Cardiovascular Flashcards
What is located more cranial - the pulmonary valve or the aortic valve?
The pulmonary valve
Normal dog size:
Lateral:
- 70% height
- 2.5-3.5 rib spaces
VD:
- 60-65% thoracic width
In the clock analogy where does the aorta live?
11-1 o’clock
In the clock analogy where does the PA live?
1-2 o’clock
In the clock analogy where does the left auricle live?
2-3 o’clock
In the clock analogy where does the left ventricle live?
2-6 o’clock (dog) 3-6 o’clock (cat)
In the clock analogy where does the right ventricle live?
6-9 o’clock
In the clock analogy where does the right atrium live?
9-11 o’clock
Describe the cardiovascular structures using the “clock analogy” in lateral recumberncy.
Describe the cardiovascular structures using the “clokc analogy” in DV/VD position.
Selective angiography - right atrial injection (normmal dog)
RAA = right auricular appendage
RV = right ventricle
PSV = pulmonary sinus of valsalva
MPA = main pulmonary artery
RPA = right pulmonary artery
LPA = left pulmonary artery
Selective angiography - right atrial injection (normal dog)
6 seconds after injection
PV = pulmonary veins
LA = left atrium
LV = left venrticle
AA = ascending aorta
BT = brachipocephalic trunk
LSA = left subclavian artery
What are some differentials for aortic arch enlatrgement?
Cats (age related)
PDA = patent ductus arteriosus
Subaortic stenosis = post-stenotic dilation
Aortic aneurism (rare)
What are some differentials for caudal vena enlargement?
R-CHF
Caval syndrom (Dilofilaria)
Obstruction of CVC or RA = blood clot of mass
Artifactual = respiratory or cardiac cycle
What are some differentials for MPA dilation?
Post-stenotic dilation = pulmonic stenosis
Pulmonary hypertension
PTE
HW dz
Left to Right shunt = PDA, VSD, ASD
What are some differentials of pulmonary venous enlargement?
L-CHF
Left atrial obstruction
Fluid overload
Left to Right shunts (PDA, ASD, VSD)
What are some differentials for small pulmonary vessels?
Dehydration/hypovolemia
Addison’s dz
Right to Left shunt (shunt reversal)
Pulmonic stenosis
PTE
Decreased CO (pericaridial effusion, restrictive pericarditis, R-CHF)
What are radiographic signs of a PDA?
What are radiographic signs of Pulmonic Stenosis (PS)?
What are radiographic signs of Subaortic Stenosis (SAS)?
What are radiographic findings of VSD?
-Depends on the severity
Describe the blood flow of a VSD
Cranial vena caval injection angiogram (dog)
What are the pertinent findings and diagnosis?
Right atrial injection angiocardiogram (dog).
What are the pertinent findings and diagnosis?
Right ventricular injection angiogram (dog).
What are the pertinent findings and diagnosis?
Aortic injection angiogram in a normal dog.
Coronary anatomy.
Describe the different variations of cardiac positions
on the DV/VD projection.
- Levocardia - location of the heart in the left side of the thorax, the apex pointing towards the left
-
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 - Dextrocardia - location of the heart in the right side of the thorax, the apex pointing towards the right. The cardiac chambers are reversed
- Dextroposition - displacement towards the right
- 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.
Normal left-sided angiogram in a 5 year old Golden Retriever
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)
Normal right-sided angiocardiogram of the dog
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
Locatin of the cardiac chambers on thoracic
radiographs of a dog
(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
Location of the cardiac chambers on thoracic
radiographs of a cat
Clock face analogy to identifying the location of the
cardiac chambers
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.
Normal Golden Retriever
(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.
Normal Doberman and Greyhound
- (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.
What is the normal location of the carina on the
lateral radiogaphs?
The carina should be located within the 4th-5th intercostal space.
Caudal Vena Cava
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.
What are some causes of caudal vena cava enlargement?
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
Cranial Vena Cava
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.
Azygoys vein
- 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.
What are some causes of narrowed caudal vena cava
- Shock
- Hypovolaemia
- Addison’s disease (hypoadrenocorticism)
- Artefactual (pulmonary hyperinflation)
Causes of mineralized caudal vena cava
- Mineralized masses
- Other dystrophic mineralization
- Metastatic mineralization:
- Hyperadrenocorticism (Cushing’s disease)
- Secondary hyperparathyroidism
- Renal disease
Differentials for enlarged main pulmonary artery
- Pulmonic stenosis (post-stenoic dilation)
- Increased circulating volume (PDA, AS, VSD)
- Pulmonary hypertension
- Severe heartworm disease and angiostrongylosis
- Artefactual:
- VD position
- Systole
- Positional rotation
Differentials for small pulmonary arteries and veins
- 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
Differentials for pulmonary arterial dilation
- Pulmonary hypertension
- PTE
- HW dz
- Left-to-right shunts (PDA, VSD, ASD)
- Angiostongylosis (but not often a feature)
- Peripheral arteriovenous fistula
Patent Ductus Arteriosus
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:
- 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
- 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
- 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.
Left-to-Right shunting PDA
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)
Right-to-left shunting PDA
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.
*
Pulmonic Stenosis
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:
- 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
- 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
- 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
Pulmonic Stenosis Angiocardiography
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 branchesfrom this single artery a few millimetres distal to its aortic origin (Figure 7.58).
Aortic Stenosis
Aortic Stenosis:
- 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.
- 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.
- 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.
Aortic Stenosis Angiography
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.
Ventricular Septal Defect
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.
Atrial Septal Defect
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:
- High in the atrial septum, near the entrance of the pulmonary veins. These are sinus venosus ASDs and are very rare
- 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
- 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.
Tetralogy of Fallot
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:
- Pulmonic stenosis leading to right ventricular outflow obstruction (main pulmonary artery atresia may also be present)
- Secondary right ventricular hypertrophy
- A subaortic VSD
- 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 is 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
Vascular Ring Anomaly
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.
Aortic Coarctation
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 takes 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.
Dilated Cardiomyopathy
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
Hypertrophic Cardiomyopathy
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.
Restrictive Cardiomyopathy
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 .
What are some causes of secondary myocardial disease?
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- strongylus 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.
Pericardial Effusion
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.
Right Artial Hemangiosarcoma
- 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.
Heart Base Masses
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 wrap 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 .
Heartworm Dz
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 interstitial to alveolar infiltrates may be seen , associated with pulmonary thromboembolism
Cats (Figure 7.154):
- Most commonly enlargement of the caudal lobar pulmonary arteries (>1.6 times the ninthrib 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
Angiostrongylosis
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.
Pulmonary Thromboembolism
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 pulmonary 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.
Bud-Chiari-like syndrome
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 invasion 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.
Cranial Caval Syndrome
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
Normal Cranial Mediastinal Width
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.
Differentials for increased perihilar opacity
(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.
Causes of mediastinal shift
- 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.
Mediastinal Masses
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
Causes of Pneumomediastinum
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
Mediastinal Effusion
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.
Mediastinitis
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.
