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10. Congenital Heart dz > PS > Flashcards

PS Flashcards

1
Q

Patterson et al. typical valvular lesions

A
  • Fused valve leaflets w/o thickening
  • Dome-shaped valve with central orifice
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2
Q

Patterson et al. grade 1 PV dysplasia lesions

A
  • Less common → marked thickening of valve leaflets w/o fusion
    o Grade 1: slight thickening of valve leaflets
     Little/no fusion or hypoplasia
     Minimal or no pulmonary outflow obstruction
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3
Q

Patterson et al. grade 2 PV dysplasia lesions

A

o Grade 2: moderate to severe thickening of valve leaflets
 With fusion or hypoplasia or both
 Moderate to severe pulmonary outflow obstruction

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4
Q

Patterson et al. valvular pathology

A
  • PV annulus normal or slightly ↓ size
  • Thickening
    o Some degree of thickening in all affected dogs
     Slight thickening
     Bulky, non-flexible, cushion-like leaflets filling valve orifice
    o Equal involvement frequency among 3 leaflets
    o Small irregular nodules on leaflets surface
  • Hypoplasia
    o Smaller size leaflet vs normal dog
    o Variable degree from slight reduction to complete absence
     Often mishapen
    o Usually 1 or 2 leaflet involved, most often L involved > anterior > R
  • Fusion
    o Adjacent leaflets do not insert separately on intimal surface of PA
    o Variable degree from slight (<1/4) to complete fusion
    o 3 commissures affected w equal frequency
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5
Q

Histo of normal PV

A

o Fibrosa layer on arterial side
 Covered by layer of flat endothelial cells
 May contain elastic fibrils
 Not completely separated from spongiosa
o Spongiosa layer
 Variable thickness
 Loose fibrillar material, fragments of collagen and widely separated cells
o Ventricularis layer on ventricular side
 Fibroelastic layer
 Covered by layer of flat endothelial cells

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6
Q

Histo lesions PS

A
  • PS: thickening of spongiosa w loosely arranged collagen tissue
    o Similar cell population
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7
Q

Embryology DORV

A
  • Etiology: uncertain
    o Localized growth of trabeculated myocardium early in development
    o RV subdivision/obstruction from arrested incorporation of primitive bulbus cordis into RV body
     Incomplete fusion of bulbar or endocardial cushions → associated VSD
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8
Q

gross exam DORV

A
  • Obstructive fibrous band
    o Jct of RV body and proximal infundibulum
    o Below crista supraventricularis
  • Anomalous muscle bundles traversing middle of RV: supraventricular crest → RV apex
    o Proximal hypertrophied chamber → sinus portion of RV
    o Distal low pressure chamber → infundibulum portion
  • Pyramidal mass of muscle below TV from IVS → RVFW
    o 2 bundles
     Ventral bundle: attach RVFW → IVS
     Dorsal bundle: larger, attach to base of anterior pap muscle
    o Near the base of TV ring (vs moderator band is usually more apical, no obstruction)
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9
Q

Types of DORV

A

o Type I: fibromuscular band of tissue at jct of RV cavity and pulmonary infundibulum (proximal RVOT)
o Type II: fibromuscular thickening of pulmonary infundibulum → just below PV

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10
Q

Signalment DORV

A

asymptomatic animal with heart murmur
o Can also present in R sided CHF

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11
Q

PE DORV

A

loud pansystolic crescendo-decrescendo murmur

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12
Q

ECG DORV

A
  • ↑ QRS duration
  • R axis deviation
  • Junctional tachycardia
  • APC/VPCs
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13
Q

CTX DORV

A
  • Cardiomegaly, R sided
  • Cardiac silhouette can also be normal
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14
Q

2D echo DORV

A

o RVH
o RAE
o Anomalous muscle bundles: muscle proliferation causing obstruction of flow
o Abnormal fluttering of PV

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15
Q

Doppler echo DORV

A

o PG across mid RV: obstruction is proximal to infundibulum
 Vs TOF: obstruction at infundibulum
 Degree of obstruction can vary
o VSD

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16
Q

Cardiac KT angio DORV

A

o Filling defects w/I RV below crista supraventricularis
o VSD

17
Q

Cardiac KT pressure stury DORV

A

o ↑ pressure in proximal/sinus portion of RV vs lower cavity
o Pressure in distal chamber = PAP
 Unless concommittant PS

18
Q

Natural hx and tx DORV

A
  • Severity increase in time
  • Treatment: balloon valvuloplasty, surgical division
19
Q

PS embryology

A
  • Valve development: 3 endocardial swellings → excavation forms cusps
20
Q

Gross exam grading system PS

A

o Grade 1:
 Slight thickening of PV leaflets w little to no fusion/hypoplasia
 Minimal to no pulmonary OT obstruction

o Grade 2: dysplastic valve
 Moderate/severe thickening of PV leaflets
 Fusion, hypoplasia, dome shaped PV leaflets
 Moderate/severe PV flow obstruction

21
Q

Breeds abn CA PS

A

o English Bulldogs and Boxers

22
Q

Concurrent defects PS

A

TVD (large breeds), PFO

23
Q

Histo PS

A
  • Overproduction of normal valve element: 2nd to failure of conversion of embryonic valve primordia
    o Thickening of the valve spongiosa
    o Bands of fusiform 
    o Dense collagen network
  • Blood filled spaces lined w endothelium found in cusps
24
Q

Pathophys PS

A
  • ↑ RVOT resistance to blood flow → ↑RV systolic P → RVH
    o Proportional to severity of obstruction
    o Infundibulum hypertrophy → dynamic RVOTO
  • Myocardial response to ↑ wall stress
    o Neonatal: hyperplasia + ↑# of capillaries
    o Adult: hypertrophy of existing fibers
  • RAE:
    o TR
    o ↑RV filling P
    o ↓ CO → activates RAAS
  • RVE: RV failure from
    o ↓ RV SV
    o R-CHF
25
Q

Signalment PS

A

o Predisposed breeds: Bulldogs, Beagle, Samoyed, Chihuahua, Miniature Schnauzer, Lab, Mastiff, Chow chow, Newfoundland, Basset Hound, Keeshond, WHWT, Terrier, Spaniels
 Genetics: heritable in Keeshonds and Beagles
o Rare in cats

26
Q

C/s PS

A

most asymptomatic or
o Signs related to ↓ CO: syncope, lethargy
o R-sided CHF
o Cyanosis if R → L shunting defect

27
Q

PE PS

A

o Systolic ejection murmur at L base
 +/- systolic apical (TR)
 +/- diastolic basilar (PI)
 +/- pulmonary ejection click → doming of PV
 +/- split S2 → ↑ RV ET
o Jugular pulse

28
Q

ECG PS

A
  • R axis deviation
  • Tall/peaked P waves
  • Transient RBBB following BV reported
29
Q

CTX PS

A
  • MPA dilation
  • R sided cardiomegaly
  • Pulmonary underperfusion
30
Q

2D echo PS

A

o Abnormal PV
 Systolic doming
 Thickened/fused leaflets w ↓ motion
 ↑ echogenicity
 Type A (Typical)
* Commissural fusion
* Normal PA annulus
* Aortic:pulmonic ratio of <1.2
* Post stenotic dilation
 Type B (Dysplastic)
* Dysplastic, immobile leaflets
* Narrow annulus/hypoplastic
* Aortic:pulmonic ratio of >1.2
o Flattening/paradoxical IVS motion
o RVH w prominent pap muscles
o Muscular narrowing of RVOT
o ↑ endocardium echogenicity (fibrosis)
o Post stenotic MPA dilation

31
Q

Dopper echo PS

A

o High velocity/turbulent flow across stenosis
o PG across PV: Mild 30-50mmHg, Moderate 50-80mmHg, Severe >80mmHg
o PI: secondary to abnormal valve apparatus and PA annular dilation
 Diastolic fluttering of TV
 ↑ velocity if PH (>2.5m/s)
o TR

32
Q

Cardiac KT angio PS

A

o Post stenotic dilation of MPA
o Features of PV dysplasia
 Narrowed valve orifice
 Asymmetric valve sinuses
 Hypoplasia of annulus/valve sinus
 Systolic valve doming
 Filling defect → from thickening of leaflets
o RVH
o Levophase: look for single RCA

33
Q

Cardiac KT pressure study PS

A

o Systolic PG across obstruction
o ↑RV systolic pressure
o ↑RAP: ↑a wave

34
Q

Natural hx PS

A
  • PV dysplasia most frequent in dogs
    o Subvalvular/supravalvular stenosis reported but unfrequent
     Supravalvular: Giant Schnauzer
    o Pulmonary atresia → most severe form
  • Mild to moderate PS may live normal lives.
  • Moderate: most dogs are ok, uncertain px long term
    o PG ↓ might be beneficial if concurrent TVD
  • Severe may develop c/s and R CHF
    o General correlation btw PG and survival
    o Progressive muscular hypertrophy can worsen PG w DRVOTO
    o Usually balloon valvuloplasty will be attempted to ↓ PG
     Single RCA → BV contra indicated, can place stent
35
Q

Decr px PS

A

when c/s develop
o Exercise intolerance
o R-CHF
o Arrhythmias (Afib)/sudden death

36
Q

Tx PS

A

o BVP: especially if dysplatic valve w/o hypoplasia
o Stent: indicated in CA anomaly of PA hypoplasia
 TR: contra indicated since will ↑ RV volume over load w/ creating PI
o Sx

37
Q

RVOTO can be associated w/

A

o HCM
o High output states: hyperT4, anemia, fever, pregnancy

38
Q

RVOTO PE

A

soft early to mid systolic high frequency murmur
o Murmur can change with HR and body position

39
Q

Echo DRVOTO

A

↑ velocity in RVOT
o No other cause of murmur on echo and normal heart

10. Congenital Heart dz (28 decks)

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