Air‐filled lungs provide an excellent opacity interface to visualize intra‐thoracic soft tissues. The ratio of gas to soft tissue in normally inflated lungs is greater than 10:1. To take full advantage of the gas‐to‐soft tissue opacity interface, make thoracic radiographs at peak inspiration. Fully inflated lungs not only enhance the visibility of intra‐thoracic structures, they also separate the structures to reduce summation and superimposition artifacts (Figures 3.1 and 3.2). Poor lung inflation can mimic or mask disease. At the end of this chapter there are extensive lists of differential diagnoses for numerous radiographic findings regarding the thorax. Figure 3.1 Inspiration vs. Expiration. Lateral views of a dog thorax made during inspiration (A) and expiration (B). Fully inflated lungs provide the gas‐to‐soft tissue opacity interfaces needed to identify the intra‐thoracic structures. The cranial lobar blood vessels are better visualized during inspiration than expiration (white arrow). During inspiration, there is a better separation between the aorta and caudal vena cava (white double‐headed arrow) and between the heart and diaphragm (black arrow and dotted triangle). The caudal vena cava is more parallel with the spine during inspiration. Figure 3.2 Inspiration vs. Expiration. VD views of a dog thorax made during inspiration (A) and expiration (B). Fully inflated lungs separate the cardiac silhouette and diaphragm and enhance the opacity interface. The costophrenic angles (white arrows) are wider and sharper during inspiration. Orthogonal views are necessary for complete evaluation. Standard orthogonal views of the thorax include a left or right lateral view (preferably both) and a ventrodorsal (VD) or dorsoventral (DV) view. Radiographs of the pharynx or larynx are useful to examine the upper respiratory tract, which may be helpful in determining the etiology of lower respiratory disease. Whenever practical, remove the endotracheal tube and any superimposed monitoring equipment prior to imaging the cervical region. Measure the thickest part of the neck, usually near the head, and center the x‐ray beam on the larynx. Collimate the FOV to the area of interest and use the small focal spot. The lateral view is made with the mouth closed and the head and neck in a neutral position, about a 135° angle between the spine and the mandibles. Align the transverse processes of C1 in the same plane and elevate the sternum as needed to correct rotation. The VD/DV view is made with the head and neck extended. If needed, rotate the patient slightly to the left or right to eliminate superimposition of the skull and spine. The patient’s age, body type, body condition, phase of respiration, and position at the time of radiography can significantly affect the radiographic appearance of thoracic structures. Conditions outside the thoracic cavity may affect the appearance of the intra‐thoracic structures, including abdominal distention that limits lung inflation (Figure 3.4). Some of these effects are described below and discussed in more detail with each specific structure later in this chapter. Figure 3.3 Stretching the patient. Two lateral views of the same 10‐year‐old, 22‐kg dog. In radiograph A, the patient is hyperextended resulting in dorsoventral narrowing of the thorax (double‐headed arrow), less inflated lungs, a narrowed trachea, and distortion of the cardiac silhouette. In radiograph B, the patient is in a more neutral and relaxed position, allowing the lungs to expand and producing a truer representation of the trachea and cardiac silhouette. Figure 3.4 Distended abdomen. Lateral view of a dog depicting abdominal distention due to gastric bloat. The distended abdomen limits expansion of the thoracic cavity which results in poor lung inflation. Figure 3.5 Patient rotation artifacts. A. A properly positioned VD view of a dog thorax: the spine and sternum are superimposed, the dorsal spinous processes are centered in the vertebral bodies (black arrow), and the right and left ribs are equal length. B. A VD view made with the patient rotated to the right: the appearance of the thorax is distorted. The sternum is right of the spine (yellow arrow) and most of the cardiac shadow is right of midline (the heart follows the sternum). The right cardiac border is closer to the right thoracic wall (black arrowheads) which may be mistaken for right heart enlargement. The right ribs are longer than the left and the dorsal spinous processes project lateral to the vertebral bodies (black arrow). The left caudal pulmonary vessels, which normally are superimposed on the cardiac silhouette, are visible spine (white arrow) and may be mistaken for enlarged vessels or lung disease. Figure 3.6 Rib articulations. VD view of a dog thorax depicting numbered ribs and the corresponding numbered thoracic vertebrae. Figure 3.7 Costochondral junctions. Lateral view of a dog thorax depicting various appearances of costal cartilages. A. Soft tissue opacity cartilage that is not mineralized. B. Uniform mineralization of cartilage. C. Heterogenous mineralizations, common in older dogs. D. Large mineralizations at multiple costochondral junctions. Figure 3.8 Diffuse thickening of the thoracic wall. VD views of a dog thorax depicting thickening of the thoracic wall. A. Normal thoracic wall for comparison. B. Subcutaneous fat due to obesity causes diffuse thickening of the thoracic wall. The extracostal muscles are displaced and outlined by fat to create curved, soft tissue opacity lines (white arrows) that conform to the shapes of the ribs. Notice the lungs are more opaque than in image A due to summation of overlying fat. Pericardial fat surrounds the cardiac silhouette (black arrowheads). C. Subcutaneous emphysema creates a mixed pattern and outlines the extracostal muscles (white arrows). Summation of emphysema may be mistaken for gas in the thoracic cavity (black arrows). D. Subcutaneous fluid produces uniform soft tissue opacity thickening of the thoracic wall (white arrow) and obscures the fascial planes and extracostal muscles. The type of fluid cannot be determined from radiographs. Compared to image A, the thoracic cavity is overall increased in opacity due to summation of the subcutaneous fluid. Figure 3.9 Extra‐pleural sign. VD view of a dog thorax depicting a mass in the thoracic wall (white arrow) and a pulmonary nodule located near the thoracic wall (black arrow). The margins of the thoracic wall mass gradually taper cranially and caudally to form angles greater than 90° with the inner chest wall. The margins of the lung mass form acute angles less than 90° with the chest wall. Figure 3.10 Thoracic wall lipoma. VD view of a dog thorax depicting a well‐defined, fat opacity mass in the left thoracic wall (white arrow). There is no extra‐pleural sign because the lipoma does not bulge into the thoracic cavity (notice the small pulmonary vessels that are visible through the lipoma and extend to the chest wall). Part of the lipoma is superimposed on the lung to create an area of faintly increased opacity (white arrowheads). Figure 3.11 Hemivertebra. Lateral view (A) and VD view (B) of a dog thorax depicting a partially developed, wedge‐shaped vertebra in the caudal thoracic spine (black arrow). There is spinal kyphosis and crowding of the proximal ribs. In the VD view, the ribs radiate from the hemivertebra to resemble the spokes in a bicycle wheel. Figure 3.12 Inward curving ribs. VD radiograph (A) and CT image (B) of a typical dog thorax. The lungs extend to the inner margins of the ribs (arrows). VD view (C) and CT image (D) of a Bassett Hound thorax. The inward curving ribs (arrow in D) create soft tissue opacity along the inner thoracic walls (arrows in C) which may be mistaken for pleural fluid. Figure 3.13 R Types of rib fractures. Lateral view of a dog thorax depicting three types of rib fractures, including a cranially displaced segmental rib fracture (white arrows), a caudally displaced transverse rib fracture (black arrow), and a minimally displaced, overriding rib fracture (yellow arrow). In the latter, notice the increased opacity caused by overlap of the fracture ends. Figure 3.14 Rib fractures. VD view of a dog thorax depicting older, healing rib fractures (white arrows) and a new segmental rib fracture (black arrows). The margins of the healing fractures are smooth and well‐defined. The more medial fracture is healing in slight malunion. The more lateral fracture appears as an expansile area in the rib. The ends of the newer, segmental fracture are sharply marginated without evidence of periosteal new bone production. Figure 3.15 Rib tumor. Lateral view (A) and VD view (B) of a dog thorax depicting localized soft tissue swelling and osteolysis in the left eighth rib (white arrow). No periosteal response is visible. The lesion is easier to see in the VD view because it is tangential to the x‐ray beam and there is less superimposition artifact. The soft tissue swelling produces an extra‐pleural sign (black arrows). Possible causes for these radiographic findings include tumor and osteomyelitis. Figure 3.16 Flail chest. VD view of a dog thorax depicting segmental fractures in three adjacent ribs on the left side (white arrows) with soft tissue swelling and subcutaneous emphysema. The mediastinum is shifted to the right due to pneumothorax and higher pressure in the left hemi‐thorax than in the right. Figure 3.17 Flail chest. These illustrations depict the paradoxical movements of a flail chest. (A) During inspiration the thorax expands (black arrows), decreasing the intra‐thoracic pressure and allowing the lungs to expand and fill with air (white arrows). The flail section, however, is sucked inward due to the lower intra‐thoracic pressure (red arrows). (B) During expiration the thorax contracts, increasing the intra‐thoracic pressure to expel the air from the lungs. The flail part is pushed outward by the higher intra‐thoracic pressure. Figure 3.18 Fused sternebrae. Lateral view of a dog thorax depicting congenital fusion and slight misalignment of the fifth and sixth sternebrae (white arrow). No soft tissue swelling nor evidence of degenerative change or active bone remodeling is seen. Figure 3.19 Pectus excavatum. Lateral view (A) and VD view (B) of a dog thorax depicting dorsal deviation of the caudal sternum (white arrow). The caudal thorax is dorsoventrally narrowed. The cardiac shadow is displaced dorsally and to the right by the deformed sternum. Figure 3.20 Pectus carinatum. Lateral view of a dog thorax depicting ventral protrusion of the caudal sternum (white arrow). The dorsoventral dimension of the thoracic cavity is increased, allowing the cardiac silhouette to be more upright in position. Figure 3.21 Sternal lysis. Lateral view of a dog thorax depicting localized osteolysis in the fourth sternebra (black arrow) with adjacent soft tissue swelling (white arrows). Inward swelling produces an extra‐pleural sign (yellow arrow). Possible causes for the radiographic findings include tumor and infection. Figure 3.22 Parts of the diaphragm. Lateral view (A) and VD view (B) of a dog thorax depicting the parts of the diaphragm. The cupula is the central ventral “dome” of the diaphragm. The right and left crura insert on the L3 and L4 vertebrae. The ventral margins of L3 and L4 are less distinct than the adjacent vertebrae (red arrows). The yellow arrows point to the costophrenic recesses, where the diaphragm meets the thoracic wall. Figure 3.23 Left lateral vs. right lateral. Left lateral view (A) and right lateral view (B) of the same dog thorax depicting the positions of the left and right crura (L and R). In left lateral recumbency, the left crus (L) is cranial to the right crus (R), and the crura overlap. In right lateral recumbency, the right crus is cranial to the left, and the crura are more parallel. Gas in the stomach (S) is caudal to the left crus. The caudal vena cava (yellow arrows) emerges from the right crus. Figure 3.24 VD view vs. DV view. Ventrodorsal view (A) and Dorsoventral view (B) of a dog thorax. In the VD view, the diaphragm appears as three humps: (1) the right crus, (2) the cupula, and (3) the left crus. In the DV view, the diaphragm appears as one hump: the cupula (arrow). Notice that the cupula and the cardiac silhouette are in the contact in the DV view, indenting the diaphragm. Figure 3.25 Eventration of the diaphragm. Lateral view (A) and VD views (B and C) of a cat thorax depicting a cranial bulge in the ventral part of the diaphragm (white arrows). Any part of the diaphragm may be involved. As depicted in the VD views, the eventration may be centrally located (B) or more lateral (C). Figure 3.26 Tenting of the diaphragm. VD view of a dog thorax depicting hyperinflated lungs and severe caudal displacement of the diaphragm. The diaphragmatic costal attachments are visible as projections extending from the cupula (white arrows). Figure 3.27 Diaphragm hernia. Lateral view (A) and VD view (B) of a cat thorax depicting a mixed opacity mass in the right hemithorax. Fat opacity is visible, extending from the cranial abdomen into the thoracic cavity mass. Segments of gas‐filled and fluid‐filled small intestine are visible in the mass (black arrows). Also visible is the well‐defined edge of a soft tissue opacity structure (yellow arrows) which may represent displaced liver or spleen. The cardiac silhouette is completely effaced in the lateral view and partially effaced in the VD view. The left border of the cardiac shadow is visible in the VD view (white arrows). The ventral and right lateral margins of the diaphragm are not identified. The colon (C) can be followed from the abdomen into the thorax, across the level of the diaphragm. Figure 3.28 Paracostal hernia. Lateral view (A) and VD view (B) of a cat thorax depicting a swelling along the left lateral body wall (white arrow). The swelling is soft tissue opacity with curvilinear gas‐filled segments of small intestine. Notice in the lateral view that the cardiac and diaphragm borders remain visible through the extra‐thoracic swelling. This is because the intra‐thoracic opacity interface remains. Figure 3.29 Hiatal hernia. Lateral view (A) and VD view (B) of a cat thorax depicting a soft tissue opacity mass protruding from the dorsal diaphragm near midline and between the aorta and caudal vena cava (white arrows). Pulmonary vessels are visible at the mass because the hernia is located outside the lungs, in the caudal mediastinum. Figure 3.30 Peritoneal‐pericardial diaphragmatic hernia. Lateral view (A) and VD view (B) of a cat thorax depicting a large, rounded cardiac shadow with multiple, curvilinear gas‐filled segments of small intestine within the cardiac borders. The caudal cardiac and cranial diaphragmatic margins are not distinguished ventrally. The dorsal border of the PPDH is visible in the lateral view (white arrow). The caudal sternum is mildly deformed due to sternal dysraphism (black arrow). Figure 3.31 Pleural fissure lines. Illustration of a dog lung (A) and a lateral radiograph of a dog thorax (B) depicting the normal locations of pleural fissures. (1) Line produced by the cranioventral mediastinum between the right and left cranial lung lobes. (2) Right and left middle pleural fissure lines located between the right cranial and middle lung lobes and between the cranial and caudal sub‐segments of the left cranial lung lobe. (3) Right and left caudal pleural fissure lines located: between the right middle and caudal lobes and between the left cranial and caudal lobes. (4) Right and left dorsal pleural fissure lines located between the right and left cranial and caudal lobes. Figure 3.32 Pleural fissure lines. Illustration of a dog lung (A) and a lateral radiograph of a dog thorax (B) depicting the normal locations of pleural fissures. (1) Line created by the cranioventral mediastinum between the right and left cranial lung lobes. (2) Right and left middle pleural fissure lines located between the right cranial and middle lung lobes and between the cranial and caudal sub‐segments of the left cranial lung lobe. (3) Right and left caudal pleural fissure lines located between the right middle and caudal lobes and between the left cranial and caudal lobes. (4) Dorsal pleural fissure lines located between the right and left cranial and caudal lobes (not visible in the illustration A). (5) Line created by the caudoventral mediastinum between the accessory and left caudal lung lobes. Figure 3.33 Normal pleural fissure line. Lateral view of a dog thorax depicting the appearance of a normal pleural fissure line (white arrow) due to perfect alignment with the x‐ray beam. Figure 3.34 Normal pleural fissure line. Cross sectional CT image of a dog thorax depicting the patient in dorsal recumbency with the x‐ray beam (yellow arrow) aligned with an interlobar fissure (white arrow). C = cardiac silhouette, S = spine. Figure 3.35 Abnormal fluid or gas in the pleural space. VD views of a dog thorax depicting fluid (A) and gas (B) in the pleural space. Both pleural fluid and pleural gas prevent the lungs from fully expanding. In A, the lung lobes are surrounded by fluid (white arrow) which is more opaque than lung tissue. Fluid in the costophrenic recesses makes them more rounded (black arrow). In B, the lung lobes are surrounded by gas (white arrow), which is less opaque than lung tissue. Figure 3.36 Pleural fissure lines. VD view of a dog thorax. (1) A reverse fissure line created by fat between the right cranial and middle lung lobes. Notice that the fissure line made by fat is wider centrally and tapers peripherally. (2) Mineralized costal cartilage, which may be mistaken for a pleural fissure line. Notice that the cartilage curves in the opposite direction of fissure lines 1, 3, and 4. (3) Thin pleural fissure line that is uniform in width, without tapering at either end. This type of fissure line is consistent with pleural thickening or minimal pleural effusion. (4) Larger, wedge‐shaped pleural fissure line that is wider peripherally and tapers centrally, caused by pleural effusion. Figure 3.37 Pleural effusion, VD view. A. Cross‐sectional CT image of a dog thorax depicting the patient in dorsal recumbency. Fluid in the pleural space moves with gravity to the dependent (dorsal) part of the thoracic cavity (white arrows). Because the thorax is wider dorsally than ventrally, fluid moves into the spaces between the lungs and the lateral chest walls. C = cardiac silhouette; S = spine. B. VD view of a dog thorax depicting fluid between the lung edges and chest wall (black arrows) and between lung lobes (white arrows). The cardiac shadow is visible because it is adjacent to air‐filled lung, as seen in the CT image (A). Figure 3.38 Pleural effusion, DV view. A. Cross‐sectional CT image of a dog thorax depicting the patient in ventral recumbency. Pleural fluid flows with gravity to the dependent (ventral) part of the thoracic cavity where it collects adjacent to the mediastinum and cardiac silhouette (C). S = spine. B. DV view of a dog thorax depicting a small volume of pleural fluid between the lungs and chest wall (black arrow) and in the interlobar fissures (white arrows). As seen in the CT image (A), most of the fluid collects along the ventral midline where it effaces the cardiac, mediastinal, and diaphragmatic margins. The dorsal lung vessels (yellow arrows) are well‐visualized because they are surrounded by well‐inflated lung. Figure 3.39 Pleural effusion, lateral view. A. Cross‐sectional CT image of a dog thorax depicting the patient in lateral recumbency. Pleural fluid flows with gravity to collect along the dependent thoracic wall and in an interlobar fissure (white arrows); S = spine, C = cardiac silhouette. The dependent (down) lung is partially collapsed and increased in opacity. The smaller down lung allows the cardiac shadow to “fall” toward the down side and slide dorsally along the curved chest wall (black arrows). B. Lateral view of the same dog thorax. Pleural fluid outlines the lung margins (white arrows) and is visible in a dorsal interlobar fissure (black arrow). The ventral lung border appears wavy (yellow arrows). Figure 3.40 Severe pleural effusion with pleural fibrosis. Lateral view (A) and VD view (B) of a dog thorax depicting a large volume of pleural fluid surrounding lungs that are unable to expand against the fluid (black arrows). Fluid separates the individual lung lobes and outlines their rounded and slightly irregular margins. The appearance of the lungs is concerning for pleural fibrosis. The diaphragm is caudally displaced and flattened by the large effusion. Figure 3.41 Normal cat lung. A. Illustration of a normal cat lung specimen. B. Lateral radiograph of a cat thorax. The arrows point to the normal curvature of the dorsocaudal lungs due to the hypaxial muscles. In the radiograph, the soft tissue opacity muscle may be mistaken for pleural fluid in the costophrenic recess (arrow). Figure 3.42 Obesity. Lateral view (A) and VD view (B) of a dog thorax depicting an overweight patient with a large amount of subcutaneous fat and excessive fat deposits in the mediastinum (black arrows indicate the widened cranial and caudal parts of the mediastinum). The lungs do not extend all the way to the ribs (white arrows). Pericardial fat makes the cardiac margins less distinct. Fat extending into the interlobar fissure between the right cranial and middle lung lobes creates a reverse fissure line (yellow arrow). Figure 3.43 Pneumothorax. Two cross‐sectional CT images of a dog thorax depicting the patient in dorsal recumbency (A) and in ventral recumbency (B); S = spine, C = cardiac shadow. Gas always rises. In dorsal recumbency (A), gas rises to collect along the narrow ventral midline (white arrows) where it may be obscured in a VD radiograph by the spine, sternum, and mediastinum. In ventral recumbency (B), gas rises to the wider dorsal thorax where it can spread between lung and chest wall, making detection easier in a DV view than in a VD view. Figure 3.44 Pneumothorax. Lateral view (A) and VD view (B) of a dog thorax depicting free gas in the pleural space. Pleural gas outlines the lungs, the interlobar fissures, and is visible between the lungs and chest wall (black arrows). The yellow arrow points to gas between the cranial and caudal subsegments of the left cranial lung lobe. In the lateral view, the cardiac shadow is dorsally separated from the sternum with gas in‐between (white arrows). Lungs are increased in opacity because they are less inflated. Figure 3.45 Separation of the cardiac shadow from the sternum. Four cross‐sectional CT images of a dog thoraces with the patient in lateral recumbency. The dashed yellow lines represent the distance between the cardiac shadow (C) and the sternum (*); S = spine. A. Normally inflated lungs support the cardiac shadow in its central position. B. Collapse of the dependent lung allows the heart to fall toward the dependent chest wall and slide dorsally along its curved border (arrows). C. Deep‐chested conformation: the lungs are normally inflated, but the tall narrow thorax leads to greater distance between the cardiac shadow and sternum. D. Lung collapse due to pneumothorax (white solid arrow). The heart falls with gravity and slides dorsal to the sternum (white dashed arrows). Figure 3.46 Skin folds. VD view of a dog thorax depicting skin folds superimposed on the thoracic cavity (white arrowheads). These may be mistaken for the edges of the lungs, but close inspection reveals the folds can be followed beyond the limits of the thoracic cavity. Also, tiny pulmonary vessels are visible between the skin folds and the ribs (yellow arrows). Figure 3.47 Tension pneumothorax. Lateral view (A) and VD view (B) of a dog thorax depicting an expanded thoracic cavity with severe collapse of all lung lobes (white arrows). The lung edges are widely separated from the chest wall by a large volume of pleural gas. The cardiac shadow is dorsally displaced from the sternum with gas in‐between (yellow arrow). The diaphragm is caudally displaced, revealing its costal attachments (black arrows). Figure 3.48 Tension viscerothorax. Lateral view (A) and VD view (B) of a dog thorax depicting a large, gas‐distended mass in the left hemithorax (black arrows). The rounded margins are thin and well‐defined resembling. The mediastinum is shifted to the right. The normally visible gas bubble in the gastric fundus is not identified. Possible etiologies for the intra‐thoracic mass include an incarcerated stomach and a large pulmonary cyst or bulla. Figure 3.49 Mediastinal structures. Lateral view (A) and VD view (B) of a dog thorax depicting the normally visible mediastinal structures: trachea (T), cardiac silhouette (C), descending aorta (Ao) and caudal vena cava (CVC). Summation of the cranial mediastinal structures produces soft tissue opacity ventral and lateral to the trachea (white arrows). The ventral mediastinum creates a thin, curved, soft tissue opacity line between the left and right cranial lung lobes (red arrow) and between the accessory and left caudal lung lobes (yellow arrow). In the VD view, the cranioventral mediastinum begins at the T1‐2 thoracic vertebra and curves caudally toward the left cranial edge of the cardiac shadow. It follows the medial border of the right cranial lung lobe. The right cranial lobe wraps around the heart and extends across midline to the left. The caudoventral mediastinum begins at the left caudal edge of the cardiac shadow and curves toward the left diaphragm. It follows the accessory lung lobe, which extends to the left, across the midline. The caudal mediastinum is not identified in a lateral view. In the VD view, only the left border of the aorta usually is visible (black arrows). In a lateral view, fluid in the caudal esophagus (E) sometimes produces a soft tissue opacity band between the aorta and caudal vena cava, particularly in a left lateral view. Figure 3.50 Thymus. Lateral view (A) and VD view (B) of a 5‐month‐old dog thorax depicting the appearance of the thymus in the cranioventral mediastinum (yellow arrows). In the lateral view, the thymus is less distinct, appearing as an ill‐defined soft tissue opacity structure. In the VD view, the thymus appears as a triangular‐shaped soft tissue opacity structure, sometimes described as resembling the sail on a sailboat. Figure 3.51 Mediastinal lymph nodes. Lateral view of a dog thorax depicting the locations of the mediastinal lymph nodes. The sternal node (S) is dorsal to the second and third sternebrae. The cranial mediastinal nodes (CrM) are ventral to the trachea, near the large cranial mediastinal blood vessels. The tracheobronchial nodes (TB) are in the hilar region, ventral to the esophagus and near the tracheal bifurcation. Figure 3.52 Mediastinal shift. VD view of a dog thorax depicting collapse of the right lung. The cardiac shadow is displaced to the right, and the right side of the diaphragm is displaced cranially (black arrows). The right lung is more opaque than the left lung because it contains less air. The left lung is hyperinflated to compensate for right lung collapse. Notice that the patient is not rotated: the spine and sternum are superimposed, the dorsal spinous processes are centered on the vertebral bodies, and the right and left ribs are equal length. Figure 3.53 Cranial mediastinal mass. Lateral view (A) and VD view (B) of a dog thorax depicting localized widening of the cranial mediastinum (white arrows). The trachea is displaced dorsally and to the right (black dashed arrows). The margins of the soft tissue opacity mediastinal mass are more distinct in the VD view due to the opacity interface provided by air‐filled lung. The cranial cardiac border is partially effaced by the mass. Figure 3.54 Thymoma. Lateral view (A) and VD view (B) of a dog thorax depicting a large, well‐defined, soft tissue opacity mass in the cranial mediastinum (white arrows). The mediastinum is markedly widened, preventing the cranial lung lobes from reaching the thoracic inlet. The mass displaces the trachea dorsally and to the right and displaces the cardiac silhouette (C) caudally and dorsally (black dashed arrows). The cranial cardiac border is partially effaced by the mass. Figure 3.55 Mediastinal lymphadenomegaly. Lateral view (A) and VD view (B) of a dog thorax depicting enlargement of the sternal (S), cranial mediastinal (Cr), and tracheobronchial (TB) lymph nodes (yellow arrows). TB lymphadenomegaly displaces the caudal trachea ventrally and widens the tracheal bifurcation (black dashed arrows). In the VD view, superimposition of the spine and sternum obscures both the sternal and cranial mediastinal lymph nodes. Figure 3.56 Branchial cyst. Lateral view (A) and VD view (B) of a cat thorax depicting a well‐defined, soft tissue opacity mass located immediately cranial to the cardiac shadow (white arrows). In the VD view, only the left border of the mass is visible due to superimposition of the spine and sternum. Notice that the thoracic limbs are pulled caudally in the VD view to eliminate superimposition of the shoulders on the cranial thorax. Figure 3.57 Dorsal mediastinal mass. Lateral view (A) and VD view (B) of a dog thorax depicting increased opacity dorsal to the trachea and widening of the cranial mediastinum (white arrows). The trachea is displaced ventrally and to the right (black dashed arrows). Notice that you cannot determine from the VD view alone whether the mass is located dorsal or ventral to the trachea. Figure 3.58 Heart base mass. Lateral view (A) and VD view (B) of a dog thorax depicting soft tissue opacity at the base of the cardiac silhouette and focal dorsal and right lateral displacement of the distal trachea (black arrow). Figure 3.59 Caudal mediastinal mass. Lateral view (A) and VD view (B) of a dog thorax depicting a soft tissue opacity mass centered between the cardiac silhouette and the diaphragm (white arrows). The mass partially effaces the caudal cardiac and cranial diaphragm borders. The mass may be located in the caudal mediastinum or accessory lung lobe. Figure 3.60 Mediastinal mineralization. Lateral view of a dog thorax depicting (1) a mineral opacity foreign object in the esophagus, (2) mineralization of the aortic valve, (3) mineralization in the wall of the descending aorta, and (4) mineralization in the hilar lymph nodes. Figure 3.61 Pneumomediastinum. Lateral view of a dog thorax depicting a small volume of free gas in the cranial mediastinum. Gas outlines the outer margin of the trachea (black arrows) and creates a mottled pattern in the tissues ventral to the trachea (yellow arrow). Figure 3.62 Pneumomediastinum. Lateral view of a dog thorax depicting free gas in the mediastinum. Gas outlines structures that are not normally seen, such as the cranial mediastinal blood vessels (CrV), the esophagus (E), and the azygous vein (Az). Gas enhances visualization of the cardiac, aortic (Ao), and longus coli (LC) borders and the outer tracheal margin (white arrows). Figure 3.63 Tracheal rupture. Lateral view of a cat thorax depicting marked subcutaneous emphysema (white arrowheads) as well as free gas in the mediastinum, pleural space, and retroperitoneal space. Mediastinal gas sharply outlines the margins of the cardiac silhouette, aorta (Ao), cranial vena cava (CrV), azygous vein (Az), and esophagus (E). Migration of mediastinal gas leads to cervical emphysema, and pneumo‐retroperitoneum, the latter outlines the borders of the abdominal aorta (Ao) and dorsal kidneys (K) (white arrow). Gas diffusing through the mediastinal pleura causes a pneumothorax (black arrow). In this case, the origin of the free gas is a ruptured trachea. The ends of the torn trachea overlap to create a thin line of increased opacity and a slight discontinuity in the tracheal wall (yellow arrow). Figure 3.64 Normal canine esophagram. Lateral view (A) and VD view (B) of a dog thorax depicting a positive contrast esophagram. The longitudinal mucosal folds in the esophagus produce linear filling defects along its entire length. The linear defects are parallel and nearly equal in width. In the lateral view, the normal redundancy in the esophagus is visible near the thoracic inlet (white arrow). Contrast medium is visible in the stomach. Figure 3.65 Normal feline esophagram. Lateral view (A) of a cat thorax depicting a positive contrast esophagram. The mucosal folds in the proximal esophagus are longitudinal and create parallel, linear filling defects, similar to those seen in a dog esophagram. Caudal to the level of the tracheal bifurcation, the mucosal folds are oblique and produce transverse filling defects (arrow). B. In this anatomical image of a feline esophagus, you can see the mucosal folds transition from longitudinal to oblique (arrow). The contrast radiographic appearance of the oblique folds has been described as a “herringbone pattern” because it resembles the skeleton of a herring fish (C). Figure 3.66 Tracheal stripe sign. Lateral view of a dog thorax depicting gas in the esophagus dorsal to the trachea. Gas outlines the ventral mucosal margin of the esophagus (white arrows). The ventral wall of the esophagus blends with the dorsal wall of the trachea to create a soft tissue opacity stripe that may be mistaken for a thickened dorsal tracheal wall (black arrows). Figure 3.67 Esophageal foreign objects. Lateral view of a dog thorax depicting sites where ingested foreign objects frequently lodge in the esophagus. (1) thoracic inlet: an irregular‐shaped mineral opacity object is visible here. (2) base of the cardiac silhouette: the soft tissue opacity material that is lodged here causes local dilation of the esophagus and ventral displacement of the trachea. (3) cranial to the diaphragm: the cranial part of this soft tissue opacity object is partially outlined by gas in the distal esophagus. Figure 3.68 Spirocercosis. Lateral view (A) and VD view (B) of a dog thorax depicting lesions associated with spirocercosis. The pathognomonic finding with spirocercosis is a periosteal response along the caudal thoracic vertebrae. This new bone production is visible in the lateral view along the ventral bodies of T8‐10 (black arrows in the ovoid close‐up). Compare T8‐10 to the normal vertebrae on either side (T7 and T11). In both the lateral and VD views, a soft tissue opacity mass is visible on midline, located between the aorta and caudal vena cava (yellow arrows). This mass is an esophageal granuloma, but a lung mass would have a similar appearance. The two small bulges in the proximal descending aorta (white arrows) are aneurysms caused by the migrating parasites. Figure 3.69 Esophageal stricture. Lateral view (A) and VD view (B) of a cat thorax depicting an esophagram. There is a localized area of persistent narrowing in the caudal esophagus (white arrows). The mucosal margins are irregular, which may be due to severe inflammation or neoplasia. Figure 3.70 Gas‐distended esophagus. Lateral view of a dog thorax depicting a largely dilated, gas‐filled esophagus. The esophageal walls are thin and widely separated (yellow arrowheads), but converge caudally toward the diaphragm. Figure 3.71 Megaesophagus. Lateral view (A) and VD view (B) of a dog thorax depicting gas‐distention of the entire esophagus (arrows). The ventral margin of the longus coli muscles is sharp and distinct against the air‐filled esophagus (white arrow). The tracheal stripe sign is visible (yellow arrow). The trachea and cardiac base are displaced ventrally. The cardiac shadow appears shortened due to ventral displacement. In the VD view, the slight indentation along the right lateral border in the middle of the esophagus is a normal finding at the heart base. Figure 3.72 Esophageal stricture and inflammation. Two lateral views of a dog thorax depicting a barium esophagram. (A) Radiograph made immediately after administering barium reveals filling defects dorsal to the cardiac base (white arrow) and a narrowed area in the distal esophagus (black arrow). (B) Radiograph made a few minutes later reveals adherence of barium to damaged esophageal mucosa (white arrow) and persistent narrowing in the distal esophagus (black arrow). Possible etiologies for these lesions include inflammation and neoplasia. Retention of a small amount of barium at the thoracic inlet occurs frequently in normal dogs and its significance in this case is uncertain. Figure 3.73 Esophageal lesions. Lateral view of a dog thorax depicting a positive contrast esophagram. (1) A narrowed area in the esophagus which may be transient (due to peristalsis) or persistent (due to a stricture); a follow up radiograph is needed for diagnosis. (2) Esophageal ulcer; a small pocket of barium extends away from the mucosal margin. (3) Filling defects along the dorsal esophageal wall; defects are consistent with mural nodules (e.g., granulomas, tumors). (4) Irregular‐shaped filling defects in the distal esophagus caused by a mural tumor extending into the esophageal lumen. Figure 3.74 Esophageal diverticulum Lateral view (A) and VD view (B) of a dog thorax depicting a positive contrast esophagram. There is a localized, contrast‐filled bulge in the distal esophagus, just cranial to the diaphragm (white arrow). Figure 3.75 Gastroesophageal intussusception. Lateral view (A) and VD view (B) of a dog thorax depicting part of the stomach extending into the distal esophagus (white arrows). The displaced stomach appears as a mixed opacity mass in the caudodorsal thorax. The mass is continuous with the intra‐abdominal part of the stomach (black arrow). The esophagus cranial to the intussusception is dilated with gas. Gas outlines the cranial border of the displaced stomach. Figure 3.76 Vascular ring anomaly. Lateral view (A) and VD view (B) of a dog thorax depicting widening of the craniodorsal mediastinum (white arrows). The widening is soft tissue opacity and obscures the ventral margin of the longus coli muscles. The trachea is displaced ventrally and to the left (black dashed arrows). These findings are consistent with a dorsal mediastinal mass, probably involving the esophagus. (C) Barium esophagram: the proximal esophagus is dilated with barium and tapers abruptly at the base of the cardiac shadow (yellow arrow). A small amount of barium is visible in the distal esophagus. (D) This illustration depicts the anatomy of the persistent right aortic arch: the ligamentum arteriosus (LA), located between the aorta (Ao) and main pulmonary artery (MPA), constricts the esophagus (E) at the base of the heart. The proximal esophagus is distended with gas and the distal esophagus is normal size. Figure 3.77 Vascular ring anomaly. Lateral view of a dog thorax depicting marked dilation of the proximal esophagus (white arrows) due to constriction near the cardiac base. The dilated esophagus is filled with ingesta that obscures the trachea. Figure 3.78 The cardiac shadow. Lateral view (A) and VD view (B) of a dog thorax depicting the cardiac base, apex, long axis (black double headed arrows) and short axis (yellow double headed arrows). In the lateral view, the height of the thoracic cavity is measured from the dorsal border of the last sternebra to the ventral border of the perpendicular vertebra (blue double headed arrow). In the VD view, the width of the thoracic cavity is measured at the widest part of the rib cage (blue arrow). Figure 3.79 Normal canine cardiac silhouette. Lateral view (A) and VD view (B) of a dog thorax depicting a typical canine cardiac silhouette that is normal in position, size, and shape. Notice in the lateral view the normal slight ventral curvature in the distal trachea. Compare these normal radiographs with the various appearances of the cardiac silhouette depicted in other figures in this chapter. Figure 3.80 Deep‐chested conformation. (A) Lateral view of a dog thorax depicting the appearance of the cardiac silhouette within a deep, narrow thoracic cavity. Compared to Figure 3.79, the cardiac shadow is more slender and upright with less cardiosternal contact and a smaller cardiothoracic ratio. (B) Lateral view of another deep chested dog depicting fat opacity between the cardiac shadow and the sternum (arrow). Separation of the cardiac shadow from the sternum may be a normal finding in a patient with a narrow, deep chest and should not be mistaken for a pneumothorax. (C) In a VD view of a deep‐chested dog the cardiac shadow appears relatively long and narrow because in dorsal recumbency it is more parallel with the sternum. (D) In a DV view of a deep chested dog the cardiac shadow appears relatively small and rounded because in ventral recumbeny it is more perpendicular to the sternum. Figure 3.81 Barrel‐chest thoracic conformation. Lateral view (A) and VD view (B) of a dog thorax depicting the appearance of the cardiac silhouette in a wide, shallow thoracic cavity. Compared to Figure 3.79, the cardiac shadow is relatively wider and more rounded with more cardiosternal contact and a larger cardiothoracic ratio. The trachea is closer to the spine, which is expected with this type of body conformation, but may be mistaken for cardiac enlargement. Figure 3.82 Feline cardiac silhouette. Lateral view (A) and VD view (B) of a cat thorax depicting a cardiac shadow that is normal in position, size, and shape. Compared to dogs, the feline cardiac silhouette is relatively thinner and more tapered at either end. The distal trachea is straight without the distal ventral curvature that is present in some dogs. Figure 3.83 Aged feline cardiac silhouette. Lateral view (A) and VD view (B) of a cat thorax depicting common age‐related changes in the cardiovascular structures. Compared to Figure 3.82, the cardiac shadow is more inclined toward the sternum (black dotted arrow), the aortic arch is more vertical (yellow arrow), and the descending aorta is more tortuous (white arrows). In the VD view, the proximal aorta often is visible left of midline (arrow) and may be mistaken for a mass in the cranial mediastinum or lung. Figure 3.84 Vertebral heart score (VHS). Lateral view of a dog thorax depicting the VHS method to assess the size of the cardiac silhouette. The cardiac length is measured from the ventral border of the distal trachea to the cardiac apex (white double headed arrow). The cardiac width is the widest part of the cardiac shadow, measured perpendicular to the cardiac length at the level of the caudal vena cava (yellow double headed arrow). Both measurements are transposed onto the thoracic spine, each beginning at the cranial edge of the T4 thoracic vertebra. Count the number of vertebrae spanned by each measurement to the nearest 1/10th vertebra. Add the two numbers together to get the VHS. In this example, the cardiac length is 5.4 vertebrae and the cardiac width is 4.3 vertebrae which gives a VHS of 9.7 (5.4 + 4.3 = 9.7). Figure 3.85 Microcardia. Lateral view (A) and VD view (B) of a dog thorax depicting a small cardiac silhouette. The cardiac shadow is narrowed and dorsal to the sternum. The aorta, caudal vena cava, and pulmonary vessels also are small. The lungs are less opaque due to diminished pulmonary blood flow. Figure 3.86 Cardiomegaly. Lateral view (A) and VD view (B) of a dog thorax with a normal cardiac silhouette. The white dashed lines depict the typical appearance of cardiomegaly: the cardiac borders expand, becoming more rounded and moving closer to the thoracic walls. Cardiosternal contact increases and the trachea is dorsally displaced. In the VD view, the cardiac apex and caudal mediastinum are displaced to the left of midline (yellow arrow). Figure 3.87 Pericardial effusion. Lateral view (A) and VD view (B) of a dog thorax depicting a very large, rounded cardiac silhouette. The cardiac borders are smooth and even and very well‐defined (yellow arrows). The trachea is dorsally displaced (black dashed arrow) but retains its distal ventral curvature. The aorta (Ao) and pulmonary vessels (white arrow superimposed on the cardiac silhouette) are small due to low cardiac output. The caudal vena cava is dilated due to reduced venous return (blue double headed arrow). Figure 3.88 Normal anatomy of the heart. Lateral views (A, B) and VD views (C, D) of a dog thorax with illustrations that depict the locations and arrangements of structures in the right and left sides of the heart: AA = ascending aorta Ao = descending aorta AV = azygous vein BT = brachycephalic trunk CaVC = caudal vena cava CrVC = cranial vena cava LA = left atrium LAu = left auricle LPA = left pulmonary artery LS = left subclavian artery LV = left ventricle MPA = main pulmonary artery PV = pulmonary veins RA = right atrium RAu = right auricle RPA = right pulmonary artery RV = right ventricle Figure 3.89 Cardiovascular circulation. This illustration summarizes normal cardiovascular blood flow. Blood from the body returns to the heart via the cranial and caudal vena cavae and enters the right atrium (RA). It then passes through the tricuspid valve into the right ventricle (RV). The RV pumps blood past the pulmonary valve into the pulmonary arteries (PA) and to the lungs. Oxygenated blood from the lungs returns to the heart via the pulmonary veins (PV) and enters the left atrium (LA). It then passes through the mitral valve into the left ventricle (LV). The LV pumps blood past the aortic valve into the aorta and to the body. The cranial arteries from the aorta include the brachiocephalic, common carotid, and subclavian. Figure 3.90 Heart chambers. Lateral view (A) and VD view (B) of a dog thorax depicting the locations of the cardiac chambers based on the cardiac axes. The long axis (white line) divides the heart into right and left sides, normally about a 3:2 ratio. The short axis (yellow line) separates the atria above from the ventricles below. In the VD view, the left atrium (LA) is located in the middle of the cardiac silhouette (arrow and dashed circle). RA = right atrium, RV = right ventricle, LV = left ventricle, Ao = aorta, CVC = caudal vena cava. Figure 3.91 Clock face analogy. Lateral view (A) and VD view (BVD view: ) of a dog thorax depicting the locations of the cardiac chambers based on a superimposed analog clock face. The clock numbers are used to approximate the borders of individual cardiovascular structures. The curved lines depict the borders of structures when enlarged. Lateral view: VD view: Figure 3.92 Mild left atrial dilation. Lateral view (A) and VD view (B) of a dog thorax depicting expansion of the dorsocaudal cardiac border (white arrow) and dorsal displacement of the distal trachea. In the VD view, the caudal atrial border is visible (black arrows). Figure 3.93 Largely dilated left atrium. Lateral view (A) and VD view (B) of a dog thorax depicting severe left atrial dilation. In the lateral view, the dorsocaudal cardiac border is expanded (white arrows), widening the cardiac base and straightening the caudal cardiac border to make it more vertical. Overall, the cardiac shadow is more triangular in shape, tapering toward the apex. The trachea is dorsally displaced and there is splitting of the primary bronchi with the left bronchus (L) dorsal to the right (R). In the VD view, the tracheal bifurcation is widened and more rounded, resembling an inverted “U” shape rather than an inverted “V” shape (black arrows). The left bronchus is narrowed because it is compressed by the left atrium. The caudal border of the left atrium is pushed toward the caudal cardiac border (white arrows), creating the appearance of a “double cardiac border”. The bulge along the left cardiac border (yellow arrows) is the left atrial appendage, which is visible because it is either dilated or laterally displaced. Figure 3.94 Left ventricular enlargement. Lateral view (A) and VD view (B) of a dog thorax depicting expansion of the caudal and left lateral cardiac borders (black arrows) due to left ventricular enlargement. The cardiac apex is further left of midline (white arrow). Figure 3.95 Right atrial dilation. Lateral view (A) and VD view (B) of a dog thorax depicting an outward bulge along the right cranial cardiac border (black arrow). In the lateral view, the right atrium, proximal aorta, and main pulmonary artery all contribute to the cranial cardiac border. Dilation of any of these can expand that part of the cardiac shadow. In the VD view, however, the specific dilated structure often can be identified. Figure 3.96 Right ventricular enlargement. Lateral view (A) and VD view (B) of a dog thorax depicting expansion of the ventral and right lateral cardiac borders (black arrows) due to right ventricular enlargement. The cardiac apex is displaced dorsally and to the left (white dotted arrows). Right ventricular enlargement may distort the cardiac silhouette to resemble a reverse capital letter “D”, as illustrated in the lateral view (C) and the VD view (D). Figure 3.97 Dilation of the aortic arch. Lateral view (A) and VD view (B) of dog thorax depicting an outward bulge in the cranial cardiac border (black arrows) due to dilation of the aortic arch. In the lateral view, it is difficult to differentiate aortic arch dilation from dilation of either the right atrium or the main pulmonary artery. Figure 3.98 Main pulmonary artery enlargment. Lateral view (A) and VD view (B) of a dog thorax depicting a focal bulge in the left cranial cardiac border (black arrow) due to dilation of the main pulmonary artery. In the lateral view, main pulmonary artery dilation is less evident and difficult to differentiate from dilation of either the right atrium or the proximal aorta. Figure 3.99 Major vessels. Lateral view (A) and VD view (B) of a dog thorax depicting the major blood vessels commonly seen in thoracic radiographs. Visible are the descending aorta (Ao), caudal vena cava (CVC), and, in the lateral view, the right and left primary pulmonary arteries. In the lateral view, The left pulmonary artery (LPA) often appears as a soft tissue opacity “bulge” dorsal to the tracheal bifurcation. The right pulmonary artery (RPA) often is seen end‐on and appears a soft tissue opacity “nodule” ventral to the tracheal bifurcation. The caudal esophagus (E) sometimes is visible in a lateral view as a soft tissue opacity band between the aorta and caudal vena cava. In the VD view, the white arrows point to the left aortic border; the right border is not visible. Figure 3.100 Cardiovascular stenosis. Illustration A depicts normal laminar blood flow. Laminar means the blood is moving downstream in “layers”. The layers of blood move together in an even, linear motion that is parallel to the long axis of the blood vessel. Blood in the center of the vessel is moving at a higher velocity than blood at the periphery. Illustration B depicts a stenosis. The narrowed area disrupts the laminar flow of blood, causing turbulence past the stenosis. Turbulence exerts outward pressure on the vascular walls that leads to post‐stenotic dilatation. Further downstream, past the stenosis and turbulence, blood flow eventually returns to normal laminar flow. Figure 3.101 Pulmonic stenosis. Lateral view (A) and VD view (B) of a dog thorax depicting a focal dilation in the main pulmonary artery (white arrow) and right ventricular enlargement (black arrows). The caudal vena cava is enlarged, and the pulmonary blood vessels are small. Figure 3.102 Aortic stenosis. Lateral view (A) and VD view (B) of a dog thorax depicting focal dilation in the aortic arch with widening of the cranial mediastinum (white arrow). The left ventricle is enlarged (black arrows) and the cardiac apex is shifted to the left of midline. Figure 3.103 Patent ductus arteriosus (PDA). This illustration depicts oxygenated blood (red) from the aorta flowing through a PDA shunt into non‐oxygenated blood (blue) in the main pulmonary artery (MPA). Arterial blood from the higher pressure aorta mixing with venous blood in the lower pressure MPA disrupts normal laminar flow in both, leading to turbulence and focal dilation in each vessel (downstream from the shunt). As blood moves past the turbulence, it eventually returns to normal laminar laminar flow. Figure 3.104 Patent ductus arteriosus (PDA). Lateral view (A) and VD view (B) of a dog thorax depicting the classic radiographic signs of a PDA. The cardiac silhouette is enlarged and abnormal in shape due to left atrial dilation (LA), left ventricular enlargement (LV), right ventricular enlargement (RV) and the three “ductus bumps”: (1) focal dilation in the proximal descending aorta; (2) focal dilation in the main pulmonary artery; and (3) bulge created by the left atrial appendage. The aortic bulge (1) typically is seen at about the level of the fourth rib. It may be easier to find by tracing the left border of the aorta from the diaphragm cranially. The main pulmonary artery bulge (2) usually is just caudal to the aortic bulge. Both (1) and (2) are located at the site of the PDA. The left atrial appendage bulge (3) is in the middle of the left cardiac border and only visible in the VD view. The pulmonary vessels are enlarged due to overcirculation (white arrows). Figure 3.105 Atrial septal defect. Lateral view (A) and VD view (B) of a dog thorax depicting enlargement of the right atrium and right ventricle (black arrows). The pulmonary vessels are large due to over‐circulation (white arrows). Figure 3.106 Ventricular septal defect. Lateral view (A) and VD view (B) of a dog thorax depicting biventricular enlargement (black arrows) and enlarged pulmonary vessels (white arrows), the latter due to over‐circulation. Figure 3.107 Canine dilated cardiomyopathy. Lateral view (A) and VD view (B) of a dog thorax depicting generalized enlargement of the cardiac silhouette. The cardiac borders are expanded, making them more rounded and moving them closer to the thoracic walls and in greater contact with the sternum. The left atrium is largely dilated (arrow) causing dorsal displacement of the trachea. The pulmonary vessels are small due to lower left heart output and the caudal vena cava (CVC) is large due to lower right heart function. Figure 3.108 Feline dilated cardiomyopathy. Lateral view (A) and VD view (B) of a cat thorax depicting a longer, wider, and more rounded cardiac silhouette. In cats with dilated cardiomyopathy, the cardiac shadow tends to sit more upright with little sternal contact. The trachea is dorsally displaced and the caudal vena cava is large. Figure 3.109 Hypertrophic cardiomyopathy. Lateral view (A) and VD view (B) of a cat thorax depicting an enlarged, triangular‐shape cardiac silhouette. The cardiac base is widened due to left atrial dilation (white arrow) and a large or displaced right atrium (yellow arrow). There is increased cardiosternal contact. The vertebral heart width (VHW) is illustrated on these radiographs (Table 3.2). The maximum width of the cardiac shadow (black double headed arrow in the VD view) is transposed to the thoracic spine in the lateral view. Beginning at the cranial edge of T4, count the number of vertebrae spanned by the cardiac width to the nearest 1/10th of a vertebra. In this example, the VHW is 4.8 (normal range is 2.9–4.1). Figure 3.110 Mitral valve insufficiency. Lateral view (A) and VD view (B) of a dog thorax depicting an enlarged cardiac shadow, increased in both length and width due to left heart enlargement. The cardiac axes are illustrated in the lateral view to depict the measurements used to obtain a vertebral heart score (Figure 3.84). Notice that the long axis (white dashed line) extends from the cardiac apex to the ventral border of the left primary bronchus (L), which in this case is the dorsal cardiac border. Left atrial dilation (black arrows) displaces the trachea dorsally, splits the mainstem bronchi, and widens the tracheal bifurcation. In the lateral view, the left primary bronchus (L) is pushed dorsal to the right (R). The left bronchus is narrowed in both the lateral and VD views due to compression by the dilated left atrium. In the VD view, there is a focal bulge along the left cardiac border caused by dilation or displacement of the left atrial appendage (white arrow). In both views, the pulmonary veins (V) are larger than their paired arteries (A) due to venous congestion and early left heart failure. Figure 3.111 Tricuspid valve insufficiency. Lateral view (A) and VD view (B) of a dog thorax depicting a widened cardiac shadow due to enlargement of the right atrium and right ventricle (black arrows). The ventral, right cranial, and right lateral cardiac borders are expanded, and there is increased cardiosternal contact. The pulmonary vessels are small due to under‐circulated lungs. Figure 3.112 Heartworm disease. Lateral view (A) and VD view (B) of a dog thorax depicting right ventricular enlargement (black arrow) and focal dilation in the main pulmonary artery (white arrow). The pulmonary arteries (A) are larger than the corresponding veins (V). The arteries taper abruptly and appear blunted (yellow arrows). The caudal vena cava (CVC) is large due to increased central venous pressure. Figure 3.113 Left heart failure. Lateral view (A) and VD view (B) of a dog thorax depicting a large cardiac silhouette due to left atrial dilation and left ventricular enlargement (black arrows). The trachea is dorsally displaced by the dilated left atrium. The pulmonary veins (V) are larger than their paired arteries (A) due to venous congestion. Lung opacity is bilaterally increased in the hilar and central regions (*) due to cardiogenic pulmonary edema. Figure 3.114 Right heart failure. Lateral view (A) and VD view (B) of a dog thorax depicting pleural effusion. Fluid in the pleural space separates the lungs from the chest wall (white arrows) and causes a diffuse increase in thoracic opacity. The cardiac silhouette is widened due to enlargement of the right atrium and right ventricle (black arrows). The pulmonary vessels are small due to reduced right ventricular output. The caudal vena cava (CVC) is large due to increased central venous pressure. At the periphery of the radiographs, the abdomen is distended, and the serosal margins are indistinct due to peritoneal effusion (*). Figure 3.115 Trachea positioning artifact. A. Lateral view of a dog thorax with the head and neck flexed. Flexion shortens the distance between the larynx and the hilus, causing a temporary bend in the trachea (arrow). B. Lateral view of the same dog with the head and neck extended. There is no bend in the trachea (arrow). C. In this picture, a section of flexible garden hose is stretched between two hands. The middle portion is straight (arrow). D. In this picture, the same hands are holding the same garden hose, but the hands are moved closer together. Shortening the distance between the ends of the hose causes a bend in the middle (arrow). Figure 3.116 Tracheal ratio. Lateral view of a dog thorax depicting the tracheal ratio method for assessing tracheal size. This method compares the internal diameter of the trachea (D) to the width of the thoracic inlet (W). D is measured from mucosa to mucosa. W Thoracic inlet width is measure from the craniodorsal edge of the manubrium (M) to the cranioventral edge of the T1 thoracic vertebra. The Tracheal Ratio (TR) is calculated by dividing D by W (TR = D/W). TR = D/W. Normal TR for most dogs is > 0.20. For brachycephalic dogs it should be > 0.16 and for Bulldogs it should be > 0.12. Figure 3.117 Artifactual narrowing of the trachea. Lateral views of a cat thorax depicting the patient in a relaxed position (A) and hyperextended due to overstretching (B). Notice that overstretching the cat causes significant dorsoventral narrowing of the thoracic cavity (yellow double‐headed arrow) and narrowing of the trachea (white arrows). Figure 3.118 False narrowing of the trachea. Cross‐sectional CT images of a dog neck depicting the appearance of the trachea in the middle cervical region (A) and further caudally, near the thoracic inlet (B). The trachea (yellow arrow) naturally rotates in the caudal cervical region (dashed arrow). (C) Lateral view of a dog trachea. The dorsal tracheal membrane is visible in the lumen of the caudal cervical trachea (white arrow) because the trachea is rotated here. The dorsal tracheal membrane is not seen in the mid‐cervical tracheal lumen (black arrow) because here the trachea is aligned with the x‐ray beam. The soft tissue opacity created by the dorsal membrane in the caudal cervical region may be mistaken for the dorsal border of the trachea, leading to a false diagnosis of a narrowed tracheal lumen. Close inspection, however, reveals the true dorsal tracheal border (red arrow). Notice that this artifactual narrowing of the trachea is not caused by superimposition of an adjacent structure, such as the esophagus, longus coli muscles, or mediastinum. Figure 3.119 Tracheal stenosis. Lateral view of a cat thorax depicting a localized narrowing in the trachea (arrows) due to a stricture. Figure 3.120 Tracheal hypoplasia. Lateral view of a dog thorax depicting uniform narrowing of the tracheal lumen (arrows) due to congenital malformation of the tracheal rings. Figure 3.121 Tracheal collapse syndrome. Two lateral views depicting the same dog thorax. A. During inspiration, the tracheal lumen is normal size. B. During expiration, increased intra‐thoracic pressure collapses the distal trachea and primary bronchi (black arrows). Figure 3.122 Cervical tracheal collapse syndrome. Two lateral views depicting the same dog thorax. A. During inspiration, the redundant dorsal tracheal membrane in the caudal cervical region is sucked inward, narrowing the tracheal lumen (arrow). B. During expiration, the dorsal membrane balloons outward, widening the tracheal lumen (arrow). Figure 3.123 Skyline views of the trachea. A. This illustration depicts the patient positioning for a “skyline” radiograph of the trachea. B. Skyline view depicting a normal trachea (arrow). C. Skyline view depicting tracheal collapse with the characteristic crescent‐shaped lumen (arrow). D. Skyline view depicting a hypoplastic trachea with a small, round lumen (arrow). Figure 3.124 Thickened tracheal wall. Lateral view of a dog thorax depicting diffuse thickening of the tracheal wall (arrows) and uniform narrowing of the tracheal lumen. The serosal (outer) borders of the trachea are indistinct, making it difficult to identify the edges of the tracheal wall. The primary radiographic finding is a narrowed tracheal lumen. Figure 3.125 Tracheal mass. Lateral view of a dog thorax depicting mural lesions along the trachea. There is an irregular shaped, soft tissue opacity structure near the thoracic inlet (black arrow), which may represent a tumor, polyp, or foreign object. Further distally along the dorsal tracheal wall, there are three soft tissue nodules (white arrows), which are typical in appearance and location for granulomas caused by parasites. Notice that the margins of structures that project into the tracheal lumen are well‐defined because they are surrounded by gas. Figure 3.126 Tracheal foreign objects. Lateral view of a dog thorax. Soft tissue opacity objects are depicted in the tracheal lumen, one located near the thoracic inlet (black arrow) and another lodged distally at the tracheal bifurcation (white arrows). Figure 3.127 Lung lobe borders. Lateral view (A), VD view (B), and DV view (C) of a dog thorax illustrating the edges of the individual lung lobes. The lung lobe edges that are ventral to the trachea are illustrated in the VD view (B) and the lung lobe edges that are dorsal to the trachea are shown in the DV view (C). Acc = accessory lobe. Cr = cranial lung lobes. Ca = caudal lung lobes. M = middle lung lobes. RCa = right caudal lobe. RCr = right cranial lobe. RM = right middle lobe. LCa = left caudal lobe. LCr = left cranial lobe. LCr‐cr = left cranial lobe, cranial segment, LCr‐ca = left cranial lobe, caudal segment. Figure 3.128 Lung regions. Lateral view (A) and VD view (B) of a dog thorax illustrating the lung regions used to describe radiographic findings. H = hilar; the innermost lung field. C = central; the middle lungs where the larger blood vessels and bronchi are visible. P = peripheral; the outermost lungs that are mostly gas opacity, where tiny vessels and bronchi may be visible. Figure 3.129 Normal pulmonary vasculature. Lateral view (A) and DV view (B) of a dog thorax illustrating the pulmonary arteries (A, highlighted in blue for deoxygenated blood) and the pulmonary veins (V, highlighted in red for oxygenated blood). In the lateral view, the arteries are cranial and dorsal to their paired veins. In the DV view, the arteries are caudal and lateral to the veins. MPA = main pulmonary artery, LPA = left pulmonary artery, RPA = right pulmonary artery, LA = left atrium. Figure 3.130 Cranial lobar pulmonary vessels. Left lateral view of a dog thorax depicting the normal sizes and positions of the paired cranial lobar pulmonary vessels. The left cranial artery and vein (white A,V) are dorsal to the right cranial artery and vein (black A,V). The width of each vessel should not exceed the width of the narrowest part of the fourth rib (4), measured at the third or fourth intercostal space. Figure 3.131 Caudal pulmonary vessels. VD view of a dog thorax depicting the appearance of the right caudal pulmonary artery (A) and vein (V). The width of each vessel should not exceed the width of the ninth rib (9), where vessel and rib overlap (dotted circle). Figure 3.132 Artery‐bronchus‐vein. Lateral view of a dog thorax depicting the right cranial lobar bronchus (B) between the paired right cranial pulmonary artery (A) and vein (V). Notice the bronchus does not occupy the entire space between the vessels. Figure 3.133 Artery‐bronchus‐vein. VD view of a dog thorax depicting the right caudal lobar bronchus (B) between the paired right caudal pulmonary artery (A) and vein (V). The bronchus does not occupy the entire space between the vessels. Figure 3.134 Normal bronchi. Lateral view (A) and DV view (B) of a dog thorax illustrating the bronchial tree. The trachea bifurcates into the right and left primary bronchi at the carina (white arrow). The primary bronchi diverge from the trachea at a sharp angle, about 60°–90°. The left atrium (LA) is located immediately ventral and slightly caudal to the carina. The right primary bronchus branches to supply the right cranial lung lobe (RCr), the right middle lobe (RM), the right caudal lobe (RCa), and the accessory lobe (Acc). The accessory bronchus actually stems from the right caudal bronchus. The left primary bronchus branches to supply the left cranial lobe and the left caudal lobe (LCa). The branch to the left cranial lobe immediately divides to supply the cranial and caudal subsegments of the left cranial lobe (LCr‐cr and LCr‐ca respectively). Figure 3.135 Rings and tramlines. A. This illustration depicts an isolated bronchus that is aligned with the x‐ray beam. The bronchus is viewed end‐on and would appear as a “ring” in the radiograph. B. Another isolated bronchus, but this one is perpendicular to the x‐ray beam. The bronchus is viewed from the side or in profile and would appear as a “tramline” in the radiograph. Figure 3.136 Bronchial and vascular markings. A. Lateral view of a normal dog thorax depicting the area to be viewed close up (white dashed square). B. Close‐up view of A with some of the bronchial walls highlighted to produce more visible rings (white arrow) and tramlines (black arrow). C. Close‐up view of A with the caudal pulmonary blood vessels highlighted (yellow arrows); the vessels may be mistaken for bronchial walls. Figure 3.137 Abnormal size of pulmonary vessels. Close‐up lateral views of a dog thorax. The cranial lobar artery and vein are highlighted. A. Normal paired cranial vessels for comparison: artery (black arrow) and vein (white arrow) are similar in size and course. B. Dilation of both the artery and the vein due to over‐circulation in the lungs. C. Small artery and vein due to hypovolemia. D. The artery is larger than the vein due to heartworm disease; the artery tapers abruptly at the site of a thromboembolic obstruction. E. The vein is larger than the artery due to venous congestion caused by left heart failure. F. The vascular margins are less distinct due to fluid in the adjacent lung (e.g., inflammation, edema). Figure 3.138 Right lateral vs. Left lateral. These illustrations depict a dog in right lateral and left lateral recumbency and the associated radiographs. There is a soft tissue opacity mass in the dorsal part of the dog’s right caudal lung lobe (white arrows). A. In right lateral recumbency, the right lung is down and partially collapsed. The mass is poorly visualized due to a weak gas‐to‐soft tissue opacity interface. B. Right lateral radiograph: the margins of the mass are not well visualized because there is little alveolar gas adjacent to it. C. In left lateral recumbency, the right lung is up and well‐inflated. The mass is well‐visualized due to a strong gas‐to‐soft tissue opacity interface. D. Left lateral radiograph: the margins of the mass are well visualized because they are surrounded by gas. Figure 3.139 VD vs. DV. These illustrations depict the same dog as in Figure 3.138, but now in dorsal and ventral recumbency. The associated radiographs are below each illustration. Again, there is a soft tissue opacity mass in the dog’s right caudodorsal lung (white arrows). A. In dorsal recumbency, the dorsal part of the lung is down and partially collapsed. The mass is poorly visualized due to the weak gas‐to‐soft tissue opacity interface. B. VD radiograph: the margins of the mass are not well visualized because there is little to no alveolar gas in the adjacent lung. C. In ventral recumbency, the dorsal lung is up and well‐inflated. The mass is well‐visualized due to a strong opacity interface. D. DV radiograph: the margins of the mass are well visualized because they are adjacent to air‐filled lung. Figure 3.140 Partial lung lobe collapse due to gravity. Cross‐sectional CT image of a dog thorax depicting the appearance of the right and left caudal lung lobes with the patient in left lateral recumbency. The mediastinum (M) is highlighted in yellow. The down parts of both caudal lung lobes are more opaque (black arrows) than the up parts because the down parts are less ventilated and more perfused due to gravity. A lesion in the up part of the left lobe (*) may be better visualized in this left lateral view than in a right lateral because that part of the left lung lobe is better inflated. The degree of collapse in different parts of the lungs varies among individual patients and lung conditions. Four view radiographs of the thorax can be very useful. Figure 3.141 Multiple pulmonary nodules. Lateral view of a dog thorax depicting multiple, variable‐sized, pulmonary nodules distributed throughout the lungs. The margins of the soft tissue opacity nodules are even and well‐defined. Nodules sometimes are more visible when summated with the cardiac silhouette or diaphragm (white arrows). Figure 3.142 Numerous lung nodules. Lateral view of a dog thorax depicting many soft tissue opacity nodules scattered throughout the lungs (sometimes described as a “snowstorm” pattern). Nodules are superimposed on the diaphragm because lung wraps around the diaphragm. Numerous pulmonary nodules may represent metastatic tumors or mycotic granulomas. Figure 3.143 End‐on vessel. These illustrations depict a vessel (V) and a nearby nodule of similar size (N). A. When the vessel is perpendicular to the x‐ray beam, it appears as a curvilinear soft tissue opacity structure in the radiograph. The nodule appears as a round soft tissue opacity structure, similar in diameter to the vessel. B. When the vessel is aligned (parallel) with the x‐ray beam, it is seen end‐on and appears as a rounded structure that is nealy mineral opacity due to summation; the x‐rays traveled through a larger or longer amount of soft tissue/fluid. The nodule remains the same shape and opacity in both radiographs because it is spherical and the same thickness in all directions. Figure 3.144 Pseudo‐nodules. Close up VD‐oblique view of a dog thorax depicting various “nodules.” The right cranial lobar artery (A) and vein (V) are seen end‐on with the bronchus in between. The vessels produce nearly mineral opacity pseudo‐nodules and the end‐on bronchus appears as a thin, well‐defined ring. In the left hemithorax, there is a lung nodule (N), a superimposed skin tumor (T), and an end‐on blood vessel (B). The margin of the skin tumor is sharper than the lung nodule because it is extra‐thoracic. The end‐on vessel is near mineral opacity and continuous with a longitudinal vessel of the same width (white arrows). Figure 3.145 Investigating pseudo‐nodules. Two close‐up lateral views of the same dog thorax. The first radiograph (A) depicts a soft tissue opacity nodule at the cranioventral cardiac border (black arrow). In this case, the nodule was suspected to be caused by superimposition of a cutaneous growth. The radiograph was repeated (B) after dabbing a small amount of barium on the skin growth. The barium confirms the pseudo‐nodule. The white arrow points to mineralized costal cartilage, which also may mimic a pulmonary lesion. Figure 3.146 Pulmonary osteomas. Lateral view of a dog thorax depicting multiple, well‐defined, mineral opacity structures scattered in the lungs (black arrow). The nodules are slightly irregular in shape, less than 3 mm in size, and predominate in the ventral lungs, consistent with pulmonary osteomas. Mineralized granulomas may be similar in appearance. Figure 3.147 Cavitary lung mass. Lateral view of a dog thorax depicting a soft tissue mass with multiple, irregular‐shaped, gas‐filled cavities in the dorsocaudal lung (white arrows). The thick‐walled, cavitary lesion may represent a tumor or long‐standing abscess. Figure 3.148 Lung bulla. Lateral view of a dog thorax depicting a sharply‐defined, thin‐walled, gas opacity structure in the dorsocaudal lung (white arrows). The appearance is characteristic of a pulmonary bulla or cyst. Figure 3.149 Pneumatocele. Lateral view of a dog thorax depicting cavitary lesions with thin to mildly thickened walls (white arrows). The adjacent lung is more opaque due to hemorrhage. Patient history and follow‐up radiographs confirm the diagnosis of traumatic lung bullae. Figure 3.150 Normal bronchial markings. Lateral view of a dog thorax depicting normal lung. The walls of the larger bronchi in the hilar and central lung regions are visible (white arrows). When seen end‐on, the bronchi appear as well‐defined rings (black arrow). Figure 3.151 Increased bronchial markings. Lateral view of a dog thorax depicting an increase in bronchial markings. Compared to Figure 3.150, there are more visible rings (black arrow) and tramlines (white arrows) due to thickening of the bronchial walls. Figure 3.152 Lung inflammation. Lateral view of a dog thorax depicting increased bronchial markings and increased lung opacity (sometimes called a “bronchointerstitial lung pattern”). Compared to Figure 3.151, the bronchial markings are less distinct because there is more fluid in the lungs, the latter due to inflammation. Figure 3.153 Bronchiectasis. Lateral views of a dog thorax. A. Normal cranial lobar artery, bronchus, and vein (ABV). The vessels and bronchus taper together into the lung periphery (white arrow). Notice again that the bronchus does not fill the entire space between the vessels. B. Bronchiectasis: the bronchus is largely dilated with irregular‐shaped walls that do not taper normally (arrows). Figure 3.154 Severe bronchiectasis. Lateral view of a dog thorax depicting numerous greatly dilated bronchi (arrows). Figure 3.155 Progression of lung parenchyma disease. A. Lateral view of a dog thorax depicting the appearance of normal lungs. The right cranial lung lobe is outlined. B. During the initial stages of parenchymal lung disease (in this case, pneumonia), there is a diffuse increase in lobar opacity due to an influx of fluid and cells. The cardiovascular margins are less distinct, but they remain visible and readily identified. C. Continued alveolar filling leads to more effacement of the cardiac and vascular margins. Notice that the lung lobe is more opaque ventrally than dorsally due to the effects of gravity. There are faint air bronchograms. D. Complete filling of the alveoli results in a more uniform lobar opacification and more visible air bronchograms. The vascular and cranial cardiac margins are completely effaced. Note: during the regression or healing of parenchymal lung disease (resolving of the pneumonia), this sequence of radiographic findings will occur in reverse order as cells and fluid leave the alveolar spaces and interstitium. Figure 3.156 Lung parenchyma disease. These illustrations depict the microscopic appearance of lung parenchyma disease. The images are rendered in shades of gray to simulate a radiographic image. A. Normal lung tissue: depicted are a pulmonary blood vessel, a bronchus, the alveolar air spaces and the interstitial tissue that surrounds the alveoli and forms the alveolar walls. B. Thickened lung interstitium: the alveolar spaces are smaller than normal due to an infiltration of cells in the alveolar walls and other interstitial tissues. The cellular infiltration increases the amount of soft tissue in the lungs and limits alveolar expansion, both of which increase lung opacity. C. Peribronchial infiltrates: abnormal cells and fluid fill the alveoli adjacent to the bronchial wall, which may appear in radiographs as thickening of the bronchus. The outer margin of the bronchial wall is obscured by the adjacent alveolar filling, giving the impression of a very thick bronchial wall. D. Lung hemorrhage: blood cells leaking from the damaged vessel flow into the interstitium and fill the alveoli, both of which increase lung opacity. Blood, or any other fluid that fills the lungs, will obscure the adjacent soft tissue margins. E. Pulmonary edema: fluid accumulates in the interstitium and alveolar spaces, increasing lung opacity and blurring the soft tissue margins of the vessel and bronchial wall. Figure 3.157 Effacement. A. Lateral view of a dog thorax depicting normal lungs and well‐defined margins associated with the cardiac silhouette, caudal vena cava, and diaphragm. B. Lateral view of the same dog as in (A) but depicting alveolar filling in the caudal lung lobes (arrow points to lobar sign). Loss of alveolar gas eliminates the gas‐to‐soft tissue opacity interface, effacing the caudal cardiac, cranial diaphragmatic, and vena caval margins. C. Lateral view of the same dog as in (A) but depicting a soft tissue mass in the caudal lung lobe. The mass does not efface the nearby soft tissue margins because there is some air‐filled lung in between. The borders of the mass and the caudal vena cava (arrow) remain visible because there is a gas‐to‐soft tissue opacity interface. Figure 3.158 Alveolar filling. This illustration depicts an individual lung lobe with its artery (A), bronchus (B), and vein (V). Fluid is filling the alveolar spaces, to a small degree proximally and progressing toward the tip of the lobe where it effaces the margins of the pulmonary vessels and bronchial wall. Gas remaining in the bronchial lumen contrasts sharply with the soft tissue opacity lung parenchyma, forming an air bronchogram. Alveolar filling can extend throughout an entire lung lobe, but spread to other lobes is prevented by the pleura. The sharp pleural edge of the consolidated lung lobe adjacent to air‐filled lung produces a lobar sign (arrow). Figure 3.159 Alveolar filling. Lateral view (A) and VD view (B) of a dog thorax depicting alveolar filling. In the right cranial lung lobe there is homogeneous soft tissue opacity that effaces the right craniolateral cardiac border. The caudal edge of the right cranial lobe is sharply defined against the air‐filled right middle lobe, (white arrow points to the lobar sign). Air bronchograms (black arrow) and air alveolograms (black arrowheads) are visible. In the dorsal lung fields, there is patchy alveolar filling appearing as ill‐defined, soft tissue opacity areas in both the right and left caudal lung lobes (yellow arrows). Figure 3.160 Acinar nodules. Lateral view of a dog thorax depicting a mottled pattern of ill‐defined soft tissue opacity “nodules” in the caudal lungs (black arrow). The mottled lung opacification is caused by acute alveolar flooding. The appearance of the lungs is likely to change in follow‐up radiographs, either becoming more uniform due to continued alveolar filling or decreasing in opacity as fluid leaves the alveolar spaces. Actual pulmonary nodules would persist unchanged in serial radiographs. Figure 3.161 Parenchymal lung disease. Two lateral views of a dog thorax. A. Normal lungs for comparison. B. A diffuse increase in lung opacity. The soft tissue margins are partially effaced. The margins are blurry and less distinct than in (A), but the cardiovascular structures, diaphragm, and other soft tissues are easily recognized. This degree of lung opacification has been called “dirty lungs,” “ground glass opacity,” and “interstitial lung pattern”. It is caused by parenchymal lung disease. Figure 3.162 Lung interstitial disease. Lateral views of a dog thorax depicting normal and diseased lung. (A) Normal lung for comparison. (B) Parenchymal lung disease resulting in a diffuse mild increase in lung opacity with less distinct vascular and bronchial markings. (C) Reticular lung markings caused by thickening of the interstitial connective tissues; the markings resemble a lacey or honeycomb pattern. (D) Summation of interstitial markings creates a reticulonodular appearance in the lungs; however, the numerous tiny “nodules” are too small to be actual nodules and there are too many of them to be bronchi. Figure 3.163 Inspiration vs. Expiration. Lateral views of a dog thorax depicting the appearance of the lungs during inspiration (A) and expiration (B). Expiratory radiographs may be misinterpreted as lung disease because during expiration there is less air in the lungs, reducing the gas‐to‐soft tissue opacity interface and making the margins of soft tissue structures less distinct. In addition, bronchial and vascular markings are closer together which can make them appear more numerous than actual. Figure 3.164 Lung lobe collapse. Left lateral view (A), right lateral view (B), and VD view (C) of a dog thorax depicting collapse of the right cranial lung lobe. The collapsed lobe is increased in opacity and its caudal edge creates a lobar sign against the inflated right middle lobe (yellow arrow). The mediastinum, trachea, and cardiac shadow are shifted to the right, and the right side of the diaphragm is cranial to the left (black arrows). The right cranial lobar vessels and the cranial cardiac border are effaced due to loss of gas in the collapsed lobe. The left cranial vessels and cardiac border are well‐visualized due to compensatory hyperinflation of the left lung. The white arrow points to the tip of the left cranial lung lobe in each radiograph. Notice the collapsed right lung lobe is better visualized in the left lateral view (A) because it is “up” and adjacent to air‐filled lung. It is less evident in the right lateral view but still visible because the right cranial lung lobe extends across midline and wraps around the cranial border of the cardiac shadow. Figure 3.165 Cardiogenic pulmonary edema in a dog. Lateral view (A) and DV view (B) of a dog thorax depicting left heart failure. There is a bilateral and symmetrical increase in lung opacity in the hilar and central regions (*). The left atrium and left ventricle are enlarged (black arrows). The pulmonary veins (V) are larger than their paired arteries (A). Figure 3.166 Cardiogenic pulmonary edema in a cat. Lateral view (A) and VD view (B) of a cat thorax depicting increased left heart failure. There is a patchy and asymmetrical increase in lung opacity in the central and peripheral regions (white arrows). The cardiac shadow is enlarged, both in length and at the base (yellow arrows), resulting in a more triangular shape. Figure 3.167 Non‐cardiogenic pulmonary edema. Lateral view (A) and VD view (B) of a dog thorax depicting increased opacity in the dorsocaudal lungs. Lung opacification is bilateral and asymmetric, with greater opacity in the right caudal lung lobe. Cardiovascular structures are normal in size and shape. Air bronchograms are visible caudally (black arrows), which is concerning for more severe disease such as acute respiratory distress syndrome. Figure 3.168 Acute respiratory distress syndrome. Lateral view (A) and VD view (B) of a dog thorax with ARDS. Depicted in the radiographs is a diffuse increase in lung opacity caused by pulmonary edema. The distribution is bilateral and symmetrical, more severe in the central lung region. Cardiovascular structures are partially effaced by the alveolar filling, but appear normal in size and shape. In patients with ARDS, the pulmonary edema fails to respond to therapy. Figure 3.169 Chronic bronchitis. Lateral view (A) and VD view (B) of a dog thorax depicting hyperinflated lungs and an expanded thoracic cavity. In the VD view, the intercostal muscles bulge slightly outward (yellow arrow) due to repeated episodes of forced expiration. There are numerous bronchial rings (white arrow) and tramlines (black arrow). Many of the rings appear incomplete because not all of the bronchi are well‐aligned with the x‐ray beam. Figure 3.170 Feline asthma. Lateral view (A) and VD view (B) of a cat thorax depicting numerous bronchial markings within hyperinflated lungs. The thoracic cavity is expanded and the diaphragm is caudally displaced and flattened. The right middle lung lobe is collapsed, creating a triangular‐shaped, soft tissue opacity structure that blends with the cardiac silhouette (arrows). In the lateral view, the collapsed lobe is superimposed on the cardiac shadow. It is visible because of the lobar sign created by its caudal border. In the VD view, the collapsed lobe partially effaces the right cardiac border. Compensatory hyperinflation of the right cranial and caudal lung lobes prevents a mediastinal shift to the right. Figure 3.171 Eosinophilic pneumonia. Lateral view (A) and VD view (B) of a dog thorax depicting increased lung opacity that is diffuse and slightly patchy. There are multiple, small, indistinct nodules widely scattered in the lungs (arrows). Figure 3.172 Pulmonary emphysema. Lateral view (A) and VD view (B) of a dog thorax depicting hyperexpansion of the left lung. There is a mediastinal shift to the right. These findings are readily evident in the VD view, but in the lateral view, the only finding is well‐inflated lungs. Figure 3.173 Aspiration pneumonia. A. Lateral view of a dog thorax depicting aspiration of positive contrast medium. Contrast is visible in the right middle lobar bronchus and also along the ventral trachea. B. Lateral view of a dog thorax depicting soft tissue opacity in the right middle lung lobe with lobar sign (arrow) and an air bronchogram extending into the lobe from the tracheal bifurcation. Alveolar filling in this lobe is due to bacterial pneumonia secondary to aspiration. C. VD view of same dog thorax depicting alveolar filling in the right middle lung lobe. There is partial effacement of the right cardiac border and a caudal lobar sign (arrow). The air bronchogram is again visible. Figure 3.174 Bacterial pneumonia. Left lateral view (A), right lateral view (B), and VD view (C) of a dog thorax depicting multiple areas of increased lung opacity (white arrows). Parenchymal disease is bilateral and lobar in distribution but not symmetrical. The degree of alveolar filling in the right caudal and left cranial lung lobes completely effaces the adjacent soft tissue margins and produces lobar sign (black arrows) and air bronchograms (yellow arrows). Filling is more complete ventrally due to gravity. Alveolar filling in the left caudal lobe is less complete and appears as an ill‐defined, “fluffy” area of opacification that remains dorsal at this time. Notice that disease in the left lung is better visualized in the right lateral view and disease in the right lung is more evident in the left lateral view. Recall that the “up” lung is better inflated, which provides a stronger gas‐to‐soft tissue opacity interface. Notice also that the cranial cardiac border remains visible through the opacified left cranial lung lobe. This is because the inflated right cranial lung lobe wraps around the cardiac silhouette. In the left lateral view, the only evidence of pneumonia in the left cranial lobe is opacification in the cranial tip (LCr) and a lack of visualization of the left cranial lobar vessels; only the right cranial vessels are visible. Figure 3.175 Paragonimiasis. (A) Lateral view of a dog thorax depicting pulmonary lesions associated with paragonimus infection. There is a diffuse increase in lung opacity that partially effaces the soft tissue structures (soft tissue margins appear hazy but remain visible). The soft tissue opacity nodules (black arrows) are fluid‐filled cysts. The cavitary lesions (yellow arrows) are pneumatocysts. The white arrow points to a pneumatocyst that resembles a bulla. (B) Close‐up of the dorsocaudal lung field in (A). The arrows point to adult flukes in the pneumatocysts. A fluke that is outlined by gas has been described as resembling a signet ring (the inset photograph (C) is a signet ring). There are reticulonodular markings in the lung caused by thickening of the interstitial connective tissues. Figure 3.176 Mycotic pneumonia. Lateral view (A) and VD view (B) of a dog thorax depicting a diffuse increase in lung opacity with multiple small nodules (white arrows). The nodules are fungal granulomas. There is tracheobronchial lymphadenomegaly (black arrows) which increases the opacity in the hilar region. The trachea and primary bronchi are compressed (narrowed) and displaced ventrally by the enlarged lymph nodes. Figure 3.177 Blastomycosis. The initial radiographs of a dog with blastomycosis are on the left and the three‐year follow up radiographs are on the right. In the initial lateral view (A) and VD view (B), there is a diffuse increase in lung opacity with numerous bronchial markings and increased hilar opacity. In the follow‐up lateral view (C) and VD view (D) the lungs are less opaque, there are fewer bronchial markings, cardiovascular margins are more distinct, and hilar opacity is normal. Figure 3.178 Thoracic trauma. Lateral view (A) and VD view (B) of a dog thorax depicting diffuse, patchy, lung opacification that effaces the cardiovascular and diaphragmatic borders. Subcutaneous emphysema is visible along the dorsal and lateral thorax and is superimposed on the pulmonary and mediastinal structures. In the lateral view, a pneumomediastinum enhances visualization of the outer tracheal margin (white arrow). There are multiple rib fractures, easiest to see in the VD view (black arrows). Radiographic findings and patient history support a diagnosis of pulmonary hemorrhage. Figure 3.179 Pulmonary embolism. A. VD view of a dog thorax depicting the classic signs of pulmonary embolism. A left caudal pulmonary artery is enlarged and tapers abrubtly (white arrows), leading to a less opaque area in the left caudal lung lobe. There are few vascular markings here. B. Follow‐up VD view of the same dog. There is now a localized, ill‐defined area of increased lung opacity caused by pulmonary edema (yellow arrow). Figure 3.180 Lung lobe torsion. Lateral view (A) and VD view (B) of a dog thorax depicting a torsion of the right middle lung lobe. There is increased lobar opacity and lobar sign (white arrows). The right cardiac border is partially effaced. Foci of gas are visible in the right middle lobe (blue arrow) due to retained alveolar gas. In the lateral view, the right middle lobar bronchus is cranially displaced, narrowed and blunted (yellow arrow) due to twisting of the bronchus. Pleural fluid is present (black arrows) and there is a pleural fissure line between the cranial and caudal segments of the left cranial lung lobe. The thoracic wall is composed of bones, soft tissues, and fat. The bony thorax includes the ribs, vertebrae, and sternebrae. Soft‐tissue structures are skin, muscle, blood vessels, nerves, and pleura. The average number of ribs in both dogs and cats is 26 or (13 pair). The head of each rib articulates with the cranial aspect of the same numbered thoracic vertebra (Figure 3.6). For example, the third rib attaches to the cranial end of the third thoracic (T3) vertebra. The ribs in chondrodystrophic dogs (e.g., Bassett Hound, Dachshund) normally curve inward and indent the lungs at the costochondral junctions (Figure 3.12). Inward curving ribs may be mistaken for pleural fluid. The gaps between ribs are the intercostal spaces. Comparing the right and left sides, the intercostal spaces (ICS) are relatively symmetrical; however, the symmetry may temporarily be lost due to oblique positioning or muscular contractions. Each ICS is numbered according to its cranial rib (e.g., the third ICS is caudal to the third rib). The sternum contains 8–9 sternebrae, which are similar in appearance to the vertebrae. The first sternebra is the manubrium, which is the longest. The last sternebra is the xyphoid, which can vary significantly in size and shape. Located between the sternebrae are cartilaginous discs. These discs are similar in appearance and function to intervertebral discs. Two or more sternebrae may be fused or malaligned due to a congenital or developmental abnormality. Congenital abnormalities usually are asymptomatic and may be differentiated from pathology of the sternum by the lack of soft tissue swelling and absence of a periosteal response. Costal cartilages extend from the distal end of each rib to the sternum. Cartilages from the first 8 ribs join the intersternebral discs. Cartilages from the caudal ribs attach at the xyphoid or merge together. Mineralization of the costal cartilages normally begins at a few months of age. Mineralization has been described as heterogenous, mottled or granular and frequently becomes more sclerotic and irregular over time (Figure 3.7). Mineralized costal cartilages can become quite large, especially in chondrodystrophic and large breed dogs. Large mineralizations may be mistaken for lesions in the lungs or thoracic wall. Costal cartilage mineralization sometimes occurs in short segments, appearing as transverse lines of increased and decreased opacity. These lines may be mistaken for fractures. Carefully inspect the costal cartilages when interpreting radiographic findings to avoid an erroneous diagnosis. The normal thickness (width) of the thoracic wall varies with the patient body condition. The wall is thicker in obese and heavily muscled patients and thinner in lean animals. Abnormal thickening usually is extracostal (outside the ribs) and may be unilateral or bilateral, focal or diffuse. Focal thickening is due to a mass (see thoracic wall mass below), whereas diffuse thickening may result from subcutaneous accumulation of fat, gas, or fluid (Figure 3.8). Subcutaneous fat may represent obesity or a large lipoma. Obesity is bilateral and lipomas tend to be unilateral. The extracostal muscles may be outlined and displaced by fat, appearing as thin, curved, soft tissue opacity lines that resemble the shapes of the ribs. Subcutaneous emphysema may be unilateral or bilateral, typically producing a mixed pattern of gas and soft tissue opacities. Emphysema may result from a penetrating wound or migration of gas from a ruptured trachea or pneumomediastinum. Superimposition of subcutaneous gas may compromise evaluation of the thoracic cavity and may mask or mimic free gas in the mediastinum or pleural space. Subcutaneous fluid may be unilateral or bilateral and can obscure the margins of the extracostal muscles. Fluid may represent edema, inflammation, hemorrhage, or it may be iatrogenic (i.e., fluid therapy). Summation of subcutaneous fluid may increase the opacity of the thoracic cavity. Masses in the thoracic wall can involve any osseous or soft tissue structure. They produce localized, defined areas of thickening. The margins of a mass may be well‐defined or indistinct, depending on the opacity interface. Masses that are walled‐off and surrounded by a different opacity may be well‐visualized, provided they are large enough to be distinguished. Adjacent inflammation or other fluid accumulation can obscure the margins of soft tissue opacity masses. A mass in the thoracic wall may not be physically palpable or radiographically visible until quite large. Large masses can displace the adjacent ribs and widen the intercostal spaces. The ribs near a mass should be carefully examined for evidence of a periosteal response, osteolysis, and/or expansile remodeling. A thoracic wall mass that grows inward, toward the thoracic cavity, can produce a bulge that displaces the adjacent lung. The bulge creates an extra‐pleural sign. The extra‐pleural sign helps differentiate masses that originate outside the pleura from those that originate in the lung or pleural space (Figure 3.9). The edges of an extra‐pleural mass gradually taper toward the inner chest wall, forming angles greater than 90°. Pulmonary and pleural masses form acute angles (less than 90°) with the chest wall. Pleural effusion is absent with extra‐pleural masses (unless the pleura is damaged), but fluid is common with masses that originate in the pleural space. The opacity of a thoracic wall mass provides clues to its etiology. Gas opacity may result from a penetrating wound or infection with a gas‐producing bacteria. Herniation of a gas‐filled GI structure can produce a defined area of gas opacity. A fat opacity mass may represent a lipoma (Figure 3.10) or contents in a hernia. Lipomas can become very large, often with well‐defined margins. Indistinct margins suggest fluid adjacent to the lipoma (e.g., inflammation, edema) or a dissecting lipoma (or liposarcoma). Soft tissue opacity masses include tumors, abscesses, granulomas, seromas, and hematomas. Mineral opacity in a mass may be foreign material or dystrophic mineralization, the latter occurring in long‐standing abscesses, granulomas, or tumors. A paracostal hernia can create an extra‐pleural mass that is mixed in opacity due to the presence of displaced viscera, gas‐filled bowel, and fat (Figure 3.26). Congenital skeletal abnormalities are common in dogs and cats. Most are benign and asymptomatic. It is important to recognize benign conditions because they can alter the shape of the thorax, distort the positions of intra‐thoracic structures, and vary the locations of landmarks used during surgical and advanced imaging procedures. Benign conditions often can be differentiated from pathology by a lack of soft tissue swelling and an absence of active bone remodeling. Poor patient positioning also can alter the appearance of the bony thorax, such as making the curvature of the spine appear abnormal and distorting the sizes and shapes of the ribs. Congenital spinal abnormalities such as transitional vertebrae and hemivertebrae occur frequently in dogs and cats. Transitional vertebrae can affect the number of vertebrae and ribs (Figures 5.202 and 5.203). Hemivertebrae can alter the curvature of the spine, as well as cause narrowing of the intercostal spaces and crowding of the ribs (Figure 3.11). Spinal abnormalities are discussed further in Chapter 5: Musculoskeletal. The ribs are thin and sometimes indistinct in radiographs due to summation with other structures. To make the ribs more conspicuous, try altering your viewing perspective. Inverting the radiograph, either by turning the image upside down or by reversing the black‐and‐white scale of a digital image, tends to draw more attention to the ribs. Supplemental radiographs also can be helpful. Many rib lesions are easier to see when viewed tangentially (in profile rather than en face). Follow‐up radiographs often aid in confirming or refuting suspected rib lesions. Keep in mind that in a lateral view, the “up” ribs (furthest from the image receptor) will be larger and less distinct due to magnification distortion. Congenital rib abnormalities may alter the number or shape of the ribs. Abnormalities may be unilateral or bilateral. Extra ribs occur more often at the first cervical and first lumbar vertebrae. Fewer ribs are seen more often in the caudal thorax. Congenital alterations that affect the shapes of ribs include flaring at the ends, fusion of adjacent ribs, and bipartite development. In chondrodystrophic breeds, notably Bassett Hounds, the distal parts of the ribs normally curve inward at the costochondral junctions (Figure 3.12). Inward curving ribs also can occur in animals with pectus excavatum. An acquired absence of one or more ribs may be due to disease or surgical removal and can occur anywhere along the thorax. Diseases include nutritional, metabolic, neoplastic, and infectious disorders. Rib fractures typically result from blunt force trauma. Fractures tend to be transverse or oblique and often involve multiple ribs, usually sequentially (Figure 3.13). Other signs of trauma may be concurrent with rib fractures, such as subcutaneous emphysema, pneumothorax, and pulmonary contusions. Minimally displaced rib fractures may be difficult to detect unless the x‐ray beam is aligned with the fracture line. Oblique views sometimes are helpful. Follow‐up radiographs often reveal osseous remodeling at the fracture site(s). Healing that has progressed without complication produces a localized area of expansile remodeling with smooth, well‐defined margins and little or no soft tissue swelling (Figure 3.14). Respiratory motion during healing may lead to larger than expected callus formation. A lot of motion at a fracture site can result in a malunion or non‐union rib fracture. Spontaneous rib fractures have been reported in patients with prolonged dyspnea, severe coughing, or metabolic disease. In these cases, there is no history of trauma. Spontaneous fractures most often occur in the caudal ribs, particularly in older cats with underlying respiratory or renal disease. Pathologic rib fractures frequently are associated with neoplasia or severe osteomyelitis. Neoplasia is a more common cause than osteomyelitis, but the two cannot be differentiated in radiographs. Both can produce a productive or/and lytic bone response (Figure 3.15). Swelling in or near a rib without history or radiographic evidence of trauma should be investigated for neoplasia. Rib tumors in dogs and cats more often are secondary than primary. Metastatic rib tumors typically are small, slow‐growing, and arise in the middle (shaft) of a rib. Slow‐growing tumors tend to create expansile areas of osseous remodeling that may be difficult to distinguish from healing fractures. Any solitary rib lesion should be monitored with serial radiographs until proven benign. Primary rib tumors often arise further distally in a rib, near the costochondral junction. They can become quite large and may mineralize. Pleural effusion is absent unless a tumor erodes through the pleura. Primary rib tumors more often are reported in large‐breed dogs. Flail chest is a condition that results from segmental fractures in two or more adjacent ribs (Figure 3.16). The middle fragments become functionally free and move paradoxically with respiration. The fragments are pulled inward during inspiration and pushed outward during expiration (Figure 3.17). The conflicted movement of the chest wall leads to ineffective breathing and can quickly become an emergency, life‐threatening situation. In some patients, pain and muscle contractions may limit respiration and initially hide the paradoxical movements. Intercostal spaces (ICS) that are significantly wider or narrower than nearby ICS should be investigated. Abnormal widening may be due to traumatic swelling, a space‐occupying mass, or uneven hyperexpansion of the thorax. Trauma that widens ICS often is accompanied by other signs of injury (e.g., fractured ribs, subcutaneous emphysema). An intercostal mass generally widens one ICS and causes narrowing in the adjacent ICS. Hyperexpansion of the thorax may be due to emphysema or a tension pneumothorax and widens multiple ICS. Abnormal narrowing of ICS may be due to muscle contractions, poor lung inflation, or previous thoracotomy. Muscle contractions secondary to pain or struggling cause transient ICS narrowing, which changes in appearance in serial radiographs. As mentioned earlier, congenital fusion or malalignment of two or more sternebrae often are incidental findings that may be differentiated from pathology by a lack of soft tissue swelling and an absence of bone remodeling (Figure 3.18). Sternal dysraphism is a rare congenital abnormality that causes a “split sternum.” The split typically begins in the xyphoid and extends cranially to involve one or more additional sternebrae. The splitting itself is asymptomatic, but sternal dysraphism may be associated with peritoneal‐pericardial diaphragmatic hernia. Pectus excavatum is a congenital dorsal deviation of the sternum. It is also called funnel chest or sunken chest. The sternum curves inward, which results in dorsoventral narrowing of the thorax and a concave ventrum (Figure 3.19). Part or all of the sternum may be involved. The caudal sternebrae tend to be more severely affected, with the caudal ribs and costal cartilages usually curving inward, too. Moderate to severe pectus excavatum can reduce lung volume and displace the cardiac shadow dorsally and laterally. Cardiac displacement may be mistaken for a mediastinal shift. In a lateral view, the dorsally curving sternebrae may be superimposed on the cardiac silhouette. A temporary pectus excavatum can result from severe inspiratory efforts that draw a normal sternum inward. This is a rare occurrence that is more likely to happen in immature animals with less rigid sternums. Swimmers syndrome is a congenital abnormality that may appear similar to pectus excavatum. In affected puppies and kittens, the thorax is dorsoventrally flattened and the associated muscles are so weak that the animals are unable to stand. Their movements resemble a paddling or swimming motion. Pectus carinatum is a congenital ventral deviation of the sternum. It also is called pigeon chest or keel chest. Typically, the caudal sternum protrudes outward or caudoventrally, resulting in dorsoventral widening of the thorax and a more upright cardiac shadow (Figure 3.20). In a VD/DV view, the thorax may appear laterally narrowed. Rarely, pectus carinatum may result from severe cardiomegaly in an immature animal. Acquired sternal abnormalities may result from trauma, infection, or neoplasia. These conditions usually are accompanied by soft tissue swelling and frequently include bony abnormalities (Figure 3.21). Traumatic fractures and luxations more often are reported in younger animals, particularly cats and small‐breed dogs. Causes include blunt force injuries and bite wounds. A soft tissue mass on the sternum may represent an abscess, granuloma, hematoma, seroma, or tumor. Sternal masses that protrude inward, toward the thoracic cavity, may produce an extra‐pleural sign. The diaphragm physically separates the abdominal and thoracic cavities and provides nearly 50% of the force needed for respiration. It consists of a cupula and two crura (Figure 3.22). The cupula is the convex, dome‐shaped part of the diaphragm that bulges centrally and ventrally into the thoracic cavity. It is anchored to the sternum and ribs by fibrous tissue and connected to the spine by the crura. The crura are the two muscular “legs” of the diaphragm (singular crus). The word crus is used to describe an anatomical structure that resembles a leg. Crus is the name given to the distal part of a pelvic limb, the part between the stifle and the tarsus. Each diaphragmatic crus extends dorsally and caudally from the cupula to an attachment on the L3‐4 lumbar vertebrae. The ventral margins of L3 and L4 frequently are less distinct than the adjacent vertebral bodies, a normal finding that may be mistaken for a periosteal response. There are three natural openings in the diaphragm. Each opening, or hiatus, allows certain structures to normally pass through, but also serves as a potential site for a diaphragmatic hernia. Ventrally and to the right of midline is the caval hiatus, through which the caudal vena cava and lymphatic vessels pass. The lymphatics carry fluid in one direction, from the abdominal cavity to the sternal lymph node in the thoracic cavity. Centrally and left of midline is the esophageal hiatus, through which the esophagus and vagal nerves pass. Dorsally and near midline is the aortic hiatus, through which the aorta, azygos vein, and thoracic duct pass. The costophrenic recesses are the well‐defined, wedge‐shaped junctions between the diaphragmatic crura and the thoracic wall (Figure 3.22). The appearance of these recesses may be helpful to assess the degree of lung inflation and to detect pleural fluid. Fluid that collects in a costophrenic recess makes that recess appear more rounded, more opaque, and less distinct. The cranial or “thoracic” margin of the diaphragm tends to be sharply‐defined due to the opacity interface with lung air. The caudal or “peritoneal” margin often is only partially visible because it blends with the liver and stomach. Ventrally, the caudal margin of the diaphragm may be visible when adjacent to fat in the falciform ligament. The position of the diaphragm is determined by the degree of lung inflation and the forces exerted by the abdominal contents, both of which are affected by patient position and gravity. When the patient is recumbent, the dependent (down) lung partially collapses and the weight of the abdominal viscera push the down side of the diaphragm cranially. The greater the abdominal contents, the greater the push against the diaphragm. In left lateral recumbency (left lateral view), the left crus commonly is seen cranial to the right crus. In right lateral recumbency, the right crus often is cranial to the left (Figure 3.23). The left crus often can be identified by the nearby gas in the fundus of the stomach (the stomach is located just caudal to the left crus). Note: a full stomach can push the left crus cranial to the right, even with the patient in right lateral recumbency. The right crus can be identified by the caudal vena cava, which emerges from the right side of the diaphragm. Another difference between right and left lateral views is that the diaphragmatic crura tend to cross or overlap when in left lateral recumbency and they tend to be more parallel in right lateral recumbency (Figure 3.23). In dorsal recumbency (VD view), both crura are dependent (down) and both move cranially. The diaphragm typically appears as three humps in a VD view: right crus, cupula, and left crus. In ventral recumbency (DV view), the cupula is down and moves cranially. The diaphragm typically appears as a single hump in a DV view because the cupula obscures both crura (Figure 3.24). In some DV views, the cupula moves so far cranially that it contacts the heart. The dome of the diaphragm may appear indented by the cardiac silhouette and its margin may be indistinct. The effects of patient orientation and gravity on the position of the diaphragm tend to be more evident in large dogs than in cats and small dogs. A diaphragm may not appear as expected due to an error in radiographic technique. Errors that can distort the apparent position of the diaphragm inlcude rotation of the patient and off‐centering of the x‐ray beam. If the appearance of the diaphragm is not as you expect, first look for a normal cause of the discrepancy before diagnosing disease. When in doubt, repeat the radiographs paying special attention to proper imaging techniques. Pathologic displacement of part or all of the diaphragm may be due to an increase or decrease in lung volume, abnormal abdominal content, or a defect in the diaphragm. Non‐visualization of the diaphragm may be due to lack of an opacity interface or loss of diaphragmatic integrity. Any soft tissue opacity material between the diaphragm and air‐filled lung will obscure the margin of the diaphragm (e.g., pleural fluid, pulmonary disease, mass or fluid in the caudal mediastinum). Loss of diaphragm integrity may be due to a rupture or hernia (discussed on the next page). Cranial diaphragm displacement most often is due to partial or complete lung collapse. Displacement may be unilateral or bilateral. Unilateral cranial displacement often is accompanied by a mediastinal shift. A physiologic or pathologic increase in the size of the abdominal contents can displace the diaphragm cranially (e.g., full stomach, advanced pregnancy, organomegaly, large tumor, severe effusion). Defects in the diaphragm that allow cranial displacement include hernias, ruptures, and eventration. Eventration of the diaphragm produces a cranial bulge, usually involving only part or one side of the diaphragm (Figure 3.25). It most often is due to a congenitally thin and weak diaphragm, but may be caused by an injury to the phrenic nerve. Many patients with diaphragm eventration have no recent history or radiographic evidence of trauma and most are asymptomatic. In very severe cases, breathing can become compromised. The cranially protruding part of the diaphragm typically appears even, well‐defined, and relatively unchanged in serial radiographs. Differential diagnoses for an apparent eventration include diaphragmatic hernia, diaphragmatic mass, and a mass in the adjacent lung or caudal mediastinum. Caudal displacement of the diaphragm may be due to an expanded thoracic cavity or absence of abdominal content. Expansion may be caused by hyperinflated lungs (e.g., emphysema, inspiratory dyspnea), severe pleural effusion, severe pneumothorax, or a large intra‐thoracic mass. Absence of abdominal content may be due to emaciation or loss of body wall integrity (e.g., hernia, rupture). Severe caudal displacement of the diaphragm can reveal its costal attachments, particularly in a VD/DV view (Figure 3.26). The attachments appear as sharp projections extending cranially from the cupula, sometimes described as “tenting” of the diaphragm. Protrusion of viscera through a natural opening in the diaphragm is a hernia and protrusion through an acquired opening is a rupture. Because the two are difficult to differentiate in radiographs, we will use the term “hernia” for both. Typical radiographic findings of a diaphragmatic hernia include a mixed opacity mass in the thoracic cavity and an indistinct or absent diaphragm margin (Figure 3.27). The most commonly displaced structures are the stomach, small intestine, liver, and fat. It may be difficult to identify the displaced viscera unless structures are visibly absent from their normal locations or there is a distinctive shape or pattern associated with the herniated content. Intestines may be recognized as gas or fluid‐filled tubes that extend beyond the limits of the abdominal cavity. Visualization of rugal folds helps identify the stomach. Large protrusions into the thoracic cavity can displace and/or obscure the lungs and the cardiac silhouette. Pleural effusion is a frequent finding with diaphragmatic hernias. Fluid may be unilateral or bilateral and can obscure the displaced viscera and compromise diagnosis. Follow‐up radiographs made after thoracocentesis or may improve visualization of the displaced structures and diaphragm margins. Horizontal beam radiography also may be useful (Figure 2.15). The abdominal cavity may appear “empty” due to less viscera. Structures that remain in the abdomen often are cranially displaced or otherwise malpositioned. Radiographic diagnosis of a diaphragmatic hernia is difficult when the protrusion of viscera is transient or intermittent. Some structures may only be partially displaced. Rarely, a hernia may extend between the soft tissue layers of the thoracic wall instead of into the thoracic cavity. These paracostal hernias can present with an extra‐thoracic swelling that may be difficult to differentiate from other causes of a thoracic wall mass. The opacity of the hernia mass varies depending on the amount of fat, soft tissue organs, and gas‐filled GI structures it contains (Figure 3.28). A hiatal hernia occurs when abdominal contents protrude through a hiatus in the diaphragm. The esophageal hiatus most often is involved and the gastroesophageal junction most often protrudes. Other types of esophageal hiatal hernias include para‐esophageal, in which part of the stomach is displaced alongside the esophagus without involving the gastroesophageal junction, and gastroesophageal intussusception, in which part of the stomach enters the esophagus (see gastroesophageal intussusception). Protrusion through the aortic hiatus is called a para‐aortic hiatal hernia and protrusion through the vena caval hiatus is a para‐venous hiatal hernia. Fat or part of the stomach usually is involved in each of these hiatal hernias. Diagnosis of hiatal hernia frequently is difficult because, in many cases, the abdominal contents are only intermittently displaced, which is called a sliding or dynamic hiatal hernia. Positioning the patient with the head tilted down may aid in detection. The classic radiographic appearance of a hiatal hernia is an oval or semicircular mass near the left crus of the diaphragm (Figure 3.29). The mass generally is located near midline, between the caudal vena cava and the aorta. The size, shape, and opacity of the mass vary with the type and quantity of displaced viscera. Most hiatal hernias are soft tissue or fat opacity. The intra‐abdominal part of the stomach may be abnormal in shape and the expected gas bubble in the fundus may be absent. The stomach may appear continuous with the hiatal hernia mass if there is only partial gastric displacement. The caudal esophagus may or may not be dilated. A strangulated hernia that traps the stomach can lead to a tension viscerothorax (Figure 3.48). A peritoneal‐pericardial diaphragmatic hernia (PPDH) is a congenital condition in which there is an abnormal opening between the peritoneal cavity and the pericardial sac that. The opening allows abdominal viscera to move into the pericardial sac (Figure 3.30). Structures commonly displaced include falciform fat, liver, gall bladder, stomach, and small intestine. The characteristic radiographic finding is a large, rounded cardiac silhouette composed of various displaced opacities, such as fat, soft tissues, and gas‐filled GI structures. The border of the cardiac silhouette may be irregular or even, but usually it is sharply defined because there is less cardiac motion blur. The cardiac and diaphragm borders frequently merge together without the normal overlap or edge distinction. The dorsal border of a PPDH may be visible in a lateral view as a thin horizontal line between the cardiac silhouette and the diaphragm, located just ventral to the caudal vena cava. This line is seen more often in cats with PPDH than in dogs. PPDH differs from other diaphragm hernias in that the displaced viscera are confined to the cardiac silhouette. Pleural effusion is uncommon unless secondary right heart failure occurs. If needed, an upper GI study may be useful to identify the contents of the pericardial sac and help differentiate PPDH from pericardial effusion or cardiomegaly. PPDH is always congenital, never acquired. A sternal deformity such as pectus excavatum or sternal dysraphism may be concurrent with a PPDH. Many affected animals are asymptomatic. When clinical signs are present, they tend to be more GI related in dogs and respiratory related in cats. PPDH most often is reported in long‐haired cats and Weimaraner dogs. Masses on the caudal side of the diaphragm usually blend with abdominal structures such as the liver and stomach and therefore are not identified in radiographs. A mass on the cranial side, however, often is outlined against the lung making it visible as a rounded or semi‐circular mass. The mass can appear semi‐circular because its caudal part is obscurred by the abdominal contents. Possible causes of a diaphragm mass include neoplasia, abscess, granuloma, hernia, and eventration. The pleura are thin membranes that cover the lungs, line the thoracic cavity, and help form the mediastinum. The visceral or pulmonary pleura covers the lungs, blood vessels, and bronchi. It does not contain any sensory nerves and receives blood supply from the pulmonary circulation. The parietal pleura lines the walls of the thoracic cavity, the mediastinum, and the diaphragm. It contains many sensory nerves and receives blood supply from the systemic circulation. Between the pulmonary and parietal pleura is the pleural space. The pleural space is essentially a “potential” space because it normally contains only a capillary thin layer of fluid. The fluid serves to moisten the pleural surfaces and reduce friction. Except for this fluid, the pulmonary and parietal pleura are in virtual contact with each other. The pressure in the pleural space is less than atmospheric pressure, which helps the lungs expand with the chest during inspiration. Pleural fluid is produced continuously by the parietal pleura and resorbed by the visceral pleura. The turnover is about 75% every hour. Any condition that increases the volume of fluid entering the pleural space or prevents its absorption can increase the volume of pleural fluid. Excess fluid in the pleural space can interfere with lung expansion and convert the potential space into a true cavity. The same is true for gas that accumulates in the pleural space (i.e., pneumothorax). Each lung is divided into individual lobes by the pulmonary pleura. The divisions between the lobes are created by inward extensions of the pleura, called pleural fissures. Normal pleural fissures rarely are identified in radiographs because the pleura is so thin. The fissures become visible when filled with gas or fluid and when the pleura is thickened. The locations of the pleural fissures are known (Figures 3.31 and 3.32). When visible in radiographs, they appear as thin, curved, soft tissue opacity lines. Pleural fissure lines that are uniform in thickness with no tapering at either end, generally are caused by pleural thickening (lines that taper suggest pleural fluid as described on the next page). Pleural thickening may result from inflammation, edema, or fibrosis. Pleural fissure lines sometimes are seen in radiographs of older, clinically normal patients. In these patients, pleural thickening likely is a remnant of previous disease that is now inactive. Fissure lines in older animals often are considered to be incidental findings and have been referred to as an “aging change.” Occasionally a normal pleural fissure is visible in a radiograph (Figure 3.33). This occurs when the x‐ray beam is perfectly aligned with the fissure (Figure 3.34). Unlike pleural lines caused by disease, normal pleural lines rarely repeat in radiographs because it is unlikely that the x‐ray beam will be aligned with the lung fissure every time. Free fluid or gas in the pleural space is the most common cause of visible pleural fissures. Pleural fluid or gas outlines the lungs and separates the individual lung lobes (Figure 3.35). Separation of the lobes makes the interlobar fissures wider peripherally and narrower centrally. Pleural fluid produces wedge‐shaped fissure lines that are more opaque than air‐filled. Pleural gas produces wedge‐shaped fissure lines that are less opaque than lung (Figure 3.36). A “reverse pleural fissure line” may be created by fat in the central thorax that extends into a lung fissure. Fat fissure lines are wider centrally and taper peripherally (Figures 3.36 and 3.42). They occur most often between the right cranial and middle lung lobes in overweight dogs. Fluid in the pleural space is called pleural effusion. In general, the volume of fluid must exceed 10 ml/kg body weight to be detected in radiographs. This is about 50 ml in a cat or small dog and at least 100 ml in a medium‐size dog. As mentioned earlier, pleural effusion may result from excess fluid production, decreased absorption, or both. The type of fluid cannot be determined from radiographs. There are numerous causes of pleural effusion, many of which are associated with disease outside the pleural space (see Differential Diagnoses at the end this chapter). Fluid in the pleural space usually is freely movable and bilateral in distribution, the latter due to mediastinal fenestrations that are present in most dogs and cats. Unilateral or asymmetric effusion may result from a congenital absence of fenestrations, disease that plugs the existing fenestrations, or fluid so viscous that it cannot pass through the fenestrations. Diseases that can obstruct the fenestrations include severe or chronic inflammation, fibrosis and neoplasia. The earliest radiographic sign of pleural fluid is pleural fissure lines. Fissure lines created by small volumes of pleural fluid may be indistinguishable from pleural thickening. Small volume pleural effusions tend to be easier to see in a VD view than in a DV view. This is because in dorsal recumbency the pleural fluid is more likely to flow with gravity into the interlobar fissures and move laterally away from the mediastinal structures, where it often is easier to see (Figures 3.37 and 3.38). Horizontal beam radiography also may be useful to detect small volumes of pleural fluid (Figure 2.15). As the volume of pleural fluid increases, the lungs are less able to expand. The lung edges become further separated from the thoracic wall with fluid opacity in between. This finding sometimes is described as “retraction” of the lung lobes. Vascular and bronchial markings do not extend all the way to the ribs. Compared to fully inflated lungs, retracted lungs are more rounded and more opaque. Summation of pleural fluid further increases lung opacity. Pulmonary vessels remain visible in patients with pleural effusion, which is an important finding to help differentiate fluid outside the lungs from fluid inside the lungs (latter may result from pneumonia, pulmonary edema, or hemorrhage). Fluid in the lungs will obscure the vessels because both are soft tissue opacity and there will be no opacity interface. The central position of the heart within the thoracic cavity is maintained by fully inflated lungs. Less inflated lungs allow the heart to move to one side or the other. Pleural fluid limits lung inflation. When a patient with pleural effusion is placed in lateral recumbency, the heart “falls” toward the dependent side and slides dorsally along the curved thoracic wall (Figure 3.39). In a lateral radiograph, the cardiac shadow will be dorsally separated from the sternum. Pleural fluid between the heart and sternum often outlines the ventral lung border to create a wavy or “scalloped” appearance (Figure 3.39). Fluid in the costophrenic recesses makes them more rounded and less distinct. Fluid that collects adjacent to the mediastinum often makes it appear widened. A large volume of pleural fluid can lead to very small lungs and widely separated lung lobes. The individual lobes may resemble “leaves on a tree” (Figure 3.40). Large pleural effusions can displace the diaphragm caudally and make it appear flattened and stationary in serial radiographs. Large effusions also expand the thoracic cavity, making the ribs more perpendicular to the spine and the chest more rounded or “barrel‐shaped.” The overall opacity of the thoracic cavity may be increased to the degree that it resembles an underexposed radiograph; however, underexposure is not the cause if the vertebrae and other extra‐thoracic structures are properly exposed. Large volumes of pleural fluid may efface the cardiac and diaphragmatic borders and hide intra‐thoracic lesions. Follow‐up thoracic radiographs made after removing as much fluid as possible may yield additional diagnostic information. Chronic pleural effusions and inflammatory pleural fluid should be removed with caution because pleural fibrosis may be present. Pleural fibrosis reduces lung elasticity, which means the lungs could rupture if they re‐expand too quickly. A typical radiographic finding of pleural fibrosis is multiple rounded lung lobes with irregular margins (Figure 3.40). In patients with unilateral pleural effusion, lung not surrounded by fluid tends to be better inflated than the one that is surrounded by fluid. Unilateral effusions may not be evident in a lateral view alone because the edges of the inflated lung typically extend to the thoracic wall. The orthogonal VD/DV view often is needed to confirm the diagnosis. Variations in body conformation may be mistaken for pleural effusion. As described, the normal inward curvature of the ribs in chondrodystrophic breeds can give the false impression of pleural fluid in a VD/DV view (Figure 3.12). Also, the normal hypaxial muscles in cats may resemble rounding of the costophrenic recess in a lateral view (Figure 3.41). Thin, mineralized costal cartilages may be mistaken for pleural fissure lines (Figure 3.36). Cartilages, however, tend to be straighter or curve in the opposite direction than pleural fissure lines. Most costal cartilages can be traced to the end of a rib. Usually, there are multiple mineralized cartilages, most of which are not located in the area of a pleural fissure. In overweight patients, the thoracic walls are thick and the edges of the lungs may not extend all the way to the ribs (Figure 3.42). In addition, summation of overlying fat increases the overall thoracic opacity and excess mediastinal fat causes widening of the mediastinum. These findings in overweight patients may be mistaken for pleural effusion. Free gas in the pleural space is a pneumothorax. A pneumothorax may result from a penetrating thoracic wound, a ruptured airway, or a ruptured lung. Free gas in the pleura space increases the pleural pressure, which leads to lung collapse. The severity of lung collapse depends on the volume of gas and the pressure in the pleural space. As with pleural fluid, the earliest radiographic sign of pleural gas is pleural fissure lines. Gas fissure lines are more difficult to detect than fluid fissure lines because they produce less contrast with air‐filled lung. In most cases, lung collapse is the initial radiographic finding of pneumothorax. The lungs become separated from the chest wall and there is gas opacity in between. The vascular and bronchial markings do not extend to the ribs. The tiny vessels and bronchi in the peripheral lung may not be visible without brightening the radiograph (use a “hotlight” with film radiographs). Pneumothorax tends to be easier to see in lateral and DV views. A DV view may be more diagnostic than a VD view because in ventral recumbency pleural gas rises to the dorsal thorax. The dorsal thorax is wider than the ventral thorax so the gas will be more spread out and less likely to be obscured by the midline structures (Figures 3.43 and 3.44). Horizontal beam radiography may be useful to detect a smaller volume of pleural gas (Figure 2.15). As the volume of pleural gas increases, the degree of lung collapse increases. Smaller lungs contain less air and are more opaque than inflated lungs. Small lungs also cannot maintain the central position of the heart and other mediastinal structures, which means the mediastinum can shift laterally (see mediastinal shift in the next section of this chapter). In a lateral view, a mediastinal shift may appear as dorsal displacement of the cardiac silhouette. Dorsal separation of the cardiac shadow from the sternum sometimes is described as “elevation of the heart”. The term “elevation”, however, is a misnomer. Without the support of an inflated lung, the heart actually falls with gravity toward the dependent thoracic wall and slides dorsally along the normal curvature of the inner chest wall (Figure 3.45). Free gas in the pleural space increases the opacity interface with the diaphragm, making its cranial margin appear sharper and more distinct. A large volume of pleural gas can caudally displace the diaphragm, making it appear flattened and stationary in serial radiographs. Severe pneumothorax can reduce the overall opacity in the thoracic cavity to the degree that the thorax appears to be overexposed. However, overexposure is not the cause if the extra‐thoracic structures are properly exposed. Conditions that can mimic pneumothorax include emaciation, hyperinflated lungs, hypovolemia, and superimposed skin folds (see Differential Diagnoses). With emaciated patients, there is relatively little tissue overlying the thorax and the lungs tend to be well‐inflated, both of which can lead to a thoracic cavity that is less opaque than expected. Hyperinflated lungs also can lead to a less opaque thoracic cavity (e.g., emphysema, manual inflation). Similarly, hypovolemia that results in small cardiovascular structures can diminish overall lung opacity. Hypovolemia also can lead to separation of the cardiac shadow from the sternum. A skin fold superimposed on the thoracic cavity may be mistaken for the edge of a retracted lung (Figure 3.46). The skin fold usually can be traced beyond the limits of the thoracic cavity. Each of these conditions of mimicry is differentiated from pneumothorax by the absence of free gas between the lungs and chest wall. More common than missing a pneumothorax is an erroneous diagnosis of pneumothorax. This is especially dangerous when the clinician introduces gas into the thorax via chest tap after making an incorrect diagnosis, thus producing a pneumothorax when none existed. A favorite radiographic sign of pneumothorax is “elevation of the heart”. Rather than consider it an “elevation”, one should more accurately describe it as separation of the cardiac shadow from the sternum. The problem is that there are at least 3 causes for separation of the cardiac shadow from the sternum in addition to pneumothorax. (Figure 3.45). If it is a true pneumothorax, there will be other evidence for that diagnosis in addition to separation of the cardiac shadow. Small volumes of pleural gas usually are resorbed within 48 hours, provided that gas does not continue to enter the pleural space. A hydropneumothorax occurs when both fluid and gas are in the pleural space, The most common cause is severe thoracic trauma. Radiographic findings frequently include other signs of damage (e.g., fractured ribs, subcutaneous emphysema). The mixture of fluid and gas opacities in the pleural space can be challenging to interpret. Horizontal beam radiography may be helpful because fluid flows with gravity to the dependent side and gas rises to the “up” side. A tension pneumothorax is present when pleural pressure exceeds atmospheric pressure. Pleural pressure this high can prevent the lungs from expanding, both during inspiration and expiration, which can quickly become an emergency situation. A tension pneumothorax occurs when gas enters the pleural space during inspiration (usually from a ruptured lung) but cannot exit during expiration because the thoracic wall is intact. The lung rupture acts like a one‐way valve, allowing gas to continue flowing in but not out. In radiographs, the lungs often are markedly collapsed with very small lobes (Figure 3.47). The lung lobes may be abnormal in shape. Cardiovascular structures usually are small due to hypovolemia and may appear even smaller due to an expanded thoracic cavity. The large volume of pleural gas displaces the diaphragm caudally, sometimes revealing it costal attachments. A tension viscerothorax may develop following herniation and subsequent entrapment of a GI structure within the thoracic cavity. The trapped structure, usually the stomach, can become severely gas‐distended to resembles a large, cyst‐like mass with rounded, well‐defined margins (Figure 3.48). The mediastinum may be displaced to the opposite side. The part of the diaphragm through which the GI structure was displaced may be indistinct, which can help differentiate a viscerothorax from a unilateral pneumothorax. Gas in a pneumothorax outlines the lung, whereas gas in a viscerothorax is confined to the GI structure. Masses that originate in the pleura or pleural space usually are accompanied by pleural effusion. Pleural fluid can hide the lesion. A pleural mass may be visible in follow‐up radiographs made after removing the pleural fluid or by using horizontal beam radiography to reposition the fluid. Most pleural masses are difficult to see unless the x‐ray beam is tangential to the base of the mass. The mediastinum is the central compartment in the thoracic cavity. It is located between the right and left lungs. The mediastinum extends along the midsagittal plane from the thoracic inlet to the diaphragm and from the sternum to the spine. For descriptive purposes, it commonly is divided into cranial, middle, caudal, and dorsal parts. The cranial mediastinum extends from the thoracic inlet to the cranial border of the cardiac shadow. The middle mediastinum contains the cardiac shadow. The caudal mediastinum extends from the caudal border of the cardiac shadow to the diaphragm. The dorsal mediastinum lies dorsal to the level of the trachea. There are several openings in the mediastinum that allow communication with other parts of the body. Fluids, gases, and diseases can easily pass through these openings to enter or exit the mediastinum. Cranially, the mediastinum communicates with the cervical fascia via the thoracic inlet. Caudally, it opens to the retroperitoneal space via the aortic hiatus in the diaphragm. Centrally, it communicates with each lung through the pulmonary root or hilum. The lateral pleural walls that line the mediastinum are delicate and often fenestrated, providing an incomplete barrier between the right and left sides of the thoracic cavity. Normally visible structures in the mediastinum include the cardiac silhouette, the trachea, the aorta, the caudal vena cava, and in young animals, the thymus (Figure 3.49). The mediastinum is a site for fat deposits, so variable amounts of fat usually are visible, too. The other mediastinal structures either are too small to be seen or lack the opacity interface to be distinguished in survey radiographs. These include the esophagus, lymph nodes, vessels and nerves (e.g., cranial vena cava, left subclavian artery, brachiocephalic trunk, azygous vein, thoracic duct, phrenic nerves). The normal esophagus may be identified when it contains gas or fluid. In overweight patients, mediastinal structures not normally visible may be identified because excess fat provides the contrast needed to distinguish them. Structures may also be visible in emaciated patients because the absence of fat leads to a thinner mediastinum through which the soft tissue opacity structures may be discernable against air‐filled lungs. The thymus often is visible in young dogs and cats. It is located in the ventral part of the cranial mediastinum. In dogs, the thymus may be visible up to about six months of age, rarely up to a year of age. It generally shrinks quickly after the deciduous teeth are lost. The canine thymus tends to be easiest to see in a VD/DV view, appearing as a triangular‐shaped, soft tissue opacity structure in the left cranial thorax (Figure 3.50). In cats, the thymus may be visible up to two years of age. It usually is easier to see in a lateral view where it appears as an indistinct soft tissue opacity structure in the cranioventral mediastinum. Mediastinal lymph nodes may be visible when enlarged or mineralized. Knowledge of their normal locations aids in diagnosis (Figure 3.51). The cranial mediastinal lymph nodes are located ventral to the trachea and near the large cranial mediastinal blood vessels. They receive lymphatics from the neck, heart, esophagus, thymus, and thoracic wall. Enlargement of these nodes can widen the cranial mediastinum, increase mediastinal opacity, and displace the trachea dorsally and laterally. Caudal mediastinal lymph nodes frequently are absent in dogs and cats. The sternal lymph node is located immediately dorsal to the second or third sternebra. It usually is solitary but may be paired in some dogs. The sternal node receives lymphatics from the abdomen and enlargement generally is due to spread of intra‐abdominal disease or lymphoma. Tracheobronchial or hilar lymph nodes are located near the tracheal bifurcation. They receive lymphatics from the lungs and bronchi. Enlargement produces increased opacity in the hilar region and may lead to a mass effect that displaces the caudal trachea, usually ventrally. The radiographic appearance of the mediastinum varies with its thickness. In lateral views, summation of the cranial mediastinal structures produces a homogenous soft tissue opacity ventral to the trachea (Figure 3.49). The opacity quickly fades toward the sternum because there are fewer structures in the ventral part of the cranial mediastinum, and it usually is very thin. The caudal mediastinum also is thin and seldom visualized in a lateral view. In overweight animals, fat deposits often widen the mediastinum (Figure 3.42). The thin ventral mediastinum frequently produces a curved, soft tissue opacity line that resembles a pleural fissure line (Figures 3.31, 3.32, 3.49). It is visible both cranial and caudal to the cardiac silhouette and varies significantly in width depending on the amount of fat present. It is less evident in chondrodystrophic dog breeds. The cranioventral mediastinum conforms to the shapes of the right and left cranial lung lobes. It begins at the thoracic inlet and curves caudally, ventrally and to the left of midline. The caudoventral mediastinum conforms to the shapes of the accessory and left caudal lung lobes, curving caudally from the left cardiac border to the middle of the left hemi‐diaphragm. The caudoventral mediastinum is only visible in the VD/DV view and may be mistaken for the cardiophrenic ligament, which is not visible in radiographs. The position of the mediastinum is maintained by normal lung inflation. Lungs that are not evenly inflated allow the mediastinum to move or shift toward the smaller lung. Uneven lung inflation also allows the diaphragm on the side with the smaller lung to move cranially. The most common cause of a mediastinal shift is lung collapse. In cases of unilateral collapse, the opposite lung generally is well expanded due to compensatory hyperinflation. Collapse of part of a lung may or may not result in a mediastinal shift; it depends on the degree of compensatory inflation in the unaffected lobes. Other causes of a mediastinal shift include a large intra‐thoracic mass and a large volume of unilateral fluid or gas in the pleural space. In general, the position of the mediastinum is assessed in a VD/DV view based on the position of the cardiac shadow (Figure 3.52). Rotation of the patient during radiography may be mistaken for a mediastinal shift because the heart follows the sternum. It is important to assess patient positioning before diagnosing a mediastinal shift. The spine and sternum should be superimposed and the right and left ribs equal length in a properly positioned VD/DV view. The dorsal spinous processes should be centered on their vertebral bodies. The width of the mediastinum is assessed in a VD/DV view. In dogs, the normal width of the cranial mediastinum is about twice the width of a thoracic vertebra. In cats, the cranial mediastinum is about as wide as the spine. A wider than expected mediastinum may be localized due to a mass or it may be diffuse, involving the entire mediastinum. A mediastinal mass may arise in the cranial, dorsal, middle, or caudal part of the mediastinum. Cranial mediastinal masses that arise ventral to the trachea create increased opacity dorsal to the sternum. When large enough, the mass may displace the trachea dorsally and laterally, usually to the right (Figure 3.53). Very large masses can displace the cardiac shadow caudally and push the tracheal bifurcation caudal to the sixth intercostal space (Figure 3.54). Caudal cardiac displacement usually is accompanied by dorsal cardiac displacement. Possible sites of origin for a cranioventral mediastinal mass include thymus, lymph node, sternum, and ectopic thyroid or parathyroid tissue. A mass may represent a tumor, cyst, abscess, or hematoma (see Differential Diagnoses). A large thymus in a mature dog or cat may be due to neoplasia or sometimes hemorrhage. Thymic tumors can grow to a very large size, particularly thymomas (Figure 3.54). A large sternal lymph node creates a soft tissue opacity mass dorsal to the second or third sternebra (Figure 3.55). Sternal lymphadenomegaly produces an extra‐pleural sign, easiest to see in a lateral view. Rarely, a cranial mediastinal mass will involve one or more sternebrae and may cause osteolysis, a periosteal response, or/and adjacent soft tissue swelling. Cranial mediastinal cysts or branchial cysts are congenital, fluid‐filled cavities of embryologic origin. They usually are too small to be seen in radiographs of young animals but gradually enlarge over time. Branchial cysts are more common in cats than in dogs and typically produce a well‐defined soft tissue opacity mass just cranial to the cardiac shadow (Figure 3.56). An aspirate of the cyst generally yields clear, acellular fluid with low specific gravity. Conditions that may mimic a cranial mediastinal mass include fat deposits and errors in patient positioning. Older, small breed dogs normally store fat in the cranial mediastinum, which may be mistaken for a mass. During positioning for radiography, many patients will tuck their heads and flex their necks which can produce a bend in the trachea that resembles a mass effect (Figure 3.115). Superimposition of the thoracic limb musculature also can mimic a cranial mediastinal mass. When in doubt, repeat the radiograph paying special attention to patient positioning. Dorsal mediastinal masses occur dorsal to the trachea and most often are associated with the esophagus. Large masses can displace the trachea ventrally and laterally, usually to the right (Figure 3.57). A dilated esophagus can do the same and may be caused by abnormal retention of gas, fluid, food, or a combination of these. The type of esophageal content will affect the opacity of the dorsal mediastinum. An uncommon type of dorsal mediastinal mass is a large vertebral lesion (e.g., paraspinal tumor, severe lordosis, severe spondylosis). Middle mediastinal masses or hilar masses most often represent enlarged tracheobronchial lymph nodes or a heart base tumor. Both of these produce soft tissue opacity along the distal trachea and both can become large enough to displace and compress the trachea. Tracheobronchial lymphadenomegaly occurs at the tracheal bifurcation (Figure 3.55). The enlarged lymph nodes can displace the trachea in any direction, but most often it is ventrally. Dorsal displacement of the trachea most often is due to left atrial dilation. Tracheobronchial lymphadenomegaly may be caused by lymphoma or a mycotic infection. Neoplasms other than lymphoma rarely cause hilar lymph node enlargement. Mineralization in a hilar lymph node typically is a healing response that most often is seen with histoplasmosis. Heart base masses generally arise cranial to the tracheal bifurcation (Figure 3.58). The margins of a heart base mass often are indistinct due to effacement by pericardial fluid or the adjacent cardiovascular structures. Displacement of the trachea may be the only radiographic finding with a heart base mass. The trachea typically is pushed dorsally and laterally, usually to the right. Heart base tumors frequently are associated with the aorta (e.g., chemodectoma), but may involve the main pulmonary artery or the right atrium (e.g., hemangiosarcoma). End‐on visualization of the right pulmonary artery in a lateral view may be mistaken for a hilar mass. This artery, whether normal size or enlarged, can appear as a round, soft tissue opacity “nodule” located ventral to the tracheal bifurcation (Figure 3.99). Caudal mediastinal masses typically are associated with the esophagus or diaphragm (see Differential Diagnoses). They usually are located on midline or just left of midline (Figure 3.59). Large masses may efface the caudal cardiac and/or cranial diaphragmatic borders. A mass in the accessory lung lobe can be difficult to distinguish from a caudal mediastinal mass. Diffuse widening of the mediastinum may be due to abundant fat in the mediastinum (i.e., obesity), dilation of the esophagus, or fluid in the mediastinum. Excess mediastinal fat is common and must be differentiated from the other disorders. In overweight animals without mediastinal disease, the width of the cranial mediastinum should not exceed the thickness of the thoracic wall, measured at the same level (Figure 3.42). Dilation of the esophagus is discussed in the next section under “Esophagus”. Fluid in the mediastinum may result from a ruptured esophagus, severe inflammation, or hemorrhage (see Differential Diagnoses). Keep in mind that abundant fat or fluid can obscure a mediastinal mass. Conditions that may mimic diffuse widening of the mediastinum include summation with pleural or pulmonary fluid and superimposition of a thoracic mass. Orthogonal radiographs are necessary to avoid misinterpreting a structure located outside the mediastinum as something abnormal inside the mediastinum. Summation of dirt, debris, or medication on the skin or hair coat may be mistaken for mineral or metal in the mediastinum. The same is true with summation of a costal cartilage or a mineralized mass in the chest wall. Summation of subcutaneous gas not caused by pneumomediastinum may be mistaken for gas in the mediastinum. Mineral opacity in the mediastinum may represent esophageal content or dystrophic mineralization (Figure 3.60). Dystrophic mineralization may be associated with a lymph node, a long‐standing mass, or a cardiovascular structure. Lymph node mineralization usually is a healing response, most often following a mycotic infection (e.g. histoplasmosis). It is rare with neoplasia. A chronic abscess, hematoma, or tumor may mineralize, either focally or diffusely. Cardiovascular mineralization may be incidental or caused by a disease, such as hypercalcemia. Heart valve mineralization usually is small, sharp, and linear. In blood vessels, mineralization tends to be curvilinear and heterogenous, most often in the wall of the aorta or a coronary artery. Pneumomediastinum means there is free gas in the mediastinum. The gas provides an opacity interface to visualize structures that are not normally seen in survey radiographs. Radiographic signs vary with the amount of gas present. The signs tend to be easier to see in a lateral view where the spine and sternum are not superimposed. Small volumes of mediastinal gas may outline only the outer margin of the trachea and produce subtle, patchy areas of gas opacity (Figure 3.61). Larger volumes of gas may outline the cranial mediastinal blood vessels, the esophagus, and sharpen the margins of the aorta and cardiac silhouette (Figure 3.62). Gas can easily migrate in and out of the mediastinum through the normal openings at the thoracic inlet and aortic hiatus. Through these openings, gas can enter the cervical region and retroperitoneal space, respectively. Cervical gas readily spreads into the subcutaneous tissues along the thorax and abdomen (Figure 3.63). Retroperitoneal gas can outline the kidneys, abdominal aorta, and abdominal vena cava. Mediastinal gas also can diffuse through openings in the mediastinal pleura to enter the pleural space. Pneumomediastinum can progress to pneumothorax via the mediastinal fenestrations or a tear in the mediastinum. A pneumomediastinum may result from a ruptured trachea or ruptured esophagus. It may also be caused by migration of gas from the cervical region or pleural space. Cervical gas may result from a penetrating wound in the neck. Pleural gas may result from a penetrating wound in the thorax or from a tear in a bronchus or lung. Dyspnea is uncommon with pneumomediastinum unless a secondary pneumothorax develops. Iatrogenic causes of pneumomediastinum include faulty intubation, over‐distention of a tracheal tube cuff (especially in cats), and faulty venipuncture. An uncomplicated pneumomediastinum often is self‐limiting and gas typically is resorbed in 2–10 days. Serial radiographs are useful to monitor the patient’s progress and response to therapy. Conditions that can mimic a pneumomediastinum include both an abundance of mediastinal fat and a lack of mediastinal fat. Abundant fat can separate and outline the mediastinal soft tissues. A lack of fat (e.g., emaciated patient) may allow the mediastinal soft tissues to become more visible against air‐filled lungs. The esophagus is relatively fixed in position at the caudal pharynx and at the diaphragm. The portion in between is freely moveable and quite distensible. The esophagus seldom is identified in survey radiographs because it usually is empty and collapsed. Small volumes of swallowed gas or fluid sometimes are visible, but these tend to be transient and variable in appearance in serial radiographs. The cervical part of the esophagus runs from the cricopharynx (cranial esophageal sphincter) to the thoracic inlet. It lies dorsal and left lateral to the trachea. At the level of the first and second ribs, there is a slight ventral curvature or redundancy in the esophagus (Figure 3.64). The redundancy adds length to the esophagus to allow for movements of the head and neck. During flexion, the ventral curvature is more pronounced and may be mistaken for an esophageal diverticulum, (i.e., a pseudodiverticulum). Esophageal redundancy is accentuated in brachycephalic breeds where the length of the esophagus is confined to a shorter body. The thoracic part of the esophagus extends from the thoracic inlet to the diaphragm. It runs caudally in the median plane, dorsal and left of the trachea, right of the aortic arch, and between the descending aorta and the caudal vena cava. Occasionally, the normal esophagus is visible in a lateral view as a horizontal, soft tissue opacity band between the aorta and caudal vena cava (Figure 3.49). The vagal nerves run alongside the esophagus and follow it through the diaphragm into the abdominal cavity. The abdominal part of the esophagus runs left of midline from the diaphragm to the cardia of the stomach. The esophagus ends at the gastroesophageal junction. It is important to make both thoracic and cervical radiographs when examining the esophagus. Abdominal radiographs may be indicated as well because disease in the upper GI tract can affect the esophagus. Complete evaluation of the esophagus often requires an esophagram. The procedure for esophagography, as well as its indications and contraindications, is described in Chapter 2, Contrast Radiography. Esophagrams differ in appearance between dogs and cats. In dogs, all of the esophagus contains striated muscle and the mucosal folds are longitudinal (Figure 3.64). The folds produce multiple linear filling defects along the entire length of the esophagus. In cats, the cranial 2/3 of the esophagus contains striated muscle and longitudinal mucosal folds, but in the caudal 1/3 there is smooth muscle and the mucosal folds are transverse or oblique in orientation. From about the level of the tracheal bifurcation to the stomach, the feline mucosal folds produce a pattern of filling defects commonly is described as “herringbone” (Figure 3.65). In both dogs and cats, contrast medium in the esophagus should be transient and not retained. In some normal dogs, a small amount of contrast may persist for a short period of time near the larynx or thoracic inlet. Persistence of gas, fluid, soft tissue opacity material, or mineral opacity structures in the esophagus needs to be investigated. Abnormal opacity may be localized or diffuse, heterogenous or homogenous. Possible causes of retained gas, fluid, or solid material include physical obstruction, motility disorders, lodged foreign material, and a mass in the esophagus. Gas in the esophagus may or may not be due to pathology. A small volume of esophageal gas often is incidental and transient. Transient gas commonly is seen between the thoracic inlet and the tracheal bifurcation. Esophageal gas that is dorsal to the trachea may produce a tracheal stripe sign. The tracheal stripe results from the soft tissue opacity wall of the esophagus lying against the soft tissue opacity wall of the trachea with no different opacity between them (Figure 3.66). The two walls blend together to mimic a thickened dorsal tracheal wall. The tracheal stripe sign may be mistaken for a pneumomediastinum. However, free gas in the mediastinum generally outlines both the dorsal and ventral tracheal walls as well as other mediastinal structures. Larger volumes of transient esophageal gas sometimes are seen in patients that are sedated, anesthetized, or have swallowed a lot of air (e.g., panting, struggling, coughing, vomiting). Aerophagia usually is accompanied by abundant gas in the GI tract. Persistent gas in the esophagus may indicate a motility problem. A gas‐distended esophagus sometimes is difficult to recognize in radiographs because the esophageal lumen is the same opacity as the lungs (Figure 3.70). In addition, the esophageal walls tend to be thin, faint, and widely separated (Figure 3.71). The walls of a dilated esophagus may be easier to recognize in the caudal thorax where they converge toward the diaphragm. Cranially, the ventral border of the longus coli muscles tends to be more distinct against a gas‐distended esophagus. Foreign materials can lodge in the esophagus of a dog or cat. Common sites include the cranial cervical region, the thoracic inlet, the base of the heart, and just cranial to the diaphragm (Figure 3.67). Metal and mineral opacity objects usually are readily identified in radiographs. Soft tissue opacity materials must be outlined by gas or large enough to be distinguished. Objects that obstruct the esophagus may lead to dilation of the esophagus cranial to the object. The dilated esophagus may fill with gas, fluid, food, or a combination of these. Dilation may not be evident if the patient regurgitated and emptied the esophagus prior to radiography. Masses associated with the esophagus may be intraluminal, mural, or extraluminal. A large esophageal mass may be difficult to distinguish from a mass in the adjacent lung. Many esophageal masses are soft tissue opacity (e.g., tumor, abscess, granuloma, hematoma). A soft tissue opacity mass in the esophagus often is difficult to detect unless surrounded by gas or a positive contrast medium. In an esophagram, an esophageal mass may appear as a localized thickening of the esophageal wall and/or a filling defect in the esophageal lumen (Figure 3.73). The mucosal margin of the thickened wall may be smooth or irregular, depending on the amount of mucosal damage. Ulcers sometimes are present, appearing as contrast‐filled outpouchings that extend away from the esophageal lumen. If the esophagus is obstructed by a mass, contrast fills the dilated lumen cranial to the obstruction. Spirocercosis is a parasitic infection caused by Spirocerca lupi, a nematode with worldwide distribution. It is endemic in warm climates where the incidence can be as high as 85%. After being ingested, the parasites penetrate the gastric mucosa and travel along arteries to the thoracic aorta. They migrate through the aorta and end up in the caudal esophagus where they can produce granulomas along the dorsal esophageal wall. Parasite migration can produce small aneurysms in the wall of the aorta. Spirocera granulomas can grow quite large and may undergo malignant transformation to osteosarcoma. Osteosarcomas can mineralize and they can metastasize to the lungs. Large intra‐thoracic granulomas also can cause hypertrophic osteopathy. The pathognomonic sign of spirocercosis is new bone production along the ventral margins of the thoracic vertebrae (Figure 3.68). New bone occurs in about 25% of affected dogs, most often caudal to the T5 thoracic vertebra. One or more vertebrae may be involved. The border of the new bone may be solid, lamellar, or brush‐like and may be well‐defined or ill‐defined. Diagnosis of spirocercosis is confirmed by endoscopy or finding parasite eggs in the feces. An abnormally narrowed or dilated esophagus seldom is detected in survey radiographs unless there is persistent retention of gas, fluid, or food. Usually, an esophagram is needed for diagnosis and to evaluate the mucosal margin. Abnormal narrowing persists in multiple radiographs and may be focal or regional. Possible causes of a narrowed esophagus include stricture, mural thickening or mass, and external compression, the latter may be the result of a vascular ring anomaly or hiatal hernia (see Differential Diagnoses). Liquid contrast media may be used to evaluate esophageal width and to visualize the mucosal margin. Barium provides the best mucosal coating. An irregular mucosal margin may be due to severe inflammation or neoplasia (Figure 3.69). If the esophageal narrowing does not obstruct the passage of liquids, it may not be evident in a standard esophagram. Mixing the contrast medium with food may aid in diagnosis. Abnormal dilation of the esophagus commonly is called megaesophagus. Although megaesophagus is used as a general term to simply describe esophageal dilation, it is also the name given to flaccid dilation of the esophagus due to one of several congenital or acquired causes of weak or absent peristalsis. Congenital megaesophagus is more common in dogs than in cats, particularly in German shepherds. Acquired megaesophagus may result from numerous conditions, including severe or chronic inflammation, neuromuscular disease, immune‐mediated disease, chronic obstruction, and others (see Differential Diagnoses). Severe or chronic esophagitis usually is due to gastric reflux and can affect esophageal motility in animals at any age. Neuromuscular and immune‐mediated motility disorders often are idiopathic. They tend to occur in older animals (7–15 years of age) and many are incurable. Any cause of acquired megaesophagus may begin as mild or intermittent dilation and progress in severity. Many esophageal obstructions initially present with localized or regional dilation, but any persistent narrowing can progress to general dilation. Certain strong sedatives and anesthetic agents can cause transient esophageal dilation that usually resolves during recovery. Radiographic diagnosis of esophageal dilation depends on size and content. As mentioned earlier, a large, gas‐filled esophagus can easily be missed in survey radiographs because the lumen is the same opacity as the adjacent lungs and the esophageal walls are thin, faint, and widely separated (Figures 3.70 and 3.71). In the lateral view, look for the tracheal stripe sign and a more distinct ventral border to the longus coli muscles. Widening of the mediastinum may or may not be evident with a gas‐filled esophagus. A dilated esophagus may displace the trachea ventrally and laterally, usually to the right. The base of the cardiac silhouette may also be displaced ventrally, making the cardiac shadow appear shortened (Figure 3.71). Many patients with a dilated esophagus have concurrent aerophagia and aspiration pneumonia. A gastric outflow problem should always be investigated as a possible etiology of a dilated esophagus. Performing an esophagram in a patient with megaesophagus carries increased risk of aspiration, but sometimes the procedure is needed to help determine the etiology and full extent of the dilatation. A severely dilated esophagus may require a larger than expected volume of contrast medium for complete opacification. Inadequate dosing can result in an erroneous diagnosis of local esophageal dilation in a patient with general dilation. Inflammation of the esophagus may or may not be evident in radiographs. A normal esophagram does not rule out esophagitis. Characteristic radiographic findings include local or regional dilation and variable thickening of the esophageal wall. The mucosal margin may be smooth or irregular. If irregular, rule out neoplasia. Inflammation and neoplasia in the esophagus cannot be reliably differentiated with radiographs. Muscle spasms are common with esophagitis and may be mistaken for an esophageal stricture. Muscle spasms can last longer than normal peristalsis, but they are transient and vary in appearance between radiographs. Strictures persist relatively unchanged. Barium may adhere to damaged mucosa creating a mottled pattern (Figure 3.72). Mucosal ulcers appear as barium‐filled out‐pouches that extend away from the esophageal lumen (Figure 3.73). A diverticulum is an abnormal outpouching in the esophageal wall. It may result from a weakness in the wall that allows the mucosa to protrude through (pulsion diverticulum) or from an external adhesion that pulls the wall outward (traction diverticulum). Esophageal diverticula are reported most often either at the thoracic inlet or just cranial to the diaphragm. They may be visible in survey radiographs when the esophagus contains gas or ingesta. In an esophagram, a diverticulum appears as a contrast‐filled bulge that extends outward, away from the lumen (Figure 3.74). The lumen may be dilated or it may deviate ventrally or laterally. As stated earlier, the normal redundancy in the esophagus may be mistaken for a diverticulum at the thoracic inlet, particularly in brachycephalic dogs. To distinguish a true diverticulum from a pseudodiverticulum, repeat the radiograph with the patient’s neck extended. There will be little difference in the appearance of a true diverticulum between extension and flexion of the neck, whereas the normal esophageal redundancy will be less apparent with the patient’s neck extended. Invagination of the stomach into the lumen of the esophagus is rare in dogs and cats. It most often is reported in young dogs, particularly German Shepherds. Many affected animals have preexisting megaesophagus. Many gastroesophageal intussusceptions occur intermittently which makes them difficult to diagnose with radiographs. The displaced part of the stomach typically creates a well‐defined mass in the caudal esophagus (Figure 3.75). The mass may be soft tissue opacity or mixed opacity, the latter due to gas or ingesta in the stomach. Sometimes other viscera is displaced with the stomach (e.g., omentum, spleen, duodenum, pancreas). Often it is difficult to identify the displaced viscera. The stomach may be recognized by its rugal folds or if there is a visible connection between the intra‐thoracic mass and the intra‐abdominal part of the stomach. The stomach that remains in the abdomen frequently is abnormal in shape or position. Sometimes the area normally occupied by the stomach appears to be empty or contains only small intestine. An incarcerated stomach can become greatly distended with gas and present as an emergency situation (Figure 3.48). Gastroesophageal intussusception usually leads to caudal esophageal obstruction and cranial esophageal dilation. Dilation may be evident in survey radiographs if there is sufficient gas, fluid, or food in the esophagus. Otherwise an esophagram may be needed for diagnosis. Rarely, contrast medium may enter the stomach during an esophagram to outline the gastric rugae and confirm the diagnosis. Anomalous development of the aorta can lead to constriction of the esophagus at the base of the heart. The most common anomaly is a persistent right fourth aortic arch. In this situation, the aorta develops on the right side of the trachea instead of the left side and the esophagus is trapped in a tight ring formed by the ligamentum arteriosum and the trachea (Figure 3.76). The result is a functional stenosis that partially or completely obstructs the esophagus. The esophagus proximal to the vascular ring may retain gas, fluid, or food and may be dilated well into the cervical region (Figure 3.77). The esophagus distal to the vascular ring usually is normal size. The dilated proximal esophagus often is large enough to widen the cranial mediastinum and to displace the trachea. Tracheal displacement usually is ventral and to the left (leftward displacement because the anomalous aortic arch usually is on the right). In an esophagram, the proximal esophagus generally fills with contrast medium and then tapers quickly at the heart base, ending near the fourth intercostal space. Contrast medium may or may not be seen in the distal esophagus, depending on the degree of obstruction. What commonly is called the “heart” in a radiograph is actually an image of the pericardial sac and its contents. The contents include pericardial fluid, the origins of major blood vessels, the heart, and blood, all of which are soft tissue opacity and not individually distinguished. Because radiographs reveal only the outer margin of the pericardial sac, the terms cardiac silhouette or cardiac shadow are more accurate. The word “heart” will be used to describe the actual heart itself. Normal cardiovascular anatomy and circulation are depicted in Figures 3.88 and 3.89. The pericardial sac consists of two layers. The inner visceral layer is called the epicardium and blends with the surface of the heart. The outer parietal layer is tough and fibrous. Between the visceral and parietal layers is a tiny volume of pericardial fluid for lubrication. The pericardiophrenic ligament forms a strong attachment to the diaphragm. It is not visible in radiographs, but the caudal mediastinum sometimes is mistaken for the pericardiophrenic ligament (VD/DV view). The central position of the cardiac silhouette is maintained by normally inflated lungs. In most dogs and cats, the cardiac shadow is located between the T3 and T8 thoracic vertebrae, with its base at about the fifth or sixth intercostal space (base refers to the dorsum or “top” of the cardiac shadow). The cardiac base is formed by the atria, proximal aorta, main pulmonary artery, and cranial vena cava. Enlargement of any of these can alter the size or shape of the cardiac base. Immediately dorsal to the base lies the tracheal bifurcation and carina. The position of the carina relative to the spine is used to assess cardiac size. The ventrum or “bottom” of the cardiac shadow is called the apex. The cardiac apex is formed by the interventricular septum. In a lateral view, the cardiac silhouette sits dorsal to the sternum with its long axis tilted cranially about 45° off perpendicular. The long axis is the apex‐to‐base dimension or length of the cardiac shadow. The short axis is the width of the cardiac silhouette; the widest dimension perpendicular to the long axis, often at about the level of the caudal vena cava (Figure 3.78). In a lateral view of most healthy dogs and cats, the cardiac base is situated at about 2/3 the height (dorsoventral dimension) of the thoracic cavity (Box 3.1). In most dogs, the cardiac shadow occupies about 2.5–3.5 intercostal spaces. In most cats, it occupies about 2.0–2.5 spaces. In a VD/DV view, the normal position of the cardiac silhouette is on midline with its long axis tilted about 30° off parallel with the spine (Figure 3.78). In most dogs, the width of the cardiac shadow is about 2/3 the width of the thoracic cavity. The cardiac apex generally points left of midline. The canine cardiac silhouette may touch or overlap the diaphragm (Figure 3.79). In most cats, the width of the cardiac shadow is about 1/2 the width of the thoracic. The feline cardiac apex is variable in position (may be right or left of midline) and usually separated from the diaphragm by one or two intercostal spaces of lung (Figure 3.82). The shape and apparent size of the cardiac shadow are related to the shape of the thorax and the size of the thoracic cavity. In dogs with a narrow, deep‐chested conformation (e.g., Doberman Pinscher, Irish Setter), the cardiac silhouette is more narrow and upright with relatively little sternal contact and a smaller cardiac‐to‐thoracic ratio (Figure 3.80). The cardiothoracic ratio is a subjective assessment of the size of the cardiac silhouette in relation to the size of the thoracic cavity. In dogs with a wide, shallow thorax or a “barrel‐chested” conformation (e.g., Bulldog, Pug), the cardiac shadow is wider and more rounded with greater sternal contact and a larger cardiothoracic ratio (Figure 3.81). Athletic dogs (e.g., Greyhound) also tend to have a relatively large cardiothoracic ratio (the heart appears relatively large in relation to the size of the thoracic cavity). In cats, thoracic conformation is more uniform and the size and shape of the cardiac shadow are more consistent among different cat breeds. The feline cardiac silhouette is thinner and more elongated than in dogs with a relatively smaller cardiothoracic ratio (Figure 3.82). In lateral radiographs of older animals, the cardiac shadow may be tilted further cranially and more parallel with the sternum. This is particularly true in older cats. Also in aged cats, the aortic arch tends to become more vertical and elongated and often bulges to the left (Figure 3.83). In a VD/DV view, the bulge in the proximal aorta cat may be mistaken for a mass in the cranial mediastinum or in the left lung.
3
Thorax
Introduction
Procedure for making thoracic radiographs
Radiographic views of the thorax
Patient factors
Immature animals
Aged animals
Obese animals
Emaciated animals
Breed conformation
Effects of positioning
Thoracic wall
Normal radiographic anatomy
Thickened thoracic wall
Thoracic wall mass
Abnormal bony thorax
Vertebral abnormalities
Rib abnormalities
Abnormal intercostal spaces
Sternal abnormalities
Diaphragm
Normal radiographic anatomy
Abnormal position of the diaphragm
Diaphragmatic hernia
Diaphragm mass
Pleura and Pleural Space
Normal radiographic anatomy
Pleural fissure lines
Pleural fluid
Pleural gas
Pleural mass
Mediastinum
Normal radiographic anatomy
Mediastinal shift
Abnormal width of the mediastinum
Abnormal opacity in the mediastinum
Esophagus
Normal radiographic anatomy
Contrast radiography of the esophagus
Abnormal content or opacity in the esophagus
Abnormal size and margination of the esophagus
Esophagitis
Esophageal diverticulum
Gastroesophageal intussusception
Vascular ring anomaly
Heart
Normal radiographic anatomy

Stay updated, free articles. Join our Telegram channel

Full access? Get Clinical Tree

