Figure 9-10 Kerley B lines.

Interlobular septae are not visible on a normal chest radiograph but can become visible if they accumulate excessive fluid. First described by neurologist/radiologist Peter James Kerley, they are very short (1-2 cm long), very thin (about 1 mm) horizontal lines perpendicular to and abutting the pleural surface (white oval).

Figure 9-11 Kerley A lines.

The A lines (circle) appear when connective tissue near the bronchoarterial bundle distends with fluid. They extend from the hila for several centimeters in the midlung and do not reach the periphery of the lung like Kerley B lines do. A network of Kerley lines is produced in the lungs in patients with congestive heart failure producing the “prominence of the pulmonary interstitial markings” seen in that disease.

Figure 9-12 Peribronchial cuffing.

Normally the bronchus is invisible when seen on-end in the periphery of the lung. When fluid accumulates in the interstitial tissue around and in the wall of a bronchus as it does in CHF, the bronchial walls become thicker and can appear as ringlike densities when seen on-end (solid white arrows). Peribronchial cuffing may not always produce perfectly round circles.

Figure 9-13 Normal fissures and fluid in the fissures.

A, The major (solid white arrow) and minor fissures (dashed white arrow) may be barely visible normally but are almost never thicker than a line you could draw with the point of a sharpened pencil. B, Fluid can collect in the fissures in CHF and distend them, making them appear thicker and more irregular in contour and more visible than normal. The major fissure is more prominent (solid white arrow) as is the minor fissure (dashed white arrow). When the patient’s heart failure clears, the fissures will return to normal appearance, but after repeated and prolonged bouts of failure, fibrosis may result in permanent thickening of the fissures.

Figure 9-14 Fluid in inferior accessory fissure.

In addition to thickening the major and minor fissures, fluid may also distend accessory fissures in the lung. Here, the inferior accessory fissure that separates the medial from the other basilar segments of the lower lobe and is usually barely visible when present is markedly thickened (solid black arrow). Peribronchial thickening (white circle) is also seen.

Figure 9-15 Pleural effusions in congestive heart failure.

Bilateral pleural effusions (dotted and solid black arrows) are present in this patient with CHF. Effusions in CHF are most often bilateral but may be asymmetrical, the right side invariably being slightly larger. While a unilateral, left pleural effusion may occur with CHF, a large left effusion should draw suspicion to another possible cause, such as metastatic disease.

Figure 9-16 Bat-wing pattern of pulmonary edema.

The radiographic findings of pulmonary alveolar edema include fluffy, indistinct, patchy airspace densities frequently centrally located and sparing the outer third of the lung. This is called the bat-wing (angel-wing) or butterfly pattern, and it suggests pulmonary edema versus other airspace diseases such as pneumonia. The patterns of cardiogenic and noncardiogenic pulmonary edema overlap considerably, but the absence of pleural effusions, absence of fluid in the fissures, and the normal-sized heart favor a noncardiogenic cause in this case. The patient was in septic shock from an overwhelming urinary tract infection.

Figure 9-17 Rapidly clearing pulmonary edema.

Pulmonary edema generally is both abrupt in its onset and quick to clear. A, This patient demonstrates bilateral, perihilar airspace disease with diffuse prominence of the interstitial markings characteristic of pulmonary edema. B, Four days later, the lungs are clear. Patients with adult respiratory distress syndrome are not likely to clear this quickly, nor are patients who have coexisting diseases such as renal or hepatic failure or superimposed pneumonia.

Figure 9-18 Reexpansion pulmonary edema.

Unilateral airspace disease affects the entire right lung (solid black arrow). In addition, a chest tube (dotted black arrow) is seen on the same side. The chest tube was inserted for a large, right-sided, tension pneumothorax that was rapidly reexpanded. Reexpansion pulmonary edema results from the overly rapid expansion of a lung that has typically been chronically collapsed by pneumothorax or a large pleural effusion. Its exact cause is unknown. In general, unilateral pulmonary edema can occur either because of an abnormality on the same side as the pulmonary edema (e.g., prolonged positioning with the affected side dependent) or an abnormality on the opposite side (e.g., large pulmonary embolus occluding flow to the opposite lung).

Figure 9-19 Noncardiogenic pulmonary edema.

Even though this airspace disease has a perihilar distribution similar to cardiogenic pulmonary edema (solid white arrows), there is no pleural fluid, fluid in the fissures or cardiomegaly. In general, noncardiogenic pulmonary edema is less likely to demonstrate pleural effusions and Kerley B lines, more likely to demonstrate a normal pulmonary capillary wedge pressure (PCWP) of less than 12 mm Hg, and more likely to be associated with a normal-sized heart than cardiogenic pulmonary edema.

Figure 9-20 Hypertensive cardiovascular disease.

Systemic hypertension can lead to hypertrophic cardiomyopathy. The left ventricle (dotted white arrow) is only slightly enlarged, but other modalities would demonstrate marked concentric hypertrophy of the left ventricular wall that has occurred at the expense of the lumen. The aorta itself is uncoiled (solid white arrows) due to increased systemic blood pressure (see also Fig. 9-7C).

Figure 9-21 Chronic mitral stenosis with tricuspid regurgitation.

The left atrium is enlarged (solid white arrow). Pulmonary venous hypertension has produced a redistribution of flow in the lungs so that the upper lobe vessels have become more prominent than the lower lobe (cephalization) (white circle). Due to increased pulmonary vascular resistance and subsequent pulmonary arterial hypertension, the right heart also undergoes changes, eventually including tricuspid regurgitation with enlargement of the right atrium (solid black arrow).

Figure 9-22 Pulmonary arterial hypertension.

Normally, the main pulmonary artery (MPA) is about the same diameter as the ascending aorta (A). In this patient, with pulmonary arterial hypertension, the MPA is much larger than the aorta. There is also a rapid attenuation in the size of the pulmonary arteries (solid white arrows) called pruning, which is also seen in pulmonary arterial hypertension.

Figure 9-23 Dilated alcoholic cardiomyopathy.

The cardiac silhouette is markedly enlarged, primarily as a result of biventricular enlargement. The patient had a long history of alcohol abuse. Dilated cardiomyopathy is frequently associated with congestive heart failure.

Figure 9-24 Constrictive pericarditis.

There is extensive pericardial calcification (solid white arrows), most likely post-inflammatory in etiology. Although restrictive cardiomyopathy and constrictive pericarditis can have identical clinical findings, the presence of pericardial calcifications excludes restrictive cardiomyopathy. If indicated, pericardiectomy holds the potential for cure for patients with constrictive pericarditis.

Figure 9-25 Aortic aneurysm.

The entire thoracic aorta is enlarged in this 67-year-old man. The ascending aorta (solid white arrow) should normally not project farther to the right than the right heart border (dashed white arrow) on a nonrotated chest radiograph. The descending thoracic aorta should normally parallel and almost disappear with the thoracic spine; as it becomes larger, it swings farther away from the spine (dotted white arrows).

Figure 9-26 Aortic aneurysm, conventional chest radiograph and CT.

Close-up view of a frontal radiograph of the chest (A) demonstrates a large mediastinal soft tissue mass (solid white arrow). This soft tissue density represents a large aneurysm of the proximal descending aorta seen also in the CT scan (B). The aneurysm measured 6.7 cm, which placed it at significant risk for rupture. Calcification in the wall of an aneurysm is common (dotted white arrow). Contrast material mixes with blood flowing in the lumen of the aorta (solid white arrow), but the flowing blood is separated from the intimal calcification by a considerable amount of noncontrast-containing thrombus adherent to the wall (closed black arrow).

Figure 9-28 Aortic dissections, types A and B.

A, An intimal flap is seen to traverse both the ascending (solid black arrow) and descending aorta (dotted black arrow). This is a Stanford type A dissection. B, There is a normal-appearing ascending aorta (dotted white arrow) while an intimal flap is noted by the black line traversing the descending aorta (solid black arrow). The intimal flap is the characteristic lesion of an aortic dissection. The smaller lumen is usually the true (original) lumen, and the larger, false lumen is actually a channel that has been produced by blood dissecting through the media.

Figure 9-29 Cardiac MRI, short axis view.

This is a standard view of the heart using MRI called the short axis view. The right ventricle (RV) lies anterior to the left ventricle (LV), separated by the interventricular septum (solid white arrow). Note the wall of the left ventricle (dotted white arrow) is normally thicker than the right ventricle. (A is anterior and P is posterior.)

Figure 9-30 Cardiac MRI, horizontal long axis view.

This is another standard view of the heart using MRI called the horizontal long axis or four-chamber view. The right (RV) and left ventricles (LV) are separated by the interventricular septum (solid white arrow). Posterior to each of them are the right atrium (RA) and left atrium (LA) separated by the regions of the tricuspid (dotted white arrow) and mitral valves (solid black arrow), respectively. (A is anterior and P is posterior.)

Figure 9-31 Cardiac MRI, vertical long axis view.

The vertical long axis or two-chamber view demonstrates the left ventricle (LV) separated from the more posterior left atrium (LA) by the mitral valve area (solid black arrow). Pulmonary veins drain into the left atrium (solid white arrow). The aorta (Ao) sits atop the pulmonary artery (PA). (A is anterior and P is posterior.)

Figure 9-32 Cardiac MRI, bright blood and black blood images.

Using different imaging algorithms, MRI is capable of displaying the same tissues with differing appearances. (A) and (B) are both axial sections through the heart, showing the right ventricle (solid white arrows), the left ventricle (dotted white arrows) and the aorta (Ao). The bright blood technique (A) is utilized to assess cardiac function while the black blood technique (B) is usually better at depicting cardiac morphology. (A is anterior and P is posterior.)

Figure 9-33 Cardiac CT, coronary artery calcification.

CT scan through the heart without intravenous contrast demonstrates calcified plaque in the left anterior descending coronary artery (solid black arrows). The amount of calcium detected on a cardiac CT scan and calculated by computer can be a helpful prognostic tool for coronary artery disease.