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10. Congenital Heart dz > PDA > Flashcards

PDA Flashcards

1
Q

Normal anatomy PDA

A
  • Bifurcation of main PA → ventral aspect of descending Ao btw L subclavian and intercostal arteries
    o Distinct muscular cylinder btw 2 elastic arteries
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2
Q

Function of DA during fetal life

A

o Allow blood flow to bypass lungs during fetal life

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3
Q

Histo DA

A
  • 98% smooth muscle + subadventitial elastic fibers +adventitial loose collagen
    o Circumferential distribution of muscle mass
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4
Q

What happens after birth

A

o Constriction in response to ↑ arterial O2 tension → close w/I min to hrs after birth
o Apobiosis: non inflammatory muscle degeneration starts after 48h
 Complete cytolysis after 1mo → ligamentum arteriosum
* Remnant adventitial elastic fibers

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5
Q

Difference in Hu DA

A

intimal cushions of fetal DA contribute to closure = not in dogs

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6
Q

Gross pathology

A
  • Most dogs: funnel shaped ductus
    o Narrowest segment at PA
    o Internal orifice is narrowed by fibrous ridge from maximal contraction of small amount of ductus muscle
  • Intra-aortic wall segment: ductus course w/I wall of Ao before opening in Ao lumen
    o Separated from the lumen by thin flap
    o May bulge and form aorto-ductal aneurysm
     Caused by lack of ductus muscle in Ao wall segment
     Size varies inversely w length of surgical segment → larger aneurysm = shorter surgical segment
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7
Q

Histopathology changes

A
  • Shorter ductus
  • Hypoplasia of ductal muscle mass AT PA END
    o Primary abnormality
    o Muscle present: contraction and degeneration → partial constriction and ductal closure
     Asymmetric: Failure to encircle lumen precluded complete closure
  • Replacement by non contracting, Ao like elastic segments AT AO END
    o Secondary abnormality → from absence of ductus muscle promoter/inducer
  • Both abnormalities contribute to failure to close
    o Hypoplastic muscle: ↓ strength to close against systemic BP
    o Elastic segment prevents sphincteric action
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8
Q

Histo lesions grades

A
  • 6 grades based on presence/extent of elastic tissue
  • Grade abnormality inversely related to ductus length
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9
Q

Breed predispositions and epidemio

A

Toy, miniature Poodles, Collies, Pomeranians, Shetland Sheep dogs, Maltese, English Springer Spaniel, Keeshond, Yorshire Terrier

o Females > males

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10
Q

PE and clinical evaluation: type 1

A

small PDA
 Asymptomatic L to R shunt
 High frequency continuous murmur only at L base, faint/no thrill
 Normal HR, pulse, CTX, ECG
 Sx not urgent but recommended for normal life span

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11
Q

PE and clinical evaluation: type 2

A

medium PDA
 Asymptomatic L to R shunt
 Coarse continuous murmur at L base + thrill
 Pulse normal to slight bounding
 Echo: Mild to moderate L heart enlargement before 1y
 CTX: Borderline ↑ pulmonary vascular marks
 ECG: R wave >3mV
 Sx recommended but can wait couple weeks

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12
Q

PE and clinical evaluation: type 3a

A

large PDA before CHF
 ↓ exercise capacity
 Coarse continuous murmur and thrill + systolic murmur at L apex from MR
 Bounding pulses
 CTX: medium to large ductal aneurysm, left enlargement, significant ↑ pulmonary vascular marks
 Echo: marked L enlargement before 6mo
 ECG: Sx recommended w/o delay

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13
Q

PE and clinical evaluation: type 3b

A

large PDA +CHF
 Same as 3a + dyspnea from pulmonary edema
 ECG: Afib ca be present
 Sx: clear CHF prior

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14
Q

PE and clinical evaluation: type 4

A

large PDA + PH → R to L shunting
 Hind leg weakness, collapse with exercise
 Differential cyanosis: limited to caudal body
 Pulses normal to weak
 Polycythemia
 Usually no murmur
* Split, prominent S2 can be present
 ECG: R axis deviation from RVH

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15
Q

Angio classification: Type I

A

o Gradually tapered from Ao → point of insertion on PA
o No abrupt change in diameter
o Angle typically <15

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16
Q

Angio classification: Type II

A

o Abrupt/marked distal narrowing of >50% ductal diameter
o Type IIA: constant dimension of proximal portion
 Most common
o Type IIB: conical chape, angle from 30-60 degrees

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17
Q

Angio classification: Type III

A

o Tubular appearance w/o attenuation of ductal diameter (<20%)
o Common in German Shepherd
o Difficult for KT occlusion

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18
Q

Embryology/birth

A
  • DA: muscular blood vessel btw Ao and PA
    o Fetal patency maintained by ↓partial O2 pressure + PGE2/PGI2 → SM relaxation
  • Birth:
    o ↓PGE2 production + ↑ metabolism by lungs
    o Aeration of lungs → ↓ PVR → reversal of DA flow
     Ao blood → ↑pO2 in DA
    o Functional closure: DA SM vasoconstriction
    o Anatomical closure: fibrosis of SM cell 2nd to hypoxia
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19
Q

Histology and lesions grades

A
  • Primary abnormality: hypoplastic ductal mass
  • Secondary abnormality: ↑ elastic fibers
  • 6 grades of lesions
    o 1&2: enough muscle to close PA end, lack at Ao end
     Ductal aneurysm
     Ductus diverticulum: outpouching of ventral aspect of Ao
  • Form frustra of PDA, possess genes for defect
    o 3, 4, 5: partial closure at PA end
     Small, medium, large PDA size
    o 6: no ductal constriction
     Large L → R shunt
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20
Q

Pathophys L to R PDA

A
  • Flow across PDA depend on
    o Size of smallest PDA orifice → restrictive PDA
    o Relative PVR and SVR: AoP > PA → L to R shunting
  • Continuous flow: systolic + diastolic PG btw Ao and PA
  • ↑ pulmonary blood flow
    o Pulmonary overcirculation
    o ↑ venous return to L heart → LV volume overload → 2nd LAE and LVEH
     Normal contractility (Frank Starling): ↑ SV
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21
Q

Genetics

A

hereditary, polygenic
o 2 dogs w/ PDA → 80% offspring affected
o 1 PDA w/ offspring → 70% offspring affected
o 1 PDA w/ normal → 20% offspring affected

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22
Q

Signalment

A

o Predisposed breeds include: chihuahua, poodles, collie, sheltie, maltese, pomeranian, Toy, Yorkie, English Springer Spaniels, Keeshond, Bichon, CKCS, Shetland Sheep dog
 Reported in some large breeds including German Shepherd, Newfoundland, Labs
o Females > males

23
Q

C/s L to R PDA

A

L-CHF

24
Q

PE L to R PDA

A

o Murmur
 Continuous cardiac murmur with thrill
* Diastolic component may be faint/absent if ↑ pulmonary pressures
* Peak intensity in systole
 +/- Systolic murmur at L apex (MR)
o Bounding pulses, hyperkinetic, water-hammer
 ↑ pulse pressure
 ↓ diastolic pressure from diastolic runoff
 ↑ systolic pressure from ↑ SV

25
Q

ECG

A
  • LAE: wide P waves
  • LVE: ↑ R wave amplitude
26
Q

CTX

A
  • LAE/LVE
  • Pulmonary overcirculation
  • 3 bulge: ductal aneurysm, Ao, MPA dilation
27
Q

2D echo L to R PDA

A

o LAE and LVE
o MPA dilation

28
Q

Doppler echo L to R PDA

A

o Continuous flow in PA region
o MR and PI from annular dilation
o ↑ Ao flow (from ↑SV)

29
Q

Cardiac KT angio L to R shunt

A

o Ductus diverticulum: blind, funnel shaped outpouching of ventral aspect of ascending Ao
 Fruste form of the defect
 Indicate genetic for PDA

30
Q

Cardiac KT pressure study L to R shunt

A

o ↑LV end diastolic pressure, PCWP, LAP
o Normal RVP

31
Q

Cardiac KT oximetry L to R shunt

A

O2 step up in PA >5% from RV

32
Q

DDX L to R shunt PDA

A

o AP window
o Anomalous systemic to pulmonary shunt

33
Q

PX L to R shunt PDA

A

closure recommended in all cases
o 64% would die w/I 1y w/o correction
o Excellent px after closure

34
Q

Complications L to R shunt PDA

A

 L CHF
 Afiib
 PH
 MR

35
Q

Branham reflex

A

↑ diastolic P
* ↓ pulse pressure
* Bradycardia

36
Q

Treatment L to R PDA

A

closure always recommended
o Surgical ligation: excellent px
 Complication 5-8%
 Residual flow 2-3%
o KT occlusion: ACDO

37
Q

PDA R to L shunt gross path

A
  • Usually grade 6 lesions: large, short, tubular PDAs
38
Q

R to L shunt PDA histo

A
  • Muscular and small pulmonary arteries changes
    o Intimal thickening
    o Medial hypertrophy
    o Plexiform lesions → irreversible
  • Narrowing of vessel lumen
39
Q

Pathophys R to L shunt PDA

A
  • Large PDA: no resistance to flow
    o ↑ pulmonary blood flow → ↑PAP → pulmonary vessel injury → ↑PVR
     Medial hypertrophy
     Intimal proliferation
    o OR persistence of fetal pulmonary circulation → ↑PAP → ↑PVR
    o ↑PVR leads to shunt reversal
  • Deoxygenated blood in systemic circulation
    o ↓O2 tension → ↑ EPO → polycythemia → ↑ blood viscosity → ↑ resistance to blood flow
    o ↓ blood flow and O2 delivery
40
Q

What happens w/ exercise if R to L shunt PDA

A

↓ SVR → exacerbate shunting

41
Q

C/s R to L shunt PDA

A

o Exercise intolerance/collapse: ↓ SVR with fixed ↑ PVR
o Pelvic limb weakness
o Seizure
o Differential cyanosis: hindlimbs
 Location of shunting in Ao is distal to cranial vessels

42
Q

Signalment R to L shunt PDA

A

usually young, before 6mo/o

43
Q

PE R to L PDA

A

o Usually no continuous murmur, but PH can cause
 Soft L basilar ejection murmur
 Split S2 (PH)
o Normal/weak pulses

44
Q

BW R to L PDA

A

polycythemia
o Perfusion of kidneys w hypoO2 blood → EPO production → polycythemia → hyperviscosisty if PCV >65%

45
Q

ECG R to L shunt PDA

A
  • R axis deviation from RVH
46
Q

CTX R to L PDA shunt

A
  • Usually no cardiomegaly, if so = R sided
  • Dilated MPA
  • Dilated PAs
  • Ductal aneurysm
47
Q

Echo R to L PDA shunt

A
  • Small LA/LV → ↓ pulmonary venous return
  • RVH + signs suggestive of PH
  • Flow in ductal region
48
Q

Contrast echo R to L PDA shunt

A

agitated saline injected into peripheral vein → opacify descending Ao but not LV
o Need to confirm absence of intracardiac shunting

49
Q

Cardiac KT R to L PDA pressure study

A

o ↑RV systolic pressure
o Equilibration of Ao and PA pressures

50
Q

Cardiac KT R to L PDA angio

A

o Aortic + LV selective angiogram: bidirectionnal shunting commonly observed
o Importance of R to L shunting is assessed by RVH and L heart size

51
Q

Cardiac KT R to L PDA oximetry

A

O2 step down in descending Ao vs ascending

52
Q

Eisenmenger physiology

A

reversal of L to R shunting 2nd to ↑ PVR
o ↑ flow rates and transmission of systemic pressures into pulmonary circulation
o Uncommon: 1-6%

53
Q

Treatment R to L PDA shunt

A

o Exercise limitation
o Avoid stress
o ↓ PCV <65%: phlebotomy or hydroxyurea
 Hydroxyurea is myelosuppressive agent
* Side effects: A-, V+, bone marrow hypoplasia, sloughing of nails
o Sildenafil

54
Q

Natural hx R to L PDA

A
  • Can live 2-5y if PCV well controlled and stress avoided
  • Shunt closure is contraindicated → would stop access of RV blood to systemic circulation
    o ↑ RV afterload
    o ↓ CO → shock → death

10. Congenital Heart dz (28 decks)

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