Transcript VALVULAR HEART DISEASE

VALVULAR HEART DISEASE
Goals and Objectives
• Discuss the common etiologies of valvular
stenosis and regurgitation.
• Recognize the signs and symptoms of
severe valvular stenosis and regurgitation
• Be able to quickly identify and treat acute
mitral and aortic regurgitation
• Identify patients who should be referred for
surgical replacement of their valves
Mitral Stenosis
Etiology of Mitral Stenosis
• Rheumatic heart disease: 77-99% of all
cases
• Infective endocarditis: 3.3%
• Mitral annular calcification: 2.7%
• Congenital: rare
Mitral Stenosis Overview
• Definition: Obstruction of LV inflow that
prevents proper filling during diastole
• Normal MV Area: 4-6 cm2
• Transmitral gradients and symptoms begin
at areas less than 2 cm2
• Rheumatic carditis is the predominant cause
• Prevalence and incidence: decreasing due
to a reduction of rheumatic heart disease.
MS Pathophysiology
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Progressive fibrosis ,thicking ,calcifications of of valve
leaflets and fusion of commisures leads to gradual
narrowing of mitral valve orifice,symptoms begin at
areas less than 2 cm2
 restricted blood flow from LA to LV and LA pressure
rises -Leads to left atrial enlargement and atrial
fibrillation(very common)….. pulmonary
congestion(reduced lung compliance) pulmonary venous
hypertension –Progressive and gradual rise in
pulm.venous HTN leads to increase pulm.vascular
resistance and pulm.arterial HTN leading to RVH-later
RV dilatation and RT heart Failure .
SYMPTOMS
• Breathlessness (pulmonary congestion) dominant •
• Fatigue (low cardiac output) •
• Palpitation (atrial fibrillation) •
• Haemoptysis (pulmonary congestion, pulmonary
embolism) •
• Cough (pulmonary congestion) •
• Chest pain (pulmonary hypertension) •
• Oedema, ascites (right heart failure)
• Thromboembolic complications (e.g. stroke, ischaemic
limb)
SIGNS
• Dyspneaic,Mitral facies -malar flush(pinkishpurple patches on the cheeks)
• JVP normal or raised
• Pluse usually irregular due to Atrial fibrillation
LOCAL:
• Palpation : Apex tapping(loud S1), • RV heave, loud P2
(pulmonary hypertension)-diastolic thrill.
• • Auscultation Loud first heart sound, opening snap ,Middiastolic murmur •
• Crepitations, pulmonary oedema, effusions
• Signs of right-sided heart failure: in advanced disease
Heart Sounds in MS
• Diastolic murmur:
– Low-pitched diastolic rumble most prominent at
the apex.
– Heard best with the patient lying on the left side
in held expiration
– Intensity of the diastolic murmur does not
correlate with the severity of the stenosis
Heart Sounds in MS
• Loud S1-Opening snap: heard at the apex when
leaflets are still mobile
– Due to the abrupt halt in leaflet motion in early
diastole, after rapid initial rapid opening, due to
fusion at the leaflet tips.
– A shorter S2 to opening snap interval indicates
more severe disease.-
Investigations
• ECG: may show atrial fibrillation and LA
enlargement
• CXR: LA enlargement and pulmonary
congestion. Occasionally calcified MV
• ECHO: The GOLD STANDARD for
diagnosis. Asses mitral valve mobility,
gradient and mitral valve area,other lesions
• Cardiac catheterization
Management of MS
Serial echocardiography:
– Mild: 3-5 years
– Moderate:1-2 years
– Severe: yearly
• Medications: MS is a mechanical problem and
medical therapy does not prevent progression
– -blockers, CCBs, Digoxin which control heart rate
in atrial fibrillation
– Anticoagulant to prevent thromboembolization in
atrial fib.
– Duiretics for fluid overload and pulm .congestion
Management of MS
• Rheumatic fever prophylaxis
• IE prophylaxis: Patients with prosthetic valves or
a Hx of IE for dental procedures.
Nonmedical managment
• Mitral balloon valvuloplasty and valve
replacement(MVR)
• Symptomatic mod/sever MS +favorable anatomy
• Asymptomatic mod/sever MS +pulm.HTN
+favorable anatomy(Isolated mitral stenosis • No
mitral regurgitation, Mobile, non calcifiedvalve/subvalve
apparatus on echo • LA free of thrombus )
• Valve replacement(MVR)
Mitral Regurgitation
Chronic Mitral Regurgitation
Overview
• Definition: Backflow of blood from the LV to
the LA during systole
• Mild (physiological) MR is seen in 80% of
normal individuals.
Acute MR
• Endocarditis
• Acute MI:
• Malfunction or disruption of prosthetic
valve
Etiologies of Chronic Mitral
Regurgitation
-Mitral valve prolapse
-Dilatation of the LV and mitral valve ring
(e.g. coronary artery disease, cardiomyopathy)
-Rheumatic fever
-Ischaemia or infarction of the papillary
muscle
-Myocardial infarction
Mitral valve prolapse
• Occurs in 5% of adults
• Floppy MV, caused by congenital
anomalies or degenerative myxomatous
changes, Marfans syndrome.
• Asymptomatic,atypical chest pain ,benign
arrythmia ,small risk of embolic stroke
• Mid systolic click and late systolic murmur
• Prognosis is good
Pathophysiology of MR
• Pure Volume Overload
• Compensatory Mechanisms: Left atrial
enlargement, LVH and increased
contractility,LV dilatation.
– Progressive left atrial dilation and right ventricular
dysfunction due to pulmonary hypertension.
– Progressive left ventricular volume overload leads to
dilation and progressive heart failure.
SYMPTOMS
Asymptomatic
• Dyspnoea (pulmonary venous congestion)
Fatigue (low cardiac output)
• Palpitation (atrial fibrillation, increased
stroke volume)
• Oedema, ascites (right heart failure)
Systemic embolization { stroke , ischaemic
limb etc.. }
Signs
• Pulse :Atrial fibrillation/flutter
• Cardiomegaly: displaced hyperdynamic
apex beat
• Apical pan.systolic murmur ± thrill • Soft
S1, apical S3.
• Signs of pulmonary venous congestion
(crepitations, pulmonary oedema, effusions)
• Signs of pulmonary hypertension and right
heart failure.
Investigations in MR
• ECG: May show, LA enlargement, atrial
fibrillation and LV hypertrophy with severe MR
• CXR: LA enlargement, central pulmonary
artery enlargement.
• ECHO: Estimation of LA, LV size and
function. Valve structure assessment
– TEE if transthoracic echo is inconclusive
– Cardiac catheterization.
Management of MR
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Medications
Mild –moderate MR can be treated
medically
a) Vasodilator such as hydralazine,ACE inhibitors
b) Rate control for atrial fibrillation with blockers, CCB, digoxin in AF
c) Anticoagulation in atrial fibrillation and flutter
d) Diuretics for fluid overload
•
Serial Echocardiography:
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Mild: 2-3 years
Moderate: 1-2 years
Severe: 6-12 months
IE prophylaxis: Patients with prosthetic
valves or a Hx of IE for dental procedures.
Surgical
• Repair or MVR
• Sever even asymptomatic
• Progressive cardiomegaly or progressive
deterioration of LV function by ECHO
Treatment of Acute MR
• Balloon Pump
• Nitroprusside even if hypotensive
• Emergent Surgery
Aortic Stenosis
Aortic Stenosis Overview:
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Normal Aortic Valve Area: 3-4 cm2
Symptoms: Occur when valve area is
1/4th of normal area.
• Types:
– Supravalvular
– Subvalvular
– Valvular
Etiology of Aortic Stenosis
• Congenital(Bi-cusped).
• Rheumatic.
• Degenerative/Calcific.
Patients under 70: >50% have a congenital
cause
Patients over 70: 50% due to degenerative
Evaluation of AS
Cardiac catheterization: Should only be done for a direct
measurement if symptom severity and echo severity don’t
match OR prior to replacement when replacement is planned.
Pathophysiology of Aortic Stenosis
• A pressure gradient develops between the
left ventricle and the aorta. (increased
afterload)
• LV function initially maintained by
compensatory pressure hypertrophy
to maintain the cardioac output
• When compensatory mechanisms
exhausted, LV function declines and
pulm.edema supervenes.
Presentation of Aortic Stenosis
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Asymptomatic mild/moderate
Syncope: (exertional)
Angina: (increased myocardial oxygen
demand; demand/supply mismatch)
Dyspnea: on exertion due to heart failure
(systolic and diastolic)
Sudden death
Physical Findings in Aortic Stenosis
• Slow rising carotid pulse (pulsus tardus)
• Thrusting apex beat (LV pressure overload) • Narrow
pulse pressure
• Heart sounds- soft and split second heart
sound, S4 gallop due to LVH.
• Systolic ejection murmur- cresendodecrescendo character. This peaks later as
the severity of the stenosis increases.
– Loudness does NOT tell you anything about
severity
Investigations
• ECG Left ventricular hypertrophy ,LBBB
• Chest X-ray May be normal; sometimes enlarged
LV and dilated ascending aorta on PA view,
calcified valve on lateral view.
• Echo Calcified valve with restricted opening,
hypertrophied LV) Doppler • Measurement of
severity of stenosis • Detection of associated aortic
regurgitation.
• Cardiac catheterisation • Mainly to identify
associated coronary artery disease • May be used
to measure gradient between LV and aorta.
Management of AS
• General- IE prophylaxis in dental procedures
with a prosthetic AV or history of endocarditis.
• Medical - limited role since AS is a mechanical
problem. Vasodilators are relatively
contraindicated in severe AS
• Aortic Balloon Valvotomy- shows little
benefit.
• Surgical Replacement: Definitive treatment
Simplified Indications for Surgery
in Aortic Stenosis
• Any SYMPTOMATIC patient with severe
AS (includes symptoms with exercise)
• Any patient with decreasing EF
• Any patient undergoing CABG with
moderate or severe AS
Aortic Regurgitation
Aortic Regurgitation Overview
• Definition: Leakage of blood into LV during
diastole due to ineffective coaptation of the
aortic cusps.
Etiology of Acute AR
• Endocarditis
• Aortic Dissection
• Physical Findings:
– Wide pulse pressure
– Diastolic murmur
– Florid pulmonary edema
Treatment of Acute AR
• True Surgical Emergency:
• Positive inotrope: (eg, dopamine,
dobutamine)
• Vasodilators: (eg, nitroprusside)
• Avoid beta-blockers
• Do not even consider a balloon pump
Etiology of Chronic AR
Cusps defects
• Congenital -Bicuspid aortic valve
• Rheumatic
• Infective endocarditis
Aortic root dilatation Marfan.
Pathophysiology of AR
• Combined pressure AND volume overload
• Compensatory Mechanisms: LV dilation,
LVH. Progressive dilation leads to heart
failure.
Symptoms
• Asymptomatic until 4th or 5th decade
• Progressive Symptoms include:
- Dyspnea: exertional, orthopnea, and
paroxsymal nocturnal dyspnea
- Nocturnal angina: due to slowing of heart rate
and reduction of diastolic blood pressure.
- Palpitations: due to increased force of
contraction.
Signs
 Peripheral
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signs
Pulses Large volume or ‘collapsing’ pulse.
Corrigan pulse
Increased pulse pressure
Bounding peripheral pulses
Capillary pulsation in nail beds: Quincke’s sign •
Femoral bruit (‘pistol shot’)
Duroziez’s sign •
Head nodding with pulse: de Musset’s sign.
Hill’s sign
JVP may be normal or elevated
Central Signs
• Apex : Hyperdynamic and displaced apical
impulse.
• Diastolic thrill.
• Auscultation
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High pitched, blowing, decrescendo diastolic
murmur at LSB, best heard at end-expiration
& leaning forward.
 Austin-Flint murmur indicates severity (mid to
late diastolic murmur)
 Systolic murmur related to high flow state
Investigations
• ECG Initially normal, later left ventricular
hypertrophy and T-wave inversion
• Chest X-ray Cardiac dilatation, maybe aortic
dilatation Features of left heart failure
• Echo Dilated LV •Hyperdynamic LV • Doppler
detects reflux • Fluttering anterior mitral leaflet
• Cardiac catheterisation (may not be required) •
Dilated LV • Aortic regurgitation • Dilated aortic root.
Management of AR
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General: IE prophylaxis in dental procedures
with a prosthetic AV or history of
endocarditis.
Medical: Vasodilators (ACEI’s), Nifedipine
improve stroke volume and reduce
regurgitation only if pt symptomatic or HTN.
Serial Echocardiograms: to monitor
progression.
Surgical Treatment: Definitive Tx
Simplified Indications for Surgical
Treatment of AR
• ANY Symptoms at rest or exercise
• Asymptomatic treatment if:
– EF drops below 50% or LV becomes
dilated.
Tricuspid stenosis
Almost always rheumatic
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 in patients with a valve area
<2.0cm and a mean pressure gradient >5mmHg.
Tricuspid regurgitation
Most common cause is annular dilatation due to RV failure of
any cause
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.
Pulmonary stenosis
Most commonly due to congenital malformation
Survival into adulthood is the rule, infective
endocarditis is a risk and right ventricular failure is
the most common cause of death.
Carcinoid plaques may lead to constriction of the
pulmonary valve ring.
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 present and well-tolerated for
many years
• The clinical manifestations of the primary disease
tend to overshadow the pulmonary regurgitation.
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