ABUAD Cardio PPT PDF

 CORONARY ATHEROSCLEROSIS  This is the narrowing of the coronary arteries due to tunica intima plague formation.  It is the accumulation of fats in the wall of the blood vessels.  It is common in old age.  The net effect of it is the reduction of blood flow through the vessels that...

 CORONARY ATHEROSCLEROSIS  This is the narrowing of the coronary arteries due to tunica intima plague formation.  It is the accumulation of fats in the wall of the blood vessels.  It is common in old age.  The net effect of it is the reduction of blood flow through the vessels that supplied the heart.  Causes  Hyperlidaemia,  Obesity,  Hereditary,  Hypertension,  Smoking,  Diabetes mellitus,   Causes (End)  Aging,  Sedentary lifestyle  (Physical inactivity),  Stress,  Use of Contraceptives,  Metabolic disturbances.  Pathology  The deposition of fatty plague in the tunical intima of the coronary artery.  This will lead the intima cells to form a fibrous cap and consequential reduction in the blood flow through the heart.  The process can induce the vessels to thrombus formation and embolism leading to myocardiac infaction.  Clinical manifestation  Nausea and vomiting  Diaphoresis,  Cold clammy skin,  Fatigue,  Reduction in cardiac output  Shortness of breath,  Apprehension,  Chest pain (Angina)  Diagnostic evaluation  Normal ECG reading  High blood levels of cardiac enzymes  Dysrhythmias  Coronary angiography  Management  Antilipidaemic agents: It lowers the cholesterol level in the blood. E.g Clofibrate, cholestyramine and colestipol  HMG Coa reducatse ihibitors e.g Lovastaton (Mevacor), Prevastating (Prevachol), Simvastatin (Lescol) and Atorvastin (Calcium).  Nitrate compound e.g Nitroglycerin: Promotes vasodilation and improve oxygenation to the myocardiac muscle.  Analgesic: Acetaminophen/ Ibuprofen to relief pain.  Nursing management  Admission: Close to nurses’ station for close observation.  Nurses the patient in a comfortable position e.g Sitting up position  Observation: Monitor the vital signs and ECG to ensure proper functioning.  Rest: Low fat, low cholesterol, low salt, increased fibre are indicated to decrease cholesterol level and prevent constipation.  Lifestyle adjustment: Smoking and Inactivity should be avoided.  Teach patient and family to participate in the rehabilitation process.  Encourage the patient to join a support group.  ANGINA PECTORIS  This is chest pain caused by inadequate oxygen delivery to the myocardiac muscles due to reduced or blockage in the blood supply to the myocardium.  The pain can be relieved by rest and nitrates (Nitroglycerin)  Types  Stable angina (Exertional angina): It happens during engagement in exercise or emotional stress. It has a stable pattern of onset, duration, severity and relieving factors. It can be relieved by Nitroglycerin.  Unstable angina(Pre-infarction): It occues with unpredictable degree of exertion and increase in occurrence. The pain may not be relieved by Nitroglycerin.  Intractable angina: This is a chronic incapacitating angina that is unresponsive to intervention.  Pathology  The cause lead to insufficient oxygen to the myocardium which result in myocardiac ischaemia. The myocardial cells becomes cyanotic and the left ventricular pumping function decreases.  The cyanosis will cause accumulation of lactic acid leading to aerobic metabolism replacement by anaerobic.  The myocardial muscles becomes irritated by the lactic acid accumulation bringing pain transmission felt in the left shoulder and arm and breathlessness. The pain is usually in form of tightness or strangling sensation.  Features  Pain (Burning, crushing and squeezing pain that radiates to the shoulder, arm, jaw, neck and back. Most times, it lasts for less than 5 minutes),  Dyspnoea,  Pallor,  Increased perspiration,  Palpiation,  tachycardia,  weakness/Fatigue, hypertension, dizziness/fainting,  Diagnosis  1. Cardiac catherization to provide detail on patency of the coronary artery.  2. exercise stress will induce the pain.  3. Radiological examination reveals occluded coronary artery  4. EEG shows altered PQRS wave.  Nursing management  Goal: To relief chest pain and stabilize respiration.  Drug of choice is Nitroglycerin (Monitor BP before the administration)  Serve the prescribed Thrombolytics, anticoagualnts and antilipemics  Continuous cardiac monitoring  Administer oxygen as prescribed  Assist patient to identify aggravating factors e.g Exercise/activities, emotional excitement, exposure to cold and consumption of heavy foods  Inform patient to always take Nitroglycerin prior to or during activities to avoid pain.  Complication  Heart failure  Shock (Neurological)  Hypertension  Acidosis  MYOCARDIAC INFARCTION  This is the destruction of myocardial tissues of the heart with severe and prolonged deprivation of blood and oxygen because of insufficient coronary blood flow. The areas or zones involved in the damage are as follows.  Zone of necrosis: Death of muscles caused by the extensive oxygen deprivation. It is irreversible.  zone of injury: The area is inflamed and injured. It surrounds the necrosed area and it is reversible.  Zone of ischaemia: This is the region surrounding the area of injury. It is reversible.  Types  1. Transmural infarction: The tissue damage extends through all the myocardial layer of the heart. This type is also termed Q-waves.  2. Sub-endocardial infarction: Only innermost layer is damaged. The area of necrosis is confined to the innermost layer of the heart. It is also termed non-Q wave type.  Causes  Coronary thrombosis (Partial or Total), coronary artery disease,  Embolism, anaemia, hypoxia, atheriosclerosis, coronary artery spasm, hypertension, arterial inflammation, embolism  Predisposition: Aging, stress, smoking, sedentary lifestyle, diabetes mellitus, Elevated triglyceride and cholesterol level, Obesity, Excessive intake of saturated fats.  Pathology Occlusion of the coronary arteries as a result of the cause result in inadequate blood supply to the heart muscles. The deprivation in oxygen and nurtients leads to myocardiac ischaemia and cellular necrosis in the affected area thereby leads to loss of myocardiac contractility and reduced cardiac output. There is intense pain in the area and it is described as tightness, heaviness. Dysponea from pain and coronary congestion. The constriction in the chest may last for about 20 minutes or more. Stimulation of the vomiting centre in the brain will result in nausea and vomiting. There will be levated blood pressure due to heart compensation. In the long run, the blood pressure will drop because of decreased pumping efficiency of the heart  Features  Anxiety,  Severe chest pain,  Increased heart rate,  Elevated blood pressure and respiration (Initial),  Nausea and vomiting,  Diaphoresis, cold clammy pale skin,  Fainting attack and palpiation,  weakness and fatigue, dyspnea, Tachycardia or Bradycardia.  Diagnosis  Electrocardiogram: Myocardial ischaemia causes the T wave to be larger and inverted.  Serum enzyme studies: Reveals elevated level of creatinine.  Elevated White blood cell  Electrocardigraphy: Abnormal ventricular walls.  Management  Goal: Relief pain, stabilize heart rhythm and reduce cardiac workload.  Oxygen therapy should be established.  Thrombolytic agent and anticoagulant such as Streptokinase and Urokinase to dislodge the clot.  Beta-adrenergic blockers e.g Propanolol to improve oxygenation by promoting blood flow n small arteries.  Pain control by Opiates e.g Morphine  Management  Nitroglycerine and Aspirin may also be administered  I.V atropine is given for heart block and bradycardia  Surgical: A temporary pacemaker is inserted to check heart block or bradycardia.  Mechanical opening of the coronary arteries to get rid of the occlusions (Percutaneous Transluminal Coronary angiography).  Nursing management  Patient is admitted in a comfortable position (Fowler)  Encourage bed rest to decrease cardiac workload  Reassure patient and explain procedure as situation warrants to minimize the anxiety.  Provide ongoing assessments, monitor vtal signs and cardiac enzymes.  Institute a liquid diet. Advance to a low sodium, low cholesterol, low fats, solid diet as tolerated.  Nursing management  Ensure pre- and post nursing care is rendered if surgery is indicated  Teach family and client on the nature of the illness.  Ensure a close relation take a course in Cardiopulmonary rescuscitation.  Advise the patient to avoid smoking  Encourage patient to wear medical bracelet.  Complication  Cardiogenic shock,  Ventricular aneurysm,  Pericarditis,  Rupture of the atrial or ventricular septum,  Ventricle wall or valve, heart failure,  HEART FAILURE  This is the inability of the heart to maintain adequate circulation due to decreased myocardial contractility.  It can also be defined as the inability of the heart to carry out its pumping function to meet up with metabolic needs of the body.  Types  Left ventricular failure(Left sided).  Right ventricular failure (Right sided or Congestive heart failure)  Causes  Hypertension,  Obesity,  Valvular defect,  Infusion overload,  Septicaemia,  Pulmonary occlusion,  Hyperthyroidism,  pericarditis  Causes  Dysrhythmia,  kidney dysfunction,  Excessive salt intake,  Myocardiac infarction,  Drug abuse,  Pregnancy with underlying disease.  Pathology  The cause elevate the heart rate based on compensatory mechanism. There is increased stroke volume and cardiac output. Persistence contraction of the heart over a long period lead to failure.  There is back flow through pulmonary veins into the lungs resulting in pulmonary congestion. The will cause difficulty in breathing and there will be cough due to irritation.  Pathology (End)  If the condition persist, the compensation will slow down and contractions will reduce causing decreased cardiac output which diminishes circulation to the vital organs of the body.  Congestion of the lungs will impair pulmonary circulation (no place for pulmonary artery to empty) leading to failure of the right side of the heart. There is enlarged jugular veins, oedema, ascites, which is characteristics of CCF.  Features  (Left Heart failure)  Dyspnea, coughing (Frothy blood tinged sputum), Fatigue, Mental confusion (Insomnia & Restlessness), Oliguria, Exercise, Rapid and irregular pulse, Anorexia, Orthopnea, pale cool extremities.  (Right Heart failure)  Eodema (Dependent pitting edema), Fullness, ascites, weight gain, jugular vein distention, cardiomegaly, hepatomegaly, abdominal pain, weakness.  Diagnostic evaluation  Radiological examination reveals cardiomegaly and vascular congestion.  Arterial Blood Gas reveals decreased partial pressure of arterial oxygen.  Elevated blood sodium.  Elevated blood urea nitrogen  Pulse oximeter will reveal decreased oxygen saturation.  Elevated central venous pressure in right sided heart failure.  Management  The goal is to; Reduce the work load on the heart, improve heart pumping activity and prevent factors that lead to heart failure. The medications used in managing the condition are;  1. Cardiac glycosides: It increases the force of myocardial contraction. Example of the drug is Digoxin. It should be noted that the drug must not be administered if the pulse is less than 60 beats/mins.  2. Diuretics: Used to get rid of excess fluid and accumulated sodium.  Management  Vasodilator therapy: Decrease peripheral resistance thereby decrease workload on the heart.eh Hydralizine. (If BP is less than 90/60mmHg, do not give)  4. Bronchodilators e.g Aminophiline  5. Expectorants e.g Benylin with codein.  6. Antilipidemic agents used to lower the serum cholesterol.  7. Angiotensin Converting Enzyme Inhibitors  Nursing management  Admit in a cardiac bed to attain a Fowler’s position.  Observation: Routne vital signs is necessary. Weigh the daily (Monitor fluid retention)  Nutrition/Diet: low sodium diet to decrease fluid retention.  Physical care: Bed bath/care of pressure area to prevent pressure sore.  Psychological care: Reassure client of the relief of the symptoms through the care.  Education/advise: Stop smoking, adhere to low salt diet, reduce stress, keep to medical check up.  Complication  Absence of heartbeat,  Brain damage,  Cardiomegaly,  Deep vein thrombosis,  Coma etc  CARDIAC ARREST  Cardiac arrest is the sudden caesation of the heartbeat and heart pumping action resulting in ineffective cardiac output and circulation.  It is an emergency condition that requires prompt management.  Causes  Myocardiac infarction,  Near drowning,  Hypoxia,  Heart failure,  Pulmonary embolism,  Acute haemorrhage (Hypovolaemia),  Ventricular irritation,  Drug overdose, Anaphylaxis,  Respiratory acidosis, Electric shock, Cardiac tamponade, Surgery (General anaesthesia).  Predisposing factors: Smoking, Family history of coronary heart disease, High Blood Pressure, Obesity, Diabetes, Sedentary lifestyle, Aging, Nutritional imbalance e.g Low calcium, low potassium or magnesium, use of hard drugs like Cocaine.  Pathophysiology: An abrupt disruption of vasomotor response to the myocardium resulting in sudden drop in myocardium contraction leading to caesation of heartbeart. The pulse become flat and partial pressure of CO2 superceeds that of O2 resulting in absence of breath which manifest as cyanosis, cold and clammy skin.  Features  Palpitations,  Sudden collapse,  Absence of breath,  absence of pulse,  chest pain,  dizziness, fainting,  weakness,  cyanosis,  cold clammy skin. Vomiting.  Diagnosis  1. Electrocardiography shows abnormal electrical pattern such prolong QT interval  2. Reduced electrolyte level e.g Low Potassium, Low calcium and low magnesium.  3. chest X-ray  4. Angiogram (Coronary catherization) will reveal blocked coronary arteries.  5. Elevated cardia enzymes (Troponin and Creatinin phosphate CPK) that helps in myocardiac contraction.  Management  Immediate Cardiopulmonary resuscitation (CPR) is instituted to restore flow of oxygen in blood to the vital organs.  Loose tight clothing  Place the patient in a flat surface and tilt the head back.  Wipe off secretions from the upper respiratory tracts.  If ambu bag is available, oxygen should be delivered 4-6 litres per minute.  Management  Start CPR immediately: Place the heel of one of your hand at the centre of the persons chest (at the lower sternum, top of the xiphoid process) covering the hand with the other hand and keeping the elbow straight. Use your upper body weight to push down hand and fast on the persons chest at the rate of 30 compressions and tilt the head backwards lifting the chin up to open the airway and give two rescue breaths.  Watch to see if the chest rises. If it does not rise, repeat the process until the patient recovers consciousness and breathing is normal/until emergency medical personnel takes over. For a child, 60 compressions are required and one hand may be required to prevent damage to the ribs. If an automated external defibrillator (AED) is available deliver one shock before carrying out CPR.  Management  Chemotherapy: Beta blockers ACE inhibitors and calcium channel blockers are used to relieve the condition.  Surgical intervention  Coronary angioplasty: It is used to open blocked coronary arteries to allow blood to freely flow to the heart.  Coronary bypass surgery: It is the bypassing the narrowed or blocked artery with the patent artery (artificial)  Corrective heart surgery, if the cause is due to congenital heart deformity or valvular disease.  Nursing management  Observation of vital signs during emergency.  Check input and output regularly  Assess for signs of cyanosis.  Psychological support to reassure the patient.  Active and passive exercises are required.  HYPERTENSION  Hypertension is the persistent, intermittent or sustained elevation of blood pressure usually above 140/90mmHg.  Represents a quantitative rather than a qualitative deviation from the normal  Hypertension is a condition in which arterial BP is chronically elevated.  Types  1. Primaryor essential/Idiopathic hypertension  2. Secondary Hypertension  Primary hypertension  It has no identifiable medical cause but there are some risk/predisposing factors which includes the following;  Aging, Race (Common among blacks), Gender (Common in men than women),  Family history, Stress, Obesity, Sedentary lifestyle, Hormonal contraceptive use,  High dietary intake of sodium or saturated fats, excessive caffeine, alcohol or tobacco use.  Secondary hypertension  It is the type caused by disease conditions of the organs of various systems in the body.  Some of the causes include; Renal disease, Phaechromocytoma, Cushing syndrome, Thyroid, parathyroid or pituitary dysfunction, Pregnancy induced hypertension, Coartation of the aorta, Diabetes mellitus.  Pathology  The cause stimulates vasomotor centre in the medullar of the brain. This lead to the release of acetycholine, epinephrine and norepinephrine resulting in the constriction of blood vessels and vasoconstrictions of peripheral vessels.  This will result in increased peripheral resistance leading to elevated blood pressure continuous peripheral resistance results in compensatory mechanism of the heart thereby increasing heart rate and cardiac output.  If the condition persist, there will be hypertrophy of the myocardial tissue and arteriosclerotic changes in the tiny blood vessels are susceptible to rupture, there will be epistaxis and retina bleeding.  Pathology  This further occlude the vessels thereby depriving vital organs of blood supply. Reduced blood supply to the brain will cause headache, dyspnea and confusion.  Reduced blood supply to the kidneys due to vasoconstriction will lead to the release of renin. Renin leads to the formation of angiotensin 1 which converts to angiotensin 2 that will further increased vasoconstriction.  Secretion of aldosterone by the cortex will lead to reabsorption of sodium and water which will further elevate the blood pressure and cause oliguria. Rupturing of the tiny blood vessels of the brain will lead to Stroke (CVA).  Features  Headache (Occipital),  Flushed face,  Elevated blood pressure,  Insomnia, fainting,  Chest pain (angina),  Dyspnea, oliguria, weakness/fatigue, dizziness, apprehension, confusion.  Diagnosis  Chest radiography shows left ventricular hypertrophy.  Electrocardiogram will show altered waves.  Blood urea nitrogen and creatinine levels are increased because of renal involvement  Urinalysis  Nursing management  Admit in a comfortable position/ noiseless position.  Adequate rest with relaxation technique  Observation: Vital signs especially blood pressureto be monitored regularly.  Nutrition; Prevent overweight by reducing calorie intake and restrict sodium intake to reduce heart overload.  Physical care: Assist in Activities of Daily Living, self care,  Nursing management  Monitor side effect of drugs  Advise patient to reduce weight by restricting calorie intake.  Urge the client to stop smoking.  Encourage client to conduct a reglar physical exercise  Encourage importance of regular blood pressure monitoring.  Instruct patient to to restrict sodium, alcohol and caffeine intake.  Complication  Myocardial infarction,  Retinal hemorrhage,  Renal insufficiency,  Stroke,  Heart failure,  Left ventricular hypertrophy,  Transient Ischemic attack,  Blindness  ENDOCARDITIS  This is an infection of the endocardium of heart valves resulting from invasion of bacteria or other organism. Since the endocardium is continuous with the cardiac or heart valves any infection or inflammation that occurs is likely to affect the valves resulting in valvular damage.  Type  Acute endocarditis: It has rapid onset, short course and more virulent with increased toxicity.  Sub acute: It has gradual onset, large course and low virulence with less toxicity.  Causes  1. Bacteriale.g Streptococcus, staphylococcus aureau  2. Fungi e,g candid albicans and aspergillus  3. E.coli  4. Pseudomonas  Predisposition  History of valvular heart disease  Congenital heart disease  Prosthetic valve replacement  Prolonged IV antibiotic therapy  Intravenous drug abuse  Patient with recent cardiac surgery  Congenital heart diseases e.g Ventricular septal defect, patent ductus artheriosus and coartation of the aorta.  Pathology  Microorganism in the blood travel to the heart valves and endocardium during systemic circulation. Organisms have high affinity for these regions.  This process trigger off fibrin and platelet aggregation forming a lesion called vegetations and collagen. The vegetation invade the heart valves leading to valve damage and infilteration or spread to the endocardium that can lead to heart failure.  The break off of this vegetation or the sepsis can lead to embolism in different parts of the body like the lungs, brain, liver and spleen causing various complications.  Features  Weakness/fatigue  Arthralgia  Fever with chills  Splenomegaly  General malaise,  weight loss, anorexia,  diaphoresis, cough, headache, Myalgia, Cardiac murmur, abdominal discomfort, local tenderness, flank pain, decreased level of consciousness.  Diagnosis  Blood analysis: Reveals positive blood cultures for causative organism  Elevated WBC count.  Echocardiogram reveals valvular damage  Electrocardiogram shows arrhythmias  Chest x-ray shows cardiomegaly  Nursing management  Admission to ensure proper bed rest.  Observation: assess invasive line and wounds for redness, warmth, tenderness, swelling, drainage and other signs of infection daily.  Nutrition: Well balanced or adequate diet is necessary to maintain resistance to infection.  Drugs: Give prescribed antibiotics and prophylaxis.  Nursing management  Psychological care: Provide patient and family with emotional support and facilitate coping startegies during the prolonged course of the infection and antibiotic treatment.  Provide complete pre and post opeative care if surgery is involved  Provide patient and family with teaching on discharge  Management  Antibiotics e.g aminoglycode, penicillin and tetracycline  Surgical intervention: Valvular debridement or excision of the vegetation is required in severe cases.  Complication: Heart failure, Unconsciousness and Brain damage.  PERICARDITIS  This is the inflammation of the pericardium, the outermost or fibrous serous sac or the layer that envelope, support and protects the heart is inflamed.  Type  Acute pericarditis (Produces serous or hemorrhage exudate)  Chronic pericarditis (This is marked with pericardial thickening).  Causes  Bacterial, fungal or viral infection,  Neoplasm, injury to the pericardium e,g Myocardial infaction, trauma or cardiac surgery,  High dose of radiation to the neck,  Uraemia,  Drugs overdose,  Aortic aneurysm with pericardial leakage,  Autoimmnue disease, Myxoedema, Rheumatoid arthritis, Pace maker insertion.  Pathology  The cause leads to accumulation of fluid in the pericardial during the inflammatory process (pericardial effusion), leading to increased pressure on the heart which results in cardiac tamponade.  Prolonged occurrence with prompt management will result in thicknening and reduced elasticity of the pericardium. This lead to reduced ability of the heart chambers to be filled with blood.  As a result of less filling, the ventricle pump less blood into the systemic circulation leading to reduced cardiac output and signs and symptoms of heart failure.  Features  Chest pain,  Tachycardia  Dyspnoea  Orthopnoea  Fever  Aneamia  Cough, pericardial friction rub  Cardiac dullness on percussion, pallor, cool/clammy skin, hypotension, jugular vein distension, oedema and ascites.  Medical management  Analgesic: Morphine, NSAIDs  Antibiotics are prescribed based on the result from culture and sensitivity.  Surgical pericardiocenthesis to drain the chambers or pericardium of excess fluid.  Pericardial window (an opening) is made in pericardium to allow continuous drainage of fluid into chest cavity.  Nursing management  Admission in a quiet environment and placed in an upright postion  Place the client on a complete bed rest to conserve energy  Observation of vitals igns and symptoms of cardiac tamponade such as hypotension, irregular heart sound.  Psychological care: Reassure patient and family to alley anxiety.  Nursing management  Nutrition: Giving high fibre diet to avoid constipation which may endager the heart.  Physical care: Assist the patient in carrying out activities of daily living.  Carryout every pre and post operative care for periocardiocentensis.  Complication: Pericardial effusion, cardiac tamponade,Heart failure, cardiac arrest  MYOCARDITIS  This is the inflammation of the Myocardium. Causes  Bacteria  Viral infection  Protozoa infection  Parasitic infection  Rheumatic fever  Immunosuppressive therapy  Infective endocarditis.  Pathology  Inflammation of the myocardium as a result of invasion by infectious micro-organism will lead to cardiac enlargement.  The pumping or contraction function of the myocardium will reduce or fail causing low stroke volume and cardiac output. Inability of the heart muscle to pump blood into heart vessel (aorta and pulmonary artery) will lead to stasis and back flow of blood resulting in congestive heart failure and pulmonary congestion.  Pathology (End)  There is pain because of innervations and this lead to vomiting when the vomiting centre is affected.  Difficulty in breathing or dyspnea may be observed because of pulmonary congestion and signs of Congestive heart failure will follow.  Features  Cardiac enlargement  Faint heart sound  Gallop rhythm,  Fever, tachycardia,  Jugular vein congestion,  Oedema, ascites, dyspnea, chest pain.  Treatment is based on the cause.  Nursing management  Admission, observation, nutrition, physical care, psychological care, patient education/ discharge.  Complication: Hepatomegally, Splenomegally, cardiomegaly, coma.  RHEUMATIC HEART DISEASE  This is the permanent damage of the heart valve resulting from systemic inflammatory condition following A-beta haemolytic streptococci invasion (Rheumatic fever).  It is common in children between age 6 and 15.  Causes  Causes: Group A-beta haemolytic streptococci (Streptococcus pyrogen)  Predisposition: Lower socioeconomic group, Run in family (Gentic), Age: 6-15, Malnutrition, Crowded living condition.  Pathology  Systemic invasion of streptococcus will lead to rheumatic fever which creates a body temperature of about 380c. Antibodies are produced to combat the streptococci.  This produce characteristic lesions at specific tissue sites. This result in the destruction of mitral and aortic valves.  This will lead to heart inflammation called carditis, pericardial effusion and cardiac failure. The process lead to rashes and nodules near tendons and bony prominence of joints.  Features  Fever  Carditis,  Nodules over bones or tendons,  Rash on the trunk or hands,  Weight loss, fatigue, stomach ache,  Polyarthritis  Diagnosis  1. White blood cell count  2, Blood studies shows anaemia  3. Cardiac enzymes are levated in carditis  4. Throat culture will reveal group A haemolytic streptococci  5. Electrocardiograph reveal prolong PR interval in some patients  6. chest x-ray shows enlargement of the heart in severe case.  7. cardiac catheterization evaluates valvular damage and left ventricular dysfunction in severe cardiac dysfunction.  Medical management  1. Drug of choice include; Penicilin or erythromycin.  2. NSAID to control inflammation and minimize joint swelling and pain.  Nursing management  Admission, observation, nutrition, physical care, psychological care, patient education/ discharge.  Complication: Congestive heart failure, Valvular heart damage, Pericardial effusion and chronic valvular disease.