INFECTIOUS & INFLAMMATORY DISORDERS OF THE HEART AND BLOOD VESSELS RHEUMATIC FEVER AND RHEUMATIC CARDITIS Systemic

inflammatory disease Follows after group A beta hemolytic strep infection Rheumatic Carditis: Inflammatory manifestations of rheumatic fever in either the acute or later stage Cardiac Structures: Heart valves (mitral) Endocardium myocardium pericardium PATHOPHYSIOLOGY Inflammatory response as a result of antibodies against group A beta hemolytic beta streptococcus Antibodies cross react against proteins of the connective tissues of the heart Causes damage of the valves and layers of the heart Antibody response cause migration of WBC Inflammatory debris accumulate around valves Fibrous tissues thicken and shorten the valves Chordae tendianeae replace damaged areas Loses its ability to open and close fully Surface irregularities around the valves prone to future colonization Antibodies attack cardiac myosin Leads to heart failure Pericardium loses its ability to stretch and fill the heart with blood Tachydysrhythmias occur Oropharyngeal inflammations

Antistreptococcal antibodies attack normal heart cells

Myocarditis and valvulitis develop

Rheumatic Carditis develops

SIGNS & SYMPTOMS: Common in children 2-3 weeks after strep infection Carditis Polyarthritis Rash Subcutaneous nodules Chorea Tachydysrhythmias Red, spotty rash on the trunk COMPLICATIONS: valve damage (heart murmurs) pericardial friction rub CHF DIAGNOSTIC FINDINGS: Antistreptolysin O titer Erythrocyte Sedimentation Rate (ESR) (15-30 mm/hr; 0-2 mm/hr; 3-13 mm/hr) C-reactive Protein (<10 mg/L) ECG echocardiography MEDICAL AND SURGICAL MANAGEMENT: IV antibiotics (Penicillin, cephalosporins, azithromycin, clindamycin, vancomycin) Bed rest Aspirin Steroids Surgery for constrictive pericarditis Prophylactic treatment before any invasive procedures

INFECTIVE ENDOCARDITIS Bacterial endocarditis Inflammation of the inner layer of the heart Considered an autoimmune response Valvular changes are susceptible to bacterial colonization SUSCEPTIBLE PATIENTS: Artificial heart valves Repaired congenital heart defects Prolapsed mitral valve Hypertrophic cardiomyopathy IV drug users Immunosuppressed patients with central venous catheters BACTERIA THAT CAUSE ENDOCARDITIS: Group A beta hemolytic strep (S. bovis and S. viridans) Staphylococcus aureus Staphylococcus epidermidis Staphylococcus faecalis Enterococcus faecalis HACEK group Candida Escherichia coli Klebsiella pseudomonas PATHOPHYSIOLOGY: S. viridans and S. aureus most frequently responsible Pathogens enter the body through invasive procedures involving mucus membranes Pathogens attach to the vegetations of platelets and fibrin surrounding heart valves, chordae tendineae and papillary muscles Mitral valve most common location of microbial deposits Valve leaflets erode and slough, blood leaks between heart chambers Vegetation can break off and form emboli ASSESSMENT FINDINGS Acute onset (<1 week) Fever, chills Muscle pain, joint pains Headache, malaise, sleep disturbance (over weeks and months) Osler nodes (fingers and toes) Splinter hemorrhages (black lines on nails) Janeway lesions (painless red-blue macular lesions on feet) Roths spots (white areas on the retina surrounded by hemorrhage) Splenomegaly Heart murmurs Petechiae (embolization) Heart failure (from emboli) CVA Flank pain and renal failure Chest pain Dyspnea DIAGNOSTIC FINDINGS Blood culture Transesophageal echocardiography to reveal vegetations ECG MEDICAL & SURGICAL MANAGEMENT IV antibiotics (2-6 weeks) Valve replacement Bed rest Limit activity Periodic antibiotic therapy MYOCARDITIS Inflammation of the myocardium Viral - coxsackie virus A & B - influenza A & B - measles - mumps

- rubella and rubeola - Epstein-Barr virus - cytomegalovirus Alcohol and cocaine abuse Radiation therapy Autoimmune disorders Use of ipecac Cardiac muscle inflame myocardial stretch and recoil blood supply cardiac output Tachycardia and dysrhythmias cardiomyopathy ASSESSMENT FINDINGS: Angina (relieved by sitting up) Low grade fever Tachydysrhythmias Dyspnea Neck vein distention Ascites Peripheral edema Crackles S1 gallop (pericardial friction rub) DIAGNOSTIC FINDINGS Electrolyte levels Thyroid function tests C-reactive protein Cardiac isoenzymes Chest x-ray Cardiography Myocardial biopsy MANAGEMENT: Antibiotics Sodium restricted diet Cardiotonic drugs Heart transplant CARDIOMYOPATHY Chronic condition characterized by structural changes in the heart muscle TYPES OF CARDIOMYOPATHY Dilated Cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy OTHER TYPES: Arrhythmogenic Cardiomyopathy cardiac muscles replacement with fatty tissues Peripartum Cardiomyopathy develops in women shortly after giving birth PATHOPHYSIOLOGY: Follows another medical problem (myocarditis, SLE, muscular dystrophy, alcoholism, cancer chemotherapy Heart muscle loses its ability to pump ASSESSMENT FINDINGS: DILATED CARDIOMYOPATHY: - Dyspnea on exertion - Fatigue - Peripheral edema - Palpitations - Chest pain RESTRICTIVE CARDIOMYOPATHY: - exertional dyspneA - Dependent edema - Ascites - hepatomegaly HYPERTROPHIC CARDIOMYOPATHY: - syncope - fatigue - shortness of breath - chest pain

heart murmur first sign Forceful heart contractions palpated over chest wall

DIAGNOSTIC FINDINGS: Chest x-ray ECG Echocardiogram Cardiac cath - pressure in the verntricles Endomyocardial biopsy myocardial disarray (alteration in the alignments of myofibrils) lack of coordination during ventricular contraction (systole0 and impaired relaxation (diastole) MANAGEMENT: Diuretics Cardiac glycosides Antihypertensive drugs Antidysrhythmic drugs Anticoagulant drugs Antiinflammatory drugs (steroids) Sodium restriction Artificial pacemaker or Implanted automatic defibrillator Ventriculomyomectomy (hypertrophic) to enlarge the left ventricle; mitral valve may also be replaced Oxygen administration I & O; weight Activity restriction Avoid caffeinated beverages Avoid smoking Vaccines to prevent pulmonary complications

PERICARDITIS Inflammation of the pericardium Can occur with or without effusion Usually secondary to endocarditis, myocarditis,, chest trauma, MI, post cardiac surgery Perciardial cells are inflamed Membranes are permeable ICF fluid leaks into interstitial space (effusion or exudate) Exudates can be: - serous - fibrinous - purulent - sanguineous Fluid accumulation results in Cardiac Tamponade Results to Pulsus paradoxus or Paradoxical pulse PARADOXICAL PULSE: Difference of 10 mmHg or more between the first korotkoff sound sound heralding systolic blood pressure heard during expiration and the first heard during inspiration Reduction in the volume capacity of the left ventricle during inspiration Impaired expansion of the left ventricle stroke volume, cardiac output death ASSESSMENT FINDINGS: Inflammatory response Dyspnea Precordial pain (mistaken for esophagitis) deep breathing worsens the pain Friction rub scratchy, high pitched sound Heart sounds difficult to hear Hypotension Weak pulse DIAGNOSTIC FINDINGS: Elevated ST segment Cardiomegaly Echocardiogram wide gap between pericardium and epicardium Abnormal hemodynamics monitoring values Elevated WBC and ESR MANAGEMENT: rest, analgesics, antipyretics NSAIDs, corticosteroids

Pericardiocentesis between visceral and parietal pericardium Pericardiostomy Pericardiectomy or Decortication allow adequate filling and contraction of the heart (constrictive pericarditis) NURSING PROCESS: Assessment - assess pericardial friction rub - note s/s of cardiac tamponade and CO Diagnosis - pain related to pericardial inflammation and myocardial perfusion Expected outcome - be free of pain or tolerable 30 minutes after intervention Interventions - upright and leaning forward - antiinflammatory drugs - Analgesics

VALVULAR DISEASES: Aortic, mitral, pulmonic and tricuspid valves Promote forward blood circulation Affecting Factors: - malformations - inflammatory ds - infections - age related degenerations - injury Common: valves of the left side of the heart DISORDERS OF THE AORTIC VALVE: AORTIC STENOSIS Narrowing of the opening of the aortic valve Valve cusps are rigid and stiff Age related (calcium deposits) Consequence of congenital defect (2 cusps) valvular damage related to rheumatic carditis and infective endocarditis Causes ventricular hypertrophy Result to left sided CHF In MI and CAD infarct may enlarge ASSESSMENT FINDINGS: Dizziness, fainting Angina - CO Dyspnea and fatigue Heart pulsations are displaced laterally or distally from the PMI at the 5th intercostal medial to the left MCL Weak carotid pulse ( SV) Split S2 sound (definite separation between the sounds of pulmonic and aortic valves closing) DIAGNOSTIC FINDINGS CXR ventricular enlargement ECG elevated R wave (large mass and force of contracting muscle) Cardiac cath LV has pressure MANAGEMENT: GOAL: maintain CO Digitalis Antihypertensive drugs Antidysrhythmic drugs Diuretics Nitrates/beta blockers Sodium restriction Antibiotics Balloon valvuloplasty (temporary) Aortic valve replacement AORTIC REGURGITATION: Aortic valve does not close tightly Aortic incompetence From damage to the cusps or papillary muscles

Fenfluramine and dexfenfluramine cause AS Blood is leaked into the LV CO; LV fluid overload fluid pressure in the LV causes the mitral valve to shut early Causes ischemia ASSESSMENT FINDINGS: Tachycardia 1st sign Palpitations Dyspnea Chestpains Water-hammer pulse or Corrigans pulse (strong radial pulse followed by sudden collapse of force) Wide pulse pressure Enlarged heart displaces the PMI Heart murmur DIAGNOSTIC FINDINGS Cardiac cath - LV pressure CXR cardiomegaly ECG tall R waves; depressed ST segments (ischemia) MANAGEMENT: Cardiac glycosides Beta blockers; diuretics Prophylactic antibiotics Avoid strenous activities Aortic valve replacement DISORDERS OF THE MITRAL VALVE: A bicuspid valve Attached to chordae tendineae Functions to open widely to allow oxygenated blood to enter the LV From LV, aorta receives 50-70 ml bolus of oxygenated blood (SV) Disorders: - mitral stenosis - mitral regurgitation - mitral prolapsed Valve does not open properly to facilitate filling of the LV Incomplete emptying of the LA Sequelae of rheumatic carditis MS worsens with each recurrence of RC Cusps calcify at the commissures Chordae tendineae shortens Creates pulmonary HPN and PE Pulmonary HPN the work of RV as it pumps against the pressure in the pulmonary vascular system RV enlarges Results in right sided CHF ASSESSMENT FINDINGS: Takes 20-40 years for a patient who has had RF to develop MI 4-5 cm2 normal valve opening Fatigue and dyspnea on exertion Tachydysrhythmias Pulmonary HPN Pink, froth sputum, crackles systolic bp from CO may affect RV causes CHF DIAGNOSTIC FINDINGS CXR enlarged LA; mitral valve calcification ECG P wave is notched (LA takes longer to depolarize than the RA) MEDICAL/SURGICAL MANAGEMENT Antibiotics Daily anticoagulant (aspirin, dipyridamole) Antidysrhythmic drugs Cardioversion (allow the SA node to reestablish itself) Percutaneous balloon valvuloplasty separate the fused leaflets PERCUTANEOUS BALLOON VALVULOPLASTY: Catheter with uninflated balloon is passed through the femoral vein to the RA Septum is punctured between the RA and LA Balloon is inflated in the MV Atrial puncture allows blood to shunt from LA to RA (closes)

COMPLICATIONS OF VALVULOPLASTY: Mitral regurgitation Residual atrial-septal defect Perforation of LV Embolization MI MANAGEMENT OF VALVULOPLASTY: Echocardiogram within 72 hrs Oral anticoagulants Prophylactic antibiotics MITRAL REGURGITATION: Mitral insufficiency Valve does not close completely Associating Factors: - rheumatic carditis - MVP - post MI - connective tissue disorder - Malfunction of a replaced valve Backward flow of blood into the LA during ventricular systole Leaks into the LV during atrial diastole Heart compensates by increasing the size of the LA and LV facilitates ejection of blood Rapid regurgitation: - forward output from the LV - develops cardiogenic shock - pulmonary congestion ASSESSMENT FINDINGS: Chronic fatigue Dyspnea on exertion Palpitations (attempts to empty the LV) Diminished S1 sound CO HPN Tachycardia (compensates for SV Loud blowing murmur throughout ventricular systole Shortness of breath DIAGNOSTIC FINDINGS Transesophageal Echocardiography identify structural changes of the MV Radionuclide angiography determine the amount of blood regurgitated ECG - cardiomegaly MEDICAL/SURGICAL MANAGEMENT: Annual echocardiograms ACE inhibitors ( AL) Digitalis CCBs, BBs, antidysrhythmic drugs Prophylactic antibiotics Intra-aortic balloon pump (provide counterpulsation to the contraction of the LV) Annuloplasty repair of valve leaflets and fibrous ring NURSING MANAGEMENT: Monitor bp, HR, PR Assess heart sounds, lung sounds Monitor F & E Na restriction MITRAL VALVE PROLAPSE: Classified as idiopathic Valve cusps enlarge Floppy valve and bulge backward into the LA Mitral regurgitation may occur More common in young women Associated with CAD MVP accompanies the valvular changes of rheumatic carditis Mitral valve prolapse syndrome associated with ANS dysfunction - catecholamines - abnormal catecholamine regulation - intravascular vol (activate RAAS) - mimic severe anxiety

- cusps distend and balloon backward to the LA ASSESSMENT FINDINGS: May be asymptomatic Chest pains not correlated with exertion Palpitations Fatigue Resembles anxiety or panic Auscultation: click during ventricular systole Presumptive diagnosis: murmur when the patient squats during auscultation Echicardiogram: abnormal movement of the cusps ECG: appears normal MEDICAL/SURGICAL MANAGEMENT: Periodic antibiotic therapy before invasive procedures Drugs: digitalis, BBs, CCBs, anticoagulants, antiplatelets, antianxiety Valve replacement Avoid caffeine Restrict fluid and sodium intake Eliminate alcohol (suppress antidiuretic hormone) NURSING MANAGEMENT: Chestpain: supine with legs at 90 degree angle for 3-5 minutes activity during tachycardia - eliminate the initiation of extra beats - make up for CO - levels of cathecolamines Deep breathing through pursed lips NURSING CARE PLAN: ASSESSMENT: Determine: VS Episodes of dizziness Chest pain Lung and heart sounds I&O Weight and fluctuations Activity tolerance Occupational activities Knowledge of medical conditions NURSING DIAGNOSIS: Risk for CO related to diminished cardiac muscle contractility, tachycardia and hypertension EXPECTED OUTCOME: CO will be adequate as evidenced by no chest pain, hypotension or dizziness. NURSING INTERVENTIONS: Monitor cardiac rhythm and rate Monitor I & O Bed rest Responding to requests and attention to anxiety Substitute sources of caffeine and sodium Promote ease Reduce fever

OTHER NURSING DIAGNOSES: Activity intolerance related to CO Pain related to myocardial ischemia Risk for infection related to susceptibility secondary to previous endocardial inflammatory or infectious disorders DRUG THERAPY: Penicillin G Potassium (Pfizerpen) Warfarin sodium (coumadin) Digoxin (Lanoxin) Ticlopidine hydrochloride (Ticlid) Quinidine (Quinaglute)