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10. Congenital Heart dz > AS > Flashcards

AS Flashcards

1
Q

Supravalvular stenosis embryology

A
  • ↑ development of Ao wall above sinus of Valsalva
    o ↓/abn expression of elastin genes: ↓ elasticity, ↑media thickness, collagen deposition
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2
Q

Supravalvular stenosis lesions

A
  • Discrete obstruction just distal to sinus of Valsalva
  • CA are proximal to obstruction: ↑ pressure in systole
    o Stenosis: ↓ flow
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3
Q

Supravalvular stenosis breeds

A
  • Rare in dogs, least common form
  • Described in cats
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4
Q

valvular stenosis lesions

A

Uncommon
Lesions
* Valvular malformations can include
o Bicuspid AoV: partial/complete fusion of 2 cusp
 Most common in Hu
o Unicuspid valve
o Dysplatic AoV leaflets
* Stenosis is due to incomplete opening, doming of the valve → ↓ effective valve area
* Annular hypoplasia also possible, seen most often with concurrent congenital defects

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5
Q

Embryology SAS

A
  • SAS 2nd to abn development of one LVOT component
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6
Q

LVOT formed by

A

o Conotruncal septum
o IVS
o MV septal leaflet

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7
Q

Etiology SAS

A

o Primary developmental fault of region btw conus and truncus
o Persistent embryonal tissue: retain proliferative capacity + chondrogenic potential after birth
o Abn flow pattern: shear stress in LVOT
 Endothelial damage
 Cell proliferation
 Collagen deposition

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8
Q

Forms of SAS

A

o Fribrous membrane proximal to AoV: usually very thin and just below AoV
o Fibromuscular ridge: slightly lower, thicker
o Tunnel type obstructive lesion: muscular hypertrophy/narrowing of LVOT

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9
Q

Gross exam SAS: grades described in Newfoundland

A

o 1: Mildest form
 Small, whitish slightly raised nodules on endocardial surface of IVS, below AoV
 Thickened endocardium
 Only identified from 3-12weeks
o 2: narrow ridge of whitish, thickened endocardium
 Extending partially around LVOT from base of MV septal leaflet → IVS
o 3: Most severe form
 Fibrous band, ridge or collar encircling LVOT below AoV
 Raised above endocardium
 Extend to/involve cranioventral leaflet of MV + base of AoV
 Usually >6mo

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10
Q

Gross exam SAS associated lesions

A

o Concentric LVH: severity reflect PG
o LAE: from ↓LV compliance, myocardial failure, MR
o Dilation of ascending Ao and Ao arch: turbulent flow
o Abnormalities of MV can also be present: minor to severe MVD, attachments to septal leaflets
o Thickened AoV: from turbulent flow
 Can result in AI
o Focal areas of myocardial fibrosis/infarction
o Intramural coronary arterial changes

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11
Q

Histology lesions

A
  • Stenotic ring:
    o Large, uni/multinucleated rounded connective  → resemble chondrocytes
    o Loosely arranged reticular fibers
    o Mucopolysaccharide ground substance
    o Elastic fibers
  • Advanced lesions: bundles of collagen + cartilage
  • Intramural coronary artery pathology and remodeling (PG >35mmHg)
    o Luminal narrowing
    o Intimal proliferation of connective tissue/SM cell
    o Medial degeneration and hypertrophy, SM cell disorganization
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12
Q

Cause of CA pathology

A

not known
 ↑LV systolic P
 ↑ systolic wall tension
 Abnormal coronary blood flow
* ↓ baseline diastolic flow
* Reversal of coronary flow in systole
* Minimal coronary flow reserve

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13
Q

Pathophys SAS

A

LVOT obstruction: same for all level of obstruction → ↑ LV afterload
* ↑PG across stenotic region → ↑LV systolic P → ↑ wall stress → LVCH
o Wall stress is proportional to LVP and inversely proportional to wall thickness
o LVH: compensatory response to ↑ thickness → ↓ wall stress
 Preserve SV and CO
* Persistent/chronic P overload → ventricular remodeling
o Hypertrophy → fibrosis →  death
o LVH: ↑ ventricular stiffness → ↓ diastolic fct → ↓ ventricular relaxation → ↓diastolic filling
 Proportional to degree of LVH
o Subendocardial ischemia:
 2nd to ↑intracardiac compressive forces in systole and ↑ O2 consumption
 Minimal coronary flow reserve: can’t keep up w/ exercise and ↑ HR (short diastole)
 ↓ coronary perfusion
 Hu: ↑ prevalence of CA ostium obstruction may contribute

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14
Q

Wall stress equation

A

Wall stress = P x r/2th

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15
Q

Signalment: breeds SAS

A

o Most common in larger breeds: boxer, newfoundland, German shepherd, Golden retrievers, Bull Terrier, Rottweiler
 Overrepresented: Samoyed, Great Dane
 Rare in cats

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16
Q

Particularity of lesion development SAS

A

o Not present at birth → develop in 1st 3-8 weeks of life
 Gradient can ↑ in rapidly growing giant breed dogs
 Mechanism for ↑ severity: uncertain
* Fibrocartilagenous ring of SAS derived from embryonal endocardial tissue w proliferative capacity and chondrogenic potential after birth
* ↑ body size and LVH may contribute to progression

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17
Q

Genetic SAS

A

 Inherited in Newfie: polygenic, autosomal dominant w/ gene modification
 Heritable in other breeds

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18
Q

C/s SAS

A

asymptomatic or
o Exertional syncope: exercise induced ↑ LVP → activation of ventricular mechanoR → bradycardia + vasodilation
o Sudden death (arrhythmias)
o L CHF: myocardial failure, ↑ ventricular stiffness, MR, Afib
 Rare since LVH keep normal SV
 Usually 2nd to complicating factor: myocardial infarct, MR, AI

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19
Q

PE SAS

A

o Hypokinetic, late rising arterial pulse → obstruction to ejection
 Pulsus parvus et tardus
 Normal pulse pressure
o Murmur
 Systolic ejection L basilar murmur → high velocity and turbulent flow across lesion
* Can radiate in carotid artery
 To and fro murmur: if concurrent AI present
 Paradoxical split S2: delayed AoV closure from ↑ET
 S3-S4 gallop

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20
Q

ECG SAS

A
  • Often normal
  • LVH and myocardial ischemia responsible for changes in QRS and ST segment
    o ↑ R wave amplitude
    o L axis deviation
  • VPCs in dogs with severe PG
  • ST segment deviation: slurred, depressed, elevated
    o ST segment depression: LVH or myocardial ischemia
    o Exercise induced ST segment deviation + VPCs → suspect ischemia/abnormal coronary blood flow
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21
Q

CTX SAS

A
  • Post stenotic dilation of Ao (ascending, arch + brachiocephalic trunk)
    o Widening of mediastinum on VD
    o Lost of cranial waist on lateral
  • Cardiomegaly: LVH + LAE
22
Q

Echo 2D SAS

A

o LVH: moderate to severe PG
o Subvalvular fibrous ring:
 Narrowing btw IVS and base of anterior MV leaflet
* Can involve MV
 Proximal to AoV on LAX views
 Discrete membranous/fibromuscular ridge
o Post stenotic dilation of Ao
 Secondary thickening of AoV cusps
 Mid systolic partial closure of AoV
o LA hypertrophy/enlargement: ↑LAP to fill stiff, hypertrophied LV
o Bright, hyperechoic regions in LV → severe focal replacement fibrosis
 LV papillary muscles and endocardium

23
Q

Echo M-Mode SAS

A

o Mid systolic partial AoV closure
o Diastolic MV valve fluttering (AI)
o ↓ mitral E-F slope

24
Q

Doppler echo SAS

A

o Pressure gradient present across LVOT
 Mild: 2.2 – 2.5m/s is equivocal
 Fixed obstruction pattern
o E/A reversal if diastolic dysfct
o MR
 Concurrent MVD
 Involvement of anterior MV leaflet in subaortic ridge
 Geometric changes in LV
 SAM may be present → dynamic LVOTO
* Some dogs will have isolated DLVOTO → Golden retreivers
o Diastolic dysfunction: reversal of E and A waves
 From LVH or myocardial ischemia
AI

25
Q

Causes of AI w/ SAS

A

o Involvement of valve leaflets w fibrous ring → thickening of leaflets
o Jet lesions leading to thickening of leaflets
o Dilation of ascending Ao
o Bacterial endocarditis

26
Q

Cardiac KT SAS pressure study

A

o Localization of obstruction by withdrawing KT from LV → LVOT → AoV → Ao
o Systolic PG across obstruction
 ↓ by anesthesia by 40-50%
 Dynamic obstruction: PG will diverge later in systole
 Fixed obstruction: PG will diverge early
o ↑ LV end diastolic P

27
Q

Cardiac KT angio SAS

A

o LV ventriculogram:
 Small LV cavity + LVCH
 Subvalvular obstruction
 MR
 Post stenotic dilation
o Supravalvular Ao injection: r/o or assess AI
 Prominent LCA and major extramural branches
* ↑ myocardial O2 demand

28
Q

Natural hx: when do CHF develop

A
  • CHF most likely if
    o AI
    o Concurrent MV abnormalities
29
Q

Natural hx: risks

A
  • Sudden death
    o ↑ risk with severe SAS in first 3y of life (70%)
  • ↑ risk for bacterial endocarditis
30
Q

Natural hx mild SAS

A

o Mild LVH, mild PG (<75mmHg)
o Not use for breeding

31
Q

Natural hx SAS: who develops c/s

A

30% of severe cases

32
Q

Treatment to reduce c/s

A
  • Restrict exercise if moderate to severe gradient
33
Q

Embryology Ao Coarct: 2 theories

A
  • Hypothesized to occur from ectopic ductal tissue or abnormal ductal flow
  • Abn development of 4th and 6th Ao arch
    o Ductal tissue theory: migration of SM from ductus into Ao → constriction
    o Hemodynamic theory: ↓LV outflow leads to coarctation
34
Q

Gross exam Ao Coarct

A
  • Narrowing of the aorta
    o Distal to subclavian artery, adjacent to ductus arteriosus
     Jct of the arch and descending Ao
    o Discrete narrowing of Ao in area of DA insertion → juxtaductal
     Vs tubular hypoplasia
    o Ridge like thickening of the media of Ao wall
     Protrude into lumen from posterior and lateral wall
  • Ascending/descending Ao can be abn
  • Collaterals may develop: ↑ perfusion of caudal body
35
Q

Histo Ao Coarct

A
  • Disorganized intimal medial hyperplasia
    o Thick intimal and medial ridge protrude in Ao lumen
  • Posterior infolding extending around circumference of Ao
  • Dissection/aneurysm of distal portion can occur
36
Q

Pathophys Ao Coarct

A
  • Form of aortic stenosis: ↑LV systolic P → LVH
    o When lumen ↓ >45-55% of CSA
  • Depend on stenosis severity
    o Associated lesions: PDA, VSD, AS, MS
    o Rapid development: sudden DA constriction after birth
     CHF: no time for LVH to develop
  • PDA can remain patent and provide blood flow to caudal body
37
Q

Signalment Ao Coarct

A

o Rare in dogs, not reported in cats

38
Q

PE Ao Coarct

A

o Inequality of pulse pressure = HALLMARK of dz
 Proximal Ao: ↑systolic > diastolic pressure → ↑ pulse pressure in forelimbs
 Distal to obstruction: ↓systolic < diastolic pressure → ↓ pulse pressure in hindlimbs
o Weak/absent femoral pulses
o Pelvic limb weakness
 Differential perfusion
* Poor perfusion of caudal limbs
* Hypertension of cranial limbs
o Murmur loudest in systole, can last into mid diastole
 From defect itself
 Systolic ejection HM
 Continuous if well developed collaterals
o Gallop sound

39
Q

ECG Ao Coarct

A
  • LVH: ↑ R wave amplitude
40
Q

CTX Ao Coarct

A
  • Indentations/notching of ribs (Hu): enlarged intercostal arteries
    o Caused by the erosion of the inferior surfaces of the posterior ribs by dilated and tortuous intercostal collateral vessels
    o Internal mammary and spinal arteries also enlarge to provide collateral flow
  • Indentation of the Ao at the site of coarctation (“3 sign”)
  • Post stenotic dilation of the descending aorta may be seen
41
Q

Echo Ao Coarct

A
  • LVH
    o ↑ systolic pressure
  • In Hu: detailed 2D and Doppler studies of Ao
    o Narrowing visualized
    o PG across defect
42
Q

Cardiac KT pressure study Ao Coarct

A

o ↑ systolic pressure in ascending Ao
o ↓ systolic pressure distal to obstruction

43
Q

Cardiac KT angio Ao coarct

A

confirm diagnosis

44
Q

Natural hx Ao Coarct

A
  • Px variable depending on
    o Degree of Ao narrowing
45
Q

Treatment Ao Coarct

A
  • Treatments include surgical repair (anastomosis of Ao segments), balloon angioplasty, endovascular stents
    o Maintain DA patency until repair: PGE
46
Q

Tubular hypoplasia or interruption of the aorta

A
  • Ascending and descending Ao do not communicate
    o Rare in dogs
    o Most die 1st day/weeks of life
    o 2 reports: life maintained by PDA and marked collateral flow
47
Q

Tubular hypoplasia or interruption of the aorta Hu classification

A

o Type A: distal to L subclavian artery
o Type B: btw L subclavian and carotid arteries
o Type C: btw L and R carotid arteries

48
Q

Gross exam dextrocardia

A
  • Heart is positioned in R hemithorax
    o Apex pointing toward the R
    o R/L asymmetry remains present
  • Situs inversus → all organs are mirror image of normal
    o Usually no other cardiac abnormalities
  • Situs solitus → associated with major intracardiac abnormalities in Hu
    o AV discordance
    o TGA
  • Atrial situs: can be solitus, inversus or ambiguous
49
Q

Etiology dextrocardia

A

o Primary congenital abnormality
 Congenital developmental malposition
o Secondary to fluid, tissue, air pushing the heart to the R = cardiac DEXTROPOSITION

50
Q

Associated lesions/dz dextrocardia

A
  • Respiratory abnormalities: if situs inversus
    o Bronchitis, sinusitis, bronchiectasis
51
Q

ECG dextrocardia

A
  • Inverted voltage of atrial and ventricular depolarization (negative P and QRS)
  • P wave axis: to the R and inferiorly
52
Q

CTX dextrocardia

A
  • Apex of the heart is directed to the R

10. Congenital Heart dz (28 decks)

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