly every body organ.
- Types:
1) Macrophage
2) Neutrophil


2) Natural Killer (NK) cells
- Unique group of defensive cells running in the blood stream and lymph that can lyse and kill
cancer cells and virus-infected body cells before the immune system are enlisted in the fight.
INFLAMMATORY RESPONSE:
- Bodys second line of defense, triggered when body tissues are injured.
- Cardinal signs:
1) Redness (rubor)
2) Heat (calor)
3) Pain (dolor)
4) Swelling (tumor)
- Process of inflammation























FEVER
INJURY
Damaged cells secretes inflammatory chemicals (histamine and kinins)
Dilatation of blood vessels capillary permeability (leaky) Attraction of phagocytes
and WBC into the injured
area (chemotaxis)
blood flow into the area
Leak of plasma from
the blood stream into
the tissue spaces
Entrance of clotting
proteins from the
blood into the area
Removal of damaged /
dead tissue cells and
pathogens from the area.
Redness
Heat
O
2
&
nutrient supply
metabolic rate of
tissue cells
Edema
Swelling
Activation of
pain receptors
Pain
Possible temporary limitation of
joint movement
Fibrin barrier
formation
Walls off the damaged area to
prevent the spread of pathogen
Healing

- A systemic response to invading microorganisms.
- Pyrogens reset the normal setting of the thermostat to high levels.
- Pyrogens = chemicals secreted by WBC and macrophages exposed to foreign cells or
substances in the body.
- Good effects of fever: (Low and moderate)
1. Prevents/retards bacterial proliferation
fever causes liver and spleen to gather iron and zinc during fever, since bacteria
require large amounts of iron and zinc to multiply.
2. Facilitation of repair
- Fever increases metabolic rate of tissue cells.

B. Specific defense system
(Immune system)
- Attack against particular foreign substances
- Considered as functional system rather than an organ/anatomical system because it recognizes antigens and
abnormal cells to inactivated or destroy it.
- Bodys third line of defense.
- Types of Immunity:
1. Humoral Immunity (Antibody-mediated Immunity)
- Provided by antibodies present in the bodys fluids (humor)
2. Cellular Immunity (cell-mediated immunity)
- Protection provided by the lymphocytes (because the protective factor is living cells).
Immune Response
- Immune systems response to threat that tremendously increases
- Provides protection that is carefully targeted against specific antigen.

3 important Aspects of Immune Response:
1. Antigen specific it recognizes and acts against particular pathogens.
2. Systemic immunity is not restricted to the initial infection site.
3. Presence of Memory - it recognizes and mounts even stronger attacks on previously encountered
pathogens.
Antigens
- any substance capable of exciting the immune system and provoking an immune response.
Types:
non-self antigens
self-antigen protein molecules of own body cells.
- Do not trigger an immune response in own body, but strongly antigenic to other people
Hapten (incomplete antigen) troublesome small molecule causing an immune response in the body
- But when small molecules link with the bodies proteins, the immune system recognizes the
combination as foreign and mount an attraction that is harmful rather than protective.
Types of lymphocytes
a. B cells- resides in the lymph nodes, spleen, and other lymphoid tissues.
- Forms plasma cells and memory cells
- Descendants:
- Plasma cell- production of antibodies
- Memory cell- quick and efficient reaction to subsequent infections or meetings with the
same antigen
b. T cells- becomes immune competent in the thymus gland and can differentiate to the several types of
effector cells.
- Types:
1. Helper T cell- to stimulate production of killer T cells and B cells
2. Cytotoxic T cell- produce by helper T cell during cellular immunity.

- killing virus infected cells, and foreign graph cells
3. suppressor T cell- slow or stops the activity of B or T once the infection has been conquered
- helps prevent uncontrolled unnecessary immune system activity by winding down and finally
stopping the immune system after an antigen has been successfully destroyed.
4. Delayed hypersensitivity T cells- plays a major role in cell mediated allergies and inflammation
- Promotes intense inflammatory response
Macrophages
- Engulf foreign particles and present fragments of the engulfed antigens under surfaces, where
they can be recognized by immuno competent T cells
- Remain fixed in the lymphoid organ














CARDIOVASCULAR SYSTEM


Four compartments

The heart is divided into 4 chambers: 2 on the right hand side and 2 on the left. Each upper chamber is known as
an atrium and each lower chamber as a ventricle. The 4 compartments are known as: the right atrium; the right
ventricle; the left atrium and the left ventricle. Blood comes into the heart via the atria, which are the smaller
chambers, and is pumped out via the larger ones the ventricles.

The right atrium,
Located in the upper right side of the heart, and a small appendage, the right auricle, act as a temporary storage
chamber so that blood will be readily available for the right ventricle. Deoxygenated blood from the systemic
circulation enters the right atrium through three veins, the superior vena cava, the inferior vena cava, and the
coronary sinus.
The right ventricle
is the pumping chamber for the pulmonary circulation. The ventricle, with walls thicker and more muscular than
those of the atrium, contracts and pumps deoxygenated blood through the three-cusped pulmonary semilunar
valve and into a large artery, the pulmonary trunk. The pulmonary trunk immediately divides into two
pulmonary arteries, which lead to the left and right lungs, respectively.
The left atrium

and its auricle appendage receive oxygenated blood from the lungs though four pulmonary veins (two from each
lung). The left atrium, like the right atrium, is a holding chamber for blood in readiness for its flow into the left
ventricle. When the ventricles relax, blood leaves the left atrium and passes through the left AV valve into the
left ventricle. The left AV valve is also called the mitral or bicuspid valve, the only heart valve with two cusps.
The left ventricle
is the pumping chamber for the systemic circulation. Because a greater blood pressure is required to pump
blood through the much more extensive systemic circulation than through the pulmonary circulation, the left
ventricle is larger and its walls are thicker than those of the right ventricle. When the left ventricle contracts, it
pumps oxygenated blood through the aortic semilunar valve, into a large artery, the aorta, and throughout the
body. The following events occur in the left ventricle, simultaneously and analogously with those of the right
ventricle.

Interventricular septum - Muscle that separates two ventricle from each other.
Interatrial septum -Cardiac Muscle that separates two atrium from each other.
Coronary sulcus (artioventricular groove) - marks the junction of the atria and ventricles.
Anterior interventricular sulcus and posterior interventricular sulcus- mark the junction of the ventricles on the
front and back of the heart, respectively.

Superior and inferior vena cava
These are the 2 large veins which enter the heart on the right hand side and bring blood low in oxygen into the
right atrium. The superior (top) vena cava brings in blood from the head and arms and upper body; the inferior
(lower) vena cava brings in blood from the trunk and legs the lower body.
Arteries
Carry blood away from the heart. They are the thickest blood vessels, with muscular walls that contract to keep
the blood moving away from the heart and through the body.
Arterial walls have three layers:

The endothelium is on the inside and provides a smooth lining for blood to flow over as it moves through the
artery.
The media is the middle part of the artery, made up of a layer of muscle and elastic tissue.
The adventitia is the tough covering that protects the outside of the artery.
Types of arteries:
a. Coronary arteries
The heart is just a big muscle which pumps blood around the body. This oxygen is brought to the heart by the
coronary arteries. The right and left coronary arteries branch off the aorta the large main blood vessel which
leaves the heart with fresh oxygen-rich blood so they are ensured of a good blood supply rich in oxygen.
b. Pulmonary arteries
The right and left pulmonary arteries branch off the main pulmonary trunk. Blood that needs oxygen is pumped
into them from the right ventricle and they take it to the lungs where it is loaded up with oxygen.
Veins
Carry blood back to the heart. They're not as muscular as arteries, but they contain valves that prevent blood
from flowing backward. Veins have the same three layers that arteries do, but are thinner and less flexible. The
two largest veins are the superior and inferior vena cava.
Pulmonary veins
The right and left pulmonary veins bring the oxygen-rich blood back from the lungs to the heart into the left
atrium.
Aorta
The aorta is the largest artery in the body. Fresh blood full of oxygen is pumped by the left ventricle into the
aorta, round the aortic arch and out into the upper body via the 3 main arteries branching off the aortic arch
and into the thorax, trunk and lower body via the descending aorta.
Valves
Valves are one-way doors. There are valves separating the chambers of the heart. As the heart beats, the valves
open and blood is pumped from one chamber to another chamber.


Layers of the heart

Pericardium
The pericardium is the double walled sac that contains the heart and the roots of the great vessels that leave
from or enter the heart. There are two layers of the pericardial sac, which are the fibrous pericardium and the
serous pericardium. The serous pericardium is further divided into two layers, which are the parietal
pericardium and the visceral pericardium. The parietal pericardium is inseparably fused to the fibrous
pericardium, while the visceral pericardium is actually a part of the epicardium, which is the outermost single
layer of the pericardium. The visceral layer extends into the starting point of great vessels, thus, becoming one
with the parietal layer of the serous pericardium.
Myocardium
The myocardium is the basic muscle that makes up the heart. This muscle is involuntary and, this is striated in
nature. The cardiac muscle structure consists of basic units of cardiac muscle cells known as myocytes.
Coordinated contraction of the cardiac muscles is what makes the heart propel blood to various parts of the
body.
Endocardium
The endocarium is the innermost, thin and smooth layer of epithelial tissue that lines the inner surface of all the
heart chambers and valves. This layer is made of thin and flat cells that are in direct contact with the blood that
flows in and out of the heart. Each heart valve is formed by a fold of endocardium with connective tissue
between the two layers.






Blood flow







Superior and
inferior vena
cava
Right
atrium
Right
ventricle
Pulmonary semi
lunar valve
Tricuspi
d valve
Pulmonary
trunk
Pulmonar
y vein
Lung tissue
(pulmonary
circulation)
Pulmonary
arteries
Left
atrium
Aorta
Aortic
semilunar
valve
Left
ventricle
e
Bicuspid
valve
Body tissue
(systemic
circulation)

Valves begin to heal w/ scar tissue forming Inflammation subsides
Heart valve tissues become inflamed
Unmanaged, subsequent exposure to the antigen
Unmanaged, subsequent exposure to the antigen
PATHOPHYSIOLOGY




















Predisposing factors:
- 15 yrs. Old
- Exposure to GABHS (his auntie
has the same dse)
- (-) immunization
Precipitating factors:
- Malnutrition
- Poor living conditions
- Congested neighborhood
- Improper food handling
Presence of Group A beta-hemolytic streptococcus
Attach to epithelial cells of the upper respiratory tract
Activated antigen-presenting cells present the bacterial antigen to helper T-cells.
Activated B-cells
Production of antibodies against the cell wall of streptococcus
Antibodies cross react with cardiac myosin and antigens of tissue glucoprotein in the joints, skin, brain and other connective tissue.
Induces cytokines release
Inflammatory response
WBC count
FEVER
ARTHRALGIA
ESR
Activity intolerance






















Restriction of leaflet motion
Impeding to full swing action
Mitral Valvular stenosis
Leaflets may become deformed by healing tissue
Valve fails to close completely
Mitral Regurgitation
blood volume and pressure in the LA
cardiac output pulmonary venous
blood flow & pressure
Pulmonary congestion
Stimulate SNS
Release of epinephrine and
norepinephrine
vasoconstriction
Further damage
to the heart
muscles Release of
renin by
kidneys
Dyspnea Non
producti
ve
cough
Orthopnea
GIT Skin Kidney
Cold clammy, pallor
HR & Contractility
gastric secretions
digestion
BM
Renal perfusion
Formation of angiotensin I
S
3
Heart sound
Wide pulse pressure
cyanosis
Murmurs
RR Use of accessory muscles
RBC
Hypertrophy of LA Impaired LV filling
Dyspnea Arrythmia CHF


















ACE converts angiotension I to II
Promotes the release of aldosterone
Promotes retention of
Na
+
and water

Fluid volume
overload
Preload and afterload
Further stress on the ventricular wall
Further in the workload of the heart
Thickness of the heart muscle
ventricular pressure and resistance to
ventricular filling
Subsequent in cardiac output
JVD
workload of the heart
contraction
Elasticity
Fatigue
Activity intolerance
Stimulates ADH
production

Peripheral edema


Fail to contract
Death
bp
UO
Fast, bounding
pulse
Weakness
Hypertrophy CHF

PRIORITIZATION
Diagnosis Scientific explanation Rationale Score
Impaired gas exchange
related to fluid shifting in
the pleural space
secondary to pulmonary
congestion
It is the deficit in oxygen
and carbon dioxide
elimination at the
alveolar capillary
membrane due to
accumulation of fluid in
the pleural space
It is first prioritized
problem because certain
vital tissues such as
those of the brain and
the heart cannot survive
for a long without
continuous supply of
oxygen if gas exchange is
impaired, it could lead to
life threatening condition
of the patient
1st
Decrease cardiac output
The amount of blood
pump by each ventricles
during a given period,
cardiac output must be
responsive to changes in
metabolic demands of
the tissue
It is our second
prioritized problem
because decrease cardiac
output may lead to
diminish ability of the
patient to response to
stress
2nd
Excessive fluid volume
related to sodium and
water retention
It is refers to an isotonic
expansion caused by
abnormal retention of
water and sodium. This
may be related to simple
fluid overload or
diminished function of
homeostatic mechanism
responsive for regulating
fluid balance
This is our third
prioritized problem,
because retention of
fluid and sodium can
lead to more severe
complication that could
be life threatening to the
patient. The goal of
treatment is to preserve
or restore the
intravascular fluid
volume and treating the
cause of fluid retention
3rd




















NURSING CARE PLANS
Assessment Diagnosis Goals Intervention Rationale Evaluation
Subj:
Hindi siya masyado
makakilos kasi ang
bilis niya mapagod
as verbalized by the
guardian.






Obj:
-murmur S
3
-peripheral
edema(+3)
- cold clammy skin
- 4 sec. capillary
refill
- BP: 140/20 mmHg
-





Decrease cardiac
output related to
incompetent valve
stenosis as
manifested by
arrhythmia,
prolonged capillary
refill and generalized
edema.


Analysis:

Aortic regurgitation

Decreased CO

Decreased systemic
blood pressure

Decrease perfusion
to the kidney

Activation of renin

Activation of AI and
AII

Released aldosterone

arginine vasopressin

vasoconstriction
After 2 of nursing
intervention pt will
lessen/ eradicate
streessors that can
help in reducing the
workload of the
heart participate in
activities that
reduce the workload
of the heart like
stress management,
therapeutic
medication, and
balanced activity
rest pattern.

Obj:
- To be able to
decrease
edema
- To be able to
promote blood
circulation
- To be able to
demonstrate
an increase in
activity
tolerance
Independent:
- Monitor VS, note for cardiac
rate and blood pressure


- Keep client on bed, promote
rest, semi fowler position is
preferred and may elevate
feet in shock situations
- Encourage slowly dangling of
legs before standing
- Limit visitors
- Review diagnostic studies like
CXR, ECG
- Encourage relaxation
techniques such as deep
breathing exercises
Dependent:
- Administer O
2
as indicated


- Provide F and E as indicated

Collaborative:
- Collaborate with the dietician
to adjust ind. Diet plan such
as LSLF, bland diet with
frequent small feeding
- Discuss sign and symptoms
that require prompt reporting
to health care provider (
muscle cramps, headache
and dizziness)


- Provide baseline data for
comparison to follow trends
and evaluate response to
intervention
- Decrease O
2
consumption and
promote venous return


- To prevent orthostatic
hypotension
- To promote adequate rest and
sleep

- Helps to determine underlying
causes
- To reduce anxiety



- To increase O
2
available for
cardiac function and for tissue
perfusion
- To minimize DHN and
dysrhythmias

- To maintain adequate
nutrition balance


- Immediate consultation
because this could be sign of
drug toxicity and mineral loss
esp. Potassium
GOAL PARTIALLY
MET
After 2 of nursing
intervention pt was
able to participate
in activities that
reduced the
workload of the
heart


Assessment Diagnosis Goals and Objective Intervention Rationale Evaluation

Subjective:
sobrang
nagmamanas na nga
ako, mula mukha
hanggang paa ko as
verbalized by the
patient

Objective:
Edema
Weight gain
Abdominal girth
of 30cm
Urine output:























Excess fluid volume
related to increased
ADH production and
sodium/water
retention as
manifested by pitting
edema (grade 3) and
weight gain from 35-
40 kgs.

Analysis






















Goal:
After 8hrs of
continuous nursing
intervention the
patient will be able to
reduce recurrence of
fluid excess as
manifested by
decrease abdominal
girth, reduce edema
from (+3) to (+1).

Objective:
To be able to
reduce
accumulation of
fluid (edema) on
feet and different
part of the body
To be able to
increase output.
Independent:
Monitor VS.

Note presence of
underlying condition
that potential fluid
excess
Note presence of
edema and calculate
its grade
Measure abdominal
girth everyday

Note pattern of
urination
Elevate edematous
part (feet) and change
position frequently

Measure I and O

Promote ambulation


Dependent:
Restrict Na and Fluid
as indicated
Administer diuretics as
prescribed

Collaborative:
Assist with procedure
as indicated
(paracentesis)

Establish baseline data
for further comparison
To assess precipitating
factor


To evaluate degree of
edema

To evaluate changes that
may indicate increase
fluid retention
To know if there is fluid
retention in the body
To reduce tissue
pressure and decrease
risk of skin breakdown

To measure intake of
fluids accurately
To promote circulation
and to mobilize excess
fluid

GOAL MET
After 8 hrs of
continuous nursing
intervention,
patient was able to
reduce recurrence
of fluid excess as
manifested by
decreased
abdominal girth and
decreased edema
from grade 3 to
grade 1.
Low cardiac output
Renal perfusion
Vasoconstriction
Release of renin by
the kidney
Formation of
angiotensin I
Convert to
angiotensin II
Release of
aldosterone
Sodium/water
retention


ASSESSMENT DIAGNOSIS GOALS AND OBJECTIVES INTERVENTION RATIONALE EVALUATION
S: Nahihirapan akong
huminga as verbalized by
the patient

Objective data:
Respiratory rate of
33 bpm
Cyanosis
Use of accessory
muscle
Orthopnea
Crackles
Non-productive
cough
Impaired gas exchange
related to fluid shift on
alveoli secondary to
pulmonary edema as
manifested by respiratory
rate of 33 bpm and
cyanosis
GOALS:
After 1 day of nursing
intervention, the patient
will improve respiration
OBJECTIVES:
To be able to
decrease respiratory
rate from 33 bpm to
atleast 30 bpm by
positioning the
patient in semi fowler
position and
administration of
oxygen inhalation
To be able to change
cyanosis to pinkish
skin, lips and nail bed
color by providing
adequate oxygen for
better circulation of
blood
Monitor vital sign


Monitor color of the
skin, use of accessory
muscle oxygen
saturation, depth,
pattern and rate of
respiration
Position patient in semi
fowler position


Secure oxygen at
bedside



Minimize activities and
energy expenditures by
assisting ADLs
DEPENDENT
Give oxygen as
prescribed by the
physician



Give bronchodilator as
prescribed by the
physician
COLLABORATIVE
Review laboratory and
diagnostic results such
as ECG, Chest xray,
CBC, Blood chemistry
For baseline data and
for further comparison
This assessment data
alert the healthcare
provider to potential
hypoxemia or
hypercapnea
To promote lung
expansion and
decreasing the work of
breathing
Oxygen support
alveolar gas exchange
and improve oxygen in
blood and tissue
Rest is vital to reduce
oxygen and energy
demand


Oxygen support
alveolar gas exchange
and improve oxygen in
blood and tissue
It relaxes bronchial
smooth muscle leading
to brochodilation
To note any
incongruence and
alteration in the
results
Goal partially met.
After a day of nursing
intervention the patient
respiratory rate decrease
from 33 bpm to 30 bpm
but the skin, remain
cyanosis
INFERENCE

Pulmonary congestion

Pulmonary edema

Increase capillary pressure

Plasma leak out

Accumulation of excessive
fluid in the alveoli

Impaired gas exchange







DRUG STUDY
Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
Dopamine drip D
5
W
92.8 cc


Indications:
Correction of
hemodynamic
imbalances present in
the shock syndrome due
to MI, trauma,
endotoxic septicemia,
open heart surgery,
renal failure and chronic
cardiac decompensation
in CHF.
Drug acts directly and by
the release of
norepheniphrine from
sympathetic nerve
terminals; dopaminergic
receptors mediate
dilation of vessels in the
renal and splanchnic
beds, which maintains
renal perfusion and
function; alpha receptor
which are activated by
higher doses of
dopamine, mediate
vasoconstriction, which
can override the
vasodilating effects;
beta 1 receptors
mediate a positive
inotropic effect on he
heart
>Contraindicated with
pheochromocytomas,
tachyparrythmias,
ventricular fibrillation,
hypovolemia (dopamine
is not a substitute for
blood, plasma, fluids,
electrolytes, which
should be restored
promptly when loss as
occurred), general
anesthesia with
halogenated
hydrocarbons or
cyclopropane, which
senthesize the
myocardium to
catecholamines.
>use cautiously with
atherosclerosis, arterial
embolism, Raynouds
disease, cold injury,
frost bite, diabetic
endarteritis, Burgers
disease (monitor color
and temperature of the
extremities), pregnancy,
lactation
CV: ectopic beats,
tachycardia, anaginal
pain, palpitations,
hypotension,
vasoconstriction,
dyspnea, bradycardia,
hypertension, widened
QRS.
GI: nausea and vomiting
Other: headache,
piloerection, azotemia,
gangrene with
prolonged used.
>Monitor body weight,
skin color, urine output,
serum electrolytes, Hct
and ECG.
>Drug should always be
diluted before use if not
prediluted.
>Monitor cardiac output
and BP closely during
infusion.




Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities

captopril

Capoten, Novo-Captopril
(anti-hypersensitive)

25 mg/tab tab BID

Indication :
>hypertension
>CHF
>left ventricular
dysfunction (LVD) after MI
>diabetic nephropathy

Selectively suppresses
reninangiotensin-
aldosterone system,
inhibits ACE; prevents
conversion of angiotensin I
to angiotensin II.

>hypersensitivity
>pregnancy (2
nd
/3
rd

trimester)
>lactation
>heart block
Children
>K-sparing
>diuretics
>bilateral renal artery
stenosis

CNS: fever, chills
CV: hypotension, postural
hypotension, tachycardia,
angina
GI: loss of taste, liver
function tests
GU: impotence, dysuria,
nocturia, proteinuria,
nephrotic syndrome, acute
reversible renal failure,
polyuria, oliguria
frequency
HEMA: neutropenia,
agranulocytosis,
pancytopenia,
thrombocytopenia,
anemia
INTEG: rash
MISC: angioedema,
hyperkalemia
RESPI: bronchospasms,
dyspnea, cough



>may be crushed or mixed
with food
>monitor blood studies;
decrease platelet count,
and WBC with different
baseline and periodically
q3 months, if neutrophils
<1000/mm^3, d/c
treatment.
>monitor BP, check for
orthostatic hypotension,
syncope, and if changes
occur dosage change may
be required.
>monitor renal studies;
protein, BUN, creatinine;
watch for decrease levels
that may indicate nephritic
syndrome and renal
failure; monitor renal
symptoms: polyuria,
oliguria frequency, dysuria
>established baseline and
renal, liver function tests
before therapy begin and
check periodically;
monitor for increase liver
function studies, watch for
increase uric acid, glucose
>check K levels throughout
treatment, although
hyperkalemia rarely occurs
>check regularly for

edema in feet and legs;
monitor weight daily in
CHF
>assess for allergic
reactions; rash, fever,
priritus, urticaria; drug
should be d/c if
antihistamine failed to
help
>reach pt. not to use OTC
products (cough,
cold,allergy) unless
dictated by prescriber;
serious side effects can
occur; xanthines such as
coffee, tea, chocolate, cola
can prevent action of drug
>teach patient to notify
prescriber of mouth sores,
sore throat, fever, swelling
of hands or feet, irregular
heartbeat, chest pain,
coughing, SOB.
>caution patient to report
excessive perspiration,
DHN, vomiting, diarrhea:
may lead to fall in BP.
>caution patient that drug
may cause dizziness,
fainting, lightheadedness;
may occur during first few
days of therapy, to avoid
activities that may be
hazardous.







Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
Ranitidine hydrochloride
40 mg TIV now.

Indication:
>Short-term treatment of
active duodenal ulcer.
>Maintenance therapy for
duodenal ulcer at reduced
dosage.
>Short term treatment of
GERD.
>Treatment of heartburn,
acid indigestion, sour
stomach.
Competitively inhibits the
action of histamine at the
H2 receptors of the
parietal cells of the
stomach, inhibiting basal
gastric acid secretion and
gastric acid secretion that
is stimulated by food,
insulin histamine,
cholinergic agonists,
gastrin and pentagstrin
>Contraindicated with
allergy to ranitidine,
lactation.
>Use cautiously with
impaired renal or hepatic
function, pregnancy
CNS: headache, malise,
dizziness, somnolence,
insomnia, vertigo.
CV: tachycardia,
bradycardia, PVCs (rapid
IV administration).
DERM: rash, alopecia.
GI: constipation, diarrhea,
nausea, vomiting,
abdominal pain, hepatitis,
increased ALT levels.
GU: gynecomastia,
impotence or decreased
libido.
HEMA: leukopenia,
granulocytopenia,
thrombocytopenia,
pancytopenia.
LOCAL: pain at IM site,
local burning or itching at
IV site.
OTHERS: athralgias

>Administer oral drug with
meals at bedtime.
>Decrease doses in renal
and liver failure.
>Provide concurrent
antacid therapy to relieve
pain.
>Arrange for regular
follow-up including blood
tests, to evaluate effects.
>If you are also using an
antacid, take it exactly as
prescribed, being careful
of the times of the
administration.
>Report sore throat, fever,
unusual bruising or
bleeding, tarry stools,
confusion, hallucinations,
dizziness, severe
headache, muscle or joint








Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
Apo-Furosemide, Furoside
Lasix, Lasix Special,
Myrosemide (Loop
diuretics)
40 mg tab BID

Indication
>edema in CHF, nephritic
syndrome, ascites, caused
by hepatic disease, hepatic
cirrhosis; may be used
alone or adjunct with
antihypertensives such as
spirolacone, triamference,
should not be used with
ethacrynic acid.
Acts on the ascending loop
of Henle in the kidney,
inhibiting reabsorption of
electrolytes sodium
chloride causing excretion
of Na, Mg, Cl, H2o and
some K; reabsorption of
sodium chloride and and
decrease excretion of K in
the distal tubule of the
kidney; responsible for
slight antihypertensive
effect and peripheral
vasodilation.
>Hypersensitivity to
sulfonamides, anuria,
hypovolemia, infants,
lactation, electrolyte
depletion
CNS: fatigue, weakness,
vertigo, paresthesias.
CV: orthostatic
hypotension, chest pain,
ECG changes, circulatory
collapse
EENT: loss of hearing, ear
pain, tinnitus, blurred
vision.
ELECT: hypkalemia,
hypochloremic alkalosis,
hypomagmesemia,
hyperuricemia,
hypocalcemia,
hyponatremia, metabolic
alkalosis.
ENDO: hyperglycemia
GI: nausea and vomiting,
diarrhea, dry mouth,
anorexia, cramps,
orpancreatitis.
GU: plyuria, renal failure,
glycosuria.
HEMA: thrombocytopenia,
agranulocytosis,
leukopenia, neutropenia,
anemia.
INTEG: rash, pruritus,
purpura, Stevens Johnson
Syndrome, sweating,
photosensitivity, urticaria.
MS: cramps, stiffness.
>assess patient for
tinnitus, hearing loss, ear
pain, periodic testing of
hearing is needed when
high doses of this drug are
given by IV route.
>monitor for renal,
cardiac, neurologic, GI,
pulmonary manifestations
of hypokalemia: acidic
urine, reduced urine
osmolality, nocturia,
polyuria and polydypsia;
hypotension, broad T
wave, U-wave, ectopy,
tachycardia, weak pulse;
muscle weakness, altered
LOC, drowsiness, apathy,
lethargy, confusion,
depression, anorexia,
nausea, cramps,
constipation, distention,
paralytic ileus,
hypoventilation,
respiratory muscle
weakness.
>monitor for CNS, GI, CV,
integumentary and
neurologic.




Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
Cefuroxime 1.5 grm. TIV
q8

Indication:
> Pharyngitis, tonsillitis
caused by streptococcus
pyogenes.
>Otitis media
>Lower respiratory
infection.
>UTI
>Uncomplicated
gonorrhes.
>Skin and skin structure
infections, including
impetigo
>Treatment of early Lyme
disease.
>Meningitis
>Septicemia
Bactericidal. Inhibits
synthesis of bacterial cell
wall, causing cell death.
>Contraindicated with
allergy to cephalosporins
or penicillins.
>Use cautiously with renal
failure, lactation,
pregnancy
CNS: headache, dizziness,
lethargy, paresthesias.
GI: nausea and vomiting,
diarrhea, anorexia,
abdominal pain,
flatulence,
pseudomembranous
colitis, hepatotoxicity
GU: nephrotoxicity
HEMA: bone marrow
depression (decrease
WBC, decrease platelets,
decrease Hct,)
LOCAL: pain, abscess at
injection site, phlebitis,
inflammation at IV site.
OTHER: superinfections,
disulfiram-like reaction
with alcohol.

>Assess skin status, LFTs,
renal functions tests,
culture of affected area,
sensitivity tests,
>Culture infection, and
arrange for sensitivity
tests before and during
therapy if expected
response is not seen.
>Give oral drug with food
to decrease GI upset and
enhance absorption.
>Give oral drugs to
children who can swallow
tablets; crushing the drug
results in a bitter,
unpleasant taste.
>Have vitamin K available
in case
hypoprothrombinemia
occurs.
>Discontinue if
hypersensitivity reaction
occurs.
>Teach patient to report
severe diarrhea with
blood, pus or mucus; rash;
DOB; unusual tiredness,
fatigue; unusual bleeding
or bruising; unusual
itching or irritation.




Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
prednisone 20 mg/tab 1
tab TID after meals

Indication
>Replacement therapy in
adrenal cortical
insufficiency.
>Hypercalcemia
associated with cancer.
>Short term management
of various inflammatory
and allergic disorders such
as rheumatoid arthritis,
collagen disease,
dermatologic diseases,
status asthmaticus, and
autoimmune disorder.
>Hematologic disorders.
>Ulcerative colitis, acute
exacerbations of MS, and
palliation and some
leukemias and
lymphomas.
>Trichinosis with
neurologic or myocardial
involvement.






Enters target cells and
binds to intracellular
corticosteroid receptors,
initiating many complex
reactions that are
responsible for its anti-
inflammatory and
immunosuppressive
effects.
>Contraindicated with
infections especially
tuberculosis, fungal
infection, amoebiasis,
vaccinia and varicella, and
antibiotic resistant
infections, lactation.
>Use cautiously with renal
or liver disease
hypothyroidism, ulcerative
colitis with impending
perforation, diverticulitis,
active or latent peptic
ulcer, inflammatory bowel
disease, heart failure,
hypertension,
thromboembolic
disorders, osteoporosis,
seizure disorder, DM,
hepatic disease, pregnancy
(monitor infants for
adrenal insufficiency).
CNS: vertigo, headache,
paresthesias, insomnia,
seizures, psychosis,
cataracts, increase IOP,
glaucoma (long term
therapy), euphoria,
depression
CV: hypotension, shock,
hypertension and heart
failure secondary to fluid
retention,
thromboembolism,
thrombophlebitis, fat
embolism, cardiac
arrhytmias
ELECTROLYTES
IMBALANCE: Na + and
fluid retention,
hypokalemia,
hypocalcemia
ENDOCRINE: amenorrhea,
irregular menses, growth
retardation, decrease CHO
tolerance, DM,Cushingoid
state (long term effect),
increase blood sugar,
increase serum
cholesterol, decreased T3
and T4 levels, HPA
suppression with systemic
therapy longer than 5 days
GI: peptic esophageal
>administer once a day
doses before 9 AM to
mimic normal peak
corticosteroid blood levels
>increase dosage when pt.
is subject to stress
>do not stop taking the
drug without consulting
your health care provider;
take once daily doses at
about 9 AM
>avoid exposure to
infections
>report unusual weight
gain, swelling of the
extremities, muscle
weakness, black or tarry
stool, fever, prolonged
sore throat, colds or other
infections, worsening of
the disorder for which the
drug is being taken

ulcer, pancreatitis,
abdominal distention,
nausea, vomiting, increase
appetite, weight gain (long
term therapy)
HYPERSENSITIVITY:
hypersensitivity on
anaphylactoid reactions
MS: muscle weakness,
steroid myopathy, loss of
muscle mass,
osteoporosis, spontaneous
fractures (long term
therapy)
OTHER:
immunosuppression
aggrevation or masking of
infections; impaired
wound healing; thin fragile
skin; petechiae,
ecchymosis, purpura,
striae, subcutaneous fat
atrophy












Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
Lanoxin 0.25 mg/tab tab
BID

Indication:
>heart failure
>atrial fibrillation

Increases intracellular
calcium and allows more
calcium to enter the
myocardial cell during
depolarization via a Na-K
pump mechanism; this
increases force of
contraction (positive
inotropic effect), increases
renal perfusion (seen as
diuretic effect in patients
with heart failure),
decreases heart rate
(negative chronotropic
effect), decreases AV node
conduction velocity
Increases intracellular
calcium and allows more
calcium to enter the
myocardial cell during
depolarization via a Na-K
pump mechanism; this
increases force of
contraction (positive
inotropic effect), increases
renal perfusion (seen as
diuretic effect in patients
with heart failure),
decreases heart rate
(negative chronotropic
effect), decreases AV node
conduction velocity
>CNS: Headache,
weakness, drowsiness,
visual disturbances,
mental status change.
>CV: Arrhythmias
>GI: GI upset, anorexia
> Assess patient for allergy
to digitalis preparations.
> Monitor apical pulse for I
min. before administering;
Hold dose if pulse is lower
than 60 in adults and 90 in
infants. Notify prescriber if
the same PR was assessed
after 1 hr.
> Check dosage and
preparations carefully
> Avoid IM injections; w/c
may be very painful.
> Avoid giving with meals;
This will delay absorption.
> Have emergency
equipment ready; have K+
salts, lidocaine, phenytoin,
atropine, and cardiac
monitor readily available
in case toxicity develops.
> Advise patient not to
stop taking this drug
without notifying the
healthcare provider.
> Advise patient to report
slow or irregular pulse,
rapid weight gain, loss of
appetite, nausea, diarrhea,
vomiting, blurred vision

and DOB.



Name of drug,route,
dose and indications
Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities
Isoniazid
Isotamine, Nydrazid
Antituberculotic
200mg/tab 1 tab OD

Indication:
> Tuberculosis, all forms in
w/c organisms are
susceptible.
> Prophylaxis in specific
patients who
aretuberculin reactors or
household members of
recently diagnosed
tuberculars or who are
considered to be a high
risk.
> Bactericidal: Interferes
with lipids and nucleic acid
biosynthesis in actively
growing tubercle bacilli.
> Contraindicated in
patients with allergy to
isoniazid, isoniazid-
associated hepatic injury
or other severe adverse
reactions to isoniazid,
acute hepatic disease.
> Use cautiously with renal
impairment, lactation,
pregnancy
> CNS: Peripheral
neuropathy, seizures,
toxic encephalitis, and
optic neuritis.
> GI: nausea, vomiting,
epigastric distress,
biliribinemia, elevated AST
and ALT levels and
hepatitis
> Hema: Agranulocytosis,
haemolytic or aplastic
anemia,
thrombocytopenia,
eosinophilia,
hyperglycemia and
metabolic acidosis.
> Hypersensitivity: Fever,
skin eruptions,
lympadenopathy,
vasculitis.
> Other: Gynecomastia,
rheumatic syndrome.

> Assess patient for any
allergy to isoniazid.
> Give drug on an empty
stomach, 1 or 2 hr before
meal: May be given w/
food if GI upset occurs.
> Decrease foods
containing histamine in
patients diet.
> D/C drug if signs of
hypersensitivity occur.
> Monitor Liver and kidney
function; risk of serious
fatal hepatitis.
> Advise strict compliance
to pharmacological
therapy.
> Instruct patient to report
any signs of weakness,
fatigue, loss of appetite,
nausea and vomiting,
jaundice, darkening of
urine.


















DISCHARGE PLANNING
D- Diet
Encourage patient to eat nutritious foods, limiting intake of food and sodium.
F- Follow- up
Instruct patient to have a follow-up visit after 1 week at his doctors clinic.
A- Activity Level
Encourage following activity with restrictions, resuming activity gradually, and resting whenever
tired.
Advise patient to have assistance and support as tolerated when ambulating and to perform
ADLs involving hygiene and self-care, with support if needed.
T- Treatment
Emphasize the importance of prophylaxis against recurrent streptococcal pharyngitis and
continuous therapy to prevent recurrent rheumatic fever and rheumatic heart disease.
D- Discharge Plan
Explain to the patient and parents the disease process and its treatment to promote
understanding of acute and lifelong prophylactic treatment.
Teach patient and parents to prevent further streptococcal infections b good hand washing and
avoiding people with sore throat.
Encourage the patient and parents to contact the primary healthcare provider if a sore throat
occurs.
Advise patient to return to physical education classes gradually, with the guidance of the
physician.
Encourage patient to take frequent naps and rest periods.
Encourage relaxing environment using relaxation techniques, listening to music and quiet
activities
Teach patient and parents about the importance in keeping their environment clean and
practicing proper food handling and sterilizing kitchen utensils.
Advise the parents that child cannot return to school until health care provider assesses that all
disease activity is gone. Parents may need to discuss with teachers how the child can catch up
with school..

M- Medications
Make sure that the patient understands the purpose, dosage, route, and possible side effects of
all prescribed home medications.
Instruct patient and the family to strictly follow the orders for take home meds upon discharge
as prescribed by the physician.