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1. Give the pathophysiology, sign / symptoms and nursing care for the following disorders. Inflammatory Heart Disease Rheumatic Fever/ Rheumatic Heart Disease Pathophysiology Endocarditis Inflammation of the endocardium (can involve any portion of the endothelial lining of the heart). • Relatively uncommon (1.5 to 6.2 cases per 100,000 people in developed countries) • Not fully understood • Thought to result from an abnormal immune response to M proteins of group A β- hemolytic streptococcal bacteria • Carditis, inflammation of the heart, develops in about 50% of people with RF; usually involve 3 layers of the heart: pericardium, myocardium and endocardium. • As inflammatory resolves, fibrous scarring occurs causing deformity (RHD). • Results to stenosis and regurgitation Sign and Symptoms Nursing Care • Fever and migratory join pains – initial manifestation Cardiac: chest pain, friction rub, heart murmur, S3, S4, cardiomegaly, pericardial effusion • Musculoskeletal: migratory polyarthritis: redness, heat, swelling, pain, and tenderness of more than one joint; usually affects large joint of extremities. • Integumentary: erythema marginatum: transitory pink, nonpruritic, macular lesion on trunk or inner aspect of upper arms or thighs; subcutaneous nodules over extension or wrist, elbow, ankle, and knee joints • T 39.4°C (101.5°F) + flulike symptoms, accompanied by cough, SOB, and join pain • Embolic complications • Heart murmur (90% in infective endocarditis); may Healht promotion • Prompt identification and treatment of streptococcal throat infections (red, fierylooking throat, pain with swallowing, enlarged and tender cervical lymph nodes, fever rage 38.3°C to 40°C) to decrease spread of pathogen and the risk for rheumatic fever. Assessment • Health history: assess risk for RF (prolonged, untreated or recurrent pharyngitis), complaints of sore throat with fever, difficulty swallowing, and general malaise Healht promotion • Prevention of endocarditis • Education is the key part of prevention Assessment • Physical examination: V/S, apical pulse and heart sounds; rate and ease of respirations, • Classified by its acuity and disease course Myocarditis • Infectious agent infiltrate interstitial Pericarditis Pericardial damage worsen or new murmur develop lung sound; skin color, temperature, and presence of petechiae or splinter hemorrhages. • Depends on the degree of myocardial damage of abscesses • Chest pain • Inflammatory • Abnormal heart process damage the sound: muffled S1, S3, murmur, local or diffuse pericardial friction swelling and damage. rub • Frequently assess for manifestations of heart failure: activity intolerance, UO, heart and breath sounds • During acute phase: hemodynamic monitoring and the ECG • Both physical and emotional rest are indicated, because anxiety increased myocardial oxygen demand • Classic manifestations: -release of chest pain, pericardial friction inflammatory rub (characteristic sign of pericarditis) vasodilation, and fever. hyperemia, and • Chest pain – the edema; increase most common is capillary permeability abrupt onset; -Escape of plasma caused by inflammation of proteins and nerve fibers in the fibrinogens into the lower parietal pericardial space pericardium and - influx of WBC to the pleura covering diaphragm. (Refer site of injury to to page 10 of this destroy the causative sheet.) Relieved by agent sitting upright and leaning forward as - exudate formation the heart moves away from the - inflammatory diaphragmatic side resolve without long- of the lung pleura. term effects or may • Low grade fever Healht promotion • Early identification and treatment of the disorder can reduce the risk of complications. • Promptly report a pericadial friction rub or othe rmanifestations of pericarditis in client with recent AMU, cardiac surgery, or systemic disease associated with a risk for pericarditis. Assessment produce scar tissue and adhesions between the pericardial layers - restrict cardiac function Valvular Heart Disease Mitral Stenosis • Dyspnea and tachycardia Chronic constrictive pericarditis • Tissue scarring of pericardial layers that leads contract, restricting diastolic filling and elevating venous pressure. • May follow viral infection, radiation therapy, or heart surger • Health History: complain of acute substernal or precordial chest pain, effect of movement and breathing on discomfort, pain radiation, associated symptoms; recent AMI, heart surgery, or other cardiac disorder; current medications; chronic conditions (e.g., RF, or connective tissue or autoimmune disorder) • Physical examination: V/S; variation in systolic BP with respirations; strength of peripheral pulses, variations with respiratory movement; apical pulse, clarity changes with respiratory movement, presence of a friction rub; neck vein distension; LOC, skin color, and other indicators of cardiac output. Pathophysiology Sign and symptoms Nusring Care • RHD or bacterial endocarditis; • Typical earliest manifestation: dyspnea on exertion (DOE) • Cough, hemoptysis, frequent pulmonary infections • Loud S1, split S2, mitral opening • the cardio-care six • observe closely for findings of heart failure, pulmonary edema, and reactions to drug therapy. • if client has had surgery, watch for hypotension, arrhythmias, and thrombus formation. reduces blood volume to left rising pressure in the left atrium; calcification of the valve leaflets (due to blo atrial hypertrophy and pulmonary congestion, increasing pressure in the hypertrophy of the R ventricle and Mitral Regurgit ation allowing blood to regurgitate during systole form L ventricle atrial hyperthrophy and pulmonary enlargement of the R ventricle. Mitral Valve Prolapse Excess tissue in the valve leaflets and ventricular blood regurgitates into the L atrium snap, diastole murmur: lowpitched, rumbling, crescendodecrescendo, heard best in the apical region; palpable thrill • Atrial dysrhythmias • explain the need for long-term antibiotic therapy and the need for additional antibiotics before dental care. • report early findings of heart failure such as dyspnea or a hacking, nonproductive cough. • Fatigue, weakness, DOE, orthopnea • Murmur: loud, highpitched, rumbling, and holosystoli c (occurring throughou t systole); accompani ed by palpable thrill, heard most clearly at the cardiac apex • May be asymptom atic • Severe or acute regurgitation: pulmonary congestion and edema • Tachydysr hythmias causing palpitation • the cardiocare six • monitor the cardio seven • if client has surgery, monitor postoperativel y for hypotension, arrhythmias and thrombus formation • diet restrictions and drugs • explain tests and treatments • prepare client for longterm antibiotic and follow-up care. • stress the need for prophylactic antibiotics during dental care. • Assess mental status (Restlessness, severe anxiety and confusion). s, lightheade dness, syncope • Progressiv e worsening : leads to heart failure, embolizati on may cause transient ischemic attacks (TIAs) • Most common symptom – atypical chest pain: left sided or substernal , frequently related to fatigue, not exertion • Usually asymptom atic • Audible midsystolic ejection click or murmur; high pitched last systolic murmur Aortic Stenosis The increased pressure load imposed by aortic stenosis results in compensatory hypertrophy of the left ventricle (LV) without cavity enlargement (concentric hypertrophy). With time, the ventricle can no longer compensate, Chest pain: Angina pectoris in patients with aortic 1. Assist the patient in bathing, if necessary. 2. Provide a bedside causing secondary LV cavity enlargement, reduced ejection fraction (EF), decreased cardiac output, and a misleadingly low gradient across the aortic valve (low-gradient severe AS). Patients with other disorders that also cause LV enlargement and reduced EF (eg, myocardial infarction, intrinsic cardiomyopathy) may generate insufficient flow to fully open a sclerotic valve and have an apparently small valve area even when their AS is not particularly severe (pseudosevere AS). Pseudosevere AS must be differentiated from low-gradient severe AS because only patients with low-gradient severe AS benefit from valve replacement. Elevated shear stress across the stenosed aortic valve degrades von Willebrand factor multimers. The resulting coagulopathy may cause GI bleeding in patients with angiodysplasia (Heyde syndrome). stenosis is typically precipitate d by exertion and relieved by rest Heart failure: Symptoms include paroxysm al nocturnal dyspnea, orthopnea, dyspnea on exertion, and shortness of breath Syncope : Often occurs upon exertion when systemic vasodilatat ion in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline 3. 4. 5. 6. commode because using a commode puts less stress on the heart than using a bedpan. Offer diversional activities that are physically undemandi ng. Alternate periods of rest to prevent extreme fatigue and dyspnea. To reduce anxiety, allow the patient to express his concerns about the effects of activity restrictions on his resposibilitie s and routine. Keep the patient’s legs elevated while he sits in a chair to improve venous return in the heart. 7. Place the patient in an upright position to relieve dyspnea. 8. Administer oxygen as needed to prevent tissue hypoxia. 9. 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. 10. Allow the patient to express his fears and concerns about the disorder, it’s impact on his life, and any impending surgery. 11. Monitor the patient’s vital signs, weight, and intake and output for signs of fluid overload. 12. Evaluate patient’s activity tolerance and degree of fatigue. 13. Monitor the patient for chest pain that may indicate cardiac ischemia. 14. Regularly assess the patient’s cardiopulmo nary function. 15. Observe the patient for complicatio ns and adverse reactions to drug therapy. Aortic Regurgit ation Incompetent closure of the aortic valve can result from intrinsic disease of the leaflets, cusp, diseases of the aorta, or trauma. Diastolic reflux through the aortic valve can lead to left ventricular volume overload. An increase in systolic stroke volume and low diastolic aortic pressure produces an increased Mild aortic regurgitation may produce few symptoms. People with more severe aortic regurgitation may notice heart palpitations, chest pain, fatigue, or shortness of breath. Other symptoms include difficulty breathing when lying down, weakness, fainting, or swollen ankles and feet. 1. Electrocardiogram ECG is rarely normal in chronic aortic regurgitation and often exhibit significant changes in repolarization. On acute aortic regurgitation ECG may be normal. Visible image of left ventricular hypertrophy, increased amplitude QRS, ST-Tshaped type of diastolic overload, meaning that the average vector showed that ST is great, and and T wave vector parallel to the average of pulse pressure. The clinical signs of AR are caused by the forward and backward flow of blood across the aortic valve, leading to increased stroke volume. [5] The severity of AR is dependent on the diastolic regurgitant valve area, the diastolic pressure gradient between the aorta and LV, and the duration of diastole. 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 Acute AR of significant severity leads to increased blood volume in the LV during diastole. The LV does not have sufficient time to dilate in response to the sudden increase in volume. As a result, LV enddiastolic pressure increases rapidly, causing an increase in pulmonary venous pressure and altering coronary flow dynamics. As pressure increases throughout the pulmonary circuit, the patient develops dyspnea and pulmonary the QRS complex. Figure shows the P-R interval lengthening. 2. Thorax Radiography Shows a progressive enlargement of the heart. Namely an enlarged left ventricle, left atrium, and aortic dilatation. The shape and size of the heart was unchanged in acute insufficiency but looks pulmonary edema. 3. Transthoracic Echocardiography Exposing the base of the proximal aorta on imaging. 4. Aortography. 5. Increased cardiac isoenzyme (CPK and ck mb) 6. Cardiac catheterization 7. Transesophageal Echocardiography (TEE) edema. In severe cases, heart failure may develop and potentially deteriorate to cardiogenic shock. Decreased myocardial perfusion may lead to myocardial ischemia. Early surgical intervention should be considered (particularly if AR is due to aortic dissection, in which case surgery should be performed immediately). Chronic aortic regurgitation Chronic AR causes gradual left ventricular volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through the addition of sarcomeres in series (resulting in longer myocardial fibers), as well as through the rearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume. The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that result from LV dilation (Laplace law). During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased (due to the increased preload and the Frank-Starling mechanism). Patients may remain asymptomatic during this period. As AR progresses, LV enlargement surpasses preload reserve on the Frank-Starling curve, with the EF falling to normal and then subnormal levels. The LV end-systolic volume rises and is an indicator of progressive myocardial dysfunction. Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may worsen during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Grossly, the LV gradually transforms from an elliptical to a spherical configuration. Tricuspid Stenosis 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 There are few symptoms to report. Many patients with this condition at times report feeling: tired and lethargic fragility a quivering In the treatment of tricuspid stenosis, medical care consists of assessment and treatment of the underlying cause of the valvular 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 become shortened. The restricted valve opening hampers blood flow into the right ventricle and, subsequently, to the pulmonary vasculature. Right atrial enlargement is observed as a 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, end omyocardial fibrosis, systemic lupus erythematosus, and congenital tricuspid atresia Tricuspid Regurgit ation The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetence can result from primary structural abnormalities of the leaflets and chordae or, more often, be secondary to myocardial dysfunction and dilatation. [1] Tricuspid valve insufficiency feeling in the neck a rapid, irregular heartbeat called a palpitation, or both. pain in the upper right part of their abdomen which may be caused by an enlarged, congested liver. Symptoms are rarely dramatic enough to require surgery to replace the tricuspid valve. Dyspnea on exertion Orthopn ea Paroxys mal nocturnal dyspnea Ascites Peripher pathology, as follows: Treat bacterial endocarditis with the appropriate antibiotics as determined by the sensitivity of the organisms cultured. Medically address cardiac arrhythmias depending on their characterizati on. Decreasing right atrial volume overload with diuresis and salt restriction helps decrease symptoms and improve hepatic function. 1. Assess mental status (Restlessness , severe anxiety and confusion). 2. Check vital signs (heart rate and blood due to leaflet abnormalities may be secondary to endocarditis or rheumatic heart disease. When due to the latter, it generally occurs in combination with tricuspid stenosis. Ebstein anomaly is the most common congenital form of tricuspid regurgitation. Inspiration increases the severity of tricuspid regurgitation. Inspiration induces widening of the RV, which enlarges the tricuspid valve annulus and thus increases the effective regurgitant orifice area. [2] Chronically, tricuspid regurgitation leads to RV volume overload, which results in right-sided congestive heart failure (CHF). This manifests as hepatic congestion, peripheral edema, and ascites al edema 3. 4. 5. 6. 7. pressure). Assess heart sounds, noting gallops, S3, S4. Assess manually peripheral pulses (with weak rate, rhythm indicated low cardiac output). Assess lung sounds and determine any occurrence of Paroxysmal Nocturnal Dyspnea (PND) or orthopnea. Monitor central venous, right arterial pressure [RAP], pulmonary arterial pressure(PA P) Routinely Assess skin colour and temperature (Cold, clammy skin is secondary to compensator y increase in sympathetic nervous system stimulation and low cardiac output and desaturation) . 8. Carefully maintain intake output and daily check weight. 9. Administer medication as prescribed, noting response and watching for side effects and toxicity. 10. Administer stool softeners as needed(s training for a bowel movement further impairs cardiac output). 11. Explain drug regimen, purpose, dose, and side effects. 12. Maintain adequate ventilation and perfusion (Place patient in semito highFowler’s position or supine position). 13. Administer O2 as ordered. 14. Assess response to increased activity and help patient in daily activities. 15. Maintain physical and emotional rest (restrict activity and provide quiet and relaxed environment ). 16. Monitor sleep patterns; administer sedative. 17. If invasive adjunct therapies are indicated (e.g., intraaortic balloon pump, pacemaker), maintain within prescribed protocol and prepare patient. 18. Explain diet restrictions (fluid, sodium). Pulmonic Stenosis Congenital pulmonary stenosis occurs due to improper development of the pulmonary valve in the first 8 weeks of fetal growth. It can be caused by a number of factors, though most of the time this heart defect occurs by chance, with no clear reason evident for its development. Some congenital heart defects may have a genetic link that causes heart problems to occur more often in certain families. Heavy or rapid breathing Shortness of breath Fatigue Rapid heart rate Swelling in the feet, ankles, face, eyelids, and/or abdomen Chest Xray. A diagnostic test that uses X-ray beams to produce images of internal tissues, bones, and organs onto film. Electrocardio gram (ECG or EKG). A test that records the electrical activity of the heart, shows abnormal rhythms (arrhythmias), and detects heart muscle stress. Echocardiogr am (echo). A procedure that evaluates the structure and function of the heart by using sound waves recorded on an electronic sensor that produce a moving picture of the heart and heart valves. Pulmonic Regurgit ation Incompetence of the pulmonic valve occurs by 1 of 3 basic pathologic processes: dilatation of the pulmonic valve ring, acquired alteration of pulmonic valve leaflet morphology, or congenital Most patients with mild to moderate pulmonary valve regurgitation do not experience any symptoms. They may lead a normal life. Patients with a more severe Cardiac catheterization. A cardiac catheterization is an invasive procedure that gives very detailed information about the structures inside the heart. Under sedation, a small, thin, flexible tube (catheter) is inserted into a blood vessel in the groin, and guided to the inside of the heart. Blood pressure and oxygen measurements are taken in the four chambers of the heart, as well as the pulmonary artery and aorta. Contrast dye is also injected to more clearly visualize the structures inside the heart. Pulmonic regurgitation is seldom severe enough to warrant special treatment because the right ventricle normally adapts to lowpressure volume overload without absence or malformation of the valve. degree of PR may experience some of these symptoms: difficulty. Highpressure volume overload leads to right-sided heart strain and, Fatigue ultimately, heart Shortness of failure. Underlying breath, especially etiologies causing during exertion severe pulmonic Chest pain regurgitation, whether congenital Palpitations or acquired, must Enlarged liver be treated to Fainting with prevent or reverse exercise right-sided heart Exercise strain and failure intolerance that may further complicate the clinical picture. 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. 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. 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 Cardiomyopathy Dilated cardiomyopathy is characterized by ventricular chamber enlargement and systolic dysfunction with greater left ventricular (LV) cavity size with little or no wall hypertrophy. Hypertrophy can be judged as the ratio of LV mass to cavity size; this ratio is decreased in persons with dilated cardiomyopathies. The enlargement of the remaining heart chambers is primarily due to LV failure, but it may be secondary to the primary cardiomyopathic process. Dilated cardiomyopathies are associated with both systolic and diastolic dysfunction. The Symptoms are a good indicator of the severity of dilated cardiomyopathy and may include the following: Fatigue Dyspnea on exertion, shortness of breath, cough Orthopnea, paroxysmal nocturnal dyspnea Increasing edema, weight, or abdominal girth On physical examination, look for signs of heart failure and volume overload. Assess vital signs with specific attention to the following: Tachypnea Tachycardia Hypertension or hypotension 1. 2. 3. 4. 5. 6. Provide oxygen at 2 to 4 L/min to maintain or improve oxygenation. Minimize oxygen demand by maintaining the patient at bed rest. Provide liquid diet on acute phase, Administer diuretic as prescribed to reduce preload and afterload. Monitor serum potassium before and after administration of loop diuretics. Prophylactic heparin may be ordered to prevent thromboembolu s formation decrease in systolic function is by far the primary abnormality due to adverse myocardial remodeling that eventually leads to an increase in the end-diastolic and end-systolic volumes. Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further diminish the cardiac output and increase endsystolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction. Early compensation for systolic dysfunction and decreased cardiac output is accomplished by increasing the stroke volume, the heart rate, or both (cardiac output = stroke volume × heart rate), which is also accompanied by an increase in peripheral secondary to venous poisoning. 7. Institute pressure ulcer prevention strategies secondary to hypoperfusion or vasoconstrictio n agents. vascular tone. The increase in peripheral tone helps maintain appropriate blood pressure. Also observed is an increased tissue oxygen extraction rate with a shift in the hemoglobin dissociation curve.