OBJECTIVES

PLACEMENT: Nursing Care Management 104 Level IV AREA OF EXPERIENCE: Holy Child Hospital Surgery Ward TIME ALLOTMENT: 1 hour CASE: Congestive Heart Failure secondary to Rheumatic Heart Disease TOPIC DESCRIPTION: This topic deals with the case of an early adulthood client who has been diagnosed with Congestive Heart Failure secondary to Rheumatic Heart Disease. This will focus on the clients psychosocial profile composed of demographic data, health history, genogram together with her growth and development. This will also tackle the anatomy and physiology of the major organs and the systems affected; specifically, the heart, lungs and the integument. Also included are the laboratory and diagnostic exam results and medications in relation to the clients condition. The concept map, functional health patterns, nursing care plans as well as journal/article readings regarding the disease condition will also be dealt with. CENTRAL OBJECTIVES: At the end of the case presentation, the learners shall enrich their knowledge base, improve their immediate skills, and manifest positive attitude and behaviour towards the care of patients who have Congestive Heart Failure secondary to Rheumatic Heart Disease. SPECIFIC OBJECTIVES: After the case presentation with the aid of various resources, the learners shall: Clearly grasp of the psychosocial and demographic profile and physical assessment of our client. Familiarize the anatomy and physiology of the body systems and organs related to the disease conditions. Correlate the results of diagnostic and laboratory tests to the disease condition of the patient. Trace the pathophysiology of the disease conditions in focus and also their related concepts in accordance to the patients condition. Analyze why a certain medication is prescribed for the patients disease condition and identify its classification, action, ideal dosage, indications and contraindications, side effects and adverse reactions, and the nursing responsibilities associated with its administration. Evaluate the accuracy of the functional health pattern, the suitability of the constructed nursing care plan and the summary of nursing diagnoses related to the patients condition. Evaluate and provide constructive criticisms in the case presentation as a whole. Incorporate the new discoveries from the journals to the analysis and actual care of the patients having these disease conditions.

ACKNOWLEDGEMENT
Laurenn Cecilia S. Bael and Hel Rhea B. Belarmino, as presentors responsible for this case study, we would like to thank the following: First and foremost is our heavenly dear Father God, the source of our strength, endurance and wisdom to pursue this case study. Words are not enough in showing our endless gratitude to You, our almighty creator. We also thank You for the blessings, graces and miracles that You willingly and lovingly bestowed upon us during our second rotation. Thank you. Second are the amazing authors of the books and journals that guided us throughout the case study. Without them, we would have never fully understood this case. Third is to our client and her family. Thank you for sharing and entrusting us vital information regarding this case. We appreciate your full cooperation and support for the days weve given our care; this has greatly helped in enhancing our skills, knowledge and attitudes in molding us to be a more competent and professional nurse the future. Fourth are our ever-loving parents. Thank you for your endless support; for without you, we will not be here today. We offer to you our handwork and this case study. May God bless you all and keep you safe always. Lastly, our clinical instructor Mrs. Renee Felisa O. Teh. We thank you for guiding us throughout the whole rotation and for being our second parent. Indeed, we learned a lot of things from you. You encourage us by being a role model of a professional nurse. Despite being stressed out by our mistakes, you always smile at us giving us an assurance that we can do this; wonderful and loud cheers for you maam. May God bless you all!

INTRODUCTION
Good day everyone, we are here today to present our case with the diagnosis of Congestive Heart Failure secondary to Rheumatic Heart Disease. While being in this rotation, caring for our client has become one of the most unforgettable experiences. With her full cooperation, we have learned a lot regarding her disease condition. Rheumatic heart disease is a condition in which the heart valves are damaged by rheumatic fever. Rheumatic fever is an inflammatory disease. It can affect many of the body's connective tissues especially those of the heart, joints, brain or skin. Anyone can get acute rheumatic fever, but it usually occurs in children five to 15 years old. In our clients case, she is 26 years old. The rheumatic heart disease that results can last for life. The incidence of rheumatic fever/rheumatic heart disease is low in the United States and most other developed countries. However, it continues to be the leading cause of cardiovascular death during the first five decades of life in the developing world. (http://www.americanheart.org/presenter.jhtml?identifier=4709, 2010). Rheumatic heart disease eventually leads to congestive heart failure. Out of the 86, 241, 697 people in the Philippines, 1,521, 912 have congestive Heart Failure. CHF is the 6 th leading cause of mortality in the Philippines, affecting males more than females. (http://www.slideshare.net/davejaymanriquez/right-and-left-congestive-heart-failurepresentation, 2008) Now we will be presenting to you the case of our patient who is suffering from Congestive Heart Failure. This case analysis we will be dealing with the concepts of Congestive Heart Failure and Rheumatic Heart Disease. Aside from that, we will also be presenting the clients demographic profile, the risk factors, the pathophysiology and the treatment. Nursing and medical management, the necessary diagnostic exams and laboratory exams will also be included. So sit back and relax as we go along with our case presentation.

ANATOMY and PHYSIOLOGY

THE LUNGS The human lungs are the organs of respiration in humans. Humans have two lungs, with the left being divided into two lobes and the right into three lobes. Together, the lungs contain approximately 1500 miles (2,400 km) of airways and 300 to 500 million alveoli, having a total surface area of about 70 m2 in adults roughly the same area as a singles badminton court. The surface area is roughly the same area as one side of a tennis court[1] Furthermore, if all of the capillaries that surround the alveoli were unwound and laid end to end, they would extend for about 620 miles! Organization The conducting zone contains the trachea, the bronchi, the bronchioles, and the terminal bronchioles The respiratory zone contains the respiratory bronchioles, the alveolar ducts, and the alveoli. The conducting zone and the respiratory zone (but not the alveoli) are made up of airways. The conducting zone has no gas exchange with the blood, and is reinforced with cartilage in order to hold open the airways. The conducting zone warms the air to 37 degrees Celsius and humidifies the air. It also cleanses the air by removing particles via cilia located on the walls of all the passageways. The lungs are surrounded by the rib cage. The respiratory zone is the site of gas exchange with blood. The smooth muscle tone in bronchioles, and therefore bronchiolar diameter, is controlled by: the sympathetic nervous system via noradrenaline acting on the beta receptors and causes bronchodilation the parasympathetic nervous system via acetylcholine which acts on the M-1 muscarinic receptors and maintains the resting tone of the bronchiolar smooth muscle. This action is related, although considered distinct from bronchoconstriction many other non-autonomic nervous and biochemical stimuli including, for example, carbon dioxide. The pleural cavity is the potential space between the parietal pleura lining the inner wall of the thoracic cage and the visceral pleura lining the lungs.

CIRCULATORY SYSTEM The circulatory system is an organ system that moves nutrients, gases, and wastes to and from cells to help fight diseases and help stabilize body temperature and pH to maintain homeostasis. This system may be seen strictly as a blood distribution network, but some consider the circulatory system as composed of the cardiovascular system, which distributes blood, and the lymphatic system, which distributes lymph. While humans, as well as other vertebrates, have a closed cardiovascular system (meaning that the blood never leaves the network of arteries, veins and capillaries), some invertebrate groups have an open cardiovascular system. The most primitive animal phyla lack circulatory system. The lymphatic system, on the other hand, is an open system. The main components of the human circulatory system are the heart, the blood, and the blood vessels. The circulatory system includes: the pulmonary circulation, a "loop" through the lungs where blood is oxygenated; and the systemic circulation, a "loop" through the rest of the body to provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7 litres) of blood, which consists of plasma, red blood cells, white blood cells, and platelets. Also, the digestive system works with the circulatory system to provide the nutrients the system needs to keep the heart pumping. Two types of fluids move through the circulatory system: blood and lymph. The blood, heart, and blood vessels form the cardiovascular system. The lymph, lymph nodes, and lymph vessels form the lymphatic system. The cardiovascular system and the lymphatic system collectively make up the circulatory system. Pulmonary circulation Pulmonary circulation is the portion of the cardiovascular system which transports oxygen-depleted blood away from the heart, to the lungs, and returns oxygenated blood back to the heart. Oxygen deprived blood enters the right atrium of the heart and flows into the right ventricle where it is pumped through the pulmonary arteries to the lungs. Pulmonary veins return the now oxygen-rich blood to the heart, where it enters the left atrium before flowing into the left ventricle. Also, from the left ventricle the oxygen-rich blood is pumped out via the aorta, and on to the rest of the body.

Systemic circulation Systemic circulation is the portion of the cardiovascular system which transports oxygenated blood away from the heart, to the rest of the body, and returns oxygen-depleted blood back to the heart. Systemic circulation is, distance-wise, much longer than pulmonary circulation, transporting blood to every part of the body except the lungs. Coronary circulation The coronary circulatory system provides a blood supply to the heart. As it provides oxygenated blood to the heart, it is by definition a part of the systemic circulatory system. Heart View from the front, which means the right side of the heart is on the left of the diagram (and viceversa)

The heart pumps oxygenated blood to the body and deoxygenated blood to the lungs. In the human heart there is one atrium and one ventricle for each circulation, and with both a systemic and a pulmonary circulation there are four chambers in total: left atrium, left ventricle, right atrium and right ventricle. The right Atrium, which is the upper chamber of the right side of the heart, receives blood from the upper body through the Superior Vena Cava, and from the lower body through the Inferior Vena Cava. The blood that is returned to the right atrium is oxygen-poor and passed into the right ventricle to be pumped through the pulmonary artery to the lungs to be re-oxygenated. The left atrium receives newly oxygenated blood from the lungs which is passed into the strong left ventricle to be pumped through the aorta to the tissues of the body.

THE INTEGUMENTATRY SYSTEM The integumentary system does not only include the three layers of your skin, but also all of its accessory structures, such as nails, hair, and glands. There are many disorders that can occur, but many ways to prevent them as well. Structure of the Skin The skin covers the entire exterior of the human body. In an adult, the skin has a surface area of about 1.8 square meters, or 20.83 square feet. Usually, the skin is only loosely attached to underlying muscle tissue, but where there are no muscles, the skin attaches directly to bone. The skin is sometimes called the cutaneous membrane or the integument, and since the skin has several accessory organs, it is also possible to speak of the integumentary system. The skin has three regions: the epidermis, the dermis, and the subcutaneous layer. The subcutaneous layer, however, actually lies below the skin. Epidermis This is the outer and thinner region of the skin. It is made up of stratified squamous epithelium that is capable of keratinizing, or becoming hard and tough. Cells divide and grow quickly, push older epidermal cells farther away from nutrient supply and older cells die.
Epidermis serves protective functions: - Shields moist tissues against water loss, mechanical and chemical injuries, and can keep out disease causing agents - Some cells in epidermis are melanocytes, which produce pigment melanin-this pigment absorbs sunlight and helps protect melanin-this deeper layers from UV radiation

Two main layers: the stratum germinativum and the stratum corneum.

Stratum Germinativum The basal cells of the stratum germinativum lie just superior to the dermis and are constantly dividing and producing new cells that rise to the surface of the epidermis in two to four weeks. As the cells push away from the dermis, they move progressively farther away from the blood vessels in the dermis. Since these cells are not being supplied with nutrients and oxygen, because the epidermis itself lacks blood vessels, they eventually die and are sloughed off. Langerhan's cells are specialized cells produced in red bone marrow and found in the lower epidermis. These cells phagocytize microbes and then travel to lymphoid organs, where they stimulate the immune system to react. Melanocytes are another type of specialized cell located in the lower epidermis. Melanocytes produce melanin, the pigment primarily responsible for skin color. Since the number of melanocytes is about the same in all individuals, variation in skin color is due to the amount of melanin produced and its distribution. When Caucasians sunbathe, melanocytes produce more melanin in an attempt to protect the skin from the damaging effects the ultraviolet (UV) radiation in sunlight. The melanin is passed to other epidermal cells, and the result is tanning, or in some people, the formation of patches of melanin called freckles. Another pigment, called keratin, is present in epidermal cells and in the dermis and gives the skin of people of Asiatic origin its yellowish coloration. The pinkish color of fair-skinned people is due to the blood in the capillaries of the dermis. Stratum Corneum As cells are pushed toward the surface of the skin, they become flat and hard, forming the tough, uppermost layer of the epidermis, the stratum corneum. Hardening is caused by keratinization, the cellular production of a fibrous, waterproof protein called keratin. Over much of the body, keratinization is minimal, but the palms of the hands and the soles of the feet normally have a particularly thick outer layer of dead, keratinized cells. The waterproof nature of keratin protects the body from water loss and gain. The stratum corneum also serves as a mechanical barrier against microbe invasion. This is a region of fibrous connective tissue that is deeper and thicker than the epidermis. The upper layer of the dermis has finger-like projections called dermal papillae. These project into and anchor the epidermis. In the overlying epidermis, they cause ridges, resulting in spiral and concentric patterns. The function of the epidermal ridges is to increase friction and thus provide a better gripping surface. Because they are unique to each person, fingerprints and footprints can be used for identification purposes. Dermis The dermis contains collagenous and elastic fibers. The collagenous fibers are flexible but offer great resistance to overstretching; they prevent the skin from being torn. The elastic fibers stretch to allow movement of underlying muscles and joints, but they maintain normal skin tension. The dermis also contains blood vessels that nourish the skin. Blood rushes into

these vessels when a person blushes and is reduced in them when a person turns cyanotic or blue. There are also numerous sensory nerve fibers in the dermis that take nerve impulses to and from the accessory structures of the skin. Subcutaneous Layer The subcutaneous layer, or hypodermis, lies below the dermis. It is composed of loose connective tissue, including adipose (fat) tissue. Fat is an energy storage form that can be called upon when necessary. Adipose tissue also helps insulate the body from either gaining heat from the outside or losing heat from the inside. A well-developed subcutaneous layer gives the body a rounded appearance and provides protective padding against external assaults. Excessive development of this layer results in obesity Accessory Structures of the Skin Hair, nails, and glands are structures of the epidermal origin, even though some parts of hair and glands are largely found in the dermis. Hair Hair is found on all body parts except the palms, soles, lips, nipples, and portions of the external reproductive organs. Most of this hair is fine and downy, but the hair on the head includes stronger types as well. After puberty, when sex hormones are made in quantity, there is noticeable hair in the axillary and pelvic regions of both sexes. In the male, a beard develops, and other parts of the body may also become quite hairy. Females also experience an increase in the amount of hair found on the body. Hairs project from complex structures called hair follicles. These hair follicles contain numerous epidermal cells but are located in the dermis of the skin. Certain hair follicle cells continually divide, producing new cells that form a hair. At first, the cells are nourished by dermal blood vessels, but as the hair grows up and out of the follicle, they are pushed farther away from this source of nutrients, become keratinized, and die. They portion of a hair within a follicle is called the root, and the portion that extends beyond the skin is called the shaft. The life of any particular hair is usually three to four months for an eyelash and three to four years for a scalp hair; then it regrows. Baldness occurs when the hair on the head fails to regrow. Each hair has one or more oil, or sebaceous, glands, whose ducts empty into the follicle. A smooth muscle, the arrector pili, attaches to the follicle in such a way that contraction of the muscle causes the hair to stand on end. If a person has had a scare or is cold, goose bumps develop due to contraction of these muscles. A pocket of stationary air develops between the skin and the extended hairs. Nails Nails grow from special epithelial cells at the base of the nail in the region called the nail root. These cells become keratinized as they grow out over the nail bed. The visible portion of the nail is called the nail body. The cuticle is a fold of skin that hides the nail root. Ordinarily, nails grow only about 1 millimeter a week. The pink color of nails is due to the vascularized dermal tissue beneath the nail. The whitish color of the half moon-shaped base, or lunula, results from the thicker germinal layer in this area. Glands The glands in the skin are groups of cells specialized to produce and secrete a substance into ducts. There are three types: sweat glands, sebaceous glands, and mammary glands.

Sweat glands These glands, also called sudoriferous glands, are present in all regions of the skin. There can be as many as ninety glands per square centimeter on the leg, four hundred glands per cubic centimeter on the palms and soles, and an even greater number on the fingertips. A sweat gland is a tubule that is coiled, particularly at its opening. Some sweat glands--apocrine glands--open into hair follicles in the anal region, groin, and armpits. These glands begin to develop at puberty, and some believe that their secretion acts as a sex attractant. These glands become active when a person is under stress. Other sweat glands--eccrine glands--open onto the surface of the skin. They become active when a person is hot and help lower body temperature. The sweat (perspiration) produced by these glands is mostly water, but it also contains salts and some urea, a waste substance. Therefore, sweat is a form of excretion. Ears contain modified sweat glands, called ceruminous glands, which produce cerumen, or earwax. Sebaceous glands Most sebaceous glands are associated with a hair follicle. These glands secrete an oily substance called sebum that flows into the follicle and then out onto the skin surface. This secretion lubricates the hair and skin, and helps waterproof them. Particularly on the nose and cheeks, the sebaceous glands may fail to discharge sebum and the secretions collect, forming whiteheads or blackheads. If pus-inducing bacteria are also present, a boil or pimple may result.

PHARMACOLOGIC MANAGEMENT
1. GENERIC NAME: CARVEDILOL

BRAND NAME: CARVID, COREG CLASSIFICATION: Alpha- and beta-adrenergic blocker, Antihypertensive INDICATIONS: Hypertension, alone or with other oral drugs, especially diuretics Treatment of mild to severe CHF of ischemic or cardiomyopathic origin with digitalis, diuretics, ACE inhibitors Left ventricular dysfunction (LVD) after MI ACTION: Competitively blocks alpha-, beta-, and beta2-adrenergic receptors and has some sympathomimetic activity at beta2-receptors. Both alpha and beta blocking actions contribute to the BP-lowering effect; beta blockade prevents the reflex tachycardia seen with most alpha-blocking drugs and decreases plasma renin activity. Significantly reduces plasma renin activity. DOSAGE AND ROUTE: 6.25 1tab TID PO ADVERSE REACTIONS: CNS: Dizziness, vertigo, tinnitus, fatigue, emotional depression, paresthesias, sleep disturbances. CV: Bradycardia, orthostatic hypertension, CHF, cardiac arrhythmias, pulmonary edema, hypotension

GI: Gastric pain, flatulence, constipation, diarrhea, hepatic failure Respiratory: Rhinitis, pharyngitis, dyspnea Other: Fatigue, back pain, infections

CONTRAINDICATIONS AND CAUTIONS: Contraindicated with decompensated CHF, bronchial asthma, heart block, cardiogenic shock, hypersensitivity to carvedilol, pregnancy, lactation. Use cautiously with hepatic impairment, peripheral vascular disease, thyrotoxicosis, diabetes, anesthesia, major surgery. NURSING CONSIDERATIONS: Do not discontinue drug abruptly after chronic therapy (hypersensitivity to catecholamines may have developed, causing exacerbation of angina, MI, and ventricular arrhythmias); taper drug gradually over 2 wk with monitoring. Consult with physician about withdrawing drug if patient is to undergo surgery (withdrawal is controversial). Give with food to decrease orthostatic hypotension and adverse effects. Monitor for orthostatic hypotension and provide safety precautions. Monitor patients with diabetes closely; drug may mask hypoglycemia or worsen hyperglycemia. WARNING: Monitor patient for any sign of liver dysfunction (pruritus, dark urine or stools, anorexia, jaundice, pain); arrange for LFTs and discontinue drug if tests indicate liver injury. Do not restartcarvedilol. PATIENT TEACHING: Take drug with meals. Do not stop taking drug unless instructed to do so by a health care provider. Avoid use of over-the-counter medications. You may experience these side effects: Depression, dizziness, light-headedness (avoid driving or performing dangerous activities; getting up and changing positions slowly may help ease dizziness). Report difficulty breathing, swelling of extremities, changes in color of stool or urine, very slow heart rate, continued dizziness.
2. GENERIC NAME: CAPTOPRIL

BRAND NAME: CAPOTEN CLASSIFICATION: ACE inhibitor, Antihypertensive INDICATIONS: Treatment of hypertension alone or in combination with thiazide-type diuretics Treatment of CHF in patients unresponsive to conventional therapy; used with diuretics and digitalis Treatment of diabetic nephropathy Treatment of left ventricular dysfunction after MI

ACTION: Blocks ACE from converting angiotensin I to angiotensin II, a powerful vasoconstrictor, leading to decreased BP, decreased aldosterone secretion, a small increase in serum potassium levels, and sodium and fluid loss; increased prostaglandin synthesis also may be involved in the antihypertensive action. DOSAGE AND ROUTE: tab BID PO ADVERSE REACTIONS: CV: Tachycardia, angina pectoris, MI, Raynaud's syndrome, CHF, hypotension in salt- or volume-depleted patients Dermatologic: Rash, pruritus, scalded mouth sensation, pemphigoid-like reaction, exfoliative dermatitis, alopecia, photosensitivity GI: Gastric irritation, aphthous ulcers, peptic ulcers, dysgeusia, cholestatic jaundice, hepatocellular injury, anorexia, constipation GU: Proteinuria, renal insufficiency, renal failure, polyuria, oliguria, urinary frequency Hematologic: Neutropenia, agranulocytosis, thrombocytopenia, hemolytic anemia, pancytopenia Other: Cough, malaise, dry mouth, lymphadenopathy CONTRAINDICATIONS AND CAUTIONS: Contraindicated with allergy to captopril, history of angiodema, second or third trimester of pregnancy. Use cautiously with impaired renal function; CHF; salt or volume depletion, lactation. NURSING CONSIDERATIONS: Administer 1 hr before or 2 hr after meals. WARNING: Ensure that patient is not pregnant before beginning treatment. Encourage use of contraceptives; if pregnancy is detected, stop drug. WARNING: Alert surgeon and mark patient's chart with notice that captopril is being taken; the angiotensin II formation subsequent to compensatory renin release during surgery will be blocked; hypotension may be reversed with volume expansion. Monitor patient closely for fall in BP secondary to reduction in fluid volume (due to excessive perspiration and dehydration, vomiting, diarrhea); excessive hypotension may occur. Reduce dosage in patients with impaired renal function. PATIENT TEACHING: Take drug 1 hour before meals; do not take with food. Do not stop without consulting your health care provider. Be careful of drop in blood pressure (occurs most often with diarrhea, sweating, vomiting, dehydration); if light-headedness or dizziness occurs, consult your health care provider. Severe fetal damage can occur if captopril is taken during pregnancy. Use of contraceptives is advised; if pregnancy should occur, stop drug and notify your health care provider. Avoid over-the-counter medications, especially cough, cold, allergy medications that may contain ingredients that will interact with ACE inhibitors. Consult your health care provider.

 You may experience these side effects: GI upset, loss of appetite, change in taste perception (limited effects, will pass); mouth sores (frequent mouth care may help); rash; fast heart rate; dizziness, light-headedness (usually passes after the first few days; change position slowly, and limit your activities to those that do not require alertness and precision). Report mouth sores; sore throat, fever, chills; swelling of the hands, feet; irregular heartbeat, chest pains; swelling of the face, eyes, lips, tongue, difficulty breathing.
3. GENERIC NAME: FUROSEMIDE

BRAND NAME: LASIX CLASSIFICATION: Loop diuretic INDICATIONS: Oral, IV: Edema associated with CHF, cirrhosis, renal disease IV: Acute pulmonary edema Oral: Hypertension ACTION: Inhibits the reabsorption of sodium and chloride from the ascending limb of the loop of Henle, leading to a sodium-rich diuresis. DOSAGE AND ROUTE: 10mg IVTT q6h PO ADVERSE REACTIONS: CNS: Dizziness, vertigo, paresthesias, xanthopsia, weakness, headache, drowsiness, fatigue, blurred vision, tinnitus, irreversible hearing loss CV: Orthostatic hypotension, volume depletion, cardiac arrhythmias, thrombophlebitis Dermatologic: Photosensitivity, rash, pruritus, urticaria, purpura, exfoliative dermatitis, erythema multiforme GI: Nausea, anorexia, vomiting, oral and gastric irritation, constipation, diarrhea, acute pancreatitis, jaundice GU: Polyuria, nocturia, glycosuria, urinary bladder spasm Hematologic: Leukopenia, anemia, thrombocytopenia, fluid and electrolyte imbalances, hyperglycemia, hyperuricemia Other: Muscle cramps and muscle spasms CONTRAINDICATIONS AND CAUTIONS: Contraindicated with allergy to furosemide, sulfonamides; allergy to tartrazine (in oral solution); anuria, severe renal failure; hepatic coma; pregnancy; lactation. Use cautiously with SLE, gout, diabetes mellitus. NURSING CONSIDERATIONS: Administer with food or milk to prevent GI upset. Reduce dosage if given with other antihypertensives; readjust dosage gradually as BP responds. Give early in the day so that increased urination will not disturb sleep.

Avoid IV use if oral use is at all possible. WARNING: Do not mix parenteral solution with highly acidic solutions with pH below 3.5. Do not expose to light, may discolor tablets or solution; do not use discolored drug or solutions. Discard diluted solution after 24 hr. Refrigerate oral solution. Measure and record weight to monitor fluid changes. Arrange to monitor serum electrolytes, hydration, liver and renal function. Arrange for potassium-rich diet or supplemental potassium as needed.

PATIENT TEACHING: Record intermittent therapy on a calendar or dated envelopes. When possible, take the drug early so increased urination will not disturb sleep. Take with food or meals to prevent GI upset. Weigh yourself on a regular basis, at the same time and in the same clothing, and record the weight on your calendar. Blood glucose levels may become temporarily elevated in patients with diabetes after starting this drug. You may experience these side effects: Increased volume and frequency of urination; dizziness, feeling faint on arising, drowsiness (avoid rapid position changes; hazardous activities, like driving; and consumption of alcohol); sensitivity to sunlight (use sunglasses, wear protective clothing, or use a sunscreen); increased thirst (suck on sugarless lozenges; use frequent mouth care); loss of body potassium (a potassium-rich diet or potassium supplement will be needed). Report loss or gain of more than 3 pounds in 1 day, swelling in your ankles or fingers, unusual bleeding or bruising, dizziness, trembling, numbness, fatigue, muscle weakness or cramps.
4. GENERIC NAME: DIGOXIN

BRAND NAME: LANOXIN CLASSIFICATION: Inotropics INDICATIONS: Heart Failure, paroxysmal supraventricular tachycardia, atrial fibrillation and flutter ACTION: Inhibits sodium-potassium-activated adenosine triphosphate, promoting movement of calcium from extracellular to intracellular cytoplasm and strenghthening myocardial contraction. Also acts on CNS to enhance vagal tone, slowing conduction through the SA and VA node. DOSAGE AND ROUTE: 0.25 tab OD ADVERSE REACTIONS: CNS: fatigue, generalized muscle weakness, agitation, hallucinations, headache, malaise, dizziness, vertigo, stupor, paresthesia CV: arrhythmias

 EENT: yellow-green halos around visual field, light flashes, photophobia, diploplia GI: anorexia, nausea, vomiting, diarrhea. CONTRAINDICATIONS AND CAUTIONS: Contraindicated in patients hypersensitivity to drug and to those with digitalis-induced toxicity, ventricular fibrillation, or ventricular tachycardia unless caused by heart failure Use with extreme caution in elderly patients and in those with acute MI, incompetent AV block, sinus bradycardia, PVCs, chronic constructive pericarditis, hypertrophic cardiomyopathy, renal insufficiency, severe pulmonary disease, or hypothyroidism. NURSING CONSIDERATIONS: Drug-induced arrhythmias may increase the severity of heart failure and hypotension. Before giving drug, take the apical-radial pulse for 1 minute. Record and notify prescriber for significant changes. Toxic effects of the heart may be life-threatening and may require attention. Monitor digoxin level. WARNING: Excessive slowing of the pulse rate (60 beats/minute) may be a sign of digitalis toxicity. Withhold drug and notify prescriber. Monitor potassium level carefully. Take corrective action hypokalemia occurs. Reduce drug dose for 1 or 2 days before elective cardioversion. PATIENT TEACHING: Teach the patient and a responsible family member about drug action, dosage regimen, how to take pulse, reportable signs, and follow-up care. Tell patient to report pulse less than 60 beats/minute, or skipped beats or other rhythm changes. Instruct patient to report adverse reactions immediately. Encourage patient to eat potassium-rich foods. Tell the patient not to substitute one brand from another. Advise patient to avoid the use of herbal drugs or to consult prescriber before taking any.

5. GENERIC NAME: RANITIDINE HYDROCHLORIDE

BRAND NAME: ZANTAC CLASSIFICATION: Antiulcer drug INDICATIONS: Active duodenal and gastric ulcers Maintenance therapy for duodenal and gastric ulcers Pathologic hypersecretory conditions, such as Zollinger-Ellison syndrome

 Erosive esophagitis Heartburn

ACTION: Competitively inhibits action of histamine on the H2 at the receptor sites of the parietal cells, decreasing gastric acid secretion. DOSAGE AND ROUTE: 0.5 tab HS OD SQ ADVERSE REACTIONS: CNS: vertigo, malaise, headache EENT: blurred vision Hepatic: jaundice Other: burning and itching at the injection site, anaphylaxis, angioedema CONTRAINDICATIONS AND CAUTIONS: Contraindicated in patients hypersensitivity to drug and those with acute porphyria Use cautiously in patients with hepatic dysfunction. Adjust dosage in patients with impaired renal function. NURSING CONSIDERATIONS: Assess patient with abdominal pain. Note presence of blood in emesis, stool, or gastric aspirate. Drug may be added to total parenteral nutrition solutions. PATIENT TEACHING: Instruct patient proper use of OTC preparation, as indicated. Remind patient to take once-daily prescription drug at bedtime for best results. Instruct patient to take without regard to meals because absorption isnt affected by food. Tell the patient taking 150mg EFFERdose to dissolve drug in 6-8ounces of water before taking drug. Tell parent to dissolve 25mg EFFERdose tablet in at least 5ml of water and give with dosing cup, medicine dropper, or oral syringe. Urge patient to avoid cigarette smoking because this may increase gastric secretion and worsen disease. Advise the patient to report abdominal pan and blood in stool and emesis. Warn patient with phenylketonuria that the EFFER dose granules and tablets contain aspartame.
6. GENERIC NAME: SPIRONOLACTONE

BRAND NAME: ALDAZIDE CLASSIFICATION: Diuretic INDICATIONS: Edema

Hypertension Diuretic-induced hypokalemia To detect or to hyperaldosteronism Heart failure, as adjunct to ACE inhibitors or loop diuretic, with or without cardiac glycoside Hirsutism in women Premenstrual syndrome in women Familial male precocious puberty

ACTION: potassium-sparing diuretic; antagonizes aldosterone in the distal tubules, increasing sodium and water excretion. DOSAGE AND ROUTE: tab OD PO ADVERSE REACTIONS: CNS: headache, drowsiness, lethargy, confusion, ataxia GI: diarrhea, gastric bleeding, ulceration, cramping, gastritis, vomiting, cramping GU: ability to maintain erection, menstrual disturbances Hematologic: agranulocytosis Metabolic: hyponatremia, hyperkalemia, dehydration, mild acidosis Skin: urticaria, hisutism, Other: gynecomastia, breast sorenesss, drug fever, anaphylaxis CONTRAINDICATIONS AND CAUTIONS: Contraindicated in patients hypersensitivity to drug Contraindicated with those who anuria, acute progressive renal insufficiency, or hyperkalemia. Use cautiously inpatients woth fluid or electrolyte imbalances, impaired renal function, or hepatic disease. Use with extreme caution in pregnant women. NURSING CONSIDERATIONS: To enhance absorption, give drug with meals. Protect drug from light. Monitor electrolyte levels, fluid intake and output, weight and blood pressure. Monitor elderly patients closely, who are more susceptible to excessive dieresis. Inform laboratory that the patient is taking spironolactone because drug may interfere with tests that measure digoxin levels. Drug is less potent than thiazide and loop diuretics and is useful as an adjunct to other diuretic therapy, Diuretic is delayed for 2-3 days when used alone. Maximum antihypertensive response may be delated up to 2 weeks. Watch for hyperchloremic metabolic acidosis, which may occur during therapy, especially in patients with hepatic cirrhosis.

PATIENT TEACHING: Instruct patient to take drug in the morning to prevent the need to urinate at night. If second dose is needed, tell patient to take it with food in the afternoon. ALERT: T prevent serious hyperkalemia, warn patient to avoid excessive ingestion of potassium-rich foods (such as citrus fruits, tomatoes, bananas, dates, asparagus), potassium-containing supplements. Caution patient not to perform hazardous activities if adverse CNS reactions occur. Advise men about possible breast tenderness or breast enlargement.
7. GENERIC NAME: METOCLOPRAMIDE

BRAND NAME: PLASIL CLASSIFICATION: Anitemetic INDICATIONS: To prevent or reduce nausea and vomiting from emetogenic cancer chemotherapy T prevent or reduce postoperative nausea and vomiting To facilitate small-bowel intubation, to aid in radiologic examinations Delayed gastric emptying secondary to diabetic gastroparesis Gastroesophageal reflux disease ACTION: Stimulates mobility of upper GI tract, increases lower esophageal sphincter tone, and blocks dopamine receptors at the chemoreceptor trigger zone. DOSAGE AND ROUTE: 10mg IVTT q6h ADVERSE REACTIONS: CNS: restlessness, anxiety, drowsiness, fatigue, lassitude, fever, depression, akathisia, insomnia, confusion, suicide ideaton, seizures, neuroeptic malignant syndrome, hallucinations, headache, dizziness, extrapyramidal syndrome, dyskinesia, dystonic reactions CV: transient hypertension, hypotension, supraventricular tachycardia, bradycardia. GI: nausea, bowel disorders, diarrhea/ GU: urinary frequency, incontinence. Hematologic: neutropenia, agranulocytosis Skin: rash, urticaria. Other: prolactin secretion, loss of libido CONTRAINDICATIONS AND CAUTIONS: Contraindicated in patients hypersensitivity to drug and those with pheochromocytoma or seizure disorders.

 Contraindicated in patients for whom stimulation of GI motility might be dangerous (those with hemorrhage, obstruction or perforation. Use cautiously in patients with history of depression, Parkinsons disease, or hypertension. NURSING CONSIDERATIONS: Monitor bowel sounds. Safety and effectiveness of drug havent been established for therapy lasting longer than 12 weeks. ALERT: Use 25 mg of diphenhydramine IV to counteract adverse effect form high doses. PATIENT TEACHING: Tell patient to avoid activities that require alertness for 2 hours after doses. Urge patient to report persistent or serious adverse reactions promptly. Advise patient not to drink alcohol during therapy.
8. GENERIC NAME: SODIUM CHLORIDE

BRAND NAME: Slo-Salt, Sustain CLASSIFICATION: Electrolytes and replacement solution INDICATIONS: Fluid and electrolyte replacement in hyponatremia caused by electrolyte loss or in severe salt depletion Heat cramp caused by excessive perspiration ACTION: Replaces sodium and chloride and maintains levels. DOSAGE AND ROUTE: 1 tab BID PO ADVERSE REACTIONS: CNS: aggravation of heart failure, thrombophlebitis, edema when given too rapidly or in excess. Metabolic: hyponatremia, aggravation of existing metabolic acidosis with excessive infusion Respiratory: pulmonary edema Skin: local tenderness, tissue necrosis at injection site Other: abscess CONTRAINDICATIONS AND CAUTIONS: Contraindicated in patients with conditions in which sodium and chloride administration is detrimental. Sodium 3% and %% injections, contraindicated in patients with increased, normal, or only slightly decreased electrolyte levels.

 Use cautiously in elderly or postoperative patients with heart failure, circulatory insufficiency, renal dysfunction, or hypoprotenemia. NURSING CONSIDERATIONS: Monitor electrolyte levels. PATIENT TEACHING: Explain use and administration of drug to patient and family. Tell patient to report adverse reactions promptly.
9. GENERIC NAME: KALIUM DURULE/POTASSIUM CHLORIDE

BRAND NAME: KALIUM CLASSIFICATION: Electrolytes and replacement solution INDICATIONS: Hypokalemia. Prophylaxis during treatment w/ diuretics. Severe hypokalemia. Acute MI. ACTION: Replaces sodium and chloride and maintains potassium levels. DOSAGE AND ROUTE: 1 tab x 3 days ADVERSE REACTIONS: CNS: paresthesia of limbs, listlessness, confusion, weakness or heaviness of limbs, flaccid paralysis. GI: nausea, vomiting, abdominal pain, diarrhea. Metabolic: hyperkalemia Respiratory: respiratory paralysis CONTRAINDICATIONS AND CAUTIONS: Contraindicated in patients with conditions in with severe renal impairment with oliguria, anuria, or azotemia; with untreated ADDISONs disease; or with acute dehydration, heat cramps, hyperkalemia, hyperkalemic form of familial periodic paralysis, or other conditions linked to extensive tissue breakdown Use cautiously in patients with cardiac disease or renal impairment. NURSING CONSIDERATIONS: Look-alike or sound-alike: Potassium preparations arent interchangeable; verify preparation before use and dont switch products. Make sure powders are completely dissolved before giving.

 Enteric-coated tablets arent recommended because of increased risk of GI bleeding and small bowel ulcerations. Tablets in wax matrix sometimes lodge in the esophagus and cause ulceration in cardiac cardiac patients with esophageal compression from an enlarged left atrium. Drug is commonly used orally with potassium-wasting diuretics to maintain potassium levels. Dont crush sustaines-released potassium products. Monitor ECG and electrolyte levels during therapy. Monitor renal function. After surgery, dont give drug until urine flow is established. Manu adverse reactions may reflect hyperkalemia. PATIENT TEACHING: Tell patient how to prepare powders and how to take drug, Tell patient to take with or after meals with a full-glass of water or fruit juice to lessen GI distress. Teach patient signs and symptoms of hyperkalemia, and tell patient to notify prescriber if they occur. Tell patient to report discomfort at IV insertion site. Warn patient not to use salt substitutes concurrently, except with the prescribers permission, ALERT: Tell patient not to be concerned if wax matrix appears in stool because the drug has already been absorbed.
10. GENERIC NAME: SENNA - RECTAL

BRAND NAME: SENOKOT CLASSIFICATION: Laxative, peristaltic stimulant - stool softener INDICATIONS: Constipation Clear the intestine before rectal or bowel examinations. ACTION: The laxative principles of the senna plant have been identified as sennosides (senna glycosides). Enzymatic action by colonic bacteria converts the glycosides into aglycones, which induce colonic peristalsis through stimulation of the intrinsic peristaltic mechanism in the colonic wall. This action is virtually colon-specific, since these compounds have little or no action in the stomach and small intestine. The stimulant effect on the Myenteric (Auerbachs) plexus in the colonic wall is reportedly free of mucosal injury. Senna also has effects on electrolyte and water transport. DOSAGE AND ROUTE: 2 tabs HS ADVERSE REACTIONS: CNS: weakness, dizziness, fainting, sweating CV: rapid heart rate GI: diarrhea, nausea, vomiting, rectal irritation, stomach cramps or bloating, unrelieved constipation GU: rectal bleeding; this medication may cause the urine to turn pink, red or brownish in color.

 SKIN: skin rash CONTRAINDICATIONS AND CAUTIONS: The acute abdomen NURSING CONSIDERATIONS: If griping occurs, subsequent dosage should be reduced. Administer with caution to nursing mothers. Do not use in the presence of abdominal pain, nausea, fever or vomiting. Overuse or extended use may cause dependence for bowel function. Do not administer concomitantly with mineral oil since the docusate sodium component of SenokotS (senna and docusate sodium) tablets may increase absorption of oil. Rectal bleeding or failure to have a bowel movement after use of a laxative may indicate a serious condition. Discontinue use and consult a physician. PATIENT TEACHING: Do not take any type of laxative for more than one week, unless your physician has ordered a special schedule. Laxatives should not be taken within two hours of another medicine because the desired effect of the other medicine may be reduced. If there has been a sudden change in bowel movements that persists over a period of 2 weeks, consult a physician before using a laxative. Laxative products should not be used for a period longer than 1 week unless directed by a doctor. MEDICATIONS 1. CARVEDILO L (COREG) DOSAGAE 6.25 1tab TID PO ACTION Competitively blocks alpha-, beta-, and beta2adrenergic receptors and has some sympathomimetic activity at beta2-receptors. Both alpha and beta blocking actions contribute to the BP-lowering effect; beta blockade prevents the reflex tachycardia seen with most alpha-blocking drugs and decreases plasma renin activity. Significantly reduces plasma renin activity. Blocks ACE from converting angiotensin I to angiotensin II, a powerful vasoconstrictor, leading to decreased BP, decreased aldosterone secretion, a small increase in serum potassium levels, and sodium and fluid IMPLICATIONS Activation of the clients SNS d/t decreased cardiac output triggered the release of catecholamines, thus an increase in the clients HR, myocardial contractility and vasoconstriction. This medication is given to block the negative effects of SNS. Client has been experiencing increase in BP, increase CO, increase in potassium and sodium levels and fluid excess. This medication is given to decrease these effects.

CAPTOPRIL (CAPOTEN)
2.

tab BID PO

3.

FUROSEMID 10mg IVTT q6h PO

E (LASIX)

loss; increased prostaglandin synthesis also may be involved in the antihypertensive action. Inhibits the reabsorption of sodium and chloride from the ascending limb of the loop of Henle, leading to a sodium-rich diuresis. Client has edema; fluid shifting has occurred. This medication is given to mobilize edematous fluid , reduce pulmonary venous pressure and reduce preload, thus reducing hypertension. Client has been experiencing atrial flutter as a result of CHF. This medication is given to increase the force of cardiac contraction (inotropic) and decrease conduction of speed within the myocardium and slow HR (chronotropic). Client has been on NPO status. This medication is given to decrease risks of ulcer. Blocks the harmful neurohormonal effects of aldosterone in the distal renal tubules, thus decreasing the clients manifestations of hypertension. Also used to potentiate the effects of ACEinhibitors and adjunct to other diuretics. Client has also been losing potassium, thus this is also used to increase/maintain potassium levels. Client has been experiencing nausea and vomiting, This medication is given to reduce nausea and vomiting.

DIGOXIN (LANOXIN)
4.

0.25 tab OD Inhibits sodium-potassium-activated adenosine triphosphate, promoting movement of calcium from extracellular to intracellular cytoplasm and strenghthening myocardial contraction. Also acts on CNS to enhance vagal tone, slowing conduction through the SA and VA node. Competitively inhibits action of histamine on the H2 at the receptor sites of the parietal cells, decreasing gastric acid secretion. Potassium-sparing diuretic; antagonizes aldosterone in the distal tubules, increasing sodium and water excretion.

5.

RANITIDINE HYDROCHLORIDE (ZANTAC)

6.

0.5 tab HS OD SQ

SPIRONOLA tab OD PO

CTONE (ALDAZIDE)

7.

METOCLOPRAMID E (PLASIL)

10mg IVTT q6h Immobility of upper GI tract, increases lower esophageal sphincter tone, and blocks dopamine receptors at the chemoreceptor trigger zone. Replaces sodium and chloride and maintains level. 1 tab x 3 days

1 tab BID PO
8.

SODIUM CHLORIDE (Slo-Salt, Sustain)

KALIUM DURULE/POTASSIU M CHLORIDE (KALIUM)

9.

Replaces sodium and chloride and maintains potassium levels. 2 tabs HS The laxative principles of the senna plant have been identified as sennosides (senna glycosides). Enzymatic action by colonic bacteria converts the glycosides into aglycones, which induce colonic peristalsis through stimulation of the intrinsic peristaltic mechanism in the colonic wall. This action is virtually colon-specific, since these compounds have little or no action in the stomach and small intestine. The stimulant effect on the Myenteric (Auerbachs) plexus in the colonic wall is reportedly free of mucosal injury. Senna also has effects on electrolyte and water transport.

Client has been experiencing decrease in electrolytes, such as sodium and potassium. This is given to increase sodium levels. Client has been experiencing decrease in electrolytes, such as sodium and potassium. This is given to increase potassium levels. Client has not defecated. This is given to increase peristalsis, thus promote defecation.

SENNA RECTAL (SENOKOT)

10.

RELATED READINGS
Is Primary Prevention of Rheumatic Fever the Missing Link in the Control of Rheumatic Heart Disease in Africa?
Ganesan Karthikeyan, MBBS, MD, DM; Bongani M. Mayosi, MBChB, DPhil Prevention of Rheumatic Fever and RHD: Rationale and Strategies Rheumatic fever (RF) occurs in _0.3% to 3% of patients who have pharyngitis due to group A streptococcal (GAS) infection, as an autoimmune response to the infecting agent.9 Involvement of heart valves during an acute episode of RF (carditis) leads to valve damage and chronic RHD. In studies from developing countries in the postpenicillin era, 50% to 80% of patients who have carditis develop chronic RHD at long-term follow-up. Patients who have had carditis in the past are more likely to develop carditis during recurrencesand, presumably, suffer cumulative valve damage. There are no proven treatments that alter the natural history of RF. Therefore, prevention is the key to reducing the burden of disease in the community. Given our understanding of the pathogenesis of RHD, 2 broad strategies for prevention are applicable. Primary prevention involves the detection of symptomatic GAS sore throats in susceptible individuals in the community (mainly children) and treatment with a course of oral or parenteral penicillin.6 Secondary prophylaxis is achieved by periodic administration of penicillin to individuals who have had previous episodes of RF or have RHD, with the aim of preventing recurrent GAS sore throat.5 Secondary prevention reduces the risk of recurrences of rheumatic fever, but it has not been shown to reduce the development of chronic RHD or mortality due to RHD. Several arguments have been made against adopting primary antibiotic prophylaxis for the prevention of

RF and RHD as a public health intervention in the community. The principal objection to such an approach is the expense and logistic difficulty of providing accurate bacteriologic diagnosis before instituting antibiotic therapy. The cost of a strategy of performing a throat swab culture for confirming GAS infection, followed by treatment with penicillin, was recently estimated to be about $ 50 per person.16 This translated to a total cost of $ 252.1 million for a population of 5 million children. In another analysis, the cost per disability-adjusted life year (DALY) gained using a strategy of primary prevention was $1049, and the cost per life saved was $40 920. Similarly, using a decision analysis model, other investigators have calculated the incremental cost of treating based on culture (compared with no treatment) to be $ 88 246 per additional life saved.18 In contrast, secondary prophylaxis using 3- or 4-weekly injections of benzathine penicillin has been found to be cost-effective at $142 per DALY gained and $5520 per death averted.17 It must, however, be noted that these findings are based on cost estimates from developed countries and may not be applicableto the situation in Africa. Other reasons for not favouring such primary prophylaxis relate to the poor health-seeking behavior in people with sore throats in resource-poor countries and the suggestion that a large proportion of patients who develop RF do not report having had a recent sore throat. Why Is Secondary Prevention Not Sufficient for Preventing RHD? Unlike in developed countries, where access to health care is good and the health-seeking behavior of people favors early presentation, in poor countries, the first inciting episode of streptococcal pharyngitis goes largely undiagnosed and untreated. As a result, susceptible patients have already suffered substantial valve damage from unrecognized episodes of RF by the time they come to clinical attention. Often patients present for the first time with symptoms due to the hemodynamic consequences of the resulting valve disease. The subsequent clinical course of these patients is largely determined by the natural history of the valve lesions. Although secondary prophylaxis reduces recurrent RF episodes,14 there is no evidence to suggest that such treatment alters natural history once significant valve damage has occurred.5 Moreover, the early episodes of acute RF in children in Africa often follow a fulminant course, which may require surgery inthe acute phase of illness. Therefore, it is crucially important to prevent the first episode of rheumatic carditis if any headway is to be made in reducing the number of people with rheumatic valve disease. Is Primary Prevention an Effective Strategy? The proof of principle for the effectiveness of primary antibiotic prophylaxis as a strategy (ie, treatment of symptomatic patients in high-risk groups) comes from the successful use of intramuscular penicillin in US army personnel more than half a century ago.22 Subsequently, in the 1960s, reductions in the incidence of RF were documented by several investigators, with the introduction of facilities for the prompt diagnosis and treatment of streptococcal sore throat. In an inner city area of Baltimore, the establishment of a health center charged with identifying and treating episodes of sore throat reduced the incidence of RF from 27 per 100 000 inhabitants to 11 per 100 000 inhabitants. The incidence remained unchanged in areas of the city without a neighborhood health center.23 A systematic review of hospital-based studies of primary prophylaxis found that antibiotic treatment of GAS sore throat reduced the attack rate of RF by 70%, with intramuscular penicillin reducing it by as much as 80%.6 This translated into 1 case of RF prevented for every 50 to 60 patients treated. Although the number needed to treat is likely to be much higher when primary prophylaxis is applied to the community, these studies provide convincing biological rationale for such a strategy. Further, a recent controlled trial among school children in China showed that a strategy of systematic identification and treatment of GAS infections may also reduce GAS carriage rates and the incidence of subsequent GAS infections.24 Primary prophylaxis may therefore contribute to cumulative reductions in RF incidence over time. However, several authorities have suggested that a substantial proportion of streptococcal sore throats that lead to RF may be asymptomatic.9,15 But this supposition is based entirely on evidence from retrospective data, with a high likelihood of recall bias. Further, there are issues related to interpretation of the data as well. For instance, the study by Veasy et al4 (which is often cited to support the occurrence of asymptomatic episodes) reported only the proportion of patients who had a sore throat severe enough that the parents considered seeking medical care and not all patients who had any sore throat. Education of patients (and the parents of susceptible children) from high-risk communities on the potential seriousness of a sore throat can be expected to improve reporting rates. Finally, incontrovertible evidence that primary prevention really works comes from the remarkable success of Costa Rica and Cuba in almost completely eradicating rheumatic fever with comprehensive programs incorporating a component of primary prevention.25,26 Although these were not controlled studies, they were applied to whole communities, thereby eliminating any selection bias. Further, the declines in RF incidence were not observed in otherwise similar populations in adjoining countries o provinces that did not have such programs. This suggests that the decline in RF was over and above any favorable temporal trends that may have occurred as a result of improvement in living conditions. The success of these programs therefore provides strong evidence that a strategy of primary antibiotic prophylaxis is effective in reducing the incidence of RF. The issue that remains is that of feasibility. This line of reasoning assumes that the principal streptococcal infection preceding RF is that of the throat and not the skin. Although streptococcal pyoderma is believed to be an important cause of RF in aboriginal communities in Australia, there is little evidence for such a relationship among Africans. Is Primary Prevention a Feasible Strategyin Africa?

Analyses performed in developed country settings suggestthat the cost and logistics of a primary prevention program involving bacteriologic diagnosis of GAS infection may be prohibitive. However, costs may be lower in developing countries because of lower wages. And because a strategy of primary prevention is more labor intensive (manpower for plating, processing, and interpreting culture results) than secondary prevention, the differences in cost between the 2 strategies may be much less in developing than in developed countries. Some preliminary data from India suggest that primary prevention may in fact be affordable relative to secondary prevention.28 In a population serviced by a tertiary care public hospital, Soudarssanane et al28 found that the output to input ratios were greater for primary than for secondary prevention (1.56 versus 1.07). This was partly because throat swab culture was inexpensive (approximately $ 2) and physician consultation fees are very low (approximately $ 0.5) in public hospitals in India. Lower personnel costs may similarly make primary prevention an affordable and efficient strategy in Africa; this needs to be tested in formal cost-effectiveness analyses. Even under the assumption that the costs of delivery ofprimary prevention are higher in Africa, substitution of bacteriologic diagnosis (which is the most expensive aspect of such a strategy) with sensitive, alternative methods of diagnosis of bacterial sore throat can substantially reduce costs and improve feasibility. One such alternative is theapplication of clinical decision rules to diagnose GAS pharyngitis. Clinical Diagnosis of Streptococcal Sore Throat Clinical algorithms for diagnosing bacterial pharyngitis, although far less accurate than throat swab culture, can conceivably substantially reduce the number of patients receivingunnecessary antibiotic therapy. Several clinical decision rules are available for the diagnosis of streptococcal sore throat.2935 In order to be an effective replacement for bacteriologic diagnosis, the decision rule must be easy to apply and must correctly diagnose most cases of streptococcal sore throat while keeping overtreatment of viral sore throats to a minimum. Walker et al36 studied the diagnostic performance of several clinical decision rules as applied to data obtained from Egyptian childrenwith symptoms of sore throat. Some clinical decision rules proved to be highly sensitive (_90%) and at the same time reduced overtreatment of culturenegative cases by as much as 40%.36 Two of the rules tested, those proposed by McIsaac et al33 and Steinhoff et al,35 were found to detect 92% of culture-positive cases and avoided treating 31% to 38% of culture-negative cases. Other investigators have suggested an alternative strategy of identifying non-GAS sore throat using decision rules in order to improve diagnostic accuracy.37 In a study conducted among children in Brazil, Smeesters et al37 showed that the use of a 3-question ruleto identify nonGAS throat infection would have reduced unnecessary antibiotic treatment by up to 55%.37 Clinical decision rules reduce unnecessary antibiotic use in some children, but they also fail to detect varying proportions of children with positive cultures, with the implication that they would not receive antibiotic therapy. The decision rule with the worst performance in this regard is the one advocated by the WHO. When applied to children in Brazil, Croatia, and Egypt, this rule missed up to 96% of children with positive cultures.38 The McIsaac et al33 and Steinhoff et al35 rules performed much better. In the study by Walker et al,36 they missed 9% and 16% of the children with a throat culture positive for GAS, respectively. The algorithm developed by Smeesters et al37 missed 16% of children with positive cultures. Some investigators have suggested that a 16%false-negative rate is acceptable because this figure is much lower than the general pediatric GAS carriage rates of 20% to 50%.37,39 They argue that because serologic evidence of infection was not sought in most of the studies, the positive throat cultures among patients not detected using clinical rules might not represent true infections. Nevertheless, despite the false-negative results, the systematic implementation of a primary prevention program incorporating any of these algorithms would represent a major improvement over the existing situation in Africa. However, even the validated decision rules are likely to have different performance characteristics depending on the populations in which they are used.40 Tailoring decision rulesto a specific population allows for improvement in performance characteristics. A version of the WHOs Integrated Management of Childhood Illness program adapted to Turkey introduced and tested guidelines for empirical antibiotic therapy for sore throat.41 A simple clinical decision rule incorporating common symptoms and signs had high sensitivity for detecting culture-positive GAS pharyngitis.41 Optimizinghe pretest probability of GAS infection using risk stratification schemes may also improve the performance of clinical decision rules. As an example, the New Zealand guidelines for management of sore throat recommend risk stratification of patients using demographic (eg, Maori or Pacific peoples) characteristics before application of clinical decision rules to guide decisions about empirical antibiotic use.42 Delivery of Primary Prevention The most crucial elements of any program are the logistics ofimplementation. The successful campaigns in Costa Rica andCuba are models worth emulating in this regard (Figure). In Costa Rica, a comprehensive program was launched beginningin the 1970s.26 Three important aspects of this program are worth emphasizing: (1) The need for throat swab culture to confirm streptococcal sore throats was eliminated and diagnosis was made entirely on clinical grounds, (2) sore throats were treated with a single intramuscular injection ofbenzathine penicillin, and (3) an educational campaign was launched to inform physicians, nurses, health technicians, andmedical students about the need to treat streptococcal sore throats. Over the next 2 decades, there was a dramatic decline in the incidence of RF to 1 per 100 000 inhabitants in 1991. The campaign in the Pinar del Rio province of Cuba was similar in that it involved the detection and treatment of sore throats combined with increasing community awareness, in addition to secondary prevention, and was associated with an identical decline in the incidence of RF.25 Another important feature of the programs in these countries was that both were integrated into the existing healthcare systems and used existing infrastructure, thus incurring little incremental cost. In the Cuban province,

the additional cost incurred was just $2000 per year, which was mainly spent on the educational campaign.25 Moreover, with the reduction in RF incidence, the direct spending on RF/RHD care decreased progressively from a high of $145 000 per year at the beginning of the program to _$22 000 per year after 10 years.25 Safety of Primary Prevention The 2 principal concerns of a primary antibiotic prophylaxis program, particularly one where a substantial proportion of individuals without streptococcal sore throats may receive benzathine penicillin, are (1) the problem of anaphylaxis and (2) the emergence of bacterial resistance. Contrary to popular belief, serious allergic reactions and anaphylaxis with benzathine penicillin prophylaxis for RHD are rare. The International Rheumatic Fever Study Group reported that after more than 32 000 injections and 2736 patient-years of follow up, the incidence of anaphylaxis was 1.2/10 000 injections, and the incidence of death was 0.31/10 000 injections (1 death in all).43 During the Costa Rican campaign, no deaths due to penicillin were reported, and anaphylaxis was reported only sporadically.26 In the same vein, strains of GAS, Streptococcus pneumoniae, and Hemophilus influenzae isolated at the National Childrens Hospital in Costa Rica continued to be 100% sensitive to penicillin 2 decades after the RHD control program was implemented.26 Indeed, despite the widespread use of penicillin worldwide, GAS infections have continued to remain susceptible to the antibiotic. Primary Prevention in Africa Treatment of sore throat is already part of the Integrated Management of Childhood Illness program in Africa, and penicillin is on the essential drug list of the WHO. Therefore, our call is for the implementation of existing policy within existing health systems, which we believe is within the reach of most African countries. The Awareness Surveillance Advocacy Prevention (ASAP) Program is an ongoing prevention program being implemented under the auspices of the Pan African Society of Cardiology (www.pascar.co.za)44 with the support of the national Departments of Health of South Africa, Ghana, and Egypt and the World Heart Federation. In addition to the objectives of raising awareness about the disease in the community and among physicians, ASAP aims to implement primary prevention strategies in tandem with secondary prevention within the existing primary healthcare system. Pilot programs will be developed at selected sentinel/ demonstration sites in the participating countries, which will ultimately serve as the basis for the establishment of national programs for the control of RF/RHD in these countries.45 Conclusions We believe that a preventive program that relies almost exclusively on secondary prevention, such as the one advocatedby the WHO, is unlikely to reduce the burden of RF and RHD in Africa. A strategy consisting of educating health personnel to recognize bacterial sore throat using simple clinical algorithms (instead of relying on a bacteriologic diagnosis), followed by a single injection of benzathine penicillin for the treatment of suspected cases, has been shown to be effective. The implementation of such a strategythrough the existing healthcare infrastructure may be efficientand cost-effective and has the potential to reduce the burden of RF/RHD. The recently devised ASAP program is the first step toward implementing such a comprehensive preventive strategy in Africa.44 The initial effort and expense in integrating primary prevention into national RHD programs can be expected to be more than offset by the reduction in the number of patients with severe valvular disease who will subsequently require expensive tertiary care. Finally, it cannot be overemphasized that RF/RHD is a disease of poverty. Therefore, over and above the preventive strategies, living conditions and access to healthcare must improve substantially in order to reduce disease burden in sub-Saharan Africa.

Prevalence of Rheumatic Heart Disease Detected by Echocardiographic Screening

Eloi Marijon, M.D., Phalla Ou, M.D., David S. Celermajer, Ph.D., F.R.A.C.P., Beatriz Ferreira, M.D., Ph.D., Ana Olga Mocumbi, M.D., Dinesh Jani, M.D., Christophe Paquet, M.D., M.P.H., Sophie Jacob, Ph.D., Daniel Sidi, M.D., Ph.D., and Xavier Jouven, M.D., Ph.D. Background Epidemiologic studies of the prevalence of rheumatic heart disease have used clinical screening with echocardiographic confirmation of suspected cases. We hypothesized that echocardiographic screening of all surveyed children would show a significantly higher prevalence of rheumatic heart disease. Methods Randomly selected schoolchildren from 6 through 17 years of age in Cambodia and Mozambique were screened for rheumatic heart disease according to standard clinical and echocardiographic criteria.

Results Clinical examination detected rheumatic heart disease that was confirmed by echocardiography in 8 of 3677 children in Cambodia and 5 of 2170 children in Mozambique; the corresponding prevalence rates and 95% confidence intervals (CIs) were 2.2 cases per 1000 (95% CI, 0.7 to 3.7) for Cambodia and 2.3 cases per 1000 (95% CI, 0.3 to 4.3) for Mozambique. In contrast, echocardiographic screening detected 79 cases of rheumatic heart disease in Cambodia and 66 cases in Mozambique, corresponding to prevalence rates of 21.5 cases per 1000 (95% CI, 16.8 to 26.2) and 30.4 cases per 1000 (95% CI, 23.2 to 37.6), respectively. The mitral valve was involved in the great majority of cases (87.3% in Cambodia and 98.4% in Mozambique). Conclusions Systematic screening with echocardiography, as compared with clinical screening, reveals a much higher prevalence of rheumatic heart disease (approximately 10 times as great). Since rheumatic heart disease frequently has devastating clinical consequences and secondary prevention may be effective after accurate identification of early cases, these results have important public health implications.

BIBLIOGRAPHY
Rheumatic heart disease / rheumatic fever. American Heart http://www.americanheart.org/presenter.jhtml?identifier=4709. Association. (2010).. Retrieved September 19, 19, 2010, 2010, from from

Manriquez, D.J.S. (2008) Right and left congestive heart failure. Retrieved http://www.slideshare.net/davejaymanriquez/right-and-left-congestive-heart-failure-presentation. Nursing2007: drug handbook (2007). Philippines: Lippincott Williams &n Wilkins.

September

Karthikeyan, G. & Mayosi, Bongani (2009 August 1). Is primary prevention of rheumatic fever the missing link in the control of rheumatic heart disease in Africa? Circulation: Journal of the American Heart Association. Sept. 19, 2010, from http://circ.ahajournals.org/cgi/content/full/120/8/709. Marijon, E. &et.al., (2007). Prevalence of rheumatic heart disease detected by echocardiographic screening. Th e new engl and journa l o f medicine. Retrieved September 19, 2010, http.://www.nejm.org/doi/pdf/10.1056/NEJMoa065085