Cardiovascular Flashcards

Question

Right ventricular injection angiogram (dog). What are the pertinent findings and diagnosis?

Answer 1

1. **Levocardia** - *location of the heart in the left side* of the thorax, the apex pointing towards the left 2. **Levoposition** - *displacement towards the left* Situs inversus - the thoracic and abdominal viscera are reversed (Le. a mirror image of the normal arrangement) snus solnus - the thoracic and abdominal viscera are in a normal location 3. **Dextrocardia** - location of the heart in the **right side** of the thorax, the apex pointing towards the right. The cardiac chambers are reversed 4. **Dextroposition** - *displacement towards the right* 5. **Dextroversion** - version (tuming) to the right. In terms of the heart, dextroversion means the location of the heart in the right thorax, the LV lying in the correct posnion on the left but lying cranial to the RV \*\*\*There is some controversy over the exact definnions but those listed above are most commonly accepted.

Answer 2

The catheter has been placed into the **LV via the femoral artery and aorta** ready for the contrast medium injection. _Positive contrast medium outlines the_: * Left ventricle (LV) * Aortic valve (arrowed) * Ascending aorta (Ao) * Brachiocephalic trunk (B) * Left subclavian artery (S)

Answer 3

The catheter has been placed into the **RV via the CdVC** ready for the contrast medium injection. * (b) Positive contrast medium is present within the RV and has started to enter the RVOT and main pulmonary artery (MPA). * (c) The contrast medium has now reached the left and right pulmonary artery branches (arrowed) and the smaller pulmonary arterial branches In the lungs

Answer 4

(a) Lateral view. (b) Ventral view. * Ao =Aortic arch * BR =Brachiocephalic trunk * CdVC =Caudal vena cava * CrVC =Cranial vena cava * IT = Internal thoracic arteries and veins * LA = Left atrium * LAu = Left auricular appendage * LPA = Left pulmonary artery * LS = Left subclavian artery * LV = Left ventricle * MPA = Main pulmonary artery * RA = Right atrium * RAu =Right auricular appendage * RPA =Right pulmonary artery * RV = Right ventricle

Answer 5

_Lateral view:_ * **12-2 o'clock:** left atrium * **2-5 o'clock:** left ventricle * **5-9 o'clock:** right ventricle * **9-10 o'clock:** main pulmonary artery and right auricular appendage * **10-11 o'clock:** aortic arch _Dorsoventral view:_ * **11-1 o'clock:** aortic arch * **1-2 o'clock:** main pulmonary artery (left auricular appendage in cat) * **2.30-3 o'clock:** left auricular appendage * **2-5 o'clock:** left ventricle * **5-9 o'clock:** right ventricle * **9-11 o'clock:** right atrium _Species differences:_ * On a VD/DV view the cardiac apex points more to the left in the dog. In the cat the apex is more variable, but usually closer to the midline. * **In the dog the left auricular appendage (LAu)** is located at **02.30-03.00 o'clock** on the **DV/VD view. In the cat the LA and LAu** are located at **1-2 o'clock** on this view and the main pulmonary artery may be cranial to this or not seen at all. * In the cat the more cranial location of the LA may make it difficult to see on the lateral view. * **In the dog, when the LA is enlarged** on the **DV/VD view** is superimposed over the cardiac silhouette in the **5-7 o'clock position** (between the caudal mainstem bronchi), whereas in the **cat, it is located more cranially at the 1-2 o'clock position**. This explains the so-called 'valentine heart shape' seen only in the cat and created by left ± right atrial enlargement.

Answer 6

(a) Lateral and (b) DV radiographs of a **normal Golden Retriever.** This breed *often appears to have right-sided cardiomegaly* on the lateral view due to the large amount of sternaI contact (similar to wide shallow-chested dog breeds) and the rectangular shape of the cardiac silhouette. On the DV view the cardiac size appears normal and the apex is moderately displaced into the left hemithorax.

Answer 7

* (c) Lateral radiograph of a **normal Dobermann.** The cardiac silhouette is *extremely upright* due to the deep narrow-chested nature of this breed. * (d) DV radiograph of a **normal Greyhound.** The cardiac silhouette is very rounded in shape (compared with b) and the apex lies in the midline.

Answer 8

The carina should be located within the 4th-5th intercostal space.

Answer 9

The CdVC receives blood from the abdomen, pelvis and hindlimbs. * The final abdominal tributaries are the hepatic veins. * The CdVC enters the thorax by crossing the diaphragm on the right side within the plica vena cava. It then traverses between the accessory and right caudal lung lobes to enter the RA dorsal to the inlet of the coronary sinus. It lies in close association with the right phrenic nerve.

Answer 10

CdVC:A0 \> 1.5 (strongly suggestive of right-sided heart abnormality). Differentials: * Right sided heart disease * Hypovolemia * CVC obstructive condistions (caval syndrome, masses, etc.) * Acquired vascular disease

Answer 11

The cranial vena cava (CrVC) receives blood from the head, neck, thoracic wall and forelimbs. * The axillary veins (from the forelimbs) , together with the internal and external jugular veins, converge to form the right and left brachiocephalic veins. * These then unite to create the CrVC. It travels in the cranial mediastinum and receives the costocervical and internal thoracic veins, as well as the azygos vein just cranial to the RA; it finally empties into the RA. The CrVC is not seen as an individual structure on a radiograph unless a pneumomediastinum is pre- sent. It forms the ventral border of the cranial mediastinum on the lateral view.

Answer 12

* The azygos vein forms from the first lumbar veins and passes through the aortic hiatus into the thorax. * It then receives intercostal, subcostal , oesophageal and broncho-oesophageal veins and terminates in the CrVC. It is not seen on a radiograph unless a severe pneumomediastinum is present or it is markedly enlarged. It then appears as a wavy vessel immediately ventral to the thoracic spine, receiving tributaries from every intervertebral space (Figure 7.24). It may rarely be seen in very deep-chested, narrow breeds, such as the Greyhound , in the absence of a pneumomediastinum.

Answer 13

* Shock * Hypovolaemia * Addison's disease (hypoadrenocorticism) * Artefactual (pulmonary hyperinflation)

Answer 14

* Mineralized masses * Other dystrophic mineralization * Metastatic mineralization: * Hyperadrenocorticism (Cushing's disease) * Secondary hyperparathyroidism * Renal disease

Answer 15

* Pulmonic stenosis (post-stenoic dilation) * Increased circulating volume (PDA, AS, VSD) * Pulmonary hypertension * Severe heartworm disease and angiostrongylosis * Artefactual: * VD position * Systole * Positional rotation

Answer 16

* Dehydration * Shock * Hypoadrenocorticism (Addison's disease) * Positive pressure ventilation (and other causes of pulmonary hyperinflation) * Pericardial effusion with tamponade * Constrictive pericarditis * Severe pulmonary stenosis * Right-to-left shunts (tetrallogy of Fallor, reverse PDA) * Focal due to PTE

Answer 17

* Pulmonary hypertension * PTE * HW dz * Left-to-right shunts (PDA, VSD, ASD) * Angiostongylosis (but not often a feature) * Peripheral arteriovenous fistula

Answer 18

**PDA** is the **most common** congenital cardiac disease in **dogs**. **Small-breed** dogs (including, but not limited to, Chihuahua, Maltese, Poodle, Pomeranian, Bichon Frise, Shetland Sheepdog) and **German Shepherd** Dogs are predisposed. Bitches are more affected than dogs. Cats are also affected but the condition is less common than in dogs. The ductus arteriosus is an important part of normal fetal circulation. It extends from the **main pulmonary artery** to the **descending aorta** and in the fetus functions to divert blood away from the lungs back into the systemic circulation . **After birth, pulmonary vascular resistance falls** and flow in the ductus reverses . The ductus then **closes by constriction of smooth muscle** within its wall , brought about by **increased arterial oxygen** tension that **inhibits local prostaglandin release**. The ductus is usually **closed by 7- 10 days after birth**. It remains in the adult as the ligamentum arteriosum. PDA results from failure of normal closure of the ductus arteriosus, resulting in a shunting vessel between the descending aorta and the main pulmonary artery. _There are three main types of PDA:_ 1. The **mildest form** of the condition results in closure of the ductus at the **pulmonary arterial end only.** This produces a clinically insignificant blind-ended pouch called a 'ductus diverticulum'. **No shunting** of blood occurs and this anomaly may only be identified as an incidental finding on postmortem 2. The **commonest** clinically presenting patent ductus is a **complete tapering funnel-shaped** tube with blood shunting from **left-to-right**. Volume overloading of the left side of the heart causes left atrial dilatation and left ventricular dilatation and hypertrophy 3. The third and **least common** form for the ductus to take is a **non-tapering cylindrical tunnel.** This is associated with **persistent postnatal pulmonary hypertension** and **bidirectional** *or* **right-to-left** shunting (Eisenmenger's syndrome) . These are sometimes known as 'reversed PDAs' and are discussed further, below. The condition results in decreased pulmonary blood flow, a normal to small LV and right ventricular concentric hypertrophy.

Answer 19

Clinically, a left-to-right shunting PDA is characterized by a **continuous machinery-type heart murmur** (continuous systolo-diastolic murmur) heard best over the main pulmonary artery. A bounding or 'waterhammer' arterial pulse may also be present. Most animals are usually asymptomatic when the murmur is discovered. **Surgical ligation** is recommended in almost all cases. _Radiographic findings include:_ * **Classically left-sided** changes are present, but generalized cardiomegaly may be seen * Prominent aortic arch * Prominent LA * Left ventricular enlargement, leading to straightening of the caudal margin of the heart * Increased vascular lung pattern, with increased size of both the pulmonary arteries and veins; very distally located vessels are visible due to enlargement (the **vascular pattern** is due to increased blood flow to the lung, caused by the left-to-right shunt) * Eventually signs of left-sided cardiac failure _DV view (Firgure 7.46):_ * Prominence of the **aortic arch , pulmonary trunk and LAu** at 11-1, 1-2 and 2-3 o'clock, respectively: this triad has been reported to be **pathognomonic** for PDA but is not present in all patients (only around 20% of cases) * Occasionally an aortic bulge (,ductus bump') may be seen near the level of the ductus. This is caused by the abrupt narrowing of the descending aorta beyond the level of the ductus origin * Enlarged LA with splayed caudal mainstem bronchi with or without double opacity sign * Increased vascular lung pattern (Figure 7.46b)

Answer 20

Occasionally, right-to-left shunting occurs through a PDA due to **high pulmonary vascular resistance**. This is thought to occur because the **non-tapering tubular shape of the ductus** in these animals **permits aortic pressures to be transmitted to the pulmonary arterial system**. The resulting extremely increased pulmonary perfusion eventually leads to intimal arteriolar damage and muscular proliferation, causing marked pulmonary hypertension and reversed flow through the ductus arteriosus (Eisenmenger's syndrome). This change has usually been shown to occur in the first few weeks of life. The pulmonary vascular changes are poorly understood, but are known to be **irreversible, thereby precluding surgical treatment** for this condition. The anomaly is quite different in presentation to a left-to-right shunting PDA. Clinical signs include fatigue, shortness of breath and weakness. **No murmur or only a soft systolic murmur** is heard on auscultation and a split second heart sound may be detected. **Differential cyanosis** may be seen with normal pink cranial mucous membranes but cyanotic caudal mucous membranes, due to the fact that the **PDA originates distal to the brachiocephalic trunk and left subclavian artery**. The animal may be **polycythaemic.** _Radiographic findings include:_ * Dilatation of the main pulmonary artery (seen best on the DV view) * A 'ductus bump' may be seen * Underperfusion of the lung fields may be evident (hypovascular pattern, hyperlucent lung fields). * **Right heart enlargement** on both lateral and DV views _Angiocardiography:_ * Right-to-Ieft shunting can be demonstrated by an injection of contrast medium in the RV or main pulmonary artery. * The contrast medium then shunts from the main pulmonary artery to the descending aorta through the wide ductus (Figure 7.52). * Pulmonary arteries may be normal or appear tortuous . * Left-sided injections may show an extensive broncho-oesophageal collateral circulation. *

Answer 21

Pulmonic stenosis encompasses any obstruction of blood flow from the RV to the main pulmonary artery. The prevalence is higher in English Bulldogs, but also Beagles, Boxers, Chihuahuas, Schnauzers and all terriers. Pulmonic stenosis is a rare condition in cats. The condition usually occurs in isolation but on occasion other cardiac anomalies, such as tricuspid dysplasia, ASD, patent foramen ovale or VSD, may be present. _The stenosis may occur at different levels:_ 1. **Valvular stenosis (most common form):** a variety of anomalies may occur including hypoplasia of the valve, thickened valve leaflets, asymmetric valve leaflets and incomplete commissural separation . A fibrous ring may also be present below the valve 2. **Subvalvularstenosis** (less common) : a specific form of this occurs in *English Bulldogs and Boxers* due to an *anomalous origin of the left main coronary artery* (Figure 7.55). Many variations are possible most commonly the *left and right coronary arteries* branch from a **single large coronary artery** that arises from the **right aortic sinus** of Valsalva and wraps around the right ventricular outflow tract (RVOT). These cases cannot be treated with balloon valvuloplasty 3. Supravalvularstenosis (rare): may be seen more often in Giant Schnauzers. The stenosis leads to a **pressure overload** and **concentric hypertrophy** of the **RV**. This in turn leads to **decreased right ventricular diastolic compliance, ventricular filling impairment and increased right atrial pressure**. Tricuspid regurgitation may result and further raises right atrial pressure with eventual right- sided heart failure. The condition is usually asymptomatic at the time of diagnosis. However, it eventually leads to exercise intolerance, syncope and possible right-sided heart failure if functional tricuspid insufficiency is present. On clinical examination pulmonic stenosis is characterized by a left-sided systolic heart murmur, most audible at the heart base (ejection type of murmur). Therapy for the condition includes both medical and surgical options and the appropriate choice depends on the severity of the stenosis and the clinical status of the patient. The condition should be monitored over time as some dogs can gradually develop more severe obstructions . _Radiographic findings include:_ * Right-sided cardiomegaly: * Increased sternal contact on the lateral view * Rounding of the heart with reverse D shape on the DV view * Prominence of the main pulmonary artery (post-stenotic dilatation), best seen on the DV view (between 1-2 o'clock) * In a minority of dogs, the dilated post-stenotic main pulmonary artery segment is seen superimposed over the caudal trachea on the lateral view. This has been termed the 'hat sign' * In very severe cases, pulmonary hyperlucency and small pulmonary vessels (due to decreased pulmonary arterial outflow) may be seen * There may be signs of right-sided cardiac failure: * right ventricular and atrial enlargement * enlarged CdVC * hepatomegaly * ascites and pleural effusion

Answer 22

_Angiocardiography:_ This is not usually used for diagnosis but is often used **prior to surgical intervention**. Diagnosis can be established after selective catheterization of the **RVOT using a jugular approach**. Right atrial injections of contrast medium are not suitable for the diagnosis of pulmonic stenosis, since the pulmonic valve area is usually superimposed upon the opacified RA. * Stenosis is visible at the level of the valve, the infundibulum or at the subvalvular level (muscular hypertrophy, creating a filling defect in the outflow tract). * Post-stenotic dilatation of the main pulmonary artery can be identified. * In cases of functional tricuspid insufficiency, regurgitation of contrast medium is seen from the RV to the RA. * In **English Bulldogs and Boxers**, it is vital to **search for an abnormal origin of the left coronary artery** as an underlying cause of the stenosis (see Figure 7.55). Ideally, coronary arteriography should be performed. Alternatively, the aortic root and coronary arteries should be examined in the late levophase after a right ventricular injectionof contrast medium, or just after a left ventricular injection of contrast medium. In affected animals **a single coronary artery is seen wrapping around the RVOT and a right coronary artery branches**from this single artery a few millimetres distal to its aortic origin (Figure 7.58).

Answer 23

Aortic Stenosis: 1. The **vast majority** of aortic stenosis occurs in the **subvalvular region** (subvalvular aortic stenosis). This is the most common congenital cardiac malformation in **large-breed dogs**. 2. Valvular stenosis (thickened valves and hypoplastic annulus) is rare, but Bull Terriers are predisposed. A bicuspid valve may also rarely cause a mild valvular stenosis. 3. Supravalvular stenosis is also very rare. The remainder of this section relates to subvalvular aortic stenosis. Large-breed dogs are more commonly affected by subvalvular aortic stenosis. Breed predisposition includes Golden Retrievers, Newfoundlands, German Shepherd Dogs, Boxers, Rottweilers and English Bull Terriers. It occurs occasionally in cats. The condition may be accompanied by other congenital cardiac disorders, such as mitral valve dysplasia and PDA. The lesion is usually a fixed ridge or ring of **fibrous tissue in the LVOT just below the aortic valve.** The outflow obstruction leads to increased left ventricular systolic pressure, and **concentric left ventricular hypertrophy** results. A **post-stenotic dilatation of the aorta** and **sometimes brachiocephalic trunk occurs**. Mild aortic regurgitation is often present. Animals with subvalvular aortic stenosis are predisposed to **aortic endocarditis, abnormal coronary arterial flow and myocardial infarctions.** The functional and clinical consequences vary with the severity of the obstruction. This ranges from minor obstructions with minimal hypertrophy and no clinical signs, to significant obstructions with concentric hypertrophy of the LV, left-sided heart failure, syncope or sudden death. _Radiography_ Radiography is often unremarkable in mild cases. Changes may be seen in more severe cases: * **Lateral view** (Figure 7.64a): * Elongated cardiac silhouette, with dorsally displaced trachea and carina and straightened caudal margin of the heart due to left ventricular enlargement * Prominent ascending aorta and aortic arch (post-stenotic dilatation) * Sometimes mild left atrial enlargement (if severe, suggests concurrent mitral regurgitation) * In cases with left-sided heart failure: left atrial dilatation, pulmonary venous congestion and pulmonary oedema. * **DV view** (Figure 7.64b): * Rounding of the left contour of the heart * Aortic bulge at the 11.00--01 .00 o'clock position * There may be left atrial enlargement (see above) * In cases with left-sided heart failure: left atrial dilatation, pulmonary venous congestion and pulmonary oedema.

Answer 24

Subaortic stenosis is demonstrated by a **left ventricular injection of contrast medium.** * Narrowing of the outflow tract is usually obvious on lateral views (Figure 7.65). * Varying degrees of post-stenotic dilatation of the ascending aorta can be identified: in a normal dog, the maximum diameter of the ascending aorta distal to the sinus of Valsalva is always less than the diameter of the sinus of Valsalva.

Answer 25

VSD is a common congenital disorder in both dogs and cats. Breed predispositions include English Springer Spaniels, West Highland White Terriers and Lakeland Terriers, amongst others. VSD is known to have a genetic basis in the Keeshond with malformations of the conotruncal septum. Anomalous development of any part of the ventricular septal components may lead to a VSD (see above). However, **most commonly** the defect occurs at the point of fusion of the **membranous and muscular parts** of the septum, resulting in a perimembranous lesion. Thus, the defect is most often located **'high' or dorsally on the septum**. Occasionally, the defect occurs lower down in the muscular part of the septum. _On the left side_ the defect is usually located in the **subaortic septum** , just below the aortic valve and typically between the right coronary and non-coronary cusps. _On the right side_ the location is **more variable.** * Typically, the VSD opens under the **septal cusp** of the tricuspid valve (also known as infracristal or under the crista supraventricularis). * Less commonly, the opening on the right is in a more cranial location and opens directly into the RVOT above the tricuspid valve (also known as supracristal or above the crista supra- ventricularis). \*\*\*The full classification of VSOs is complex and is beyond the scope of this manual. The septal defect allows **left-to-right shunting** of blood unless other significant abnormalities are present, which result in shunt reversal (such as pulmonic stenosis , tricuspid dysplasia or severe pulmonary arterial hypertension). Pathophysiological and clinical effects of the VSD depend upon the size and location of the defect, and the presence or absence of associated malformations. _VSDs may be classed as resistive or non-resistive:_ * **Resistive** VSDs are **small** and provide resistance to flow between the right and left sides * **Non-resistive** VSDs are **large** (approximately the same size as the aortic orifice) , and there is no resistance to flow between the two sides. The most common type of VSD in the dog is a small resistive VSD. However, these are often large enough to have clinical significance. With resistive lesions the flow across the defect depends both on its size and the pressure difference between the left and right sides. Blood is shunted from the high pressure left side to the right side across the defect (in the absence of other abnormalities). _In most cases_ it has been shown that the shunted volume moves **directly into the RVOT**, hence **right-sided enlargement is not usually a feature** of the condition. The shunted blood then enters the pulmonary circulation and finally returns to the left side of the heart. This results in **overcirculation of the pulmonary system and left-sided heart enlargement** (eccentric hypertrophy) if the shunt is significant. If left ventricular end-diastolic pressure increases sufficiently as a result, then **left-sided heart failure** will ensue. _Less commonly_, the **defect is lower in the septum** and a **significant volume** of shunted blood enters the **RV**, rather than exiting immediately via the out-flow tract. In this case, **right-sided heart enlargement may occur.** Non-resistive VSOs result in the two ventricles functioning as a single chamber. The volume of blood that is shunted, and the direction that it is shunted in, depends purely on the difference between the systemic and pulmonary resistance. In most cases the systemic resistance is much higher and a huge left-to-right shunt occurs. However, this large shunt to the pulmonary circulation will result in increased pulmonary pressure. The RV hypertrophies concentrically in response to this. Both ventricles also hypertrophy eccentrically. If pulmonary hypertension worsens (pulmonary vascular pathology, reactive pulmonary hypertension) then there will be increased resistance to the right ventricular outflow. The shunt fraction from left-to-right will decrease and eventually shunt reversal may occur should right ventricular systolic pressures exceed left ventricular systolic pressures. The latter is known as Eisenmenger's complex; and right-to-Ieft shunting and cyanosis are observed. The clinical presentation, **prognosis and recommended treatment vary** enormously with the **type of VSD**. * In general, small, uncomplicated VSDs have a good prognosis and clinical signs may not be seen. * Animals with larger shunts and cardiomegaly have a poorer prognosis. * Those with Eisenmenger's complex have a very guarded long-term prognosis. _Radiographic findings include:_ * Small defects: thoracic radiographs can be totally normal * Larger defects: left atrial and left ventricular enlargement with or without increased vascular pattern in the lungs * In cases with left-sided congestive heart failure: pulmonary oedema * In cases with biventricular heart failure: pulmonary oedema, pleural and peritoneal effusion * Varying degrees of right ventricular and main pulmonary artery enlargement are also possible, depending on the level and size of the defect (as explained above) * Main pulmonary arterial enlargement and an underperfused lung periphery suggests pulmonary hypertension or pulmonic stenosis and shunt reversal.

Answer 26

ASDs are **uncommon** congenital abnormalities in the dog. Breeds at risk include the Samoyed, Boxer, Newfoundland and Old English Sheepdog. They are also infrequently seen in cats (mostly endocardial cushion defects) . _ASDs can occur at three main locations:_ 1. **High** in the atrial septum, near the entrance of the pulmonary veins. These are sinus venosus ASDs and are very **rare** 2. In the **middle** of the septum. These are **ostium secundum** ASDs and are the **most common** type. They vary in size. Some authors consider a patent foramen ovale to be a small ostium secundum defect. Conversely, other authors do not consider a patent foramen ovale to be a true ASD, as the atrial septum forms normally but the foramen walls are pushed apart, usually by conditions that increase right atrial pressure 3. At the **base** of the septum. These are either **ostium primum** defects **or endocardial cushion defects**. Various types of endocardial cushion defects exist and they are often accompanied by abnormal atrioventricular valve development. These defects are usually big and are more commonly reported in cats . A complete endocardial cushion defect comprises a large ASD in the lower atrial septum, a high VSO and fusion of the septal leaflets of the two atrioventricular valves. This results in a communication between all four cardiac chambers and is also known as an atrioventricular valve canal defect. _Most ASDs_ are associated with **left-to-right shunting**, unless there is a reason for reversal of the flow, with increased right atrial pressure (pulmonic or tricuspid valve malformation or pulmonary hyper- tension) . Just as with VSDs , the defect may be classed as resistive or non-resistive. The shunting occurs during diastole. Large defects result in significant left-to-right shunting and **eccentric hypertrophy of the RV, pulmonary overcirculation and sometimes right atrial dilatation. Right-sided heart failure** may result. If left atrial enlargement is identified then the examiner should look for an additional defect, such as an endocardial cushion defect with mitral regurgitation. These animals may develop left-sided or bilateral heart failure. Shunt reversal may occur in certain conditions, such as pulmonic stenosis or pulmonary hypertension (Eisenmenger's syndrome/physiology). Most ASDs are not clinically significant and **treatment is usually not necessary.** _Radiographic findings include:_ * Often normal radiographs * Right-sided cardiomegaly: dilatation of the RV with or without dilatation of the RA * There may be enlarged pulmonary arteries * Left atrial changes are seen with some endocardial cushion defects.

Answer 27

Tetralogy of Fallot is a complex congenital disorder, resulting from a **failure of the conotruncal septum to align properly** at the embryonic stage. The **Keeshond and English Bulldog** are predisposed and the condition is also seen in cats. Tetralogy of Fallot is the most common cause of **cyanotic cardiac disease** in young animals. _The disease is characterized by four features:_ 1. **Pulmonic stenosis** leading to right ventricular outflow obstruction (main pulmonary artery atresia may also be present) 2. Secondary **right ventricular hypertrophy** 3. A **subaortic VSD** 4. **Dextroposition of the aorta** (rightward positioning or overriding aorta). The right ventricular outflow obstruction and increased right ventricular pressure lead to **shunting** of blood from the **right side to the left** via the septal defect. Deoxygenated blood mixes with left-sided oxygenated blood and hypoxaemia results. The **LA and LV are small** and the **pulmonary arteries and veins are underperfused**. The bronchial arteries increase the systemic collateral circulation that they provide to the lungs. Animals present with exercise intolerance, failure to grow, shortness of breath, syncope, cyanosis and secondary polycythaemia. Note that since shunting occurs at the level of the ventricles the **cyanosis is generalized** and not differential as in reverse PDA. Medical and surgical treatment options exist and the prognosis is variable. _Radiographic findings include:_ * The overall size of the **heart i**s usually **small to normal** * **Right ventricular enlargement** may be apparent * The overriding of the aorta may produce a foss of the cranial indentation on the cardiac silhouette on the lateral view * The main pulmonary artery is not enlarged (unlike the situation in pulmonic stenosis without a septal defect) * **Hypovascularization of the lungs** may be identified: hyperlucent lung fields, decreased size of the pulmonary lobar vessels

Answer 28

A vascular ring anomaly results from an abnormal embryonic development of the primordial aortic arches **(aortic arches Ill, IV or VI)** around the embryonic pharynx. This leads to postnatal **constriction** of the **thoracic oesophagus** and development of a **secondary megaoesophagus** (see also Chapter 8). Dogs and cats are affected; in dogs, **German Shepherd** Dogs and Irish Setters are predisposed to this condition. _A spectrum of abnormalities may be encountered, the most common ones being:_ * Persistance of the **right fourth** aortic arch (PRAA) with a **left-sided ligamentum arteriosum** (most common anomaly) **and/or a retro-oesophageal left subclavian** artery * **Double aortic arches** * Normal fourth aortic arch with **retro-oesophageal (aberrant) right subclavian** artery (usually not a major problem from a clinical stand-point). * Rarely, a PDA is associated with a vascular ring anomaly. _Radiographic findings include:_ * If the vascular ring anomaly has entrapped the oesophagus, then oesophageal dilatation may be seen cranial to the heart base. Oesophagography may be required to identify this * A soft tissue or heterogenous granular opacity, cranial to the heart base with general ventral displacement of the trachea may be seen on survey radiographs * There may be a ventral alveolar pattern if aspiration pneumonia has occurred * Moderate or marked focal **leftward** curvature of the **trachea** near the cranial border of the heart in DV or VD radiographs (see Figure 9.18, p. 208) is a reliable sign of PRAA in young dogs with consistent clinical signs (as opposed to the normal right-sided tracheal curvature in normal animals) * **In cases of PRAA** the **leftward margin of the descending aorta is not visible** * **If** a well defined, normal left descending aortic margin is **clearly identified** on the VD or DV view, **a less common vascular ring anomaly may be suspected**: angiography is warranted in such cases, to confirm the diagnosis and plan the best surgical approach. _Oesophagography:_ * Oesophageal contrast studies show accumulation of the contrast medium in a distended oesophagus cranial to the heart base and abrupt tapering at the level of the sixth pair of ribs. * Occasionally, the oesophageal dilatation is generalized and these cases carry the worst prognosis. _Angiocardiography:_ This is not necessary in all cases, as an adequate presurgical diagnosis of vascular ring constriction of the oesophagus can be made with barium studies of the oesophagus. It may be valuable to identify animals that have a normal left fourth aortic arch but abnormal formation of the right fourth and/or right sixth aortic arch: in these cases a right thoracotomy is the best surgical approach as opposed to the more common left approach. A left ventricular injection of contrast medium is usually performed: * **Persistent right fourth aortic arch** is more consistently demonstrated on DV views, where the opacified aortic arch can be seen **coursing to the right of the trachea** * A **retro-oesophageal left subclavian artery** can be demonstrated in lateral views as it **courses cranially from its origin dorsally and to the left of the aorta** at about the level where the thoracic aorta begins to parallel the vertebral column. The persistent left subclavian artery compresses the oesophagus dorsally when it begins running ventrally to the thoracic inlet.

Answer 29

Aortic coarctation is a very **rare condition** in dogs and even more rare in cats. The disease consists of a **narrowing of the aortic lumen** that usually occurs at the **aortic isthmus**, the segment of the aorta **between** the origin of the **left subclavian artery** and the insertion of the **ductus arteriosus.** It is believed to be due to **spreading of the specialized contractile ductal tissue into the aorta** to form a sling around it, which after birth becomes part of an obstructive curtain of tissue. The narrowing is responsible for obstruction to the flow into the descending aorta and **aneurysmal dilatation** of the aorta **distal to the obstruction**. The narrowing process t**akes weeks to develop**, which leaves time for the LV to adjust to the increased pressure load and for **collateral circulation to develop**; this is why there are often no clinical signs associated with the disease. _Radiographic findings are non-specific:_ * An exaggerated and **enlarged aortic arch** is visible, creating a soft-tissue opacity bulging out from the mediastinum into the left cranial thorax * The **trachea can be displaced ventrally** (lateral view) and to the **right** (VD or DV view) by the soft tissue opacity * **Notching of the ribs** (small indentation surrounded by fine rim of sclerotic bone) is highly suggestive of aortic coarctation in humans and has also been reported in dogs. It occurs due to **enlargement of the intercostal arteries**. These carry collateral circulation in a retrograde direction from both the costocervical trunk and internal thoracic arteries to supply the distal aorta. _Angiocardiography:_ * Cardiac catheterization and aortography are indicated to localize accurately the site of obstruction, determine the length of the coarctation and identify associated malformations.

Answer 30

**Dilated cardiomyopathy** * DCM is characterized by **left-sided or four-chamber dilatation** and **impaired left ventricular systolic function.** * DCM is a major cause of morbidity and mortality in various large and giant breeds of dog, including Deerhounds, Dobermanns, Great Danes, Irish Wolfhounds, Newfoundlands, * St Bernards and spaniel breeds (Cocker and American Cocker, English Springer). * Presentation is usually associated with the onset of congestive heart failure, with coughing or dyspnoea. Exercise intolerance may be marked. It may be associated with episodic tachyarrhythmias, such as ventricular tachycardia, resulting in syncopal episodes. There is a long, presymptomatic phase of this disease and the onset of congestive heart failure is merely the 'tip of the iceberg'. Thoracic radiographs should be obtained in all dogs where left-sided congestive heart failure is suspected clinically, or is imminent. Radiographs are exquisitely sensitive at documenting the volume load associated with left-sided congestive heart failure (pulmonary oedema). A pulmonary infiltrate associated with left atrial enlargement and pulmonary venous congestion is consistent with cardiogenic pulmonary oedema. In clinical symptomatic DCM, the cardiac silhouette is almost always abnormal. Possible findings include : * Left atrial and left ventricular enlargement * Right atrial and right ventricular enlargement * The cardiac silhouette may have a sharp 'static' In left-sided congestive failure: * Triad of signs: LA enlargement, pulmonary venous distension and pulmonary infiltrate * The pulmonary infiltrate due to pulmonary oedema is normally predominantly perihilar. It may be interstitial, alveolar or mixed. In right-sided congestive failure: * Evidence of abdominal effusion (ascites) in the cranial abdomen * Distended CdVC * Pleural effusion

Answer 31

HCM is the most common form of myocardial disease affecting cats. It is genetically transmitted as an acquired, **autosomal dominant** trait (proven in **Maine Coons**). It is characterized by **concentric left ventricular hypertrophy**, which may be **regional or asymmetrical**. The wall thickness:LV chamber diameter ratio (= relative wall thickness) is greatly increased. Evidence of **diastolic dysfunction** is documented by Doppler studies. This is manifested by progressive left atrial enlargement. Symptomatic cats present with signs of **left-sided congestive heart failure** (dyspnoea due to pulmonary oedema). This is often of sudden onset , and may be preceded by a stressful incident or fluid loading. There is a **long presymptomatic phase.** Affected cats may fortuitously have a heart murmur detected, which leads to an early diagnosis. Other cats may be detected by echocardiographic screening schemes in breeds, such as Maine Coons and Persians. _Radiography:_ * Left atrial enlargement * Pulmonary venous distension * Pulmonary infiltrate, which may affect any region of the lung field, and be patchy, interstitial, alveolar or mixed. This is consistent with pulmonary oedema. Radiography does not differentiate between the various myocardial diseases. In asymptomatic HCM, there **may be no gross radiographic evidence of cardiomegaly** or specific chamber enlargement. In symptomatic HCM, left atrial enlargement is evident. Radiographically, apparent biatrial enlargement may be documented, but in most cases, echocardiography shows that the marked left atrial enlargement pushes the interatrial septum and the right atrial wall more to the right and cranially, giving this impression on the cardiac silhouette. The apparent biatrial enlargement gives the classical 'valentine' shaped heart on the DV view (Figure 7.102b). A pleural effusion may be present, associated with biventricular failure.

Answer 32

_Restrictive cardiomyopathy_ RCM is much more poorly understood than other forms of cardiomyopathy in the cat. It is characterized by **relatively normal wall thickness,** **LV chamber size and systolic function, but marked left atrial enlargement** is apparent. The pathophysiology is associated with **reduced LV compliance and diastolic dysfunction**. With elevated filling pressures, there is a restrictive filling pattern on mitral inflow (however, note that this diastolic abnormality is not specific for RCM). _There are two main forms:_ * **An endomyocardial form:** believed to be **post-inflammatory** (feline endomyocarditis) . There is irregular endocardial thickening * **A myocardial form:** the initiating factor is unknown and the endocardium appears normal. A consequence of the marked left atrial enlargement may be **thromboembolism**. ReM is usually not detected until the cat presents with **left-sided congestive heart failure or thromboembolic complications.** _Radiography:_ This does not differentiate between the various myocardial diseases. * In RCM, there is **usually dramatic left atrial enlargement** (which may appear radiographically to reflect biatrial enlargement) . Signs of **left-sided congestive heart failure** include pulmonary venous distension and a pulmonary infiltrate .

Answer 33

**Secondary myocardial disease**: The myocardium is influenced by other systemic factors, including: * Systemic hypertension * Hyperthyroidism * Hypothyroidism * Chronic renal failure * Acromegaly * Respiratory disease (cor pulmonale) These may result in significant cardiac disease or congestive heart failure. Diagnostic tests other than imaging are required to make the diagnosis of a secondary myocardial disease. _Systemic causes of myocardial depression:_ In the presence of **impaired systolic function,** it **should not be merely presumed** that this represents, for example, a preclinical phase of **DCM**. Conditions which should be excluded are: * **Tachyarrhythmia.** An animal which is tachycardic (e.g. supraventricular tachycardia) may develop a phenotype similar to DCM (called a tachycardiomyopathy). Control of rate (and/or rhythm) should result in improved systolic function * Assessment of systolic function or chamber dimensions should not be carried out in the presence of a dysrhythmia, if possible. Altered electrical activation of the ventricles or abnormal rate can give misleading results * **Hypothyroidism.** There have been several case reports of dogs with hypothyroidism and DCM, with improvement in systolic function associated with thyroid supplementation. It is not clear that the association is cause and effect; many breeds show prevalence of both conditions * Systemically ill animals may show myocardial depression possibly associated with elevated cytokine levels. _Systemic hypertension:_ Systemic hypertension results in **increased afterload** (arterial resistance) on the LV; LV pressure then increases to maintain cardiac output. To normalize wall stress, **concentric LV** hypertrophy occurs. Therefore, the walls are thick and the LV chamber may be proportionately small. Systemic hypertension is normally believed to be **secondary to a primary problem** in animals. Essential hypertension is considered to be rare. Conditions which may result in hypertension include: * Chronic renal failure * Hyperthyroidism * Hyperadrenocorticism * Acromegaly * Phaeochromocytoma * Hyperaldosteronism (Conn's syndrome). Note that some of these conditions are associated with factors that have a **direct trophic effect on the myocardium** (see previously), so not all changes are related to the hypertension. _Pulmonary hypertension (cor pulmonale):_ Pulmonary hypertension is a consequence of primary respiratory disease or abnormalities of the pulmonary vasculature. Mild degrees of pulmonary hypertension are recognized in brachycephalic breeds of dogs and in obesity (Pickwickian syndrome). Severe pulmonary parenchymal disease, such as **idiopathic pulmonary fibrosis** in **West Highland White Terriers**, can result in more significant pulmonary hypertension, although the cardiac manifestations are not usually clinically relevant to the presentation. Pulmonary vascular disease may be secondary to **parasitism,** such as **Dirofilaria immitis or Angio- strongylu**s vasorum infection. Pulmonary vascular disease may be a consequence of an initially left-to-right shunting congenital heart disease, leading to **Eisenmenger's physiology** (e.g. **reverse-shunting PDA or VSD**). It is the pulmonary hypertension which results in reversal of the shunting from the pulmonary into the systemic circulation, for those phases of the cardiac cycle where pulmonary pressures exceed systemic pressures, resulting in cyanosis. Sometimes, the cause of the pulmonary vascular disease is unknown (essential or primary pulmonary hypertension) . _Myocardial infiltrative disease:_ Unusually, the myocardium can be affected by infiltration. These infiltrations are normally neoplastic, such as **lymphoma.** Other, non-cardiac signs usually result in the presentation of the patient. Cardiac dysrhythmias, such as ventricular tachycardia, may be clinically important.

Answer 34

Findings vary with the amount of fluid and the rate at which it developed. Rapid accumulation of fluid may cause tamponade without radiographic signs of cardiomegaly. The classic appearance is a **generally enlarged** and **globoid cardiac silhouette** with: * Sharply defined margins * No specific chamber enlargement. A careful examination for heart base masses and right atrial mass effect should be performed; however, often no radiographic evidence is seen. A search for **pulmonary metastases** and **thoracic lymphadenopathy** should be performed. There may be hypoperfused lung fields due to tamponade and radiographic features of right-sided heart failure.

Answer 35

* There are usually radiographic features of **pericardial effusion**. * It is **unusual to see focal right atrial enlargement**. * The lungs should be evaluated for evidence of **metastasis** (most commonly these are **poorly defined small coalescing nodules** (see Figure 12.56, p. 268), less commonly they are well circumscribed nodules or an **alveolar infiltrate secondary to haemorrhage**). * **Hepatosplenomegaly** may be seen: in this case **right-sided heart disease** or **metastatic neoplasia** should be considered.

Answer 36

Heart base masses are usually **chemodectomas**, but **ectopic thyroid and parathyroid tumours** may be found less commonly in this location. * **Chemodectomas** (also known as non-chromaffin paragangliomas, members of the APUDoma (amine precursor uptake and decarboxylation)) group of neoplasms) are **tumours of the aortic bodies**. These are congregations of neuroendocrine cells **responsible for detecting blood pressure changes**. * **Brachycephalic** breeds are predisposed to chemodectomas and this is thought to have an association with **chronic hypoxia.** * Occasionally, chemodectomas are seen in **other locations**, such as the **cranial mediastinum**. * In the heart, they w**rap around the aortic root and main** **pulmonary artery**. * They are **locally invasive** and **expansile**. * **Metastasis** is seen in dogs and cats but is not common (occurs in approximately 10-20% dogs) and is **slow to occur.** * Metastatic sites include the **lung, LA, pericardium, liver and kidney.** _Radiographic findings include:_ * There is often minimal or no change in the appearance of the cardiac silhouette * **Mass border effacing or silhouetting** with **cranial aspect of the cardiac silhouette** * **Focal elevation of the terminal** (caudal) part of the **trachea** on the lateral view (Figure 7.150) * Focal deviation of the terminal trachea on the DV/ VD view in association with a soft tissue mass * There **may be radiographic features of pericardial effusion .**

Answer 37

The manifestations of heartworm disease depend on the number of worms, the chronicity of infection and on interactions between the parasite and host. Most dogs with heartworm infection are asymptomatic. Presenting signs in symptomatic dogs may include lethargy, coughing , poor condition, ascites and syncope. More **serious consequences** of heartworm disease, such as **parasitic eosinophilic pneumonitis,** may occur. **Rare complications** include: * Eosinophilic granulomatosis * Thromboembolic disease * Pulmonary hypertension * Glomerulonephritis * Caval syndrome * Disseminated intravascular coagulation (DIC) Clinical signs in cats are often chronic and non-specific . These include anorexia, weight loss, vomiting, dyspnoea and coughing. **More acute signs** are usually due to **aberrant worm migration** (more common in cats than dogs) or **worm embolization**, and include shock, salivation , haemoptysis, neurological signs, vomiting, syncope and even death _Radiographic findings include:_ **Dogs** (Figure 7.153). Changes primarily reflect the pulmonary hypertension that results from physical obstruction to outflow by adult worms living in the RV and pulmonary outflow tract, as well as changes to the walls of the pulmonary arteries : * Enlargement of the right side of the heart ('reverse D ' appearance on VD/DV view) * Enlargement of the main pulmonary artery segment * Enlargement and tortuosity of the (particularly caudal) lobar pulmonary arteries * Right heart failure may be evident in advanced disease * There may be **diffuse bronchointerstitial pulmonary pattern** due to **eosinophilic infiltrates** associated with an allergic response * Patchy dense i**nterstitial to alveolar infiltrates** may be seen , associated with p**ulmonary thromboembolism** **Cats** (Figure 7.154): * Most commonly enlargement of the **caudal** **lobar pulmonary arteries (\>1.6 times the ninth****rib on the VD view)** * Tortuosity of these vessels and enlargement of the right side of the heart is much less common than in dogs * Bronchointerstitial or even alveolar pulmonary infiltrates and pulmonary hyperinflation, mimicking feline bronchial disease have also been reported * Changes may also be seen in cats that ultimately resist heartworm infection and are eventually negative for the disease

Answer 38

Angiostrongylus vasorum is a **metastrongylid nematode** that infects domestic **dogs**. A. vasorum has a worldwide distribution and within Europe is endemic in southern England, France, Ireland and Denmark. **Foxes** are presumed to act as a **wildlife reservoir** for the parasite. The **adult worm** is oviparous and lives in the **right side of the heart or the pulmonary arteries,** from where the **eggs are carried to the pulmonary capillaries.** The eggs hatch and first-stage (L 1) larvae migrate through the alveolar epithelium, are **coughed up, swallowed and passed in the faeces**. The life cycle is indirect and larvae undergo subsequent moults within a molluscan intermediate host, to become third-stage (L3) larvae. When a dog ingests an intermediate host, infective L3 larvae are liberated into the dog's small intestine. The L3 larvae undergo two further moults in the **mesenteric lymph nodes** and the L5 larvae migrate via the **liver to the right side of the heart,** completing the life cycle. * The most common clinical signs associated with angiostrongylosis are **coughing and dyspnoea** caused by the **inflammatory response to the eggs and migrating larvae** at the level of the alveolar membrane. * The second common manifestation of angiostrongylosis is a **coagulopathy.** * ****Subcutaneous, mucosal and internal haemorrhages may all be seen. * Neurological signs associated with cerebral haemorrhage may also occur. * Bleeding may occur with or without concurrent respiratory disease and the pathogenesis of the coagulopathy is undetermined. * A minority of dogs suffer collapse episodes or sudden death, possibly due to aberrant larval migration into the myocardium. The majority of affected dogs are **young** and **Cavalier King Charles Spaniels** appear particularly predisposed to clinical disease. _Radiography_ Significant thoracic radiographic abnormalities are present in almost all clinically affected dogs. * Most common findings are **alveolar infiltrate** and **bronchial thickening** (seen in approximately 80% and 70% of dogs, respectively). Typically, the **alveolar infiltrate** has a **multifocal or peripheral distribution**. Less commonly a **mild, generalized interstitial pattern may be seen** * Note that the same thoracic radiographic changes are also seen in most dogs with A. vasorum-associated coagulopathy, even in the absence of clinical signs of respiratory disease * Less common findings include a **small volume pleural effusion** and **right ventricular enlargement** * Although A. vasorum is a pulmonary vascular parasite, significant radiographic changes affecting the pulmonary arteries are not usually seen * Radiographic improvement may lag behind clinical resolution * Residual alveolar infiltrate may still be present * 1 month after successful treatment and an **interstitial pattern may persist for up to 3 months**. Angiostrongylosis should be suspected in any young dog presenting with compatible clinical signs and a typical radiographic pattern (see below). The diagnosis is confirmed by demonstrating the presence of L1 larvae in the **faeces or airway cytology** samples. Other diagnostic findings are variable. Eosinophilic inflammation in airway cytology samples is less common than might be expected. The results of coagulation function testing are inconsistent and in some cases may be normal.

Answer 39

Pulmonary thromboembolism (PTE) results in **interruption of the blood supply to a portion of the lung** due to **obstruction of a pulmonary artery(ies)** by _embolic material:_ * Blood clots * Parasites * Tumour fragments * Bacterial aggregates * Bone marrow fat, * etc. delivered by the blood stream. _Primary thrombosis_ (formation in situ) may result from: * Local stasis * Turbulent blood flow * Vascular injury _Hypercoagulable states_, such as those that exist with: * Glomerulonephritis * Cushing's disease * Pancreatitis * DIC also predispose to thrombus formation in both the pulmonary and systemic circulation. The consequences of PTE depend on the magnitude of the obstruction and the pre-existing condition; they may range from insignificant to severe ventilation-perfusion mismatching, development of pulmonary hypertension and right heart failure. _Radiography:_ * **Most commonly** there are **no** survey radiographic **abnormalities.** * **Enlargement of the hilar** portion of the p**ulmonary arteries** may be identified; there may be **abrupt reduction in size or termination.** * **Poor perfusion** to part or all of a lung lobe may result in a **hyperlucent** appearance in the absence of hyperinflation. * There may be **atelectasis of a lung lobe**, resulting in a **mediastinal shift** and **displacement of the diaphragm.** * **Focal pleural effusion** may be seen around the **affected lobe.** * Occasionally, there are **peripheral triangular areas** of consolidated lung extending to the pleural margin, **particularly in the caudal lung lobes.** _Contrast studies:_ * Pulmonary angiography **may delineate abrupt termination or filling defects** in **large pulmonary arterial segments**, or areas of decreased or absent perfusion. * Interpretation may be difficult in lungs with abnormal findings on plain films; abnormal perfusion to areas of lung that appear radiographically normal is much less equivocal.

Answer 40

In animals, this term describes **post-sinusoidal hypertension** and the development of a **high-protein peritoneal effusion** due to the **obstruction of hepatic venous return to the heart**. _The obstruction may involve the:_ * Junction of the hepatic veins with the CdVC * CdVC itself between the entry of the hepatic veins and the heart * RA. _Causes include:_ * **Thrombosis**, associated with **heartworm disease** * **Compression or invasio**n of the cava by tumours or other masses * **Trauma**-induced **stricture, fibrosis, diaphragmatic hernia** * **Congenital** cardiac (e.g. CTD) or caval (e.g. membranous obstruction) anomalies. _Radiography_ * Other than **ascites**, radiographic features are not specific. * **Absence** (congenital) of the ***CdVC,*** **masses, hernias** or other abnormalities in the region of the caudal mediastinum, diaphragm or liver may be seen. _Contrast studies:_ * A caudal vena cavagram (lateral saphenous injection) may demonstrate invasion, compression or obstruction of the CdVC. _Ultrasonography:_ * Abdominal ultrasonography may identify abnormalities of the liver or the abdominal Portion of the CdVC. * **Doppler** interrogation may identify abnormal or **retrograde flow**. Colour Doppler evaluation of the hepatic veins and CdVC provides the most information regarding the presence and direction of blood flow within the hepatic veins and CdVC. _Computed tomography:_ * CT may demonstrate structural abnormalities or masses * CT angiography may be necessary to demonstrate vascular abnormalities.

Answer 41

CrVC syndrome results from **obstruction of the CrVC** with resulting impairment of the venous return from the cranial parts of the body to the heart. _Reported causes include:_ Great vessel **invasion/compression**: * ****Tumour (e.g. thymoma) * Granuloma (e.g. blasto- mycosis) * Thromboembolism. _Predisposing factors include:_ Conditions that contribute to a hypercoagulable state: * Immune-mediated disease * Sepsis * Glomerulonephritis * Cardiac disease * Neoplasia * Corticosteroid administration * Central venous catheters with these pre-existing conditions The clinical signs include **symmetrical, simultaneous swelling of the head, neck and forelimbs.** _Radiography:_ * Radiographs **may be normal or may demonstrate the cause of the obstruction** (e.g. cranial mediastinal mass) _Contrast studies:_ * Angiography may demonstrate **intraluminal filling defects, extraluminal compressive masses or other** causes of CrVC obstruction. * Non- selective angiography via the **jugular vein** is preferred but may be difficult in the face of swelling of the soft tissues of the neck; cephalic vein administration of contrast medium should also provide excellent opacification

Answer 42

The width of the cranial mediastinum * In **dogs**, the maximum width of the cranial mediastinum on a VD/DV view should be **less than twice the width** of the **vertebral column** at this level. * In **cats**, the cranial mediastinum should be **no wider than the width of the superimposed thoracic spine** on a VD/DV view.

Answer 43

(i) The normal perihilar structures are seen on lateral and DV views. Note that the angle between the caudal mainstem bronchi can vary with breed and centring of the X-ray beam. (iI) The mass effect created by simultaneous enlargement of the **left and right tracheobronchial lymph nodes** is demonstrated. Both nodes can accentuate the ventral deflection of the trachea at the carina. The left and right nodes can be separated by looking for the adjacent bronchus. The left bronchus bifurcates Immedialely ventral to the carina. (iii) The mass effect created by an enlarged **middle tracheobronchial lymph node.** Note that the caudal lobar bronchi are separated on the DV view and pushed ventrallyon the lateral view. (Iv) The mass effect created by the **cranial mediastinal lymph nodes**. If these nodes are large enough they can elevate the trachea. Note that heart base tumours are often located in this region and can produce a similar effect. (v) **Enlarged pulmonary arteries** (and somellmes veins) can sometimes be mistaken for enlarged lymph nodes. This is a diagram of enlargement of the main pulmonary artery in dirofilariasis. (vi) **Letf atrial enlargement** can be easily distinguished from middle tracheobronchial node enlargement. Both separate the caudal mainstem bronchi on a VD/DV view, but on the lateral view the bronchi are depressed ventrally with node enlargement and dorsally (especially the left) with left atrial enlargement.

Answer 44

* Unilateral lung collapse (concomitant signs should be looked for: increased opacity of the lung, cranial displacement of the diaphragm on affected side, etc .) * Pleural disease with pleural adhesions * Unilateral pleural effusion * Unilateral pneumothorax * Unilateral lobar overinflation due to unilateral pulmonary emphysema or compensatory hyperinflation * Large single or multiple pulmonary masses * Unilateral diaphragmatic hernia/rupture * Deformities of the thoracic wall or spine, such as scoliosis or pectus excavatum.

Answer 45

Mediastinal masses may be located anywhere within the mediastinum, depending on their aetiology and tissue of origin. Mediastinal masses have been divided into **five main locations** (Figure 8.19). As with other parts of the body, location may suggest the organ or tissue of origin. For example, a perihilar mass is likely to be due to either enlargement of the tracheobronchial lymph nodes or a mass at the heart base. Often masses can be so large at presentation that their origin is difficult to determine. Assessment of displacement of other intrathoracic structures is useful to determine the origin of such masses. The majority of masses are of soft tissue opacity, thus not permitting further differentiation on the basis of radiological appearance, but occasionally masses may be **mineralized (e.g. teratoma)** or of **fat opacity (e.g. mediastinal lipoma)**. Ultrasonography can be very useful in further assessment of these lesions, either using the heart or liver as an acoustic window, or, if the mass is large enough, by a direct transthoracic technique. Occasionally, it is difficult to decide whether a mass near the midline originates from the mediastinum or from a lung lobe adjacent to the mediastinum. This can be a challenging distinction to make. Factors that may assist in differentiation are: * The DV or VD view may provide an immediate answer as to whether or not the mass is in the midline * Extrapleural sign may be seen with mediastinal mass * A **mediastinal mass will usually be equal in size and similar in appearance on both left and right lateral** views whereas a **pulmonary mass may change with altered magnification** and inflation of the surrounding lung * Displacement and effacement of mediastinal structures suggests a mediastinal origin, but may occur if a pulmonary mass is large enough and close enough to the midline * Ultrasonography may be useful in evaluation of motion of the mass with lung movement if a suitable window can be obtained

Answer 46

_Thoracic, tracheal , oesophageal and cervical injury:_ * Blunt thoracic trauma resulting in bronchial or alveolar rupture * Perforating injury to skin or neck (e.g. puncture wounds, pharyngeal stick injuries) * Iatrogenic cervical or tracheal injury (e.g. jugular venepuncture, transtracheal washing, tracheostomy) * Tracheal rupture (e.g. secondary to overinflation of endotracheal tube cuff) Oesophageal rupture (e.g. foreign body, bite wound, iatrogenic) _Spontaneous:_ following * Cough * Respiratory disease, such as paraquat toxicity * Pulmonary emphysema _Lung lobe Torion causing bronchial tear_ (rare) _Idiopathic_

Answer 47

Mediastinal effusion or fluid is **uncommon**. Effusions include pus, lymph, blood, chyle, transudate and modified transudate. In **chylomediastinum**, effusion from the **thoracic duct** will initially be limited to the mediastinum, but the fluid has usually entered the pleural space by the time the animal shows clinical signs. **Haemomediastinum** may result from **trauma**. This may occur due to bleeding from one of the great vessels (usually rapidly fatal) or the haemorrhage may extend into the mediastinum from trauma to the neck. Other causes of mediastinal haemorrhage include **coagulopathy, neoplastic erosion of vessels and, rarely, rapid involution of the thymus** (which is usually fatal). **Oesophageal perforation** results in **mediastinitis**, and initially small volumes of fluid may distribute evenly throughout the mediastinum. Some neoplastic masses may produce a modified transudate. _Radiography:_ A DV view is the most useful: * **Reverse fissures** are visible at the heart base * Some widening of both the cranial mediastinum and the caudoventral mediastinal reflection is seen . On the lateral view, the apex of the heart and the cranioventral mediastinal reflection may be obscured, but changes may be minimal.

Answer 48

Mediastinitis implies **infection** or **inflammation** in the mediastinum and results in thickening of the mediastinal pleurae and exudate production. It can develop from a _primary disease process_, such as: * Chronic fungal - Histoplasma or Cryptococcus species * Bacterial - including Actinomyces and Nocardia species * Granulomatous mediastinitis * Spirocercosis has also been associated with mediastinitis Mediastinitis may also occur _secondary to:_ * Perforation of the trachea or oesophagus * As an extension of an infectious or inflammatory process from the cervical soft tissue, pericardium, pulmonary parenchyma or pleural space. The **most common** cause is **oesophageal perforation**, Clinical features may include tachypnoea, dyspnoea, pain, cough, regurgitation, voice change (secondary to recurrent laryngeal nerve involvement) and head and neck swelling. _Radiography:_ * Widening and perhaps increase in opacity of the mediastinum may be seen, particularly on the DVNDview. * If the inflammation is focal then discrete thickenings or mass lesions may be seen, which must then be differentiated from neoplastic mediastinal masses. * Pneumomediastinum may be present if the mediastinitis is secondary to tracheal or oesophageal perforation. _Contrast studies:_ * **If oesophageal perforation** is suspected then oral administration of a small volume (5-10 ml) of **non-ionic water-soluble iodine-containing** contrast medium, such as iohexol, may identify the site. Both lateral and DV/VD views should be taken to look for evidence of extravasation of the contrast medium. If no extravasation is seen on initial films then repeat films should be taken 5-10 minutes later to look for slow leakage. * In cases of chronic oesophageal per1oration, the original perforation may have closed and no contrast leakage will be evident.