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Inflammatory Disorders Updated Spring 2012 by Nancy Jenkins Layers of the Heart Muscle TISSUES SURROUNDING THE HEART Infective Endocarditis • Infection of the inner layer of the heart • Usually affects the cardiac valves • Was almost always fatal until development of penicillin • Around 15,000 cases diagnosed annually in the U.S. Causative Organisms Causative organism more virulent Streptococcus viridans Staphylococcus aureus Viruses Fungi Etiology and Pathophysiology Occurs when blood turbulence within heart allows causative agent to infect previously damaged valves (congenital or acqired valvular disease) or other endothelial surfaces May occur in people with a history of rheumatic heart disease May occur in people with normal valves with increased amounts of bacteria Etiology/Pathophysiology Endocarditis – – – When valve damaged, blood is slowed down and forms a clot. Bacteria get into blood stream Bacterial or fungal vegetative growths deposit on normal or abnormal heart valves Vegetation – – – Fibrin, leukocytes, platelets, and microbes Adhere to the valve or endocardium Embolization of portions of vegetation into circulation Classifications of Endocarditis Acute Infective Endocarditis – – – Subacute Infective Endocarditis SBE- most common – – Abrupt onset Rapid course Staph Aureus Gradual onset Systemic manifestations Prosthetic Valve Endocarditis Bacterial Endocarditis of the Mitral Value Fig. 37-2 Sequence of Events in Infective Endocarditis Fig. 37-3 Risk Factors- endocarditis Hx of rheumatic fever or damaged heart valve Prior history of endocarditis Invasive procedures- (introduce bacteria into blood stream) (surgery, dental, etc) Recent Dental Surgery Permanent Central Venous Access IV drug users Valve replacements Nursing Assessment Subjective Data – – – – – History of valvular, congenital, or syphilitic cardiac disease Previous endocarditis Staph or strep infection Immunosuppressive therapy-(HIV) Recent surgeries and procedures Nursing Assessment Functional health patterns – – – – IV drug abuse Alcohol abuse Weight changes Chills Nursing Assessment – – – – – – – Diaphoresis Fever Bloody urine Exercise intolerance Generalized weakness Fatigue Cough Nursing Assessment – – – Dyspnea on exertion Night sweats Chest, back, abdominal pain Collaborative Care Fungal and prosthetic valve endocarditis – – Responds poorly to antibiotics Valve replacement is adjunct procedure Assesment endocarditis Infection and emboli – – – – – – – – – – Emboli-spleen most often affected (splenectomy) Osler’s nodes- painful, red or purple pea-sized lesions on toes and fingertips Splinter hemorrhages- black longitudinal streaks on nail beds Janeway lesions- flat, painless, small, red spots on palms and soles Roth spots- hemorrhagic retinal lesions Murmur- 90% have murmurs Heart Sounds Assessment Video T above 101(blood cultures) and low-grade Chills Anorexia Fatigue Splinter hemorrhage • small areas of bleeding under the fingernails or toenails. • due to damage to capillaries by small clots Janeway Lesions • flat, painless red spots on palms and soles Osler’s Nodes Painful, pea-size, red or purple lesions On finger tips or toes Osler’s nodes Roth spots Roth’s Spots • hemorrhagic retinal lesions Diagnostic Tests Blood CulturesEchocardiogram-TEE best- see vegetations Other- WBC with differential, CBC,ESR, serum creatinine,CXR, and EKG Echocardiogram-video Mitral Valve involvement Echocardiogram- Diagnostic Criteria Duke criteria 2 major – Blood cultures and vegetations present 5 minor – symptoms Treatment- Medications Antibiotics – – – – IV for 2-8 weeks Monitor peaks and troughs of certain drugs Monitor BUN and Creat. Unclear success of oral antibiotics if not a good candidate for IV. Oral antibiotics are considered when dealing with endocarditis: – Of the tricuspid valve – With a causative organism sensitive to oral agents – Long-term IV therapy difficult or impossible – Outpatient f/u can be arranged Nursing Diagnoses Risk for Imbalanced Body Temperature Risk for Ineffective Tissue Perfusion-emboli Ineffective Health Maintenance Complications Emboli (50% incidence) – – CHF- 80% incidence with involvement of aortic valve – Right side- pulmonary emboli (esp. with IV drug abuseWhy??) Left side-brain, spleen, heart, limbs,etc check edema, crackles, VS Arrhythmias- A-fib Death . Prevention Eliminate risk factors Patient teaching Risk Stratisfication for IE High Risk– – – – – Mechanical prosthetic heart valve Natural prosthetic heart valve Prior infective endocardititis Valve repair with prosthetic material Most congenital heart diseases Moderate Risk– – – – Valve repair without prosthetic material Hypertrophic cardiomyopathy Mitral valve prolapse with regurgitation Acquired valvular dysfunction Low Risk– Innocent heart murmurs – Mitral valve prolapse without regurgitation Coronary artery disease People with pacemakers/ defibrillators – – • Prophylactic antibiotics are generally recommended only for people in the “High Risk” category Collaborative Care Prophylactic treatment for patients having – Removal or drainage of infected tissue Renal dialysis Ventriculoatrial shunts Dental, oral, or upper respiratory tract procedures – Endocarditis video review – – – Video Review Layers of the Heart Muscle Myocarditis Myocarditis is an uncommon inflammation of the heart muscle (myocardium). This inflammation can be caused by infectious agents, toxins, drugs or for unknown reasons. It may be localized to one area of the heart, or it may affect the entire heart. (effects like pounding the heart get inflammation and swelling) Etiology/Pathophysiology Myocarditis-video – – – – – – Virus, toxin or autoimmune response causes necrosis of the myocardium Most often caused by viral infection Frequently caused by Coxsackie B virus Frequently follows an upper respiratory infection or viral illness Get decreased contractility Can become chronic and lead to dilated cardiomyopathyheart transplant or death •This is an infection in the muscles of the heart, most commonly caused by the Coxsackie B virus that follows upon a respiratory or viral illness, bacteria and other infectious agents. Risk factor-myocarditis Hx of upper respiratory infection Toxic or chemical effects (radiation, alcohol) Autoimmune or immunosuppresents- 10% HIV develop it Metabolic-lupus Heat stroke or hypothermia Assessment myocarditis Infection and CHF – – – – – – Fatigue,DOE Tachycardia Arrhythmias- PVCs, PACs, Atrial Tachycardias, Chest pain Signs of heart failure (S3, etc.) Pericarditis frequently occurs with myocarditischeck friction rub Diagnostic Tests EKG- Non-specific T-wave abnormalities CK-MB and Troponin may be elevated Endomyocardial biopsy- there are risks and not used for every case but is definitive for myocarditis Chest X-Ray- Variable (Normal to Cardiomegaly) Echocardiogram Cardiovascular Magnetic Resonace A safe and sensitive noninvasive diagnostic test to confirm the diagnosis is not available Chest X-Ray in Myocarditis Endomyocardial Biopsy (EMB) Medications Antibiotics Antiviral with interferon-a IVIG- experimental trials Corticosteroids or immunosuppressents HF drugs- ACE, diuretics, beta blockers etc Antiarrhythmics Anticoagulants- Why?? Other Treatments Bedrest and activity restrictions- Why important?? **Activities may be limited for 6 months- 1 yr. O2 GOAL- Decrease workload of the heart so it can heal Nursing Diagnoses Activity Intolerance Decreased CO Anxiety Excess fluid Volume Pericarditis Pericarditis is an inflammation of the pericardium, the thin, fluid-filled sac surrounding the heart. It can cause severe chest pain (especially upon taking a deep breath) and shortness of breath. Pericardial Sac Anatomy-video Etiology/Pathophysiology Pericarditis – – – – bacterial, fungal or viral infection Heart loses natural lubrication(10-30cc’s) and layers roughen and rub Inflammatory process causes lymphatic fluid build-up- if sudden may have cardiac tamponade Pericardial Effusion- usually 250 cc’s before show up on x-ray. Can have 1000cc’s. Risk Factors/pericarditis Post MI (Dressler’s syndrome) Radiation Infection Trauma Cancer Drugs and toxins Rheumatic diseases Trauma or cardiac surgery Can be chronic disorder-pericardium becomes rigid Assessment pericarditis Inflammation and pain Pericardial friction rubdiaphragm at LL sternal border in knee chest position – Fever – Substernal, sharp, pleuritic chest pain – Inc. with coughing, breathing,turning,lying flat Dec. with sitting up and leaning forward Referred to trapezius muscle Dyspnea Diagnostic Tests- to R/O CBC-inc. WBC, ESR, and CRP Cardiac Enzymes- elevated but not as much as with MI EKG- ST elevation, PR changes Echo- for wall movement CXR CT or MRI- for pericardial effusion Pericardiocentesis fluid for analysis- attempt to determine cause ECG in Pericarditis Medications ASA or tylenol NSAIDS- ibuprofen Corticosteroids Pericarditis video review Livestrong Pericarditis Video Complications of Pericarditis Pericardial Effusion- an accumulation of excess fluid in the pericardium Cardiac Tamponade- an increase in intracardial pressure caused by pericardial effusion that results in compession of the heart Pericardial Effusion-video Can occur rapidly or slowly Pulmonary compression-cough, dyspnea, and tachypnea Phrenic nerve involvement- hiccups Laryngeal nerve- hoarseness Pericardial Effusion- EKG Electrical Alternans-video Pericardial effusion with electrical alternans •The QRS axis alternates between beats. In this example it is best seen in the chest leads where the QRS points in different directions! •This is rarely seen and is due to the heart moving in the effusion. Cardiac Tamponade- Compression of the heart Can occur acutely (trauma) or sub-acutely (malignancy) Symptoms- chest pain, confusion, anxious and restless Later- tachypnea, tachycardia, and dec. CO, NVD and pulsus paradoxus present With slow onset dyspnea may be only symptom cardiac tamponade with aortic dissection PERICARDIUM CARDIAC TAMPONADE Original heart size Excess pericardial fluid Cardiac tamponade Definition- a decrease in systolic BP with inspirations that is exaggerated in 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 Determination of Pulsus Paradoxus 1.Place the patient in a position of comfort and take their systolic blood pressure during baseline respiration. 2.Raise sphygmomanometer pressure until Korotkoff sounds disappear. 3.Lower pressure slowly until first Korotkoff sounds are heard during early expiration with their disappearance during inspiration 4.Record this pressure. 5.Very slowly lower pressure (1mm at a time) until Korotkoff sounds are heard throughout the respiratory cycle with even intensity. 6.Record this pressure. 7.The difference between the two recorded pressures is the Pulsus Paradox. 8.Hemodynamically significant pulsus paradox is greater than or equal to 10 but we look at trends. People with COPD may have a paradox due to increased thoracic pressures. Surgical/invasive Interventions Pericardiocentesis-now use echo or fluoroscopy – – – – Hook needle to V lead- guided by EKG and echo Look for ST elevation Withdraw fluid Afterward watch for cardiac tamponade (PP), arrhythmias, and pneumothorax Pericardiectomy Pericardial window Sclerosing agent- tetracycline (Bonds layers together) Pericardial Window A procedure in which an opening is made in the pericardium to drain fluid that has accumulated around the heart. A pericardial window can be made via a small incision below the end of the breastbone (sternum) or via a small incision between the ribs on the left side of the chest. Cardiac Tamponade and treatment Chronic Constrictive Pericarditis Starts with acute then scarring and fibrosis occur See signs of HF and cor pulmonale; most relate to decreased cardiac output Most prominent finding is jugular vein distention (JVD) Treatment of choice pericardectomy- with use of cardiopulmonary bypass Nursing Diagnoses for Pericarditis Acute Pain Ineffective Breathing Pattern Risk for Decreased Cardiac Output Activity Intolerance Review Specific Nursing Assessment for Inflammatory Heart Disorders Paradoxical pulse Murmur Pericardial friction rub Emboli Chest pain CHF Comfort Measures O2 Bedrest Positioning Prevent complications of immobility Psychological support Review- animations Endocarditis Myocarditis Pericarditis Case Study- Endocarditis J.F. is a 50 year-old married homemaker with a genetic autoimmune deficiency; she has suffered from recurrent bacterial endocarditis. The most recent episodes were a Staphylococcus aureus infection of the mitral valve 16 months ago and a Streptococcus mutans infection of the aortic valve 1 month ago. During this latter hospitalization, an ECG showed moderate aortic stenosis, moderate aortic insufficiency, chronic valvular vegetations, and moderate left atrial enlargement. Two years ago J..F. received an 18month course of TPN for malnutrition caused by idiopathic, relentless N/V. she has also had CAD for several years, and 2 years ago suffered an acute anterior wall MI. In addition, she has a history of chronic joint pain. Now, after being home for only a week, J.F. has been readmitted to your floor with endocarditis, N/V, and renal failure. Since yesterday she has been vomiting and retching constantly; she also has had chills, fever, fatigue, joint pain, and headache. As you go through the admission process with her, you note that she wears glasses and has a dental bridge. She is immediately started on TPN at 125 ml/hr and on penicillin 2 million units IV q4h, to be continued for 4 weeks. Other medications are furosemide 80 mg PO qd, amlodipine 5 mg PO qd, K-Dur 40 mEq PO qd (dose adjusted according to laboratory results), metoprolol 25 mg PO bid, and prochlorperazine (Compazine) 2.5 to 5 mg IVP prn for N/V. Admission VS are 152/48 (supine) and 100/40 (sitting), 116, 22, 37.9 degrees Celsius. When you assess her, you find a grade II/VI holosystolic murmur and a grade III/VI diastolic murmur; 2+ pitting tibial edema but no peripheral cyanosis; clear lungs; orientation x3 but drowsy; soft abdomen with slight left upper quadrant (LUQ) tenderness; hematuria; and multiple petechiae on skin of arms, legs, and chest. What is going on? Significance of orthostatic hypotension, wide pulse pressure and tachycardia? – Decreased cardiac output, aortic insufficiency Significance of abdominal tenderness, hematuria, joint pain, and petechia? – Indicates embolization. Clinical Manifestations in relation to J.F. Primary manifestations – – – – – – – – – – – – – – – – Fever Chills Weakness Malaise Fatigue Anorexia Arthralgia Myalgia Back pain Abdominal discomfort Weight loss HA Clubbing Oslers Nodes Janeway’s lesions Petechiae Secondary due to embolization – – – – – – – – – – – – – LUQ pain Splenomegaly Local tenderness and abdominal rigidity Flank pain Hematuria Azotemia *Gangrene Hemiplegia Ataxia Aphasia Visual changes Change In level of consciousness Pulmonary emboli (Right side) What do J.F.’s lab values mean? J.F.’s lab values: Na 138, K 3.9, Cl 103, BUN 85, Creatinine 3.9, glucose 185, WBC 6.7, Hct 27%, Hgb 9.0. Her abnormal values and their indication? Acute Viral Myocarditis 12/11/ 26 y/o wife, mother of two and student presented to a clinic with flu-like symptoms twice. She received antibiotic and steroids with poor results. Two weeks later she presented to the Community Memorial Hospital of Ventura emergency room where they treated her again with antibiotics, then discharged her. Four days later, she presented back to the Ventura Emergency room with flu-like symptoms, shortness of breath, nausea and weakness, as well as, chest tightness upon physical exam. Myocarditis cont. She had elevated cardiac enzymes and was taken urgently to the cath-lab for a potential angioplasty. Her cardiac catheterization showed that her coronary arteries were clean, however, her ejection fraction (EF) was <10%, with a cardiac output of 1.5 L/min. Her blood pressure (BP) was 97/49 Echo showed severe left ventricle dysfunction. She was diagnosed with Acute Viral Myocarditis. She was placed on a biVAD and transplant list