Infective diseases of heart


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  • Findings include:Progressive, frequently severe sharp chest pain , worse on deep inspiration and especially when lying supine: pain relieved by sitting.Pain referred totrapezius muscle (shoulder, upper back).*Hallmark finding in acute pericarditis- pericardial friction rub(click to hear);leathery grating sound produced by inflamed layers rubbing together; heard most clearly at left lower sternal border with client sitting and leaning forward.. *It is caused by the beating of the heart against an inflamed pericardium or lung pleura, which itself has a wide variety of etiologies…sound is usually continuous, and heard diffusely over the chest. It typically has three components, one systolic and two diastolic. The systolic occurs with ventricular contraction, and the diastolic occurs during both rapid ventricular filling and atrial contraction. It is accentuated when the patient sits up and leans forward, and may be accentuated during inspiration. If the rub completely disappears when the patient holds his breath it is more likely due to pleural, not pericardial, origin.
  • Place patient in position of comfort; take systolic BPduring baseline respiration.Raise sphygmomanometer pressure until Korotkoff sounds disappear.Lower pressure slowly until first Korotkoff sounds are heard during early expiration with their disappearance during inspirationRecord this pressure.Very slowly lower pressure (1mm at a time) until Korotkoff sounds heard throughout respiratory cycle with even intensity.Record this pressure.The difference between the two recorded pressures is Pulsus Paradox.Hemodynamically significant pulsus paradox is greater than or equal to 10 but look at trends. People with COPD may have a paradox due to increased thoracic pressures.
  • Infective diseases of heart

    1. 1. INFECTIVE DISEASES OF HEART MS. MINU SHARMA MSc Nursing 2nd yr. Himalayan College of Nursing, Dehradun
    2. 2. INFECTIVE DISEASES OF HEART The infections are named for the layer of heart most involved in the infectious process:  Pericarditis (pericardium)  Myocarditis (myocardium)  Endocarditis (endocardium)
    3. 3. PERICARDITIS  Pericarditis refers to the inflammation of the pericardium, the membraneous sac enveloping the heart.
    4. 4. Incidence  Incidence varies with the cause.  Pericarditis occurs after pericardectomy in 5 % - 30% patients.  1% - 3 % of cases develop after 10 days to 2 months after acute myocardial infarction.  Pericarditis may be acute or chronic.
    5. 5. Pericarditis Acute Pericarditis Chronic Pericarditis
    6. 6. Acute pericarditis Serous pericarditis Fiberous pericarditis Purulent pericarditis Hemorrhagic pericarditis Chronic pericarditis Adhesive mediastino pericarditis Constrictive pericarditis
    7. 7. Acute pericarditis  Serous pericarditis is usually caused by noninfectious inflammation such as occurs in rheumatoid arthritis and systemic lupus erythematosus .
    8. 8.  Fibrous and serofibrinous pericarditis represent the same basic process and are the most frequent type of pericarditis. Common causes include acute myocardial infarction (MI), postinfarction (including Dressler syndrome), uremia, radiation and trauma
    9. 9.  Purulent or suppurative pericarditis due to causative organisms may arise from direct extension, hematogenous seeding, or lymphatic extension, or by direct introduction during cardiotomy. Immunosuppression facilitates this condition. Clinical features include fever, chills, and spiking temperatures. Constrictive pericarditis is a serious potential complication.
    10. 10.  Hemorrhagic pericarditis involves blood mixed with a fibrinous or suppurative effusion, and it is most commonly caused by tuberculosis or direct neoplastic invasion. This condition can also occur in severe bacterial infections. Hemorrhagic pericarditis is common after cardiac surgery and may cause tamponade. The clinical significance is similar to suppurative pericarditis
    11. 11. Chronic pericarditis Adhesive mediastino pericarditis is a reaction that usually follows suppurative or caseous pericarditis, cardiac surgery, or irradiation.  This condition is rarely caused by a simple fibrinous exudate.  The pericardial potential space is obliterated, and adhesion of the external surface of the parietal layer to surrounding structures occurs.
    12. 12.  Clinically, systolic contraction of the ribcage and diaphragm and pulsus paradoxus may be observed.  The increased workload may cause massive cardiac hypertrophy and dilatation, which can mimic an idiopathic cardiomyopathy.
    13. 13.  Constrictive pericarditis is usually caused by suppurative, caseous, or hemorrhagic pericarditis. The heart may become encased in a 0.5-cm–thick to 1-cm–thick layer of scar or calcification, resembling a plaster mold.
    14. 14. Etiology  INFECTION Viral infection :  Accounts for 1-10% of cases.  The disease is usually a short self-limited disease that lasts 1-3 weeks and can occur as seasonal epidemics, especially coxsackievirus B and influenza.
    15. 15.  Causative viruses include coxsackievirus B, echovirus, adenoviruses, influenza A and B viruses, enterovirus, mumps virus, Epstein-Barr virus, human immunodeficiency virus (HIV), herpes simplex virus (HSV) type 1, varicella-zoster virus (VZV), measles virus, parainfluenza virus (PIV) type 2, and respiratory syncytial virus (RSV), cytomegalovirus (CMV), and hepatitis viruses A, B, and C (HAV, HBV, HCV).
    16. 16. Bacterial infections  Accounts for 1-8% of pericarditis cases Result from direct pulmonary extension, hematogenous spread, myocardial abscess or endocarditis, penetrating injury to chest wall from either trauma or surgery, or a subdiaphragmatic suppurative lesion.
    17. 17. Parasitic : Parasitic organisms include Entamoeba, Echinococcus, and Toxoplasma. Fungal : Fungal organisms that may cause acute pericarditis include Histoplasma, Blastomyces, Coccidioides, Aspergillus, and Candida. Myocardial injury
    18. 18. Cont...  Myocardial injury Myocardial infarction Cardiac trauma Post cardiac surgery Hypersensitivity
    19. 19. Cont...  Collagen diseases Rheumatic fever: Pericarditis in those with rheumatic fever occurs more commonly in lower socioeconomic groups and in children, often accompanying endocarditis and myocarditis, with a worse prognosis. Consider rheumatic fever as an etiology in any child with pericarditis.
    20. 20. Scleroderma :Scleroderma refers to a group of rare chronic autoimmune diseases in which the skin and connective tissues tighten and harden; it is a progressive disease. Inflammation of the lining around the heart (the pericardium)develops pericarditis ; causes chest pain and fluid build-up around the heart (pericardial effusion). Systemic lupus erythematosus Rheumatoid arthritis
    21. 21.  Drug reaction Procainamide : Pericarditis can also develop from a drug-induced lupus syndrome caused by medications including procainamide, hydralazine, methyldopa, isoniazid, mesalazine, and reserpine. Doxorubicin: The anthracycline antineoplastic agents, such as doxorubicin and cyclophosphamide, have direct cardiac toxicity and can cause acute pericarditis Penicillin : Penicillin and cromolyn sodium, induce pericarditis through a hypersensitivity reaction
    22. 22.  Methysergide: Methysergide antimigraine drug belongs to the group of medicines known as ergot alkaloids. It causes constrictive pericarditis through mediastinal fibrosis
    23. 23.  Smallpox vaccination infrequently leads to myocarditis. IN A REVIEW of a large vaccination program in the US military, approximately 12 per 100,000 vaccinated troops developed myopericarditis within 14 days of vaccination. Whether this was due to a direct viral cytopathic effect or an immune-mediated phenomenon is unclear.
    24. 24. Cont...  Radiation therapy  Cobalt therapy  Metabolic disorders Uremia Myedema  Chronic anemia  Neoplasm  Aortic dissection
    25. 25. Acute pericarditis. fibers covering surface of heart.
    26. 26. Clinical Manifestations  PHYSICAL EXAMINATION FINDING Dyspnea/tachypnea, particularly in patients with sizable effusions Pericardial friction rub : Pericardial friction rubs are triphasic : (1) An atrial systolic rub that precedes S1 (2) A ventricular systolic rub occurs between S1 and S2 and is coincident with the peak carotid pulse (3) An early diastolic rub occurs after S2 (usually the faintest). Diaphragm at LL sternal, lean forward, listen at inspiration
    27. 27. • Ewart sign: Ewart's sign is a set of findings on physical examination in people with large collections of fluid around their heart (pericardial effusions).Dullness to percussion ("woody" in quality), egophony, and bronchial breath sounds may be appreciated at the inferior angle of the left scapula when the effusion is large enough to compress the left lower lobe of the lung • Fever usually low grade but occasionally reach 104°F [40°C] • Varying degrees of consciousness may also be present
    28. 28. ◦ Tachycardia and cardiac arrhythmias, such as premature atrial and ventricular contractions, are occasionally present ◦ Pulsus paradoxus occurs in 70-80% of patients with pericardial tamponade and is measured by careful auscultation with a blood pressure cuff. The first sphygmomanometer reading is recorded at the point when the beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the respiratory cycle.
    29. 29.  A difference of more than 10 mm Hg defines pulsus paradoxus. This decrease is important in patients with more slowly developing tamponade, because they may lack findings of the Beck triad. If an associated hemorrhage is outside pericardial sac, hypotension and tachycardia without elevated jugular venous distension may be found.
    30. 30. In Constrictive Pericarditis : -  Pedal edema  Hepatomegaly  Ascites  JVD  Kussmaul’s sign  Pericardial knock (early diastolic sound) heard at the apex  Usually - no friction rub
    31. 31.  CLINICAL FINDING  Palpitations may be the presenting complaint, but chest pain is the cardinal symptom of pericarditis  Common associated signs and symptoms include low-grade intermittent fever, dyspnea/tachypnea
    32. 32. In uremic patients, heart rates may be deceptively slow with tamponade, fever, and hypotension due to autonomic impairment. Patients with cardiac tamponade may present subacutely with symptoms of anxiety, dyspnea, fatigue, or altered mental status. They may have a history of medical illnesses associated with pericardial involvement, particularly end-stage renal
    33. 33. Complications of Pericarditis  Pericardial Effusion  Cardiac Tamponade
    34. 34. Pericardial Effusion  Can occur rapidly or slowly  Pulmonary compression-cough, dyspnea, and tachypnea  Phrenic nerve art sounds distant, muffled  Slow build-up; no immediate effects  If rapid  compression of heart  tamponade!
    35. 35. Cardiac Tamponade  Compression of heart  Occur acutely (trauma) or sub-acutely (malignancy)  Symptoms- chest pain, confusion, anxious, ^ CVP, restless, muffled heart sounds  Later- tachypnea, tachycardia, and dec. CO, NVD and pulsus paradoxus  With slow onset dyspnea may be only symptom
    36. 36. PERICARDIUMCARDIAC TAMPONADE Original heart size Excess pericardial fluid
    37. 37. Cardiac tamponade Physiology- Paradoxical pulse is a pulse that markedly decreases in amplitude during inspiration. On inspiration, more blood is pooled in the lungs and so decreases the return to the left side of the heart; this affects the consequent stroke volume. Definition- a decrease in systolic BP with inspirations that is exaggerated in cardiac tamponade
    38. 38. Collaborative Care -Pericarditis, Pericardial Effusion, Cardiac Tamponde  Diagnostic Tests  Medications  Surgical/Therapeutic Interventions  Nursing Diagnosis/Interventions
    39. 39. Diagnostic Tests- to R/O  CBC-inc. WBC, ESR, and CRP  Cardiac Enzymes- inc. but not as much as with MI  EKG- diffuse St elevation *important to different from MI changes (acute pericarditis)  Echo- for wall movement  CXR; Doppler imaging  CT or MRI- for pericardial effusion  Pericardiocentesis fluid- determine cause; treat cardiac tamponade
    40. 40. Medications-  ASA or tylenol Acetaminophen decreases fever and pain , but does not help inflammation.Adult dosing is 2 regular strength (325 mg) every 4 hours or 2 extra-strength (500 mg) every 6 hours. Maximum dose is 4,000 mg per day.  NSAIDS : Drug-induced pericarditis treatment includes stopping the administration of the offending agent and anti-inflammatory therapy as needed. Treatment is with aspirin or NSAIDs
    41. 41.  NSAID regimens — The 2004 European Society of Cardiology guidelines recommended the use of an NSAID for the treatment of acute pericarditis. Commonly used NSAID regimens include :  Ibuprofen — Depending on the severity of the pericarditis and individual medication response, a dose of 400 to 800 mg of ibuprofen three times daily is usually adequate for symptom relief. Ibuprofen can be the preferred NSAID because of its rare side effects, favorable impact on coronary artery blood flow, and large
    42. 42.  Indomethacin — Indomethacin can be administered at a dose of 50 mg three times daily for one to two weeks followed by slow tapering.  Aspirin — Aspirin can be given at a dose of 750 to 1000 mg every six to eight hours followed by gradual tapering every week for a treatment period of three to four weeks.
    43. 43.  Corticosteroids  Anti-anxiety medication proton pump inhibitors
    44. 44. Surgical/invasive Interventions (remove fluid-treat tamponade)  Pericardiocentesis ◦ Hook needle to V lead- guided by EKG and echo ◦ Look for ST elevation ◦ Withdraw fluid ◦ Afterward watch for cardiac tamponade (PP), dysrhythmias, pneumothorax  Pericardial window  Percutaneous balloon pericardiotomy  Sclerosing agent- tetracycline (Bonds layers together)
    45. 45. Pericardiocentesis
    46. 46. Procedure in which opening is made in pericardium to drain fluid that has accumulated around heart-ericardial window can be made via a small incision below end of the breastbone (sternum) or via a small incision between the ribs on the left side of chest. Pericardial Window
    47. 47. Nursing Diagnosis for Pericarditis  Acute pain related to tissue ischemia secondary to arterial occlusion, tissue inflammation as evidenced by patient facial expression .  Ineffective Breathing Pattern related to inflammatory process as evidenced by dyspnea  Risk for Decreased Cardiac Output related to structural abnormalities of the heart  Activity Intolerance related to imbalance between oxygen supply and metabolic
    48. 48. Nursing Management  Collaboration of oxygen and delivery of analgesic drugs and drug side effects observed.  Observation of vital signs.  Perform 12 lead ECG, 24 lead if necessary  Recognize complications  Bed rest with Fowler position / semi- Fowler position client with pillows.  Positioning/sit up/lean forward
    49. 49.  Instruct client to deep breathe or use incentive spirometer every 1 - 2 hours  Space activities  Prevent complications of immobility  Psychological support  Appropriate medication selection
    50. 50. Research study  A systematic review was performed in Europe to assess the efficacy and safety of colchicine for pericarditis prevention. Randomised clinical trials on pharmacological prevention of pericarditis were included. study found that colchicine 0.5-1.0 mg daily was safe and efficacious for the primary and secondary prevention of pericarditis and should be considered as first line therapy for pericarditis prevention.
    51. 51. Myocarditis Myocarditis-uncommon inflammation of heart muscle
    52. 52. Etiology  Virus  Bacterial infection  HIV infection  Lyme’s disease  Giant cell  Chagas’ disease
    53. 53.  Other agents are also able to provoke myocarditis, such as alcohol, radiation, chemicals, and drugs
    54. 54.  A recent study also showed that severe emotional stress could produce heart failure that starts abruptly, with evidence of inflammation of heart muscle as well.
    55. 55. Myocarditis- infection in muscles of heart; most commonly caused by Coxsackie B virus that follows a respiratory or viral illness, bacteria and other infectious agents
    56. 56. Risk factor-myocarditis  Treatment of URI  Toxic or chemical effects  Autoimmune disorders  Post pericarditis  Metabolic-lupus  Heat stroke or hypothermia
    57. 57. PATHOPHYSIOLOGY Viral, bacterial, mycotic, parasitic, protozoal, or spirochetal infection. Myocarditis
    58. 58.  It also may occur in patient after acute systemic infection such as rheumatic fever, in those receiving immunosuppressive therapy, or in those with infective endocarditis
    59. 59. Clinical Findings  Systemic signs/symptoms  Chest pain due to coexisting pericarditis  Pericardial friction rub  In severe cases - symptoms of progressive heart failure like CHF, pulmonary rales, pedal edema  Frequent manifestation are fatigue, dyspnea, palpitation and chest pain
    60. 60.  Tachycardia, dysrhytmia  Fatigue  Joint pain or swelling  Leg swelling  Shortness of breath
    61. 61.  Pericarditis frequently occurs with myocarditis- check friction rub  Congestive heart failure  Pulmonary involvement  Sudden death
    62. 62. Diagnostic Tests A physical examination may show no abnormalities, or may reveal the following:  Abnormal heartbeat  Fever  Tachycardia  Edema in the legs
    63. 63.  An Electrocardiogram : T wave inversions; saddle-shaped ST- segment elevations may be present.  A Chest X-Ray
    64. 64.  Echocardiogram  Magnetic resonance imaging (MRI) scan  Heart biopsy  Elevated C-reactive protein (CRP) and/or Erythrocyte sedimentation rate (ESR)
    65. 65.  Markers of myocardial damage  Biopsy
    66. 66. Medications  In the acute phase, supportive therapy  For symptomatic patients, digoxin and diuretics.  For patients with moderate to severe dysfunction, cardiac function can be supported use of :  Antibiotics  Oral therapy with ACE inhibitors (Captopril, Lisinopril)
    67. 67.  Inotropes  Antiviral with interferon-a  Corticosteroids or immunosuppressents  HF drugs-  Diuretic  Beta blockers  Antiarrhythmics  Anticoagulants  Heart transplantation
    68. 68. COMPLICATION  Atrial fibrillation  Ventricular tachyarrhythmias  Dilated cardiomyopathy  Sudden cardiac death  Multisystem organ failure
    69. 69. ARTICLE REVIEW  Myocarditis is an uncommon cause of cardiac disease that can result in arrhythmia, congestive heart failure, and death. Myocardial injury in myocarditis is due in part to activated cellular and humoral immune components directed toward normal cardiac tissue. Although numerous therapies for myocarditis, including corticosteroids and immunosuppressive agents, have been applied in animal experiments and in human studies, none have demonstrated survival benefit over untreated controls. In many patients, myocarditis may spontaneously resolve. Information about myocarditis pathogenesis, manifestations, and treatment
    70. 70. Endocarditis  Endocarditis is an inflammation of the inner layer of the heart , the endocardium.
    71. 71. Types of Endocarditis  Sub acute bacterial endocarditis  Acute bacterial endocarditis  Native wall endocarditis  Prosthetic wall endocarditis
    72. 72.  Nonbacterial thrombotic endocarditis  Rheumatic endocarditis  Infective endocarditis
    73. 73. RHEUMATIC ENDOCARDITIS  Acute rheumatic fever, which occurs most often in school age children, may develop after an episode of group A beta haemolytic streptococcal pharyngitis. Patients with rheumatic fever may develop rheumatic heart disease.
    74. 74. Pathophysiology Tissue are not invaded and directly damaged by destructive organism Leukocytes accumulate in affected tissue and nodule Myocardium involve in inflammatory process Rheumatic myocarditis develops Rheumatic endocarditis,result in permanent side effect
    75. 75. CLINICAL MANIFESTATION  Tiny vegitations or growth  Pin head sized beads arranged in a row along valve flap  Valvular regurgitation  Rheumatic fever  Heart murmur
    76. 76. ASSESSMENT AND DIAGNOSTIC FINDING  Shortness of breath  lung cracles and wheezes in lung  Systemic symptoms  Lung : Pneumonia, Pulmonary abscess
    77. 77.  Kidney : Hematuria,Renal failure  Spleen : Left upper quadrant pain  Heart : Myocardial infraction  Brain : Stroke
    78. 78. PREVENTION  Early adequate treatment of streptococcal infection familiar with sign and symptom of streptococcal pharyngitis Fever Chills Sore throat Diffuse redness of throat with exudates on oropharynx
    79. 79. MEDICAL MANAGEMENT  Long term antibiotic therapy is recommended treatment and penicillin administration.
    80. 80. INFECTIVE ENDOCARDITIS  Infective endocarditis is an infection of valves and endothelial surface of the heart.  Endocarditis usually develops in people with cardiac structural defects
    81. 81.  High Risk- ◦ Mechanical prosthetic heart valve ◦ Natural prosthetic heart valve ◦ Prior infective endocardititis ◦ Valve repair with prosthetic material ◦ Most congenital heart diseases
    82. 82.  Moderate Risk- ◦ Valve repair without prosthetic material ◦ Hypertrophic cardiomyopathy ◦ Mitral valve prolapse with regurgitation ◦ Acquired valvular dysfunction
    83. 83.  Low Risk- ◦ Heart murmurs ◦ Mitral valve prolapse without regurgitation ◦ Coronary artery disease ◦ People with pacemakers/ defibrillators
    84. 84. Clinical manifestation  Stroke ,aphasia or ataxia  Loss of vision from embolization to the brain or retinal artery  Petechiae  Splinter hemorrhages  Osler nodes
    85. 85.  Janeway lesions  Roth spots  Myocardial infraction  Pulmonary embolous  Finger clubbing
    86. 86. Pathophysiology
    87. 87. Diagnostic test  History  Laboratory tests ◦ Blood cultures ◦ WBC with differential  Complete blood count (CBC)  Electrolytes  Creatinine
    88. 88.  BUN  Glucose  Coagulation panel ◦ ESR, CRP  Echocardiography  Chest x-ray
    89. 89. Treatment  Prophylactic treatment for patients ◦ Removal or drainage of infected tissue ◦ Renal dialysis ◦ Ventriculoatrial shunts  Antibiotic administration ◦ Monitor antibiotic serum levels ◦ Subsequent blood cultures ◦ Renal function monitored  BUN, Creatinine
    90. 90.  Antibiotic therapy  Fever ◦ Comfort with ASA, Ibuprofen etc  Surgical ◦ Early valve replacement.
    91. 91. Complications  Emboli (50% incidence) ◦ Right side- pulmonary emboli ◦ Left side-brain, spleen, heart, limbs,etc  CHF-check edema, rales  Arrhythmias  Death
    92. 92. RESEARCH STUDY A study was conducted by AHA on prevention of infective endocarditis concluded the major changes in the recommendations these are : (1) Only an extremely small number of cases of infective endocarditis might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100% effective. (2) Infective endocarditis prophylaxis for dental procedures is reasonable only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis. (3) For patients with these underlying cardiac conditions, prophylaxis is reasonable for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa
    93. 93. (4) Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of infective endocarditis. (5) Administration of antibiotics solely to prevent endocarditis is not recommended for patients who undergo a genitourinary or gastrointestinal tract procedure. These changes are intended to define more clearly when infective endocarditis prophylaxis is or is not recommended and to provide more uniform and consistent global recommendations.
    94. 94. RHEUMATIC HEART DISEASE  Rheumatic fever is an inflammatory disease of heart potentially involving all layers of the heart.  Rheumatic heart disease is a chronic condition resulting from rheumatic fever that is characterized by scarring and deformity of the heart valves.
    95. 95.  Rheumatic fever is an inflammatory disease that occurs following a Streptococcus pyogenes infection, such as streptococcal pharyngitis  Caused by antibody cross-reactivity that can involve the heart, joints, skin, and brain, the illness typically develops two to three weeks after a streptococcal infection.  Acute rheumatic fever commonly appears in children between the ages of 6 and 15, with only 20% of first-time attacks occurring in adults
    96. 96. CLINICAL MANIFESTATION  Modified Jones criteria were first published in 1944 by T. Duckett Jones, revised by the American Heart Association in collaboration with other groups.
    97. 97. Major criteria  Carditis
    98. 98.  Subcutaneous nodules  Polyarthritis
    99. 99.  Sydenham's chorea  Erythema marginatum
    100. 100. Minor criteria  Fever  Arthralgia  Raised erythrocyte sedimentation rate or C reactive protein  Leukocytosis  ECG showing features of heart block, such as a prolonged PR interval  Previous episode of rheumatic fever or inactive heart disease
    101. 101. Other signs and symptoms  Abdominal pain  Nose bleeds  Preceding streptococcal infection: recent scarlet fever, raised antistreptolysin O or other streptococcal antibody titre, or positive throat culture.  mitral valve disease
    102. 102.  Aortic valve disease  The mechanical valve problems  Atrial fibrillation
    104. 104. DIAGNOSTIC TEST  Medical history  Physical examination for signs of rheumatic fever, including joint pain and inflammation. Abnormal rhythms or murmurs that may signify that the heart has been strained.
    105. 105.  Throat culture & blood test  Chest X-ray  Electrocardiogram (ECG)  Echocardiogram,
    106. 106. COMPLICATIONS  Endocarditis  Heart failure
    107. 107. TREATMENT  Bed rest  Hospital admission to treat heart failure  Antibiotics for infection  NSAIDS
    108. 108.  Corticosteroids  Salicyclates  Balloons inserted through a vein to open up stuck valves  Heart valve surgery to repair or replace damaged heart valves.
    109. 109. NURSING DIAGNOSIS 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.
    110. 110.  4) Hyperthermia related to: inflammation of the synovial membrane, and inflammation of the heart valves. 5) Imbalanced Nutrition, Less Than Body Requirement related to: an increase in stomach acid caused by the sympathetic nervous system compensation. 6) Activity intolerance related to: muscle weakness, prolonged bed rest or immobilization. 7) Self-Care Deficit related to: Musculoskeletal Disorders: polyarthritis / arthralgia and therapy bed rest.
    111. 111. 8) Impaired Skin Integrity related to: inflammation of the skin and tissue subcutan. 9) Risk for Impaired Gas Exchange related to: the accumulation of blood in the lungs due to increased atrial filling. 10) Risk for Injury related to: involuntary movements, irregular, rapid and muscle weakness / chorea
    112. 112. NURSING INTERVENTION  Monitor blood pressure, pulse apical and peripheral pulse  Monitor cardiac rhythm and the frequency  Sleeping position 45º semifowler  Instruct the client to do stress management techniques (quiet environment, meditation)  Collaboration and providing oxygenation therapy
    113. 113.  Energy saving clients during the acute  Maintain a sleep until the results of laboratory and clinical status improved  In line with the better situation, monitor the gradual increase in the level of activity  Create a schedule of activity and rest  Teach to participate in activities.  Teach the children / parents who do not realize that the movement is connected with the Korean and temporary.  In case of chorea, protect from accidents, bedrest and provide appropriate sedation program.
    114. 114. RESEARCH STUDY  Two-dimensional echocardiographic studies were performed in 293 patients with rheumatic heart disease who underwent open-heart mitral valve surgery during an 18-month period. Diagnostic confirmation of a left atrial thrombus was based on direct inspection of the left atrium during surgery and histopathologic examination. Two- dimensional echocardiographic recordings were reviewed. Of the 293
    115. 115.  This diagnosis was confirmed at surgery and histopathologic study in 30 (specificity 98.8%). A thrombus was not found in three patients. In 21 other patients, left atrial thrombi were present but were not detected by two-dimensional echocardiography (sensitivity 58.8%). Ten of these 21 had thrombi in the left atrial cavity. In 11 patients, thrombi were located in the left atrial appendage, all of which were missed by two-dimensional echocardiography. Excluding these 11 left atrial appendage thrombi, the sensitivity of two-dimensional echocardiography for detecting left atrial cavity thrombi was 75.0 %. 
    116. 116. Reference  Black JM,Hawks JH medical surgical nursing 7th ed.elsevier ; Missouri, 2005 vol:2; 1612- 24.  Suzzane ,Brenda Suddarth’s B ,textbook of medical surgical nursing 12th ed. Lippincot Williams and Wilkins; vol:1;2012; 814-21  Suzzane ,Brenda Suddarth’s B ,textbook of medical surgical nursing 10th ed. Lippincot Williams and Wilkins; vol:1; 2004; 778-84.  Chintamani,Levis’s medical surgical nursing 7th ed.Elsevier;2011; 860-71  Mohan H Patholology quick review 2nd ed. Jaypee brothers New delhi 2005; 222-33,
    117. 117.  Tripathi KD Essentials of medical pharmacology 6th ed. Jaypee brothers New delhi 2008; 493-554  overview#showall   DSECTION=treatments-and-drugs   /  htm  /   Groups/cmp/education/papers/Pages/colchicine- pericarditis-prevention.aspx#.ULOH24Z9DKt