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3 LOBAR COLLAPSES
Lobar collapses occur due to occlusion of major bronchi. This occurs secondary
to sputum plugs/ inhaled foreign bodies or tumours.
Understanding the appearance of collapsed lung is simply a case of under
standing the anatomy involved.
Important anatomy of the bronchi.
The right main bronchus is more vertically orientated than the left main bronchus
which is almost horizontal in orientation. The angle between them averages out
at about 65 degrees. This means inhaled foreign bodies are ore likely to go
down the right main bronchus.
The right main bronchus divides into and gives off the upper lobe bronchus, it
then continues downwards as the bronchus intermedius. The bronchus
intermedius then divides into middle and lower lobe bronchi.
A blockage of the bronchus intermedius therefore causes simultaneous lower
and middle lobe collapse.
The left main bronchus divides andgives off the upper lobe bronchus and then
continues downwards as the lower lobe bronchus. It is the upper lobe bronchus
that gives off the bronchi to the lingula (the tongue shaped middle lobe equivalent
abutting onto the left heart border).
This means a left upper lobe collapse would look very different to a right
upper lobe collapse as effectively a middle lobe is collapsing (lingula).
Some general features of a collapse
The collapsed lobe becomes denser (more radio-opaque) and smaller.
The remaining lung becomes darker (more radio-lucent) as it expands to fill the
space lost due to the collapse.
If the lobe is big enough (the largest lobes being the lower lobes), you may see
crowding of the ribs, a raised hemi-diaphragm and sometimes mediastinal shift to
the side of collapse.
Left upper lobe collapse
The appearance of left upper lobe collapse is often misinterpreted even by
fairly senior clinicians. I think this is because it is assumed that it should look
like an area of increased density defined by a straight line.
1
As the left upper lobe collapses, it collapses forwards, this results in a lobe that
gradually thins out as you move peripherally from the mediastinum (a veil type
appearance). There is no sharp line of a horizontal fissure to define it. The
delineation of the oblique fissure that defines the area of collapse is only seen on
the lateral radiograph. The outline of the left heart is lost as this corresponds to
lingula. Usually most of the superior mediastinal outline is also lost as it
corresponds to the anterior and apico-posterior segments of the upper lobe.
Delineation of the
major fissure on
the lateral
This is called a juxta-phrenic peak it is
caused by pleura attached to the
diaphragm pulling it upwards due
volume loss
Occasionally the appearance is further confused by aeration of much of the left
superior chest with lung outlining the left superior mediatinum. This is caused by
the right upper lobe crossing the midline and filling the space previously occupied
by the left upper lobe.
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Left upper lobe collapse with aeration caused by the Right upper lobe
expanding across the midline.
Right upper collapse(RUL)
RUL collapse is usually much easier to recognize and understand. It is well
delineated by the horizontal fissure. The horizontal fissure has been pulled
upward due to volume loss and the outline of the right superior mediastinum is
lost as it is in contact with the anterior aspect of the upper lobe.
RUL collapse less obvious on this
AP lordotic view
Classic RUL collapse the relative
expansion and convexity near the
hilum is indicative of tumour (Golden’s
S sign)
Middle lobe collapse/Consolidation
The middle lobe is quite small and you seldom see evidence of volume loss.
3
In this radiograph there is clearly consolidation in the middle lobe although it is
not delineated by the horizontal fissure superiorly. Note the loss of the right heart
border can also occur with pectus excavatum.
The sternal compression means that the heart is
rotated to the left. The anterior ribs are sharply
angled downwards in a 7 configuration.
Left lower lobe collapse
This is easy to spot when it is big. It is much more difficult when the lobe has
collapsed down into a very small volume. As the lower lobe is a big lobe,
evidence of loss of volume may be very useful.
Clearly we should be looking for loss of the outline of the descending aorta and
loss of the left hemi-diaphragm. The lower lobe collapses essentially cause a
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triangle behind the heart with its apex at the appropriate hilum as seen on this
radiograph. The triangle is formed by the major fissure abutting onto descending
aorta (normally in contact with the posterior aspect of the lower lobe) and
henidiaphragm (normally in contact with anterobasal segement of lower lobe).
The right shoulder is rotated back
and hence if the radiograph was
normal more mediastinum would
be seen on the right.
There is crowding of the ribs on
the left.
There is loss of the outline of the
descending aorta and left hemidiapragm.
The is a double heart border. The
more medial is the outline of the
solid lower lobe.
This is as classic a left lower lobe
collapse.
The endotracheal tube is in a
satisfactory position and the
cardiac monitoring is noted.
Subtle LLL collapse.
The right shoulder is back and so
on the PA radiograph the right
side of the chest should be
darker,it isn’t.
There is very slight crowding of
ribs on the left.
There is loss of outline of the
lower descending aorta and
medial aspect of the left
hemidiaphragm.
Right lower lobe and bronchus intermedius collapse
Many causes of collapse are due to tumour and I think that I see as many middle
and lower lobe collapses (due to bronchus intermedius obstruction) as I do pure
lower lobe collapses (due to lower lobe bronchus obstruction).
Apart from the signs of volume loss, we expect to see a sharp boundary
superiorly caused by major fissure in lower lobe collapse, and a horizontal and
major fissure in middle and lower lobe collapse. If the middle lobe is involved we
should lose the outline if the right atrium as well.
5
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4 INFECTIONS
Lobar pneumonia
A lobar pneumonia is what one thinks of as a typical chest infection. It is a
process originating in the airspaces and spreads via the pores of Khon. (These
are openings in the alveolar wall allowing gas and fluid transfer). This process
often produces large areas of consolidation, often lobar in distribution typically
with air bronchograms. It is frequently caused by a Strep Pneumonaie infection
in a young patient.
Lobar pneumonias should not occur in patients beyond their 40s but If they do
complete resolution must occur.
Some clinicians see it as an indication for a bronchoscopy in this subgroup of
patients, as a lobar pneumonia in these patients suggests a bronchial lesion.
Apart from strep.pneumoniae , the other organism that classically causes a lobar
pneumonia is Klebsiella. This classically causes bulging fissures and is
commonly associated with cavitation and commonly occurs in alcoholics.
Before discussing broncho pneumonias, we need to revise a liitle anatomy.
The secondary pulmonary lobule
Each lobe can be divided into broncho-pulmonary segments. These are then
divided into secondary pulmonary lobules. These are separated by thin
septations which are hardly visible even on high resolution CT. The lymphatics
and pulmonary veins travel in these septa. Each lobule has about 10 terminal
bronchioles, which leads to smaller units of the lung called acini.
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acinus
Terminal bronchiole
and accompanying
artery
Pulmonary vein and
lymphatics in the
septa
Secondary pulmonary lobule
Bronchopneumonia
This is caused by consolidation in multiple overlapping secondary pulmonary
lobules. The process is thought to be centered on the airways and therefore air
bronchograms are much less common. After considering the anatomy of the
secondary pulmonary lobules you will understand why some people think of it as
a patchwork quilt pattern of shadowing. Probably the archetypal
bronchopneumonia occurs with Staphylococcus Aureus which is often bilateral
and commonly secondary to influenza. Staphylococcus Aureus is also associated
with cavitation. This pattern of disease is usually bacterial.
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Staph pneumonia
p
Arrows point to multiple small cavities.P indicates a pneumatocoele
Some pneumonias present with a more diffuse pattern of disease and cause
either interstitial shadowing and associated ground glass shadowing (alveolar
oedema).These tend to be viral pneumonias, pneumocystis or bacterial
pneumonias in a immunosuppressed patient (e.g. legionella or pseudomonas).
Cavities and Pneumatocoeles
Pneumatocoeles occur secondary to bronchiole obstruction (they are much more
common in paediatrics). This causes air trapping .Both alveolar and mass effect
are also rarely seen.
Cavitation on the other hand is a hole secondary to central necrosis.
Both however are secondary to infection (mnemonic SHITES).
Staphylococcus
Haemophilus influenzae
Tuberculosis
Enteric bacteria
Streptocooccus
pneumatocoeles and abscesses)
(pneumatocoeles)
(cavitation)
(cavitation)
(pneumatocoeles)
Other conditions associated with holes in the lungs.
1. Bronchogenic Carcinoma-usually large upper lobe squamous cell tumour
caused by central necrosis.
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2. Infarction (rare due to dual blood supply)-secondary to a large area of
infarction, often secondarily infected and in the lower lobes.
3. Metastases-squamous, colonic and sarcomas (cavitating metastases are
associated with pneumothoraces)
4. Bronchogenic cysts (rare)
5. Sequestrated lung- (rare) Left lower lobe preponderance.
6. Rheumatoid nodules. These may rarely cavitate.
7. Wegeners Granulomatosis (rare).Multiple lesions associated with patches of
haemorrhage and inflammatory change.
8. Sarcoid- Cavitating nodules are rare in sarcoidosis.
9. Bullous disease
Lung abscess
This abscess was located in the apical segment of the right lower lobe
Radiologists by and large are hopeless at guessing the organism. We can
usually locate the site of the pathology. We are able to say if the picture is
essentially one of a bronchopneumonia, a lobar pneumonia or if it is mainly in the
interstitium.
Some organisms that are worth knowing about and why
Streptococcus Pnemonaie. It is the most prevalent and a cause of broncho
and lobar pneumonias in all patients (immunosuppressed or otherwise).
Staphylococcus Aureus. It usually presents as a bilateral bronchopneumonia
with cavitation and pneumatocoeles (most commonly in children).Commonly post
influenza (together with strep pneumonaie and Haemophilus Influenzae). It is
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importantAlso in drug addicts, the immunosuppressed, those with indwelling
catheters and in patients with bacterial endocarditis. It is a relatively common
cause of empyemas (walled off pleurally based infection).
Haemophilus Influenzae. It causes a bilateral patchy bronchopneumonia and is
seen particularly inpatients with COPD.
Mycoplasma. It causes A lower lobe patchy/peribronchial consolidation.
Frequently, it starts as a lower lobe process associated with ground glass or
interstitial shadowing with small irregular nodules. Bilateral involvement is not
uncommon and can cause lymphadenopathy in paediatric patients.
Pseudomonas. Often seen in a debilitated patient who require mechanical
ventilation. It causes a patchy often bilateral bronchopneumonia with nodular
infiltrates
Legionella. Usually occurs in elderly, male patients and accounts for 3% of
pneumonias in the UK. It has a sub lobar, lower lobe distribution and a 30%
association with effusions. It often rapidly spreads to other sites within the chest.
Cavitation tends only to be a feature in the immunosuppressed patient.
Moxarella Cattarrhalis. It usually causes tracheo-bronchitis or a mild pneumonia.
Particularly in patients with carcinoma or COPD. It causes lobar or segmental
consolidation and in some patients it causes a bi-basal interstitial pattern..
Streptococcus Pyogenes. It is an uncommon infection that looks like a
staphylococcal bronchopneumonia. It usually follows viral infections but tends not
to cause pneumatocoeles.
Brucella. Acquired from farm animals, it can rarely present with consolidation and
effusion. Less than 1% of cases.
Pneumocystis Carinii(PCP). This commonly occurs in patients with AIDs
(usually the CD4 count is less than 200).Classically bilateral ground glass or
interstitial shadowing is present (cysts do occur but this is a CT rather than a
plain film finding). It also occurs in other immunosuppressed patients.
.
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Bilateral ground glass/airspace shadowing.
In itself consistent with any number of
diseases processes of alveolar oedema
/consolidation.Consistant with
mycoplasma,alveolitis etc . This was
pneumocystis
Chlamydia Pneumonaie. Person to person spread. Often asymptomatic and
makes up about 10% of community acquired pneumonia. Usually patchy, and
unifocal consolidation. About half have effusions.
Chlamydia Psittaci. It occurs in patients exposed to birds (especially parrots). It
is Indistinguishable from a bacterial pneumonia. The appearances vary, from
patchy consolidation to lobar pneumonia and sometimes bi-basal interstitial
infiltrates. It can be associated with lymphadenopathy and radiological features
are often slow to clear
Coxiella Burnetti. There is a history of contact with farm animals. Causes a rounded or
segmental/lobar consolidation in the lower lobes.
Varicella. A serious pneumonia in young adults with a 10-20% mortality. Usually
presents with bilateral ill defined nodules measuring 5-10mm in diameter. It may
leave calcified nodules in the lower zones (chronic venous hypertension in heart
failure is another cause).
AIDS AND CHEST INFECTIONS
They have a higher incidence of bacterial and TB infections.
Pneumocystis Carinii pneumonia occurs when the CD4 count drops below 200 or
so. The incidence of fungal infections is also higher.
TB only presents typically in less than ½ of patients with PCP infection.
Anaerobic infections
These almost invariably occurs secondary to aspiration.
They are spread by the airways to dependant areas and therefore. The right side
of the chest is more commonly affected.
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We usually think of the basal segments of the lower lobes being involved, but
these patients are often supine and so we need to think about which regions are
supine in a supine position.
These are often anaerobic infections and can be associated with cavitation.
Posterior (RUL)
Apico-posterior (LUL)
Apical (RLL)
Apical
(LLL)
Posterior (RLL)
Posterior
(LLL)
Dependant segments in the supine position
TUBERCULOSIS
This is a relatively common infection with increasing prevalence.
Primary TB
Primary TB in adults can present with a large pleural effusion. It may however
appear as an infective focus anywhere in the lungs with 30% of cases appearing
as increased localized nodular shadowing .
The classic appearance in a child is that of the primary complex. This consists of
a small focus of consolidation (often difficult to see) in the mid or lower zones of
the lungs. This focus is associated with lymphadenopathy in the paratracheal or
hilar region to give you the primary complex. It is this focus that often heals and
forms a calcified granuloma. 90% of cases these become quiescent and10%
reactivate.
Child with primary TB. There is right paratracheal
lymphadenopathy. The primary focus is not seen. The
chronic cough which this child developed has resulted
in a pneumomediastinum.
Secondary (reactivation) TB
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By far the most common presentation of TB in adults is secondary or reactivation
TB. This affects predominantly the upper lobes and apical segments of the lower
lobes. What is seen is a combination of cavitation and consolidation in these
areas. The normal evolution of these cavities is to start off thick walled. They may
expand as they become quiescent but then become thin walled.
Lymphadenopathy is also often evident and compression of the bronchi can arise
secondary to lymph node enlargement. Endobronchial spread of TB is common.
TB may also result in empyemas (infected pleural effusions) which often calcify
on healing.
Healing in TB is associated with scarring and fibrosis and this is obviously seen
primarily in the upper zones. TB is therefore one of the few causes of upper lobe
fibrosis. We might as well deal with this differential diagnosis of upper lobe
fibrosis now.
Secondary TB in the Right upper
lobe and apical segment of left
lower lobe.
Upper lobe fibrosis differential (mnemonic TRASH)
1. TB (common)
2. Radiation (bilateral radiation changes are uncommon)
3. Ankylosing spodylitis (rare) associated with marked kyphosis)
4. Alveolitis, extrinsic allergic (uncommon) associated with mid zone fibrosis
rather than upper lobe fibrosis in reality
5. Aspergillous. Broncho-pulmonary (uncommon)
6. Sarcoidosis (relatively common)
7. Histiocytosis X (rare)
Classic bilateral upper lobe fibrosis
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All the other causes of fibrosis cause predominantly increased mid and lower
zone fibrosis and hence shadowing.
Miliary TB
Another form of primary TB that needs discussion is miliary TB. This looks has
the appearance of nodular shadowing. The nodules are typically small (3-5mm)
and can be ill or well defined and may take up to a month to develop.
The nodulation is secondary to blood borne spread of infection to the interstitium
of the lungs; these nodules are also present in the meninges, adrenals, kidneys
etc.
Urgent treatment is required and there is a differential diagnosis to this
appearance.
A patient with Miliary TB Not
obvious until you look hard at
the lung parenchyma
Miliary shadowing in a patient with COAD
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Miliary shadowing differentials
1. Other infections-Mycoplasma, Histoplasmosis, candida and atypical infections
2. Sarcoidosis (patient not as unwell as the chest radiograph suggests)
3. Lymphoma
4. Metastatic disease. renal, thyroid, bone sarcomas, prostate,
chorioncarcinoma, pancreas and bronchus.
5. Extrinsic allergic alveolitis-fluffy small nodules which represent centri-acinar
(centri-lobular) consolidation.
6. Silicosis- evidence of fibrosis and usually there is a clear history of exposure.
Atypical Mycobacterium
They are usually of low pathogenicity and ubiquitous. M Kansasii is the only
atypical mycobacterium that when cultured on its own is likely to be pathogenic.
Usually looks like TB. There is a subgroup of elderly females that tend to present
with mid and lower zone nodulation associated with bronchiectasis.
ASPERGILLOUS INFECTIONS
This is as good a place to cover it. It presents in one of three ways:Aspergilloma
These are cavities in the lung which are occupied by fungal balls of aspergillous.
Any cause of cavity formation can be responsible (all the causes of upper lobe
fibrosis and also cavitation within malignancy). The most common cause overall
will be old TB. They are often asymptomatic but may present with massive
haemoptysis.
Bilateral upper lobe fibrosis with
bilateral aspergilloma
Invasive Aspergillosis
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This occurs in immunosuppressed patients. They often have one or more
rounded areas of consolidation in the lung. On CT these often have a halo of
lower attenuation change around them. This is not pathognomonic, but is highly
suggestive of the diagnosis.
Bronchopulmonary Aspergillosis
These patients present with cough and asthma. They have a eosinophilic picture
on their blood film. Flitting areas of consolidation are often seen (these represent
eosinophilic infiltrates). These areas tend to be segmental and recur over time.
Central bronchi become distended (bronchiectasis) with mucous and spores.
This occurs mainly in the mid zones and can cause associated fibrosis, collapse
and bronchocoeles (occluded bronchi distend due to central occlusion and dilate
into dilated cystic areas from collateral aeration.
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5 HEART FAILURE
This is the inability of the heart to maintain a normal output at normal filling
pressures. The inability to maintain a sufficient output for the body’s needs
is cardiogenic shock.
With a PA radiograph and a good inspiratory effort we can make a reasonable
attempt at assessing cardiac size.
CARDIOTHORACIC RATIO
GIVEN BY A+B/C
B
A
C
Remember that heart size can be larger in some populations. West Indian males
may have a ratio of 0.6 and still be normal. In addition if there is hyperinflation of
the lungs, the failing heart may not be enlarged. Also the measurements of A and
B may be inaccurate, if there are significant pericardial fat pads being included in
the measurements. Note that with an acute myocardial infarction or a
dysrhythmia there may be no cardiac enlargement.
Other features that may be helpful when looking at the cardiac silhouette are
calcification of heart valves (usually mitral and aortic most commonly).
Calcification of the left ventricle especially may represent an old area of
infarction. A bulge in this area may represent a left ventricular aneurysm.
Calcification of the left atrium tends to occur in old rheumatic heart disease.
aortic
mitral
Position of aortic and mitral valves
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Signs of raised left atrial pressure
Upper lobe blood diversion
For upper lobe blood diversion to be a useful sign, the film must be an erect film.
Conditions that cause fibrosis or emphysema in the lower lobes cause upper lobe
blood diversion. In these conditions it does not necessarily mean that there is
raised left atrial pressure. In addition upper lobe emphysema (the normal pattern
of smokers) emphysema can also prevent upper lobe blood diversion.
What you do is eyeball the radiograph. Is the lung phlethoric anyway (Are you
seeing lung markings out to the periphery?)? The vessels are also less well
defined as their walls are oedematous.
Do the upper lobe vessels generally look more prominent then the lower lobe
vessels. Theoretically you should measure the diameter of upper and lower zone
vessels which are equidistant from the hila point (The hila point is the point where
the superior pulmonary artery crosses the main pulmonary artery and is often
not well seen) and establish if the upper lobe vessel is of a larger diameter.
Finding an inferiorly placed vessel equidistant from the hila point is often very
difficult).
Look at the blood vessels between the 1st and 2nd ribs anteriorly they should be
less than 3mm in diameter. They should certainly be smaller than the
accompanying bronchus.
Ground glass shadowing and consolidation
Look for alveolar oedema or consolidation which is usually symmetrical and
dependant and pleural effusions (fluid in the pleural cavity). Note that bilateral
consolidation or ground glass consolidation is a non specific sign of oedema and
consolidation for whatever cause.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Heart failure/fluid overload
Inhaled toxins. Smoke and inhaled gases
Near Drowning
ARDS
Cerebral oedema
Aspiration and bilateral bronchopneumaonia.-usually unilateral
Circulating toxins and drugs reactions.
Prolonged dependence on one side
Aspiration
Rapid expansion of a collapsed lung
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The meniscus sign of an effusion?
A
B
C
A B C
The meniscus sign comes about due to the depth of fluid /soft tissue that
absorbs x-rays. It has nothing to do with surface tension and does not
distinguish fluid from pleural thickening. Clearly the meniscus would
change if it was fluid and the patient lay supine or on their side
Other general comments about effusions
1. The right hemi-diaphragm is more permeable
Therefore ascites is often associated with right sided effusions
2. Liver abscesses cause right sided effusions
3. Sub-phrenic abscesses are often a cause right sided effusions
4. In general it is said that left sided effusions are more worrying and assoc with
pericardial disease, thoracic aneurysm, oesophageal rupture, pulmonary
embolism and pneumonia.I think this is over emphasized and I have seen
several patients with mediastinal bleeds and right sided effusions.
5. Remember in the context of infection an effusion (particularly if bulging) may
represent an empyema.
Bilateral consolidation secondary to failure.
The are of lucency is due to a bulla unmasked
by the surrounding consolidation.
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Lymphatic overload
The lymphatics are often working flat out to clear the excess fluid. Look for
evidence of lymphatic overload (swollen septa between pulmonary lobules
(septal lines/ Kerley B lines). Subpleural fluid also sometimes accumulates.
Septal lines/Kerley B lines. Engorged lymphatics which run
in the septa.
Although they do occur in other conditions (Lymphangitis
Carcinomatosa),
they usually indicate heart failure/overload.
There is also a small subpleural fluid collection.
Pericardial Fluid
This can result in enlargement of the cardiac silhouette which can be massive. It
is important to remember certain points.
It is the speed of accumulation of the pericardial fluid rather than quantity that
dictates how symptomatic the effusion is. Usually there is a relatively rapid
increase in diameter of cardiac contour with no particular pattern of chamber
enlargement.
A Flask like appearance is typical, sometimes overlying the hila. A lack of
pulmonary congestion is also a pointer (restriction of right and left sided cardiac
output).
There are many cause usually viral (cocsackie in particular), Dressslers
syndrome (usually1-2 weeks after MI), uraemia, collagen vascular disease,
hypothyroidism, CCF ,and rarely tumour (mesothelioma especially). Aortric
dissections involving the arch (and in particular the ascending aorta) can also
cause bleeding into the pericardium.
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Some notes on cardiac enlargement
Being able to tell which chamber of the heart is predominantly enlarged from the
cardiac contour is less important than ever. This is because echocardiography
and now MR have taken over this role.
Rather than try and remember each outline associated with defects.
Remember what enlargement of different chambers look like and then put it
together.
Apex turns up with right ventricular enlargement.
A child with Tetralogy of Fallot –upturned apex in
keeping with Right Ventricular Hyppertrophy
The Apex goes down with left ventricular enlargement.
Right atrial enlargement causes bulging on the right side.
Left atrial enlargement causes enlargement of the atrium behind the heart. The
carina is often splayed,a double heart border arises on the right and the left atrial
appendage enlarges.
In Mitral stenosis, you would expect left atrial enlargement and pulmonary
congestion. Left ventricular hypertrophy would occur with mixed mitral valve
disease.
Left atrial
appendage
Double heart
border
Mixed mitral valve disease. Enlarged left atrial appendage
and left atrium (splayed carina, Double right heart border).
There is left ventricular hypertrophy (apex down
secondary to mitral regurgitation.
Thus in an ASD, you would expect right atrial and ventricular enlargement.The
lungs would be phlethoric. Left ventricular enlargement would only occur with
Eisenmengers syndrome(reversal of flow form right to left).
In a VSD, you would expect right ventricular enlargement. The lungs would be
phlethoric.
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