INFLAMMATORY & VALVULAR HEART DISEASE

Objectives Compare and contrast inflammatory and valvular heart disease Evaluate a comprehensive plan of care for the client with inflammatory and valvular heart disease.

Layers of the Heart Fig. 37-1. Layers of the heart muscle and pericardium. The section of the heart wall shows the fibrous pericardium, the parietal and visceral layers of the serous pericardium (with the pericardial sac between them), the myocardium, and the endocardium.

Inflammatory Heart Disease Infective Endocarditis Pericarditis Rheumatic Fever Myocarditis

Infective Endocarditis Infection of the inner layer of the heart that usually affects the cardiac valves Almost always a fatal condition until development of penicillin 15,000 new cases diagnosed in the United States each year Subacute form Preexisting valve disease Longer clinical course Insidious onset Caused by enterococci Acute form Healthy valves Shorter clinical course Rapid onset

Etiology & Pathophysiology Occurs when blood turbulence within heart allows causative agent to infect previously damaged valves or other endothelial surfaces

Cont’d Principal risk factors Age Intravenous drug abuse (IVDA) Prosthetic valves Use of intravascular devices Renal dialysis

Cont’d Vegetation Fibrin, leukocytes, platelets, and microbes Adhere to the valve or endocardium Embolization of portions of vegetation into circulation

Fig. 37-2. Bacterial endocarditis of the mitral valve Fig. 37-2. Bacterial endocarditis of the mitral valve. The valve is covered with large, irregular vegetations (arrow).

Causes Streptococcus viridans Staphylococcus aureus Viruses Fungi

Clinical Manifestation Nonspecific Fever occurs in 90% of patients. Chills Weakness Malaise Fatigue Anorexia Murmur http://www.easyauscultation.com/heart- sounds.aspx Subacute form Arthralgias Myalgias Back pain Abdominal discomfort Weight loss Headache Clubbing of fingers Vascular manifestations Splinter hemorrhages in nail beds Petechiae Osler’s nodes on fingers or toes Janeway’s lesions on palms or soles Roth’s spots Murmur in most patientsThe onset of a new or changing murmur is noted in most patients with IE, with the aortic and mitral valves most commonly affected. Murmurs are often absent in tricuspid endocarditis because right-sided heart pressures are too low to be heard. Heart failure in up to 80% with aortic valve endocarditis Manifestations secondary to embolism Clinical manifestations secondary to embolization in various body organs may also be present. Organs involved may be the spleen, kidney, peripheral blood vessels of the arm and leg, brain, and lung.

Diagnosis Thorough H&P Dental Procedures Invasive Procedures IV devices Other recent infections Labwork & Dx Studies History Recent dental, urologic, surgical, or gynecologic procedures Heart disease Recent cardiac catheterization or surgery Intravascular device placement Renal dialysis Skin, respiratory, or urinary tract infection Laboratory tests Blood cultures WBC with differential Echocardiography Chest x-ray Two blood cultures drawn 30 minutes apart from two different sites will be positive in more than 90% of patients. A mild leukocytosis occurs in acute endocarditis (uncommon in subacute), with average white blood cell (WBC) counts ranging from 10,000 to 11,000 μL (10 to 11 × 109/L). Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels may be elevated. Echocardiography is valuable in the diagnostic workup for a patient with IE when the blood cultures are negative, or for the patient who is a surgical candidate and has an active infection. A chest x-ray examination is done to detect the presence of cardiomegaly (an enlarged heart).

Collaborative Care What could be done for patients having procedures involving: Certain dental procedures Respiratory tract incisions GI wound infection Urinary tract infection ___________________________________ ___?? Antibiotic administration Monitor antibiotic serum levels (e.g., peak and trough). Subsequent blood cultures Monitor renal function. Accurate identification of the infecting organism is the key to successful treatment of IE. Long-term treatment is necessary to kill dormant bacteria clustered within the valvular vegetations. Complete eradication of the organism generally takes weeks to achieve, and relapses are common.

Acute Pericarditis Inflammation of the pericardium, the membranous sac enveloping the heart. It may be a primary illness or it may develop during various medical and surgical disorders. Asymptomatic or chest pain/friction rub Motrin/bedrest/maybe pericardiocentesis/watch for cardiac tamponade

Myocarditis Inflammatory process involving the myocardium Results from infection, usually asymptomatic Frequently associated with acute pericarditis Treat underlying cause

Rheumatic Fever Inflammatory disease of the heart potentially involving all layers of the heart RHEUMATIC HEART DISEASE: Chronic condition resulting from rheumatic fever, charachterized by scarring and deformity of the heart valves

Valve Disorders Regurgitation (re-GUR-jih-TA- shun) Stenosis (ste-NO-sis) When valves do not close completely, blood flows backward through the valve in a process called regurgitation. When valves do not open completely, a condition called stenosis, the flow of blood through the valve is reduced. Atresia occurs if a heart valve lacks an opening for blood to pass through. Stenosis Valve orifice is restricted. Forward blood flow is impeded. A pressure gradient is created across open valve. Pressure gradient differences reflect the degree of stenosis. Regurgitation Incomplete closure of valve leaflets Results in backward flow of blood Valvular disorders occur in children and adolescents primarily from congenital conditions and in adults from some form of cardiovascular disease.

Valve Dysfunction When any of the heart valves do not close or open properly, blood flow is affected. How the Heart Works: http://youtu.be/WXwYYsi6z7Q Tricuspid valve, separates the right atrium from the right ventricle, Mitral valve, which separates the left atrium from the left ventricle. Tricuspid valve has three leaflets; the mitral valve has two. Both valves have chordae tendineae that anchor the valve leaflets to the papillary muscles and ventricular wall. Semilunar valves are located between the ventricles and their corresponding arteries. The pulmonic valve lies between the right ventricle and the pulmonary artery The aortic valve lies between the left ventricle and the aorta.

Normal Heart

Valvular Stenosis and Regurgitation Fig. 37-8. Valvular stenosis and regurgitation. A, Normal position of the valve leaflets, or cusps, when the valve is open and closed. B, Open position of a stenosed valve (left) and position of closed regurgitant valve (right). C, Hemodynamic effect of mitral stenosis. The stenosed valve is unable to open sufficiently during left atrial systole, inhibiting left ventricular filling. D, Hemodynamic effect of mitral regurgitation. The mitral valve does not close completely during left ventricular systole, permitting blood to reenter the left atrium.

Mitral Valve Stenosis Rheumatic mitral stenosis is widespread in developing countries. Less common causes are congenital mitral stenosis, rheumatoid arthritis, and systemic lupus erythematosus. Majority of adult cases result from rheumatic heart disease. Causes scarring of valve leaflets and chordae tendineae Contractures develop with adhesions between commissures of the leaflets. Stenotic mitral valve assumes “fish mouth” shape caused by thickening and shortening of valve strictures. Result = Obstruction ↑ left atrial pressure and volume Hypertrophy of pulmonary vessels Chronic left atrial pressure elevations Mitral stenosis is an obstruction of blood flowing from the left atrium into the left ventricle. It is most often caused by rheumatic endocarditis, which progressively thickens the mitral valve leaflets and chordae tendineae. The leaflets often fuse together. Eventually, the mitral valve orifice narrows and progressively obstructs blood flow into the ventricle. The opening narrows to the width of a pencil. The left atrium has great difficulty moving blood into the ventricle because of the increased resistance of the narrowed orifice. The left atrium dilates (stretches) and hypertrophies (thickens) because of the increased blood volume it holds. Because there is no valve to protect the pulmonary veins from the backward flow of blood from the atrium, the pulmonary circulation becomes congested. As a result, the right ventricle must contract against an abnormally high pulmonary arterial pressure and is subjected to excessive strain. Eventually, the right ventricle fails. The enlarged left atrium may create pressure on the left bronchial tree, resulting in a dry cough or wheezing Difficulty breathing Fatigue Low cardiac output Hemoptysis Cough; wheeze Experience palpitations, orthopnea, paroxysmal nocturnal dyspnea (PND), and repeated respiratory infections. Pulse is weak and often irregular because of atrial fibrillation (caused by the strain on the atrium). A low-pitched, rumbling, diastolic murmur is heard at the apex. As a result of the increased blood volume and pressure, the atrium dilates, hypertrophies, and becomes electrically unstable, and patients experience atrial dysrhythmias. Echo, cath, CHF pt’s treated accordingly Anticoagulants to avoid thrombosis Antibiotics to prevent infective endocarditis Avoid strenuous activity

Mitral Valve Regurgitation Valve patency depends on Left atrium Left ventricle Abnormality of any of these structures can result in regurgitation. Majority of cases attributed to MI Chronic rheumatic heart disease Mitral valve prolapse Acute: A low CO may mask a new systolic murmur. Rapid assessment (e.g., cardiac catheterization) and intervention (e.g., valve repair or replacement) are critical for a positive outcome. Clinical manifestations Acute: Thready peripheral pulses and cool, clammy extremities Chronic: Asymptomatic for years until development of some degree of left ventricular failure Initial symptoms include Weakness Fatigue Palpitations Dyspnea that gradually progresses to orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema Auscultatory findings of accentuated left ventricular filling leading to audible S3 Murmur is loud pansystolic or holosystolic murmur located at apex radiating to left axilla. Patients with asymptomatic MR should be monitored carefully, and surgery (valve repair or replacement) should be considered before significant left ventricular failure or pulmonary hypertension develops. Ischemic papillary muscle dysfunction Infective endocarditis Management of mitral regurgitation is the same as that for congestive heart failure Usually, patients with mitral regurgitation benefit from afterload reduction (arterial dilation) by treatment with angiotensin-converting enzyme (ACE) inhibitors, such as captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil, Zestril), ramipril (Altace), or hydralazine (Apresoline). Antibiotic prophylaxis therapy is instituted to prevent infectious endocarditis. Once symptoms of heart failure develop, the patient needs to restrict his or her activity level. Surgical intervention consists of mitral valvuloplasty (ie, surgical repair of the heart valve) or valve replacement.

Mitral Valve Prolapse Mitral valve prolapse is usually an inherited connective tissue disorder resulting in enlargement of one or both of the mitral valve leaflets. Infective endocarditis may cause perforation of a leaflet, or the scarring following the infection may cause retraction of the leaflets or chordae tendineae.

Aortic Valve Stenosis Results from a previous rheumatic fever or fibrocalcific degeneration in older adults Valve leaflets stiffen and retract, stenosis occurs Obstruction of blood flow from left ventricle to aorta during systole

Aortic Valve Regurgitation Caused by infective endocarditis, trauma, or aortic dissection Retrograde blood flow from ascending aorta into LV during diastole=volume overload=hypertrophy, decreased contractility=pulmonary HTN & RVF Acute AVR =Life threatening emergency Chronic AVR= result of rheumatic heart disease, congenital disorders;

Tricuspid & Pulmonic Valve disease Uncommon Stenosis occurs more frequently than regurgitation Increase in blood volume to RA and RV RA enlargement & elevated systemic venous pressures

Collaborative Care of Valvular Heart Disease Prevention Anticoagulant therapy Percutaneous Transluminal Balloon Valvuloplasty Surgery Valvulotomy (valve repair) Prosthetic mechanical valves (valve replacement) Prosthetic biologic valves (valve replacement)

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References Lewis, S., Heitkemper, M, & Dirksen, S. (2007). Medical Surgical Nursing, 7th Ed.. St. Louis: Mosby, Chapter 37. Lewis, S., Heitkemper, M, & Dirksen, S. (2011). Medical Surgical Nursing, 8th Ed.. St. Louis: Mosby, Chapter 37. National Heart Lung and Blood Institute. (2012). What is heart valve disease? Retrieved from http://www.nhlbi.nih.gov/health/health- topics/topics/hvd/ National Heart Lung and Blood Institute. (2012). What is endocarditis? Retrieved fromhttp://www.nhlbi.nih.gov/health/health- topics/topics/endo/ Youtube.com. (2012). How the heart works animation video. Retrieved April 6, 2012 from http://www.youtube.com/watch?v=WXwYYsi6z7Q &feature