The Dept of Anaesthesia & Intensive Care, CUHK
The right lung has 3 lobes: Right upper lobe, middle and lower lobe.
The left lung has 2 lobes: Left upper lobe (the lingula anatomically corresponds to the middle lobe on the right) and lower lobe.
Lobes are separated by fissures - the right major fissure separates the right upper and middle lobes from the right lower lobe. The right minor (horizontal) fissure separates the right upper lobe from the right middle lobe. The left major fissure separates the left upper lobe and lower lobe. Segmental anatomy has little relevance in plain chest radiography.
The position of the various lobes on the frontal CXR is illustrated below.
The figures illustrate the CXR appearance of consolidation of different lobes. Because of the loss of the solid-gas interface the heart borders or diaphragms may be obscured by consolidation of adjacent lobes
Right upper, middle and lower lobe consolidation (from left to right)
Left upper lobe,lingula and left lower lobe consolidation (from left to right)
An infiltrate is the filling of airspaces with fluid (pulmonary oedema), inflammatory exudates (white cells or pus, protein and immunological substances), or cells (malignant cells, red cells or haemorrhage) that fill a region of lung and increase the visual impression of increased soft tissue density.
Atelectasis is the collapse of the airspaces which also results in the visual impression of increased soft tissue density. This makes it impossible to distinguish infiltrates from atelectasis on the basis of visual density alone. Considering other factors is therefore required. Atelectasis must have volume loss by definition (collapse of airspaces must reduce lung volume), whereas infiltrate does not.
Atelectasis in ICU patients occurs most frequently in the left lower lobe, probably because the heart in the supine position compresses the lower lobe bronchus. The following signs of atelectasis can be seen:
Major differentiating factors between atelectasis and pneumonia:
Right upper lobe collapse (left) and consolidation (right)
Acute Respiratory Distress Syndrome (ARDS)
ARDS is an acute response to systemic inflammation. It is difficult to distinguish from cardiogenic pulmonary oedema or pneumonia. While cardiogenic pulmonary edema typically begins centrally in the bilateral perihilar areas, ARDS usually causes more uniform opacification. Pleural effusions are not typical of ARDS but often present in CHF. Kerley B lines are common in CHF but not in ARDS, while air bronchograms can be found in both. The distinction from pneumonia is on the basis of non-radiological investigations.
Acute respiratory distress syndrome. The patient is intubated and has a pulmonary artery catheter in situ
Pulmonary oedema is transudate fluid collecting in the lung tissue. Three
mechanisms lead to pulmonary edema. These are:
Any one or more often a combination of these mechanisms will cause fluid to enter the alveolar space.
When the capacity of the the lymphatic system is overwhelmed, interstitial oedema results. The classic Kerley lines are made by the thickening of the interlobular septa that carry the lymphatics (Kerley B lines are short thin lines, 1.5 to 2cm in length, seen in the periphery of the lower lung, extending to the pleura). As fluid continues to accumulate, it leaks into the pleural space resulting in pleural effusions and into the alveolar spaces causing the classic alveolar pattern of pareynchymal pulmonary edema.
Congestive heart failure is the most common cause of acute pulmonary oedema, and has additional features to the above because of the mechanism of causation that is primarily the increased hydrostatic gradient. It is often associated with cardiomegaly – difficult to determine on an AP film. Better indications are that the upper lobe blood vessels become more prominent due to vascular congestion (upper lobe blood diversion). The interstitial edema that results from transudation of fluid also affects the interstitium around the vessels and causes an apparent increase in diameter, causing an elevated arteriole to bronchiole ratio. Transudation fluid may also outline the bronchi that run with the vessels, causing peribronchial cuffing.
Note causes of non-cardiogenic pulmonary oedema include aspiration, transfusion reaction, neurogenic, ARDS, renal or hepatic disorders, inhalation of toxins, allergic alveolitis.
Note: A hallmark of pulmonary oedema is it’s ability to clear rapidly – within hours. This may help to distinguish it from pneumonia, ARDS or haemorrhage.
Presents radiographically like any other alveolar infiltrate (pneumonia, edema). Pulmonary hemorrhage is often resolves more quickly than other alveolar densities such as pneumonia, but not as quickly as improving pulmonary oedema.
Text © Gavin Joynt, June 2005; images © Charles Gomersall, June 2005
August, 2014 unless
otherwise stated. The author, editor and The Chinese University of Hong Kong
take no responsibility for any adverse event resulting from the use of this