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Cardiovascular Disorders Inflammatory Heart Disease Pathophysiology Rheumatic fever develops in some children and adolescents following pharyngitis with group A beta-hemolytic Streptococcus (ie,Streptococcus pyogenes). The organisms attach to the epithelial cells of the upper respiratory tract and produce a battery of enzymes allowing them to damage and invade human Rheumatic tissues. After an incubation period of 2-4 Fever/Rheumatic days, the invading organisms elicit an Heart Disease acute inflammatory response with 3-5 days of sore throat, fever, malaise, headache, and an elevated leukocyte count. Sign and Symptoms Common symptoms Common symptoms of rheumatic fever are described below. Arthritis Pain and swelling of the joints (arthritis) is the most common symptom of rheumatic fever, affecting three out of four people. Heart inflammation (carditis) Shortness of breath, particularly when you're physically active or when sleeping (it can often wake you up, gasping for breath). Persistent coughrapid heartbeat (tachycardia). Feeling tired all the time. Chest pain. Creditis can persist for several months, but itshould improve over Nursing Care 1) Decreased Cardiac Output Related to: a disturbance in the closure of the mitral valve (valve stenosis). 2) Ineffective Peripheral Tissue Perfusion Related to: decreased metabolism primarily due to vasoconstriction of peripheral blood vessels. 3) Acute Pain Related to: inflammation of the synovial membrane. time. Sydenham's chorea Sydenham's chorea is a term that describes a collection of symptoms related to inflammation of the nerves. These symptoms are: 4) Hyperthermia Related to: inflammation of the synovial membrane, and inflammation of the heart valves. 5) Imbalanced Nutrition, Less Than Involuntary and Body Requirements uncontrollable jerking and twitching of the body – most Related to: an increase in stomach acid caused by often, the hands and feet. difficulty with tasks requiring the sympathetic nervous fine hand movements, such as system compensation. writing. 6) Activity intolerance problems with balance. unusual emotional outbursts, Related to: muscle such as crying or laughing for weakness, prolonged bed rest or immobilization. no apparent reason. Skin rash The rash is usually painless, nonitchy and spreads slowly over the child's body. It may only be noticeable in children with fair skin. The rash usually comes and goes over the course of a few weeks or months, 7) Self-Care Deficit Related to: Musculoskeletal Disorders: polyarthritis / arthralgia and therapy bed rest. before disappearing altogether. It's rare for adults with rheumatic fever to develop a skin rash. Less common symptoms Less common symptoms of rheumatic fever include: Subcutaneous skin nodules – small painless bumps or lumps under the skin, usually found on the wrists, elbows and knees. a high temperature (fever) of 39C (102F) or above abdominal pain nosebleeds Endocarditis Endocarditis infection occurs along the edges of the heart valves. The lesions, called vegetations, are masses composed of fibrin, platelets, and infecting organisms, held together by agglutinating antibodies produced by the bacteria. As inflammation continues, ulceration may result in erosion or perforation of the valve cusps, leading to valvular incompetence, damage to the conduction pathway (if in the septal Endocarditis is rarely an obvious diagnosis for a generalist. It may present with a wide variety of clinical signs, some subtle; the diagnosis may be difficult or the signs misleading, and there is a wide differential diagnosis to consider. However, there is a wealth of clinical signs to look for. 8) Impaired Skin Integrity Related to: inflammation of the skin and tissue subcutaneous. 9) Risk for Impaired Gas Exchange Related to: the accumulation of blood in the lungs due to increased atrial filling. 10) Risk for Injury 1) Obtain a history of allergies prior to the administration of antibiotics. 2) Ensure patency of IV and prevent the complications of longterm IV therapy. area), or rupture of a sinus of Valsalva (if in the aortic area). Although endocarditis can affect native and prosthetic valves, infection seldom affects a previously normal heart – the majority (60%) of IE patients have a predisposing cardiac condition. Vegetations usually affect the left side of the heart, with the most common underlying lesions being mitral valve prolapse and degenerative mitral and aortic regurgitation. Constitutional symptoms Endocarditis should be considered in patients with vague or generalized constitutional symptoms such as fever, rigors, night sweats, anorexia, weight loss, or arthralgia. Cardiac signs The presence of a new murmur is very significant, as is a change in the nature of an existing murmur (a regurgitant murmur may disappear on worsening). Rheumatic disease is a risk factor for the Myocardial involvement or valvular development of endocarditis. Other dysfunction may both contribute to predisposing cardiac lesions include left ventricular failure. hypertrophic cardiomyopathy with associated mitral reflux, subaortic Skin lesions stenosis, and ventricular aneurysm. Endocarditis is indicated by: There are also congenital lesions that predispose adults to endocarditis: these Osler's nodes – tender include ventricular septal defect (VSD), lesions found on finger pulps bicuspid aortic valve, and coarctation of and thenar/hypothenar the aorta. eminences Janeway lesions – transient, nontender Vegetations occur when a high-pressure macular papules on palms or jet enters a low-pressure cavity through soles 3) Observe for signs and symptoms of complications such as CHF, renal failure, or emboli. 4) Educate the patient about his condition and the need for continued treatment and prophylactic antibiotics. 5) Teach the patient to recognize the symptoms of endocarditis and to seek medical assistance should symptoms recur. a narrow orifice. This explains why endocarditis complicates a small VSD, but is not associated with a large VSD, mitral stenosis, or an atrial septal defect. In the presence of a VSD, vegetations can be found on the right ventricular side of the VSD, on the tricuspid valve, or where the jet impinges on the right ventricular wall. Vegetations found in coarctation usually occur distal to the obstruction. Finally, in children, cyanotic heart disease is still the most common cause of endocarditis, and the risk does not diminish after surgical repair as prostheses carry their own risk. splinter hemorrhages petechiae (embolic or vasculitic) Clubbing– in long-standing disease. Eyes Roth spots (boat-shaped hemorrhages with pale centers, in retina) and conjunctival splinter hemorrhages may be found. Splenomegaly Splenic infarction may occur as a result of emboli. In this case, splenic palpation may be painful and tender, and a rub may be heard. Neurological An acute confusional state is common in patients with infective endocarditis (IE). Cerebral emboli, which usually affect the middle cerebral artery, result in hemiplegia and sensory dysfunction. Mycotic aneurysms also affect the middle cerebral artery, where rupture may cause a subarachnoid hematoma. Mycotic aneurysms can occur several years after endocarditis has been treated. Renal Infarction causes loin pain and hematuria. Immune complex deposition may result in glomerulonephritis. The pathogenesis of myocarditis is not entirely clear. However, in viralmediated myocarditis, animal models have implicated 3 significant mechanisms: An infectious organism directly invades the myocardium Myocarditis Local and systemic immunological activation quickly ensues Cellular (CD4+) and humoral (B-cell clonal multiplication) activation occurs, causing worsening local inflammation, anti-heart antibody production and further myonecrosis. Common myocarditis symptoms include: Chest pain Rapid or abnormal heart rhythms (arrhythmias) Shortness of breath, at rest or during physical activity Fluid retention with swelling of your legs, ankles and feet Fatigue Other signs and symptoms you'd have with a viral infection, such as a headache, body aches, joint pain, fever, a sore throat or diarrhea. Myocarditis in children When children develop myocarditis, they might have 1. Give a comfortable position (semifowler position). 2. Monitor pain characteristics and administer analgesics as needed and use salicylates around the clock. 3. Give O2 supplement and ensure saturation ˃90%. 4. Give drugs as indicated (Aspirin, Steroids). 5. Give anti pyretic drug if fever present. signs and symptoms including: Fever Fainting Breathing difficulties Rapid breathing Rapid or abnormal heart rhythms (arrhythmias) 6. Provide a calm and quite environment and give emotional support while patient is confined to hospital or home with restrictive intravenous therapy. 7. Check vital sign and record it carefully. 8. Carefully monitor intake output. 9. Closely monitor sign for cardiac tamponade. 10. Ensure bed rest to reduce myocardial oxygen requirements and reduce heart rate. 11. Ensure rest and activity according to degree of tolerance. 12. Ensure high protein, high carbohydrate, and low sodium diet to meet adequate nutrition. 13. Explain all procedures to patient that improve patient confidence. 14. Prepare patient for surgery if needed 15. If patient received surgical treatment, provide postsurgical care and instruction. 16. After surgery, monitor patient’s temperature, fever may be present for weeks. 17. Provide 4 hourly mouth cares and serve attractive meals that stimulate appetite. 18. Instruct to avoid people who have an upper respiratory tract infection. 19. Monitor for signs and symptoms of organ damage such as stroke (CVA, brain attack), meningitis, heart failure, myocardial infarction, glomerulonephritis , and splenomegaly. 20. Instruct patient and family about activity restrictions, medications, and signs and symptoms of infection. Pericarditis The pericardium consists of a 2-layered The symptoms of pericarditis pliable, fibroserous sac that covers the can include the following: surface of the heart. The inner layer, the visceral pericardium, is adherent to the Sharp pain in the chest, myocardium. It has a microvillous sometimes central, other surface that secretes pericardial fluid. times to the left; may The outer layer, or parietal pericardium, decrease in intensity when is contiguous with the inner layer. It is sitting up and leaning composed of collagen layers with forward. interspersed elastin fibrils. Both layers Palpitations are normally only 1 to 2 mm thick and a Shortness of breath, space containing 15 to 35 mL of especially when reclining. pericardial fluid separates them. The Minor fever. pericardium is perfused by the internal General weakness. mammary arteries and innervated by Swelling of the abdomen or the phrenic nerve. The pericardium legs. protects and restrains the heart. In Cough. addition, it determines cardiac filling Pain in the shoulder. patterns, limits chamber dilatation, and equilibrates compliance between the 2 ventricles. 1. Pain r/t pericardial inflammation. 2. Potential for decreased CO r/t cardiac tamponade (heart cannot fill up and pump out). 3. Knowledge deficit r/t procedures & 4. medications& f/u care. Valvular Heart Disease Mitral Stenosis Pathophysiology Sign and symptoms Mitral valve stenosis commonly The normal mitral valve has an orifice leads to shortness of breath, area of about 4 cm that permits free especially during exercise or when flow of blood from the left atrium into lying down. the left ventricle during diastole. As the Other common symptoms valve orifice becomes reduced in mitral include: stenosis, flow between left atrium and cough, with or without blood left ventricle is progressively impeded chest pain, or chest and pressure in the left atrium remains discomfort higher than that of the left ventricle. fatigue By restricting flow, mitral stenosis swelling in ankles and/or feet results in 2 primary pathophysiological respiratory infections consequences: plum-colored cheeks Increased left atrial pressure is If mitral valve stenosis is referred to the lungs, where it leads to severe, you may feel your congestion and the symptoms heart fluttering or beating associated with it rapidly. The restricted orifice limits filling of Rarely, you may feel discomfort in the left ventricle, thereby limiting your chest. Your chest might feel cardiac output. tight or constricted, or you may feel Thus, although left ventricular pain that radiates outward from contractility is usually normal, the your chest. pathophysiological effects of mitral stenosis produce a syndrome In some cases, mitral valve stenosis mimicking left heart failure. may not cause any symptoms, or the symptoms may appear only during exercise. You might develop Nursing Care Activity intolerance related to pulmonary congestion and decreased blood supply to meet the demands of the body. symptoms when your body undergoes stress such as during an infection or pregnancy. In addition to the common symptoms, children with this issue might experience slower growth. Mitral Regurgitation MR can be caused by organic disease (e.g., rheumatic fever, ruptured chordae tendineae, myxomatous degeneration, leaflet perforation) or a functional abnormality (i.e., a normal valve may regurgitate [leak] because of mitral annular dilatation, focal myocardial dysfunction, or both). Congenital MR is rare but is commonly associated with myxomatous mitral valve disease. Alternatively, it can be associated with cleft of the mitral valve, as occurs in persons with Down syndrome, or an ostium primum atrial septal defect. Acute mitral regurgitation Acute MR is characterized by an increase in preload and a decrease in afterload causing an increase in enddiastolic volume (EDV) and a decrease in end-systolic volume (ESV). This leads to an increase in total stroke volume When associated with coronary artery disease (CAD) and acute myocardial infarction (MI), significant acute MR is accompanied by the following symptoms: Dyspnea Fatigue Orthopnea Pulmonary edema (often the initial manifestation) The following may be noted with chronic MR: Some patients may remain asymptomatic for years. Patients may have normal exercise tolerance until systolic LV dysfunction develops, at which point they may experience Nursing Care Plans for Mitral insufficiency, or mitral regurgitation, Primary nursing care plans diagnosis: Activity intolerance related to diminished cardiac output (TSV) to supernormal levels. However, forward stroke volume (FSV) is diminished because much of the TSV regurgitates as the regurgitate stroke volume (RSV). This, in turn, results in an increase in left atrial pressure (LAP). According to the Laplace principle, which states that ventricular wall stress is proportional to both ventricular pressure and radius, LV wall stress in the acute phase is markedly decreased since both of these parameters are reduced. Chronic compensated mitral regurgitation In chronic compensated MR, the left atrium (LA) and ventricle have sufficient time to dilate and accommodate the regurgitant volume. Thus LA pressure is often normal or only minimally elevated. Because of the left ventricular dilatation via the process of eccentric hypertrophy, TSV and FSV are maintained. Wall stress may be normal to slightly increased as the radius of the LV cavity increases but the end-diastolic LV pressure remains normal. As the LV progressively enlarges, the mitral annulus may stretch and prevent the mitral valve leaflets symptoms of a reduced forward cardiac output. Patients may feel chest palpitations if AF develops as a result of chronic atrial dilatation. Patients with LV enlargement and more severe disease eventually progress to symptomatic congestive heart failure (CHF) with pulmonary congestion and edema. Palpation may reveal the following: Brisk carotid upstroke and hyperdynamic cardiac impulse. Prominent LV filling wave. Auscultation may reveal the following: Diminished S 1 in acute MR and chronic severe MR with defective valve leaflets. Wide splitting of S 2 as a from coapting properly during systole, thus worsening the MR and LV dilatation. Chronic decompensated mitral regurgitation In the chronic decompensated phase, muscle dysfunction has developed, impairing both TSV and FSV (although ejection fraction still may be normal). This results in a higher ESV and EDV, which in turn causes an elevation of LV and LA pressure, ultimately leading to pulmonary edema and, if left untreated, cardiogenic shock. Mitral Valve Prolapse Mitral valve prolapse (MVP) is characterized primarily by myxomatous degeneration of the mitral valve leaflets. In younger populations, there is gross redundancy of both the anterior and posterior leaflets and chordal apparatus. This is the extreme form of myoxomatous degeneration, known as Barlow’s syndrome. In older populations, however, MVP is characterized by fibroelastic deficiency, sometimes with superimposed chordal rupture due to a result of early closure of the aortic valve. S 3 as a result of LV dysfunction or increased blood flow across the MV. Accentuated P 2 if pulmonary hypertension is present. Characteristic murmur. Most people with mitral valve prolapse have no symptoms. They also never experience any health problems due to mitral valve prolapse. Consult with and refer to cardiologist for continued monitoringand follow-up. • Teach about MVP, including heart valve anatomy, physiology,and Chest pain is the most frequent symptom in people function, common manifestations of MVP, who have symptoms with and treatment mitral valve prolapse. The rationale. chest pain may be very bothersome and frightening, • Discuss symptoms of lack of connective tissue support. These anatomic abnormalities result in malcoaptation of mitral valve leaflets during systole, resulting in regurgitation. Mitral annular dilatation may also develop over time, resulting in further progression of mitral regurgitation (MR). Acute severe MR results in congestive heart failure symptoms without left ventricular dilatation. Conversely, chronic or progressively severe MR can lead to ventricular dilatation and dysfunction, neurohormonal activation, and heart failure. Elevation in left atrial pressures can result in left atrial enlargement, atrial fibrillation, pulmonary congestion, and pulmonary hypertension. Myxomatous proliferation is the most common pathologic basis for MVP, and it can lead to myxomatous degeneration of the loose spongiosa and fragmentation of the collagen fibrils. Disruption of the endothelium may predispose patients to infectious endocarditis and thromboembolic complications. However, the vast majority of patients with MVP have only but it does not increase the progressive mitral risk of heart attack, death, or regurgitation, and other heart problems. theneed to report these to the cardiologist. • Discuss recommended Mitral valve prolapse is the follow-up care and its most common cause rationale. of mitral regurgitation. • Allow to verbalize That's a condition in which some blood flows backward feelings and share concerns about MVP. through the mitral valve Encourage to attend an with each heartbeat. MVP support group meeting. Over years, moderate or • Discuss the prognosis severe mitral regurgitation for MVP, emphasizing can cause weakness of the that most clientslive heart muscle, known normal lives using diet as congestive heart failure. and lifestyle Symptoms of congestive management. heart failure include: • Instruct to keep a Shortness of breath with weekly record of exertion Swelling in the legs and feet symptoms and their frequencyfor 1 month. • Discuss lifestyle changes Mitral valve prolapse has to manage symptoms: also been associated with aerobic exercisewith other symptoms: Fluttering or rapid heartbeat warmup and cooldown periods; maintaining called palpitations adequatefluid intake, Shortness of breath, a minor derangement of the mitral valve structure that is usually clinically insignificant. especially with exercise Dizziness Passing out or fainting , known as syncope Panic and anxiety Numbness or tingling in the hands and feet especially during hot weather or exercise; relaxation techniques (e.g., meditation, deepbreathing exercises,music therapy, yoga, guided imagery, heat therapy, orprogressive muscle relaxation) to perform daily; avoiding caffeineand crash diets; forming healthy eating habits. • Teach about infective endocarditis risk and prevention withprophylactic antibiotics. Encourage notifying dentist and otherhealth care providers of MVP before dental or any invasive procedure. Aortic Stenosis The human aortic valve normally consists of three cusps or leaflets and has an opening of 3.0-4.0 square centimeters. When the left ventricle contracts, it forces blood through the valve into the aorta and subsequently to the rest of the body. When the left ventricle expands again, the aortic valve closes and prevents the blood in the aorta from flowing backward (regurgitation) into the left ventricle. In aortic stenosis, the opening of the aortic valve becomes narrowed or constricted (stenotic) (i.e., due to calcification). Degenerative aortic stenosis, the most common variety, and bicuspid aortic stenosis both begin with damage to endothelial cells from increased mechanical stress. Inflammation is thought to be involved in the earlier stages of the pathogenesis of AS and its associated risk factors are known to promote the deposition of LDL cholesterol and a highly damaging substance known as Lipoprotein(a) into the aortic valve resulting in significant damage and stenosis over time. Symptoms related to aortic stenosis Assist the patient in depend on the degree of stenosis. bathing, if necessary. Most people with mild to moderate 1. Provide a bedside aortic stenosis do not have commode because symptoms. Symptoms usually using a commode present in individuals with severe puts less stress on aortic stenosis, though they may the heart than occur in those with mild to using a bedpan. moderate aortic stenosis as well. 2. Offer diversional activities that are Angina physically Angina in setting of heart failure undemanding. also increases the risk of death. In 3. Alternate periods of people with angina, the 5-year rest to prevent mortality rate is 50% if the aortic extreme fatigue valve is not replaced. and dyspnea. 4. To reduce anxiety, Syncope allow the patient to Syncope(fainting spells) from express his aortic valve stenosis is usually concerns about the exertional. In the setting of heart effects of activity failure it increases the risk of death. restrictions on his In people with syncope, the 3 year resposibilities and mortality rate is 50%, if the aortic routine. valve is not replaced. 5. Keep the patient’s legs elevated while Congestive heart failure he sits in a chair to Congestive heart failure (CHF) improve venous As a consequence of this stenosis, the left carries a grave prognosis in people return in the heart. ventricle must generate a higher pressure with each contraction to effectively move blood forward into the aorta. Initially, the LV generates this increased pressure by thickening its muscular walls (myocardial hypertrophy). The type of hypertrophy most commonly seen in AS is known as concentric hypertrophy, in which the walls of the LV are (approximately) equally thickened. In the later stages, the left ventricle dilates, the wall thins, and the systolic function deteriorates (resulting in impaired ability to pump blood forward). Morris and Innasimuthu et al. showed that different coronary anatomy is associated with different valve diseases. Research is ongoing to see if different coronary anatomy might lead to turbulent flow at the level of valves leading to inflammation and degeneration. with AS. People with CHF attributable to AS have a 2-year mortality rate of 50% if the aortic valve is not replaced.[citation needed] CHF in the setting of AS is due to a combination of left ventricular hypertrophy with fibrosis, systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV). Associated symptoms In Heyde's syndrome, aortic stenosis is associated with gastrointestinal bleeding due toangiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve. 6. Place the patient in an upright position to relieve dyspnea. 7. Administer oxygen as needed to prevent tissue hypoxia. 8. Keep the patient in a low sodium diet. Consult with a dietitian to ensure that the patient receives foods that he likes while adhering to the diet restrictions. 9. Allow the patient to express his fears and concerns about the disorder, it’s impact on his life, and any impending surgery. 10. Monitor the patient’s vital signs, weight, and intake and output for signs of fluid overload. 11. Evaluate patient’s activity tolerance and degree of fatigue. 12. Monitor the patient for chest pain that may indicate cardiac ischemia. 13. Regularly assess the patient’s cardiopulmonary function. 14. Observe the patient for complications and adverse reactions to drug therapy. The pathophysiology of AR depends on whether the AR is acute or chronic. In acute AR, the LV does not have time to dilate in response to the volume load, whereas in chronic AR, the LV may undergo a series of adaptive (and maladaptive) changes. Acute aortic regurgitation Aortic Regurgitation Symptoms of aortic insufficiency Assess mental status are similar to those of heart (Restlessness, severe failure and include the following: anxiety and confusion). 1. Check vital signs (heart rate and Dyspnea on exertion blood pressure). Orthopnea 2. Assess heart Paroxysmal nocturnal sounds, noting dyspnea gallops, S3, S4. Palpitations Acute AR of significant severity leads to 3. Assess manually Angina pectoris increased blood volume in the LV during peripheral pulses Cyanosis (in acute cases) diastole. The LV does not have sufficient (with weak rate, time to dilate in response to the sudden rhythm indicated increase in volume. low cardiac output). Chronic aortic regurgitation 4. Assess lung sounds and determine any Chronic AR causes gradual left occurrence of ventricular volume overload that leads Paroxysmal to a series of compensatory changes, Nocturnal Dyspnea including LV enlargement and eccentric (PND) or hypertrophy. LV dilation occurs through orthopnea. the addition of sarcomeres in series 5. Monitor central (resulting in longer myocardial fibers), venous, right as well as through the rearrangement of arterial pressure myocardial fibers. [RAP], pulmonary arterial pressure(PAP) 6. Routinely Assess skin colour and temperature (Cold, clammy skin is secondary to compensatory increase in sympathetic nervous system stimulation and low cardiac output and desaturation). 7. Carefully maintain intake output and daily check weight. 8. Administer medication as prescribed, noting response and watching for side effects and toxicity. 9. Administer stool softeners as needed(s training for a bowel movement further impairs cardiac output). 10. Explain drug regimen, purpose, dose, and side effects. 11. Maintain adequate ventilation and perfusion (Place patient in semi- to high-Fowler’s position or supine position). 12. Administer O2 as ordered. 13. Assess response to increased activity and help patient in daily activities. 14. Maintain physical and emotional rest (restrict activity and provide quiet and relaxed environment). 15. Monitor sleep patterns; administer sedative. 16. If invasive adjunct therapies are indicated (e.g., intra-aortic balloon pump, pacemaker), maintain within prescribed protocol and prepare patient. 17. Explain diet restrictions (fluid, sodium). Tricuspid stenosis results from alterations in the structure of the tricuspid valve that precipitate inadequate excursion of the valve leaflets. The most common etiology is Tricuspid stenosis rheumatic fever, and tricuspid valve involvement occurs universally with mitral and aortic valve involvement. With rheumatic tricuspid stenosis, the valve leaflets become thickened and sclerotic as the chordae tendineae There are few symptoms to report. Many patients with this condition at times report feeling: tired and lethargic fragility a quivering feeling in the neck A rapid, irregular heartbeat called a palpitation, or both. Pain in the upper right part of their abdomen which may Assessment and treatment of the underlying aetiology for the valvular pathology (e.g., antibiotics for bacterial endocarditis or somatostatin analogues for carcinoid syndrome) 1. Fluid and sodium become shortened. The restricted valve be caused by an enlarged, opening hampers blood flow into the congested liver. right ventricle and, subsequently, to the Symptoms are rarely dramatic pulmonary vasculature. Right atrial enough to require surgery to enlargement is observed as a replace the tricuspid valve. consequence. The obstructed venous return results in hepatic enlargement, decreased pulmonary blood flow, and peripheral edema. Other rare causes of tricuspid stenosis include carcinoid syndrome, endocarditis, endomyocardial fibrosis, systemic lupus erythematosus, and congenital tricuspid atresia. In the rare instances of congenital tricuspid stenosis, the valve leaflets may manifest various forms of deformity, which can include deformed leaflets, deformed chordae, and displacement of the entire valve apparatus. Other cardiac anomalies are usually present. Tricuspid Regurgitation Normal tricuspid valves develop dysfunction with elevation of right ventricular systolic and/or diastolic pressure, right ventricular cavity enlargement, or tricuspid annular dilation with leaflet tethering. View image The pathological consequences of restriction 2. Medicines to treat cardiac arrhythmias secondary to right atrial distension (usually atrial fibrillation and/or flutter) 3. Pharmacotherapy with diuretics to reduce morbidity associated with systemic venous congestion. Activity is usually selflimited by the patient due to easy tiring and diminished pulmonary blood flow. Mild tricuspid regurgitation may 1. For patients in not cause any symptoms. whom tricuspid Symptoms of heart failure may regurgitation is occur, and can include: secondary to leftsided heart failure, Active pulsing in the neck veins treatment centers Decreased urine output on adequate advanced tricuspid regurgitation (TR) are related to a reduced cardiac output and elevated right atrial pressure, which, if long-standing, leads to atrial distension with reduced contractile reserve and atrial fibrillation. Often, patients with chronic severe TR will present with ascites from advanced liver disease from chronic congestion or fibrosis (cardiac cirrhosis), gut congestion with symptoms of dyspepsia or indigestion, and fluid retention with leg oedema. Fatigue, tiredness General swelling Swelling of the abdomen Swelling of the feet and ankles Weakness control of fluid overload and failure symptoms (eg, diuretic therapy). Patients should be instructed to reduce their intake of salt. Elevation of the head of the bed may improve symptoms of shortness of breath. 2. Digitalis, diuretics (including potassium-sparing agents), angiotensinconverting enzyme (ACE) inhibitors, and anticoagulants are all indicated in the care of these patients. Antiarrhythmics are added as needed to control atrial fibrillation. PS can be due to isolated valvular (90%), subvalvular, or peripheral (supravalvular) obstruction, or it may be found in association with more complicated congenital heart disorders. The characteristics of the various types of PS are described in this section. Valvular pulmonic stenosis Isolated valvular PS comprises approximately 10% of all congenital heart disease. Typically, the valve commissures are partially fused and the Pulmonic Stenosis 3 leaflets are thin and pliant, resulting in a conical or dome-shaped structure with a narrowed central orifice. Poststenotic pulmonary artery dilatation may occur owing to "jet-effect" hemodynamics. Subvalvular pulmonic stenosis Subvalvular PS occurs as a narrowing of the infundibular or subinfundibular region, often with a normal pulmonic valve. This condition is present in individuals with tetralogy of Fallot and can also be associated with a ventricular septal defect (VSD). Pulmonary valve stenosis affects the body’s ability to get oxygenated blood. Many children do not show symptoms until adulthood. Examples of pulmonary valve stenosis symptoms include: Sometimes, treatment may not be needed if the disorder is mild. When there are also other heart defects, medications may be used to: heart murmur Help blood flow prominent and enlarged jugular through the heart vein (prostaglandins) bluish tint to the skin Help the heart beat chest pain stronger fainting Prevent clots (blood heart palpitations thinners) unexplained fatigue Remove excess fluid failure to thrive (water pills) difficulty breathing Treat abnormal Pulmonary valve stenosis can cause heartbeats and sudden death in severe instances. rhythms This is why diagnosis and treatment is vital to your health. Percutaneous balloon pulmonary dilation (valvuloplasty) may be performed when no other heart defects are present. This procedure is done through an artery in the groin. The doctor sends a flexible tube (catheter) with a balloon attached to the end up to the heart. Special xrays are used to help guide the catheter. The balloon stretches the opening of the valve. Some patients may need heart surgery to repair or replace the pulmonary valve. The new valve can be made from different materials. If the valve cannot be repaired or replaced, other procedures may be needed. Double-chambered right ventricle is a rare condition associated with fibromuscular narrowing of the right ventricular outflow tract with right ventricular outflow obstruction at the subvalvular level. Pulmonic Regurgitation Incompetence of the pulmonic valve occurs by 1 of 3 basic pathologic Because pulmonic regurgitation is the result of other factors in the Pulmonic regurgitation is seldom severe enough to processes: dilatation of the pulmonic valve ring, acquired alteration of pulmonic valve leaflet morphology, or congenital absence or malformation of the valve. body, any noticeable symptoms are ultimately caused by an underlying medical condition rather than the regurgitation itself. warrant special treatment because the right ventricle normally adapts to low-pressure volume overload without However, more severe difficulty. High-pressure regurgitation may contribute to volume overload leads to right ventricular enlargement by right-sided heart strain dilation, and in later stages, right and, ultimately, heart heart failure. failure. 1. Underlying A diastolic decrescendo murmur etiologies causing can sometimes be identified,( heard severe pulmonic best) over the left lower sternal regurgitation, border whether congenital or acquired, must be treated to prevent or reverse right-sided heart strain and failure that may further complicate the clinical picture. 2. A discussion of therapeutic interventions in pulmonary hypertension by etiology is beyond the scope of this article. Refer to the articles for each entity under Differentials for a detailed discussion of treatment options. 3. If pulmonary hypertension is identified with pulmonic regurgitation, determining the etiology is essential to institute appropriate therapy as expeditiously as possible. For instance, primary pulmonary hypertension, secondary pulmonary hypertension due to thromboembolism, severe mitral stenosis, and pulmonary carcinomatosis can all manifest as severe pulmonary hypertension with pulmonic regurgitation. 4. No aspect of medical management of heart failure is uniquely applicable to pulmonic regurgitation, and the discussion of management of right-sided heart failure is beyond the scope of this article. In general, similar approaches to those used in the treatment of patients with leftsided congestive heart failure can be useful. In some circumstances, such as in patients with pulmonary hypertension, vasodilator therapies must be very carefully considered and monitored. In addition, therapies aimed toward the underlying etiology may also reduce pulmonic regurgitation (see Heart Failure). 5. The American Heart Association and the American College of Cardiology have published guidelines on the management of patients with valvular heart disease. The pathophysiology of cardiomyopathies is better understood at the cellular level with advances in molecular techniques. Mutant proteins can disturb cardiac function in the contractile apparatus (or mechanosensitive complexes). Cardiomyocyte alterations and their persistent responses at the cellular level cause changes that are correlated with sudden cardiac death and other cardiac problems. Cardiomyopathy Symptoms may appear at any age and usually include signs of pulmonary congestion and/or low cardiac output. There is often a history of fatigue and exertional symptoms for months or even years prior to diagnosis (Elliott, 2000). Symptoms are often progressive and can necessitate cardiac transplantation. Arrhythmias, thromboembolism and sudden death are common and may occur at any stage. Symptoms include dyspnoea, palpitations, reduced exercise capacity, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea, oedema and syncope. The presentation within a family may range from the asymptomatic patient, who requires no treatment, to heart failure and in some cases, sudden cardiac death. Cardiomyopathy is a chronic condition with extensive emotional and social ramifications. Anxiety levels are high, especially in symptomatic patients (Cox et al, 1997). Cardiomyopathy is genetically inherited in many cases, giving rise to fear of transmission and issues surrounding genetic counselling. Parents may feel guilty for passing on the condition and it can change family dynamics. The nurse is in an ideal position to help guide the family through the difficult stages of diagnosis and treatment and support the family through the screening process.