Tetralogy of Fallot Case Presentation

MANISHA COLLEGE OF NURSING

CASE PRSENTATION ON TETRALOGY OF FALLOT

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Submitted by

Submission on

General objectives: At the end of class students will able to understand and gain knowledge regarding Tetralogy of Fallot and implementing the patient in clinical area.

Specific objectives: Students will able to  to introduce the Tetralogy of Fallot  to define the definition of Tetralogy of Fallot  to enumerate the etiological and risk factors, classification/ types of Tetralogy of Fallot  to explain the pathophysiology of Tetralogy of Fallot  to know the diagnostic evaluation of Tetralogy of Fallot  to list out the clinical manifestation of Tetralogy of Fallot  to describe the medical management of Tetralogy of Fallot  to discuss the nursing management of Tetralogy of Fallot

INTRODUCTION I am Nimisha Rajan, studying 2nd year M.Sc (N) in Manisha College of Nursing Dept of child health Nursing. I am going to speciality practical’s in R.K.childrens Hospital, there I am posted in CICU there I find one case i.e; Tetralogy of Fallot. So as felt to this s my case presentation Mr M.Harish, 5 years, male from Gajuwaka admitted in R.K.childrens Hospital in CICU on 29-3-13 at 4:30pm under the consultant of Dr. Naveen with the complains of poor maternal nutrition, viral illness.

IDENTIFICATION Student Profile Name Of The Student: Mrs. Nimisha Rajan

Patient Profile Name of the patient:

Mr. M.Harish

2nd year M.Sc(N) Age:1 years

Subject: child health Nursing

Sex: male

Topic: tetralogy of fallot

Address: 6-57-6/1; road no:9

Submitted to: Mrs. TulasiMadam

sramikanagar, gajuwaka

M.Sc(N); Lecturer

Dept.of Medical Surgical Nrsing

E.P NO: 11794104

Bed no:1

Submitted on:

Ward:ICU

Venue:

Education: nil

Time duration:

Occupation: nil

No.of.persons attended

Marital status:single

date of care started

Date of admission:

29/03/13 at 4:30pm

total days of nursing care

Name of the doctor: Dr. Naveen

Diagnosis: tetralogy of fallot

HISTORY COLLECTION Chief complains: My patient Mr. M.Harish,1years, male admitted in R,K Hospital complains poor maternal nutrition, viral illness.. Present medical history: he admitted in CICU due to poor maternal nutrition, viral illness with complain of tetralogy of fallot as diagnosed by physician Past medical history: he was admitted in hospital due to poor maternal nutrition, viral illness Present surgical history: Not significant of surgical history

Family history: Family profile: Slink

name of the family members

age

sex

relation ship

occupation

remark

1

M.samba murthy

29y

M

Father

employ

-

2

M.rathnam

26y

F

Mother

house wife

-

3

M.pushpa

3y

F

sister

-

--

Nutritional history: Sl.no

Time

Diet

Amount

Caloric

Protein Carbohydrate

Fat

1.

8am

milk

150ml

110k.cal

3.0

4.0

3.8

2.

9am

idly -2

2nos

372k.cal

6.9

58.9

0.2

with 200 grms 690k.cal

6.9

74.5

5.2

3.0

4.0

3.8

20.8

58.9

0.2

with chutney 3.

12:30pm rice curry

4.

4:00pm

5.

8:30pm

tea rice curry

150ml with

15.0k.cal

150 grms 372k.cal

Personal history: Diet: patient diet includes vegetarian a. he takes food in per day 3 times. Rest & sleep: disturbed sleep pattern Elimination: abnormal bowel & bladder (bowel – constipation & urination is frequently & small amount of urine is passing) Socio economic history: Environmental history:Housing: building and own house Ventilation: adequate ventilation Electricity: present Water supply: municipality tap

Physical examination: vitals signs

patient value

normal value

remarks

98.60F

98.60F

normal

Pulse

92b/min

72b/min

abnormal

Respiration

22b/min

16-18b/min

abnormal

120/60mmhg

120/80mmhg

abnormal

93%

100%

normal

Temperature

Blood pressure Spo2

Genarl appearance: Consciousness: conscious Orientation: oriented time, place, and date Nourishment: moderate nourished Health: un healthy Body build: moderate Activity: dull Look: anxious Hygiene: moderately hygiene Speech: clear

REVIEW OF SYSTEMS Skin /integumentary system: Colour: black Texture: wrinkles skin/dry skin

Skin turgor: present Hydration: well hydrated Discolouration: no discolouration of skin Subjective symptoms: dry skin is present Nails: Nail beds: pale in colour Nail plates: flat, absnce of clubbing Cyanosis: no central and peripheral cyanosis Colour: black Texture: dry Eyes: eye brows: symmetric Eyelashes: equally distributed Papillary reflex: abnormal Conjunctiva: abnormal Vision: abnormal vision (blurred vision) Ears: Pinna: normally placed Cerumen: no defect Otarrhea: no discharges from ear Hearing: no defect in hearing process Nose: Nasal septum: no deviation of nasal septum Nasal pathway: clear nasal pathway

Smell: no defect Mouth & pharynx: Lips: absence of cracks and pale in colour Tongue: coated tongue Bleeding : no history of bleeding Tooth decay: history of tooth decay Dental care: no history of dental caries Neck: ROM: not possible Lymph nodes: not palpable Trachea: present in midline Thyroid gland: not enlarged Jugular vein: not distended.

SYSTEMIC EXAMINATION Heart:

Cardiovascular system: H/O hypertension: hypertensive Varicose veins: no H/o varicose veins Dysponea: present Orthopnea: not evident Chest pain: evident Palpitation: present

Heart sounds: present S1 S2 sounds Pluse:92b/min Heart beat: abnormal rate and rhythm Inspection: on inspection the thoracic cavity is normal and clear, no lesions detected, sutured mark presented Palpation: no palpable masses detected Percussion: no percussion performed Auscultation: on auscultation at 5 areas , pulmonic, aortic, erbs point, mitral, apical area. S1 S2 sounds are clear and gallop sounds present

INVESTIGATIONS Slink

Name of the investigation

Pt value

Normal value

1.

Hb%

11.1gms

2.

TWBC

8300cells/cumm 1,500000cells/cumm abnormal

3.

DC

P

86%

L

11%

E

0.3%

12-14gms

Remarks abnormal

4,5000c/cumm

abnormal

4.

platelet count

1.7 laks/cumm

5.

bil.urea

47mg/dl

10-40mg/dl

abnormal

6.

sr. creatine

1.0

0.5-1.4mg/dl

normal

7.

ECG

normal  Extreme tachycardia  lt.ant. hemi block  invented T wave  ST-T

abnormal

abnormality  excessive overload of lt. atrium, lt. ventricular hypertrophy abnormal

8.

x-ray

abnormal

abnormal

MEDICATIONS Slink

Medications

Dose

Route

Time

1.

Inj. Dytor20

1gm

IV

BD

2.

Inj. Taxim

1gm

IV

8th hrly

3.

Inj. PNZ

40mg

IV

4.

T. Ivas

10mg

oral

5.

T.Mtoprolol

25mg

oral

6.

oxygen inhalation

7.

floret} nitrofix} nebulisation duolin}

OD BD OD

Nursing responsibility  assess the patient general condition of client  observe the client for side effects  immediate nursing intervention are to be done  administration of alternatives agonist to prevent the sid effects  administer continuous oxygen inhalation

Tetralogy of fallot Introduction: Tetralogy of Fallot (TOF) is one of the most common congenital heart disorders (CHDs). This condition is classified as a cyanotic heart disorder, because tetralogy of Fallot results in an inadequate flow of blood to the lungs for oxygenation (right-to-left shunt) (see the following image). Patients with tetralogy of Fallot initially present with cyanosis shortly after birth, thereby attracting early medical attention.

Normal heart

Tetralogy of Fallot

Louis Arthur Fallot, after whom the name tetralogy of Fallot is derived, was not the first person to recognize the condition. Stensen first described it in 1672; however, it was Fallot who first accurately described the clinical and complete pathologic features of the defects.

ANATOMY AND PHYSIOLOGY: ANATOMY OF HEART:

 The heart is a hallow muscular organ located in the center of the thorax where it occupies the space between the lungs (mediastinum) and rests on the diaphragm.  It weights approximately 3oogrms (10.6oz) the weights and size of the heart are influenced by age, gender, body weight, extent of physical exercises and conditioning and heart disease.  The hart pumps to the blood to the tissues, supplying them with oxygen and other nutrients.  The heart composed of 3 layers  The inner layer or endocardium consists of endothelial tissue and lines the inside of the heart valves.  The middle layer or myocardium is made up of muscles fibbers and is responsible for the pumping action.  The exterior layer of the heart is called the epicardium.  The heart is encased in a thin fibrous sac called the pericardium, which is composed of to layers.  Adhering to the epicardium is the visceral pericardium  Enveloping the visceral pericardium is the parietal pericardium, tough fibrous tissues that attaches to the great vessels, diaphragm, sternum and vertebral column and supports the heart in the mediastinum.  The space between 2 layers (pericardial space) is normally filled with about 20ml of fluid which lubricates the surface of the heart and reduce friction during systole.

FUNCTIONS OF THE HEART: Electophysiogic properties: The cardiac electrophysiologic properties of cardiac muscle regulates the heart rate and rhythm. The properties of cardiac include:  Exacitability  Automaticity  Contractility  Refractoriness  Conductivity

Exacitability: the ability of cardiac muscle cells to depolarize in response to stimuli/responses to electrical impulses Automaticity: ability to initiate an electrical impulse. Ability of cardiac pacemaker cells to initiate an impulse spontaneously and repetitively with out external neuro hormonal control. Contractility: the heart muscle is composed of long narrow cells or fibers. The action of potential initiates the muscles contraction by releasing calicium through the tubules of the cell membrane. Refractoriness: refractoriness is the heart inability to response to a new stimulus while still in a state of depolarization from an earlier stimulus. Conductivity: ability to transmit an electrical impulses from one cell to another.

DEFINITION: Heart failure is a significant cardiac functional disorder that can results in reduced oxygen delivery to the body’s organs tissues. The in ability of heart to supply blood circulation for the body needs. Heart failure is an abnormal clinical condition involving impaired cardiac pumping. It results in the characteristics pathophysiologic changes of vasoconstriction and fluid retension. Heart failure formerly called as congestive heart failure. Heart failure I not a disease.

INCIDENCE: Heart failure is association with high rest of morbidity, mortality and economic costs. In hospital mortality for these patients is 4% with a men length of hospital stay of 6.5 days. Hospital re-admission for 20 to 30 days 50%at 6 to 12 months mortality rate increases. Heart failure can affect both women and men alough the mortality is higher among women Heart failure affects about 5million people in U.S with 5000,000 new cases diagnosed each year It is mainly affected in aging people age below 75 years of age. In India mainly affected 33% of people in the year diagnosed as chronic heart failure.

ETIOLOGY AND RISK FACTORS: The performance of heart depends on 4 essential components: 1) Contractility of the muscle

2) Preload (amount of blood in the ventricles at the end of diastole) 3) After load (the pressure against which the left ventricles ejects) 4) Heart rate The causes of heart failure can be divided into 3 subgroups  Abnormal loading conditions  Abnormal muscle function  Conditions or disease that limit ventricular filling

Abnormal loading condition: conditions that increases preload

conditions that increases after load

 Regurgitation of mitral or tricuspid  Hypertension valve  Hyper volemia

 Pulmonary or systemic aortic or plumonic stenosis

 Congenital defect (left-right shunts)  High peripheral vascular resistance  Ventricular septal defect  Atrial septal defect  Patent ductus arteriosus

Abnormal muscle function:  Myocardial infraction  Myocarditis  Cardiomyopathy  Ventricular aneurysm

 Long term alcohol consumption  Coronary heart disease  Metabolic heart disease  Endocrine heart rate Limited ventricular filling:  Mitral or tricuspid stenosis  Cardiac tamponade  Constrictive pericarditis  Hypertrophic obstructive cardiomyopathy

Causes of heart failure: chronic heart failure

acute heart failure

 Coronary heart disease

 Acute myocardial infraction

 Hypertension

 Dysrhythmias

 Rheumatic heart disease

 Pulmonary mboli

 Congenital heart disease

 Thyrotoxicosis

 Corpulmonale

 Hypertensive crises

 Cardiomyopathy

 Rupture of papillary muscle

 Anemia

 Ventricle septal defect

 Bacterial endocarditis

 Myocarditis.

 Val uvular disorder

RISK FACTORS:      

Primary risk factor CAD and advancing age Hypertension Diabetes mellitus Cigarette smoking Obesity High serum cholesterol level.

PATHOPHYSIOLOGY: The cause(s) of most congenital heart diseases (CHDs) are unknown, although genetic studies suggest a multifactorial etiology. A study from Portugal reported that methylene tetrahydrofolate reductase (MTHFR) gene polymorphism can be considered a susceptibility gene for tetralogy of Fallot. Prenatal factors associated with a higher incidence of tetralogy of Fallot (TOF) include maternal rubella (or other viral illnesses) during pregnancy, poor prenatal nutrition, maternal alcohol use, maternal age older than 40 years, maternal phenylketonuria (PKU) birth defects, and diabetes. Children with Down syndrome also have a higher incidence of tetralogy of Fallot, as do infants with fetal hydantoin syndrome or fetal carbamazepine syndrome. As one of the conotruncal malformations, tetralogy of Fallot can be associated with a spectrum of lesions known as CATCH 22 (cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia). Cytogenetic analysis may demonstrate deletions of a segment of chromosome band 22q11 (DiGeorge critical region). Ablation of cells of the neural crest has been shown to reproduce conotruncal malformations. These abnormalities are associated with the DiGeorge syndrome and branchial arch abnormalities. The hemodynamics of tetralogy of Fallot depend on the degree of right ventricular (RV) outflow tract obstruction (RVOTO). The ventricular septal

defect (VSD) is usually nonrestrictive, and the RV and left ventricular (LV) pressures are equalized. If the obstruction is severe, the intracardiac shunt is from right to left, and pulmonary blood flow may be markedly diminished. In this instance, blood flow may depend on the patent ductus arteriosus (PDA) or bronchial collaterals.

BOOK PICTURE CLINICAL MANIFESTATION: The manifestations of heart failure depends on the specific ventricular involved the precipitating cause of failure, the degree of impaired, the rate of progression the duration of the failure and the clients underlying conditions. The signs and symptoms of heart failure can be related to which ventricles are affected. Left sided heart failure causes different manifestations then right sided heart failure. In chronic heart failure. Patient may have right and left ventricular failure. left side heart failure:  Pulmonary congestion includes:dysnea, cough, pulmonary crackles low oxygen saturation levels heart sounds s3 or ventricular gallop detected on auscultation, orthopnea, paraxymal nocturnal dysnea, adventitious breath sounds heard in various areas of lungs, oliguria,

PATIENT PICTURE CLINICAL MANIFESTATION:

     

breathlessness cough fever oedema in lower extremities tachycardia increased pulse and respiration rate  oliguria  insomnia

insomnia, tachycardia, palpitations right side heart failure:  Congestion in peripheral tissues and the viscra predominates  Increased jugular venous distension  Systemic clinical manifestation:  oedema of lower extremities  hepatomegaly  as cites  anorexia and nausea, weakness and Assessing for heart failure: weight gain due to retention of fluid Assessing for heart failure: general:  fatigue  decreased activity tolerance  dependent edema

general:  fatigue  decreased activity tolerance  dependent edema  weight gain cardiovascular:

cardiovascular:

 third heart sound s3  apical impulses enlarged with leftlateral displacement  pallor and cyanosis  jugular venous distension(JVD) respiratory:  dysnea on exertion  pulmonary crackles that don’t clear with cough  orthopnea  paroxysmal nocturnal dysnea (PND) cerbro vascular:  un explained confusion altered mental status  light headedness renal:

 apical impulses enlarged with left lateral displacement  jugular venous distension(JVD)

respiratory:  dysnea on exertion  pulmonary crackles that don’t clear with cough  paroxysmal nocturnal dysnea (PND)

or cerbro vascular:

 un explained confusion altered mental status  light headedness  oliguia and decreased frequency renal:

or

 oliguia and decreased frequency during the day

during the day  nocturia gastro intestinal:    

anorexia and nausea enlarged liver ascites hepato jugular reflux

gastro intestinal: no significance

DIAGNOSTIC EVALUATIONS DIAGNOSTIC EVALUATIONS  history collection and physical examination  assessment of ventricular function  serum chemistries, cardiac enzymes, BNP levels, liver function tests, serum electrolytes, BUN,CBC.  Chest x-ray  12 lead ECG  Echocardiography  Exercise stress testing  Nuclear imagaing studies  Hemodynamic monitoring  Cardiac catherization  Routine uninalysis MEDICAL MANAGEMENT

 The goal of management of heart failure to relieve patient symptoms, to improve functional status and quality of life and to extend survival.  medical management based on type , severity and cause of heart failure  specific objectives of medical management includes the following  eliminates or reduce any etiologic contributory factors such as

 history collection and physical examination  Hemoglobin  Total White Blood Count  Direct count –P;L;E  Platelet count  Bilirubin urea  Serum creatinine  ECG  Chest x- ray  Routine urinalysis

MEDICAL MANAGEMENT

       

Inj. Dytor 20- 1gm, IV,BD Inj. Taxim 1grm, IV 8th hrly Inj. PNZ 40mg, IV, OD T. IVAS10mg oral, BD T. Metoprolo 25mg, oral, OD Continuous O2 inhalation Floret Nitrofix nebulisation

controlled hyprtension or aterial  duolin fibrillation with a rapid ventricular response  optimize pharmacologic and other therapeutic regimens  reduce the work load on the heart by reducing preload and after load  promote a life style conducive to cardiac health  prevent episodes of acute decompensate heart failure  managing the patient with heart failure includes providing comprehensive education and counselling to the patient and family  it is important that patient and family understand the nature of heart failure and the importance of their participation in the treatment regimen  life style recommendations include restriction of dietary sodium, avoidance of excessive fluid intake, alcohol and smoking weight reduction when indicates and regular exercises pharmacologic therapy  angiotensin I- converting enzyme inhibitors  angiotensin II receptor blockers  hydralazine and isosorbid dinitrate  betablockers and calcium channel blockers  diuretics  digitalis  intravenous infusion - nesiritide - milrinome - dobutamine  medications for diastolic dysfunction

other medications for heart failure:  anticoagulants  non steroidal inflammatory drugs Nutritional therapy:  a low sodium (2-3g/day) diet and avoidance of drinking excessive amount of fluid are usually recommended  dietary restriction of sodium reduces fluid retention and the symptoms of peripheral and Nutritional therapy: pulmonary congestion  diet needs to be made with  Provided a low sodium (2-3g/day) diet and avoidance of drinking consideration of good nutirion as excessive amount of fluid are well s the patients likes and dislikes usually recommended and cultural food patterns  dietary restriction of sodium Additional therapy: reduces fluid retention and the symptoms of peripheral and  supplemented oxygen pulmonary congestion  other interventions  coronary artery revascularization  diet needs to be made with consideration of good nutirion as with PTCA; CABG surgery may well s the patients likes and dislikes be considered and cultural food patterns  ventricular function may improve in some patients when coronary Additional therapy: flow is increased.  Cardiac resynchronization therapy  supplemented oxygen  Cardiac transplantation  Mechanical circulation assistance with an implanted ventricular assist device  ultra filtration COLLABORATIVE THERAPY:  treatment for underlying cause  o2 therapy at 2-6l/min by nasal cannula  rest activity period

    

drug therapy daily weights sodium restricted diet circulatory assisted devices cardiac resynchronization therapy with internal cardio ventricular COLLABORATIVE THERAPY: defibrillator  treatment for underlying cause  cardiac transplantation  o2 therapy at 2-6l/min by nasal cannula Complication:  rest activity period  drug therapy based on assessment data, potential  daily weights complication that may develop sodium restricted diet including the following :  hypotension, poor perfusion and cardiogenic shock  dysrhythmias  thrombo embolism  pericardial effusion and cardiac tamponade. Complication: NURSING MANAGEMENT: not significant Assessment: Subjective data:  importance health information Past health history: CAD,HTN, cardiomyopathy, congenital heart disease or valvular, DM, thyroid or lung disease rapid or irregular heart NURSING MANAGEMENT: rate. medications: use of an compliance with any cardiac medications, use of Assessment: diuretics, estrogens, corticosteroids, non steroidal inflammatory drugs, over Subjective data:

the counter drug, herbal supplements.  Functional health pattern:  Health perception –health management:- fatigue, anxiety, depression.  Nutritional metabolic- usual sodium intake, nausea, vomiting, anorexia, stomach bloating, weight gain, ankle swelling  Elimination: nocturia, decreased day time urinary output, constipation  Activity exercises: dysnea, orthopne, cough, palpitations, dizziness, fainting  Sleep and rest: number of pillows used for sleeping, paroxysmal nocturnal, dysnea, insomnia.  Cognitive perceptual: chest pain or heaviness, abdominal discomfort; behavioural changes; visual changes. objective data:  Integumentary: cool, diaphoretic skin, cyanosis or pallor, peripheral oedema.  Respiration: tachypnea, crackles, rhonchi, wheezes, frothy, blood tinged sputum.  Cardiovascular: tachycardia, s3 &s4 murmurs, pulses alterations, PMI displaced inferiorly and posterior jugular vein distension  Gastro intestinal: abdominal distension, hepatosplenomegaly, ascites.  Neurologic: restlessness, confusion, decreased alteration or memory.

 importance health information Past health history: CAD,HTN, rapid or irregular heart rate.

medications: use of an compliance with any cardiac medications, use of diuretics, corticosteroids, non steroidal inflammatory drugs, over the counter drug  Functional health pattern:  Health perception –health management:- fatigue, anxiety, depression.  Nutritional metabolic- usual sodium intake, ankle swelling  Elimination: decreased day time urinary output, constipation  Activity exercises: dysnea, cough, palpitations, dizziness, fainting  Sleep and rest: dysnea, insomnia.  Cognitive perceptual: chest pain or heaviness, abdominal discomfort; behavioural changes; visual changes.

objective data:

 Integumentary: cool, peripheral oedema.  Respiration: tachypnea, wheezes, tinged sputum.  Cardiovascular: tachycardia, s3 &s4 murmurs, pulses alterations, increased jugular vein pressure  Gastro intestinal: abdominal distension  Neurologic: restlessness, confusion, decreased alteration or memory.

NURSING DIAGNOSIS: 1. Risk for Decreased cardiac output related to structural abnormalities of the heart. 2. Activity Intolerance related to imbalance in the fulfillment of oxygen to the body's needs. 3. Impaired growth and development related to inadequate oxygenation, tissue nutrisis needs, social isolation. 4. Risk for infection related to the general conditions is inadequate.

Theory application Roy’s adaptation model Introduction:  Sister callista Roy began her nursing career in 1963. After receiving B.Sc(N) noting from moult saint marry college.  1960receives Ms in nursing  1977 her doctorate in sociology  Roy’s model is characterised as a system theory with a strong analogies of intervention. General system: Due to set of organized components released to form a whole employee feedback cycle of input, through put, output.  INPUT: Input includes tensions adaption level (the range of stimuli to which persons adaptation early)

 THROUGH PUT: through put makes use of a person processes and effect ions. Process refers to control mechanism that a person uses as a adaptive system. Effectors refers to the physiologic function, self concept and role function involved in adaptation.  OUTPUT: output is the outcome of the system when system is a person. Output refers to person’s behaviour. Metaparadigm and RAM:  Human being:Person is a bio psychological being in constant interaction with changing environment and recipient the nursing care as living system  Environment: Environment and surrounding and effect the development and behaviour of the persons group. The internal and external are the part of the person’s environment. For ex: elderly person admitted to hospital all the conditions of influence on him/her.  Health: heath is a process whereby individual are striving to achieve their maximum potential. It can be seen in healthy people, exercises regularly, not smoking pay attention dietary pattern. It is a process to relieve acute and chronic illness and terminal stages of diseases & to control the sign and symptoms, to promote health of the persons by promoting adaptive responses. 

Nurses: the nurses to reduce the ineffective responses as output behaviour of the person. The nurse promotes the health in all life processes. The nurses suggested by the model include approaches aimed at maintaining adaptive responses that support the person’s effort to creativity use his or her coping mechanism. INPUT

THROUGH PUT

OUT PUT

- Early detection and screening programs

Demoraghpical variables of the patient      

-The client will have knowledge regarding disease process

-monitor the vital signs

name age, sex, education, occupation income

Adequate knowledge in disease process

-Administer continuous oxygen & medication

Rehabilitation & follow up

- health education about disease condition Feed back NURSES NOTES

Name of the patient: M. Harish

Ward: CICU

Age: 1years

Diagnosis: tetralogy of fallot

Sex: Female

Dr. Name: Dr. Naveen

E.p no: 794143 Time

Diet

730

Idly with chutney

830 8

00

Bed. no: 1 Medication

observation: 1/4/13

water 50ml Inj. Dytor 20 1gm IV BD coconut water

Nurses Care Plan

Inj. Taxim 1gm IV 8th hrly Inj. PNZ 40mg IV OD

Patient is very thin & less activity and

weakness;

cough;

breathlessness.  Monitored vital signs  Temp:98.60 F

fever;

100ml

T.Ivas 10mg oral BD

rice porage T. Metoprolo 25mg Oral 30

10

1 cup

OD

 Pluse:92b/min  Resp:22b/min  Blood pressure:120/60mmhg  SpO2: 93%

floret}

 Provide

nitrofix} nebulisation

position

changing

frequently  Provide complete bed rest

duolin}

 Provide calm environment

o2 inhalation

 Administer medication as per physician prescribed  Administered O2  Provide nebulisation  History collection and performed physical examination  Provide psychological support  Provided health education about  Diet  Exercises  Personal hygiene  Relaxation therapy. lakshmi/St.N

HEALTH EDUCATION

Bibliography:  Brunner &Suddarth’s “text book of Medical Surgical Nursing”, 12 th edition; volume:1; page no:825-838 & 685-690  Lewis “text book of Medical Surgical Nursing”, Elsevier publication; page no:820-837  Joyce. M. Black “text book of Medical Surgical Nursing”, 7 th edition; volume:2; page no:1649-1669 & 1548-559  Ross & Willison “anatomy & physiology” 2nd edition,2001; pageno:678-682.  Mosby doug consult for nurses, 2006, mosby publication