Congenital Heart Defects Flashcards

1
Q

Three shunts in fetal circulation?

A

ductus venosus, foramen ovale, & ductus arteriosus

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2
Q
A
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3
Q

What happens to the fetal shunts?

A

as soon as baby is born, fetal shunts & umbilical vessels are no longer needed & become occluded

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4
Q

What happens w/ severe fetal cardiac malformations ?

A

They are incompatible w/ intrauterine life resulting in either embryonic death or fetal abortion

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5
Q

What happens w/ cardiac malformations that are compatible w/ intrauterine life?

A

result in post natal heart failure or sudden death

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6
Q

What happens w/ minor cardiac malformations?

A

they are well compensated by physiologic adaptive mechs & cause no clinical signs. in these cases, defects are purely incidental finding @ slaughter or post-mortem

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7
Q

The etiological diagnosis of congenital heart defects is rarely reached. What are some etiologies?

A
  1. genetic: single or multiple gene effects, chromosomal abnormalities
  2. maternal infections: parvo, bluetongue virus, BVD, rubella
  3. nutritional deficiencies: vit A, pantothenic acid, riboflavin, zinc
  4. drugs: thalidomide, ethanol, salicylates
  5. other teratogens: radiation, fetal hypoxia, maternal diabetes
  6. multifactorial (genetic & enviro factors)
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8
Q

What are most common congenital heart defects (categories)?

A
  1. defects that cause vol overload
  2. defects that cause press overload
  3. defects that cause early cyanosis
  4. miscellaneous
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9
Q

What are the most common congenital heart defects that cause volume overload?

A

Left to right shunts
1. Patent Ductus Arteriosus (PDA)
2. Atrial Septal Defect (ASD)
3. Ventricular Septal Defect (VSD)

valvular regurgitation
1. Valvular dysplasias

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10
Q

What is a left to right shunt?

A

When a defect is present btwn the right and left cardiac chambers, blood flows down the pressure gradient from L to R side

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11
Q

What is valvular regurgitation?

A

regurgitated blood from the ventricles to the atria leads to progressive atrial dilation & eccentric ventricular hypertrophy of the affected side

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12
Q

What are the most common congenital heart defects that cause press overload?

A

Aortic & pulmonic stenosis

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13
Q

Pathogenesis of pressure overload?

A

ventricular outflow obstruction causes a progressive/chronic increase in intraventricular pressure resulting in concentric hypertrophy of the affected side

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14
Q

What are the most common congenital heart defects that cause early cyanosis?

A

Right to L shunts
1. Tetralogy of Fallot
2. Transposition of Great Arteries

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15
Q

What are the most common miscellaneous congenital heart defects?

A
  1. persistent right aortic arch
  2. ectopia cordis
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16
Q

What is a right to left shunt?

A
  • in these diseases, nonoxygenated blood from the right heart compartments flow into the left heart compartments or directly into the systemic circulation
  • this also occurs in cases of PDA & VSD when there is reversal of shunting from R to L
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17
Q

What is the ductus arteriosis?

A

Normal communication btwn pulmonary artery & aorta in fetal circulation. normally closes after birth forming LIGAMENTUM ARTERIOSUM.

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18
Q

Species where patent ductus arteriosus is seen?

A

all spp but particularly in dogs (> poodles, collies, pomeranians)

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19
Q

diagnosis of patent ductus arteriosus can only be made when?

A

if ductus fails to close 3 wks after birth

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20
Q

Hemodynamics of patent ductus arteriosus ?

A

L to R shunt btwn aorta & pulmonary artery -> increased pulmonary blood flow (hyperflux) -> pulmonary hypertension -> press overload in RV & vol overload in LV

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21
Q

MD?

A

patent ductus arteriosus

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22
Q

MD?

A

patent ductus arteriosus

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23
Q

MD?

A

patent ductus arteriosus

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24
Q

How long may closure of ductus arteriosus take in foals?

A

several days

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25
Q

Is there a difference between structural and functional closure of the ductus arteriosus?

A

yes

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26
Q

steps of L to R shunts?

A

high pulmonary vascular resistance -> medial hypertrophy or irreversible obstructive intimal lesions “plexogenic arteriopathy” -> shunt reverses (R to L) -> late cyanosis (Eisenmenger syndrome)

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27
Q

What is atrial septal defect and what are two main forms?

A

communication btwn L & R atrium in postnatal life
1. persistence of fetal FORAMEN OVALE (probe-patent foramen ovale)
2. true atrial defect in which there is failed closure of atrial septum

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28
Q

Clinical significance of minor atrial defects?

A

little clinical significance; no clinical signs

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29
Q

In which species is atrial septal defect most common?

A

dogs & cats

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30
Q

MD?

A

patent foramen ovale

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31
Q

MD?

A

patent foramen ovale

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32
Q

MD?

A

atrial septal defect

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33
Q

MD?

A

atrial septal defect

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34
Q

Probe- patent foramen ovale?

A

in 20% of people, probe can be passed through patent foramen ovale but this opening is not fxnal (no shunt)

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35
Q

hemodynamics of atrial septal defects?

A
  • large defect: excessive blood flow from LA -> RA; volume overload of RV -> RV hypertrophy
  • pulmonary congestion (oxygenated blood is returned to lungs)
36
Q

What is a ventricular septal defect?

A

communication btwn R & L ventricle

37
Q

Ventricular septal defects are one of the most common cardiac defects in …

A

domestic animals (> Eq, Cattle)

38
Q

MD?

A

ventral septal defect

39
Q

MD?

A

ventral septal defect

40
Q

How does a ventricular septal defect result?

A

embryologically, muscular septum grows up, membranous septum grows down, & infundibulum meets both muscular & membranous septums

41
Q

Relative to position in septum, ventricular septal defects could be…?

A
  1. high, when septal defect is close to AV valve
  2. low, when septal defect is close to apex (rare)
42
Q

MD?

A

Low ventricular septal defect

43
Q

MD?

A

ventricular septal defect

44
Q

hemodynamics of ventricular septal defect?

A

L to R shunt -> RV press & vol overload -> RV hypertrophy -> R heart fail (if uncompensated) -> LV hypertrophy as well

blood shunting could later reverse to R -> L & cause cyanosis (Eisenmenger complex)

45
Q

What is valvular dysplasia?

A

congenital malformation that is often difficult to assess in post-mortem exams. requires experienced practitioner or pathologist

46
Q

What should you do if you suspect valvular dysplasia?

A

always submit whole heart to diagnostic lab or take good digital pics of valves

47
Q

What are two types of valvular dysplasia?

A

Tricuspid & Mitral dysplasia

48
Q

What spp are tricuspid dysplasia most common in?

A

Cats, followed by dogs (particularly retrievers)

49
Q

What features do dysplastic tricuspid valves show one or more of?

A
  1. diffuse or focal thickening of leaflets
  2. missing or short chordae tendineae
  3. thick or short papillary muscles
  4. direct fusion of leaflets to papillary muscles/ventricular wall
50
Q

What does tricuspid dysplasia cause?

A

eccentric hypertrophy of R ventricle & massive distension of R atrium

51
Q

What are some other names for mitral dysplasia?

A

left atrioventricular valvular insufficiency or stenosis

52
Q

What species is mitral dysplasia most common in?

A
  • cats
  • in dogs (Cavaliers, great danes, & english bull terriers)
53
Q

Features of dysplastic mitral valves?

A
  1. short thick leaftlets & enlarged annulus
  2. short thick chordae tendineae
  3. upward malposition of atrophic or hypertrophic papillary muscles
54
Q

what does mitral dysplasia cause?

A

eccentric hypertrophy of L ventricle & distension of L atrium

55
Q

What is mitral valve displasia often accompanied by?

A

tricuspid dysplasia, VSD, ASD

56
Q

MD? on R side of heart

A

tricuspid dysplasia (shorter or absent chordae tendineae, thickened valve)

57
Q

MD? Right side of heart

A

tricuspid dysplasia (shorter or absent chordae tendineae, thickened valve)

58
Q

MD? right side of the heart?

A

tricuspid dysplasia (shorter or absent chordae tendineae, thickened valve)

59
Q

MD? right side of the heart

A

tricuspid dysplasia (shorter or absent chordae tendineae, thickened valve)

60
Q

MD?

A

dilation of right atrium

61
Q

MD?

A

tricuspid dysplasia (thickened valves, absent chordae tendineae, direct fusion of the leaflet to the papillary muscle)

62
Q

What is pulmonic stenosis?

A

narrowing of pulmonic valve orifice

63
Q

What sp is pulmonic stenosis common in?

A

Dogs (beagle, english bulldogs)

64
Q

3 classifications of pulmonic stenosis depending on location?

A
  1. valvular
  2. subvalvular
    3.supravalvular
65
Q

What is a stenotic site typically formed by ?

A

a constricting band of fibrous or muscular tissue

66
Q

What strange feature causes pulmonic stenosis in some dogs?

A

anomalous coronary artery obstructs the right outflow tract

67
Q

where is post-stenotic arterial dilation often found?

A

in artery, distal to stenosis

68
Q

hemodynamics of pulmonic stenosis?

A

obstruction of the right ventricular outflow -> press overload of RV -> RV hypertrophy -> post stenotic dilation of the pulmonary artery -> if uncompensated, R heart failure

69
Q

What would you find on necropsy with pulmonic stenosis?

A
  • heart has broad base
  • internal exam of heart reveals notably hypertrophic R ventricle
  • exam of pulmonary artery reveals narrow lumen due to sub-valvular constrictive fibrosis or abnormal fusion of cusps commissures
  • pulmonary artery may show post-stenotic dilation
70
Q

MD?

A

pulmonic stenosis

71
Q

What spp is aortic & subaortic stenosis most commonly seen?

A

aortic valvular stenosis is distinctly uncommon in animals, dogs (bull terriers, boxers, german shepherds, & newfies) and pigs

72
Q

Hemodynamics of subaortic stenosis?

A

obstruction of the LV outflow -> press overload of LV -> LV hypertrophy -> post-stenotic dilation of aorta. if uncompensated, L heart fail w/ pulmonary congestion & edema.

73
Q

Stenosis can cause turbulence in aorta, leading to…

A

jet lesions (trauma to aorta)
- inflammation & appearance of platelets/deposits of fibrin

74
Q

What do dogs with subaortic stenosis often have concurrently?

A

mitral valve disease & myocardial necrosis & fibrosis

75
Q

MD?

A

sub-aortic stenosis

76
Q

MD?

A

sub-aortic stenosis with jet lesion

77
Q

MD?

A

subaortic valve stenosis

77
Q

MD?

A
78
Q

What is Tetralogy of Fallot?

A

combo of 4 heart changes present @ birth:
1. VSD
2. overriding aorta
3. pulmonic stenosis
4. right ventricular stenosis

79
Q

What is transposition of great arteries?

A

aorta arises from R ventricle & pulmonary artery arises from L ventricle. there is separation of systemic & pulmonary circulations that is incompatible w/ postnatal life unless shunt exists for adequate mixing of blood (R to L shunt; early cyanosis)

80
Q

another name for transposition of great arteries?

A

ventriculoarterial discordance

81
Q

What sp is persistent R aortic arch most seen in?

A

dogs

82
Q

What causes persistent R aortic arch?

A

a cardiac malformation, where aorta is incorrectly formed frm R 4th (rather than L 4th) aortic arch in embryo.
trachea & esophagus are enclosed by aortic arch, pulmonary artery, & ligamentum arteriosum which results in localized esophageal constriction

83
Q

What does esophageal constriction from persistent R aortic arch result in?

A

dysphagia, regurgitation, megaesophagus. no hemodynamic abnormalities, no signs of heart failure

84
Q

What is ectopia cordis?

A

congenital displacement of heart outside body

85
Q

viability of ectopia cordis?

A

mostly found in stillbirths or aborted fetuses; sporadically animals survive for days, weeks, or more!