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Valvular Heart Disease


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Rheumatic fever

Rheumatic fever (RF) is generally classified as a

connective tissue or collagen-vascular disease

It is an inflammatory reaction that causes damage to

collagen fibrils and to the ground substance ofconnective tissue

Involves multiple organs: primarily the heart, the

joints, and the central nervous system

Recurrent attacks of RF may cause fibrosis of heart

valves, leading to chronic valvular heart disease


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Epidemiology

Peak incidence ages 5~15 years

Rare before age 4 years and after age 40 years

The incidence of RF and prevalence of rheumatic

heart disease (RHD)are markedly variable in

different countries:

In developed country, such as the united states,

the incidence of RF

2/100,000In many developing countries, the incidence of

acute RF approaches or exceeds 100/100,000


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Etiology and Pathogenesis

Multiple factors contribute to the pathogenesis,

including -hemolytic streptococcal pharyngitisand immunological status of the human body

Cross immune response between host and

streptococcal antigens

Streptococcal pharyngitis

Abnormal reaction-autoimmunity disease


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Pathology

Pathological characters:

Exudative and proliferative inflammatory reactions

involving connective or collagen tissue

Affects primarily the heart, joints, brain, cutaneousand subcutaneous tissues

Pathological processExudative stage

Proliferative stage: Aschoff nodule (pathognomonic)Fibrosis and calcification (scar formation)


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Recurrent attacks of RF (rheumatic carditis,

valvulitis) scar formation and deformity of

heart valves chronic RHD

Valvular involvement:

Mitral valve: 75%~80%

Aortic valve: 30%

Tricuspid & pulmonary valves: 5%


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Clinical findings

1Major manifestations Carditis: pericarditis, cardiomegaly, congestive heart

failure, and mitral or aortic regurgitation murmurs

Migratory polyarthritis: involves large jointslasts 1~5 weeks, subsides without residual deformity

prompt response to salicylates or nonsteroidal agents

Erythema marginatum: rare Subcutaneous nodules: uncommon Chorea: least common, most diagnostic


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2Minor manifestations Clinical findings: fever, polyarthralgias Laboratory findings

Elevated acute phase reactants:

ESR (erythrocyte sedimentation rate)

CRP (C reactive protein)

ECG change: prolonged P-R intervalA history of RFSupporting evidence of an antecedent group A

streptococcal infection: Positive throat culture or rapid streptococcal antigen test Elevated or rising titers of antistreptococcal antibodies(anti-streptolysin O and anti-DNase B)


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DiagnosisBased on Jones criteria and confirmation of

streptococcal infection

Guidelines for the diagnosis of initial attacks of RF

(Jones criteria, updated 1992)

If supported by evidence of preceding group A

streptococcal infection, the presence of two major

manifestations or of one major and two minor

manifestations establishes the diagnosis of acute RF


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TreatmentGeneral Measures

Strict bed rest

Medical Measures

1. Control streptococcal infection

Penicillin is of choice

benzathine penicillin, 1.2 million units im once,

or procaine penicillin, 600,000 units im daily, 10 days

If allergic to penicillin, erythromycin be given


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2. Antirheumatic therapy

(1) Salicylates

Of choice in patients with little or no cardiac involvement;

Particularly effective in reducing fever and relieving joint

pain and swellingAspirin 0.6~0.9 g / 4h in adults; lower doses in children

(2) Corticosteroids

Used in patients who do not respond well to adequate

doses of salicylates

Prednisone 40~60 mg orally daily, tapering over 2 weeks


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3. Treatment of symptoms and complications

If heart failure is present, digitalis preparations should be

used cautiously because cardiac toxicity may occur with

conventional dosages

Prevention

Primary prevention

Early treatment of streptococcal pharyngitis

Penicillin or erythromycin

Secondary prevention

To prevent recurrence of rheumatic activityLong-acting penicillin (benzathine penicillin)

1.2 million units im, every 4 weeksSulfonamides or erythromycin may be substituted


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Mitral stenosis (MS)EtiologyMost commonly rheumatic fever

rheumatic heart diseaseRHDSymptoms commence mostly in 2nd~4th decade

2/3 of all patients are female25% of all patients with RHD have pure MS

40% have combined MS and mitral regurgitation (MR)


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Other rare causesFar less frequently, MS is congenital in etiology

observed primarily in infants and young children

Calcification of mitral annulus (when subvalvular or

intravalvular extension is extensive)

observed in old patients

Very rarely, MS is a complication of carcinoid

disease or connective tissue disease (systemic lupus

erythematosus, SLE; rheumatoid arthritis)


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PathologyFibrosis, thickening, rigid and calcification of the valve

apparatus

Rheumatic fever results in four forms of fusion of themitral valve apparatus leading to stenosis:

Commissural, cuspal, chordal, and combined

Characteristically, mitral valve cusps fuse at their

edges, and fusion of the chordae results in thickeningand shortening of these structures


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Commissural adherent and fusion

restricted opening of mitral valve

fish mouth shape of mitral valve orifice

Thickening, fusion and shortening of the

chordae or papillary muscles

funnel-shaped change of valve apparatus


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Secondary changesChronic MS Dilatation of the left atrium

Fibrosis of the atrial wallDevelopment of mural thrombi

Hypertrophy and dilation of RV


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Hemodynamic changes

MS involves mainly LA and RV

1. Effect of MS on left atrioventricular pressure

gradient and left atrial pressure (LAP)

MVA transvalvular gradient LAP

Normal 46cm2Mild MS 1.5cm2 5-10mmHg Moderate 1.01.5cm2 10-20mmHg Severe 1.0cm2 20mmHg 25mmHg


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2. Effect of elevated LAP on pulmonary circulation

The elevated LAP in turn raises pulmonary venous and capillary

pressures (PVP, PCP), resulting in exertional dyspnea

LAP PVPPCP DyspneaLung compliance

Pulmonary hypertension results from:

1. Passive backward transmission of the elevated LAP

2. Reactivepulmonary arteriolar constriction, which presumablyis triggered by left atrial and pulmonary venous hypertension

3. Organic obliterative changes in the pulmonary vascular bed,

which may be considered to be a complication of longstanding and

severe MS


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3. Effect of pulmonary hypertension on RV

Pulmonary hypertension

RV hypertrophy & dilationsecondary TR, PR

Right ventricular failure


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Clinical manifestationsSymptoms

Onset in patients with moderately severe MSMVA1.5 cm2Dyspnea:Principal symptom, appears at early stage

Precipitated by exertion, fever, AF or pregnancyExertional dyspnea, orthopnea,paroxysmal

nocturnal dyspnea, acute pulmonary edemaHemoptysis

Profuse hemorrhage: rupture of bronchialsubmucosal varices

Blood-stained sputum

Pink, frothy sputum

Cough occurs frequentlyrespiratory infection, compression of left bronchus

Hoarseness(Ortners syndrome), less commonCompression of left recurrent laryngeal nerve


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Physical examinationCardiac signs of MS

Changes of heart sounds:

Accentuated S1

Opening snap (OS) sharp, follows A2 along left

sternal border or at apex

Both suggest MV leaflets flexible

Marked calcification or thickening of the MV leaflets

S1 becomes softer, and OS may disappear

probably because of diminished motion of the leaflets


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Diastolic murmur of MS

A low-pitched, diastolic rumbling murmur,

localized at or near apex, with pre-systolic

accentuation in patients with sinus rhythm

Auscultation of the murmur is facilitated byplacing the patient in the left lateral position and

auscultate during expiration

When the patient is in the left lateral

recumbent position, a mid-diastolic or presystolicthrill may be palpable at apex


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Cardiac signs secondary to pulmonary

hypertension and RV dilationRV pulsation is present at the left parasternal region

Accentuated or splitting of P2 may be heard in the

second left intercostal space

Other signs of pulmonary hypertension:

Pulmonic ejection sound, owing to dilation of the PA

Graham Steell murmur of PR: a decrescendo diastolic

murmur along the left sternal border

When RV dilation is companied by TR, a pansystolicmurmur may be audible in the 4th or 5th intercostalspace in the left parasternal region


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Other signs

Mitral face: malar flush

Signs of right heart failure:Systemic venous hypertension, hepatomegaly, edema,

and ascites are all signs of severe MS with elevated

pulmonary vascular resistance and right heart failure


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Laboratory examinationElectrocardiography (ECG)

Left atrial enlargement

Mitral valve P waveP-wave duration in lead II 0.12 sLarge terminal negative P force in lead V1

Right ventricular hypertrophy

ArrhythmiaPremature atrial contraction atrial fibrillation


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Radiological findings

Mitral valve heartMarked enlargement of LA

Enlargement of RV

Dilatation of PA

Pulmonary congestion

Interstitial edema (manifested as Kerley B lines)


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EchocardiographyThe most valuable technique for diagnosing MS,

and determining its severity

M-mode echoThickened, calcified leaflets

open poorly, close slowly (EF slope)

The double peaks disappear

Both leaflets move anteriorly during early diastole

Two-dimensional echo:

Fusion, thickening, doming of the valve leaflets, and poorleaflet separation in diastole; mitral orifice area


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Doppler echoMost accurate noninvasive technique for quantifying the

severity of MS

Spectrum Doppler: measure transvalvular gradient, MVA

Color Doppler: display high velocity color jet

Provide other important informationCardiac chamber size (LA, RV)

Left ventricular contractility

Pulmonary arterial pressure

Other coexisted valvular or congenital abnormalities

Mural thrombi


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Cardiac catheterization

Its value in assessment of patients with MS or

suspected MS has been largely superseded by

echocardiography

If surgery is planned, coronary angiography is

performed to ascertain whether or not bypass

grafting is indicated in patients at risk of having

coexisting coronary artery disease


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Diagnosis and differential diagnosis

Diagnosis Diastolic rumbling murmur at apex

ECG or X ray reveals LA dilatationConfirmed by echocardiography

Differential diagnosis Diastolic murmur at apex

Increased flow across mitral valveSevere MR

Massive left to right shuntsVSD, PDAHyperdynamic circulationhyperthyroid, anemia

Austin-Flint murmursevere ARLeft atrial myxoma postural change of the murmur

other signs of myxoma

Graham Steell murmurshould be differentiated from aortic regurgitation


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Complication

Atrial fibrillation Commoncardiac output by about 20%

LA, age Incidence

Acute pulmonary edema Severe

Dyspnea and cyanosis; unable to lie on backpink, frothy sputum; both lungs filled with rales

ThromboembolismDevelop in 20% of patients

About 2/3 found in the cerebral vesselsRecurrent and multiple

Risk factors: AF, LA55mm, a history of recentembolism or a low cardiac output


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Late stage, main cause of deathDyspnea and hemoptysisprotective effect(RV CO pulmonary circulationLAP;

thickening of alveolus & pulmonary capillary walls)

Infective endocarditisOccurs less frequentlyon rigid, thickened, calcified

valves and is therefore more common in patients

with mild than with severe MS

Respiratory infectionCommon

Induce and aggregate heart failure


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Management

General treatment

Patients with RHD should receive penicillinprophylaxis to prevent recurrence of RF and

prophylaxis for IE

Avoid and control anemia and infectionsAsymptomatic patients: avoid strenuousexertion Patients with dyspnea should reduce physicalactivity, restrict sodium intake, and take oral

diuretics


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Treatment of complications

Profuse hemoptysisMeasures designed to reduce pulmonary venous pressure,

including sedation, assumption of the upright posture, and

aggressive diuresis, are used to treat hemoptysis

Acute pulmonary edemaDilate venous system, reduce preload (nitrates)

Avoid dilating small artery

Digitalis glycosides do not benefit patients with MS and sinus

rhythm, but are of great value in slowing the ventricular rate

in patients with AF and in the treatment of right-sided HF


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Treatment of Arrhythmias

AF with rapid ventricular rate:

Ventricular rate (70~80 bpm)Digitalis glycosidesiv cedilanid, oral digoxin-blockers

In patients with mild MS without marked LA dilation

who have been in AF less than 6~12 months, elective

cardioversion (electrical or pharmacological) should

be considered


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Prophylactic anticoagulant treatment

AF

Previous embolic episodes

LA thrombus revealed by echocardiographyLong term anticoagulant treatment with warfarin is

necessary in patients without contraindication


Restriction of sodium intake

Diuretics

Nitrates


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Indications for relieving stenosis

Symptomatic patients with moderate to severe MS

(MVA1.5 cm2), or evidence of pulmonaryhypertension with RV hypertrophy

Recurrent systemic emboli despite anticoagulation

with moderate or severe stenosis

Percutaneous balloon mitral valvuloplastyPBMVProcedure of choice for pure MS with pliable and

noncalcific valve


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Surgical techniques

Open mitral commissurotomy

Indication:

Patients without significant MR

valvular calcification, involvement of chordae and

papillary muscle, left atrial thrombus or restenosis

Mitral valve replacement

Indication:Severe distortion and extensive calcification of the valve

and subvalvular apparatus;Associated with significant MR or aortic valve disease


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Mitral regurgitation (MR)

Etiology

Mitral valve apparatus and/or LV structural

and functional abnormality

RHD: common(1/3); + MS and/ or aortic valve disease

Mitral valve prolapse (MVP)myxomatous degeneration, floppy and redundancy

Ischemic heart disease (or CAD)

papillary muscle dysfunction

Mitral annular calcification


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Severe dilatation of LVresult in dilatation of the mitral annulus and

lateral movement of papillary muscle

Infective endocarditisvalve leaflets destruction, perforation, retraction;

valve closure interfered by vegetation

Other causes:

Rupture of the chordae

congenital abnormalities

obstructive hypertrophic cardiomyopathy


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Hemodynamic changes

MR involves mainly LA and LVChronic MRCompensation: MRLV volumeLV, LA

LVEDV SV CO, EF

Decompensation:

Left HF, LAP and LVEDP pulmonary congestion,pulmonary hypertension, right HF

(hepatomegaly, edema, and ascites)

CO

Acute MRMRLA, LV volumeLVEDPLAP

pulmonary congestion, pulmonary edema

SV and CO


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Clinical manifestations

SymptomsChronic MR

Mildno symptom

Severeleft-sided heart failureWeakness, fatigue (CO)

Dyspnea (pulmonary congestion)RHD:symptoms occur late, once present, LV

dysfunction is usually irreversible

MVP:asymptomatic, or atypical chest pain,palpitation, fatigue; in severe MR, left

HF occur at late stage

Acute Mildmild exertional dyspneaSevereacute left HF, pulmonary edema,

or cardiac shock


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Physical examination

Cardiac impulse at apexHyperdynamic

Displaced laterally, inferiorly (Chronic)

Changes of heart soundsS1(RHD) or normal (MVP, CAD)

S3 (severe MR): prominent

Mid or late systolic clickMVPAcute: P2S4


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Systolic murmur

RHDPansystolic, blowing, high-pitched murmurmaximal at the apex

Anterior valve lesion, radiate to the axilla and back

Posterior leaflet abnormality, radiate to the base

MVPmid- to late-systolic murmurDysfunction of papillary muscles:

Variable (early, mid, late or holosystolic)

Rupture of the chordae: musical

(Acute MR: not pansystolic murmur, but lower-pitched,

decrescendo, and softer than the murmur of chronic MR)


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Laboratory examination

ECGChronic (severe) MR:LA dilation, Atrial fibrillation

LV enlargement and non-specific ST-T changes

Acute MR: sinus tachycardia

Radiological findingsChronic (severe) MR:

Cardiomegaly with LA, LV; pulmonary congestion,

interstitial edema with Kerley B lines (left HF)

C-shaped calcification of mitral annulus

Acute MR:Normal cardiac silhouette or mild LA dilation

overt pulmonary congestion, edema


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Echocardiography1Display anatomy of the mitral valve apparatus

Useful in determining the etiology of MR (2D)

2Confirm the existence of MRDoppler (color, spectrum): reveal high-velocity jet into

LA during systole

Sensitivity~100%Estimate the severity of MR4 cm2 MildColor flow jet area 4~8 cm2 Moderate8 cm2 Severe

3Measure cardiac chamber sizes, evaluate LVfunction, pulmonary artery pressure, provide

data concerning other valvular lesions


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Radionuclide angiography and MRI

Evaluate LV function

Estimate the severity of regurgitation

The regurgitant fraction can be estimated from

the ratio of LV to RV (LV/RV) stroke volume

Cardiac catheterizationConfirm the diagnosis of MR and estimate

its severity, evaluate cardiac function and

pulmonary artery pressureCoronary angiography is performed to

determine presence of CAD prior to surgery


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Diagnosis

Chronic MRTypical systolic murmur at apex associated

with enlargement of LA and LV

Acute MRSudden onset of dyspnea

Systolic murmur at apex

Normal cardiac silhouette, but obvious

pulmonary congestion

etiology existed

Confirmed by Echocardiography


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Differential diagnosis

Tricuspid regurgitation (TR)

SM heard best along the left sternal border

augmented during inspiration

Ventricular septal defect (VSD)

SM loudest at the left sternal border

accompanied by a parasternal thrill

Systolic ejecting murmur at left sternal border:

aortic or pulmonic stenosis

hypertrophic obstructive cardiomyopathy

Echocardiography


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Complication

Atrial fibrillation

seen frequently in severe cases

Infective endocarditis

more common than in MSSystemic embolism

less common than in MS

Heart failure

occur early in acute MRbut late in chronic MR


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Management

Chronic MR

Medical treatment

Prevention: same as in MSAsymptomatic patients with normal cardiac

functionfollow-up regularlyManagement of AFsimilar to that in MS

(slow ventricular rate, anticoagulation)

Treatment of heart failurerestriction of sodiumintake, angiotensin-converting enzyme inhibitors

(ACEI), diuretics, digitalis glycosides


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Surgical treatment

Mitral valve replacementIndications

Severe MR and in functional Class or Functional Class associated with LV dilation

(LVESD45mm on echocardiography)Severe MR, progressive deterioration of LVEF,LVESD and LVEDD

Mitral valve repair

IndicationsMVP

Chordal rupture

Mitral annulus dilation


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Acute MR

Principle

Reduce pulmonary venous pressure

Increase cardiac output

Correct etiology

Medical treatmentIntravenous nitroprusside

Intravenous diuretics

ACEI and other vasodilators

Surgical treatmentMitral valve replacementMitral valve repair


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Aortic stenosis (AS)

Etiology

RHD

Common, + AR and mitral valve disease

Degenerative calcific AS

Common in the elderly, accompanied by calcification of

the mitral annulus

Congenital abnormalities

Calcific stenosis of congenitally bicuspid aortic valve

Congenital aortic stenosis


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Hemodynamic changes

Normal aortic orifice area (AOA): 3.0~4.0 cm2

AOA 1.0cm2, LVSP, with significant transvalvulargradient

Compensation

ASLV pressure load

Concentric LVHcomplianceLVEDPLAH

Maintain systolic wall stress and CO LVEDV

Decompensation

LVEDVwall stress, myocardial ischemia, fibrosis

left HF


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Symptoms

Cardinal symptoms: dyspnea, angina and syncope

1. Dyspnea: exertional dyspnea

orthopneaparoxysmal nocturnal dyspnea

acute pulmonary edema

(varying degrees of pulmonary venous hypertension)

2. Angina pectoris:occurs frequently in patients with critical AS,

>1/3 associated with coronary artery disease


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Mechanisms of ischemiaMyocardial oxygen consumption: LVH, LVSP, LVET Relative decrease in myocardial capillary densitySubendocardial coronary artery compression: LVDPCoronary perfusion pressure: AO pressure, LVDP

Imbalance between myocardial oxygen demand and supply

3. Syncope: typically exertional

Arterial pressure cerebral perfusion

Mechanisms:

Increase blood flow to exercising muscle without compensatoryincrease in cardiac output

Severe arrhythmias


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Physical examinationSystolic ejection murmur

Blowing, harsh, crescendo-decrescendo

Maximal at aortic area (R2 or L3, 4)

Transmitted to the neck and apexMay be associated with systolic thrill

The more severe the AS, the longer the duration

of the murmur

When the LV fails and the CO falls, the murmur

becomes softer or disappear


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Heart sound changesS1 normal or soft

A2 weak or absent

paradoxical splitting of S2

prominent S4

Aortic ejection soundcongenital AS or pliable valve AS

Other signsLeft ventricular heave

Systolic and pulse pressures

Delayed and diminished carotid pulses


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ECG

Severe: LVH and secondary ST-T changes,

LAarrhythmiasRadiological findings

Normal size or slightly enlarged heart

Calcification of the aortic valve

Poststenotic dilatation of the ascending aortaPulmonary congestion


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Echocardiography

Establish a diagnosis, and determine the

severity of AS

M-mode and 2D echo

Observe aortic valve opening, thickening andcalcification

Helpful in determining the etiology of AS

Also invaluable in detecting associated mitral

valve disease and in assessing LV performance,hypertrophy, and dilatation


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Doppler echoAllows calculation of the aortic valve gradient

Estimate the severity of the stenosis 30 mmHg Mild ASMPG 30~50 mmHg Moderate AS50 mmHg Severe AS

Color Doppler flow imaging is helpful in the

detection and determination of the severity of

any accompanying aortic regurgitation


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Cardiac catheterizationDetermine the severity of AS by measuring

systolic LV and aortic pressure simultaneously,

and calculating the valve area

An average pressure gradient of50mmHg orpeak pressure gradient of 70mmHg represent

severe AS

Coronary angiography is performed in most

adults to assess for concomitant coronary disease


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Diagnosis

Typical systolic murmur of AS

Associated with AR and/or mitral valve damageRHD

Pure AS:

Infants and young childrenunicuspid malformation

Childhood ~65 yearscalcification of bicuspid AV

65 yearsdegenerative calcificationConfirmed by echocardiography


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Differential diagnosis

Transmitted murmurMR, TR, VSDOther LVOT obstructive disease

Congenital supravalvular AS

Congenital subvalvular AS

Hypertrophic obstructive cardiomyopathy


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Management

Medical treatment Treatment of Arrhythmias: prevent AF with an

antiarrhythmic agent when premature atrial

contractions are frequent; when AF does occur,

restore sinus rhythm

Treatment of angina pectoris: nitrates

Treatment of heart failure: diuretics must be

used with caution; vasodilators should be

avoided


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Surgical treatment

Valve replacementIndications:

Repeated occurrence of syncope, angina pectoris orsignificant left heart failure

Asymptomatic patients with progressive LV dysfunctionand/or LV hypertrophy, and very high transvalvular

gradient (80mmHg) Severe ASAOA0.7 cm2Commissural incision under direct vision

In children and adolescents with noncalcific

severe congenital AS


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Percutaneous balloon valvuloplasty

Indications

Children and adolescents with congenital noncalcific AS

Adults with severe calcific AS who are poor candidates

for surgery or as an intermediate procedure prior tosurgery:

Patients with cardiogenic shock due to critical ASPatients with critical AS who require an urgent noncardiac

operation

Pregnant women with critical ASPatients with critical AS who refuse surgical treatment


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Aortic regurgitation (AR)

Etiology

Primary disease of the aortic valves

and/ or aortic root


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Aortic valve disease

RHD most common, about 2/3+ AS and/or mitral valve diseaseInfective endocarditis Congenital deformity: bicuspid valves

Myxomatous degeneration of the aortic valveAortic root dilatationMarfan syndromeAortic dissection(involve annulus or leaflets) Syphilitic aortitis


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Hemodynamic changes

Chronic AR

CompensationARLV volume LV, LVEDV SV(CO)

Decompensation:

LV systolic dysfunction LV failure (EF, LVESV)

Acute ARAR LV volume LVDP LAP

CO pulmonary congestion

pulmonary edema


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SymptomsChronic ARAsymptomatic for many years

Palpitation, precordial discomfort, head pounding

(related to SV)LV failure (dyspnea, fatigue):occur at late stage

Angina pectoris or chest pain: less common

Acute ARmildno symptom

severeAcute LV failure and hypotension

(pulmonary edema)


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Physical examination

Chronic, severe AR

Peripheral arterial signs: Owing to wide pulse pressure:SBP, DBP

Water-hammer pulse (rapid rise and fall)

Pistol shot sounds (booming systolic & diastolic soundsheard over femoral artery)

Duroziezs sign (systolic, diastolic murmur over partiallycompressed femoral artery)

Quinckes sign (subungual capillary pulsations)

de Mussets sign (head bobs with each heartbeat )

Apical impulse: diffuse and forceful, displaced laterallyand inferiorly (hyperactive, enlarged LV) Heart sound: An S3 gallop is common with LV failure


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Heart murmursAortic diastolic murmur:

High-pitched, blowing, decrescendo pattern

When AR is due to primary valvular disease, the diastolic

murmur is best heard along the left sternal border in the

3rd and 4th intercostal spaces

However, when it is due mainly to dilatation of the ascending

aorta, the murmur is often more readily audible along the

right upper sternal border

Austin-Flint murmur:

apical mid or late diastolic low-pitched murmur:common in severe AR, owing to partial closure of MV by

the regurgitant jet


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Ejection systolic murmur:

common

harsh

at the base of the heart

accompanied by a systolic thrill

Acute AR

S1 soft or absentP2S3 and S4AR murmur: lower pitched and shorter than

that of chronic ARAustin-Flint murmur: brief


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ECGAcute: sinus tachycardia; nonspecific ST-T changes

Chronic: LV enlargement and hypertrophy, arrhythmias

Radiological findings

Acute AR: cardiac size normal or slightly enlargedsigns of pulmonary congestion, pulmonary edema

Chronic: LV enlargement, associated with dilatation ofthe ascending aorta

Severe, aneurysmal dilatation of the aorta suggestsaortic root diseaseMarfan syndrome

Pulmonary congestionLV heart failure


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Echocardiography

Confirm diagnosis, estimate severity, identify the cause

2-D echo:Structural changes of the valve leaflets and/or aortic root

M mode echo:Diastolic fluttering of the anterior leaflet of the mitral

valve is an important echocardiographic finding in ARSerial assessments of LV size and function

Doppler echo:Sensitive, accurate noninvasive technique for detecting AR

LVOT diastolic regurgitant jet, estimate the severity of AR

Cardiac catheterizationQuantify the severity of AR

Evaluate the coronary and aortic root anatomy


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DiagnosisCharacteristic diastolic murmur associated with peripheral

arterial signs, make a diagnosis of AR

Combined with other information, etiology is usually found

Differential diagnosisGraham Steell murmur (pulmonary hypertension associated

with dilatation)

Austin-Flint murmur: differentiated from that of MS


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Management

Chronic AR

Medical treatment

Asymptomatic patients withsevere AR and LV dilation:Vasodilators (ACEI, et al) reduce the severity of AR,should be used to prolong the compensated period

-blocker: slow the rate of aortic dilation in MarfansPatients with HF:

Vasodilators (ACEI), diuretics and digitalis glycosides


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Surgical treatmentValvular replacement

Indications:

Symptomatic patientsAsymptomatic patients with LV dysfunction,

with persistent or progressive LVESVor

EFat rest

Repair or replacement of the root

Aortic root disease


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Acute AR

Medical treatmentPrinciple: reduce pulmonary venous pressure, increase

cardiac output, and stabilize hemodynamics

Intravenous nitroprusside

DiureticsPositive inotropic agent

Antibioticsactive IESurgical treatment

Urgently requiredValvular replacement or aortic valve repair


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