PDA Flashcards
Normal anatomy PDA
- Bifurcation of main PA → ventral aspect of descending Ao btw L subclavian and intercostal arteries
o Distinct muscular cylinder btw 2 elastic arteries
Function of DA during fetal life
o Allow blood flow to bypass lungs during fetal life
Histo DA
- 98% smooth muscle + subadventitial elastic fibers +adventitial loose collagen
o Circumferential distribution of muscle mass
What happens after birth
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
Difference in Hu DA
intimal cushions of fetal DA contribute to closure = not in dogs
Gross pathology
- 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
Histopathology changes
- 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
Histo lesions grades
- 6 grades based on presence/extent of elastic tissue
- Grade abnormality inversely related to ductus length
Breed predispositions and epidemio
Toy, miniature Poodles, Collies, Pomeranians, Shetland Sheep dogs, Maltese, English Springer Spaniel, Keeshond, Yorshire Terrier
o Females > males
PE and clinical evaluation: type 1
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
PE and clinical evaluation: type 2
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
PE and clinical evaluation: type 3a
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
PE and clinical evaluation: type 3b
large PDA +CHF
Same as 3a + dyspnea from pulmonary edema
ECG: Afib ca be present
Sx: clear CHF prior
PE and clinical evaluation: type 4
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
Angio classification: Type I
o Gradually tapered from Ao → point of insertion on PA
o No abrupt change in diameter
o Angle typically <15
Angio classification: Type II
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
Angio classification: Type III
o Tubular appearance w/o attenuation of ductal diameter (<20%)
o Common in German Shepherd
o Difficult for KT occlusion
Embryology/birth
- 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
Histology and lesions grades
- 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
Pathophys L to R PDA
- 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
Genetics
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
Signalment
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
C/s L to R PDA
L-CHF
PE L to R PDA
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
ECG
- LAE: wide P waves
- LVE: ↑ R wave amplitude
CTX
- LAE/LVE
- Pulmonary overcirculation
- 3 bulge: ductal aneurysm, Ao, MPA dilation
2D echo L to R PDA
o LAE and LVE
o MPA dilation
Doppler echo L to R PDA
o Continuous flow in PA region
o MR and PI from annular dilation
o ↑ Ao flow (from ↑SV)
Cardiac KT angio L to R shunt
o Ductus diverticulum: blind, funnel shaped outpouching of ventral aspect of ascending Ao
Fruste form of the defect
Indicate genetic for PDA
Cardiac KT pressure study L to R shunt
o ↑LV end diastolic pressure, PCWP, LAP
o Normal RVP
Cardiac KT oximetry L to R shunt
O2 step up in PA >5% from RV
DDX L to R shunt PDA
o AP window
o Anomalous systemic to pulmonary shunt
PX L to R shunt PDA
closure recommended in all cases
o 64% would die w/I 1y w/o correction
o Excellent px after closure
Complications L to R shunt PDA
L CHF
Afiib
PH
MR
Branham reflex
↑ diastolic P
* ↓ pulse pressure
* Bradycardia
Treatment L to R PDA
closure always recommended
o Surgical ligation: excellent px
Complication 5-8%
Residual flow 2-3%
o KT occlusion: ACDO
PDA R to L shunt gross path
- Usually grade 6 lesions: large, short, tubular PDAs
R to L shunt PDA histo
- Muscular and small pulmonary arteries changes
o Intimal thickening
o Medial hypertrophy
o Plexiform lesions → irreversible - Narrowing of vessel lumen
Pathophys R to L shunt PDA
- 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
What happens w/ exercise if R to L shunt PDA
↓ SVR → exacerbate shunting
C/s R to L shunt PDA
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
Signalment R to L shunt PDA
usually young, before 6mo/o
PE R to L PDA
o Usually no continuous murmur, but PH can cause
Soft L basilar ejection murmur
Split S2 (PH)
o Normal/weak pulses
BW R to L PDA
polycythemia
o Perfusion of kidneys w hypoO2 blood → EPO production → polycythemia → hyperviscosisty if PCV >65%
ECG R to L shunt PDA
- R axis deviation from RVH
CTX R to L PDA shunt
- Usually no cardiomegaly, if so = R sided
- Dilated MPA
- Dilated PAs
- Ductal aneurysm
Echo R to L PDA shunt
- Small LA/LV → ↓ pulmonary venous return
- RVH + signs suggestive of PH
- Flow in ductal region
Contrast echo R to L PDA shunt
agitated saline injected into peripheral vein → opacify descending Ao but not LV
o Need to confirm absence of intracardiac shunting
Cardiac KT R to L PDA pressure study
o ↑RV systolic pressure
o Equilibration of Ao and PA pressures
Cardiac KT R to L PDA angio
o Aortic + LV selective angiogram: bidirectionnal shunting commonly observed
o Importance of R to L shunting is assessed by RVH and L heart size
Cardiac KT R to L PDA oximetry
O2 step down in descending Ao vs ascending
Eisenmenger physiology
reversal of L to R shunting 2nd to ↑ PVR
o ↑ flow rates and transmission of systemic pressures into pulmonary circulation
o Uncommon: 1-6%
Treatment R to L PDA shunt
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
Natural hx R to L PDA
- 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
