Congenita heart disease: ATRIAL AND VENTRICULAR SEPTAL DEFECTS: Ettinger Flashcards

(45 cards)

1
Q

ATRIAL AND VENTRICULAR SEPTAL DEFECTS

During cardiac embryonic development the atria and ventricles begin as a common chamber. The heart is subsequently partitioned into the normal four-chambered heart by the growth of cardiac septa.15a The atria are partitioned by a wall formed mainly from two septa: the septum………….., which forms first, and the septum ………….., which develops to the ……………t of the septum primum. The ……………, a slitlike passageway, which persists between these septa, permits ………..to……….. atrial shunting in the fetus, but functionally and anatomically closes in the neonate when ……………. pressure rises.

A

The atria are partitioned by a wall formed mainly from two septa: the septum primum, which forms first, and the septum secundum, which develops to the right of the septum primum. The foramen ovale, a slitlike passageway, which persists between these septa, permits right-to-left atrial shunting in the fetus, but functionally and anatomically closes in the neonate when left atrial pressure rises.

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2
Q

The major portion of the ventricular septum forms by inward growth from the ventricular walls. The area of atrioventricular confluence, including the upper ventricular septum, lower atrial septum, and atrioventricular valves, is formed primarily by growth and differentiation of the ………………………..

A

The major portion of the ventricular septum forms by inward growth from the ventricular walls. The area of atrioventricular confluence, including the upper ventricular septum, lower atrial septum, and atrioventricular valves, is formed primarily by growth and differentiation of the endocardial cushions.

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3
Q

Defects in the development of the embryonic ventricular septum, the primum or secundum atrial septa, or the endocardial cushions, may result in atrial and/or ventricular septal defects. Congenital septal defects are common in both dogs and cats as isolated lesions and as components of more complex lesions such as tetralogy of Fallot.4a-13a,62a-79a

A

Defects in the development of the embryonic ventricular septum, the primum or secundum atrial septa, or the endocardial cushions, may result in atrial and/or ventricular septal defects. Congenital septal defects are common in both dogs and cats as isolated lesions and as components of more complex lesions such as tetralogy of Fallot.4a-13a,62a-79a

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4
Q

PATHOGENESIS

Except for the proven genetic basis of ventricular septal defect in Keeshonden with conotruncal malformation,124a there are no data on the cause(s) of spontaneous septal defects in dogs or cats.[28],4a Atrial septal defects (ASD) are usually classified based on the anatomic region of the malformation.15a,16a Defects at or near the foramen ovale are referred to as ostium (or septum) ………….. defects (Figure 249-11), while defects of the lower atrial septum are called ostium primum defects. Rarely observed ………………. ASD are found dorsocranial to the fossa ovalis near the entrance of the cranial vena cava.

A

PATHOGENESIS

Except for the proven genetic basis of ventricular septal defect in Keeshonden with conotruncal malformation,124a there are no data on the cause(s) of spontaneous septal defects in dogs or cats.[28],4a Atrial septal defects (ASD) are usually classified based on the anatomic region of the malformation.15a,16a Defects at or near the foramen ovale are referred to as ostium (or septum) secundum defects (Figure 249-11), while defects of the lower atrial septum are called ostium primum defects. Rarely observed sinus venosus ASD are found dorsocranial to the fossa ovalis near the entrance of the cranial vena cava.

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5
Q

Since the endocardial cushions are responsible for partitioning the lowermost atrial septum, defects in the region immediately adjacent to the AV valves (septum primum) are often included in the term “endocardial cushion defects.” A defect in this area may also include anomalous development of the atrioventricular valves such as a “cleft” in the septal leaflet of the mitral valve.

A complete endocardial cushion defect is a large defect of the lower atrial septum and upper ventricular septum with fusion of the septal leaflets of both AV valves. This is also referred to as an AV canal defect, since the embryonic atrioventricular canal area never partitions and there is communication between all four cardiac chambers.

A

Since the endocardial cushions are responsible for partitioning the lowermost atrial septum, defects in the region immediately adjacent to the AV valves (septum primum) are often included in the term “endocardial cushion defects.” A defect in this area may also include anomalous development of the atrioventricular valves such as a “cleft” in the septal leaflet of the mitral valve.

A complete endocardial cushion defect is a large defect of the lower atrial septum and upper ventricular septum with fusion of the septal leaflets of both AV valves. This is also referred to as an AV canal defect, since the embryonic atrioventricular canal area never partitions and there is communication between all four cardiac chambers.

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6
Q

Patent foramen ovale is not a true ASD inasmuch as the atrial septum forms normally but the walls of the foramen are pushed apart, usually by conditions which increase right atrial pressure. A patent foramen ovale achieves clinical significance when it allows right-to-left shunting, as may occur with severe pulmonic stenosis or tricuspid valve dysplasia.

A

Patent foramen ovale is not a true ASD inasmuch as the atrial septum forms normally but the walls of the foramen are pushed apart, usually by conditions which increase right atrial pressure. A patent foramen ovale achieves clinical significance when it allows right-to-left shunting, as may occur with severe pulmonic stenosis or tricuspid valve dysplasia.

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7
Q

Most ventricular septal defects (VSD) are located in the upper ventricular septum (Figure 249-12). Muscular apical or mid-ventricular septal defects are uncommon in small animals.
On the left side, the typical location of a VSD is just below the ……………, most often centered between the ………. ……………. and …………………. cusps.

A

Most ventricular septal defects (VSD) are located in the upper ventricular septum (Figure 249-12). Muscular apical or mid-ventricular septal defects are uncommon in small animals.
On the left side, the typical location of a VSD is just below the aortic valve, most often centered between the right coronary and noncoronary cusps.

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8
Q

On the right side, the opening is often described by its position relative to the crista supraventricularis muscular ridge. A subcristal (infracristal) VSD is located proximal to the crista supraventricularis near the cranial aspect of the septal leaflet of the tricuspid valve, which may partially cover it. A supracristal VSD is located distal to the crista supraventricularis just below the pulmonic valve.

A

On the right side, the opening is often described by its position relative to the crista supraventricularis muscular ridge. A subcristal (infracristal) VSD is located proximal to the crista supraventricularis near the cranial aspect of the septal leaflet of the tricuspid valve, which may partially cover it. A supracristal VSD is located distal to the crista supraventricularis just below the pulmonic valve.

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9
Q

Large defects may obliterate the crista and are usually associated with additional defects, as in tetralogy of Fallot (see Figure 249-12).2a,4a The right side of the root of the aorta, including the right coronary and noncoronary cusps, may be displaced to the right so that the aorta straddles the defect. The altered geometry of the aortic root that accompanies many VSDs sometimes results in substantial aortic valve regurgitation.17b

A

Large defects may obliterate the crista and are usually associated with additional defects, as in tetralogy of Fallot (see Figure 249-12).2a,4a The right side of the root of the aorta, including the right coronary and noncoronary cusps, may be displaced to the right so that the aorta straddles the defect. The altered geometry of the aortic root that accompanies many VSDs sometimes results in substantial aortic valve regurgitation.17b

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10
Q

PATHOPHYSIOLOGY

Shunting across small (resistive) defects depends primarily on the size of the communication and the pressure difference between the ……………., while shunting across large (nonresistive) defects depends primarily on …………..

A

Shunting across small (resistive) defects depends primarily on the size of the communication and the pressure difference between the two chambers, while shunting across large (nonresistive) defects depends primarily on relative resistances of the systemic and pulmonary circulations.

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11
Q

In the absence of other abnormalities, left heart pressures exceed those on the right and the direction of shunting is …………………
Cardiac chambers in the circuit of the shunt enlarge to accommodate the excess blood volume and the pulmonary vasculature is overcirculated. Large volume left-to-right shunts eventually result in myocardial failure, elevated filling pressures, and the development of overt congestive heart failure.

A

In the absence of other abnormalities, left heart pressures exceed those on the right and the direction of shunting is left-to-right.
Cardiac chambers in the circuit of the shunt enlarge to accommodate the excess blood volume and the pulmonary vasculature is overcirculated. Large volume left-to-right shunts eventually result in myocardial failure, elevated filling pressures, and the development of overt congestive heart failure.

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12
Q

Right-to-left shunting occurs via a septal defect when …………,…………,or…………….. (3) raise pressures on the right side of the heart. The consequences of “reversed” shunting include cyanosis from arterial ……………., ………………… ……………….., and sudden death.

A

Right-to-left shunting occurs via a septal defect when pulmonic stenosis, tricuspid dysplasia, or pulmonary arterial hypertension raise pressures on the right side of the heart. The consequences of “reversed” shunting include cyanosis from arterial hypoxemia, polycythemia, hyperviscosity, and sudden death.

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13
Q

Atrial Septal Defect

Flow across an ASD occurs primarily during ……………. The pressure difference across the defect is ……. and the direction and magnitude of the shunt is determined mainly by the relative ……….. resistance to inflow for each ventricle.

Normally, the right ventricle is more compliant than the left and offers little resistance to filling, causing blood to preferentially shunt from the left atrium into the right atrium and ventricle. The result is ………….. of the right atrium, …………… hypertrophy of the right ventricle, and pulmonary …………………

A

Atrial Septal Defect

Flow across an ASD occurs primarily during diastole. The pressure difference across the defect is low and the direction and magnitude of the shunt is determined mainly by the relative diastolic resistance to inflow for each ventricle.
Normally, the right ventricle is more compliant than the left and offers little resistance to filling, causing blood to preferentially shunt from the left atrium into the right atrium and ventricle. The result is dilation of the right atrium, eccentric hypertrophy of the right ventricle, and pulmonary overcirculation.

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14
Q

ASD: …………… saturation in the right heart and pulmonary arteries is increased. The …………atrium receives the shunted blood, but most of the increased pulmonary venous return is shunted immediately into the right ………….., resulting in minimal ………………..

A

Oxygen saturation in the right heart and pulmonary arteries is increased. The left atrium receives the shunted blood, but most of the increased pulmonary venous return is shunted immediately into the right atrium, resulting in minimal left atrial dilatation.

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15
Q

If considerable left atrial enlargement is observed in an animal with an ASD, an additional defect, such as an …………………………… defect with mitral regurgitation, should be suspected. ………………………….. defects are more commonly detected in cats and may cause left sided or bilateral congestive heart failure.

A

If considerable left atrial enlargement is observed in an animal with an ASD, an additional defect, such as an endocardial cushion defect with mitral regurgitation, should be suspected. Endocardial cushion defects are more commonly detected in cats and may cause left sided or bilateral congestive heart failure. Endocardial cushion defects are reported in dogs, but are rare.

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16
Q

The flow across an ASD does not usually generate an audible heart murmur because the pressure gradient and flow velocity across the defect are …….. When the shunted blood joins with blood entering from the ……………, the volume and velocity of flow through the right heart is increased resulting a murmur of relative …………….(common) or …………………..(uncommon). Delayed closure of the ……………… (and ………………… closure of the aortic valve) causes splitting of the second heart sound.

Since the volume overload affects the…… ventricle and not the ….. large shunts culminate in the development of …….. heart failure.

A

The flow across an ASD does not usually generate an audible heart murmur because the pressure gradient and flow velocity across the defect are low. When the shunted blood joins with blood entering from the vena cava, the volume and velocity of flow through the right heart is increased resulting a murmur of relative pulmonic stenosis (common) or tricuspid stenosis (uncommon). Delayed closure of the pulmonic valve (and early closure of the aortic valve) causes splitting of the second heart sound.

Since the volume overload affects the right ventricle and not the left, large shunts culminate in the development of right heart failure.

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17
Q

Ventricular Septal Defect

Flow across VSD occur primarily during ventricular ……….. In the absence of other cardiovascular defects LV systolic pressure is …………….. times that of the right ventricle and flow proceeds from the left to the right ventricle. The magnitude of left-to-right shunting with small (resistive) defects is mainly determined by the …………….. of the defect and the systolic ……………… (…………….) between the …………….

A

Ventricular Septal Defect

Flow across VSD occur primarily during ventricular systole. In the absence of other cardiovascular defects LV systolic pressure is 4 to 5 times that of the right ventricle and flow proceeds from the left to the right ventricle. The magnitude of left-to-right shunting with small (resistive) defects is mainly determined by the diameter of the defect and the systolic pressure difference (gradient) between the ventricles.

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18
Q

The peak pressure difference across the defect can be estimated noninvasively by Doppler echocardiography. Using the peak flow velocity (meters/second) of the blood flow passing through the defect, the pressure gradient is calculated using the simplified Bernoulli equation (ΔP = 4V2). A resistive defect with normal right and left ventricular pressures (approximately 20 mm Hg and 100 mm Hg, respectively) is expected to have a peak jet velocity of …………. than …….m/s, corresponding to a peak pressure gradient across the defect of greater than ……mm Hg.

A

The peak pressure difference across the defect can be estimated noninvasively by Doppler echocardiography. Using the peak flow velocity (meters/second) of the blood flow passing through the defect, the pressure gradient is calculated using the simplified Bernoulli equation (ΔP = 4V2). A resistive defect with normal right and left ventricular pressures (approximately 20 mm Hg and 100 mm Hg, respectively) is expected to have a peak jet velocity of greater than 4.5 m/s, corresponding to a peak pressure gradient across the defect of greater than 80 mm Hg.

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19
Q

If the peak velocity is lower than predicted, right ventricular ………………. pressure is most likely increased, caused either by the presence of ……………….. or increased ……………………… (pulmonary arterial hypertension).

A

If the peak velocity is lower than predicted, right ventricular systolic pressure is most likely increased, caused either by the presence of pulmonic stenosis or increased pulmonary vascular resistance (pulmonary arterial hypertension).

20
Q

When a small VSD is located high in the membranous septum, blood is ejected by the left ventricle directly into the RV outflow tract and out the main pulmonary artery: the right heart experiences only a very modest volume load and right heart enlargement is minimal.

A

When a small VSD is located high in the membranous septum, blood is ejected by the left ventricle directly into the RV outflow tract and out the main pulmonary artery: the right heart experiences only a very modest volume load and right heart enlargement is minimal.

21
Q

Right heart enlargement is more prominent when the VSD is …………… or located in the …………….. region of the ………………. septum.

A

Right heart enlargement is more prominent when the VSD is large or located in the muscular region of the interventricular septum.

22
Q

With a typical, small, high VSD, oxygen saturation in the right ventricular outflow tract (RVOT) and pulmonary artery is higher than in the ………………..
Large shunts (pulmonary to systemic flow ratio greater than … : …) may overload the left and/or right heart enough to increase ventricular …………….. pressures and cause signs of left, right or biventricular failure. Very large, nonresistive VSDs cause the pressures in both ventricles to equilibrate and the two ventricles behave as a common pumping chamber.

Unless the pulmonary circulation is protected by a …………………. valve, the development of pulmonary hypertension is unavoidable.

A

With a typical, small, high VSD, oxygen saturation in the right ventricular outflow tract (RVOT) and pulmonary artery is higher than in the right atrium or apex of the right ventricle. Large shunts (pulmonary to systemic flow ratio greater than 3 : 1) may overload the left and/or right heart enough to increase ventricular diastolic pressures and cause signs of left, right or biventricular failure. Very large, nonresistive VSDs cause the pressures in both ventricles to equilibrate and the two ventricles behave as a common pumping chamber.

Unless the pulmonary circulation is protected by a stenotic pulmonic valve, the development of pulmonary hypertension is unavoidable.

23
Q

Eisenmenger’s Syndrome

In newborn animals with a large VSD, pulmonary …………….may not decline after birth, resulting in sustained pulmonary arterial hypertension. If right ventricular ……………..and ………………. pressures equilibrate at or above systemic (left ventricular) levels, bidirectional or right-to-left shunting may occur.
The development of pulmonary hypertension associated with a shunting cardiac defect is known as Eisenmenger’s physiology or syndrome. When the defect is a VSD, the term “Eisenmenger complex” is often employed.

A

Eisenmenger’s Syndrome

In newborn animals with a large VSD, pulmonary vascular resistance may not decline after birth, resulting in sustained pulmonary arterial hypertension.13b,14b If right ventricular systolic and diastolic pressures equilibrate at or above systemic (left ventricular) levels, bidirectional or right-to-left shunting may occur. The development of pulmonary hypertension associated with a shunting cardiac defect is known as Eisenmenger’s physiology or syndrome. When the defect is a VSD, the term “Eisenmenger complex” is often employed.

24
Q

Sustained pulmonary hypertension is characterized by progressive and irreversible changes in the pulmonary ………….. similar to those mentioned in the section on reversed PDA.
As in dogs with a PDA, reversed (right to left) shunting through a VSD is usually established before ……. months of age. In contrast to human patients, gradual development of pulmonary vascular disease and progressive pulmonary hypertension is relatively common in dogs and cats.

A

Sustained pulmonary hypertension is characterized by progressive and irreversible changes in the pulmonary arteries similar to those mentioned in the section on reversed PDA.
As in dogs with a PDA, reversed (right to left) shunting through a VSD is usually established before 6 months of age. In contrast to human patients, gradual development of pulmonary vascular disease and progressive pulmonary hypertension is relatively common in dogs and cats.

25
CLINICAL FINDINGS Breed predispositions for atrial and ventricular septal defects are indicated in Table 249-1. Clinical findings of the typical left-to-right ASD include a soft, grade 2-3/6, systolic ejection murmur over the left heart base and splitting of the second heart sound (Figure 249-13).[30],[31],23c-25c The murmur is often misinterpreted as mild pulmonic stenosis or as an innocent murmur.
CLINICAL FINDINGS Breed predispositions for atrial and ventricular septal defects are indicated in Table 249-1. Clinical findings of the typical left-to-right ASD include a soft, grade 2-3/6, systolic ejection murmur over the left heart base and splitting of the second heart sound (Figure 249-13).[30],[31],23c-25c The murmur is often misinterpreted as mild pulmonic stenosis or as an innocent murmur.
26
A low pitched, right-sided diastolic murmur of relative tricuspid stenosis may occur, but it is usually not audible, especially in smaller patients. Cyanosis is absent unless there is an additional defect such as pulmonic stenosis or tricuspid valve dysplasia,15b or the infrequent complication of pulmonary hypertension.26c Signs of right heart failure develop in dogs or cats with large defects. Differential diagnosis includes anomalous pulmonary venous return, which is an extremely rare anomaly in dogs and cats.80a
A low pitched, right-sided diastolic murmur of relative tricuspid stenosis may occur, but it is usually not audible, especially in smaller patients. Cyanosis is absent unless there is an additional defect such as pulmonic stenosis or tricuspid valve dysplasia,15b or the infrequent complication of pulmonary hypertension.26c Signs of right heart failure develop in dogs or cats with large defects. Differential diagnosis includes anomalous pulmonary venous return, which is an extremely rare anomaly in dogs and cats.80a
27
Figure 249-13 Phonocardiogram recorded at the left heart base from a dog with a primum atrial septal defect. The lead II electrocardiogram has a negative, slightly prolonged QRS complex, which is indicative of a right ventricular conduction disorder (partial or incomplete right bundle branch block). The phonocardiogram shows a systolic ejection murmur (SM) that ends well before the second heart sound, which is widely split. S1, First heart sound; A2, aortic component of the second heart sound; P2, pulmonic component of the second heart sound.
Figure 249-13 Phonocardiogram recorded at the left heart base from a dog with a primum atrial septal defect. The lead II electrocardiogram has a negative, slightly prolonged QRS complex, which is indicative of a right ventricular conduction disorder (partial or incomplete right bundle branch block). The phonocardiogram shows a systolic ejection murmur (SM) that ends well before the second heart sound, which is widely split. S1, First heart sound; A2, aortic component of the second heart sound; P2, pulmonic component of the second heart sound.
28
The main cardiac structural changes caused by an ASD include dilatation of the right atrium and eccentric hypertrophy of the right ventricle.
The main cardiac structural changes caused by an ASD include dilatation of the right atrium and eccentric hypertrophy of the right ventricle.
29
The electrocardiogram may indicate right ventricular enlargement (right axis shift, increased S wave depth in leads I, II, III), but intraventricular conduction disturbances, especially partial or complete right bundle branch block (Figure 249-14), are also common, especially with ostium primum atrial or atrioventricular septal defects.4a,64a,66a
The electrocardiogram may indicate right ventricular enlargement (right axis shift, increased S wave depth in leads I, II, III), but intraventricular conduction disturbances, especially partial or complete right bundle branch block (Figure 249-14), are also common, especially with ostium primum atrial or atrioventricular septal defects.4a,64a,66a
30
Thoracic radiographs show enlargement of the right heart, main pulmonary artery, and pulmonary hypervascularity proportional to the magnitude of the shunt (Figure 249-15). The left atrium is only modestly enlarged unless there is concurrent mitral regurgitation from a cleft mitral valve or a more extensive endocardial cushion defect.
Thoracic radiographs show enlargement of the right heart, main pulmonary artery, and pulmonary hypervascularity proportional to the magnitude of the shunt (Figure 249-15). The left atrium is only modestly enlarged unless there is concurrent mitral regurgitation from a cleft mitral valve or a more extensive endocardial cushion defect.
31
Echocardiography permits direct imaging of ASD,[31] but false positive impressions of an ASD are common because of imaging artifacts caused by beam orientation and the thinness of some portions of the normal interatrial septum. Doppler evidence of transatrial shunting is more reliable and typically shows laminar or mildly turbulent.............flow through the ASD (Figure 249-16), and increased RV outflow and pulmonary artery velocities. Doppler studies are also helpful for demonstrating associated problems such as mitral regurgitation or other associated defects.[24],16b Contrast echocardiography is helpful, particularly when the defect is large or when elevated right heart pressures cause reversed flow across the defect.
Echocardiography permits direct imaging of ASD,[31] but false positive impressions of an ASD are common because of imaging artifacts caused by beam orientation and the thinness of some portions of the normal interatrial septum. Doppler evidence of transatrial shunting is more reliable and typically shows laminar or mildly turbulent diastolic flow through the ASD (Figure 249-16), and increased RV outflow and pulmonary artery velocities. Doppler studies are also helpful for demonstrating associated problems such as mitral regurgitation or other associated defects.[24],16b Contrast echocardiography is helpful, particularly when the defect is large or when elevated right heart pressures cause reversed flow across the defect.
32
Cardiac catheterization of animals with an ASD is helpful for evaluating the magnitude and direction of shunting. In cases of left-to-right shunting, oximetry samples from the venae cavae, right atrium, and right ventricle indicate an increase in oxygen saturation between the ................ and the atrium and/or ventricle, and the magnitude of systemic to pulmonary shunting can be estimated.
Cardiac catheterization of animals with an ASD is helpful for evaluating the magnitude and direction of shunting. In cases of left-to-right shunting, oximetry samples from the venae cavae, right atrium, and right ventricle indicate an increase in oxygen saturation between the venae cavae and the atrium and/or ventricle, and the magnitude of systemic to pulmonary shunting can be estimated.
33
Central venous and right ventricular diastolic pressures are ................ when congestive heart failure is present or imminent. ................. systolic flow across the pulmonic valve may result in “relative” pulmonic stenosis, identified by a mild systolic pressure gradient (.......to .........mm Hg) between the ..................and pulmonary artery.
Central venous and right ventricular diastolic pressures are elevated when congestive heart failure is present or imminent. Increased systolic flow across the pulmonic valve may result in “relative” pulmonic stenosis, identified by a mild systolic pressure gradient (5 to 15 mm Hg) between the right ventricle and pulmonary artery.
34
Flow through the ASD can be demonstrated by angiocardiography. When introduced via a femoral vein, a catheter can often be easily passed from the right atrium through an ASD or patent foramen ovale into the left atrium to perform the injection of contrast and visualize left-to-right shunting. Alternatively, contrast injection into the pulmonary artery will outline left-to-right shunting defects during the left-sided phase of the study. Following pulmonary venous return, the atrial septum usually can be seen between the left atrium and aorta on the lateral projection. Passage of dye from the left atrium into the right atrium and vena cavae confirms the presence of the defect.
Flow through the ASD can be demonstrated by angiocardiography. When introduced via a femoral vein, a catheter can often be easily passed from the right atrium through an ASD or patent foramen ovale into the left atrium to perform the injection of contrast and visualize left-to-right shunting. Alternatively, contrast injection into the pulmonary artery will outline left-to-right shunting defects during the left-sided phase of the study. Following pulmonary venous return, the atrial septum usually can be seen between the left atrium and aorta on the lateral projection. Passage of dye from the left atrium into the right atrium and vena cavae confirms the presence of the defect.
35
With more extensive endocardial cushion defects are suspected, a left ventricular injection can be performed to demonstrate the VSD, mitral regurgitation, and occasionally left ventricular-to-right atrial shunting.
With more extensive endocardial cushion defects are suspected, a left ventricular injection can be performed to demonstrate the VSD, mitral regurgitation, and occasionally left ventricular-to-right atrial shunting.
36
The clinical features of VSD depend on the magnitude of the shunt and presence of complications or other defects. In animals with a typical small, subcristal VSD, a harsh, holosystolic murmur is heard best over the ...... mid- to ........... precordium. In rare cases of supracristal VSD, the defect opens just under the pulmonic valve and the systolic murmur may be heard best at the .......base. Splitting of the second heart sound can occur but is often not recognized because of the imposition of the murmur on the second heart sound. If distortion of the aortic root causes significant aortic regurgitation, a blowing, decrescendo ............... murmur will be audible over the left ventricular outflow area. These combined systolic and diastolic murmurs are sometimes described as a “................." murmur. Aortic regurgitation flow into the right ventricle can produce a ....................murmur best heard on the right hemithorax. Systolic murmurs over the atrioventricular valves may also be detected if the defect is part of a more extensive endocardial cushion defect.
The clinical features of VSD depend on the magnitude of the shunt and presence of complications or other defects. In animals with a typical small, subcristal VSD, a harsh, holosystolic murmur is heard best over the right mid- to cranial precordium. In rare cases of supracristal VSD, the defect opens just under the pulmonic valve and the systolic murmur may be heard best at the left base. Splitting of the second heart sound can occur but is often not recognized because of the imposition of the murmur on the second heart sound. If distortion of the aortic root causes significant aortic regurgitation, a blowing, decrescendo diastolic murmur will be audible over the left ventricular outflow area. These combined systolic and diastolic murmurs are sometimes described as a “to-and-fro” murmur. Aortic regurgitation flow into the right ventricle can produce a diastolic murmur best heard on the right hemithorax. Systolic murmurs over the atrioventricular valves may also be detected if the defect is part of a more extensive endocardial cushion defect.
37
Electrocardiographic findings in animals with a VSD are variable. With moderate or large left-to-right shunts there is often evidence of left atrial or ventricular enlargement, but right ventricular conduction defects also occur. Frontal plane leads may demonstrate a subtle abnormality in early ventricular septal activation, characterized by a Q wave that is wide or contains high-frequency notching.69a Right axis deviation and a narrow QRS complex in a dog with VSD usually indicates right ventricular hypertrophy and a more complex lesion, such as VSD with pulmonic stenosis or pulmonary hypertension.
Electrocardiographic findings in animals with a VSD are variable. With moderate or large left-to-right shunts there is often evidence of left atrial or ventricular enlargement, but right ventricular conduction defects also occur. Frontal plane leads may demonstrate a subtle abnormality in early ventricular septal activation, characterized by a Q wave that is wide or contains high-frequency notching.69a Right axis deviation and a narrow QRS complex in a dog with VSD usually indicates right ventricular hypertrophy and a more complex lesion, such as VSD with pulmonic stenosis or pulmonary hypertension.
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Thoracic radiographs are very useful in assessing the magnitude of left-to-right shunting VSDs. Pulmonary hypervascularity and left atrial and ventricular enlargement are observed in proportion to shunt magnitude (Figure 249-17).22a-24a The main, lobar, and peripheral pulmonary arteries are usually prominent. In animals with small defects, thoracic radiographs may appear entirely normal. With large defects, the right ventricle may also enlarge. A large pulmonary artery segment, underperfused lungs, and small peripheral pulmonary vasculature suggest the possibility of pulmonic stenosis or pulmonary hypertension and right-to-left shunting.
Thoracic radiographs are very useful in assessing the magnitude of left-to-right shunting VSDs. Pulmonary hypervascularity and left atrial and ventricular enlargement are observed in proportion to shunt magnitude (Figure 249-17).22a-24a The main, lobar, and peripheral pulmonary arteries are usually prominent. In animals with small defects, thoracic radiographs may appear entirely normal. With large defects, the right ventricle may also enlarge. A large pulmonary artery segment, underperfused lungs, and small peripheral pulmonary vasculature suggest the possibility of pulmonic stenosis or pulmonary hypertension and right-to-left shunting.
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Two-dimensional color flow Doppler echocardiography usually identifies all but the smallest VSDs (Figure 249-18). Small aneurysms of membranelike tissue may occasionally be seen protruding into the RV from the margins of the VSD.[33] Spectral Doppler studies are useful to quantify the high-velocity jet through small, resistive VSDs, as previously mentioned. Contrast echocardiography may also be used to identify flow through the defect, but it is usually not necessary if a careful echocardiographic examination is performed.
Two-dimensional color flow Doppler echocardiography usually identifies all but the smallest VSDs (Figure 249-18). Small aneurysms of membranelike tissue may occasionally be seen protruding into the RV from the margins of the VSD.[33] Spectral Doppler studies are useful to quantify the high-velocity jet through small, resistive VSDs, as previously mentioned. Contrast echocardiography may also be used to identify flow through the defect, but it is usually not necessary if a careful echocardiographic examination is performed.
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Figure 249-17 Lateral (A) and dorsoventral (B) thoracic radiographs of a cat with a ventricular septal defect and a large left-to-right shunt. The cardiac silhouette is enlarged and there is rounding of the cranial border of the heart on the lateral view. The pulmonary arteries and veins are enlarged on the dorsoventral view.
Figure 249-17 Lateral (A) and dorsoventral (B) thoracic radiographs of a cat with a ventricular septal defect and a large left-to-right shunt. The cardiac silhouette is enlarged and there is rounding of the cranial border of the heart on the lateral view. The pulmonary arteries and veins are enlarged on the dorsoventral view.
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Figure 249-18 Echocardiography of a Siamese cat with a ventricular septal defect (VSD). A, The right long axis view shows the VSD (*) positioned between the left ventricular outflow tract (LVOT) and aorta (Ao) and opening into the right ventricle (RV). Note the proximity of the VSD to the root of the Ao and origin of the aortic valve (arrowheads). B, The right long axis color flow Doppler study reveals systolic left-to-right shunting across the VSD into the RV.
Figure 249-18 Echocardiography of a Siamese cat with a ventricular septal defect (VSD). A, The right long axis view shows the VSD (*) positioned between the left ventricular outflow tract (LVOT) and aorta (Ao) and opening into the right ventricle (RV). Note the proximity of the VSD to the root of the Ao and origin of the aortic valve (arrowheads). B, The right long axis color flow Doppler study reveals systolic left-to-right shunting across the VSD into the RV.
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Cardiac catheterization in animals with a VSD allows identification of the anatomic defect and estimation of the degree of shunting. Oximetry samples demonstrate a “step-up” in oxygen content between the right ventricle and pulmonary artery. Intracardiac pressures are usually normal in dogs and cats with a small VSD. Right ventricular pressures are often elevated .....to......mm Hg above the pressure in the ........................ as a reflection of increased transvalvular flow and relative pulmonic stenosis. More dramatic increases in right ventricular systolic pressure indicate ...................... or concurrent .................., and the development of elevated end-..................ventricular pressures and central venous pressure herald the onset of heart failure.
Cardiac catheterization in animals with a VSD allows identification of the anatomic defect and estimation of the degree of shunting.27c Oximetry samples demonstrate a “step-up” in oxygen content between the right ventricle and pulmonary artery. Intracardiac pressures are usually normal in dogs and cats with a small VSD. Right ventricular pressures are often elevated 5 to 15 mm Hg above the pressure in the pulmonary artery as a reflection of increased transvalvular flow and relative pulmonic stenosis. More dramatic increases in right ventricular systolic pressure indicate pulmonary hypertension or concurrent pulmonic stenosis, and the development of elevated end-diastolic ventricular pressures and central venous pressure herald the onset of heart failure.
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In uncomplicated cases, left ventricular angiocardiography serves to outlines the VSD (Figure 249-19). Bidirectional or right-to-left shunting is observed when RV systolic pressure reaches and exceeds LV systolic pressure. Anatomic changes of the semilunar valves or great vessels, especially of the aortic root, are best visualized by injection of contrast in the proximal aorta, which is also the preferred location to determine the presence and severity of aortic regurgitation.17b
In uncomplicated cases, left ventricular angiocardiography serves to outlines the VSD (Figure 249-19). Bidirectional or right-to-left shunting is observed when RV systolic pressure reaches and exceeds LV systolic pressure. Anatomic changes of the semilunar valves or great vessels, especially of the aortic root, are best visualized by injection of contrast in the proximal aorta, which is also the preferred location to determine the presence and severity of aortic regurgitation.17b
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NATURAL HISTORY The morbidity and mortality associated with atrioventricular septal defects depend on defect size and location, magnitude and direction of shunt flow, and the presence of additional lesions. Spontaneous closure of small VSDs often occurs in children, but this is an uncommon occurrence in cats and dogs.71a Animals with uncomplicated small defects (ASDs and VSDs) and modest shunts usually live a normal lifespan without ever developing recognizable clinical signs. Large shunts causing moderate to severe cardiomegaly often lead to intractable congestive heart failure. Moderate to severe aortic regurgitation, an uncommon complication of VSD, presents a very substantial risk of left heart failure and shortened survival.17b It is often difficult to predict outcome in very young animals with a VSD until they grow closer to adult size at 6 to 12 months of age. Animals that develop pulmonary hypertension (Eisenmenger syndrome) have a guarded short-term and very guarded to poor long-term prognosis, although survival beyond 7 years is possible. Cats with severe endocardial cushion defects often develop marked cardiomegaly and biventricular congestive heart failure at an early age (
NATURAL HISTORY The morbidity and mortality associated with atrioventricular septal defects depend on defect size and location, magnitude and direction of shunt flow, and the presence of additional lesions. Spontaneous closure of small VSDs often occurs in children, but this is an uncommon occurrence in cats and dogs.71a Animals with uncomplicated small defects (ASDs and VSDs) and modest shunts usually live a normal lifespan without ever developing recognizable clinical signs. Large shunts causing moderate to severe cardiomegaly often lead to intractable congestive heart failure. Moderate to severe aortic regurgitation, an uncommon complication of VSD, presents a very substantial risk of left heart failure and shortened survival.17b It is often difficult to predict outcome in very young animals with a VSD until they grow closer to adult size at 6 to 12 months of age. Animals that develop pulmonary hypertension (Eisenmenger syndrome) have a guarded short-term and very guarded to poor long-term prognosis, although survival beyond 7 years is possible. Cats with severe endocardial cushion defects often develop marked cardiomegaly and biventricular congestive heart failure at an early age (
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CLINICAL MANAGEMENT Surgical closure is the definitive treatment for all atrioventricular septal defects, but open-heart correction is uncommonly attempted in animals because of the usual requirement for cardiopulmonary bypass or other techniques to arrest the heart.76a,77a,29c-31c,24b Successful closure of both ASDs and VSDs using percutaneous closure devices has been reported in a small number of animals.[34-37] Palliative treatment of VSD may be accomplished without bypass by applying a constrictive band around the main pulmonary artery. This technique creates supravalvular pulmonic stenosis and increases the right ventricular systolic pressure, thereby reducing the magnitude of left-to-right shunting.75a This procedure is recommended for dogs and cats showing signs of rapidly progressive cardiomegaly and overt or impending congestive heart failure. Overaggressive banding should be avoided, as it can result in pressure overload, acute right heart failure or, in surviving animals, right-to-left shunting. Alternatively, systemic arterial vasodilators can be administered to reduce systemic vascular resistance and the magnitude of left-to-right shunting.79a As noted for reversed PDA, surgical correction of animals with Eisenmenger's syndrome should not be attempted. Restricted physical activity is probably the most prudent and effective strategy. Periodic phlebotomy may be useful in some patients developing extreme polycythemia. Maintenance of the PCV at 58% to 65% is recommended.
CLINICAL MANAGEMENT Surgical closure is the definitive treatment for all atrioventricular septal defects, but open-heart correction is uncommonly attempted in animals because of the usual requirement for cardiopulmonary bypass or other techniques to arrest the heart.76a,77a,29c-31c,24b Successful closure of both ASDs and VSDs using percutaneous closure devices has been reported in a small number of animals.[34-37] Palliative treatment of VSD may be accomplished without bypass by applying a constrictive band around the main pulmonary artery. This technique creates supravalvular pulmonic stenosis and increases the right ventricular systolic pressure, thereby reducing the magnitude of left-to-right shunting.75a This procedure is recommended for dogs and cats showing signs of rapidly progressive cardiomegaly and overt or impending congestive heart failure. Overaggressive banding should be avoided, as it can result in pressure overload, acute right heart failure or, in surviving animals, right-to-left shunting. Alternatively, systemic arterial vasodilators can be administered to reduce systemic vascular resistance and the magnitude of left-to-right shunting.79a As noted for reversed PDA, surgical correction of animals with Eisenmenger's syndrome should not be attempted. Restricted physical activity is probably the most prudent and effective strategy. Periodic phlebotomy may be useful in some patients developing extreme polycythemia. Maintenance of the PCV at 58% to 65% is recommended.