Canine and Feline Cardiovascular System

CHAPTER 35 

Canine and Feline Cardiovascular System

Robert Bahr

R

adiographing the cardiovascular system is indicated when staging a patient with suspected cardiac disease, deciding about cardiac therapy, and monitoring response to therapy or progression of cardiac disease. Unfortunately, radiographs are not very accurate for assessing either cardiovascular function or morphology because of the wide range of the normal cardiac appearance in dogs, the effect of radiographic positioning on the appearance of the cardiac silhouette,1 and the fact that many physiologic changes are not accompanied by morphologic changes. See Chapter 28 for a discussion of the effect of positioning on the appearance of the normal cardiac silhouette. With regard to body habitus, muscular dogs or those with a barrel-shaped thorax have a cardiac silhouette that looks large. Conversely, the normal cardiac silhouette in breeds with a laterally compressed but deep thoracic cavity, such as greyhounds and collies, can look abnormally small (Fig. 35.1). Thus the body habitus of the dog should always be considered when the heart is evaluated radiographically. If any suspicion of a cardiac abnormality exists, because of either radiographic appearance or clinical or historical information, then echocardiography is indicated.2 Cats have much less patient-to-patient variation in the radiographic appearance of the heart, and there is much less of an effect of radiographic positioning. However, body habitus will still alter the appearance of the cardiac silhouette due to fat collections around the heart. Radiographic positioning can have a profound effect on the appearance of the cardiac silhouette (see Chapter 28).1 Perhaps most important is the difference in cardiac silhouette appearance in ventrodorsal (VD) versus dorsoventral (DV) radiographs. In DV radiographs, the diaphragm is displaced cranially, which will physically deviate the heart cranially, and usually into the left hemithorax. The magnitude of this displacement is more pronounced in medium and large dogs than in cats or small dogs (Fig. 35.2).1,3 Alternately, in large-breed dogs, the cardiac silhouette will be magnified in VD views when compared to DV views due to its increased distance from the imaging plate. It is important to realize that the cardiac silhouette is not composed only of the heart. The pericardium, any fluid or tissue in the pericardial space, and any tissue or fluid in the mediastinum immediately adjacent to the heart will blend with the heart, thereby contributing to the overall size and shape of the cardiac silhouette. This principle is perhaps most important when attempting to assess heart size in obese patients because fat in the mediastinum adjacent to the heart increases the size of the cardiac silhouette. Occasionally, this fat will be visible as a region of decreased opacity immediately adjacent to the heart (Fig. 35.3). Despite these normal variations, a starting point for radiographic evaluation is necessary and what follows is a discussion of the qualitative radiographic signs of enlargement for each heart chamber, the aorta, and the caudal vena cava. 684

Although qualitative assessment of the cardiac silhouette is the preferred method, a quantitative method of cardiac measurement, called the vertebral heart scale (VHS) was devised to take the effect of body habitus on the size of the cardiac silhouette into account.4 In the VHS method, the length of the long and short axis of the heart is measured, summed, and scaled against the length of the vertebral bodies dorsal to the heart, beginning with T4, to quantify heart size in terms of vertebral number. Based on 100 clinically normal dogs, the mean normal VHS was 9.7 vertebrae, with a standard deviation of 0.5 vertebrae. By definition, 95% of any normal population lies within the mean plus or minus two standard deviations of the mean. Therefore, the normal VHS ranges from 8.7 to 10.7 vertebral body lengths. This is too much variation for the VHS to be of valid diagnostic use in individual dogs. Additionally, the combination of respiratory and cardiac cycle can lead to a difference of nearly 1.0 vertebral body lengths in an individual dog (Video 35.1).5 This adds to the already large amount of normal variation present in the normal VHS. Evidence supports the VHS not being superior to subjective radiographic assessment of heart size.6,7 There is also variation between readers in the transformation of long- and short-axis dimensions into VHS units.8 Perhaps the best use of the VHS is to compare cardiac size on serial radiographs of the same patient made over time to monitor disease progression or response to treatment.9,10 Subjective radiographic assessment of the heart will be of most value when the cardiac abnormalities are pronounced. Therefore, cardiac radiography will be most useful (1) as a screening tool for assessing marked cardiac abnormalities, (2) for evaluation of the pulmonary circulation, (3) to assess whether cardiac decompensation has occurred, and (4) to evaluate response to therapy. Any suspected cardiac abnormality must be interpreted in light of signalment and physical findings. This chapter provides examples of moderate to severe chamber enlargement and describes the features of some of the more common acquired and congenital cardiac anomalies. For ease of recognition of certain cardiac abnormalities in the DV or VD radiograph, the cardiac silhouette can be considered to represent a clockface. The origin of bulges on the cardiac silhouette caused by dilation of different parts of the heart or great vessels can be predicted by using this clockface analogy (Fig. 35.4).

RADIOGRAPHIC SIGNS Radiographic Signs of Specific Cardiac Chamber Enlargement Left Atrium

Enlargement of the left atrium is the most frequently encountered cardiac enlargement in the dog due to the high prevalence of myxomatous mitral valve disease. Left atrial enlargement is

CHAPTER 35  •  Canine and Feline Cardiovascular System

A

C

E

B

D

F Fig. 35.1  Lateral and ventrodorsal (VD) thoracic radiographs from a normal borzoi (A and B), a normal

Labrador retriever (C and D), and a normal pug (E and F), illustrating the effect of body habitus on the appearance of the cardiac silhouette.

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B Fig. 35.2  Ventrodorsal (VD; A) and dorsoventral (DV; B) thoracic radiographs of a normal dog. In the DV, the heart appears wider and is displaced into the left hemithorax. This displacement, due to cranial excursion of the diaphragm when the dog in in sternal recumbency, if often misinterpreted as abnormal.

AA

MPA

LAu RA

Fig. 35.4  The heart in a ventrodorsal (VD), or dorsoventral (DV), view Fig. 35.3  Lateral radiograph of the thorax of a Doberman pinscher. There is fat around the heart leading to the cardiac silhouette being larger than the heart itself. The less opaque fat creates contrast for visualization of the actual margin of the heart (black arrows). This dog also has left atrial dilation that causes a concavity on the dorsocaudal heart border (white arrow).

almost always caused by dilation. In addition to mitral valve disease, left atrial dilation can occur with left-to-right pulmonary overcirculation causing volume overload, but this is less common. In the lateral view, dilation of the left atrium in the dog causes a change in shape of the dorsocaudal aspect of the cardiac silhouette. Rather than curving normally toward the tracheal bifurcation, the dorsocaudal heart border tends to course more in a dorsal or dorsocaudal direction, with straightening or formation of a slight concavity on the caudal margin of

illustrating the clockface analogy. Locations of dilation of the left auricle (LAu), main pulmonary artery (MPA), aortic arch (AA), and right atrium (RA) are shown. LAu, Bulge at 2 to 3 o’clock; MPA, bulge at 1 to 2 o’clock; AA, bulge at 11:30 to 12:30 o’clock; RA, bulge at 9:30 to 11:30 o’clock.

the heart (Fig. 35.5; see Fig. 35.3). This shape change has been referred to as loss of the caudal cardiac waist. Left atrial dilation also causes dorsal displacement of the tracheal bifurcation. Some dogs with a dorsally displaced tracheal bifurcation will also have narrowing of one or both principal bronchi (Fig. 35.6). This narrowing is most likely not due solely to impingement from the subjacent dilated left atrium but more likely to coexisting bronchial chondromalacia with dynamic bronchial collapse. The enlarged pulsating left atrium will be more likely to contribute to narrowing of a malacic bronchus than a normal bronchus, and the malacic bronchus will also be subject to dynamic airway collapse (Video 35.2). Dogs with left atrial dilation and bronchial narrowing from

CHAPTER 35  •  Canine and Feline Cardiovascular System bronchomalacia will typically exhibit a cough, which often misleads the clinician to conclude erroneously that the patient is in heart failure. In fact, in an evaluation of 206 dogs with mitral valve disease, there was not a statistical association between the presence of pulmonary edema and coughing.11 Therefore, causes of a cough other than heart failure should always be considered in dogs with a heart murmur. Dilation of the left atrium may also cause divergence of the principal bronchi in the VD or DV view (Fig. 35.7, see Fig. 35.6). This appearance is similar to principal bronchial

Fig. 35.5  Lateral radiograph of a dog with a dilated left atrium. The

dilated atrium has created a concave shape change on the caudal margin of the heart (white arrow). This is a very common sign of left atrial dilation in the dog.

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displacement occurring secondary to tracheobronchial lymph node enlargement as described in Chapter 33, with the normal acute angle between the principal bronchi appearing wider because of the interposed enlarged lymph nodes. An important difference here is that the enlarged left atrium will be ventral to the tracheal bifurcation in the lateral view, whereas the enlarged tracheobronchial lymph nodes will be dorsal. A massively dilated left atrium may also lead to a region of increased opacity superimposed over the cardiac silhouette in the VD or DV view that creates the appearance of a double wall. This is caused by a summation effect of the enlarged left atrium being projected on the remainder of the heart (Fig. 35.8). Dilation of the left atrial appendage (auricle) occurs less frequently than dilation of the left atrium and, when present, appears as a focal bulge along the left cardiac border in the 2 to 3 o’clock position according to the clockface analogy (see Fig. 35.7). An extremely enlarged left atrium can also result in lateral displacement of the left auricle, resulting in a similar appearance without the auricle actually being dilated. The above descriptions of left atrial enlargement apply to the dog. Left atrial enlargement in the cat is much less conspicuous radiographically. In many cats with echocardiographically proven left atrial dilation, there is no radiographic evidence of such. In some cats, a focal concave defect will be present on the dorsocaudal aspect of the cardiac silhouette, but this is not as common as in the dog (Fig. 35.9). Another change that occurs with left atrial dilation in the cat is an increase in width of the cardiac base in the VD or DV view. Cats with marked left atrial dilation can have a so-called “valentine-shaped” cardiac silhouette in the VD or DV view due to pronounced enlargement of the cardiac base region (Fig. 35.10). A valentine-shaped cardiac silhouette is often misinterpreted as evidence of biatrial enlargement, but in most cats a valentine-shaped appearance is due to pronounced left atrial dilation without enlargement of the right atrium.12

B Fig. 35.6 Lateral (A), and dorsoventral (DV; B), radiographs of a dog with marked left atrial dilation. In A,

there is dorsal displacement of the trachea and narrowing of the left principal bronchus (black arrow). The left cranial lobe pulmonary vein is also distended (white arrow) compared with the corresponding artery, consistent with pulmonary venous hypertension secondary to mitral insufficiency. In B, the dilated left atrium appears as a region of increased opacity caudal to the tracheal bifurcation (black arrows) causing splaying of the principal bronchi around it.

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Fig. 35.7  Dorsoventral (DV) radiograph of a dog with pronounced left atrial dilation. The enlarged left atrium has caused abaxial displacement of the principal bronchi (black arrows). There is also a bulge on the left aspect of the cardiac silhouette that is consistent with left auricular dilation or lateral displacement of the left auricle by the dilated left atrium (white arrows).

Left Ventricle The following changes apply to both the cat and dog. The left ventricle may enlarge as a result of hypertrophy or dilation. Concentric hypertrophy, a likely response to increased afterload such as with aortic stenosis, mainly occurs at the expense of lumen volume and may lead to no enlargement or nonspecific enlargement. Eccentric hypertrophy is likely a response to increased preload, as in patent ductus arteriosus or mitral insufficiency, and can cause visible left ventricular enlargement. Severe, eccentric hypertrophy that results in elongation of the left ventricle can lead to elevation of the entire intrathoracic trachea in the lateral view, thus narrowing the angle between the trachea and the thoracic vertebrae. In the VD or DV view, the cardiac apex may appear more blunted, and the left heart border may appear to be more rounded than its normally straight appearance. Dilation of the left ventricle is a likely response to chronically increased preload and is often associated with cardiac failure. Dilation of the left ventricle may either contribute to an overall appearance of generalized cardiomegaly or result in the elongation of the left ventricle, causing generalized tracheal elevation. Debate has occurred, even among experienced radiologists, about the accuracy with which either left ventricular hypertrophy or dilation can be diagnosed from survey radiographs, so it is safest to describe the change as left ventricular enlargement and use echocardiography to differentiate the cause.

Right Atrium

Radiographic detection of an enlarged right atrium is uncommon in both dogs and cats but is occasionally seen in dogs with tricuspid dysplasia. As with the left atrium, enlargement of the right atrium is usually caused by dilation. When visible in the lateral view, right atrial dilation causes a bulge or mass effect in the craniodorsal aspect of the cardiac silhouette. However, dilation of the aortic arch and main pulmonary artery can also cause this radiographic appearance in the lateral view. In the VD or DV projection, an increased bulge in the right

B Fig. 35.8 Lateral (A) and dorsoventral (DV; B) radiographs of a dog with massive dilation of the left atrium. In A, there is a large mass effect in the dorsocaudal region of the cardiac silhouette and a concave shape change of the caudal cardiac margin (white arrows). When radiographed for the DV view, the dilated left atrium becomes superimposed on the remainder of the heart, creating a summation shadow that creates a double-wall effect. In B, the black arrows depict the margin of the enlarged left atrium.

heart border from the 9 o’clock to 11 o’clock position may be present (Fig. 35.11). Isolated right atrial dilation is very rare in the cat.

Right Ventricle

The right ventricle may enlarge as a result of hypertrophy or dilation. The changes described here apply mainly to the dog as identification of right ventricular enlargement in the cat is not common. The right ventricle undergoes hypertrophy in response to increased afterload, as with pulmonic stenosis or pulmonary hypertension, which is commonly seen in heartworm disease. Hypertrophy mainly occurs at the expense of lumen volume and may lead to no or minimal change in the appearance of the cardiac silhouette. However, radiographs are more sensitive for detection of right ventricular hypertrophy in dogs than for left ventricular hypertrophy. This is likely related to the normally

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Fig. 35.9  Lateral radiograph of a cat with dilation of the left atrium. There is a concave depression on the dorsocaudal aspect of the cardiac silhouette (white arrow), similar to that seen in many dogs. This is less commonly observed in cats with left atrial dilation than in dogs but is occasionally seen.

may be enlarged. Dilated cardiomyopathy is a common cause of generalized cardiomegaly. Subjectively, the cardiac silhouette appears larger than expected, but specific chamber enlargement may or may not be evident. Generalized cardiomegaly may also be misinterpreted because of underinflation of the lungs, making the thoracic cavity appear smaller than normal. This, in turn, makes the heart appear larger relative to the amount of aerated lung surrounding it. This was discussed in Chapter 28. Echocardiography should be used to confirm a cardiac abnormality when generalized cardiomegaly is suspected radiographically.

thinner wall of the right ventricle, with hypertrophy causing more obvious changes in cardiac size and shape. Because the right ventricle is normally in contact with the sternum, right ventricular enlargement, whether from dilation or hypertrophy, often causes an increased sternal contact in the lateral view (Fig. 35.12B). In the average dog, the amount of cardiac contact with the sternum ranges from 2.5 to 3 intercostal spaces; thus sternal contact in excess of 3 intercostal spaces is consistent with right ventricular enlargement. Some deep-chested breeds, such as Doberman pinschers and Irish wolfhounds, may normally have only approximately 1.5 to 2 intercostal spaces of sternal contact, so 2.5 to 3 spaces would be consistent with right ventricular enlargement for those breeds. Likewise, some barrel-chested breeds, such as the bulldog, can normally have more than 3 to 3.5 intercostal spaces of contact. Right ventricular hypertrophy can also lead to the cardiac apex being displaced dorsally from the sternum in lateral views (see Fig. 35.12C). In VD or DV views, a hypertrophic right ventricle appears more rounded and protrudes farther into the right hemithorax than normal, giving the cardiac silhouette a pronounced reversed letter D shape (see Fig. 35.12A). However, care should be taken to not over-read the more rounded appearance of the right ventricle and judge it to indicate a “reversed letter D shape,” because essentially all normal dog hearts have a somewhat rounded shape to the right ventricle with the left ventricle being straighter in shape.

The caudal vena cava is variable in size depending on the phase of respiration and cardiac cycle. It can be judged to be enlarged only if it is consistently larger in diameter than the length of the fifth or sixth thoracic vertebral bodies of the spine as measured in the lateral view. Another measure of caudal vena cava size is that enlargement can be inferred if the diameter of the caudal vena cava is more than 1.5 times the diameter of the descending aorta.13 The caudal vena cava can enlarge in response to increased central venous pressure, but the size of the caudal vena cava is not an accurate way to evaluate central venous pressure. Valid inferences on cardiovascular disease cannot typically be made on the basis of the size of the caudal vena cava only.

Generalized Cardiomegaly

Aorta

Generalized enlargement of the cardiac silhouette can result from combinations of chamber enlargement or all four chambers

Radiographic Signs of Major Vessel Enlargement Caudal Vena Cava

Widening of the precardiac mediastinum, as seen in the VD or DV views, can indicate dilation of the aortic arch. A focal

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Fig. 35.10  Dorsoventral (DV) radiograph of a cat with marked enlargement of the left atrium. There is an increase in width of the cardiac base region (black arrows). This is seen more often with left atrial dilation in the cat than the concave depression on the caudal cardiac margin. When pronounced, this widening in the base region is termed a “valentine-shaped” cardiac silhouette.

bulge in the descending aorta in VD or DV views can be seen in patients with aortic stenosis and patent ductus arteriosus (Fig. 35.13). In lateral views, an enlarged aortic arch can create increased mass at the cranial aspect of the cardiac silhouette (see Fig. 35.13).

Some older cats will have a tortuous aorta in the lateral view, with a more vertical aortic arch orientation. The aortic arch then curves upward and caudally, assuming a serpentine contour as it progresses toward the diaphragm (Fig. 35.14A). In the DV or VD views, this aortic contour may be projected

CHAPTER 35  •  Canine and Feline Cardiovascular System

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B

Fig. 35.11  Left lateral (A) and dorsoventral (DV; B) radiographs of a Labrador retriever with tricuspid dysplasia. A bulge is visible in the region of the right atrium consistent with right atrial enlargement. The extent of ventral and caudal extension of the enlarged right atrium is often greater than one might expect.

B

A

C Fig. 35.12  Right ventricular hypertrophy. A, Ventrodorsal (VD) view of a dog with pulmonic stenosis. Right ventricular hypertrophy has resulted in increased cardiac mass on the right side that creates an appearance of a reverse, or backward, letter D. Enlargement of the main pulmonary artery is also visible in the 1:00 to 2:00 o’clock position. B, Right lateral radiograph of a dog with pulmonic stenosis. The increased mass of the right ventricle has resulted in increased contact of the heart with the sternum over a longer distance than normal. C, Right lateral radiograph of a dog with heartworm infection. The increased mass on the right side of the heart has caused elevation of the cardiac apex from the sternum. Mild elevation of the cardiac apex from the sternum may be present in normal dogs in a left lateral view, but normal apex displacement should never be this marked in the right lateral view.

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B Fig. 35.13 Lateral (A) and dorsoventral (DV; B) radiographs of a dog with aortic stenosis. In A, the dilated aortic arch appears as a bulge on the craniodorsal aspect of the cardiac silhouette (black arrow). In B, the enlarged aortic arch appears as an opacity at the cranial, and slightly left, aspect of the cardiac silhouette (black arrows).

B

A

Fig. 35.14  A, Lateral radiograph of a cat with a tortuous aorta. In A, the aortic arch is more vertical than normal, and the descending aorta is tortuous. B, In another cat with a tortuous aorta, the aortic arch is located to the left of midline (black arrows) and when projected end-on can be misinterpreted as a pulmonary mass.

away lateral to the mediastinum on the left side and be misinterpreted as a pulmonary nodule when projected end-on (see Fig. 35.14B).14 A tortuous aorta is usually clinically insignificant in aged cats.

Main Pulmonary Artery

The main pulmonary artery is not seen normally as a separate structure, but when it dilates sufficiently in dogs, it will appear as a focal bulge in the 1:00 o’clock position in VD or DV views (Fig. 35.15). A dilated main pulmonary artery is not recognized routinely in lateral views. Common causes of main

pulmonary artery dilation include pulmonary hypertension, as from heartworm infection, and turbulence, as from pulmonic stenosis or patent ductus arteriosus. Enlargement of the main pulmonary artery is rarely recognized in cats. This is not because it does not occur but because the enlarged artery does not extend peripheral to the cardiac silhouette in cats as in dogs.

Radiographic Signs of Pulmonary Arterial and Venous Changes

Radiographic assessment the heart is incomplete without also evaluating the main pulmonary artery, as well as the peripheral

CHAPTER 35  •  Canine and Feline Cardiovascular System pulmonary arteries and veins. Therefore, knowing where to look for and how to differentiate parenchymal pulmonary arteries from veins is crucial. In the lung, parenchymal vessels and airways are arranged in an artery-bronchus-vein triad, with the bronchus always being positioned between the pulmonary artery and pulmonary vein. In lateral projections, when pulmonary arteries can be seen as separate structures from pulmonary veins, the arteries are dorsal and veins are ventral to the intervening bronchus.15 This applies mainly to cranial lobar arteries and veins, because the caudal lobar arteries and veins are superimposed in lateral projections and caudal lobar pulmonary arteries are difficult

Fig. 35.15  Dorsoventral (DV) radiograph of a dog with dilation of the main pulmonary artery (black arrows).

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to differentiate from veins in the lateral view. The right cranial lobar pulmonary artery and vein are valuable reference vessels, because they are best seen as individual structures when the animal is in left lateral recumbency (Fig. 35.16). In left recumbency, the right cranial lung lobe is better inflated resulting in better definition of the right cranial lobe pulmonary artery and veins. Although the left cranial lobe will be better inflated in right recumbency, the left and right pairs of cranial lobe vessels are almost always overlapped in that particular view, making their assessment much more difficult (see Fig. 35.16). It is much less common to be able to compare the left cranial lobe artery and vein as individual vessels due to their more dorsal position and cranial course. In a VD or DV projection, pulmonary arteries and veins are most conveniently compared in the caudal lobes where pulmonary arteries are lateral to pulmonary veins, with the bronchus interposed. The caudal lobe pulmonary vessels are better seen in the DV view than in the VD view, because the lungs are better inflated when the dog is in sternal recumbency for a DV radiograph (Fig. 35.17). In addition to the improved inflation of the caudal lung lobes in sternal recumbency, the caudal lobar vessels are more perpendicular to the diverging x-ray beam than they are with the patient in dorsal recumbency for VD radiography. Paired arteries and veins are less well seen in the cranial lobes or right middle lobe in either DV or VD views, although occasionally the cranial lobar vessels can be evaluated. Although a bronchus always lies between a paired pulmonary artery and pulmonary vein, the entire distance between these paired vessels is not always entirely occupied by the bronchus. The exact position of the bronchus and its actual size can only be determined if the bronchial wall either is mineralized or thickened because of disease (see Fig. 35.17B). Peripheral pulmonary arteries should be approximately the same size (matched in size) as their associated pulmonary vein.15 With regard to absolute size of the caudal lobe pulmonary artery and vein, a convenient comparison is the relative size of a caudal lobe pulmonary artery to the thickness of the ninth rib in the VD or DV view where they intersect. The summation

B Fig. 35.16  Close-up from right (A) and left (B) lateral radiographs of a normal dog. In the right lateral view A, the left and right cranial lobe arteries and veins are superimposed and distinguishing the right cranial lobe artery from the right cranial lobe vein is impossible. In the left lateral view B, the right cranial lobe artery (white arrows) and right cranial lobe vein (black arrows) are more clearly seen. The ability to distinguish the right cranial artery from the vein is typically easier in a left lateral radiograph. Note the similar size of the artery and vein in B.

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A

B Fig. 35.17  A, Dorsoventral (DV) radiograph of a normal dog. The right caudal lobe pulmonary artery (single

black arrow) is lateral to the bronchus, whereas the right caudal lobe pulmonary vein is medial (double black arrows). B, Close-up view of the right caudal lobe area giving another view of the right caudal lobe pulmonary artery and vein. On close inspection, the mineralized wall of the caudal lobe bronchus can be seen between the artery and vein. Note that in this dog, as in most, the bronchus does not occupy the entire space between the artery and vein. When the bronchus is not mineralized, inferring that it occupies the entire distance between its associated artery and vein is inaccurate.

A

A

Box  •  35.1

A R9

R9 R9

Normal

Artery enlarged

Artery small

Fig. 35.18  The principle of using the summation shadow created by

overlap of a caudal lobe pulmonary artery (A) with the right ninth rib (R9) to assess the absolute size of the pulmonary artery. In normal dogs, the summation shadow will have equal sides (left panel). When the artery is enlarged (center panel), the summation shadow will be longer in the horizontal direction. When the artery is small (right panel), the summation shadow will be longer in the vertical direction.

shadow created by overlap of a caudal lobe pulmonary artery and the ninth rib should normally have sides of equal length, meaning the vessel and rib are the same size. If the pulmonary artery is enlarged, the long axis of the summation shadow will be in a horizontal direction. If the pulmonary artery is small, the long axis of the summation shadow will be oriented in a vertical direction (Fig. 35.18). Peripheral pulmonary arteries and veins should normally be approximately the same size (matched). Pulmonary vessels

Conditions That May Increase the Size of Both Pulmonary Arteries and Pulmonary Veins Left-to-right shunt Patent ductus arteriosus Ventricular septal defect Atrial septal defect Peripheral arteriovenous fistula Iatrogenic intravenous fluid overload Fluid retention secondary to decreased cardiac output

are dynamic, however, and their size can change relatively quickly, being a function of intraluminal pressure and volume. Dehydration from diuretic administration or increased intravascular volume from overzealous intravenous fluid administration can lead to rapid changes in vessel size, so interpretation of vessel size must be made with knowledge of any recently administered medications or therapies. More meaningful information is gathered with sequential radiographic examinations, especially if therapies have changed recently. Certain diseases cause predictable changes in the size of either pulmonary arteries alone or pulmonary veins alone, or both simultaneously. Box 35.1 lists diseases where both pulmonary arteries and veins can be enlarged (Fig. 35.19). The

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B Fig. 35.19  A, Dorsoventral (DV) radiograph from a dog with a patent ductus arteriosus. The caudal lobe arteries and veins are both enlarged as a result of overcirculation of the pulmonary vascular system. Note the size of the summation shadow where the vessels cross the right ninth rib (black arrow) and compare to Fig. 35.17. The shape of these summation shadows indicates that both the right caudal pulmonary artery and vein are enlarged. B, Lateral thoracic radiograph of another dog with a patent ductus arteriosus where both the artery and vein of the right cranial lobe are enlarged.

degree of the enlargement depends on the severity and duration of the inciting cause. Differentiating these diseases depends on evaluating the history, physical examination findings, and findings from echocardiography. Pulmonary artery enlargement without venous enlargement may occur with the conditions listed in Box 35.2. The most common cause of pulmonary arterial enlargement without pulmonary vein enlargement in the dog is pulmonary hypertension secondary to heartworm infection (Fig. 35.20). In heartworm disease, arterial enlargement occurs because of pulmonary hypertension resulting from lesions in the vascular tunica intima or tunica media or because of thromboembolic disease, or both. Any or all of the pulmonary arteries may become enlarged, but the most commonly enlarged pulmonary arteries in spontaneous heartworm disease are the caudal lobar arteries with a predilection for enlargement of the right more than the left.16 In cats with heartworm disease, enlargement of the main pulmonary artery is usually not visible radiographically.17-19 The main pulmonary artery does enlarge in cats with heartworm disease, but it is more medial than in dogs and its border is therefore not visible on survey radiographic images. The peripheral pulmonary arteries can become visibly enlarged in cats with heartworm disease (Fig. 35.21). Enlargement of the caudal lobar arteries on the VD view, with normal-sized caudal pulmonary veins, can represent the earliest radiographic change seen in spontaneous feline heartworm disease. Because feline pulmonary lobar arterial enlargement can resolve and reappear over a span of 4 to 5 months in experimental heartworm infection, vascular changes cannot be relied on entirely when evaluating thoracic radiographs of cats for heartworm disease. A persistent bronchointerstitial pulmonary pattern also occurred in approximately 50% of cats experimentally infected with heartworm disease, appearing similar to the bronchial pattern seen in feline allergic/ inflammatory lung disease. The bronchial pattern persisted, even after the vascular changes had resolved. Thus cats

Box  •  35.2 Conditions That May Increase the Size of Pulmonary Arteries Without Associated Vein Enlargement Tunica intima proliferation or tunica media hypertrophy Dirofilariasis Angiostrongyliasis Aelurostrongylus (feline) Thromboembolic disease or primary thromboses Dirofilariasis Angiostrongyliasis Renal disease: Amyloidosis, glomerulonephritis Septicemia Pancreatitis Hyperadrenocorticism Severe chronic lung disease

with radiographic evidence of bronchial disease should be considered suspects for heartworm disease even in the absence of classic vascular changes.20 The diagnosis of feline heartworm disease is a challenge. Thoracic radiography and serum antibody tests are used to evaluate the index of suspicion while echocardiography and serum antigen tests are used for confirming infection.21,22 However, echocardiographic detection of heartworm infection may not be uniformly accurate, with better correlation related directly to worm burden.23 Heartworm disease is also the most common cause of pulmonary thromboembolism, due to arterial occlusion by dying worm emboli or blood clots. This results in an increase

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A

B

C

D Fig. 35.20 Lateral (A), close-up lateral (B), dorsoventral (DV; C), and close-up DV (D), radiographs of the

thorax of a dog with heartworm disease. In A, the right cranial lobe pulmonary artery is larger than the right cranial lobe vein, and there is an intense alveolar pattern in the dorsocaudal aspect of the lung. The opacity encircled (black circle) is an identification microchip. In B, the enlarged right cranial lobe pulmonary artery (black arrows) compared to the right cranial lobe vein (white arrows) is very conspicuous. In C, the main pulmonary artery is dilated, the right ventricle appears enlarged, and there are patchy alveolar opacities in both caudal lung lobes, more intense on the right. In D, the right caudal lobe pulmonary artery is tortuous (white arrows). The vein cannot be seen because of the alveolar pattern in the right caudal lobe. The alveolar pattern in this dog is likely caused by thromboembolism given its patchy intense distribution. That it is caused by an allergic reaction cannot be ruled out.

in pulmonary opacity that at first is a mixed heterogeneous pattern with a tendency to form a predominantly alveolar pattern later (Fig. 35.22). It is also possible for survey thoracic radiographs to have no evidence of pulmonary involvement in peracute thromboembolism. Although overt pulmonary infarction is possible with heartworm disease, it is rare. The differential diagnosis for pulmonary vein enlargement occurring without pulmonary arterial enlargement is listed in Box 35.3. Pulmonary vein enlargement is most commonly seen in dogs with mitral insufficiency because of pulmonary venous hypertension (Figs. 35.23 and 35.24). Diseases associated with decreased size of both the pulmonary arteries and veins are listed in Box 35.4 (Fig. 35.25). Regardless of cause, the lung fields in these diseases appear

hyperlucent because of a lesser contribution by the pulmonary arteries and veins to the overall soft tissue opacity of the lungs. Up to this point, only the size of pulmonary vessels has been considered. A change in shape of pulmonary vessels can also occur and is most commonly seen in dogs with heartworm disease where vessels become tortuous (see Figures 35.20 and 35.22D) and may also appear to terminate abruptly, which is termed truncation or pruning (Fig. 35.26). Pulmonary vascular margination should be relatively sharp. However, perivascular disease in adjacent lung results in either partial or complete loss of vascular conspicuity. This is caused by an accumulation of fluid, cells, or necrotic debris in either the interstitium or the alveoli immediately adjacent to the vessel, causing border effacement with the vessel wall and obscuring its margins (Fig. 35.27).

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Box  •  35.3 Conditions That May Increase the Size of Pulmonary Veins Without Associated Artery Enlargement Cardiac Volume or pressure overload Mitral insufficiency Mitral valvular endocardiosis Early left-to-right shunts (thinner walls of veins dilate more easily), including patent ductus arteriosus and ventricular septal defect Primary myocardial disease Myocardial failure (arrhythmias, fibrosis) Dilatory cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy

Noncardiac Dysfunction Fig. 35.21  Dorsoventral (DV) radiograph of a cat infected with heartworms. Both caudal lobe pulmonary arteries are enlarged (black arrows). Looking closely, smaller (normal) caudal lobe pulmonary veins are present medial to each artery. Enlargement of the main pulmonary artery is not seen in cats with heartworm disease, although it is likely present.

Left atrial obstruction Mass (neoplastic or inflammatory) at heart base Thrombosis within left atrium

Box  •  35.4 Congestive Heart Failure

Backward left-sided heart failure begins when increased end-diastolic filling pressure in the left ventricle is transmitted into the left atrium and then into the pulmonary veins creating pulmonary venous hypertension. Pulmonary venous hypertension results in pulmonary veins becoming larger than the corresponding lobar artery (see Figs. 35.23 and 35.24). Pulmonary venous hypertension is not evidence of heart failure. However, as pulmonary venous pressure continues to increase, this will ultimately result in transudation of fluid from the pulmonary capillaries into the lung interstitium, first causing a hazy, unstructured interstitial pulmonary pattern (interstitial pulmonary edema), followed by alveolar edema. It is also being recognized that pulmonary arterial hypertension is a common complication in dogs with left heart disease, mainly dogs with myxomatous mitral valve disease. Initially, pulmonary arterial hypertension develops as a consequence of pulmonary venous hypertension being transmitted backward through the pulmonary capillaries into the pulmonary arteries. Later there are morphologic changes occurring in the pulmonary capillaries as heart failure progresses, increasing resistance to blood flow resulting in further increases in pulmonary artery pressure.24 Radiographically, this could result in enlargement of both pulmonary arteries and veins in patients with left heart disease/failure when one might expect to find only pulmonary venous enlargement (Fig. 35.28). However, finding both enlarged pulmonary arteries and veins in canine myxomatous mitral valve disease is not common. Cardiogenic pulmonary edema often has a dorsocaudal distribution in dogs but any distribution is possible. A perihilar distribution is also possible but this is overemphasized. In small animals, the finding of a distinct perihilar distribution of cardiogenic pulmonary edema is not common. For example, in 61 dogs with pulmonary edema secondary to mitral regurgitation, only seven had a perihilar distribution of the

Conditions That May Decrease the Size of Pulmonary Arteries and Veins Right-to-left shunts Tetralogy of Fallot Ventricular septal defect with pulmonic stenosis Severe pulmonic stenosis with decreased cardiac output Hypovolemia Shock Dehydration

edema. Most dogs (43 out of 61) had focal increases in pulmonary opacity rather than a perihilar or generalized distribution.25 Lateral views are most likely related to summation artifact. Radiographic visualization of interstitial cardiogenic pulmonary edema is rare because it is short lived, and it does not create a marked increase in lung opacity. Interstitial pulmonary edema typically progresses to multifocal areas of alveolar pulmonary opacity, obscuring pulmonary vascular structures. In dogs, pulmonary edema is usually most obvious radiographically in the caudal lobes. Cardiogenic pulmonary edema could be expected to result in generalized homogeneous lung involvement, but this is not common. Cardiogenic pulmonary edema is more often patchy in cats (Fig. 35.29). The pattern of pulmonary edema distribution in dogs with mitral insufficiency has been associated with the direction of the regurgitant jet. A symmetric distribution was associated predominantly with a central mitral regurgitant jet, whereas an asymmetric distribution was usually associated with an eccentric jet.25 Some cats with left heart failure also have a component of pleural effusion in addition to pulmonary edema (see Fig. 35.29). Regardless of the distribution of cardiogenic pulmonary edema, it is important to evaluate the cardiac silhouette for evidence of enlargement.

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698

A

B

C

D

E

Fig. 35.22  Left lateral (A), close-up left lateral (B), ventrodorsal (VD; C), dorsoventral (DV; D), and close-up

DV (E) radiographs of a dog with heartworm disease. In A and B, note the enlargement of the right cranial lobe artery compared with the vein. In C, note the reversed D appearance of the cardiac silhouette, consistent with right ventricular hypertrophy. In D and E, note the enlargement of the right caudal lobe artery compared with the vein. These findings are typical of canine heartworm disease.

Right-sided heart failure usually includes some or all of the following radiographic signs: bilateral pleural effusion with varying degrees of secondary pulmonary atelectasis, ascites, and hepatosplenomegaly. If the heart is visible, some changes of right heart enlargement are likely to be present. The radiographic appearance of pleural fluid, abdominal fluid, and hepatosplenomegaly are covered elsewhere in this text.

Acquired Cardiovascular Lesions

Acquired cardiovascular lesions are much more common in clinical practice than are congenital lesions. The most common acquired lesions are mitral insufficiency, heartworm disease, and cardiomyopathy.

Mitral Insufficiency

Mitral insufficiency is the most common cause of acquired heart disease in small animal practice, primarily occurring in small-breed dogs.26 Radiographic signs can include various degrees of the following (see Figs. 35.5 to 35.8 and Figs. 35.23, 35.24, and 35.27): • Left atrial enlargement, attributable to dilation caused by volume overload from mitral valve regurgitation • Left ventricular enlargement, from dilation caused by volume overload because not as much blood is ejected from the left ventricle with each systole • Distended pulmonary veins if venous hypertension has developed

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A

C

A

B

Fig. 35.23 Lateral (A), dorsoventral (DV; B), and close-up DV (C) views of a dog with compensated mitral insufficiency. In A, the heart is enlarged, and the left atrium is dilated. In B, the heart is also enlarged, and the right caudal lobar pulmonary vein is enlarged compared with the artery. This can also be seen in a close-up (C) where the right caudal lobar vein (black arrows) is considerably larger than the artery (white arrows). This is an example of compensated mitral insufficiency. Pulmonary venous hypertension transmitted from the increased left atrial pressure causes the pulmonary vein enlargement, but there is no evidence of pulmonary edema to signify left-sided heart failure.

B Fig. 35.24  Lateral radiograph (A) and close-up lateral radiograph (B) of a dog with compensated mitral insufficiency. The left atrium and the right cranial lobe vein are enlarged, a sign consistent with pulmonary venous hypertension. The venous enlargement (black arrows) compared to the normal artery (white arrows) is clearly seen in B.

699

A

B

Fig. 35.25  Ventrodorsal (VD; A) and close-up VD (B) thoracic radiographs of a dog with pulmonary undercirculation from multiple congenital cardiac anomalies. Note the small, inconspicuous pulmonary vessels. The appearance of hypovolemia would be similar. In B, note the small size of the right caudal lobe pulmonary vein where it crosses the right ninth rib (black arrow).

Fig. 35.26  Close-up view of the left caudal thorax of a dog with

severe heartworm disease. The left caudal lobe pulmonary artery is massively dilated (black arrows). At the most caudal pair of arrows, the vessel ends abruptly; or is truncated. This is due to an intravascular thrombus completely obstructing the lumen at this level with marked reduction in vessel diameter distal to the obstruction.

A

B

C

Fig. 35.27  Left lateral (A), dorsoventral (DV; B), and close-up DV (C) radiographs of a dog with left-sided

heart failure secondary to mitral insufficiency. In A, the heart and left atrium are enlarged. Pulmonary vessels are difficult to identify because of border effacement created by edema in adjacent lung. The caudal lung lobes appear abnormally opaque in this lateral view, but this may be caused by poor ventilation, and recumbencyassociated atelectasis. Any suspicious lung opacity identified in the lateral view must be confirmed in the DV or VD view. In B, there is an alveolar pattern in the right middle and caudal lobes. This can be seen in the close-up (C). Note the poor visualization of pulmonary vessels in these lobes because of border effacement from the pulmonary edema. This patchy alveolar pattern, even without visualization of air bronchograms, is typical of cardiogenic pulmonary edema.

Fig. 35.28  Close-up of the right caudal thorax from a dog with

mitral insufficiency and left heart failure. The pulmonary arteries and veins are both enlarged (black arrows). The upper arrows are at the level of the right 9th rib, and it is apparent that the summation shadow of both the right caudal lobar pulmonary artery and vein with the rib is larger in the horizontal direction, evidence of vascular enlargement. The enlargement of both pulmonary arteries and veins in this dog with left heart failure is due to a combination of pulmonary arterial and venous hypertension. Fluid retention would be another differential for this appearance.

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SECTION IV  •  The Thoracic Cavity: Canine, Feline, and Equine

A

B

C

Fig. 35.29  Left lateral (A), ventrodorsal (VD; B), and close-up VD (C) radiographs of a cat with left-sided heart failure caused by hypertrophic cardiomyopathy. Pleural effusion is obvious in A. The heart cannot be seen clearly in this patient. One expects the heart to be enlarged in cats with hypertrophic cardiomyopathy and heart failure, but it may be normal radiographically in some cats. Pleural effusion is also noted in the DV view (B). Also, the caudal lobe pulmonary arteries and veins both appear enlarged. This is often seen in cats in heart failure and could be due to either coexisting pulmonary arterial and venous hypertension or fluid retention, or both. A heterogeneous, relatively unstructured pulmonary pattern is present in the caudal lobes that is consistent with pulmonary edema; see close-up in C. This heterogeneous pattern is typical of pulmonary edema in cats and is more common than more uniform homogenous lung opacification.

• Distended pulmonary arteries if pulmonary arterial hypertension or fluid retention is present • Pulmonary edema (left-sided heart failure)

Heartworm Infection

Despite the availability of highly effective preventive drugs, heartworm disease is still common in many parts of the United States. The radiographic changes vary depending on the duration of the infection, the number of worms, the location of the worms (normally the pulmonary arteries), the rate and degree of cardiac compensation, and the possible die-off of adult worms naturally or in response to therapy. Therefore, radiographic changes can vary from no abnormal findings or only a mildly affected cardiovascular system to severe involvement (see Figs. 35.20 to 35.22): • Right ventricular hypertrophy in response to pulmonary hypertension

• Dilation of the main pulmonary artery caused by turbulent blood flow and pulmonary hypertension and possibly the physical presence of heartworms • Parenchymal pulmonary artery enlargement and/or tortuosity from pulmonary hypertension and/or loss in laminar blood flow • Peripheral focal or multifocal alveolar pulmonary pattern from pulmonary thromboembolism caused by dead adult worm fragments or secondary allergic pneumonitis, which may only present as a generalized, unstructured interstitial pulmonary pattern opacity • Hepatomegaly, ascites, and occasionally pleural effusion caused by right-sided heart failure

Cardiomyopathy

Dilated cardiomyopathy results from weakened and dysfunctional myocardial contractility. Breeds predisposed to dilated

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A B

C Fig. 35.30 Lateral (A), close-up lateral (B), and ventrodorsal (VD; C) radiographs of a dog with dilated

cardiomyopathy and left-sided heart failure. The heart in some patients with dilated cardiomyopathy may appear normal. In this dog, there is enlargement of the left atrium and the right cranial lobe pulmonary vein (A), likely resulting from mitral valve dysfunction with secondary pulmonary venous hypertension. A and C have the appearance of increased lung opacity. In B, this opacity can be seen to have a bronchial and unstructured interstitial pattern. This lung pattern is more typical of an inflammatory etiology than cardiogenic pulmonary edema, except in dogs with dilated cardiomyopathy, where it is a typical manifestation of cardiogenic pulmonary edema due to a peribronchial accumulation of the edema fluid.

cardiomyopathy include the Doberman pinscher, Great Dane, Cocker spaniel, and Boxers. In dogs, any or all of the following radiographic signs may be seen (Figs. 35.30 and 35.31): • The radiographs may be normal in some dogs with dilated cardiomyopathy. • Generalized cardiomegaly is caused by volume overload or ventricular dilation. • Left atrial dilation may be present because of volume overload or mitral valve dysfunction from a change in shape of the mitral annulus as a result of cardiac dilation. • Pulmonary vein dilation from mitral valve dysfunction and regurgitation or from fluid retention is seen. • Parenchymal pulmonary artery dilation from fluid retention can be stimulated by decreased renal perfusion, leading to activation of the renin-angiotensin system.

• Possible pleural effusion, hepatomegaly, and/or ascites from right-sided heart failure is often seen. • Mixed interstitial and bronchial pattern caused by atypical pulmonary edema. Strictly on the basis of radiographic appearance, this radiographic pattern is more typical of inflammatory allergic airway disease, but a bronchointerstitial pattern is also common in large dogs with dilated cardiomyopathy as a manifestation of left heart failure. The pathophysiologic cause of peribronchial edema developing as opposed to alveolar edema is not understood. Hypertrophic cardiomyopathy occurs occasionally in dogs but is more common in cats. Feline hypertrophic cardiomyopathy is characterized by development of a hypertrophied, nondilated left ventricle in the absence of other cardiac diseases.

704

SECTION IV  •  The Thoracic Cavity: Canine, Feline, and Equine The poor left ventricular diastolic filling leads to reduced cardiac output with secondary increased mitral valve pressure and left atrial dilation. Radiographic signs of feline hypertrophic cardiomyopathy include the following (Fig. 35.32; see Fig. 35.29): • Moderate to extreme left atrial dilation. In cats, left atrial dilation with hypertrophic cardiomyopathy can become so large that it results in the characteristic “valentine” heart shape in the VD or DV view. Left atrial dilation may be caused by poor ventricular diastolic filling as a result of the left ventricular myocardial inward hypertrophy, systolic dysfunction, or abnormal systolic anterior motion caused by left ventricular outflow obstruction. • The left ventricle does not appear enlarged because the hypertrophy is constrictive (concentric), or inward, so the myocardium thickens at the expense of the left ventricular chamber size but does not increase its exterior dimensions. • Enlarged pulmonary veins may appear in early left ventricular decompensation, but visualization of pulmonary venous enlargement is not as common in cats with mitral dysfunction as in dogs. • Pulmonary edema will develop as left-sided heart failure progresses if not controlled by medication. • Pleural effusion is a late development.

Fig. 35.31  Close-up dorsoventral (DV) thoracic radiograph of a dog with

Pericardial Effusion

dilated cardiomyopathy and heart failure. The right caudal pulmonary artery and vein are enlarged (black arrows). This is sometimes seen in dogs with heart failure and can be caused by fluid retention. Decreased cardiac output results in activation of the renin-angiotensin pathway with secondary fluid retention.

A

Although not a myocardial or valve problem, pericardial effusion is acquired and can alter the shape and size of the cardiac silhouette. Radiographic signs include the following (Fig. 35.33): • There is a large round (globoid) cardiac silhouette in both lateral and VD or DV views if the effusion is severe enough. With mild or moderate amounts of fluid, the cardiac silhouette will not be generally round.

B Fig. 35.32 Lateral (A) and ventrodorsal (VD; B) radiographs of a cat with compensated hypertrophic cardiomyopathy; there is no evidence of heart failure. In A, the marked left atrial enlargement creates the so-called “valentine” appearance to the cardiac silhouette. This extent of left atrial enlargement is sometimes misdiagnosed radiographically as biatrial enlargement. Although one cannot be sure whether only the left atrium is dilated without echocardiography, a very large left atrium alone can create the valentine appearance. In B, the enlarged left atrium is not as obvious, because it is superimposed on the cardiac silhouette; this is dissimilar to the dog, in which an enlarged left atrium causes a mass effect in the region of the tracheal bifurcation. The enlarged left atrium in this cat does create a focal concave defect in the shape of the cardiac silhouette (black arrow in B).

CHAPTER 35  •  Canine and Feline Cardiovascular System

A

705

B Fig. 35.33  Left lateral (A) and dorsoventral (DV; B) radiographs of a dog with a globoid-appearing cardiac silhouette. This appearance is consistent with pericardial effusion, but based on the radiographs, a peritonealpericardial hernia or generalized cardiomegaly cannot be eliminated. This dog had pericardial effusion.

• The margin of cardiac silhouette may appear distinct as a result of little, if any, motion caused by cardiac contractions. • In severely affected patients, the margins of the hugely enlarged cardiac silhouette may touch the thoracic wall bilaterally. • Signs of right heart failure (enlarged caudal vena cava, hepatomegaly, ascites, and occasionally pleural effusion) may be present if pericardial tamponade is severe enough to prevent diastolic filling of the right atrium and ventricle. • Small to moderate volumes of pericardial effusion often do not have the previously described radiographic signs and can go undetected without echocardiography.

Congenital Cardiovascular Lesions

Given that congenital cardiac anomalies are encountered less commonly than acquired defects, only a brief summary is presented.

Patent Ductus Arteriosus

In patent ductus arteriosus, the ductus fails to close normally after birth. This results in an abnormal communication between the descending aorta and the main pulmonary artery. The marked pressure difference between these vessels results in continuous shunting of blood from the aorta into the pulmonary artery during both systole and diastole. This results in pressure and volume overload of the pulmonary circulation and altered myocardial workload. Radiographic signs include the following (Figs. 35.34 through 35.36; see Fig. 35.19): • Dilation of the proximal aspect of the descending aorta caused by turbulent blood flow • Enlargement of the main pulmonary artery from increased pressure and flow • Enlargement of the left atrium, and possibly the left auricle, from increased blood flow • Enlarged left ventricle, initially caused by dilation followed by hypertrophy • Enlarged parenchymal pulmonary arteries and veins caused by volume and pressure overload

Fig. 35.34  Dorsoventral (DV) radiograph from a dog with a patent

ductus arteriosus. There is a focal dilation of the descending portion of the aortic arch that is contiguous with the descending aorta (black arrows). There is also mild dilation of the main pulmonary artery (white arrows).

Pulmonic Stenosis

Pulmonic stenosis leads to restriction of flow from the right ventricle into the pulmonary artery. It is typically caused by an abnormal pulmonic valve but can also be associated with narrowing of the pulmonary outflow tract—that is, subvalvular pulmonic stenosis. Radiographic signs include the following (Fig. 35.37): • Dilated main pulmonary artery is caused by turbulence. • Enlarged right ventricle is caused by hypertrophy related to increased resistance associated with ejection.

706

SECTION IV  •  The Thoracic Cavity: Canine, Feline, and Equine

B

A

Fig. 35.35 Lateral (A) and dorsoventral (DV; B) radiographs of a dog with a patent ductus arteriosus. The heart is enlarged in both views, mostly because of left ventricular hypertrophy, although the diagnosis of hypertrophy cannot be made from these radiographs. B, A focal aortic arch dilation is visible in the DV view (white arrow), and the conspicuity of the left auricle (black arrow) is also increased slightly, either because of dilation or displacement by an enlarged left atrium. In A, the right cranial pulmonary lobar artery (black arrows) and vein (white arrows) are dilated. Left atrial dilation has created a concave shape change in the lateral view (white arrowhead). The lungs have an unstructured increase in opacity because of overcirculation within small pulmonary vessels.

• Parenchymal pulmonary vessels are usually normal in size; but if right-sided heart failure develops, the pulmonary vessels may be small because of reduced cardiac output.

Aortic Stenosis

Narrowing of the subvalvular region of the left ventricle is more common than primary valvular stenosis. The narrowing results in increased resistance to left ventricular ejection. Mitral valve dysfunction and regurgitation may occur as a result of the mitral annulus becoming misshapen. Radiographic signs include the following (Fig. 35.38; see Fig. 35.13): • Enlargement of the aortic arch from turbulent flow, appearing as widening of the precardiac mediastinum • Elongation of the left ventricle from hypertrophy • Left atrial dilation if secondary mitral valve dysfunction develops • Normal pulmonary vessels unless secondary mitral valve dysfunction develops, leading to pulmonary venous hypertension • Radiographs may be normal

Ventricular Septal Defect

Fig. 35.36  Selective left ventricular angiocardiogram of a dog with a

patent ductus arteriosus. The dilated main pulmonary artery segment (small thin arrows) and the ascending aorta (solid arrowheads) are accentuated by positive-contrast medium, and the patent ductus arteriosus (curved arrows) lies between the descending aorta and the main pulmonary artery segment and is opacified because of the left-to-right shunting of blood.

Abnormal development results in a communication between the left and right ventricle, usually located dorsally in the membranous septum just below the aortic valve. Because systolic pressure is higher in the left ventricle, blood flows from the left ventricle into the right ventricle during systole but not during diastole because of the similar diastolic pressure in the two ventricles. Because of the location of the defect, most shunted blood immediately enters the pulmonary artery and not the right ventricle. The volume of blood shunted with each contraction depends on the size of the defect, but the magnitude of shunting is typically less than with patent ductus

CHAPTER 35  •  Canine and Feline Cardiovascular System

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B

A

Fig. 35.37 Lateral (A) and dorsoventral (DV; B) radiographs of a dog with pulmonic stenosis. There is excessive contact of the heart with the sternum in the lateral view indicative of right ventricular enlargement, likely hypertrophy. The main pulmonary artery is enlarged in the DV view (white arrows). The parenchymal pulmonary arteries are normal in both views (black arrows in B).

• Pulmonary arteries and veins can be normal or mildly dilated because of a mild to moderate increase in pulmonary blood flow; enlargement is typically less than that seen with patent ductus arteriosus.

Tricuspid Dysplasia

Tricuspid dysplasia is a congenital malformation of the tricuspid valve. Radiographic signs include the following (see Fig. 35.11): • Right atrial enlargement from pressure and volume overload is seen. • Pulmonary vessels are usually normal but may become small if cardiac output decreases from the right ventricle.

Reduction in Heart Size

Fig. 35.38  Left ventricular angiocardiogram in a dog with subvalvular

aortic stenosis. Note the narrow subvalvular region and dilation of the aorta distal to the aortic sinus. The aorta should be no wider than the sinus; enlargement of the aorta distal to the sinus is caused by turbulent flow.

arteriosus. The magnitude of radiographic signs depends on the amount of blood shunting through the defect and can include the following (Fig. 35.39): • There is mild right ventricular hypertrophy from volume and pressure overload.

The cardiac abnormalities discussed to this point are all associated with either a normal heart or enlargement of a portion of the heart or associated vasculature. Reduction in heart size does occur, not as a result of primary cardiac disease but because of reduction in circulating vascular volume. Acutely, this occurs secondary to blood loss and, on a more chronic basis, as a result of dehydration or metabolic hypovolemia, sometimes because of Addison’s disease.27 Radiographically, the heart appears small subjectively and may be retracted from the sternum. The lungs will usually appear overinflated, but this is an artifact causedby the reduction in cardiac size. Pulmonary vessels also appear small, leading to increased pulmonary hyperlucency (Fig. 35.40). The magnitude of these changes depends on the severity of the hypovolemia, and there will be some threshold of fluid loss that must occur before the changes are obvious.

708

SECTION IV  •  The Thoracic Cavity: Canine, Feline, and Equine

A

B Fig. 35.39 Lateral (A) and dorsoventral (DV; B) radiographs of a dog with a ventricular septal defect. In A,

there is excessive elevation of the cardiac apex from the sternum consistent with right ventricular hypertrophy, mild dilation of the left atrium, and slight enlargement of the left cranial lobe pulmonary artery and vein, consistent with mild pulmonary overcirculation. In B, the apex is displaced to the left as a result of the dog being in sternal recumbency, and the appearance of excessive cardiac mass on the left is deceptive. Slight enlargement of the caudal lobe pulmonary arteries and veins is present, consistent with mild overcirculation. These findings are typical of, but not conclusive proof of, a ventricular septal defect.

A

B Fig. 35.40 Lateral (A) and ventrodorsal (VD; B) radiographs of a dog with hypovolemia secondary to Addison disease. The heart is subjectively small, and the reduction in cardiac mass has resulted in the heart separating from the sternum. The pulmonary vessels are also small. The lungs appear hyperinflated because of the relative reduction in cardiac size.

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