pulmonary arteries, dila2on of the upper lobe

VALVULAR HEART DISEASES pulmonary veins

• Kerley B lines - fine, dense, opaque, horizontal
Surgical Op,ons lines prominent in the lower and mid-lung fields
• Valve Replacement - result from disten2on of interlobular septae
• Characteris2cs of the ideal prosthe2c valves: and lympha2cs
1. Should have good hemodynamic - LA pressure exceeds 20 mmHg
characteris2cs; nonobstruc2ve and
completely competent Cardiac catheteriza,on-assess associated lesions
2. Non-thrombogenic
• Cardiac magne2c resonance- decrease need for
3. Not degenerate, wear out or vary
catheteriza2on
4. Not significantly alter blood components
• Coronary angiography- men older than 40 female
5. Be possible to insert without undue technical
older than 45, younger pa2ents with coronary risk
difficulty
factors
6. Not be annoyance to the pa2ent
Management
Mitral valves
• Beta-blockers , calcium channel blockers or digoxin
• highly durable
for rate control of AF, Warfarin for AF or
• permanent an2coagula2on
thromboembolism, penicillin for RF prophyaxis
• Surgical Op2ons:
Tissue Valves
- Mitral valvotomy- percutaneous or surgical
• more natural - Symptoma2c NYHA Func2onal Class II-IV ,
• less thrombogenic isolated MS, MVA<1cm/m body surface area
• structural failure
Mitral Valve replacement
Homogra8s (cadaver aor,c valve, dura mater)
• Pa2ents with MS and significant associated MR
• uncertain durability • In whom the valve has been severely distorted by
previous transcatheter or opera2ve manipula2on
Autogra8s
• Fascia lata, pulmonary valve Mitral Regurgita,on
Physical findings
Heterologous- Xenogra8s • Systolic thrill at the cardiac apex with apex beat
• Bovive, aor2c valve, Porcein aor2c valve, Bovine displaced laterally
pericardium • S1 generally absent or soM
• Wide but physiologically split S2
Mitral Stenosis • Systolic (holosystolic) murmur (Grade III/VI),
• Physical findings: S1 usually accentuated, slightly decrescendo, most prominent at the apex and
delayed radiates to the axilla
• P2 oMen accentuated , two components of second
heart sound closely split Diagnos,cs
• Opening snap of mitral valve audible at expira2on • ECG- LA enlargement , generally associated with AF
at or just medial to the cardiac apex • Chest X-ray- LA massively enlarged- forms the right
• Low-pitched , rumbling, diastolic murmur heard border of the cardiac silhoueVe
best at the apex with the pa2ent in lateral - Pulmonary venous conges2on, inters22al
recumbent posi2on edema , Kerley B lines
• Echocardiogram (transthoracic) – assess severity,
Diagnos,cs LA and LV size, annular calcifica2on, regional and
• ECG: P wave- LA enlargement global LV systolic func2on
• Severe pulmonary hypertension - right axis
devia2on, RV hypertrophy
• Chest X-ray - straightening of the upper leM border
of the cardiac silhoueVe, prominence of
Management Management
• With AF- an2coagula2on • For HPN or CAD- beta-blockers, ACE inhibitors
• Surgical Treatment • Surgical Treatment
- Repair-valve reconstruc2on – valvuloplasty - Severe AS who are symptoma2c
and inser2on of annuloplasty ring - LV dysfunc2on (EF <50%)
(percutaneous or surgical) - BAV disease and aneurysmal or expanding
o Indica2ons: aor2c root even if they are asymptoma2c
1. Once symptoms occur
2. Recent onset AF and pulmonary Surgery
hypertension (PA pressure > 50mmHg • Percutaneous balloon aor,c valvuloplasty
at rest or >60 with exercise) - children and young adults with congenital ,
3. Asymptoma2c pa2ents when LV noncalcific AS
dysfunc2on is progressive with LVEEF • Percutaneous aor,c valve replacement
below 60% and,or end systolic - transcatheter aor2c valve implanta2on
dimension increasing beyond 40 mm • Ross procedure
- replacement of the diseased aor2c valve with
Aor,c Stenosis the autologous pulmonic valve and
Physical Findings implanta2on of a homograM in the na2ve
• Rhythm is generally regular pulmonic valve posi2on
• Systemic arterial pressure
• Pulsus parvus et tardus Aor,c Regurgita,on
- peripheral arterial pulse rises slowly to a Physical Findings
delayed peak • directed toward detec2on of condi2ons
• Aor2c and pulmonic sounds may become predisposing to AR- bicuspid valve, endocardi2s,
synchronous or aor2c valve closure may even Marfan’s syndrome, ankylosing spondyli2s
follow pulmonic valve closure • ”water-hammer” pulse, Corrigan’s , Quincke’s
- paradoxical spliing Traube’s , Duroziez’s
• S4 • LV impulse is heaving and displaced laterally and
- audible at the apex , reflects LV hypertrophy inferiorly
• Ejec2on systolic murmur , low-pitched , rough, • A2 usually absent, High-pitched, blowing
rasping in character , loudest at the base of the decrescendo diastolic murmur , heard best with
heart the diaphragm and pa2ent siing up, leaning
forward and with breath held in forced expira2on.
Diagnos,cs • Aus2n flint murmur- soM, low-pitched, rumbling
• ECG - LV hypertrophy ( the absence of ECG signs LV mid- to late- diastolic murmur
hypertrophy does not exclude severe obstruc2on)
• Echocardiogram - thickening, calcifica2on and Diagnos,cs
reduced systolic opening of the valve leaflets • ECG- LV hypertrophy, S-T segment depression, T
o Severe AS - valve area of < 1 cm wave inversion in leads I, aVL, V3 and V6 (LV strain)
o Moderate AS - valve area 1-1.5 cm • Echocardiogram
o Mild AS - 1.5-2 cm - rapid, high frequency diastolic fluVering of the
• Chest X-ray - the absence of valvular calcifica2on in anterior mitral leaflet produced by the impact
an adult suggests that severe valvular AS IS NOT of the regurgitant jet
present
• Late stage - LV enlargement Management
• Catheteriza2on - pa2ents with mul2valvular • Acute
disease - Intravenous diure2cs and vasodilators
- young, asymptoma2c pa2ents with non- Opera2on indicated urgently
calcifica2on congenital AS • Chronic
- Pa2ents in whom obstruc2on to LV ouklow - Medical- diure2cs, vasodilators (ACE
may not be at the level of the aor2c valve but inhibitors,
at the sub- or supravalvular level - Dihydropyridine calcium channel blockers or
hydralazine)
Surgical Treatment Pulmonic Valve Disease
• pa2ents with chronic severe AR usually do not • Graham Steele murmur- high-pitched,
become symptoma2c un2l AFTER the decrescendo diastolic
development of myocardial dysfunc2on • Causes:
• when delayed too long (> 1year from one year of 1. Infec2ve endocardi2s
symptoms or LV dysfunc2on ) , surgical treatment 2. Carcinoid syndrome
oMen do not restore LV func2on 3. Postopera2vely from repair of TOF
• AVR- severe AR in symptoma2c pa2ents
irrespec2ve of LV func2on
• asymptoma2c pa2ents with severe AR and
progressive LV dysfunc2on : LVEF ,50% and LV end-
systolic dimension >55 mm or end systolic volume
>55mL/m or an LV diastolic dimension > 75 mm.

Tricuspid Stenosis
Physical Findings
• Findings-rela2vely liVle dyspnea for the degree of
hepatomegaly, ascites and edema
• Diastolic murmur heard best along leM sternal
border and over the xiphoid process and
prominent during presystole , augmented during
inspira2on

Diagnos,cs
• ECG - right atrial enlargement- tall, peaked T waves
in lead II
• Absence of ECG evidence of RVH in a pa2ent with
right-sided heart failure who is believed to have
MS should suggest associated TV disease
• Echocardiogram - tricuspid valve thickened and
domes in diastole

Management-
• Surgical repair
- carried out preferably at the 2me of surgical
mitral valovotomy or MVR
• Tricuspid valve replacement
- mechanical valves in the tricuspid posi2on are
more prone to thromboembolic complica2ons

Tricuspid Regurgita,on
• Most commonly secondary to marked dila2on of
the tricuspid annulus from RV enlargement
• Clinical feature results primarily from systemic
venous conges2on and reduc2on of cardiac output

Management
• Isolated TR ( ff, infec2ve endocardi2s or trauma)
does not require opera2on
• Func2onal TR - tricuspid valve annuloplasty
(inser2on of a ring) or tricuspid valve replacement