valvular heart disease Flashcards
normal blood flow:
1- right side
- tricuspid from – to —
- pulmonary from — to — ( at right ventricle )
2- left side
- mitral valve from – to —
- aortic valve from – to – ( at left ventricle )
vena cava –> right atrium
pulmonary artery –> lungs
pulmonary vein –> left atrium
systemic circulation –> body
valves:
* Maintain — blood flow
* Function depends on — , — & — integrity of leaflets /cusps
- Pulmonary & aortic require — and — of – attachments to –
tightly
Tricuspid and mitral – leaflets,
attachments and connections to
—- muscles
unidirectional
mobility, pliability , structural integrity
integrity + co-ordination
cuspal
close
ventricular papillary muscles
valvular heart disease:
May be — or —
Major valve problems are:
(1) —
(2) — / — / —
(3) Both 1 & 2
(4) – from valvular vegetations
congenital or acquired
stenosis
insufficiency / regurgitation / incompetence
emboli
stenosis:
- failure of the valve to – completly –> — forward flow of blood –> – overload
* Often a — valve or — abnormality or
* Post inflammatory — ; —
Regurgitation / Insufficiency:
Failure of valve to — completely –> Allows – flow of blood –> — overload
* May result from — disease of the valve cusps or damage to/distortion of — structures eg —
open
impedes
pressure
primary congenital
cusp
scarring
calcification
close
reverse
volume
intrinsic
supporting
papillary muscles
Aortic Stenosis:
Normal AV is tricuspid
* Usually due to — -related “wear and tear” resulting in progressive injury –> —
* — , — valves
– ↑ — , occurs
earlier
– 53% of removed AVs are –
* Other causes:—
(rarer than mitral valve)
* Other causes of aortic outlet
obstruction e.g. — – see
cardiomyopathy lecture
age related
dystrophic calcification
congenitally bicuspid
mechanical stress
bicuspid
rheumatic fever
HOCM
consequences of aortic stenosis:
1- – Pressure gradient across valve
2- LV pressure must – to
maintain cardiac output
3-Concentric left ventricular—
-Hypertrophied myocardium –>— because of diminished microcirculatory –
increase
rise
hypertrophy
ischemic
perfusion
Clinical Features of Aortic Stenosis:
At presentation
* Exertional – pectoris as Cardiac output –
–> (may occur due to LVH with normal coronary arteries)
* — on exertion. Why ?
* — or — on exertion. Why?
Advanced disease
* Non-exertional symptoms i.e. symptoms at –
* — , —
* — +/- —
angina
reduced
dysponea
sysncope or pre syncope
rest
left heart failure
arrhythmia , sudden death
Aortic Insufficiency:
* Each contraction must expel normal — plus any– blood ∴ heart must work harder
– Increased —
* Causes
– — disease (Rheumatic HD, Bicuspid, Syphilis, Infective endocarditis
etc)
– — dilatation (Hypertension, Arthritis with aortitis e.g.
Rheumatoid arthritis, Marfan’s, Dissection etc)
stroke volume
regurgitated
LV end-diastolic volume
cusp
aortic root
Consequences of Aortic Valve disease:
(1) If it develops acutely →
– —-
(2) If chronic →
– May have – symptomatology
– —- and —
Eventual — → —
- Acute left ventricular failure\
- little
-Left ventricular hypertrophy and dilatation - left ventricular failure
Mitral Valve
* Annular —
– (Causes — or — )
* Stenosis
– —
* Regurgitation
– Mitral valve –
Mitral Annular Calcification:
* Develops in the – , —
( — ) of the mitral valve.
* Usually — , however can cause — or — .
* Most common in — patients.
calcification
regurgitation or stenos
rheumatic fever
prolapse
peripheral fibrous ring ( annulus )
asymptomatic
regurtuation or stenosis
older
Consequences of Mitral Stenosis [MS]:
MS most frequently due to Prior —
* Left atrial – → — → mural —
→ —
* Pulmonary – → prolonged – pressure in pulmonary veins → pulmonary vascular and
parenchymal changes → — / —-
* Low cardiac output
* Infective — (Rare)
Rheumatic fever
dilation
arterial fibrillation
thrombus
embolus
congestion
back
right ventricular hypertrophy /
right ventricular failure
infective endocarditis
Mitral Regurgitation – Causes
* Abnormalities of— / –
–> – / Post — scarring
–> Infective —
– >Mitral valve –
* Abnormalities of — apparatus
– >Rupture of— or – [acute]
* Dilatation of – cavity and/or
annulus
– – enlargement (Cardiomyopathy or myocarditis)
– — of mitral ring
leaflets / commissures
rheumatic / inflammatory
endocarditis
prolaps
tensor
papillary muscles or chordea
LV
LV
calcification
Mitral Valve Prolapse:
* Valve — are — and
prolapse back into the – during —- .
* Spectrum of patients
– asymptomatic to severe
mitral regurgitation.
* – cause in most
cases.
– Others – mutation in —
Gene ( — syndrome).
complication:
* Mitral insufficiency
(regurgitation)
* Infective endocarditis
* Stroke or systemic infarction
from embolism of leaflet
thrombi
leaflets
floppy
left atrium
systole
unknown
fibrillar
marfan
Vegetations - Heart Valves
* —
(immune mediated)
* Infective —
* Other:
– — vegetations eg
Libmann Sacs and
terminal illness [marantic]
Rheumatic Fever:
Dominant cause of Valvular Heart Disease in middle – low-income regions
* — mediated multisystem —
disease.
* Occurs – to a few – post episode of group - A —
* Rheumatic carditis manifests during — phase and
may progress over time to — rheumatic heart
disease – valvular abnormalities.
rheumatic fever
infective endocarditis
non infective
immunologically
inflammatory
10 days to few weeks
streptococcal pharyngitis.
acute
chronic
1- clinical features of RF:
* Heart
– Pancarditis: Endocarditis,
myocarditis & pericarditis
* Joints
– Migratory polyarthritis - large
joints
* Skin
– Subcutaneous nodules
– Erythema marginatum
* Brain
– Sydenham Chorea
2- acute RF microscopic features:
* Immune mediated
inflammatory — in various tissues.
* — in the heart – foci of lymphocytes, occasional – cells and activated — (— cells)
* – inflammation and
Aschoff bodies in any of
the three heart layers
(pancarditis).
lesions
Aschoff bodies
plasma cell
macrophages
Anitschkow cells
diffuse
Features of Acute RF Endocarditis:
* Inflammation (immune
mediated) of the — [most
commonly the – sided
valves]
– typically result in — within the cusps or along the tendinous cords.
* Causes poor valve function
(usually incompetence)
* Vegetations (clumps of dead
cells and polys)
Chronic Rheumatic Heart Disease:
* Damage to valves is –
– Turbulence induced by
ongoing – causes more — .
– Manifests years later.
* – valve nearly always
involved.
* Post inflammation –> repair
by —
* Fibrosis across commissures
– mitral stenosis with “ –
mouth” deformity
endocardium
left
fibrinoid necrosis
cumulative
deformity
fibrosis
mitral valve
repair fibrosis
fish mouth
Infective Endocarditis
* — or — of heart valves or mural (wall) endocardium by an organism [usually a – ]
* Vegetations composed of thrombotic — & — ( — vegetations)
* — of valve & healing by –.
* What is the significance of the vegetations being
infective?
1* Acute
– Typically — of a previously normal / native heart valve by a—virulent organism
– eg. S. aureus, enterococcus faecalis
– — , — & – lesions
– difficult to —
2* Subacute
– — infection of – valves
by organisms of — virulence
– eg. Strep viridans
– – destructive
– Difficult to —
– – course
3* Prosthetic Valve
– – epidermidis
colonisation and invasion
bacteria
Debis and organisms
infective
destruction
fibrosis
infection
highly
necrotising , ulcerative , destructive lesions
treat
insidious
lower
less
diagnose
protracted
staph
Infective Endocarditis:
* Vegetations contain – , — cells &—
* Vegetations cause — & – valve further
* Septic Emboli may detach from the friable unstable vegetation and embolise –> septic — / abscess in —
especially –
fibrin , inflammatory , bacteria
necrosis and injure
infracts
any organ
brain
Infective Endocarditis
Aetiology & Pathogenesis:
* Normal, Damaged or Prosthetic valve
– (50-60%) in abnormal valves.
* — or – by – virulence organisms
– Staphylococcus aureus infects either damaged or normal valves (20-30%)
– Other: Enterococci & HACEK group {gram neg oropharyngeal commensals},fungi
– Culture – endocarditis
* Normal valve & high virulence organism eg IV —
* Catheter Induced Endocarditis
Clinical Presentation – Signs & Symptoms:
* Infection
– fever, weight loss, night sweats, rigors
* Immune complex deposition
– glomerulonephritis, Roth spots, Osler’s nodes,
& Janeway lesions
* — lesion
– murmur, complications of valve destruction, left
ventricular failure
* –
– Cerebral, coronary, splenic, Janeway lesions
bacteremia or septicaemia
low
-ve
iv drug abuser
cardiac
emboli
Infective Endocarditis
Diagnosis & Treatment:
* – Index of Clinical Suspicion…
* Blood cultures
* (TOE)—
* — & — antimicrobial therapy
* – may be required if very poor valve function
high
Trans oesophageal Echocardiography
aggressive and prolonged
surgery
Non-Infective Vegetations:
* Non- — Thrombotic Endocarditis (NBTE)
– Deposition of small sterile — on valve leaflets along line of closure of cusps
– May be source of –
– Debilitated patients (cancer, sepsis) so called – Endocarditis
* – (Libman-Sacks Disease)
bacteria
thrombi
emboli
marantic
SLE
Congenital Heart disease
Major Topic In Paediatrics but may present late in adulthood
* Faulty— during weeks 3 - 8 of
gestation when major cardiovascular structures seem
to form
* Three major categories:
– — shunt
– — shunt
– —
embryogenesis
categories:
– Left-to-right shunt
– Right-to left shunt
– Obstruction
Left-to-Right Shunt
* Abnormal communication allowing flow of blood
from – ( – & – pressure) side to the — ( — & — pressure) side
* Increase – blood flow & not associated initially with cyanosis.
* Eventually: ↑ flow volumes and ↑ pressures, RVH &
pulmonary vascular proliferation, ↑pulmonary
vascular resistance, ↑ Pulmonary Arterial Pressure
– Shunt reversal : — syndrome
left
systemic and high pressure
right
pulmonary and low
pulomary
Eisenmenger’s syndrome
Atrial Septal Defect
* May not be detected until —
* Abnormal – opening in
the —
* Allows — of blood between left and right
atria.
* Generally – tolerated; irreversible pulmonary hypertension is —
* BUT May be source of
— - –
Ventricular Septal Defect:
* Incomplete — of –
* Associated with other congenital cardiac abnormalities
* Only 20-30% isolated.
* Consequences depend on — of defect and associated anomalies
* Most involve muscular part of
septum.
* Over time — pulmonary
vascular disease develops in all
with large, unclosed VSDs
resulting in shunt reversal.
adulthood
fixed
atrial septum
communication
well
unusual
systemic emboli - paradoxical
closure
ventricular septum
size
irreversible
