Disease/Disor

der
Mitral Stenosis

Pathophysiology/Etiology

Pathology

*Narrowing of mitral valve, causing

*Stenotic mitral
valve (<2cm2) causes
LVLV getting less blood because of impediment/impairm
ent of blood
narrowingcausing PRESSURE
flowpressure
difference
gradient across mitral
valve increasesLV
*diastole
fill time increases
Pathophysiology/Etiology
Pathology
eventually LV
Scarring/infection injury
requires atrial kick to
causes/congenital defects/rheumatic
*Narrowing of aortic valve, causing *age-related
fill with bloodas
fever damage mitral valve2 main
obstruction of blood flow into
progressive
HR increases the
ways:
commissures
thicken/fuse
bodycausing PRESSURE
calcification of aortic
amount of time the
(cant open much if at all) & chordae valveUSA/Western
OVERLOAD ON LV
ventricle is in
tendonae shorten and fusevalve
Europe
diastole filling period
cusps
become rigidvalve
*rheumatic fever*diastole
decreases
calcification also occurs over time,
usually associated
making
valvebecomes
more
with MV disease
Aortic valve
When HR goes
narrowimpeding
blood
flow
(usually have both)
narrowedblood isnt
pumped
above certain point
*congenital bicuspid
adequatelypressure in LV
diastolic fill time is
Backward
Effect LV compensates aortic
valve (most
increasesinitially
insufficient to fill
LA pressure risespulmonary
common congenital
by thickening walls (myocardial
ventricle with blood
pressure
risespulmonary
hypertrophy/concentric
hypertrophy- heart defect 1and pressure builds
compliance
falls enlarged)
(bc of defective
1.5%of population
LV walls evenly
to
in LA
mitral
valve)exertional
dyspnea
(males more so)
maintain
adequate pumping
developscausing
pressuremaintainpulmonary
CO withoutedema
LV
*Rheumatic fever
bc
lack
of
fluid
from
the pulmonary
dilation for many years
most common cause
capillaries getting into the pulmonary Aortic
Sclerosis- can
*Congenital defect
interstitium
and
alveolileading
to
lead
to
stenosis
Severe AS
rare
pulmonary
arterial
hypertension
*Irregular leaflet
Later stagesLV dilates, wall
*chronic renal
(blood
affected
thickening and focal
things, vessels
diastolicalso
function
disease
overworked,
stiff over timefurther
increased
deterioratesturbulent
blood flow
*can be associated
increases
BP w/in lungs
echogenicity
causing inflammation
& & impedes
with mitral regurg or
blood
flow)
(calcification) are the
degeneration
aortic disease
Pulmonary HTN causes RHF
hallmarks
*present in 30%
*Mean gradient >50mm Hg (use
FORWARD
EFFECTS
people over 65
gradient to determine
extent of
CO
falls because of stenosisexercise *may have a murmur,
damage)
tolerance
low<1cm
because
heart area
cant pump NO STENOSIS
2
*Valve area
or valve
fast
enoughtired
(most
energy
2
2
*risk factors: HTN,
index <.6cm /m
exerted
in velocity
heart) > 4m/sec on
smoking, elevated
*Ejection
LDL
Doppler

Valvular Heart obstruction

Diseaseof blood flow into
normal mitral
valve size 4-6 cm2
Mnemonics
Sequence of Flow
TRIPS BIAS:
Disease/Disor
TRIcuspid
der
Pulmonary
Aortic Stenosis
Semilunar
BIcuspid
*25% of all
Aortic
valvular heart
Semilunar
disease patients
Complications
*80% male
PASTRI
Pulm BP, A fib,
Systemic
Mnemonics
embolism,
Sequence of Flow
Tricuspid regurg,
TRIPS BIAS:
Right heart failure,
TRIcuspid
Infective
Pulmonary
endocarditis
Semilunar
BIcuspid
MS-more common
Aortic
in females
Semilunar
Symptoms of
aortic stenosis
ASD
Angina 2 years }
Syncope 1 year }
prognosis
Dyspnoea 6/12 }

Disease/Disor
der

Pathophysiology/Etilogy

Pathology

History and
Clinical Signs
**Symptoms can
be a guide for
when surgery
needed**
* develop over 2030 years
*fatigue
*exertional
History and
dyspnea
Clinical Signs
*w/onset of a-fib
**Symptoms
symptoms
guide for when
increase/intensify
surgery needed**
rapidly
* severe AS can be
*hemoptysis
asymptomatic for
(coughing up blood)
years bc LVH
*pulmonary edema
maintains output
*usually
Thrombic
symptomatic 6-8
Complications
decade
*occurs esp in a-fib
*Cardinal
*form in atria, esp
symptoms
atrial appendages
-exertional dyspnea
*more in elderly
-angina-due to AS
*may be main
or associated CAD
complaint from pt
-Syncope(woman with cold
associated w/
leg)
arrhythmias or
vasodilation
*orthopnea,
fatigue, pulmonary
edema occur late

Investigation &
Treatment
Findings
*opening snap (valve
*physical exam and
stiff/rigid)
echo determine
*can hear 1st heart sound
whether surgery is
*diastolic murmur- low
needed*
pitched
-apex and lateral decubitus *antibiotic
position
prophylaxis for
-exercise may increase
further strep infection
Investigation & Findings
Treatment
noise
*signs of RH failure
*A-fib- control
*Rhythm regular until late in course
*early-none needed
(shortness of breath, edema, ventricular rate w/
(afib suggests MV disease or advances *late-valve
frequent night peeing,
warfarin/anticoag
severe AS with failing LV)
replacement
pronounced neck veins)
*delayed upstroke to carotids &
-balloon
*other murmurs
Surgical treatment
brachial pulses
valvulotomyEKG: Broad notched p*balloon valvulotomy
*reduced volume pulses
temporary (6
wave in II
*surgical
*displaced, sustained LV pulse
months)
*p mitrale (double hump) in valvulotomy-open
*Systolic thrill at base & neck
-transcatheter AV
LAE (v1-v2, v5-v6)
*valve repair or
*S4 (atrial gallop)common- due to
replacement*Signs of RVH
replacement
LVH & increased LVEDP
femoral, apical,
*A-fib=bad=need surgery
*S2 diminished (scarred, not going to
transaortic-stoke and
Chest X-ray
close)
severe AR are the
*straightening L heart
Valve Repair vs
Murmurs
major complications
border, then bulges
Replacement
*crescendo-decrescendo
but may be the best
*prominent pulmonary
Valve
*rough & raspy
choice in old person
arteries (eventually causing
*Better
*primary aortic radiating to neck,
w/comorbidity
HTN)
hemodynamics
occasionally to apex, NOT AXILLA
*enlarged heart posteriorly
*No anticoagulants
*with severe, usually grade 3 or
on esophagus (when barium Replacement
greater
swallowed)
*For severe
*late stages, murmur softer
*LV doesnt enlarge; LA
MR/severe *valve
EKG: most severe AS have LVH;
does
distortion
absence of severe LVH doesnt
*pericardial calcification
*Anticaog required
exclude severe AS
(more so in TB)
using mechanical
Chest X-ray
Cardiac Catherization
device or atrial fib
*early/late stage may be normal (LVH
*evaluate other valvular
concentric w/smaller chamber)
lesions & associated CAD
*if in a-fib, always
*dilated ascending aorta
(men over 45/women over
have them on
*late stage, heart size increased with
55
anticoagulants
LV contour (boot)
*measure gradient across
Echo
mitral valve (wedge
*thickened immobile leaflets with
pressure-LVEDP)
bright echoes (calcification)

History and
Clinical Signs

Investigation &
Findings

Treatment

Valvular Heart Disease

*CO doesnt increase normally with
exercise
*Late in course resting CO, gradient
& murmur decreases (bc LV failure)
*Increased wall tension compresses
CAsflow reduced

Disease/Disor
der
Aortic
Insufficiency (AI)
*also known as
aortic regurgitation
(AR)

Pathophysiology/Eti
ology
* aortic valve cant close
causing blood flow from
aortic valve back into
LVcausing VOLUME
OVERLOAD

AI pts male
2/3 AI pts
rheumatic

*has two inflows in diastole

(from LA and aortic valve)

Mnemonics
Sequence of Flow
TRIPS BIAS:
TRIcuspid
Pulmonary
Semilunar
BIcuspid
Aortic
Semilunar

*annuloaortic
ectasiaproximal
ascending aorta & aortic
annulus are
dilateddilation can causes
valve to be incompetent
causing obstruction of
blood flow into
LVcausing PRESSURE
difference

*no treatment
needed- normal aging

Pathology
*rheumatic AI frequently
associated with
*can be caused by primary
valve or aortic disease
Hemodynamic issues are
dependent upon rate of onset
of AI

*Marfans
*Congenital
*Valvular abnormality

Secondary Causes
Infectious endocarditis
Trauma
Aortic dissection or aneurysm
Marfans
Syphilis
ankylosing spondylitis (long
term arthritis)
Mnemonics
CREAM- Causes
Congenital
Rheumatic damage

*small orifice visible

*LVH
*Doppler demonstrates gradient by
measuring velocity of flow in systolic
across AV

History and Clinical

Signs
Signs/Symptoms
Dyspnea on exertion, orthopnea,
paroxysmal nocturnal dyspnea
Bounding pulse
Acute AI
*LV cant dilate increase in SV
*LVEDP rises rapidly
*Pulmonary edema or shock
Chronic AI
*Stroke volume increases (dilation
& LVH)
*left ventricular end diastolic
pressure slows in late diastole
*As LV dilates more forward flow
decreases
*significant LV deterioration
occurs before symptoms
Severe AI
*Bobbing of head, body shakes
*pulse rises rapidly
*quickne pulse (when squeeze
fingers you see red white red
white)
*wide pulse pressure (increased
systolic & decreased diastolic)
160/40

Investigation
& Findings
EKG: LVH w/
ST-T changes
Chest X-ray
*LVH & LAE
Echo
*early increased
EF
*Serial exams to
assess for failing
LF function
*EDD (end
diastolic
diameter) >
55mm
*Size of jet to
estimate AI
Cath
*to evaluate LF
function, confirm
amount of AI, &
assess associated
CAD

Treatment
*Nifedipine,
diuretic, ACE
inhibitors
Surgical treatment
*Rarely repair:2
degree infectious
endocarditis,
traumatic damage
*AVR usually
necessary in
chronic, rheumatic
AI
*AI second degree
dilated root
frequently requires
a valve conduit
*prognosis
dependent on LV
function @time of
surgery

Valvular Heart Disease

Endocarditis
Aortic dissection/ Aortic root
dilatation
Marfan's

*Point Maximum Impact (PMI)

heaving & displaced laterally
*diastolic thrill
*decrescendo diastolic murmur
LSB-valvular AI
*decrescendo diastolic murmur
RSB- dialted aortic root
*may have short, softer murmur

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

Disease/Dis
order
Tricuspid
Stenosis
*Rare, generally
rheumatic in
origin

Pathophysiology/Etiolo
gy
*diastolic pressure gradient b/w
RA and RV defines TS
*augmented by trasnvalvular
blood flow

History and
Clinical Signs
Dyspnea, pulmonary
congestion, and fatigue

Investigation &
Findings
Marked hepatic
congestion, cirrhosis,
jaundice, anasarca,
ascites

Treatment
Salt restriction
Bed rest
Diuretic therapy
Surgery needed

ECG: RA
enlargement, tall
peaked P waves
Chest X-ray:
prominence of RA &
superior vena cava
Echo: tricuspid valve
usually thickened,
domes in diastole
Disease/Dis
order
Tricuspid
Regurg- usually
secondary to
marked dilation
of tricuspid
annulus from
RV enlargement

Pathophysiology/Etiolo
gy
*seen in late HF due to rheumatic
or CHF
*usually functional dilation of
annulus & right heart
**endocarditis secondary to IV
drug use

History and
Clinical Signs
Systemic venous
congestion, reduction of
CO
*neck veins distended
*pulse weak

Investigation &
Findings
Marked
hepatomegaly, ,
jaundice, ascites
ECG: inferior Q
wave MI or RVH
Chest X-ray:
prominence of RA &
superior vena cava
Echo: shows RV
dilation and prolapse

Treatment
Well tolerated normally
Surgery eventually needed

Valvular Heart Disease