Congenital heart disease: PDA-Ettinger Flashcards

(52 cards)

1
Q

DEFECTS CAUSING PRIMARILY VOLUME OVERLOAD
SYSTEMIC TO PULMONARY (LEFT-TO-RIGHT) SHUNTS:

The circulation in the fetus differs from that in the adult. In fetal animals the ductus arteriosus develops from the left sixth embryonic arch and extends from the pulmonary artery to the descending aorta where it functions to divert blood from the nonfunctional fetal lungs back into the systemic circulation.
Before birth, the ductus diverts approximately 80% to 90% of the right ventricular output back to the left side of the circulation. Following parturition and the onset of breathing, pulmonary vascular ………….. falls, flow in the ductus ……………, and the resulting rise in arterial ……………….. inhibits …….. …………. release causing …………… of the vascular smooth muscle within the vessel wall and functional closure of the ductus arteriosus.

While the ductus may be probe-patent in puppies less than ….. days of age, it is usually closed securely …….to……… days after birth. a Persistence of a PDA beyond the early neonatal period is the first or second most commonly diagnosed congenital cardiac defect in dogs.

A

DEFECTS CAUSING PRIMARILY VOLUME OVERLOAD
SYSTEMIC TO PULMONARY (LEFT-TO-RIGHT) SHUNTS:

The circulation in the fetus differs from that in the adult. In fetal animals the ductus arteriosus develops from the left sixth embryonic arch and extends from the pulmonary artery to the descending aorta where it functions to divert blood from the nonfunctional fetal lungs back into the systemic circulation.
Before birth, the ductus diverts approximately 80% to 90% of the right ventricular output back to the left side of the circulation. Following parturition and the onset of breathing, pulmonary vascular ………….. falls, flow in the ductus ……………, and the resulting rise in arterial ……………….. inhibits …….. …………. release causing …………… of the vascular smooth muscle within the vessel wall and functional closure of the ductus arteriosus.

While the ductus may be probe-patent in puppies less than ….. days of age, it is usually closed securely …….to……… days after birth. a Persistence of a PDA beyond the early neonatal period is the first or second most commonly diagnosed congenital cardiac defect in dogs.

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2
Q

PATHOGENESIS

Failed ductal closure in dogs is characterized by distinct histologic abnormalities within the ductal wall. The normal fetal ductal wall contains a loose branching pattern of circumferential …………… throughout its length. In prenatal puppies bred to have a high probability of PDA, varying portions of the ductal wall are comprised of ………………….. rather than contractile smooth muscle fibers.

According to the work of Patterson and Buchanan et al.,4a increasing genetic liability to PDA results in “extension of the noncontractile wall structure of the aorta to an increasing segment of the ductus arteriosus, progressively impairing its capacity to undergo physiologic closure.” It is tempting to speculate that some defect prevents one or more of the series of processes that permits smooth muscle cells to proliferate in the wall of ductus before birth.

A

PATHOGENESIS

Failed ductal closure in dogs is characterized by distinct histologic abnormalities within the ductal wall. The normal fetal ductal wall contains a loose branching pattern of circumferential smooth muscle throughout its length. In prenatal puppies bred to have a high probability of PDA, varying portions of the ductal wall are comprised of elastic fibers rather than contractile smooth muscle fibers.

According to the work of Patterson and Buchanan et al.,4a increasing genetic liability to PDA results in “extension of the noncontractile wall structure of the aorta to an increasing segment of the ductus arteriosus, progressively impairing its capacity to undergo physiologic closure.” It is tempting to speculate that some defect prevents one or more of the series of processes that permits smooth muscle cells to proliferate in the wall of ductus before birth.

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3
Q

In its mildest form, the ductus closes at the pulmonary arterial end only and there is a blind, funnel-shaped outpouching of the ventral aspect of the aorta, called a …………………… This hidden form (forme fruste) of incomplete ductal closure can only be diagnosed by angiography or necropsy, but it indicates that the dog possesses genes for this defect.4a,39a-40a

A

In its mildest form, the ductus closes at the pulmonary arterial end only and there is a blind, funnel-shaped outpouching of the ventral aspect of the aorta, called a ductus diverticulum. This hidden form (forme fruste) of incomplete ductal closure can only be diagnosed by angiography or necropsy, but it indicates that the dog possesses genes for this defect.4a,39a-40a

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4
Q

Increasing genetic liability results in a tapering, funnel-shaped ductus arteriosus that remains patent after the early natal period and allows blood to flow from the high-pressure aorta to low-pressure pulmonary artery (Figure 249-2) and varying amounts of left-to-right shunting. The most severe, but least common, form is the cylindrical, nontapering ductus with persistent, postnatal pulmonary hypertension (Eisenmenger syndrome) and bidirectional or right-to-left shunting (see Figure 249-2).

A

Increasing genetic liability results in a tapering, funnel-shaped ductus arteriosus that remains patent after the early natal period and allows blood to flow from the high-pressure aorta to low-pressure pulmonary artery (Figure 249-2) and varying amounts of left-to-right shunting. The most severe, but least common, form is the cylindrical, nontapering ductus with persistent, postnatal pulmonary hypertension (Eisenmenger syndrome) and bidirectional or right-to-left shunting (see Figure 249-2).

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5
Q

Based on the breeding studies of Poodle-type dogs, Patterson et al. concluded that the mode of transmission of PDA in dogs is most likely polygenic but other mechanisms of inheritance are possible. For additional information regarding the morphology and pathogenesis of PDA, the reader is referred to several outstanding reviews of the subject.[12-14]

A

Based on the breeding studies of Poodle-type dogs, Patterson et al. concluded that the mode of transmission of PDA in dogs is most likely polygenic but other mechanisms of inheritance are possible. For additional information regarding the morphology and pathogenesis of PDA, the reader is referred to several outstanding reviews of the subject.[12-14]

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6
Q

PATHOPHYSIOLOGY

The direction of flow through the PDA is determined by the relative …………….. of the pulmonary and systemic vascular beds and is, in the vast majority of cases, directed from left-to-right (from the aorta to pulmonary artery). This results in a continuous cardiac murmur, increased pulmonary blood flow, and volume overloading of the ….. atrium and left ventricle.

A

PATHOPHYSIOLOGY

The direction of flow through the PDA is determined by the relative resistances of the pulmonary and systemic vascular beds and is, in the vast majority of cases, directed from left-to-right (from the aorta to pulmonary artery). This results in a continuous cardiac murmur, increased pulmonary blood flow, and volume overloading of the left atrium and left ventricle.

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7
Q

Because of the relatively …………………….. of the systemic circulation after birth, ………………..blood pressure is greater than pulmonary pressure, and blood shunts continuously across the PDA during both systole and diastole.

For a given pressure gradient, the magnitude of shunting is determined by the …………………….. (effective …………………) of the ductus arteriosus. In the majority of cases the ductus is widest at the aortic end and tapers to its narrowest (flow limiting) region at the point of attachment to the pulmonary artery. Increased left ventricular ………………. and rapid run-off of blood from the aorta to the low-pressure pulmonary circulation via the PDA causes increased aortic ………… and decreased aortic …………….. pressures. The resulting widened arterial …………….. offers a hemodynamic explanation for the bounding or hyperkinetic (waterhammer, Corrigan’s) arterial pulse detected in dogs with substantial shunts.

A

Because of the relatively high resistance of the systemic circulation after birth, aortic blood pressure is greater than pulmonary pressure, and blood shunts continuously across the PDA during both systole and diastole.

For a given pressure gradient, the magnitude of shunting is determined by the morphology (effective resistance) of the ductus arteriosus. In the majority of cases the ductus is widest at the aortic end and tapers to its narrowest (flow limiting) region at the point of attachment to the pulmonary artery. Increased left ventricular stroke volume and rapid run-off of blood from the aorta to the low-pressure pulmonary circulation via the PDA causes increased aortic systolic and decreased aortic diastolic pressures. The resulting widened arterial pulse pressure offers a hemodynamic explanation for the bounding or hyperkinetic (waterhammer, Corrigan’s) arterial pulse detected in dogs with substantial shunts.

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8
Q

All vascular structures involved in the transport of the shunted blunt enlarge to accommodate the extra volume flow. Increased volume flow causes dilatation of the ………………. aorta, main ………………., and overcirculation of the …………………..bed.
Dilation of the left ………… and eccentric hypertrophy of the …………………. develop in proportion to the volume flow of the shunt.
This mechanism permits compensation for a variable period of time but if the shunt is large, myocardial failure (cardiomyopathy of volume overload) develops together with progressive elevation of left ventricular ……………-………….. and overt pulmonary …………..

A

All vascular structures involved in the transport of the shunted blunt enlarge to accommodate the extra volume flow. Increased volume flow causes dilatation of the proximal aorta, main pulmonary artery, and overcirculation of the pulmonary vascular bed. Dilation of the left atrium and eccentric hypertrophy of the left ventricle develop in proportion to the volume flow of the shunt. This mechanism permits compensation for a variable period of time but if the shunt is large, myocardial failure (cardiomyopathy of volume overload) develops together with progressive elevation of left ventricular end-diastolic pressure and overt pulmonary edema.

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9
Q

Because the left-to-right shunt occurs at the level of the great vessels, the right ventricle and atrium never handle the shunted blood and these structures remain normal unless …………………… and ………………………. increase.

A

Because the left-to-right shunt occurs at the level of the great vessels, the right ventricle and atrium never handle the shunted blood and these structures remain normal unless pulmonary vascular resistance and pulmonary arterial pressure increase.

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10
Q

In a small percentage of cases, the lumen of the PDA remains wide open after birth. The absence of a …………….ductal orifice allows aortic pressure to be transmitted to the pulmonary circulation, precluding the normal postnatal ………………. in pulmonary vascular resistance. In this circumstance, the aortic and pulmonary artery pressures equilibrate and the right ventricle remains ………………………… hypertrophied after birth.

A

In a small percentage of cases, the lumen of the PDA remains wide open after birth. The absence of a restrictive ductal orifice allows aortic pressure to be transmitted to the pulmonary circulation, precluding the normal postnatal decline in pulmonary vascular resistance. In this circumstance, the aortic and pulmonary artery pressures equilibrate and the right ventricle remains concentrically hypertrophied after birth.

In Patterson’s colony of dogs, this pattern of pulmonary hypertension and reversed (right-to-left) shunting developed within the first few weeks of life.39a These observations fit the usual clinical presentation of most dogs diagnosed with a (reversed) PDA, in which there is usually no history of a continuous murmur and no evidence of left ventricular enlargement or large left-to-right shunt earlier in life..

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11
Q

Most dogs with reversed PDA flow exhibit ………………..pulmonary blood flow, a normal to small……………..ventricle, and marked …………………. hypertrophy of the right ventricle.

On rare occasions, dogs with a moderate to large left-to-right shunting PDA will experience a gradual increase in pulmonary resistance and gradual reversal of the direction of shunting, typically at several months to several years of age.

A

Most dogs with reversed PDA flow exhibit diminished pulmonary blood flow, a normal to small left ventricle, and marked concentric hypertrophy of the right ventricle.

On rare occasions, dogs with a moderate to large left-to-right shunting PDA will experience a gradual increase in pulmonary resistance and gradual reversal of the direction of shunting, typically at several months to several years of age.
In these dogs there is often a history of prior left heart failure. Substantial residual LV enlargement is evident on thoracic radiographs and by echocardiography. Pulmonary blood flow is reduced but right ventricular hypertrophy is less pronounced than in dogs that reverse the direction of shunting at an early age.

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12
Q

The precise pathogenesis of pulmonary hypertension is not completely understood, but anatomic descriptions of the pulmonary vasculature are similar in humans and animals. Histologic changes within small pulmonary arteries include hypertrophy of the ………., thickening of the ………. and reduction of lumen …………….., and development of ………………….lesions of the vessel wall. Most of these changes are considered to be ………………, precluding surgical correction of the reversed PDA.

A

The precise pathogenesis of pulmonary hypertension is not completely understood, but anatomic descriptions of the pulmonary vasculature are similar in humans and animals. Histologic changes within small pulmonary arteries include hypertrophy of the media, thickening of the intima and reduction of lumen dimensions, and development of plexiform lesions of the vessel wall. Most of these changes are considered to be irreversible, precluding surgical correction of the reversed PDA.

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13
Q

CLINICAL FINDINGS

The clinical features of PDA have been thoroughly characterized in both a breeding colony and in clinic populations.[16],1a-4a,37a-53a,10c Compared with male dogs, female dogs have substantially greater risk (2.49/1000 versus 1.45/1000) of developing a PDA.2a The Chihuahua, Collie, Maltese, Poodle, Pomeranian, English Springer Spaniel, Keeshond, Bichon Frise, and Shetland Sheepdog are most frequently affected, although other breeds such as the Cavalier King Charles Spaniel may also be predisposed. Many other breeds, including larger dogs such as the German Shepherd Dog, Newfoundland, and Labrador Retriever may also be prone to PDA in some regions. While severely affected pups and kittens may appear stunted, thin, or tachypneic from left heart failure, most are reported to be asymptomatic and developing normally at the time of their initial recognition. Clinical signs are rarely recognized within the first few weeks of life, and most dogs are not diagnosed until the time of initial examination at 6 to 8 weeks of age.

A

CLINICAL FINDINGS

The clinical features of PDA have been thoroughly characterized in both a breeding colony and in clinic populations.[16],1a-4a,37a-53a,10c Compared with male dogs, female dogs have substantially greater risk (2.49/1000 versus 1.45/1000) of developing a PDA.2a The Chihuahua, Collie, Maltese, Poodle, Pomeranian, English Springer Spaniel, Keeshond, Bichon Frise, and Shetland Sheepdog are most frequently affected, although other breeds such as the Cavalier King Charles Spaniel may also be predisposed. Many other breeds, including larger dogs such as the German Shepherd Dog, Newfoundland, and Labrador Retriever may also be prone to PDA in some regions. While severely affected pups and kittens may appear stunted, thin, or tachypneic from left heart failure, most are reported to be asymptomatic and developing normally at the time of their initial recognition. Clinical signs are rarely recognized within the first few weeks of life, and most dogs are not diagnosed until the time of initial examination at 6 to 8 weeks of age.

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14
Q

CLINICAL FINDINGS

The clinical features of PDA have been thoroughly characterized in both a breeding colony and in clinic populations.[16],1a-4a,37a-53a,10c Compared with male dogs, female dogs have substantially greater risk (2.49/1000 versus 1.45/1000) of developing a PDA.2a The Chihuahua, Collie, Maltese, Poodle, Pomeranian, English Springer Spaniel, Keeshond, Bichon Frise, and Shetland Sheepdog are most frequently affected, although other breeds such as the Cavalier King Charles Spaniel may also be predisposed. Many other breeds, including larger dogs such as the German Shepherd Dog, Newfoundland, and Labrador Retriever may also be prone to PDA in some regions. While severely affected pups and kittens may appear stunted, thin, or tachypneic from left heart failure, most are reported to be asymptomatic and developing normally at the time of their initial recognition. Clinical signs are rarely recognized within the first few weeks of life, and most dogs are not diagnosed until the time of initial examination at 6 to 8 weeks of age.

A

CLINICAL FINDINGS

The clinical features of PDA have been thoroughly characterized in both a breeding colony and in clinic populations.[16],1a-4a,37a-53a,10c Compared with male dogs, female dogs have substantially greater risk (2.49/1000 versus 1.45/1000) of developing a PDA.2a The Chihuahua, Collie, Maltese, Poodle, Pomeranian, English Springer Spaniel, Keeshond, Bichon Frise, and Shetland Sheepdog are most frequently affected, although other breeds such as the Cavalier King Charles Spaniel may also be predisposed. Many other breeds, including larger dogs such as the German Shepherd Dog, Newfoundland, and Labrador Retriever may also be prone to PDA in some regions. While severely affected pups and kittens may appear stunted, thin, or tachypneic from left heart failure, most are reported to be asymptomatic and developing normally at the time of their initial recognition. Clinical signs are rarely recognized within the first few weeks of life, and most dogs are not diagnosed until the time of initial examination at 6 to 8 weeks of age.

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15
Q

Left-to-Right Shunting PDA

A thorough physical examination and chest radiographs usually suffice to suggest the diagnosis. Mucous membranes are pink in the absence of heart failure. The precordial impulse is often exaggerated and more diffuse than normal because of left ventricular enlargement. A thrill may be palpated at the heart base and a continuous murmur is best heard in the same location (Figure 249-3). The murmur’s point of maximum intensity is located over the main pulmonary artery at the dorsocranial left heart base, and it may radiate cranially to the thoracic inlet and to the right base, where it is almost always softer.[16],5a,39a,47a Often, only a systolic murmur is audible over the mitral area. This murmur may simply represent radiation of the loudest portion of the continuous murmur from the heart base to this location or may indicate that secondary mitral regurgitation has developed as a consequence of severe left ventricular dilatation.

A

Left-to-Right Shunting PDA

A thorough physical examination and chest radiographs usually suffice to suggest the diagnosis. Mucous membranes are pink in the absence of heart failure. The precordial impulse is often exaggerated and more diffuse than normal because of left ventricular enlargement. A thrill may be palpated at the heart base and a continuous murmur is best heard in the same location (Figure 249-3). The murmur’s point of maximum intensity is located over the main pulmonary artery at the dorsocranial left heart base, and it may radiate cranially to the thoracic inlet and to the right base, where it is almost always softer.[16],5a,39a,47a Often, only a systolic murmur is audible over the mitral area. This murmur may simply represent radiation of the loudest portion of the continuous murmur from the heart base to this location or may indicate that secondary mitral regurgitation has developed as a consequence of severe left ventricular dilatation.

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16
Q

In cats, the continuous murmur of a PDA may be heard best somewhat more caudoventrally than in affected dogs. Increased LV stroke volume and rapid diastolic run-off through the PDA combine to produce peripheral arterial pulses that are hyperkinetic (bounding).

A

In cats, the continuous murmur of a PDA may be heard best somewhat more caudoventrally than in affected dogs. Increased LV stroke volume and rapid diastolic run-off through the PDA combine to produce peripheral arterial pulses that are hyperkinetic (bounding).

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17
Q

Figure 249-3 Phonocardiogram recorded at the left heart base from a dog with left-to-right patent ductus arteriosus. The lead II electrocardiogram is recorded simultaneously for timing purposes (ventricular mechanical systole is approximately the period from the middle of the QRS complex to the end of the T wave; the remainder of the time is diastole). The recorded murmur is continuous, increasing in intensity during systole, peaking near the end of systole, and decreasing in intensity during diastole.

A

Figure 249-3 Phonocardiogram recorded at the left heart base from a dog with left-to-right patent ductus arteriosus. The lead II electrocardiogram is recorded simultaneously for timing purposes (ventricular mechanical systole is approximately the period from the middle of the QRS complex to the end of the T wave; the remainder of the time is diastole). The recorded murmur is continuous, increasing in intensity during systole, peaking near the end of systole, and decreasing in intensity during diastole.

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18
Q

Electrocardiography typically indicates left ventricular enlargement (increased R-wave voltages in leads II, III, aVF and in the left chest leads, V2 and V4) and normal mean electrical axis (Figure 249-4). Widened P waves may also be found, indicating left atrial enlargement.

A

Electrocardiography typically indicates left ventricular enlargement (increased R-wave voltages in leads II, III, aVF and in the left chest leads, V2 and V4) and normal mean electrical axis (Figure 249-4). Widened P waves may also be found, indicating left atrial enlargement.

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19
Q

Chest radiographs indicate left atrial and left ventricular enlargement and pulmonary hypervascularity in proportion to the magnitude of the left-to-right shunt (Figure 249-5). On the dorsoventral projection, the aortic arch, left auricle, and main pulmonary artery may be abnormally prominent. The most specific radiographic finding is the appearance of an aortic bulge (“ductus bump”) near the origin of the ductus, which is caused by abrupt narrowing of the descending aorta just caudal to the ductus origin (see Figure 249-5). Moderate to severe LV enlargement sometimes causes the cardiac apex to shift to the right (common in cats).

A

Chest radiographs indicate left atrial and left ventricular enlargement and pulmonary hypervascularity in proportion to the magnitude of the left-to-right shunt (Figure 249-5). On the dorsoventral projection, the aortic arch, left auricle, and main pulmonary artery may be abnormally prominent. The most specific radiographic finding is the appearance of an aortic bulge (“ductus bump”) near the origin of the ductus, which is caused by abrupt narrowing of the descending aorta just caudal to the ductus origin (see Figure 249-5). Moderate to severe LV enlargement sometimes causes the cardiac apex to shift to the right (common in cats).

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20
Q

Figure 249-4 Electrocardiogram from a dog with left-to-right patent ductus arteriosus. The mean QRS axis is normal (+80%), but the QRS voltage (amplitude) is increased in several leads, including leads II, III, aVF

A

Figure 249-4 Electrocardiogram from a dog with left-to-right patent ductus arteriosus. The mean QRS axis is normal (+80%), but the QRS voltage (amplitude) is increased in several leads, including leads II, III, aVF

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21
Q

Figure 249-5 Thoracic radiographs from a dog with a left-to-right shunting patent ductus arteriosus. A, Lateral projection shows left atrial enlargement and enlarged cranial pulmonary arteries and veins. B, Dorsoventral projection shows moderate cardiomegaly, a characteristic bulge in the descending aorta and dilation of the main pulmonary artery. The pulmonary vasculature is prominent.

A

Figure 249-5 Thoracic radiographs from a dog with a left-to-right shunting patent ductus arteriosus. A, Lateral projection shows left atrial enlargement and enlarged cranial pulmonary arteries and veins. B, Dorsoventral projection shows moderate cardiomegaly, a characteristic bulge in the descending aorta and dilation of the main pulmonary artery. The pulmonary vasculature is prominent.

22
Q

The diagnosis of a PDA can be confirmed by echocardiography in almost all cases. 2D and M-mode echocardiography demonstrate eccentric LV hypertrophy and dilatation of the left atrium, ascending aorta, and pulmonary artery (Figure 249-6).11c Reduced myocardial contractility is often observed and is reflected by reduced fractional shortening and/or increased LV end-systolic dimension and EPSS measurements.

A

The diagnosis of a PDA can be confirmed by echocardiography in almost all cases. 2D and M-mode echocardiography demonstrate eccentric LV hypertrophy and dilatation of the left atrium, ascending aorta, and pulmonary artery (Figure 249-6).11c Reduced myocardial contractility is often observed and is reflected by reduced fractional shortening and/or increased LV end-systolic dimension and EPSS measurements.

23
Q

The ductus can usually be imaged from the left cranial parasternal window (see Figure 249-6). Doppler interrogation of the pulmonary artery consistently demonstrates high-velocity continuous ductal flow directed toward the pulmonic valve (see Figure 249-6). In the typical case, the peak velocity of this jet is about 4.5 to 5.0 m/s and occurs at end-systole. Other common echocardiographic findings include mildly increased LV outflow velocity (1.8 to 2.3 m/s) and modest secondary mitral and pulmonary valve insufficiency.

A

The ductus can usually be imaged from the left cranial parasternal window (see Figure 249-6). Doppler interrogation of the pulmonary artery consistently demonstrates high-velocity continuous ductal flow directed toward the pulmonic valve (see Figure 249-6). In the typical case, the peak velocity of this jet is about 4.5 to 5.0 m/s and occurs at end-systole. Other common echocardiographic findings include mildly increased LV outflow velocity (1.8 to 2.3 m/s) and modest secondary mitral and pulmonary valve insufficiency.

24
Q

In dogs with PDA, associated cardiac defects are uncommon; nonetheless, it is still worthwhile to exclude, via a carefully performed echocardiographic examination, the concurrent presence of other common congenital defects such as subaortic stenosis.4a,44a

A

In dogs with PDA, associated cardiac defects are uncommon; nonetheless, it is still worthwhile to exclude, via a carefully performed echocardiographic examination, the concurrent presence of other common congenital defects such as subaortic stenosis.4a,44a

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Cardiac catheterization and angiocardiography are usually not needed to confirm a diagnosis of PDA and are not advised unless the Doppler echocardiographic evaluation is ambiguous or additional congenital malformations are suspected.12c,13c
Cardiac catheterization and angiocardiography are usually not needed to confirm a diagnosis of PDA and are not advised unless the Doppler echocardiographic evaluation is ambiguous or additional congenital malformations are suspected.12c,13c
26
Figure 249-6 Echocardiography of left-to-right patent ductus arteriosus (PDA). A, The right short axis view shows eccentric dilation of the left ventricular cavity (LV) compared with the right ventricle (RV). B, Right long axis view from the same dog reveals eccentric dilation of the left ventricle (LV) and left atrium (LA). The interventricular septum (1) and left ventricular posterior wall (2) appear relatively thin compared with the dilated LV. The mitral valve (3) is in the closed position. The right ventricle (RV) and right atrium (RA) are normal. C, Continuous wave Doppler tracing of the PDA jet obtained from the left heart base demonstrating continuous flow and a peak velocity of 5.2 m/s, which is converted to units of pressure (108 mm Hg) via the modified Bernoulli equation. D, View of the ductus (D) imaged from the left heart base. The typical left-to-right ductus is widest at the aortic (Ao) end (1) and tapers near the main pulmonary artery (MPA) (2). E, Close-up view of the ductus (D), pulmonary artery (PA), and aorta (Ao). F, Color flow Doppler imaging applied to the echocardiographic view in E, demonstrating turbulent left-to-right blood flow through the ductus.
Figure 249-6 Echocardiography of left-to-right patent ductus arteriosus (PDA). A, The right short axis view shows eccentric dilation of the left ventricular cavity (LV) compared with the right ventricle (RV). B, Right long axis view from the same dog reveals eccentric dilation of the left ventricle (LV) and left atrium (LA). The interventricular septum (1) and left ventricular posterior wall (2) appear relatively thin compared with the dilated LV. The mitral valve (3) is in the closed position. The right ventricle (RV) and right atrium (RA) are normal. C, Continuous wave Doppler tracing of the PDA jet obtained from the left heart base demonstrating continuous flow and a peak velocity of 5.2 m/s, which is converted to units of pressure (108 mm Hg) via the modified Bernoulli equation. D, View of the ductus (D) imaged from the left heart base. The typical left-to-right ductus is widest at the aortic (Ao) end (1) and tapers near the main pulmonary artery (MPA) (2). E, Close-up view of the ductus (D), pulmonary artery (PA), and aorta (Ao). F, Color flow Doppler imaging applied to the echocardiographic view in E, demonstrating turbulent left-to-right blood flow through the ductus.
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PDA with Pulmonary Hypertension (Right-to-Left Shunting PDA) High pulmonary ........................... causing right-to-left shunting through a PDA defines the clinical syndrome commonly referred to as a “reversed PDA." Right-to-left shunting is observed in a very small minority of dogs with a PDA, but the prevalence of this phenomenon is probably underestimated and may be increased in dogs living at altitudes greater than 5000 feet above sea level.
PDA with Pulmonary Hypertension (Right-to-Left Shunting PDA) High pulmonary vascular resistance causing right-to-left shunting through a PDA defines the clinical syndrome commonly referred to as a “reversed PDA.” Right-to-left shunting is observed in a very small minority of dogs with a PDA, but the prevalence of this phenomenon is probably underestimated and may be increased in dogs living at altitudes greater than 5000 feet above sea level.
28
Reversed PDA: Obvious clinical signs are usually evident during the first year of life, but many owners do not recognize clinical signs in their pet during the first 6 to 12 months of life; and some animals are not diagnosed until 3 to 4 years of age or later. Reported signs include exertional fatigue, hind limb weakness, shortness of breath, hyperpnea, differential cyanosis, and, more rarely, seizures.
Obvious clinical signs are usually evident during the first year of life, but many owners do not recognize clinical signs in their pet during the first 6 to 12 months of life; and some animals are not diagnosed until 3 to 4 years of age or later. Reported signs include exertional fatigue, hind limb weakness, shortness of breath, hyperpnea, differential cyanosis, and, more rarely, seizures.
29
Reversed PDA: Clinical examination is very different from the more common left-to-right PDA. Right-to-left flow through a widely PDA exhibits little turbulence and physical examination reveals either no murmur or only a soft, systolic murmur at the left base. The most common auscultatory finding is an accentuated and split-second heart sound.
Clinical examination is very different from the more common left-to-right PDA. Right-to-left flow through a widely PDA exhibits little turbulence and physical examination reveals either no murmur or only a soft, systolic murmur at the left base. The most common auscultatory finding is an accentuated and split-second heart sound.
30
Differential cyanosis (cyanosis of the caudal mucous membranes with pink cranial membranes) may be observed, but recognition may require examination after exercise. Differential cyanosis is caused by the location of the PDA, which shunts right-to-left from the pulmonary artery into the .............. aorta (see Figure 249-2) but spares the.................... of the aorta, which provide normal oxygen delivery to the cranial portion of the body.
Differential cyanosis (cyanosis of the caudal mucous membranes with pink cranial membranes) may be observed, but recognition may require examination after exercise. Differential cyanosis is caused by the location of the PDA, which shunts right-to-left from the pulmonary artery into the descending aorta (see Figure 249-2) but spares the proximal branches of the aorta, which provide normal oxygen delivery to the cranial portion of the body.
31
Reversed PDA: Perfusion of the kidneys with ........... blood triggers elaboration of ................ and secondary ............ and ..................... as the PCV gradually increases to 65% or greater. Polycythemia may occur during the first year of life, but often does not become severe until 18 to 24 months of age.
Perfusion of the kidneys with hypoxemic blood triggers elaboration of erythropoietin and secondary polycythemia and hyperviscosity as the PCV gradually increases to 65% or greater. Polycythemia may occur during the first year of life, but often does not become severe until 18 to 24 months of age.
32
Reversed PDA: The electrocardiogram of dogs with a reversed PDA virtually always reveals evidence of right ventricular hypertrophy (right axis deviation, increased S wave amplitude in leads I, II, III, and the left precordial chest leads, CV6LL and CV6LU).
The electrocardiogram of dogs with a reversed PDA virtually always reveals evidence of right ventricular hypertrophy (right axis deviation, increased S wave amplitude in leads I, II, III, and the left precordial chest leads, CV6LL and CV6LU).
33
Thoracic radiographs indicate right heart enlargement, dilatation of the main pulmonary artery, a visible “ductus bump” and variable appearance of the lobar and peripheral arteries.
Thoracic radiographs indicate right heart enlargement, dilatation of the main pulmonary artery, a visible “ductus bump” and variable appearance of the lobar and peripheral arteries.
34
Echocardiography demonstrates right ventricular concentric hypertrophy and a dilated main pulmonary artery. In some cases, a wide and cylindrical ductus may be imaged (Figure 249-7). Pulmonary hypertension can be verified in some cases by Doppler interrogation of tricuspid or pulmonic insufficiency jets.
Echocardiography demonstrates right ventricular concentric hypertrophy and a dilated main pulmonary artery. In some cases, a wide and cylindrical ductus may be imaged (Figure 249-7). Pulmonary hypertension can be verified in some cases by Doppler interrogation of tricuspid or pulmonic insufficiency jets.
35
Contrast echocardiography, nuclear scintigraphy, oximetry, or angiography can be used to demonstrate the presence of right-to-left shunting should Doppler interrogation prove inadequate. Contrast echocardiography is performed by injecting air-agitated saline into a cephalic or saphenous vein, thereby opacifying the right heart, pulmonary artery, and the descending aorta (best observed by imaging of the abdominal aorta dorsal to the bladder).
Contrast echocardiography, nuclear scintigraphy, oximetry, or angiography can be used to demonstrate the presence of right-to-left shunting should Doppler interrogation prove inadequate. Contrast echocardiography is performed by injecting air-agitated saline into a cephalic or saphenous vein, thereby opacifying the right heart, pulmonary artery, and the descending aorta (best observed by imaging of the abdominal aorta dorsal to the bladder).
36
Vid vä till hö shuntande PDA: Varför blåsljud som högst runt 2:a hjärttonen (när semilunarklaffarna stängs)
Tryckskillnad som högst mellan aorta och a.pulmonalis då.
37
Cardiac catheterization can demonstrate pulmonary artery hypertension with equilibration of right and left ventricular and aortic systolic pressures.
Cardiac catheterization can demonstrate pulmonary artery hypertension with equilibration of right and left ventricular and aortic systolic pressures.
38
Oximetry verifies decreased oxygen saturation ........... to the entrance of the PDA in the ......................
Oximetry verifies decreased oxygen saturation distal to the entrance of the PDA in the descending aorta.
39
Right ventricular angiography demonstrates right ventricular hypertrophy and usually outlines a wide PDA that appears to continue distally as the descending aorta (Figure 249-8). The lobar pulmonary arteries may appear normal, especially during the first year of life, or may show increased tortuosity. Aortic or left ventricular contrast injections permit visualization of an often extensive bronchoesophageal collateral circulation (see Figure 249-8).
Right ventricular angiography demonstrates right ventricular hypertrophy and usually outlines a wide PDA that appears to continue distally as the descending aorta (Figure 249-8). The lobar pulmonary arteries may appear normal, especially during the first year of life, or may show increased tortuosity. Aortic or left ventricular contrast injections permit visualization of an often extensive bronchoesophageal collateral circulation (see Figure 249-8).
40
Figure 249-7 Echocardiography in right-to-left patent ductus arteriosus (PDA). A, The right long axis view from an American Eskimo dog shows enlargement of the right ventricle (RV) and atrium (RA). B, The right short axis view shows enlargement of the RV and flattening of the interventricular septum toward the LV. This finding is highly suspicious for pressure overload of the RV. C, Transesophageal echocardiogram of a dog with a right-to-left PDA. The ductus (D) connects the aorta (Ao) with the pulmonary artery (PA), and is wide and cylindrical in shape. Both the PA and left pulmonary artery (LPA) are enlarged. D, Continuous wave Doppler study of the dog in A showing bi-directional flow through the ductus. Right-to-left flow (below the baseline) occurs during systole, while left-to-right flow (above the baseline) occurs during diastole. E, Simultaneous two-dimensional and color flow Doppler study of the dog in A. Flow from the pulmonary artery (PA) can be seen moving right-to-left into the large ductus (D). F, Continuous wave Doppler study of pulmonic insufficiency from the dog in A. The peak velocity of insufficiency is 4.5 m/s, indicating a pulmonary artery diastolic pressure of approximately 80 mm Hg. This finding is consistent with a diagnosis of pulmonary arterial hypertension and the presence of a right-to-left shunt.
Figure 249-7 Echocardiography in right-to-left patent ductus arteriosus (PDA). A, The right long axis view from an American Eskimo dog shows enlargement of the right ventricle (RV) and atrium (RA). B, The right short axis view shows enlargement of the RV and flattening of the interventricular septum toward the LV. This finding is highly suspicious for pressure overload of the RV. C, Transesophageal echocardiogram of a dog with a right-to-left PDA. The ductus (D) connects the aorta (Ao) with the pulmonary artery (PA), and is wide and cylindrical in shape. Both the PA and left pulmonary artery (LPA) are enlarged. D, Continuous wave Doppler study of the dog in A showing bi-directional flow through the ductus. Right-to-left flow (below the baseline) occurs during systole, while left-to-right flow (above the baseline) occurs during diastole. E, Simultaneous two-dimensional and color flow Doppler study of the dog in A. Flow from the pulmonary artery (PA) can be seen moving right-to-left into the large ductus (D). F, Continuous wave Doppler study of pulmonic insufficiency from the dog in A. The peak velocity of insufficiency is 4.5 m/s, indicating a pulmonary artery diastolic pressure of approximately 80 mm Hg. This finding is consistent with a diagnosis of pulmonary arterial hypertension and the presence of a right-to-left shunt.
41
Figure 249-8 Angiographic diagnosis of right-to-left patent ductus arteriosus in a dog. A, The right ventricular injection opacifies the right ventricle (RV), pulmonary artery (PA), ductus (D) and descending aorta (Ao). Note that the systemic arteries to the cranial portion of the dog are not opacified. B, A left ventricular injection of the same dog opacifies the left ventricle (LV), aorta (Ao), and prominent collateral bronchoesophageal circulation (B).
Figure 249-8 Angiographic diagnosis of right-to-left patent ductus arteriosus in a dog. A, The right ventricular injection opacifies the right ventricle (RV), pulmonary artery (PA), ductus (D) and descending aorta (Ao). Note that the systemic arteries to the cranial portion of the dog are not opacified. B, A left ventricular injection of the same dog opacifies the left ventricle (LV), aorta (Ao), and prominent collateral bronchoesophageal circulation (B).
42
NATURAL HISTORY Eyster reported that approximately 64% of dogs diagnosed with left-to-right shunting PDA will die from complications within 1 year of diagnosis if surgical correction is not performed.53a Complications include left heart failure with pulmonary edema, atrial fibrillation, pulmonary hypertension secondary to left heart failure, and mitral regurgitation secondary to left ventricular dilatation.53a,58a Dogs and cats with PDA and more modest shunts often survive to maturity and some live beyond 10 years of age.10c In humans with an uncorrected PDA, gradual development of pulmonary hypertension and shunt reversal is a significant risk, but this gradual transition to right-to-left shunting is uncommon in dogs.
NATURAL HISTORY Eyster reported that approximately 64% of dogs diagnosed with left-to-right shunting PDA will die from complications within 1 year of diagnosis if surgical correction is not performed.53a Complications include left heart failure with pulmonary edema, atrial fibrillation, pulmonary hypertension secondary to left heart failure, and mitral regurgitation secondary to left ventricular dilatation.53a,58a Dogs and cats with PDA and more modest shunts often survive to maturity and some live beyond 10 years of age.10c In humans with an uncorrected PDA, gradual development of pulmonary hypertension and shunt reversal is a significant risk, but this gradual transition to right-to-left shunting is uncommon in dogs.
43
When persistent pulmonary hypertension in the neonate leads to reversed shunting, clinical signs result from hypoxemia, polycythemia, hyperviscosity, and cardiac arrhythmias. Congestive heart failure almost never develops but sudden death and complications from hyperviscosity are common. Animals with reversed PDA often live 3 to 5 years, and some survive beyond 7 years if the PCV is kept below 65%.
When persistent pulmonary hypertension in the neonate leads to reversed shunting, clinical signs result from hypoxemia, polycythemia, hyperviscosity, and cardiac arrhythmias. Congestive heart failure almost never develops but sudden death and complications from hyperviscosity are common. Animals with reversed PDA often live 3 to 5 years, and some survive beyond 7 years if the PCV is kept below 65%.
44
CLINICAL MANAGEMENT Surgical correction is recommended in virtually all young dogs and cats with a left-to-right shunting PDA. Correction may not be warranted in older pets if the shunt volume is small and cardiomegaly is minimal or absent. Consultation with a specialist may be helpful in borderline circumstances. Recommended preoperative studies include ECG and chest radiographs to help assess the severity of the shunt and to detect the presence of congestive heart failure. An echocardiogram should always be performed to verify the diagnosis and rule out additional defects. The timing of surgery is debatable, but PDA correction is typically recommended at an early age or as soon as the diagnosis is made, especially if congestive heart failure appears imminent. If pulmonary edema is found on the chest radiograph, the patient should be treated medically for heart failure (furosemide, ACE inhibitors) before surgery. Positive inotropic support should also be considered. Treatment with prostaglandin inhibitors such as indomethacin, often used in premature human infants to assist closure of a structurally normal but functionally immature PDA, is not effective in dogs and cats, most likely because of the absence of smooth muscle in the ductal wall.
Surgical correction is recommended in virtually all young dogs and cats with a left-to-right shunting PDA. Correction may not be warranted in older pets if the shunt volume is small and cardiomegaly is minimal or absent. Consultation with a specialist may be helpful in borderline circumstances. Recommended preoperative studies include ECG and chest radiographs to help assess the severity of the shunt and to detect the presence of congestive heart failure. An echocardiogram should always be performed to verify the diagnosis and rule out additional defects. The timing of surgery is debatable, but PDA correction is typically recommended at an early age or as soon as the diagnosis is made, especially if congestive heart failure appears imminent. If pulmonary edema is found on the chest radiograph, the patient should be treated medically for heart failure (furosemide, ACE inhibitors) before surgery. Positive inotropic support should also be considered. Treatment with prostaglandin inhibitors such as indomethacin, often used in premature human infants to assist closure of a structurally normal but functionally immature PDA, is not effective in dogs and cats, most likely because of the absence of smooth muscle in the ductal wall.
45
Two approaches to PDA correction are currently available. For many years, left thoracotomy and surgical closure, typically by ligation, was the only available treatment.15c Other surgical methods of repair include suture occlusion with metallic clips and surgical division. These technique and their results have been described in detail in several reports, indicating high surgical success rates and excellent prognosis following repair.48a-54a,10b-12b Complications of surgical PDA repair in dogs most often include hemorrhage, infection, pneumothorax, cardiac arrhythmias, cardiac arrest, and heart failure. Surgical mortality should be less than 3% in uncomplicated cases.53a,10b-12b Preexisting congestive heart failure dramatically increases the risk of anesthetic or operative death and the rate of serious complications, underscoring the necessity of resolving pulmonary congestion before surgery. Positive inotropic support provided via a dobutamine infusion should also be considered for patients in this circumstance. Most dogs experience an uneventful recovery following surgery and overall cardiac size gradually decreases toward normal, though the heart and great vessels often continue to retain an abnormal shape.44a Postoperative Doppler examination may indicate a small residual shunt, although the continuous murmur is usually absent and the clinical outcomes are good. A soft left apical systolic murmur, usually from residual secondary mitral regurgitation, is often heard for a variable period after ductus ligation.47a
Two approaches to PDA correction are currently available. For many years, left thoracotomy and surgical closure, typically by ligation, was the only available treatment.15c Other surgical methods of repair include suture occlusion with metallic clips and surgical division. These technique and their results have been described in detail in several reports, indicating high surgical success rates and excellent prognosis following repair.48a-54a,10b-12b Complications of surgical PDA repair in dogs most often include hemorrhage, infection, pneumothorax, cardiac arrhythmias, cardiac arrest, and heart failure. Surgical mortality should be less than 3% in uncomplicated cases.53a,10b-12b Preexisting congestive heart failure dramatically increases the risk of anesthetic or operative death and the rate of serious complications, underscoring the necessity of resolving pulmonary congestion before surgery. Positive inotropic support provided via a dobutamine infusion should also be considered for patients in this circumstance. Most dogs experience an uneventful recovery following surgery and overall cardiac size gradually decreases toward normal, though the heart and great vessels often continue to retain an abnormal shape.44a Postoperative Doppler examination may indicate a small residual shunt, although the continuous murmur is usually absent and the clinical outcomes are good. A soft left apical systolic murmur, usually from residual secondary mitral regurgitation, is often heard for a variable period after ductus ligation.47a
46
Echocardiographic LV fractional shortening declines sharply immediately after surgery because of diminished preload and increased afterload; but medical therapy is not usually needed if signs of heart failure were not evident preoperatively. Medical therapies required before surgery for congestive heart failure are often required for several months following repair.
Echocardiographic LV fractional shortening declines sharply immediately after surgery because of diminished preload and increased afterload; but medical therapy is not usually needed if signs of heart failure were not evident preoperatively. Medical therapies required before surgery for congestive heart failure are often required for several months following repair.
47
Postoperative ductal recanalization has been reported but is uncommon, occurring in less than 2% of cases and most commonly associated with infection.15c Postoperative fever and pulmonary infiltrates may indicate infection at the surgical site and hematogenous pneumonia.57a The owner should be informed of the suspected heritable nature of the defect and that the animal should not be used for breeding.
Postoperative ductal recanalization has been reported but is uncommon, occurring in less than 2% of cases and most commonly associated with infection.15c Postoperative fever and pulmonary infiltrates may indicate infection at the surgical site and hematogenous pneumonia.57a The owner should be informed of the suspected heritable nature of the defect and that the animal should not be used for breeding.
48
Less invasive alternative techniques for PDA occlusion have gained in popularity.[17-20],17c-21c Percutaneous embolization of the ductus using expandable metal devices with or without thrombogenic Dacron strands can be accomplished in most small animals with a PDA, avoiding the morbidity of surgical thoracotomy. The most commonly used embolization device is either a helical metal coil or a self-expanding pluglike device that is delivered through a small catheter via the femoral artery or other peripheral vessel. Following deployment into the ductus arteriosus, the coil's attached Dacron feathers induce thrombus formation, thereby occluding the PDA. The pluglike device expands into the lumen of the ductus, and similar to the helical coil, induces thrombus formation and PDA occlusion.[19],[20] The advantages of transvenous PDA occlusion over thoracotomy and surgical ligation include lower morbidity, shorter hospitalization, and faster recovery. The success rate of these technique has been promising and the major complication rate has been acceptably low, consisting mainly of residual shunting and pulmonary embolization of a coil.[17,19,21],17c-21c Careful pre- and intraoperative evaluation of the PDA morphology and device orientation facilitates correct placement of the devices.[22]
Less invasive alternative techniques for PDA occlusion have gained in popularity.[17-20],17c-21c Percutaneous embolization of the ductus using expandable metal devices with or without thrombogenic Dacron strands can be accomplished in most small animals with a PDA, avoiding the morbidity of surgical thoracotomy. The most commonly used embolization device is either a helical metal coil or a self-expanding pluglike device that is delivered through a small catheter via the femoral artery or other peripheral vessel. Following deployment into the ductus arteriosus, the coil's attached Dacron feathers induce thrombus formation, thereby occluding the PDA. The pluglike device expands into the lumen of the ductus, and similar to the helical coil, induces thrombus formation and PDA occlusion.[19],[20] The advantages of transvenous PDA occlusion over thoracotomy and surgical ligation include lower morbidity, shorter hospitalization, and faster recovery. The success rate of these technique has been promising and the major complication rate has been acceptably low, consisting mainly of residual shunting and pulmonary embolization of a coil.[17,19,21],17c-21c Careful pre- and intraoperative evaluation of the PDA morphology and device orientation facilitates correct placement of the devices.[22]
49
Coils that embolize to the lungs can be ignored, pushed to a peripheral location, or removed.[23] The authors prefer to remove dislodged coils which can be quite easily accomplished via heartworm extraction forceps or other retrieval devices. Since device retention within the PDA is required for successful closure, the ideal candidates for coil occlusion should possess a relatively small funnel-shaped PDA that tapers to a diameter of 2 or 3 mm at the pulmonary artery end
Coils that embolize to the lungs can be ignored, pushed to a peripheral location, or removed.[23] The authors prefer to remove dislodged coils which can be quite easily accomplished via heartworm extraction forceps or other retrieval devices. Since device retention within the PDA is required for successful closure, the ideal candidates for coil occlusion should possess a relatively small funnel-shaped PDA that tapers to a diameter of 2 or 3 mm at the pulmonary artery end
50
Occlusion of large diameter PDAs (>4 mm) can be achieved by deploying multiple coils into the ductal ampulla but coil dislodgement and residual shunting are more problematic in this circumstance (Figure 249-9).[19] Self-expanding, pluglike devices developed specifically for canine use (Amplatzer Canine Duct Occluder) have been successfully used to accomplish PDA closure in dogs. (Figure 249-10).[20] Advantages of this technique include secure retention of the device in the ductus with a correspondingly low rate of dislodgement, ease of delivery through the femoral vein, and suitability for closing large diameter PDAs with a single implant. The need for specialized equipment (i.e., coils, occluding stents, catheters, fluoroscopy) and an operator experienced in performing cardiac catheterization limits the application of transcatheter PDA closure techniques to university teaching hospitals and large specialty referral centers. Despite the growing use of transvenous occlusion devices, the historical and comparative success of the traditional PDA surgery makes thoracotomy and ligation a perfectly acceptable and, in some circumstances, a preferable alternative to transcatheter closure.[25]
Occlusion of large diameter PDAs (>4 mm) can be achieved by deploying multiple coils into the ductal ampulla but coil dislodgement and residual shunting are more problematic in this circumstance (Figure 249-9).[19] Self-expanding, pluglike devices developed specifically for canine use (Amplatzer Canine Duct Occluder) have been successfully used to accomplish PDA closure in dogs. (Figure 249-10).[20] Advantages of this technique include secure retention of the device in the ductus with a correspondingly low rate of dislodgement, ease of delivery through the femoral vein, and suitability for closing large diameter PDAs with a single implant. The need for specialized equipment (i.e., coils, occluding stents, catheters, fluoroscopy) and an operator experienced in performing cardiac catheterization limits the application of transcatheter PDA closure techniques to university teaching hospitals and large specialty referral centers. Despite the growing use of transvenous occlusion devices, the historical and comparative success of the traditional PDA surgery makes thoracotomy and ligation a perfectly acceptable and, in some circumstances, a preferable alternative to transcatheter closure.[25]
51
Animals with reversed PDA have irreversible obstructive pulmonary vascular disease. Morbidity and mortality are usually the result of complications related to polycythemia and chronic hypoxemia rather than congestive heart failure. Treatment of these patients consists of exercise restriction, avoidance of stress, and maintenance of the PCV between 58% and 65% by periodic phlebotomy. Long-term management by these techniques is possible.[26] Phlebotomy should be performed cautiously to avoid weakness or collapse, and intravascular volume may be supported during phlebotomy by administration of crystalloid solutions. Attempts to reduce the red cell volume of reversed PDA cases using drug therapy (e.g., hydroxyurea) have been reported and may be an alternative to repeated phlebotomy.[27] Activity restriction is usually advised as exercise-induced systemic vasodilation increases the degree of right-to-left shunting and predisposes to posterior paresis or collapse and cyanosis.
Animals with reversed PDA have irreversible obstructive pulmonary vascular disease. Morbidity and mortality are usually the result of complications related to polycythemia and chronic hypoxemia rather than congestive heart failure. Treatment of these patients consists of exercise restriction, avoidance of stress, and maintenance of the PCV between 58% and 65% by periodic phlebotomy. Long-term management by these techniques is possible.[26] Phlebotomy should be performed cautiously to avoid weakness or collapse, and intravascular volume may be supported during phlebotomy by administration of crystalloid solutions. Attempts to reduce the red cell volume of reversed PDA cases using drug therapy (e.g., hydroxyurea) have been reported and may be an alternative to repeated phlebotomy.[27] Activity restriction is usually advised as exercise-induced systemic vasodilation increases the degree of right-to-left shunting and predisposes to posterior paresis or collapse and cyanosis.
52
Closure of reversed PDA is strongly contraindicated, as it invariably leads to late operative or early postoperative acute right heart failure and death.
Closure of reversed PDA is strongly contraindicated, as it invariably leads to late operative or early postoperative acute right heart failure and death.