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Pamantasan ng Lungsod ng Marikina

College of Nursing
Marikina City



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.


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


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.

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 S3 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. hospitalization and health maintenance. No earnings was done for future


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.

Assessment Vital signs: Temp: RR: PR: BP: 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 Normal 36.5 37.5 C 15 20 cpm 60 90 bpm 120/80 mm Hg Actual 36C 100 36 140/120 Remarks

Increase RR due to impaired gas exchanged Due to aortic regurgitation

Eyes: Pupil: Conjunctiva: Sclera: Visual Acuity: Ear: Gross Hearing: External Canal: Nose: Septum: Gross Smell: Sinuses: Mouth: Lips: Mucosa: Teeth: Gums: Tongue: Pharynx: Uvula: Tonsils: Skin: Gen. Color: Texture: Temp: Turgor: Wound/Dreesing/drains: Abdomen: Configuration: Pinkish Smooth Warm Supple no dusky Smooth Cold clammy Supple no Due to oxygenation Normal Due to response of SNS; vasoconstriction Normal Normal Midline Not inflamed Midline Not inflamed Normal Normal 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 Midline Normal (-) tenderness Midline Normal (-) tenderness Normal Normal Normal gross hearing no discharge Grossly normal Too many ear wax Normal Due to Unhygienic practices PERLLA ( 3 7mm) Pinkish Anicteric Grossly normal PERRLA (4mm) Pale Anicteric Grossly normal Normal tissue perfusion Normal Normal

Flat not tender

Distended abdomen

Due toaccumulation of

Bowel sounds:

5-20/min, tympanic upon percussion


fluid in the peritoneal cavity Due to stimulation of SNS

Cardiovascular: Heart Sounds: Peripheral Pulse: Capillary Refill: Orthostatic hypotension: Respiratory: Breathing Pattern: Shape of the chest: Tactile fremitus: Breath sound:

regular Equal and strong 1-3 seconds none Regular, w/o cough 1:2 Symmetric No adventitious sound

Murmur sound with S3 fast bounding pulse 4 secs. Orthostatic hypotension Difficulty of breathing 1:2 Dec. vibration to both lungs Diminished breath sound

Due to regurgitation of blood Congestion of peripheral tissue Dec. tissue perfusion Dec. cardiac output Due to pulmonary congestion Normal Accumulation of fluid in the pleural space Due to pulmonary congestion and pleural effusion Due to joint pain Normal Normal Due to fatigue and inc. workload of the heart.

Back and Extremities: ROM: Spine: Gait: Muscle Tone:

full ROM straight Coordinated Equally strong

Dec.ROM Straight Coordinated Weak muscle


Before Hospitalization Psychological: Self Perception dati nakakatulong ako sa gawaing bahay at nagaalaga sa mga kapatid ko masigla ako dati medyo payat ako dati During Hospitalization madali na akong napapagod kaya di na ako nakakatulong sa kanila. ngayon hindi na tumaba ako dahil sa pamamanas siya pa rin ang sumusuporta samin. pabigat na lang ako ngayon din a kasya ung kinikita ni ni tatay dahil lagi n akong nasa ospital lagi na akong nasa ospital

Description of self Body Image Role Relationship Pattern: Support System Family Function Sufficiency of Income

tatay ko ang sumusuporta sa amin nakakatulong ako dati sa kanila dati ngpakakasya nmin ang suweldo ni tatay hindi kami ngpapacheck-up at di kami umiinom ng kahit anong vitamins dahil di n sapat ang pera maayos naman ang paningin at pandinig ko matalas ang aking memorya at nakakasagot pa nga ako sa eskwela eh dati tinutulog ko lang kapag may sakit akong nararamdaman ang mahalaga sa akin ay ang aking pag-aaral dati gusting gusto ko agad makatapos ng pag-aaral para makatulong sa pamilya ko lagi kami nagdadasal ng sabaysabay tuwing gabi lagi kaming nagsisimba tuwing linggo

Accessibility of health care and nutritional resources

Cognitive Perceptual Pattern: Hearing/visual Problem Changes in memory

maayos pa naman din ang paningin at pandinig ko wala naman ganung pagbabago

Pain management Value Belief Pattern: Things and personal values held important Family and social values that affect life Spirituality Religious practices that affect hospitalization Elimination: Bowel movement pattern (time, frequency and amount) Urinary Pattern (time, frequency, amount and color) Use of Aids (fluid, medication and food) Rest and Sleep Pattern: Activities of Daily Living: Feeding Toileting

ngayon ang mahalag sa akin ay ang gumaling ngayon gusto lang ay gumaling para di madagdagan ung gastos di na namin nagagawa iyon hindi n kami nakakapagsimba tuwing lingo dahil inaasikaso nila ako dati 1x ako dumudumi tuwing umaga ngayon konti lang ang naiihi ko at din a madalas Furosemide as diuretics 3-5 hrs kailangan ko na ng katulong kailanagan ko ng katulong

ngayon 2x akong dumudumi at tuwing umaga at hapon Dati madalas akong umiihi at marami un Umiinom lang ako ng maraming tubig 6-8 hrs makaisa ako nakakain makaisa ako dumumi

Bed Mobility Gen. mobility Hygiene Circadian Rhythms Sleep Concerns Nutrition: Daily food intake (quality, frequency, amount and quantity)

kayang kaya ko naman dati nakakakilos naman ako pero di ako masyadong nagpapagod pag may pasok lang ako naliligo madali lang ako nakakatuog dati Magana naman ako kumain at kahit ano nakakain ko.

kaya kong gumalaw kaya lang nahihirapan ako madali na akong napapagod kahit sa konting kilos lang ngayon pinupunasan ako

nahihirapan na akong maktulog dahil sa sakit 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 2nd HD, Thoracentesis was also ordered which is not done. On the 3rd HD, Furosemide was shifted to 40mg TIV Q12H. Thoracentecis was temporarily hold. On the 4th 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 6th 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 7th 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. He was ordered for repeat CXR.

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


Serology (September 09, 2010) Result C Reactive Protein CRP 33.7 H mg/dL Anti Streptolysin O Titer (ASO)
302.5 mg/dL

Normal Values 0.0 to 10.0 mg/dL


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

Urinalysis Actual Values Physical Analysis color transparency specific gravity Chemical Analysis pH protein sugar bilirubin urobilinogen blood nitrites leukocytes Ketones straw slightly cloudy 1.010 5.0 negative negative negative negative trace negative negative negative

Normal values Yellow Clear 1.015-1.025 4.6-8.0 Negative Negative Negative Negative Negative Negative Negative Negative

Urine Microscopy (IU) RBC WBC 21 4 1 (hpf) Normal values 17 3

28 5

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.

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

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.


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 INJURY

Damaged cells secretes inflammatory chemicals (histamine and kinins)

Dilatation of blood vessels blood flow into the area Heat

capillary permeability (leaky)

Attraction of phagocytes and WBC into the injured area (chemotaxis) Removal of damaged / dead tissue cells and pathogens from the area.

Redness O2 & nutrient supply

Leak of plasma from the blood stream into the tissue spaces Edema Swelling Pain Activation of pain receptors

Entrance of clotting proteins from the blood into the area Fibrin barrier formation

metabolic rate of tissue cells

Walls off the damaged area to prevent the spread of pathogen

Possible temporary limitation of joint movement



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 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 Promotes intense inflammatory response


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

Tricuspi d valve

Right ventricle

Pulmonary semi lunar valve

Pulmonary trunk

Pulmonary arteries

Body tissue (systemic circulation) Left ventricle e Bicuspid valve Left atrium

Lung tissue (pulmonary circulation)


Aortic semilunar valve

Pulmonar y vein

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

FEVER ARTHRALGIA ESR WBC count Activity intolerance

Restriction of leaflet motion Impeding to full swing action Aortic Valvular stenosis Leaflets may become deformed by healing tissue Valve fails to close completely Wide pulse pressure Aortic Regurgitation blood volume to LV cyanosis Orthopnea pulmonary venous blood flow & pressure Pulmonary congestion Dyspnea Use of accessory muscles RR vasoconstriction Stimulate SNS S3 Heart sound Murmurs

blood volume and pressure in the LA

cardiac output

Non productive cough

Release of epinephrine and norepinephrine Kidney RBC HR & Contractility Further damage to the heart muscles

Capillary permeability Plasma leaked out Accumulation of excessive fluid in the pleural space Pleural effusion

blood volume to RV Continuous flow of blood from the CVC blood volume of RV and RA Tricuspid regurgitation

Impaired sleep

Skin Cold clammy, pallor


Renal perfusion Release of renin by kidneys Formation of angiotensin I

gastric secretions digestion BM

Fast, bounding pulse Dec. vocal tactile fremitus s/sx: Dullness when percussed fever, chills, pleuritic chest pain, dyspnea JVD Fluid volume overload Peripheral edema Impaired gas exchange Pulmonary hypertension Respiratory failure R Ventricular failure Congestion of the viscera and peripheral tissue Blood backs to hepatic veins Pressure w/in portal vessels Portal hypertension Abdominal pain Forced fluid into the abdominal cavity Ascites Anorexia Nausea Weight gain Elasticity -dizziness, lightheadedness Cyanosis, pallor ventricular pressure and resistance to ventricular filling oxygenation in brain tissues ACE converts angiotension I to II Promotes the release of aldosterone Promotes retention of Na+ and water Preload and afterload Further stress on the ventricular wall Fatigue Further in the workload of the heart Weakness Thickness of the heart muscle Activity intolerance Stimulates ADH production bp


lung expansion

Subsequent in cardiac output Development of pressure workload of the heart contraction

Fail to contract Death

PRIORITIZATION Diagnosis Scientific explanation Rationale 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 It is our second prioritized problem because decrease cardiac output may lead to diminish ability of the patient to response to stress 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 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


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 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


Excessive fluid volume related to sodium and water retention



Subj: Hindi siya masyado makakilos kasi ang bilis niya mapagod as verbalized by the guardian.

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

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 -



Obj: -murmur S3 -peripheral edema(+3) - cold clammy skin - 4 sec. capillary refill - BP: 140/20 mmHg -

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

- 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 O2 as indicated

GOAL PARTIALLY Provide baseline data for MET comparison to follow trends After 2 of nursing and evaluate response to intervention pt was intervention able to participate Decrease O2 consumption and in activities that promote venous return reduced the workload of the heart To prevent orthostatic hypotension To promote adequate rest and sleep

- Helps to determine underlying causes - To reduce anxiety

- 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)

- To increase O2 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

Assessment 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:

Diagnosis Excess fluid volume related to increased ADH production and sodium/water retention as manifested by pitting edema (grade 3) and weight gain from 3540 kgs. Analysis 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

Goals and Objective 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.

Intervention 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

Rationale Establish baseline data for further comparison To assess precipitating factor

Evaluation 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.

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

Dependent: Restrict Na and Fluid as indicated Administer diuretics as prescribed Collaborative: Assist with procedure as indicated (paracentesis)

ASSESSMENT 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

DIAGNOSIS Impaired gas exchange related to fluid shift on alveoli secondary to pulmonary edema as manifested by respiratory rate of 33 bpm and cyanosis

GOALS AND OBJECTIVES 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 INFERENCE patient in semi fowler position and Pulmonary congestion administration of oxygen inhalation Pulmonary edema To be able to change cyanosis to pinkish Increase capillary pressure skin, lips and nail bed color by providing Plasma leak out adequate oxygen for better circulation of Accumulation of excessive blood fluid in the alveoli Impaired gas exchange

INTERVENTION 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

RATIONALE 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

EVALUATION 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

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

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

DRUG STUDY Name of drug,route, dose and indications Dopamine drip D5W 92.8 cc Mechanism of Action 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 Contraindications >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 Adverse Reactions 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. Nursing Responsibilities >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.

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.

Name of drug,route, dose and indications

captopril Capoten, Novo-Captopril (anti-hypersensitive) 25 mg/tab tab BID Indication : >hypertension >CHF >left ventricular dysfunction (LVD) after MI >diabetic nephropathy

Mechanism of Action

>hypersensitivity >pregnancy (2nd/3rd trimester) >lactation >heart block Children >K-sparing >diuretics >bilateral renal artery stenosis

Adverse Reactions
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

Nursing Responsibilities
>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

Selectively suppresses reninangiotensinaldosterone system, inhibits ACE; prevents conversion of angiotensin I to angiotensin II.

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

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.

Mechanism of Action
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

Adverse Reactions
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

Nursing Responsibilities
>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

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.

Mechanism of Action
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

Adverse Reactions
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.

Nursing Responsibilities
>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

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

Mechanism of Action
Bactericidal. Inhibits synthesis of bacterial cell wall, causing cell death.

>Contraindicated with allergy to cephalosporins or penicillins. >Use cautiously with renal failure, lactation, pregnancy

Adverse Reactions
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.

Nursing Responsibilities
>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

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.

Mechanism of Action
Enters target cells and binds to intracellular corticosteroid receptors, initiating many complex reactions that are responsible for its antiinflammatory 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).

Adverse Reactions
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

Nursing Responsibilities
>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

Lanoxin 0.25 mg/tab tab BID Indication: >heart failure >atrial fibrillation

Mechanism of Action
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

Adverse Reactions
>CNS: Headache, weakness, drowsiness, visual disturbances, mental status change. >CV: Arrhythmias >GI: GI upset, anorexia

Nursing Responsibilities
> 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

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.

Mechanism of Action
> Bactericidal: Interferes with lipids and nucleic acid biosynthesis in actively growing tubercle bacilli.

> Contraindicated in patients with allergy to isoniazid, isoniazidassociated hepatic injury or other severe adverse reactions to isoniazid, acute hepatic disease. > Use cautiously with renal impairment, lactation, pregnancy

Adverse Reactions
> 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.

Nursing Responsibilities
> 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.

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.