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Valvular Heart Disease 2

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The document discusses the main types of valvular heart disease including mitral stenosis, aortic stenosis, mitral regurgitation, aortic regurgitation, tricuspid regurgitation, tricuspid stenosis, pulmonary stenosis and pulmonary regurgitation.

The main types of valvular heart disease discussed are mitral stenosis, aortic stenosis, mitral regurgitation, aortic regurgitation, tricuspid regurgitation, tricuspid stenosis, pulmonary stenosis and pulmonary regurgitation.

The main causes of mitral stenosis discussed are rheumatic fever, congenital defects such as Lutembacher syndrome, and mitral valve annular calcification in elderly patients.

VALVULAR HEART

DISEASE
Dr.Alexandru Nechita
Valvular heart disease
 MITRAL STENOSIS
 AORTIC STENOSIS
 MITRAL REGURGITATION
 AORTIC REGURGITATION
 TRICUSPID REGURGITATION
 TRICUSPID STENOSIS
 PULMONARY STENOSIS
 PULMONARY REGURGITATION
 MIXED LESIONS
MITRAL STENOSIS
Definition:
The mitral valve’s incapacity to
open completely in diastole,
due to
- comisural fusion
- cusps thickenning
- remodeling of the
subvalvular structures
MITRAL STENOSIS
Etiology
Rheumatic fever - most of the patients,
Other etiologies are very rare:
– Congenital, MS+atrial septal defect=

Lutembacher syndrome.

– Mitral valve annular calcification - elderly.

– Other causes of LV inflow obstruction:

 atrial myxoma

 LA ball thrombus

 cor triatriatum.
MITRAL STENOSIS-
Pathology
Posterior
Fusion of the cusp

comissures, cusps or Mitral


annulus
chords.
Anterior
Contracture and cusp

thickening of the cusps. Chordae


tendinae
Shortening and fusion of Papillary
muscles
the chordae tendinae.
Funnel –shaped orifice.
Mitral Stenosis
Pathophysiology
*
 Obstruction between LA and
LV.

 Pressure gradient.

 Elevated LA pressure.

 LA pressure increases at
elevated HR.

 Pulmonary vascular
resistance elevated.

 Pulmonary hypertension

 Right ventricular hypertrophy,


enlargement.

 Systemic venous congestion. *LS Lilly, Pathophysiology of Heart Disease, Fifth Edition 2011
Mitral stenosis-
Classification
 Large: more than 2 sqcm.

 Medium: 1,5-2sqcm.

 Severe:<1sqcm.
Mitral stenosis-
Symptoms.
Hemoptysis – usuallydyspnea.
 Exertional pulmonary venous
hypertension
 Fatigue.
-rupture of alveolar capillaries.
 Presyncope, syncope.
-pulmonary infarction.
 Cough, wheezing.
-ruptured of dilated bronchial veins.
 Paroxysmal nocturnal dyspnea.
-chronic bronchitis.
 Orthopnea.

 Hemoptysis.

 Hoarsenes(Ortner syndrome)
Mitral stenosis
Physical findings
 Mitral facies.
 Tachypnea.

 Turgid jugulars.

 Jugular pulse.

 Pulmonary rales,

pleural fluid.
 Diastolic thrill.

 Sustained RV lift.
Mitral stenosis -
Auscultaion
Duroziez sound
RRU - FFT - TA -TA.

DIASTOLIC PRESYSTOLIC ENHANCED AORTIC COMP OPENING SNAP


RUMBLE MURMUR SOUND 1 OF S2

S1 A2,P2 OS S1
PRESYSTOLIC
MURMUR
Mitral stenosis -
auscultation
Mitral stenosis
auscultation –atrial
fibrillation
Mitral stenosis-
Complications
 Atrial fibrillation/flutter.
 Embolism: Systemic:cerebral,
coronary, preipheral; pulmonary.
 Acute pulmonary edema.
 RV heart failure.
 Infective endocarditis.
 Chest pain/angina.
Mitral regurgitation

Definition: Clinical syndrome


determined by the
incomplete closure of the
mitral valve during
systole.
MR - Causes
*

*LS Lilly, Pathophysiology of Heart Disease, Fifth Edition 2011


MR- Etiology
MR-pathophysiology
 A volume of blood is regurgitated from the LV to the LA
LV overload.

 End diastolic pressure increases


LA preassure is increased,
LA is dilated,
Pulm HTN can develop.

 LV is dilated
Syst LV dysfunction appears (may be irreversible)

 Pulmonary arterial hypertension can appear


+
RV failure during evolution.
MR-pathophysiology

*LS Lilly, Pathophysiology of Heart Disease, Fifth Edition 2011


MR-physical examination
 Carotid upstroke is brisk.
 Laterally displaced apical impulse with
enlarged LV.
 Apical thrill-severe MR.
 Left sternal border lift –RV dilation.
 S1 is included in the murmur, usually
normal, may be increased in rheumatic
heart disease.
 S3 gallop-large volume of regurgitation.
MR-physical examination
 The hallmark of MR is the
systolic murmur-most often
holosystolic, is of blowing type,
but may be harsh in mitral valve
prolapse

Irradiation to the left axilla and


tricuspid focar, but it can irradiate
to the base of the heart in
ruptured chordae tendinae with
posterior valve prolapse MR.
MR in mitral valve
prolapse.
 MR limited to telesystole.
 Frequent -5%pop. especially in young
women.
 Habitus is sometimes characteristic:
longiline- asthenic woman with mild chest
deformities: pectus excavatum, pectus
carrinatum.
 Palpation- bifid apical impulse.
 Meso or telesystolic click, followed by –in a
minority of cases – by telesystolic murmur.
Mitral Valve Repair
Aortic stenosis
Definition: obstruction to blood outflow
from the LV to the aorta.
Causes:
*
1. Congenital.
2. Acquired:- Degenerative
- Rheumatic
Rare causes:
Infective endocarditis
Paget bone disease
SLE
Rheumatoid involvement
Irradiation. *Lucina Foundation
PATHOLOGY
Pathophysiology
 Obstruction in LV outflow. *
 Gradient LV-Ao.

 LV pressure rises,.

 LV wall stress increases.

 LV dysfunction develops

 LV hypertophy develops.

 LV filling pressure increaqses.


*LS Lilly, Pathophysiology of Heart
 LV systolic failure develops Disease, Fifth Edition 2011
Aortic stenosis-
classification
Aortic stenosis-symptoms

 Angina pectoris.

 Exertional presyncope

 Syncope.

 Heart Failure

 Pulmonary edema.
AS- CLINICAL FINDINGS

 Peripheral pulse: parvus et tardus-


taking longer time to reach the peak
pressure, peak is reduced.

 Heart size increased in heart failure.

 Palpable G4(S4).

 Aortic thrill at the base of the heart.


AS-Auscultation
 Systolic ejection click(bicuspid)

 Paradoxically split S2.

 Systolic ejection murmur.

 In older patients ejection murmur is atypical, heard at


the apex as seagull sound –Gallavardin phenomenon.

 Ejection murmur decreased when LV failure occurs.


AORTIC VALVE
REPLACEMENT
Standard Surgical
Aortic Valve Replacement

TAVI=

Transcatheter
Aortic
Valve
Implantation
AORTIC REGURGITATION
Definition:
Incomplete closure of
the aortic cusps in
diastole and
regurgitation of
blood from the aorta to
the left ventricle.
Aortic regurgitation can be
acute or chronic.
AORTIC REGURGITATION-
Etiology
1. Aortic root dilatation.
2. Congenital biscuspid valve.
3. Previous infective endocarditis
4. Rheumatic
5. Other congenital connective tissue disease: - Marfan,
- Osteogenesis imperfecta
- Ehlers-Danlos syndrome.

6. Autoimmune diseases - Ankylosing spondylitis


- Rheumatoid arthirtis
- SLE.
- Aortitis and arteritis

7. Syphilis
AORTIC REGURGITATION-
Pathology
 Dilatation of the annulus
AR.
 Valves can show
*
– Thickening
– Shortening
– Comisural lesions
– Calcification, .
 LV
– dilated
– hypertrophied.
 LV dysfunction develops. *LS Lilly, Pathophysiology of Heart
Disease, Fifth Edition 2011
AORTIC REGURGITATION-
Symptoms
 Pounding of the head or palpitations.

 Dyspnea on exerton.

 Orthopnea, paroxysmal nocturanl


dyspnea.

 Fatigue and weakness.

 Angina pectoris.
AORTIC REGURGITATION-
peripheral signs
 Pulse pressure –elevated.
 Corrigan pulse- celer et altur.
 Atrerial hyperpulsatility:
 Musset sign-bobbing of the head with each heartbeat.
 Traube sign-pistol-shot heard over the femoral artery.
 Duroziez sign-systolic murmur fem.a.when compressed proximally,
diastolic distally.
 Quincke pulse-capillary pulsations detected pressing a glass over the
patients lips.
 Arterial dance- carotid pulsations.
 Waterhammer sign-pulsatons of the forearm when pressed.
 Landolfi sign – intermittant pupillary hippus – miosis in systole,
midriasis in diastole.
AORTIC REGURGITATION-
physical examination
 The chest may rock, cardiac impulse
may be visible.
 Diastolic thrill-severe AR.
 S1 usually soft.
 Systolic ejection murmur.
 Early or immediate, blowing
descrescendo diastolic murmur,
after S2.
 IN severe AR the murmur is
holodiastolic.
 Austin-Flint murmur of functional mitral
stenosis.
Tricuspid regurgitation
Definition: incapacity of the
tricuspid valve to close
completely during systole,
resulting in regurgitation of
blood from the right ventricle
to the right atrium.

Tricuspid valve structure: annulus, 3 leaflets, and chordae


tendinae. It is larger than the mitral valve-lower pressure-
, the annulus dilates in diastole and constricts during
systole.
Tricuspid regurgitation -
etiology
 Primary TV disease:
– Congenital:Ebstein anomaly
– Rheumatic, assoc. with mitral disease.
– Infective endocarditis.
– Iatrogenic: pacemaker wire trauma.
– Degenerative:TV prolapse.
 Secondary TV disease:
– RV dilatation
– Pulmonary hypertension.
– Cardiomyopathies
– Segmental RVdysf. Due to ischemia, ARVD,.
Tricuspid regurgitation-
symptoms
 TR is not associated with any
complaint until the late phases of the
disease when RV dysfunction develops
resulting in overt rihgt heart failure
syndrome.
 Symptoms: fatigue, right upper
quadrant discomfort, dyspepsia due to
gut congestion.
Tricuspid regurgitation –
physical examination
 Edema of the lower limbs.
 Ascites.
 Jugular congestion
 Cachexia due to low cardiac
output
 Right parasternal lift.
 Systolic puplsations of the liver.
Tricuspid regurgitation
Auscultation

Soft
early or holosystolic
murmur,
augumented with
inspiratory effort.
Tricuspid stenosis

 Rare condition
 Etiology: rheumatic in most of the cases.
 Simptoms and general signs similar to those
met in TR.
 Auscultation: low to medium pitched
diastolic rumble with inspiratory
accentuation, localized to the lower sternal
border.
Pulmonary valve
dissease.
 Apart from congenital conditions is very
rare.
 Congenital: PV stenosis, Pulmonary atresia,
Bicuspid valve, Infundibular(subvalvular
pulmonary stenosis), Idiopathic dilatation of
the pulmonary artery.
 Acquired: rheumatic, Infective endocarditis,
carcinoid heart disease, pulmonary
hypertension, iatrogenic-Ross operation.
Pulmonary stenosis –
physical examination
 Mild stenosis - systolic
ejection click+early systolic
murmur.

 Severity progresses the murmur


gets louder and peaks later in
systole.

 S2 is splitted with dealyed


pulmonary component, but with
further widening in inspiration
Severe PS - SP2 becomes softer, even inaudible, and the
murmur encompasses the aortic component.
FINISH

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