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VALVULAR HEART DISEASE By: JG SAMBAD IKDRC COLLEGE OF NURSING
Heart valves The heart contains two atrioventricular valves: Mitral valve Tricuspid valve Two semilunar valve 1. Aortic valve 2. Pulmonary valve
Types of valvular heart disease Types of valvular heart disease are defined according to the valve defect. Stenosis – constriction or narrowing Regurgitation – incomplete closure of the valve leaflets results in the backward flow of blood.
Etiology The majority of adult cause of mitral valve stenosis result from rheumatic heart disease. Less common include: Congenital mitral stenosis Rheumatoid arthritis Systemic lupus erythromatous (SLE)
PATHOPHYSIOLOGY Rheumatic endocarditis along with other causes Scaring of the valve leaflets &the chorde tendinee Contracture develop with adhesions between two leaflets Funnel shape of the valve because of thickening and shorting of the structure Obstruction of flow of blood from the mitral valve Pressure gradient difference between LA & LV during diastole Increase pressure and volume in LA Increase pressure in pulmonary vasculature Hypertrophy of pulmonary vessel in chronic congestion Extertional dyspnea due to decrease pulmonary compliance Reactive pulmonary hypertension Right ventricular hypertrophy Right ventricular failure
Clinical manifestation Dyspnea on extortion, orthopnea and PND. Acute pulmonary edema may be precipitate by uncontrolled AF, exercise, chest infection, anesthesia and pregnancy. fatigue is due to reduce cardiac out put reserve and is common in mild or moderate stenosis. Hemoptysis can occur for a Varity of reasons.
Investigation History and physical examination ECG chest X-ray Cardiac catheterization- increase PcWP, LAP Echocardiogram
Management Asymptomatic patient need only infective endocarditis prophylaxis Mild symptoms- sault intake restriction and oral stenosis In AF digoxin beta blocker or CCB for the rate control restoration of sinus rhythm may be attempted if appropriate. Anticoagulants- at last 1 year for those with thromboembolism and life long if in AF.
Surgical management Closed valvotomy: fused cups separated by dilator introduced through LV apex. Open valvotomy: with cardiopulmonary bypass is preferred to closed valvotomy cups separated under direct vision. Any fusion of subvalvular apparatus is loosened. Mitral valve replacement(MVR) - MVR if there is significant MR or the valve is severely or heavily calcified.
Pathophysiology Regurgitation mitral orifice Volume overload on the LV LV dilatation LV is decompressed into the LA during diastole Backward flow of blood in the LA Volume overload in LA LA enlargement Raised left atrium pressure Rise pressure in pulmonary vasculature Pulmonary oedema
Clinical manifestation Acute MR Chronic MR Symptoms related to pulmonary oedema and shock Thready peripheral pulse Cool and clammy extremities Murmur is heard during auscultation of heart sound May remain asymptomatic for may year until the development of some degree of right ventricular failure. Weakness Fatigue Dyspnea (due to decrease forward cardiac output) Paroxysmal nocturnal dyspnea Peripheral oedema in later stage
Investigation History and physical examination ECG chest X-ray Cardiac catheterization- increase PcWP, LAP Echocardiogram
Medical management Infective endocarditis prophylaxis required Asymptomatic patient with mild MR managed conservatively with serial echocardiograms. Vasodilators
Surgical management Mitral valve repair and Mitral valve replacement
Mitral valve prolapse MVP is the structural abnormality of the mitral valve leaflets and the pupillary muscles or chorade that allows the leaflets to prolapse or back into the left atrium during systole. MVP is the most common from of valvular heart disease in the united states.
Etiology Unknown but is related to diverse pathogenic mechanism of the mitral valve. Secondary to MS & MR. MVP can occur in the presence, redundant mitral valve leaflets elongated chorde tendineae (longer) Enlarged mitral annulus (right that is attached to the mitral valve leaflets) MVP is usually benign but serious complications can occur including mitral regurgitations, infective endocarditis sudden death and cerebral ischemia.
Clinical manifestation Arrhythmias most commonly ventricular premature contraction Ventricular tachycardia May cause palpitations Light headache and dizziness Chest pain may be due to abnormal tension on the pupillary muscles. This chest pain does not respond to Anti- Anginal treatment. E.g nitrate, sorbitrate .
Management Recommend antibiotic prophylaxis for endocarditis. Monitor the patient treated with B-adrenergic blockers to control palpitations. Advice the patient to adopt healthy eating pattern such as avoiding caffeine, because if it is a stimulant and any exacerbate symptoms. Counsel the patient who uses diet pills continuing stimulants that these preparations will exacerbate symptoms. Instruct the patient to take over the counter drug with caution. Develop a planned aerobic exercise program and the patient implement it.
Surgical management Mitral valve repair Mitral valve replacement in severe damage and calcifications
Patient and family teaching Teach patient the importance of antibiotic prophylaxis for endocarditis before undergoing any surgical procedure if the patient has MVP. Advise to patient to adopt healthy eating pattern and to avoid caffeine because it is stimulants and may cause exacerbate symptoms. Help to patient to develop and implement an exercise program to maintain optimal health. Instruct patient to contact 108 or health care provider if symptoms develop or worsen.
Aortic stenosis Definition: - Narrowing of the aortic valve.
Incidence Commonest valve lesion in UK. Risk increase with the age 2% of people >65 years have echo feature of aortic stenosis.
Causes Acquired causes Congenital causes Acquired degenerative calcific as rheumatic fever, Paget disease of bone end stage renal failure. Bicuspid aortic valve 1-2% live births. Bicuspid AV results in calcification and fibrosis of leaflets with reduced valve area.
Etiology As can occur at level of valve or above supravalvular stenosis or below the aortic valve. Degenerative calcified as results from years of normal stress on valve. IHD (increased BP, lipids, DM) Inflammatory changes occur with in valve with calcium deposited causing immobility reduced, excursions and reduced opening area. Rheumatic as due to adhesions and fusion of commissures.
Pathophysiology Progressive narrowing of aortic valve orifice. Increase pressure on LV. Worsening LVH to minimum stroke volume Stiff, non- compliant ventricle Elevated end diastolic pressure More pressure on LA Blood backflow into LA and pulmonary vasculature Various clinical manifestations
Clinical manifestations Angina pectoris Dyspnea Syncope Dizziness Palpitations Heart failure Sudden death BP- narrow pulse pressure in advanced as systolic BP is decreased. Systolic thrill felt at aortic area(2 nd ICP on right side). Slow rising, small volume pulse-best felt at carotid.
Investigation History and physical examination ECG chest X-ray Cardiac catheterization- increase PcWP, LAP Echocardiogram
Medical management β - blocker reduce myocardial or demand and may improve coronary blood flow. Loop diuretics for hypervolemia. Digoxin in case of heart failure. In severe as avoid drugs which reduce afterload. E.g NTG, ACE-I as this may worsen gradient and cause syncope.
Pathophysiology Failure of aortic valve More blood of LV stroke volume regurgitation into LV Increase in stroke volume to maintain cardiac output Increase in end-diastolic pressure LV dilatation and hypertrophy Back flow in pulmonary system
Investigation History and physical examination ECG chest X-ray Cardiac catheterization- increase PcWP, LAP Echocardiogram
Medical management Asymptomatic mild/ moderate AR with normal LV routine follow up every 1-2 year with echo. Asymptomatic severe AR with normal LV frequent 6 monthly follow up or sooner if symptoms intervene. Loop diuretics and digoxin for CCF. Vasodilator, ACE-I, & calcium channel blocker should be used in AR. Anginal chest pain can be treated with nitrates but use beta blocker with caution.
Investigation History and physical examination Echocardiography ECG: sinus rhythm with sign of RA enlargement. CXR: enlarge RA but normal PA size.
Treatment Salt restriction and diuretic may markedly improve symptoms. If co-existent MS is being operated on surgical valvuloplastiy can help. Tricuspid valve replacement occasionally may perform. Bio prosthetic valve give better results than mechanical valve.
Tricuspid regurgitation
Causes Any cause of RV dilatation(MV disease congenital heart disease, RV dysfunction etc..) Endocarditis Marfan's syndrome Rheumatic fever
Pathophysiology
Clinical manifestation Usually minimal as right side HF develop patient complaints of : Ascites Edema Nausea Anorexia Abdominal pain On examination: wasting, jaundice, oedema, artificial flutter is common, elevated JVP, tender pulsatile hepatomegaly, auscultation-S3 often heard and increased expiration.
Investigation History and physical examination ECG: non specific, may show evidence of underlying condition CXR: cardiomegaly in patient with functional tricuspid regurgitation, pleural effusion. Echocardiogram: color Doppler confirm diagnosis.
Treatment In absence of pulmonary hypertension. TR is well tolerated and may not require well tolerated and may not require specific treatment. Symptoms of RV failure respond to diuretic and fluid/salt restriction. TR secondary to valve pathology may require valve replacement.
Clinical manifestation Usually none If severe stenosis; exertional dyspnea and light headiness. Examination: prominent “a” wave in JVP occasionally thrill in 2 nd left in ICS.
Investigations History and physical examination ECG: right ventricular hypertrophy and RV overload CXR: dilated pulmonary arteries. Echocardiogram: confirms diagnosis and can show level stenosis. Cardiac catheterization: to severity of obstruction and hemodynamic effect.
Medical Treatment In general invasive intervention is recommended when gradient across valve is >50 mmhg at rest for when symptoms occur. Medical- supportive symptomatic treatment of RV failure is diuretics & fluid restriction.
Surgical intervention Balloon valvuloplastiy Pulmonary valve replacement is indicated if not suitable for medical treatments.
Pulmonary regurgitation
Causes Any cause of increased pulmonary BP Infective endocarditis Connective tissue disease-Marfan's syndrome
Clinical manifestation Often asymptomatic Symptoms increase when pulmonary BP increase or right ventricular failure exists. Then get dyspnea on exertion, lethargy, peripheral edema, abdominal pain. On examination: thrill in pulmonary area. Auscultation; murmur of PR is heard best in 3 rd & 4 th ICP on left adjacent to sternum and increase during inspirations.
Investigation History and physical examination ECG: right ventricular hypertrophy CXR: enlarged pulmonary arteries and right ventricle Echocardiogram: image may show RV dilatation and hypertrophy. Abnormal septal motion if RV volume overload.
Treatment Usually supportive treatment suffices treat RV failure in use of diuretics. If pulmonary regurgitation is due to PV ring dilation secondary to pulmonary HT, treating cause of increased pulmonary BP can relive and decrease the pulmonary regurgitation severity. If severe right HF then pulmonary valve replacement can be considered.
Prosthetic valve The two categories of prosthetic valve are: Mechanical valve Biologic valve MV are manufactured form man made material and consist of combination of metal alloys polite, carbon & Dacron. BV are constructed from bovine porcine and human cardiac tissue.
Mechanical valve 1. caged-ball valve: metal cage with several stratus mounted on a circular ring hollow metal or plastic ball inside cage.
2. tilting-disk valve Mobile lens-shaped disk attached to a circular sewing ring by two offset transverse stratus: pyrolytic carbon composition.
3. bi-leaflet valve Two pivoting semi-circular disk that open centrally, mounted directly onto a swing ring.
Biological valve Porcine heterograft Pericardial heterograft Homograft cadaver valve Harvested aortic valve of pig that is preserved in glutraldehyde and mounted on specially designed sewing ring. Three leaflets composed of pericardium from 16 to 18 months old that are preserved in glutraldehyde and mounted on Dacron covered frame Harvested aortic valve from human cadaver that is initially needed for replacement then sewn into with special mounting material.