Cardiothoracic Ratio

The determination of heart size, both subjectively and quantitatively, has been assessed from the chest film for more than 70 years. Then Danzer described the cardiothoracic ratio, which is still one of the most common measurements of overall heart size. This ratio was constructed to measure left ventricular dilatation. Because it measures the transverse heart diameter, the cardiothoracic ratio is usually normal when either the left atrium or the right ventricle is moderately enlarged because neither of these two chambers is reflected in the transverse dimension. The left atrium and right ventricle become border-forming when they are severely enlarged. Rose and colleagues noted that for the cardiothoracic ratio to reliably detect enlargement of the left ventricle (Table 1-1), changes in left ventricular volume up to 66% in excess of normal are needed.

TABLE 1-1 Cardiothoracic ratio

Modified with permission from Rose CP, Stolberg HO: The limited utility of the plain chest film in the assessment of left ventricular structure and function, Invest Radiol 17:139-144, 1982.

When the heart size is subjectively evaluated based on the configuration of the heart with respect to the thorax, the sensitivity and specificity are quite similar to the measured cardiothoracic ratio. For this reason and because quantitative measurements from tomographic imaging methods are commonly available, the cardiothoracic ratio is now used mainly as an adjunct in assessing heart size on the chest film. Although the cardiothoracic ratio is moderately variable among individuals, it is a useful indicator in an individual who is being watched for potential cardiac dilatation, such as in chronic aortic regurgitation. In this instance, an abrupt change in the cardiothoracic ratio suggests the need for urgent clinical reevaluation.

Marathon runners with heart rates in the range of 30 to 40 beats per minute occasionally have a cardiothoracic ratio between 0.50 and 0.55, reflecting the normal physiologic dilatation of the heart rather than any overall hypertrophy.

Several other measurements can be made from the standard posteroanterior and lateral chest film. Examples include total heart volume, left atrial dimension on the frontal film, width of the right descending pulmonary artery, and the distance of the left ventricle behind the inferior vena cava. These, however, are rarely used now in clinical evaluation.

Most measurements made from the chest film have poor correlation with left ventricular size from quantitative angiographic measurements. Therefore, the measurements of specific chamber diameters, volumes, and wall thicknesses should be made from techniques that show the chamber cavities (e.g., echocardiography, angiography, CT, and MRI).

Measurements of the heart and mediastinum are dramatically affected by the height of the diaphragm and the intrathoracic pressure and less so by the body position and status of the intravascular volume (Table 1-2).

TABLE 1-2 Typical variations of heart and mediastinum measurements on the chest film

Right Atrium

In the frontal view, the right atrium is visible because of its border with the right middle lobe (see Box 1-2). Neither subtle nor moderate enlargement can be recognized accurately because there is moderate variability of its shape in normal subjects, and in expiration the right atrium becomes rounder and moves to the right (Figures 1-4, 1-5).

FIGURE 1-4 Right atrial enlargement in rheumatic heart disease. A, The unusually large right atrium compresses the right middle lobe and extends inferiorly to intersect the diaphragm. A large left atrium usually does not have a diaphragmatic interface. B, Enlargement of the right heart creates a sharp interface with the lung (arrow). The horizontal contour suggests that this is the right atrial appendage rather than the right ventricle.

FIGURE 1-5 Superior right atrial convexity. In Ebstein anomaly, the large right atrium has a characteristic round superior border.

The right atrium and the other three chambers enlarge because of increased pressure, increased blood volume, or a wall abnormality. Common causes of right atrial enlargement are tricuspid stenosis and regurgitation, atrial septal defect, atrial fibrillation, and dilated cardiomyopathy. Ebstein anomaly may have all of these features. In pulmonary atresia, the right atrium dilates in direct proportion to the amount of tricuspid regurgitation (Fig. 1-6).

FIGURE 1-6 Right atrial enlargement in pulmonary atresia with intact ventricular septum. This patient had moderate tricuspid regurgitation. Note the decreased vascularity in the lungs.

All the signs of right heart enlargement that are implied on the chest film are directly visible on the CT scan. The right atrium and ventricle touch the anterior chest wall and rotate the heart posteriorly. The right coronary artery adjacent to the right atrial appendage lies to the left of the sternum (Fig. 1-7).

FIGURE 1-7 Right atrial enlargement in rheumatic heart disease. The appendage portion of the right atrium (RA) touches the anterior chest wall in this patient, who had a sternotomy for mitral valve replacement. The right coronary artery is visible in the fat between the right atrium and right ventricle. The left atrium is calcified and also enlarged.

Right Ventricle

On the lateral view, the normal right ventricle does not touch more than one fourth of the lower portion of the sternum as measured by the distance from the sterno diaphragmatic angle to the point at which the trachea meets the sternum. One sign of right ventricular enlargement is the filling in of more than one third of the retrosternal space. On the frontal view, the normal right ventricle is not visible, and only extreme dilatation causes recognizable signs because the heart rotates clockwise as it dilates and pushes against the sternum. In this instance, the usual contour of the left atrial appendage is rotated posteriorly and is no longer part of the left side of the mediastinum. You can recognize this sign by an unusually long convex curvature extending inferiorly from the main pulmonary artery (Fig. 1-8). In extreme instances the entire left heart border may be the right ventricle (Box 1-3).

FIGURE 1-8 Right ventricular enlargement. A, The broad convexity along the upper left heart border represents the dilated right ventricle. B, The right ventricle touches the sternum and fills one third of the retrosternal space. Shunt vascularity is also evident in this patient with atrial septal defect.

In tetralogy of Fallot when the fat pad is absent in the left cardiophrenic angle, the heart may have an uplifted cardiac apex (Fig. 1-9), which has been called the “boot-shaped heart” or the coeur en sabot. The right ventricle is not enlarged but may have hypertrophy.

FIGURE 1-9 Boot-shaped heart. In tetralogy of Fallot, the cardiac apex has an uplifted appearance. Other typical features are the concave main pulmonary artery segment and the right aortic arch.

Common causes of right ventricular enlargement are pulmonary valve stenosis, pulmonary artery hypertension (cor pulmonale), atrial septal defect, tricuspid regurgitation, and dilated cardiomyopathy; it can occur secondarily to left ventricular failure.

Left Atrium

There are many clues to left atrial enlargement on the frontal and lateral chest film. One of the earliest signs of slight enlargement is the appearance of the double density, which is the right side of the left atrium as it pushes into the adjacent lung. Because a prominent pulmonary vein or varix may also cause a vertical double density, the double density should begin to curve inferiorly (Fig. 1-10). In extreme cases, the left atrium may enlarge to the right side and touch the right thoracic wall (Fig. 1-11). The etiology of this “giant left atrium” is rheumatic heart disease, mainly from mitral regurgitation.

FIGURE 1-10 Left atrial enlargement in mitral stenosis. The double density (arrow) occurs because the large left atrium pushes into the adjacent lung. The line curves inferiorly, differentiating it from a pulmonary varix. The large pulmonary artery indicates pulmonary hypertension.

FIGURE 1-11 Giant left atrium. Rheumatic mitral valve disease has caused the left atrium to enlarge so that it almost touches the right thorax wall. The carina is splayed superiorly over the atrium, and the left atrial appendage is convex.

A convex left atrial appendage on the frontal view is abnormal and usually reflects prior rheumatic heart disease. In pure mitral regurgitation, the body of the left atrium, not the appendage, enlarges.

The indirect signs visible only when the left atrium is dilated at least moderately are highlighted in Box 1-4 and Figures 1-12 and 1-13.

FIGURE 1-12 Convex left atrial appendage. The large left atrial appendage and the redistribution of blood flow to the upper lobes indicate mitral stenosis.

FIGURE 1-13 Posterior displacement of the left main stem bronchus. The left bronchus should lie in a straight line with the trachea but is displaced posteriorly (arrow) by the large left atrium. The large left pulmonary artery is seen on top of the bronchus.

Common acquired causes of left atrial enlargement are mitral stenosis or regurgitation, left ventricular failure, and left atrial myxoma. Congenital causes include ventricular septal defects, patent ductus arteriosus, and the hypoplastic left heart complex. When atrial fibrillation occurs, the left atrial volume may increase by 20%.

Left Ventricle

Left ventricular enlargement exists if the left heart border is displaced leftward, inferiorly, or posteriorly. Inferior displacement may invert the diaphragm and cause this border to appear in the gastric air bubble. The chest film cannot reliably distinguish between left ventricular dilatation and hypertrophy. With hypertrophy, the apex has a pronounced rounding and a decrease in its radius of curvature. The elderly normal heart also has this shape. When massive hypertrophy is present, the left ventricular shape is large and appears similar to one that is only dilated (Box 1-5).

Common causes of left ventricular enlargement can be grouped into three categories: pressure overload (hypertension, aortic stenosis; Fig. 1-14); volume overload (aortic or mitral regurgitation, ventricular septal defects; Fig. 1-15); and wall abnormalities (left ventricular aneurysm, hypertrophic cardiomyopathy; Fig. 1-16).

FIGURE 1-14 Aortic stenosis. A, The left ventricle is enlarged to the left and inferiorly where it is seen through the stomach bubble. The ascending aorta has poststenotic dilatation. B, The posterior border of the left ventricle is significantly behind the inferior vena cava. Note moderate calcium in the aortic valve (arrow).

FIGURE 1-15 Aortic regurgitation. The left ventricle and the aorta are both large from moderate aortic regurgitation. The indentation in the descending thoracic aorta (arrow) and the absence of rib notching denote a pseudocoarctation. Because 50% of those with pseudocoarctation have a bicuspid aortic valve, this probably is the etiology of the aortic regurgitation.

FIGURE 1-16 Left ventricular aneurysm. A and B, This angular left ventricular border with curvilinear calcification (arrow) is characteristic of an aneurysm.

Distinguishing Characteristics

Calcium in the aortic valve is seen best in the lateral view, where it projects free of the spine. You can distinguish between aortic and mitral calcification by the following methods.

FIGURE 1-17 Location of the aortic valve on the lateral chest film. A line drawn from the junction of the diaphragm and the sternum to the carina passes through the aortic valve. The mitral valve is below and posterior.

FIGURE 1-18 Bicuspid aortic valve calcification. A, The calcification is located in the aortic valve by following the dilated ascending aorta into the heart. B, The distinctive bicuspid valve calcification is a ring with a linear bar through it.

Calcific Aortic Stenosis

Calcium in the aortic valve may extend from the valve into the adjacent interventricular septum and cause arrhythmias. In most cases of bicuspid aortic stenosis, the mitral valve is normal and the left atrium is not enlarged. When both the aortic and mitral valves are calcified, the cause is usually rheumatic heart disease. In a patient without rheumatic heart disease or a previous episode of infected endocarditis, calcification in a tricuspid aortic valve is rare before age 70. Patients with bicuspid aortic valves also may have had rheumatic heart disease or endocarditis and develop heavy central calcification.

The aortic valve is the only one that has a good correlation between the amount of calcium seen on a chest film and the amount of stenosis. If the patient is over age 35, heavy calcification in the aortic valve indicates severe stenosis that will probably require a valve replacement. Conversely, if no calcium is seen by fluoroscopy in the aortic valve, it is unlikely that aortic stenosis exists.

Distinguishing Patterns

The mitral valve ring may calcify in individuals over age 60. The incidence is four times higher in women. The calcium begins to form in or below the mitral annulus at the junction between the ventricular myocardium and the posterior mitral leaflet. More severe degrees of calcification will form a pattern resembling the letter J, the letter O, or a reversed letter C (Figure 1-19).

FIGURE 1-19 Mitral annulus calcification. The characteristic oval calcification (arrows) is located below the left atrial appendage segment.

Clinical Significance

In most instances, mitral annulus calcification has little clinical significance and is a noninflammatory chronic degenerative process. In extreme cases, the mass of calcification can grow posteriorly into the ventricular myocardium to produce heart block. It can also grow anteriorly into the leaflets of the mitral valve to cause mitral regurgitation and stenosis. Rarely, the calcification can erode through the endocardium and cause small systemic emboli. Mitral annulus calcification in the elderly is associated with a doubled risk of stroke, independent of the traditional risk factors.

Aortic stenosis and hypertension have a higher incidence of mitral annulus calcification, possibly because of increased strain exerted on the mitral valve apparatus from the left ventricular pressure overload. For the same reason, the tricuspid annulus rarely may calcify when right ventricular pressures have been chronically increased (Fig. 1-20).

FIGURE 1-20 Tricuspid annulus calcification. A, Adult tetralogy of Fallot with unusually large mediastinal collaterals to the pulmonary hila. B, The tricuspid annulus (arrows) calcified because of the chronic right ventricular hypertension.

Causes

Mitral leaflet calcification is almost always caused by chronic rheumatic valvular disease. Rarely, the leaflets are calcified from infected endocarditis or from tumors attached to the mitral valve. There is limited correlation between the hemodynamic severity of mitral stenosis and the amount of calcium in the valve. Although a severely calcified mitral valve is usually stenotic, mitral stenosis frequently exists with no calcium in the valve.

Appearance

Radiologically, the calcium first appears as fine speckled opacities and later coalesces into larger, amorphous masses (Fig. 1-21).

FIGURE 1-21 Calcified mitral valve. The barium-filled esophagus is displaced posteriorly around the large left atrium. The mitral valve (arrow) is heavily calcified.

As the rheumatic valvulitis progresses, causing commissural fusion, chordal shortening, and fibrosis, the leaflet calcification may extend into the chordae and to the tip of the papillary muscles. Tricuspid calcification from rheumatic valvulitis is rare, and pulmonary calcification from rheumatic heart disease does not occur.

Causes

Calcific deposits in the pericardium represent the end stage of a nonspecific inflammatory process. Tuberculosis, viruses and many other infectious agents, rheumatic fever, uremia, and trauma all may cause local or diffuse calcification. Large localized masses of calcification suggest that the etiology was tuberculosis.

Radiologic Appearance

The calcification radiologically appears in two forms:

FIGURE 1-25 Pericardial calcification. A, Eggshell calcification (arrows) outlines the right and left borders of the heart. B, Diffuse calcification projects over most of the heart and reflects circumferential deposits.

Use of Computed Tomography

In patients with constrictive pericarditis, 50% have calcium visible on the chest film, and most have calcium on the CT scan. Because pressure tracings from the ventricles may be identical in both restrictive cardiomyopathy and constrictive pericarditis, a CT scan that shows calcium in a thickened pericardium in a patient with elevated filling pressure is diagnostic of constrictive pericarditis (Fig. 1-26).

FIGURE 1-26 Computed tomography scan of pericardial calcification. Calcium is seen in the anterior pericardium, in the left atrioventricular groove, and along the lateral aspect of the left atrium.

Appearance

Coronary calcification represents atherosclerotic changes in the intima and in the internal elastic membrane of the coronary arteries. The left anterior descending artery is the most frequently calcified site, followed by the left circumflex artery, then the right coronary artery (Fig. 1-27). The incidence of coronary calcification increases with age and may be part of the normal aging process. Generally, in patients under age 60, there is a strong correlation between calcification and severity of atherosclerosis; the association is not as strong in older patients. Coronary calcification is influenced by risk factors such as increased cholesterol and lipids, smoking, hypertension, and a family history of coronary disease. There is correlation between calcification and the severity of coronary stenosis; however, some severe stenoses may not be calcified, and some heavy calcifications may not denote stenotic arteries.

FIGURE 1-27 Coronary artery calcification. A and B, The region just below the left atrial appendage segment is the location of the proximal left coronary artery (black and white arrows). The open arrow points to the calcified mitral annulus.

Association with Stenosis

A number of investigators have attempted to develop a test for asymptomatic coronary artery disease by screening for coronary calcification. Coronary calcium is frequently seen on routine multislice chest CT (Fig. 1-28). Ultrafast or electron-beam CT detects calcium in significant coronary artery stenoses with a sensitivity of about 95% and a specificity of 50%. Multislice coronary CT angiography has a similar detection rate of calcified coronary plaques but also shows the soft or noncalcified component of the plaque (see Chapter 7).

FIGURE 1-28 Coronary artery calcification. Computed tomography scan of dense calcification in the left anterior descending and left circumflex arteries.

Segmental Analysis

Because the pulmonary arteries and veins have a complex branching pattern and are associated with many overlapping structures on the standard chest film, there is moderate variability in interpreting which pulmonary pattern is present. Segmental analysis can help to classify pulmonary vasculature patterns. In the standard upright chest film exposed at total lung capacity, the pulmonary vasculature can be divided into the following three areas:

Pattern Recognition

The first step in analyzing the pulmonary vasculature is to classify it into one of the following five patterns:

Segmental Analysis

The size of the central, hilar, and peripheral pulmonary arteries and veins reflects the pressure, flow, and volume in the lungs in a complex way. In a high-output state, all pulmonary segments are enlarged: The central pulmonary artery segment is convex, the hilum appears engorged, and the peripheral vessels are large from apex to base.

Flow Ratios

High-output states can be separated into those that have increased blood flow in both the pulmonary and the systemic circulation and those that have increased pulmonary circulation only. The chest film usually does not detect increased pulmonary flow until the flow ratio (Q_p/Q_s) is at least 2 (i.e., the pulmonary flow is twice that in the aorta). Increased cardiac output from both the right and left ventricles occurs in metabolic and endocrine diseases, in arteriovenous fistulas and malformations, and in aortic regurgitation.

Contributing Diseases, Lesions, and Defects

Thyrotoxicosis (Fig. 1-30), beriberi, and pheochromocytoma are diseases that either increase the overall metabolic rate of the body or have a specific effect on the heart. They increase its rate and stroke volume. Extra cardial shunts, such as patent ductus arteriosus, aortopulmonary window, and arteriovenous fistulas and malformations either in the lungs or in another part of the body, provide a lower-resistance parallel circuit to the systemic capillary bed for the blood to return to the heart. (The electrical analogy is a short circuit of a battery, which causes a high current to flow across its terminals.) In Paget disease there are numerous arteriolar-venous channels within the bone. In aortic regurgitation, blood flow that is regurgitated from the aorta into the left ventricle is added to the forward output to produce an augmented forward flow in the aorta. Because the lungs are in a series circuit with the aorta, the output is also increased. Intracardiac shunts have a normal aortic size and large main, hilar, and peripheral pulmonary arteries. In babies, high-output states often result in an element of pulmonary edema (Fig. 1-31). A large pulmonary vasculature is also a feature of certain cyanotic congenital heart diseases (Fig. 1-32).

FIGURE 1-30 High-output state in Graves disease. The hilar pulmonary arteries are slightly large. The pulmonary arteries in the lung are larger than their adjacent bronchus in both the upper and lower lobes.

FIGURE 1-31 Shunt vascularity in ventricular septal defect. The large central pulmonary arteries are indistinct because of surrounding pulmonary edema.

FIGURE 1-32 Shunt vascularity in transposition of the great arteries with ventricular septal defect. Both upper and lower lobe pulmonary arteries and veins are large. The right-sided thymus obscures the upper lobe.

A convex main pulmonary artery segment suggesting a high-output state may be present in healthy individuals. Highly trained endurance athletes, such as marathon runners, women in the third trimester of pregnancy, and occasionally teenage girls frequently show mild enlargement of the main pulmonary artery (see Box 1-7).

Pressure Measurements and Patterns of Pulmonary Vasculature

Pulmonary hypertension exists when the pulmonary systolic pressure is greater than 30 mm Hg and the mean pressure exceeds 20 mm Hg. Pulmonary hypertension may occur when there is increased resistance in any part of the pulmonary circulation from the pulmonary artery to the left heart. The type of pattern of the pulmonary vasculature on the chest film depends on the location of the abnormal resistance, the chronicity, and the severity.

If the heart is structurally intact, the earliest sign of pulmonary artery hypertension is a convex main pulmonary artery segment. Severe chronic pulmonary artery hypertension also dilates the hilar branches but, unlike a left-to-right shunt, not the peripheral arteries within the lungs (Fig. 1-33). The gradient of small vessels at the apex and large vessels at the base is preserved.

FIGURE 1-33 Primary pulmonary artery hypertension. The main pulmonary artery segment is convex and the hilar arteries are large. The peripheral vessels are larger at the base, smaller at the apex, and retain their normal branching pattern.

Eisenmenger Syndrome

In adults with Eisenmenger syndrome the pulmonary vasculature is unusually striking because of the central arterial enlargement. The arteries dilate longitudinally, forming a serpentine course (Fig. 1-34). The rapid taper of the large aneurysmal hilar pulmonary arteries to the periphery looks like a “pruned tree.” This phrase is correct angiographically and pathologically: There are fewer arterial side branches than in a normal arterial tree. However, the reduced number of side branches can not be seen on a chest film. The size of the pulmonary arteries in relation to their adjacent bronchus is measurable on CT (Fig. 1-35).

FIGURE 1-34 Eisenmenger syndrome. In addition to the large main pulmonary artery segment and hilar branches, the peripheral pulmonary arteries are large and have a serpentine course.

FIGURE 1-35 Computed tomography scan of pulmonary artery hypertension. A, The diameters of the main and right pulmonary arteries are almost twice that of the adjacent aorta. B, The hilar pulmonary arteries are two to three times larger than their adjacent bronchus.

Box 1-8 lists the common causes of pulmonary artery hypertension.

FIGURE 1-36 Pulmonary artery hypertension from mitral stenosis. The central pulmonary artery is convex and the hilar arteries are large because of arterial hypertension. The large upper lobe pulmonary arteries and veins and invisible lower lobe vessels indicate pulmonary venous hypertension. Note the double density along the right side of the heart from left atrial enlargement.

Venous Hypertension

The pulmonary pattern in pulmonary artery hypertension that is secondary to pulmonary venous hypertension has a different time course and appearance. After weeks to months of increased pulmonary venous pressure, the hilar and central segments of the pulmonary arteries begin to dilate. The peripheral pulmonary branches continue to suggest pulmonary venous hypertension with large vessels at the apex and small vessels at the lung base.

Fluid and Water Exchange

Pulmonary edema has many radiologic patterns, and to analyze these more exactly, it is important to have an understanding of lung architecture and physiology for gas and fluid exchange.

In the normal lung, hydrostatic and osmotic forces provide a gradient to keep fluid within the pulmonary microvasculature. Fluid exchange mainly takes place across the alveolar-capillary endothelium and the interstitium around the precapillary and postcapillary vessels. The alveolar septum is differentiated into one side with thin cells for gas exchange and one side with thick cells for fluid exchange. When interstitial pulmonary edema develops, the water and protein accumulate predominantly on the thick side.

The lung removes excess fluid mainly by a network of pulmonary lymphatics. The mediastinal and pulmonary lymphatics serve as the major channel for fluid removal. Extensive lymphatic channels exist near the alveolar ducts and drain centrally adjacent to respiratory bronchioles, to the interstitium about the minor and major bronchi, and to the major mediastinal lymph nodes. The cortex of the lung has its own lymphatic supply, which drains the peripheral portion of the lung into pleural lymphatics. This anatomic arrangement provides a pathologic correlation that explains peribronchial cuffing and hilar haze on the chest film as two signs of pulmonary edema. When there is significant accumulation of lung water, the rate of lymph flow can increase tenfold before there is significant pulmonary edema. The excess lung fluid in the pulmonary interstitium is visible in patients with transplanted lungs because the lymphatics have been cut, blocking the major pathway of fluid transport from the lung.

Radiologic Appearance

The radiologic appearance of pulmonary venous hypertension with the later formation of pulmonary edema has a distinct time course and appearance that frequently separates it from other types of diffuse lung disease and noncardiogenic pulmonary edema. As the left atrial pressure rises from its normal value of less than 12 mm Hg, the size of the pulmonary veins changes and fluid begins to appear in the interstitium. The first two signs to appear on the upright chest film are that the lower lobe vessels become indistinct and the upper lobe vessels begin to dilate. In normal appearance of the lower lobe vasculature, vessel edges are sharp, multiple secondary branches are clearly visible, and the average size of vessels in the middle part of the lung between the hilum and cortex is 4 to 8 mm. At least five to eight arteries can be seen at the right base. This effect is predominantly a result of gravity in the upright person, giving greater blood flow and blood volume to the lower lobes.

As left atrial pressure rises, the hilar and lower lobe vasculature becomes indistinct and the edges are less sharp. Fluid begins to accumulate in the interstitium. The number of visible side branches decreases, perhaps because of a silhouette sign as water in the interstitium partially obscures the adjacent vessel wall. In response to the higher venous pressure, the upper lobe vessels handle the blood that is meeting increasing resistance as it enters the left atrium. You will recognize this increased blood flow to the upper lobes by the increased visibility of numerous upper lobe arteries and veins (Fig. 1-37). The width of these structures, normally 1 to 2 mm in the middle part of the lung, increases to 2 to 4 mm. The redistribution now is reflected by an increase in both the size and number of vessels in the apices. The development of pulmonary venous hypertension is a continuum in the gradient of vessel size from apex to base. The normal distribution of small apical and large basilar vessels becomes balanced with equal size in both locations; at higher pressures this reverses and the upper lobe vessels are larger. A CT scan of a supine person with pulmonary venous hypertension will show large anterior vessels and smaller posterior vessels. Roughly the same branching generation from the main pulmonary artery should be used when comparing the anterior and posterior arteries (Fig. 1-38).

FIGURE 1-37 Pulmonary venous hypertension. A, The upper lobe arteries and veins are dilated out to the cortex and are the same size as the lower lobe vessels. B, The dilated upper lobe arteries are larger than their adjacent bronchus. Many more vessels are now visible. C, The lower lobe arteries and veins are indistinct. Several Kerley B lines (arrows) are visible in the subpleural space.

FIGURE 1-38 Computed tomography scan of pulmonary venous hypertension. The anterior vessels are larger than the corresponding posterior vessels in this supine scan. Kerley B lines are adjacent to the right lung pleura posteriorly and a linear subpleural opacity in the posterior left lung (arrows).

There are other signs of interstitial lung water that help confirm the diagnosis of pulmonary venous hypertension. In the cortex of the lung, Kerley B lines appear and represent thickening of the interlobular septum (Fig. 1-39). Kerley A lines—3- to 5-cm lines about 1 mm thick and extending from the central part of the lung—represent distended lymphatics (Fig. 1-40). The perihilar haze probably represents a combination of distended lymphatics, alveolar transudate, and interstitial thickening in lung parenchyma that lies anterior and posterior to the hilum. Thickening of the interlobular fissures and accumulation of subpleural fluid represent excess fluid and distention of the interstitial space and lymphatics. The end-on appearance of the bronchus and its adjacent pulmonary artery also changes in pulmonary venous hypertension. The bronchial wall becomes thickened and less distinct (“cuffed”) and the pulmonary artery dilates (Fig. 1-41).

FIGURE 1-39 Kerley B lines. Bilateral linear opacities in the costophrenic sulci represent distended interlobar septa. These lines may extend along the lateral wall nearly to the apex. Mitral stenosis has enlarged the left atrium and distorted the right side of the heart. A double density (arrow) along the left heart border is the interface of the large left atrium with the lung. The convex main pulmonary artery indicates pulmonary artery hypertension.

FIGURE 1-40 Kerley A lines. Central linear opacities (arrows) that are perihilar and do not conform with fissures are distended lymphatics.

FIGURE 1-41 High-resolution computed tomography of cardiac interstitial edema. A, The secondary pulmonary lobules are outlined by the thickened interstitium in this patient with emphysema. The bronchovascular bundles (arrows) have a pulmonary artery larger than the adjacent bronchus. B, A basal section shows thickening of the major fissures with dependent posterior pleural effusions. The secondary lobules are visible because of a thickened interlobar septum. The bronchial walls are thickened, which is the plain chest film correlate of “cuffing.”

As interstitial edema proceeds to alveolar edema, roseate opacities begin to appear in the perihilar region and spread peripherally to form a butterfly pattern. This does not involve the lung cortex except in extreme cases. When the opacities involve a significant part of the lung cortex and its adjacent pleura, other disease processes, such as pneumonia and adult respiratory distress syndrome, are more likely explanations for the cortical distribution. The edema caused by a cardiac disease typically is symmetrical and perihilar and is more severe in the lung bases than in the apices. The distribution of cardiac pulmonary edema can be quite variable and asymmetric but is never completely unilateral. Asymmetric pulmonary edema is usually more severe in the right lung. These patients are often lying with their right side down so the distribution of pulmonary edema often corresponds to the gravity gradient. Patients who develop mitral regurgitation during myocardial infarction rarely may also have pulmonary edema, predominantly in the right upper lobe. The jet of mitral regurgitation is directed into the right upper pulmonary vein and augments the forces in that lung that promote fluid retention.

Pleural and pericardial effusions develop in patients with left heart failure. In edema, the subpleural interstitial pressure rises sufficiently to create a net pressure into the pleural space. Generally, the pulmonary venous pressure needs to exceed 20 mm Hg to have visible pleural effusions. Isolated elevation of pulmonary arterial pressure does not produce pleural effusions.

The width of the vascular pedicle is an indirect but reliable sign of increased intravascular fluid. The width is measured just above the aortic arch from the left subclavian artery on the left side to the superior vena cava on the right side (Fig. 1-42). Dilatation of this pedicle and the adjacent azygos vein is increased in overhydration, renal failure, and chronic cardiac failure. In contrast, the vascular pedicle is usually unchanged in capillary permeability edema.

FIGURE 1-42 Width of the vascular pedicle as an indicator of fluid status. A, The wide vascular pedicle measured above the aortic arch reflects a dilated superior vena cava. The azygos vein (arrow) is also large. B, This patient also has pulmonary edema but a small vascular pedicle, probably reflecting vigorous diuretic therapy that reduced the intravascular volume. The residual pulmonary edema represents a therapeutic time lag.

The time course of the appearance and disappearance of pulmonary edema on the chest film is variable, but in slowly progressing clinical situations, there is a rough correlation with the pulmonary capillary wedge pressure. When the wedge pressure is greater than 20 mm Hg, there are always detectable signs of pulmonary venous hypertension and pulmonary edema on the chest film.

There is only a fair correlation between redistribution of blood flow with dilatation of the upper lobe vessels and pulmonary capillary pressure between 12 and 20 mm Hg. Because the osmotic pressure of plasma protein is 25 mm Hg, it is reasonable to expect alveolar edema when the pulmonary capillary wedge pressure exceeds this number; however, alveolar opacities can be seen with pressures of only 20 mm Hg. Pulmonary edema may be visible within a few minutes after the onset of acute mitral regurgitation or left heart failure. As the pulmonary edema resolves, there may be a therapeutic lag during which the wedge pressure returns to normal while the pulmonary edema persists. This lag may exist from several hours to several days. Although it is common to compare interpretation of the pulmonary edema on the chest film with the pulmonary capillary wedge pressure, these two observations measure different parameters and therefore are not appropriate standards of comparison. The pulmonary capillary wedge pressure measures the instantaneous pulmonary venous and left atrial pressures. The radiologic signs of pulmonary edema are an integrated history of the production and resorption of lung water. Particularly in the resorption phase, these signs more accurately mirror the amount of lung water present rather than the pulmonary venous pressure. A patient with an acute myocardial infarction that has a chest film showing pulmonary edema and a normal pulmonary wedge pressure has stiff and noncompliant lungs because of the unresorbed interstitial fluid.

Box 1-9 lists the cardiac causes of pulmonary edema.

Anatomy and Relation to the Left Superior Vena Cava

The coronary sinus enters the right atrium anterior to the origin of the inferior vena cava. The eustachian valve of the inferior vena cava and the thebesian valve of the coronary sinus join to form a ridge of tissue between them. The coronary sinus extends behind the heart and becomes the great cardiac vein in the left atrioventricular groove. When a left superior vena cava is present, it joins the great cardiac vein about 2 cm from the right atrium to continue as the coronary sinus.

Location from Catheter Position

On the frontal chest film, a catheter ending in the coronary sinus usually cannot be distinguished from one ending in the body of the right ventricle. For this reason, you should use a lateral and a frontal view when placing a catheter or pacing wire into the right ventricle. A power injection suitable for right ventriculography has enough force to rupture the coronary sinus into the pericardium. A lateral view identifies the posteriorly placed coronary sinus line from the right ventricular one (Fig. 1-51).

FIGURE 1-51 Coronary sinus and right ventricular wires. A, The dual pacing wires have a similar course on the frontal film. B, The lateral view separates the anterior right ventricular (RV) electrode from the posterior coronary sinus (CS) electrode.

Mediastinal Position

A persistent left superior vena cava is a relatively common venous anomaly that usually connects to the right atrium. Rarely, it may connect to the left atrium and is then associated with the heterotaxy syndrome. The left superior vena cava begins at the junction of the left subclavian and jugular veins and descends in front of the aortic arch. It then may pass in front of the left pulmonary artery or go between the pulmonary artery and vein and connect with the left hemiazygos vein before entering the pericardium. The left superior vena cava joins with the great cardiac vein to become the coronary sinus (Fig. 1-52). Right and left superior venae cavae, as with most venous anomalies, have numerous variations. Either the right or left superior vena cava may be absent, or both may persist (Fig. 1-53). The innominate connecting vein rarely is absent.

FIGURE 1-52 Left superior vena cava. A, On a magnetic resonance image at the level of the aortic arch, the left superior vena cava (arrow) is adjacent to the left pulmonary artery in this patient with truncus arteriosus. Although an anomalous pulmonary vein from the left lung may be in this position, lower slices (B) show its course (arrow) near the left pulmonary artery before it connects to the coronary sinus.

FIGURE 1-53 Bilateral superior venae cavae. Injection into the right superior vena cava backfills the connecting innominate vein to the left superior vena cava.

Catheter Course

Although a left superior vena cava usually is discovered inadvertently on a chest film when a left-sided mediastinal catheter is noted, it can be used for central line placement and entry into the heart. The line from the left superior vena cava enters the right atrium and is redirected through the tricuspid valve (Fig. 1-54).

FIGURE 1-54 Left superior vena cava. Internal cardiovascular defibrillator with electrodes in a left superior vena cava and the right ventricle.