Table 101.

DIFFERENTIAL DIAGNOSIS OF VALVULAR HEART DISEASE

Mitral Stenosis Mitral
Re!ritation
Aorti" Stenosis Aorti" Re!ritation Tri"!s#i$
Stenosis
Tri"!s#i$
Re!ritation
Inspection Malar flush,
precordial bulge, and
diffuse pulsation in
young patients.
Usually prominent
and hyperdynamic
apical impulse to left
of MCL.
Sustained PMI,
prominent atrial
filling wave.
yperdynamic PMI to
left of MCL and
downward. !isible
carotid pulsations.
Pulsating nailbeds
"#uinc$e%s&, head bob
"deMusset%s&.
'iant a wave in
(ugular pulse
with sinus
rhythm.
Peripheral
edema or ascites,
or both.
Large v wave in
(ugular pulse) time
with carotid
pulsation.
Peripheral edema
or ascites, or
both.
Palpation *+apping* sensation
over area of e,pected
PMI. -ight
ventricular pulsation
left third to fifth ICS
parasternally when
pulmonary
hypertension is
present. P. may be
palpable.

/orceful, bris$ PMI)
systolic thrill over
PMI. Pulse normal,
small, or slightly
collapsing.
Powerful, heaving
PMI to left and
slightly below MCL.
Systolic thrill over
aortic area, sternal
notch, or carotid
arteries in severe
disease. Small and
slowly rising carotid
pulse. If bicuspid 0S
chec$ for delay at
femoral artery to
e,clude coarctation.
0pical impulse forceful
and displaced
significantly to left and
downward. Prominent
carotid pulses. -apidly
rising and collapsing
pulses "Corrigan%s
pulse&.
Pulsating,
enlarged liver in
ventricular
systole.
-ight ventricular
pulsation. Systolic
pulsation of liver.
Heart so!n$s%
r&'t&(% an$ bloo$
#ress!re
S1 loud if valve
mobile. 2pening snap
following S.. +he
S1 normal or buried
in early part of
murmur "e,ception is
0. normal, soft, or
absent. Prominent S3.
4lood pressure
S1 normal or reduced,
0. loud
S1 often loud.

0trial fibrillation
may be present.
Mitral Stenosis Mitral
Re!ritation
Aorti" Stenosis Aorti" Re!ritation Tri"!s#i$
Stenosis
Tri"!s#i$
Re!ritation
worse the disease, the
closer the S.5opening
snap interval.

mitral prolapse where
murmur may be late&.
Prominent third heart
sound when severe
M-. 0trial
fibrillation common.
4lood pressure
normal. Midsystolic
clic$s may be present
and may be multiple.

normal, or systolic
pressure normal with
high diastolic
pressure.

d. 6ide pulse pressure
with diastolic pressure
7 89 mm g.
6hen severe, gentle
compression of femoral
artery with diaphragm
of stethoscope may
reveal diastolic flow
":uro;ie;%s& and
pressure in leg on
palpation < 39 mm g
than arm "ill%s&.
M!r(!rs
Lo"ation an$
trans(ission
Locali;ed at or near
ape,. :iastolic
rumble best heard in
left lateral position)
may be accentuated
by having patient do
sit5ups. -arely, short
diastolic murmur
along lower left
sternal border
"'raham Steell& in
severe pulmonary
hypertension.
Loudest over PMI)
posteriorly directed
(ets "ie, anterior
mitral prolapse&
transmitted to left
a,illa, left
infrascapular area)
anteriorly directed
(ets "ie, posterior
mitral prolapse&
heard over anterior
precordium. Murmur
unchanged after
premature beat.
-ight second ICS
parasternally or at
ape,, heard in carotid
arteries and
occasionally in upper
interscapular area.
May sound li$e M-
at ape, "'allaverdin
phenomenon&, but
murmur occurs after
S1 and stops before
S.. +he later the pea$
in the murmur, the
more severe the 0S.
:iastolic= louder along
left sternal border in
third to fourth
interspace. eard over
aortic area and ape,.
May be associated with
low5pitched
middiastolic murmur at
ape, "0ustin /lint& due
to functional mitral
stenosis. If due to an
enlarged aorta, murmur
may radiate to right
sternal border.
+hird to fifth
ICS along left
sternal border
out to ape,.
Murmur
increases with
inspiration.
+hird to fifth ICS
along left sternal
border. Murmur
hard to hear but
increases with
inspiration. Sit5
ups can increase
cardiac output and
accentuate.
Mitral Stenosis Mitral
Re!ritation
Aorti" Stenosis Aorti" Re!ritation Tri"!s#i$
Stenosis
Tri"!s#i$
Re!ritation
Ti(in -elation of opening
snap to 0. important.
+he higher the L0
pressure the earlier
the opening snap.
Presystolic
accentuation before S1
if in sinus rhythm.
'raham Steell begins
with P. "early
diastole& if associated
pulmonary
hypertension.

Pansystolic= begins
with S1 and ends at or
after 0.. May be late
systolic in mitral
valve prolapse.

4egins after S1, ends
before 0.. +he more
severe the stenosis,
the later the murmur
pea$s.

4egins immediately
after aortic second
sound and ends before
first sound "blurring
both&) helps distinguish
from M-.
-umble often
follows audible
opening snap.
0t times, hard to
hear. 4egins with
S1 and fills
systole. Increases
with inspiration.

)&ara"ter Low5pitched,
rumbling) presystolic
murmur merges with
loud S1.

4lowing, high5
pitched) occasionally
harsh or musical.
arsh, rough. 4lowing, often faint. 0s for mitral
stenosis.
4lowing, coarse,
or musical.
O#ti(!(
a!s"!ltator'
"on$itions
0fter e,ercise, left
lateral recumbency.
4ell chest piece
lightly applied.
0fter e,ercise) use
diaphragm chest
piece. In prolapse,
findings may be
more evident while
standing.
Use stethoscope
diaphragm. Patient
resting, leaning
forward, breath held
in full e,piration.
Use stethoscope
diaphragm. Patient
leaning forward, breath
held in e,piration.
Use stethoscope
bell. Murmur
usually louder
and at pea$
during
inspiration.
Patient
recumbent.
Use stethoscope
diaphragm.
Murmur usually
becomes louder
during inspiration.
Mitral Stenosis Mitral
Re!ritation
Aorti" Stenosis Aorti" Re!ritation Tri"!s#i$
Stenosis
Tri"!s#i$
Re!ritation
Ra$iora#&' Straight left heart
border from enlarged
L0 appendage.
>levation of left
mainstem bronchus.
Large right ventricle
and pulmonary artery
if pulmonary
hypertension is
present. Calcification
in mitral valve in
rheumatic mitral
stenosis or in annulus
in calcific mitral
stenosis.
>nlarged left
ventricle and L0.
Concentric left
ventricular
hypertrophy.
Prominent ascending
aorta. Calcified aortic
valve common.
Moderate to severe left
ventricular
enlargement. 0ortic
root often dilated.
>nlarged right
atrium with
prominent S!C
and a;ygous
shadow.
>nlarged right
atrium and right
ventricle.
E)G 4road P waves in
standard leads) broad
negative phase of
diphasic P in !1. If
pulmonary
hypertension is
present, tall pea$ed P
waves, right a,is
deviation, or right
ventricular
hypertrophy appears.

Left a,is deviation or
fran$ left ventricular
hypertrophy. P waves
broad, tall, or
notched in standard
leads. 4road negative
phase of diphasic P in
!1.

Left ventricular
hypertrophy.
Left ventricular
hypertrophy.
+all, pea$ed P
waves. Possible
right ventricular
hypertrophy.
-ight a,is usual.
E"&o"ar$iora#&'
T*o+$i(ensional +hic$ened, immobile +hic$ened mitral :ense persistent 0bnormal aortic valve In rheumatic >nlarged right
Mitral Stenosis Mitral
Re!ritation
Aorti" Stenosis Aorti" Re!ritation Tri"!s#i$
Stenosis
Tri"!s#i$
Re!ritation
e"&o"ar$iora#&' mitral valve with
anterior and posterior
leaflets moving
together. *oc$ey
stic$* shape to opened
anterior leaflet in
rheumatic mitral
stenosis. 0nnular
calcium with thin
leaflets in calcific
mitral stenosis. L0
enlargement, normal
to small left ventricle.
2rifice can be traced
to appro,imate mitral
valve orifice area.
valve in rheumatic
disease) mitral valve
prolapse) flail leaflet
or vegetations may
be seen. :ilated left
ventricle in volume
overload. 2perate for
left ventricular end5
systolic dimension <
3.? cm.
echoes from the
aortic valve with
poor leaflet
e,cursion. Left
ventricular
hypertrophy late in
the disease. 4icuspid
valve in younger
patients.
or dilated aortic root.
:iastolic vibrations of
the anterior leaflet of
the mitral valve and
septum. In acute aortic
insufficiency,
premature closure of
the mitral valve before
the #-S. 6hen severe,
dilated left ventricle
with normal or
decreased contractility.
2perate when left
ventricular end5systolic
dimension < ?.9 cm.
disease, tricuspid
valve thic$ening,
decreased early
diastolic filling
slope of the
tricuspid valve.
In carcinoid,
leaflets fi,ed,
but no
significant
thic$ening.
ventricle with
parado,ical septal
motion. +ricuspid
valve often pulled
open by displaced
chordae.
)ontin!o!s an$
"olor ,lo* Do##ler
an$ TEE
Prolonged pressure
half5time across
mitral valve allows
estimation of gradient.
M!0 estimated from
pressure half5time.
Indirect evidence of
pulmonary
hypertension by
noting elevated right
ventricular systolic
pressure measured
from the tricuspid
-egurgitant flow
mapped into L0. Use
of PIS0 helps assess
M- severity. +>>
important in
prosthetic mitral
valve regurgitation.
Increased
transvalvular flow
velocity) severe 0S
when pea$ (et < 3
m@sec "83 mmg&.
!alve area estimate
using continuity
eAuation is poorly
reproducible.
:emonstrates
regurgitation and
Aualitatively estimates
severity based on
percentage of left
ventricular outflow
filled with (et and
distance (et penetrates
into left ventricle. +>>
important in aortic
valve endocarditis to
e,clude abscess. Mitral
inflow pattern
Prolonged
pressure half5
time across
tricuspid valve
can be used to
estimate mean
gradient. Severe
tricupid stenosis
present when
mean gradient <
? mm g.
-egurgitant flow
mapped into right
atrium and venae
cavae. -ight
ventricular
systolic pressure
estimated by
tricuspid
regurgitation (et
velocity.
Mitral Stenosis Mitral
Re!ritation
Aorti" Stenosis Aorti" Re!ritation Tri"!s#i$
Stenosis
Tri"!s#i$
Re!ritation
regurgitation (et. describes diastolic
dysfunction.