Valvular Heart Disease

Mardlatillah, MD
Learning Objective
• Heart Sound and cardiac cycle
• Mitral valve disease
• Mitral valve Stenosis
• Mitral valve regurgitation
• Aortic valve disease
• Aortic valve stenosis
• Aortic valve regurgitation
 Semilunar

VALVE PATHOLOGIES :

Stenosis
(FAILED TO OPEN)

Regurgitation
(FAILED TO CLOSE)

AV valves
Quiz
• Saat systole (pengosongan ventrikel) katup yang membuka adalah?
• Katup semilunar
• Katup AV
• Saat systole (pengosongan ventrikel) katup yang menutup adalah?
• Katup semilunar
• Katup AV
• Saat diastole (pengisian ventrikel) katup yang membuka adalah?
• Katup semilunar
• Katup AV
• Saat diastole (pengisian ventrikel) katup yang menutup adalah?
• Katup semilunar
• Katup AV
HEART SOUND
Auscultation Landmark
CARDIAC CYCLE
 HEART MURMUR
A murmur  the sound generated by turbulent blood flow

1. Flow across a partial obstruction (e.g., aortic stenosis)

2. Increased flow through normal structures (e.g., aortic systolic murmur associated with a high-
output state, such as anemia)
3. Ejection into a dilated chamber (e.g., aortic systolic murmur associated with aneurysmal
dilatation of the aorta)
4. Regurgitant flow across an incompetent valve (e.g., mitral regurgitation)
5. Abnormal shunting of blood from one vascular chamber to a lower-pressure chamber (e.g.,
ventricular septal defect [VSD])
• Murmurs are described by their timing, intensity, pitch, shape, location, radiation, and
response to maneuvers. Timing refers to whether the murmur occurs during systole or
diastole, or is continuous (i.e., begins in systole and continues into diastole). The intensity
of the murmur is typically quantified by a grading system.
 Sistolic Diastolic
murmur murmur

Aorta : Mitral : Mitral : Aorta :

FAILED TO FAILED TO FAILED TO FAILED TO
OPEN CLOSE OPEN CLOSE
Quiz
• Holosystolic murmur grade 3/6 at apex
• Mitral stenosis
• Mitral regurgitation
• Aortic stenosis
• Ejection systolic crescendo decrescendo murmur grade 3/6 di Right upper sternal border
• Aortic regurgitation
• Mitral regurgitation
• Aortic stenosis
• Early diastolic decrescendo murmur grade 3/4 di left sternal border ICS III
• Aortic regurgitation
• Mitral regurgitation
• Aortic stenosis
• Diastolic decrescendo crescendo murmur grade 2/4 at apex
• Mitral stenosis
• Mitral regurgitation
• Aortic stenosis
• Holosystolic murmur grade 2/6 di left lower sternal border
• Aortic regurgitation
• Mitral regurgitation
• Tricuspid regurgitation
MITRAL STENOSIS
MITRAL REGURGITATION
AORTIC STENOSIS
AORTIC REGURGITATION
HOW TO DIAGNOSE THE PATIENT WITH
VALVULAR HEART DISEASE?
MITRAL STENOSIS
Causes and pathology

The predominant cause 

Rheumatic fever
(Characteristic changes of the mitral
valve : thickening at the leaflet edges,
fusion of the commissures, and
chordal shortening and fusion )
 2/3 female
Causes and anatomic presentation
Mitral
Mitral Stenosis
Stenosis

Rheumatic Degenerative Congenital Others

Mainly commissural Mainly annular Mainly Inflammatory
fusion; calcification; abnormalities diseases (e.g.
Other anatomic Predominates at of SLE), infiltrative
lesions → chordal the base of leaflet subvalvular diseases,
shortening and apparatus carcinoid
fusion, leaflet heart disease, and
thickening, drug-induced
superimposed valve diseases
calcification
Pathophysiology
Severity of mitral valve obstruction is
the degree of valve opening in diastole,
or the mitral valve orifice area

In normal adults  4 to 6 cm2

Severe MS opening is reduced to 1 cm2  a left
atrioventricular pressure gradient of approximately
20 mm Hg

Increase the rate of blood flow across the mitral

orifice, resulting in further elevation of the left
atrial pressure The elevated left atrial pressure, in turn,
Decrease the diastolic filling time raises pulmonary venous and capillary
 resulting in a reduction in forward cardiac pressures, resulting in exertional dyspnoea
output  Fatigue
Hemodynamic Consequences

Pulmonary hypertension
• Elevated atrial pressure
• Pulmonary arteriolar constriction, triggered by left
atrial and pulmonary venous hypertension (reactive
pulmonary hypertension)
• Organic obliterative changes in the pulmonary
vascular bed, which may be considered to be a
complication of longstanding and severe MS
• RV dysfunction
• LV chamber typically is normal or small, with normal
systolic function
Hemodynamic Consequences

Left Atrial Changes

• The combination of mitral valve disease and atrial inflammation secondary
to rheumatic carditis causes :

• left atrial dilation,

• fibrosis of the atrial wall, and
• disorganization of the atrial muscle bundles.

• AF  irreversible

Left atrial enlargement and stasis of blood flow  increased risk of

thrombus formation and systemic embolism.
Clinical Presentation
Symptoms

Hemoptysis Dyspnea on Palpitations and Other Symptoms

exercise / Chest Embolic Events
Pain
Rare Often diagnosed when Fatigue
Increasing of LA pressure  they present with AF or
Sudden and severe, caused by increasing of pulmonary an embolic event
rupture of thin-walled, dilated vein pressure  pulmonary Ortner syndrome
bronchial veins, usually as a
consequence of a sudden rise in left edema
atrial pressure Right sided Heart Failure :
Not a typical symptom of MS Systemic venous hypertension;
 caused by severe RV hepatomegaly, edema, ascites
hypertension secondary to
the pulmonary vascular
disease or by concomitant
coronary atherosclerosis.
 Physical Examination

• The most common findings : irregular pulse caused by AF and signs of left-
and right-heart failure.

• Patients with severe chronic MS, a low cardiac output, and systemic
vasoconstriction may exhibit the so-called mitral facies, characterized by
pinkish-purple patches on the cheeks.

• When the patient is in the left lateral recumbent position, a diastolic thrill of
MS may be palpable at the apex.

• Often, a RV lift is felt in the left parasternal region in patients with PH. A
markedly enlarged right ventricle may displace the left ventricle posteriorly
and produce a prominent RV apex beat that can be confused with a LV lift.
 Physical Examination

An accentuated S1, correlating with the level of the left atrial pressure.

The opening snap (OS) of the mitral valve is caused by a sudden tensing of the valve leaflets after the valve
cusps have completed their opening excursion. The OS occurs when the movement of the mitral dome into the
left ventricle suddenly stops. It is most readily audible at the apex.

The diastolic, low-pitched, rumbling murmur of MS is best heard at the apex, with the bell of the stethoscope
(low-frequency mode on electronic stethoscopes) and with the patient in the left lateral recumbent position

Other signs of severe PH include a nonvalvular pulmonic ejection sound that diminishes during inspiration,
because of dilation of the pulmonary artery, a systolic murmur of TR, a Graham Steell murmur of pulmonic
regurgitation, and a S4 originating from the right ventricle.
Management

Drug Treatment
• Prevention of recurrent rheumatic
fever
• Prevention and treatment of
complications of MS
• Monitoring disease progression to
allow intervention at the optimal time
MITRAL REGURGITATION
Causes and pathology
Pathophysiology
Clinical Presentation

Symptoms

Patients with secondary MR related to LV dysfunction often present with heart

failure symptoms, but many are asymptomatic, with MR detected incidentally on
physical examination or echocardiography.
 Physical Examination

• Palpation of the arterial pulse is helpful in differentiating AS from MR, both of

which may produce a prominent systolic murmur at the base of the heart and
apex

• It is displaced to the left, and a prominent LV filling wave is frequently palpable.

Systolic expansion of the enlarged left atrium may result in a late systolic thrust
in the parasternal region, which may be confused with RV enlargement.
 Physical Examination
Auscultation

The systolic murmur is the most prominent physical finding

The holosystolic murmur of chronic MR is usually constant in intensity, blowing,

high-pitched, and loudest at the apex, with frequent radiation to the left axilla and
left infrascapular area.

The murmur of MR may be holosystolic, late systolic, or early systolic.

When the murmur is confined to late systole, the regurgitation usually is
secondary to MVP or to papillary muscle dysfunction and is not severe.
Early systolic murmurs are typical of acute MR.
Management
Case
25-year-old female who is 33 weeks into her pregnancy is becoming
increasingly short of breath with some lower extremity edema. She is
afebrile with a heart rate of 110 beats per minute, respirations 20 per minute
and blood pressure 100/60 mm Hg. Physical examination reveals a II/IV early
diastolic decrescendo murmur at the cardiac apex. Which of the following is
the likely valvular pathologies?
A. Aortic stenosis
B. Aortic regurgitation (with Austin-Flint murmur)
C. Mitral stenosis
D. Mitral regurgitation
E. Atrial septal defect
AORTIC STENOSIS
Three cusps, crescent shaped (3-4 cm2)
- 3 commissures
- 3 sinuses
- Supported by fibrous annulus
Causes and pathology
Pathophysiology
Clinical Presentation

Symptoms SAD
 Physical Examination

• Palpation of the carotid upstroke (The expected finding with severe AS is a

slow-rising, late-peaking, low-amplitude carotid pulse, the parvus and tardus
carotid impulse  specific for severe AS)

• Systolic murmur (The ejection systolic murmur of AS typically is late-

peaking and heard best at the base of the heart, with radiation to the
carotids ). In patients with calcified aortic valves, the systolic murmur is
loudest at the base of the heart, but high-frequency components may
radiate to the apex—the so-called Gallavardin phenomenon
Others:

• The cardiac impulse is sustained and becomes displaced

inferiorly and laterally with LV failure.

• A systolic thrill usually is best appreciated when the patient

leans forward during full expiration. It is palpated most readily in
the second right intercostal space or suprasternal notch and
frequently is transmit- ted along the carotid arteries. A systolic
thrill is specific, but not sensitive, for severe AS.
AORTIC REGURGITATION
Causes and pathology

Primary AR Secondary AR

• Congenital (most frequently bicuspid • Aortic aneurysm with sinotubular

aortic disease) junction dilatation (congenital:
• Rheumatic disease Infective bicuspid, Marfan,
endocarditis • inflammatory or infectious,
• Degenerative disease (frequently atherosclerosis, and hypertension)
combined with aortic stenosis) • Aortic dissection
• Aortic dissection extending into the
aortic root and disrupting the normal
leaflet attachment
• Redundant dissection flap prolapsing
through intrinsically normal leaflets
Causes and pathology
Pathophysiology
Clinical Presentation

Symptoms
• In chronic severe AR, the left ventricle gradually enlarges while the patient
remains asymptomatic.

• Symptoms of reduced cardiac reserve or myocardial ischemia develop,

most often in the fourth or fifth decade of life, and usually only after
considerable cardiomegaly and myocardial dysfunction have occurred.

• The principal manifestations—exertional dyspnea, orthopnea, and

paroxysmal nocturnal dyspnea—usually develop gradually. Angina
pectoris is prominent late in the course
Physical Examination
 Physical Examination

• In severe AR, the murmur reaches an early peak and then shows a dominant decrescendo
pattern throughout diastole.

• The severity of AR correlates better with the duration than with the intensity of the murmur.

• In mild AR, the murmur may be limited to early diastole and typically is high-pitched and
blowing.

• A third heart sound (S3) correlates with an increased LV end- diastolic volume. A mid-
diastolic and late diastolic apical rumble, the Austin Flint murmur, is common in severe AR
and may occur in the presence of a normal mitral valve.
Case

50-year-old female is becoming increasingly short of breath. She is

known as hypertension and diabetic patient with history of PCI on
2018. The heart rate is 98 beats per minute, respirations 28 times per
minute and blood pressure 160/30 mmHg. Heart physical examination
reveals a III/IV holosystolic murmur at apex, and II/IV early diastolic
decrescendo murmur at right upper sternal border. Which of the
following is the likely valvular pathologies?

A. Tricuspid regurgitation with pulmonary stenosis

B. Mitral stenosis dan aortic stenosis
C. Mitral regurgitation with aortic regurgitation
D. Tricuspid stenosis dan pulmonal stenosis
Thank You
 Physical Examination
• The head may bob with each heartbeat (de Musset sign)
• Water hammer pulses, abrupt distention and quick collapse (Corrigan pulse), are
eviden
• The arterial pulse often is prominent and can be best appreciated by palpation of the
radial artery with the patient’s arm elevated
• A bisferiens pulse may be present and is more readily recognized in the brachial and
femoral arteries than in the carotid arteries
• A variety of auscultatory findings provide confirmation of a wide pulse pressure.
• The Traube sign (also known as pistol shot sounds) refers to booming systolic and
diastolic sounds heard over the femoral artery
• The Müller sign consists of systolic pulsations of the uvula
• The Duroziez sign consists of a systolic murmur heard over the femoral artery when
it is compressed proximally and a diastolic murmur when it is compressed distally.
• Capillary pulsations (the Quincke sign) can be detected by transmitting a light through the patient’s
fingertips or exerting gentle pressure on the tip of a fingernail.

• Systolic arterial pressure is elevated, and diastolic pressure is abnormally low. Korotkoff sounds often
persist to zero even though the intra-arterial pressure rarely falls below 30 mm Hg. The point of change
in Korotkoff sounds (i.e., the muffling of these sounds in phase IV) correlates with the diastolic pressure.
•
• As heart failure develops, peripheral vasoconstriction may occur and arterial diastolic pressure may rise,
even though severe AR is present.

• The Hill sign (an exaggerated difference in systolic blood pressure between the upper and lower
extremities) is an artifact of sphygmomanometric measurements and is no longer considered a sign of
severe AR.

• The apical impulse is diffuse and hyperdynamic and is displaced laterally and inferiorly; systolic retraction
may be detected over the parasternal region. A rapid ventricular filling wave often is palpable at the apex.
The augmented stroke volume may create a systolic thrill at the base of the heart or suprasternal notch,
and over the carotid arteries.

• In many patients, a carotid shudder is palpable.