Differential diagnosis
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Transcript Differential diagnosis
Complete Cardiac Diagnosis
Congenital Heart Disease – Atrial Septal Defect;
cardiomegaly with multi-chamber
enlargement, RVH, dilated RA and main PA,
MVP-anterior mitral valve leaflet, PR; sinus
rhythm, pulmonary HPN, incomplete right
bundle branch block; Functional Class III C
AUSCULTATORY FINDINGS OF THE
PATIENT
DIFFERENTIAL DIAGNOSIS
Hx
Patient
ASD
VSD
PDA
RHD
“heart
disease” in
childhood
Prolonged
symptom-free
period
most children
with small
defects remain
asymptoma-tic
frequent URTI
Palpitations
premature
birth, perinatal
distress, or
perinatal
hypoxia may
be present
(+) upper
respiratory
tract infection
Mitral
stenosis
easy
fatigability
occasional
chest pain
Fatigue
Dyspnea on
exertion
Orthopnea
Frequent
respiratory
infections
Symptoms of
right
ventricular
failure
In patients
with
Eisenmenger
syndrome,
symptoms in
adult life
consist of
exertional
dyspnea,
syncope and
hemoptysis
R-L shunt
leads to
cyanosis,
clubbing, and
erythorocytosis
-dyspnea and
cough on
exertion
-orthopnea
and PND
-hemoptysis
Mitral
regurgitation
-dyspnea and
cough on
exertion
-orthopnea
and PND
-ankle edema
P.E.
Patient
ASD
VSD
PDA
RHD
Hyposthenic,
narrow AP chest
diameter
Prominent RV
impulse
loud, harsh, or
blowing
holosystolic
murmur is
heard best
over the lower
LSB in the 3rd
or 4th ICS
precordial
activity is
increased
Mitral
stenosis
diastolic thrill
at the apex
S1 and P2 are
accentuated
S2 is split or
fixed
OS of the
mitral valve on
expiration
(+) carvallo's
sign
Normal JVP and
CAP
Left lower sternal
lift
Normal S1 ff. by
gr. 3/6 crescendodecrescendo
murmur
S2 wide with fixed
splitting
Multiple clicks at
apex
S1 normal or split,
with accentuation
of TV closure
sound
Wide & fixed
splitting of the S2
Systolic ejection
murmur (heard in
pulmonic area)
Diastolic rumble
across the
tricuspid valve
Neck vein
distention
Ascites
Edema
displaced
cardiac apex
with a similar
holosystolic
murmur
apical impulse
is laterally
displaced
S1 normal, S2
typically
obscured by
murmur
Continuous
machinery-like
apical diastolic murmur
rumble and
third heart
Bounding
sound (S3)
peripheral
pulses
Mitral
regurgitation
(+) systolic
thrill at the
apex
holosystolic
murmur
-(+) S4
ECG
Patient
ASD
VSD
PDA
RHD
Normal sinus
rhythm
Ostium secundum
defects –
incomplete right
bundle block &
right axis deviation
May be
normal
LVH with a
larger PDA
LVH
RVH
Incomplete RBBB
Diffuse ST-T
changes
Ostium primum
defects – left
anterior hemiblock
& left axis
deviation
With larger
defects
there are
various
degrees of
right axis
deviation
associated
with right
ventricular
Enlargement
CXR
Patient
ASD
Cardiomegaly
with multichamber
enlargement and
pulmonary
congestion
Shunt vascularity
Right
(inc. pulm.
Ventricular
vascular markings) enlargement
LAE
Right ventricular
enlargement
PAE
Enlargement of
the pulmonary
artery segment in
P-A view
VSD
Increased
pulmonary
vascular
markings
PDA
LVE
PVE
RHD
Mitral stenosis
-(+) kerley B lines
-concentric
hypertrophy of left
atrium
-cephalization
-prominent main
pulmonary artery
and branches
-constriction of
arteries in the
middle and
peripheral lung
zones
Mitral
regurgitation
-eccentric
hypertrophy of the
left atrium
-LA and LV
enlargement
-equalization,
cephalization
-mitral annulus
calcification
Echo
Patient
ASD
ASD, ostium
secundum type
Enlargement of RV color
flow can
Negative-contrast
show the
image at the site
shunting of
of defect (saline
blood from
injection)
the left
ventricle to
Doppler –
the right
abnormal pressure
of left-to-right
VSD's can
blood flow across
result in a
the septum
shunt from
below the
tricuspid
valve to
below the
pulmonary
valve.
Markedly dilated
right ventricle with
adequate wall
motion and
contractility with
evidence of RV
pressure and
volume overload
Dilated RA w/o
thrombus
Dilated MPA
Severe TR
PR
Mod. Pul. HPN
Reverse E/A
across mitral valve
VSD
PDA
RHD
LAE
Mitral
stenosis
-mitral orifice
<4cm
-concentric
hypertrophy of
left atrium
-annular
calcifications
Continuous
flow from the
aorta into the
main
pulmonary
artery
Mitral
regurgitation
-eccentric
hypertrophy of
the left atrium
-LA
enlargement
-hyperdynamic
LV
-annular
calcifications/
LV dyskinesis
-ruptured
chordae
tendineae
CHEST X-RAY FINDING IN A LEFT TO
RIGHT SHUNT
DIFFERENTIATE PULMONARY ARTERIAL
HYPERTENSION FROM PULMONARY
VENOUS CONGESTION
Pulmonary Arterial Hypertension
•
Causes
– Primary/ Idiopathic
•
Genetic
– Secondary
•
•
1.
2.
3.
Cardiac
Pulmonary
hypoxic vasoconstriction
decreased area of the pulmonary vascular bed
volume/pressure overload
Secondary Pulmonary Arterial
Hypertension
• Hypoxic Vasoconstriction
– COPD and obstructive sleep apnea
– Due to down regulation of endothelial nitric oxide
synthetase
• Decreased Area of Pulmonary Bed
– Occurs when loss of vessels exceed 60% of the total
pulmonary vasculature
– Occurs in patients with collagen vascular disease like
CREST and scleroderma. And those with chronic
emboli
• Volume/ Pressure Overload
– Seen in patients with left to right intracardiac
shunts
– May passively occur in patients with left atrial
hypertension and left ventricular dysfunction,
mitral valve disease and hose with aortic stenosis
Pulmonary Arterial Hypertension
• Chest radiograph
- Classic finding is enlargement of central of
pulmonary arteries, attenuation of peripheral
vessels and oligemic lung fields
- Findings of RV and RA dilatation are possible
Pulmonary Venous Hypertension
• Secondary to increased resistance to
pulmonary venous drainage
• Associated with diastolic dysfunction of the LV
and valvular dysfunction
• Features
– Capillary congestion
– Focal alveolar edema
– Dilatation of interstitial lymphatics
•mild cardiomegaly
•normal pulmonary arterial markings
•pulmonary venous congestion
•fluid within the horizontal fissure
•prominent Kerley B lines (indicative of
lymphatic engorgement)
Lateral chest film show marked venous
congestion with fluid visible in both the
horizontal and oblique fissures
Pulmonary Arterial
Congestion
Pulmonary Venous
Congestion
“active congestion” – increased in flow Passive congestion – obstructed
of blood
venous outflow, swollen capillary beds
Physiologic
Systemic:
Pathologic
Localized
• Increase blood flow into skeletal
muscle (e.g. exercise)
• Systemic: generalized hypoxia,
metabolic activity
• Localized acute inflammation
• due to RHF
• diminution of CO and tissue
perfusion
• Hypoxia – decreased Hemoglobin
• Cyanosis
• Raised LA pressure secondary to LV
failure & MS
• Thrombotic occlusion of femoral
vein
MANAGEMENT