Transcript Inflam
Inflammatory Disorders TISSUES SURROUNDING THE HEART Layers of the Heart Muscle 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 Classifications of Endocarditis Acute Infective Endocarditis Subacute Infective Endocarditis SBE Abrupt onset Rapid course Staph Aureus Gradual onset Systemic manifestations Prosthetic Valve Endocarditis Occurs within 2 months after OR Risk Factors- endocarditis Hx of rheumatic fever or damaged heart valve Invasive procedures- dental,gyne, etc. IV drug users Valve replacements Assesment endocarditis Infection and emboli Emboli-spleen most often affected Osler’s nodes Splinter hemorrhages Janeway lesions Murmur T above 101(blood cultures),chills Anorexia Fatigue Roth spots Osler’s nodes Janeway lesions Splinter hemmorrhages Roth spots Diagnostic Tests Blood Cultures- for temp >101 Echocardiogram-TEE best- see vegetations Other- CBC,ESR, serum creatinine,CXR, and EKG Medications Antibiotics IV for 2-8 weeks Monitor peaks and troughs of certain drugs Monitor BUN and Creat. Nursing Diagnoses Risk for Imbalanced Body Temperature Risk for Ineffective Tissue Perfusionemboli Ineffective Health Maintenance Complications Emboli(50% incidence) Right side- pulmonary emboli Left side-brain, spleen, heart, limbs,etc CHF-check edema, rales, VS Arrhythmias-Afib most common Death Cardiac Tamponade . Prevention Eliminate risk factors Patient teaching Penicillin prophylaxis Etiology/Pathophysiology Myocarditis Virus, toxin or autoimmune response causes necrosis of the myocardium Frequently caused by Coxsackie B virus Get dec. contractility Can become chronic and lead to dilated cardiomyopathy •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 URI Toxic or chemical effects(radiation, alcohol) Autoimmune Metabolic-lupus Heat stroke or hypothermia Assessment myocarditis Infection and CHF Fatigue,DOE Tachycardia Arrhythmias Chest pain- maybe an MI Signs of CHF Diagnostic Tests EKG- ST segment and T wave changes CK-MB and Troponin may be elevated Endomyocardial biopsy Medications Antibiotics Antiviral with interferon-a Corticosteroids or immunosuppressents HF drugs-ACE, diuretics, beta blockers etc Antiarrhythmics Anticoagulants Other Treatments Bedrest and activity restrictions **Activities may be limited for 6 months1 yr. GOAL- Decrease workload of the heart Nursing Diagnoses Activity Intolerance Decreased CO Anxiety Excess fluid Volume A 42 year old West African man was admitted unconscious to the intensive care unit, after an out of hospital cardiac arrest and resuscitation by a friend. He had little medical history of note other than that he had had a recent upper respiratory tract infection. There were no risk factors for HIV infection. While on intensive care he had recurrent episodes of ventricular fibrillation requiring multiple dc shocks, but ultimately settled on treatment with intravenous lignocaine (lidocaine), amiodarone, and overdrive pacing. His resting ECG showed non-specific T wave changes (fig 1) and he intermittently had non-sustained episodes of a broad complex, irregular tachycardia (fig 2). Full blood count, urea and electrolytes, and liver function tests were normal. Transthoracic echocardiography showed normal left ventricular function and size. He gradually recovered without any sequelae. Electrophysiological testing revealed inducible non-sustained polymorphic ventricular tachycardia. Coronary angiography was entirely normal. A right ventricular biopsy was taken which subsequently showed healing myocarditis (fig 3). The patient declined to have an implantable cardioverter/defibrillator and was discharged on oral amiodarone. Normal Pericardium Pericarditis slit like opening between two layers contains pericardial fluid film of serous fluid lubricant that reduces friction between the beating heart and pericardial sac Etiology/Pathophysiology Pericarditis bacterial, fungal or viral infection Heart loses natural lubrication(15-50cc’s)and layers roughen and rub Inflammatory process causes lymphatic fluid build-up Pericardial Effusion- usually 250 cc’s before show up on x-ray PERICARDIUM CARDIAC TAMPONADE Original heart size Excess pericardial fluid Cardiac tamponade 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. 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 atime) 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% of the pressure at which all Korotkoff sounds are heard with even intensity. ____________________________________________________ Risk Factors/pericarditis Post MI (Dressler’s syndrome) Secondary to chemo and cancer Secondary to uremia in renal failure-4050% of ESRD Pts. Develop this Trauma or cardiac surgery Can be chronic disorder-pericardium becomes rigid Assessment pericarditis Inflammation and pain Friction rub-LLsternal border in knee chest position Cardiac Resources Fever Substernal, pleuritic chest pain Inc. with coughing, breathing,turning,lying flat Dec. with sitting up and leaning forward Diagnostic Tests- to R/O CBC-inc. WBC and ESR Cardiac Enzymes- inc. but not as much as with MI EKG Echo- for wall movement CXR CT or MRI- for pericardial effusion Medications ASA or tylenol NSAIDS Corticosteroids Surgical/invasive Interventions for all Pericardiocentesis Hook needle to V lead Look for ST elevation Withdraw fluid Afterward watch for cardiac tamponade(PP) Valve Replacement Heart Transplant 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. Nursing Diagnoses for Pericarditis Acute Pain Ineffective Breathing Pattern Risk for Decreased Cardiac Output Activity Intolerance Specific Nursing Assessment Paradoxical pulse Murmurhttp://www.music.mcgill.ca/auscult ation/heart_tables.html Pericardial rub Emboli Chest pain CHF Comfort Measures O2 Bedrest Positioning Space Activities Prevent complications of immobility Psychological support Case Studies http://www.indegene.com/Car/ClinRound/i ndCarCase2.html myocarditis Vascular Infections Case 7-endocarditis http://www.med.unsw.edu.au/pathology/Pat hmus/m1004089.htm-endocarditis http://intmedweb.wfubmc.edu/grand_rounds/1 999/tamponade.html CASE%20PRESENTATION Johns Hopkins Arthritis Case report on rheumatoid pericarditis