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Valvular Heart Disease

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Valvular Heart Disease * In developed countries, there is a long latent period of 20 to 40 years from the occurrence of rheumatic fever to the onset of symptoms. – PowerPoint PPT presentation

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Title: Valvular Heart Disease


1
Valvular Heart Disease
2
Types
  • Mitral Stenosis
  • Mitral Regurgitation
  • Mitral Valve Prolapse
  • Aortic Stenosis
  • Aortic regurgitation
  • Tricuspid valve is affected infrequently
  • Tricuspid stenosis causes Rt HF
  • Tricuspid regurgitation causes venous overload

3
Tricuspid Valve
4
Rheumatic Heart Disease
  • Inflammatory process that may affect the
    myocardium, pericardium and or endocardium
  • Usually results in distortion and scarring of the
    valves

5
Rheumatic Heart Disease, cont.
  • Subjective symptoms
  • Prior history of rheumatic fever
  • General malaise
  • Pain may or may not be present
  • Objective symptoms
  • Temperature
  • Murmurs
  • Dyspnea
  • polyarthritis

6
Rheumatic Heart Disease
  • Diagnosis
  • H/P
  • WBC and ESR
  • C-reactive protein
  • Cardiac enzymes
  • EKG
  • Chest x-ray
  • Echo
  • Cardiac cath
  • Cardiac output

7
Rheumatic Heart Disease
  • Nursing Care
  • Vital signs
  • Rest and quiet environment
  • Give antibiotics, digitalis, and diuretics
  • Provide adequate nutrition
  • Monitor I/O
  • Explain treatment and home care

8
Mitral Stenosis
  • Usually results from rheumatic carditis
  • Is a thickening by fibrosis or calcification
  • Can be caused by tumors, calcium and thrombus
  • Valve leaflets fuse and become stiff and the
    cordae tendineae contract
  • These narrows the opening and prevents normal
    blood flow from the LA to the LV
  • LA pressure increases, left atrium dilates, PAP
    increases, and the RV hypertrophies
  • Pulmonary congestion and right sided heart
    failure occurs
  • Followed by decreased preload and CO decreases

9
Mitral Stenosis, cont.
  • Mild asymptomatic
  • With progression dyspnea, orthopneas, dry
    cough, hemoptysis, and pulmonary edema may appear
    as hypertension and congestion progresses
  • Right sided heart failure symptoms occur later
  • S/S
  • Pulse may be normal to A-Fib
  • Apical diastolic murmur is heard

10
Mitral Regurgitation
  • Primarily caused by rheumatic heart disease, but
    may be caused by papillary muscle rupture form
    congenital, infective endocarditis or ischemic
    heart disease
  • Abnormality prevents the valve from closing
  • Blood flows back into the right atrium during
    systole
  • During diastole the regurg output flows into the
    LV with the normal blood flow and increases the
    volume into the LV
  • Progression is slowly fatigue, chronic
    weakness, dyspnea, anxiety, palpitations
  • May have A-fib and changes of LV failure
  • May develop right sided failure as well

11
Mitral Valve Prolapse
  • Cause is variable and may be associated with
    congenital defects
  • More common in women
  • Valvular leaflets enlarge and prolapse into the
    LA during systole
  • Most are asymptomatic
  • Some may report chest pain, palpitations or
    exercise intolerance
  • May have dizziness, syncope and palpitations
    associated with dysrhythmias
  • May have audible click and murmur

12
Aortic Stenosis
  • Valve becomes stiff and fibrotic, impeding blood
    flow with LV contraction
  • Results in LV hypertrophy, increased O2 demands,
    and pulmonary congestion
  • Causes rheumatic fever, congenital,
    arthrosclerosis
  • Atherosclerosis and calcification is primary
    cause in the elderly
  • Complications right sided heart failure,
    pulmonary edema, and A-fib
  • S/S Early dyspnea, angina, syncope
  • Late marked fatigue, debilitation,
    and peripheral cyanosis, crescendo-
    decrescendo murmur is heard

13
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14
Aortic Regurgitation
  • Aortic valve leaflets do not close properly
    during diastole
  • The valve ring that attaches to the leaflets may
    be dilated, loose, or deformed
  • The ventricle dilates to accommodate the blood
    volume and hypertrophies
  • Causes infective endocarditis, congenital,
    hypertension, Marfans
  • May remain asymptomatic for years
  • Develop dyspnea, orthopnea, palpitations, ,and
    angina
  • May have systolic pressure with bounding pulse
  • Have a high pitch, blowing, decrescendo diastolic
    murmur

15
Assessment for Valve Dysfunction
  • Subjective symptoms
  • Fatigue
  • Weakness
  • General malaise
  • Dyspnea on exertion
  • Dizziness
  • Chest pain or discomfort
  • Weight gain
  • Prior history of rheumatic heart disease

16
Assessment, cont.
  • Objective symptoms
  • Orthopnea
  • Dyspnea, rales
  • Pink-tinged sputum
  • Murmurs
  • Palpitations
  • Cyanosis, capillary refill
  • Edema
  • Dysrhythmias
  • Restlessness

17
Diagnosis
  • History and physical findings
  • EKG
  • Chest x-ray
  • Cardiac cath
  • Echocardiogram

18
Medial Treatment
  • Nonsurgical management focuses on drug therapy
    and rest
  • Diuretic, beta blockers, digoxin, O2,
    vasodilators, prophylactic antibiotic therapy
  • Manage A-fib, if develops, with conversion if
    possible, and use of anticoagulation

19
Interventions
  • Assess vitals, heart sounds, adventitious breath
    sounds
  • HOB
  • O2 as prescribed
  • Emotional support
  • Give medications
  • I/O
  • Weight
  • Check for edema
  • Explain disease process, provide for home care
    with O2, medications

20
Surgical Management of Valve Disease
  • Mitral Valve
  • Commissurotomy
  • Mitral Valve Replacement
  • Balloon Valvuloplasty
  • Aortic Valve Replacement

21
Mechanical Valve
22
Mechanical Valve
23
Porcine Valve
24
Tissue Valve
25
Tissue Valve
26
Cardiac murmurs
  • Cardiac murmurs are often the first sign of
    underlying valvular disease.
  • May be systolic or diastolic, pathological or
    benign.
  • Systolic murmurs may be due to physiological
    increases in blood velocity or might indicate as
    yet asymptomatic cardiac disease.
  • Diastolic murmurs are almost always pathological
    and require further evaluation.
  • An ECG and CXR, although readily available tests,
    provide limited diagnostic information.

27
Echocardiography
  • Echocardiography can evaluate valve function by
    the following imaging modalities
  • 2-D Valve motion and morphology
  • LV size and function.
  • Doppler Blood flow velocity valve
    gradients haemodynamic data.
  • Colour flow Valvular regurgitation

28
Management of cardiac murmurs
  • Murmur cardiac symptoms refer to cardiologist.
  • In asymptomatic patients with cardiac murmurs, an
    echo is indicated in the following
    instances
  • - Murmur abnormal cardiac signs
  • - Murmur abnormal ECG or CXR
  • - Diastolic or continuous murmurs
  • - Pansystolic or late systolic murmurs

29
Aortic stenosis
  • Aetiology
  • Aortic stenosis may be congenital or acquired.
  • Congenital malformations may be tricuspid,
    bicuspid or unicuspid.
  • Acquired causes include the following
  • - Degenerative disease
  • - Rheumatic disease
  • - Calcific e.g. end-stage renal failure, Pagets
    disease
  • - Miscellaneous e.g. rheumatoid involvement

30
Aetiology of aortic stenosis
A Normal aortic valve B Congenital aortic
stenosis C Rheumatic aortic stenosis D
Calcific aortic stenosis E Degenerative aortic
stenosis
31
Aortic stenosis
  • Grading and severity
  • Aortic valve area must be reduced to 25 of
    normal before significant circulatory changes
    occur.
  • Grading of stenosis severity is as follows
  • - Normal valve area 3-4cm2
  • - Mild stenosis 1.5-3cm2
  • - Moderate stenosis 1.0-1.5cm2
  • - Severe stenosis 1.0cm2
  • When stenosis is severe, the peak gradient across
    the aortic valve is usually gt 60mmHg.

32
Pathophysiology of aortic stenosis
  • Aortic stenosis
  • LV outflow obstruction
  • LV systolic pressure Aortic
    pressure
  • LV hypertrophy
  • LV dysfunction
    Myocardial ischaemia

  • LV failure

33
Aortic stenosis
Natural history of aortic stenosis without
operative treatment
34
Aortic stenosis
  • Physical findings
  • Slow rising pulse
  • Reduced systolic and pulse pressure
  • Systolic thrill over the aortic area
  • Ejection systolic, crescendo-decrescendo murmur
  • Soft or inaudible second heart sound
  • ECG LVH, AV node conduction defects

35
Aortic stenosis
  • Medical therapy
  • Conservative treatment should be offered for mild
    to moderate aortic stenosis and to asymptomatic
    patients with severe aortic stenosis as follows
  • - Advise to report symptoms
  • - Avoid vigorous exercise
  • - Antibiotic prophylaxis for endocarditis
  • - Regular follow-up echocardiography

36
Aortic stenosis
  • Surgical therapy
  • Aortic valve replacement should be offered to the
    following
  • - Symptomatic pts with severe AS
  • - Pts with severe AS undergoing CABG surgery
  • - Pts with moderate AS undergoing CABG surgery
  • - Asymptomatic pts with severe AS and LV
    dysfunction
  • Balloon valvuloplasty can play a temporary role
    as a bridge to surgery in haemodynamically
    unstable patients, or as palliation for patients
    with serious comorbid conditions

37
Aortic stenosis
  • Aortic valve replacement
  • In the absence of LV dysfunction, operative risk
    is
  • 2-8.
  • Indicators of higher mortality are NYHA class, LV
    dysfunction, age, concomitant coronary artery
    disease, and aortic regurgitation.
  • Valve replacement usually results in reduced LV
    volumes, improved LV performance and regression
    of LV hypertrophy.

38
Aortic regurgitation
  • Aetiology
  • Either due to primary disease of the aortic valve
    or wall of the aortic root or both.
  • Causes of primary aortic valve disease include
  • - Congenital eg. bicuspid aortic valve
  • - Acquired rheumatic valve disease, infective
    endocarditis, trauma, connective tissue
    disease.
  • Causes of primary aortic root disease include
  • - Degenerative, cystic medial necrosis (eg.
    Marfans), aortic dissection, syphilis,
    connective tissue disease, hypertension.

39
Pathophysiology of aortic regurgitation
  • Aortic regurgitation
  • LV volume stroke volume diastolic
    BP
  • LV mass systolic BP
  • LV dysfunction myocardial ischaemia
  • LV failure

40
Aortic regurgitation
  • Clinical history
  • In chronic severe AR, the left ventricle
    gradually enlarges while the patient remains
    asymptomatic. Symptoms usually develop after
    cardiomegaly and LV dysfunction have occurred.
    Dyspnoea is the principal complaint. Syncope is
    rare and angina is less frequent than in aortic
    stenosis.
  • In acute severe AR, LV decompensation occurs
    readily with fatigue , severe dyspnoea and
    hypotension.

41
Aortic regurgitation
  • Physical findings
  • Collapsing pulse.
  • Wide pulse pressure due to both raised systolic
    blood pressure and reduced diastolic blood
    pressure.
  • Displaced, diffuse and hyperdynamic apex beat.
  • Early blowing diastolic murmur.
  • ECG Left axis deviation, LV hypertrophy.
  • CXR Cardiomegaly, aortic calcification, aortic
    root dilatation.

42
Aortic regurgitation
  • Management
  • Medical treatment includes
  • - Diuretics, digoxin, salt restriction
  • - Vasodilators
  • - Endocarditis prophylaxis
  • Indications for surgical treatment depend on
    symptoms,
  • and LV size and function.
  • Without surgery, death usually occurs within 4
    years of developing angina and within 2 years
    after onset of heart failure.

43
Aortic regurgitation
  • Surgical therapy
  • Severe acute AR requires prompt surgical
    intervention.
  • Indications for valve replacement in pure,
    severe, chronic AR include
  • - Symptomatic patients with normal LV function
  • - Symptomatic patients with LV dysfunction or
    dilatation
  • - Asymptomatic patients with LV dysfunction or
    dilatation (EFlt50 or end-systolic diameter gt
    55mm)
  • Aortic valve and root replacement are indicated
    in patients with disease of the proximal aorta
    and AR of any severity when the aortic root
    diameter is 50mm.

44
Aortic valve replacement and prognosis
Relation of preoperative LV function to
postoperative survival
45
Mitral stenosis
  • Aetiology
  • Rheumatic fever is the predominant cause.
  • Rarely, mitral stenosis is congenital and
    observed almost exclusively in infants and young
    children.
  • Miscellaneous rare causes include carcinoid, SLE,
    rheumatoid arthritis and mucopolysaccharidoses.
  • Causes of left atrial outflow obstruction that
    may simulate mitral stenosis include left atrial
    myxoma, ball-valve thrombus, infective
    endocarditis with large vegetation and cor
    triatriatum.

46
Rheumatic mitral stenosis
  • Rheumatic mitral stenosis is due to four forms of
    fusion commissural (30), cuspal (15), chordal
    (10) or combined (45).
  • The stenotic mitral valve is typically
    funnel-shaped the orifice is frequently shaped
    like a fish mouth.
  • Symptoms usuually occur in the 3rd or 4th decade,
    but mild MS in the aged is becoming more common.
  • 25 of patients with rheumatic mitral valve
    disease have pure mitral stenosis and two-thirds
    are female.
  • May be associated with an atrial septal defect
    Lutembachers syndrome.

47
Mitral stenosis
  • Pathophysiology
  • Normal mitral valve area 4-6cm2.
  • Usually, a mitral valve area 2.5cm2 must occur
    before the development of symptoms.
  • A mitral valve area gt1.5cm2 usually does not
    produce symptoms at rest.
  • The first symptoms in mild mitral stenosis are
    usually precipitated by exercise, emotional
    stress, infection, pregnancy or fast atrial
    fibrillation.
  • A mitral valve area 1cm2 equates to severe
    mitral stenosis.
  • Pulmonary hypertension results from backward
    pressure, pulmonary arteriolar constriction and
    organic obliterative changes in the pulmonary
    vascular bed.

48
Mitral stenosis
  • Natural history
  • Long latent period of 20 to 40 years from the
    occurrence of rheumatic fever to onset of
    symptoms.
  • Once symptoms develop, there is a further 10
    years before symptoms become disabling.
  • Once significant limiting symptoms occur, the
    10-year survival rate is 5-15.
  • When there is severe pulmonary hypertension, mean
    survival falls to lt 3 years.
  • Mortality from untreated mitral stenosis is due
    to progressive heart failure (60-70), systemic
    embolism (20-30) and pulmonary embolism (10).

49
Mitral stenosis
  • Clinical features
  • The main symptom is dyspnoea due to reduced lung
    compliance.
  • Haemoptysis may also occur.
  • Approximately 15 of patients experience angina
    due to either coincidental coronary artery
    disease, right ventricular hypertension or
    coronary embolisation.
  • Embolic events may occur and 80 of such patients
    are in atrial fibrillation.

50
Mitral stenosis
  • Physical findings
  • Mitral facies pinkish-purple patches on the
    cheeks.
  • Tapping apex beat palpable first heart sound.
  • Right ventricular heave, loud P2 indicating
    pulmonary hypertension.
  • Loud first heart sound.
  • Opening snap.
  • Rumbling, mid-diastolic murmur with
    presystolic accentuation in sinus rhythm.

51
Mitral stenosis
  • Echo evaluation
  • Assessment of valve morphology degree of leaflet
    thickness, mobility and calcification and extent
    of subvalvular fusion.
  • Estimation of left atrial size.
  • Doppler echo estimation of mitral valve area,
    transvalvular gradient and PA pressure.

52
Mitral stenosis
  • Medical treatment
  • The asymptomatic patient with mild mitral
    stenosis should be managed medically. Medical
    therapy includes
  • - Avoidance of unusual physical stress.
  • - Salt restriction.
  • - Diuretics if needed.
  • - Control of heart rate ß-blocker or digoxin.
  • - Anticoagulation for AF or prior embolic
    event.
  • - Annual follow-up.
  • - Echocardiography if deterioration in clinical
    condition.

53
Mitral stenosis
  • Management of symptomatic mitral stenosis
  • Patients with symptoms should undergo clinical
    re-evaluation with echocardiography.
  • NYHA class II symptoms and mild mitral stenosis
    may be managed medically.
  • NYHA class II symptoms and at least moderate
    stenosis (MVA1.5cm2 or mean gradient 5mmHg) may
    be considered for balloon valvuloplasty.
  • NYHA class III or IV symptoms and severe mitral
    stenosis should be considered for balloon
    valvuloplasty or surgery.

54
Mitral stenosis
  • Balloon mitral valvuloplasty
  • The technique involves passing a balloon
    flotation catheter across the interatrial septum
    after trans-septal puncture and dilating the
    balloon within the mitral valve orifice.
  • Results of the procedure are highly dependent on
    the experience of the operator.
  • 80-95 of patients have a successful procedure.
  • Complications include severe MR, residual ASD,
    myocardial perforation, emboli, MI and death.
  • Overall event-free survival is 50 to 65 over
    3-7 years.
  • The underlying mitral valve morphology is the
    most important factor in determining outcome.
  • Relative contraindications include the presence
    of a left atrial thrombus and significant mitral
    regurgitation.

55
Mitral stenosis
  • Mitral valve replacement
  • Mitral valve replacement is indicated in patients
    with severe mitral stenosis and contraindications
    to surgical commisurotomy or balloon
    valvuloplasty
  • - Restenosis following surgical commisurotomy
    or balloon valvuloplasty.
  • - Significant mitral stenosis and
    regurgitation.
  • - Extensive calcification of the subvalvular
    apparatus.
  • Operative mortality ranges from 3-8 in most
    centres.
  • Postponement of surgery until the patient reaches
    NYHA class IV symptoms should be avoided.

56
Mitral regurgitation
  • Aetiology
  • Mitral regurgitation may be caused by
    abnormalities of the valve leaflets, chordae
    tendinae, papillary muscles or mitral annulus
  • Valve leaflets
  • - myxomatous degeneration causing mitral valve
    prolapse
  • - shortening, rigidity, deformity and
    retraction due to rheumatic heart disease
  • - vegetations due to infective endocarditis
  • Chordae tendinae
  • - congenital, infective endocarditis, trauma,
    rheumatic fever, myxomatous
  • Papillary muscles
  • - myocardial ischaemia, congenital
    abnormalities, infiltrative disease
  • Mitral annulus
  • - dilatation eg. ischaemic or dilated
    cardiomyopathy
  • - calcification due to degeneration,
    hypertension, aortic stenosis, diabetes,
    chronic renal failure

57
Mitral regurgitation
  • Clinical features
  • Symptoms usually occur with LV decompensation
    dyspnoea and fatigue.
  • Physical findings include
  • - Pulse sharp upstroke
  • - Apex displaced, hyperdynamic
  • - Heart sounds pansystolic murmur loudest at the
    apex, radiating to the axilla and accentuated by
    expiration.

58
Mitral regurgitation
  • Natural history
  • The natural history of chronic MR depends on the
    volume of regurgitation, the state of the
    myocardium and the underlying cause.
  • Preoperative LV end-systolic diameter is a useful
    predictor of postoperative survival in chronic
    MR.
  • The preoperative LV end-systolic diameter should
    be lt 45mm to ensure normal postoperative LV
    function.

59
Mitral regurgitation
  • Medical treatment
  • Symptomatic patients may benefit from the
    following drug therapy whilst awaiting surgery
  • Vasodilator therapy
  • Diuretics
  • Digoxin / Beta-blockers in presence of atrial
    fibrillation.
  • Endocarditis prophylaxis

60
Mitral regurgitation
  • Surgical treatment
  • Surgery is indicated in the presence of symptoms
    or left ventricular end systolic diameter 45mm.
  • The surgical procedure consists of either mitral
    valve repair or replacement.
  • Mitral valve repair better preserves LV function
    and avoids the need for chronic anticoagulation.
  • However, mitral valve repair is technically more
    demanding and often not possible to perform in
    severely deformed valves.

61
Mitral regurgitation
Relationship of preoperative ejection fraction
to postoperative survival
62
Acute mitral regurgitation
  • Aetiology
  • Important causes of acute mitral regurgitation
    include
  • Infective endocarditis causing disruption
  • of valve leaflets or chordal rupture.
  • Ischaemic dysfunction or rupture of papillary
    muscle.
  • Malfunction of prosthetic valve.

63
Chronic versus Acute MR
  • Finding Chronic MR Acute MR
  • Symptoms subtle onset obvious
  • Appearance normal/mildly severely ill
  • dyspnoeic
  • Tachycardia not striking always present
  • Apex beat displaced not displaced
  • Systolic thrill common absent
  • Murmur harsh pansystolic soft
    or absent early systolic component
  • ECG-LVH usually present absent
  • CXR severe cardiomegaly normal
    heart size

64
Acute mitral regurgitation
  • Medical therapy
  • The following therapies may be beneficial in
    reducing the severity of MR
  • - Vasodilator therapy
  • - Inotropic therapy
  • - Intra-aortic balloon counterpulsation
  • Surgical therapy
  • Indicated in patients with acute severe MR and
    heart failure.
  • Higher mortality rates than for elective chronic
    MR, but unless treated aggressively, the
    outcome is usually fatal.

65
Mitral valve prolapse
  • General features
  • Occurs in 2-6 of the general population
  • Twice as common in women.
  • Due to myxomatous proliferation of the mitral
    valve.
  • Usually occurs as a primary condition, but may
    be a secondary
  • finding in connective tissue diseases e.g.
    Marfans syndrome.
  • Vast majority of patients are asymptomatic.
  • Symptoms may include palpitations, dizziness,
    syncope, or chest
  • discomfort.
  • The principal physical finding is the
    mid-systolic click, followed
  • by a late systolic murmur in the presence of
    regurgitation.

66
Mitral valve prolapse
  • Echocardiographic criteria
  • M-mode criterion ? 2mm posterior displacement
    of one or both
  • leaflets.
  • 2-D echo findings Systolic displacement of one
    or both leaflets
  • within the left atrium in the parasternal
    long-axis view leaflet
  • thickening, redundancy, chordal elongation and
    annular dilatation.
  • The diagnosis of mitral valve prolapse is even
    more certain
  • when leaflet thickness is gt5mm.
  • Echocardiography is useful in the risk
    stratification of patients
  • with mitral valve prolapse.

67
Mitral valve prolapse
  • Natural history
  • In most patients, mitral valve prolapse is
    associated with a benign
  • prognosis.
  • Complications may occur in patients with a
    systolic murmur,
  • thickened leaflets an increased LV or LA size,
    especially in men
  • gt 45 years old
  • Complications include progressive mitral
    regurgitation, infective
  • endocarditis, cerebral emboli, arrhythmias and
    rarely sudden death.

68
Mitral valve prolapse
  • Management
  • Asymptomatic patients without MR or arrhythmias
    have an excellent prognosis follow-up every 3-5
    years.
  • Patients with a typical systolic murmur should
    receive endocarditis prophylaxis.
  • Patients with a long systolic murmur may show
    progression of MR and should be reviewed
    annually.
  • Patients with previous embolic events should be
    given antiplatelet / anticoagulant therapy.
  • Severe MR requires surgery, often mitral valve
    repair.

69
Prosthetic valves
  • Prosthetic valves may be divided into 2 broad
    categories
  • Mechanical valves
  • Very good durability.
  • Require long-term anticoagulation.
  • May cause mild haemolysis.
  • Bioprosthetic (tissue) valves
  • Porcine variety most commonly used.
  • Limited durability.
  • Anticoagulation for first 3 months only.

70
Mechanical valves
Designs and flow patterns of different types of
mechanical valves
71
Prosthetic valves
  • Mechanical versus tissue valves
  • No difference in survival, haemodynamics or in
    probability of
  • developing endocarditis, valve thrombosis or
    systemic embolism.
  • Valve-related failure is much more common with
    tissue valves.
  • Anticoagulant-related bleeding occurs with
    mechanical valves.
  • Elderly patients tend to receive tissue valves.

72
Tricuspid stenosis
  • Always rheumatic in origin and when present
    accompanies mitral valve involvement.
  • The anatomical changes and physiological
    principles are similar to those of mitral
    stenosis.
  • The low cardiac output state causes fatigue
    abdominal discomfort may occur due to
    hepatomegaly and ascites.
  • The diastolic murmur of tricuspid stenosis is
    augmented by inspiration.
  • Medical management includes salt restriction and
    diuretics.
  • Surgical treatment should be carried out in
    patients with a valve area lt2.0cm2 and a mean
    pressure gradient gt5mmHg.

73
Tricuspid reurgitation
  • Most common cause is annular dilatation due to RV
    failure of any cause may also be caused by
    intrinsic valve involvement
  • Well tolerated in the absence of pulmonary
    hypertension in the presence of pulmonary
    hypertension, cardiac output declines and RV
    failure may worsen.
  • Symptoms and signs result from a reduced cardiac
    output, ascites, painful congestive hepatomegaly
    and oedema.
  • The pansystolic murmur of TR is usually loudest
    at the left sternal edge and augmented by deep
    inspiration.
  • Severe functional TR may be treated by
    annuloplasty or valve replacement. Severe TR due
    to intrinsic tricuspid valve disease requires
    valve replacement.

74
Pulmonary stenosis
  • Most commonly due to congenital malformation and
    usually an isolated anomaly.
  • Survival into adulthood is the rule, infective
    endocarditis is a risk and right ventricular
    failure is the most common cause of death.
  • Rheumatic involvement of the pulmonary valve is
    very uncommon and rarely leads to serious
    deformity.
  • Carcinoid plaques may lead to constriction of the
    pulmonary valve ring.

75
Pulmonary regurgitation
  • Most common cause is ring dilatation due to
    pulmonary hypertension, or dilatation of the
    pulmonary artery secondary to a connective tissue
    disorder.
  • May be tolerated for many years unless
    complicated by pulmonary hypertension.
  • The clinical manifestations of the primary
    disease tend to overshadow the pulmonary
    regurgitation.
  • Physical examination reveals a right ventricular
    heave and a high-pitched, blowing, early
    diastolic decrescendo murmur over the left
    sternal edge, augmented by deep inspiration.
  • Pulmonary regurgitation is seldom severe enough
    to require specific treatment. Surgery may be
    required because of intractable RV failure.
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