Congenital Heart diseases Flashcards
What are some of the most common congenital heart dz in dogs
PDA (patent ductus arteriosus)
Stenoses (aortic/pulmonic)
ASD (atrail septal defect)
mitral dysplasia
What are some of the most common congenital heart dz seen in cats
AV dysplasia
VSD (ventral septal defect)
End fibroelast
PDA
Aortic stenosis
Tetralogy of Fallot
What causes a PDA congenitally in dogs?
lack of smooth muscle in ductus arteriosus to close ductus after birth
(so, normally the ligamentum arteriosus forms)
can vary in size with amt of sm. musc. there
more common to have small patency than larger
What happens in a dog with a PDA?
due to higher BP in aorta, blood from aorta will flow into PA through the lungs and back into LA.
This will create a volume overload in L heart⇒ eccentric hypertrophy! → LHF
This is a L-R shunting PDA (≈ 90% of all PDAs)
Where is a PDA murmur heard loudest?
Very load murmur!
Above the base of the heart
So much turbulence created should be able to feel palpable thrill! (Grade 6/6)
Machinery murmur (in both systole & diastolye)
Radiographic changes seen with L-R PDA?
Enlarged pulmonary vessels due to extra blood from aorta!
LV enlargement may be seen also.
If there is a lg PDA what happens? (absolutely no sm musc)
so much blood flow through to lung vasculature that trophic factors are released as the lung capillaries try to resist extra fluid that they become thickened (hypertrophy) and the pressure backs up in the PA so that the direction of the flow in PDA becomes a R-L shunting!
All PDAs are “born” L-R but after 6-8 weeks can become R-L due to above factors
what are some changes seen after PDA switches to R-L shunting
“differential cyanosis”
Since PDA is distal to brachicephalic trunk (after) the deoxygenated blood then flows into aorta to rest of body.
The mm in the front of dog will be pink (blood from LV flows into brachicephalic trunk as normal) and the back 1/2 cyanotic
erythrocytosis
due to deoxygentated blood flow to kidneys (thier response is incr EPO)
RHF
due to volume overload as in L-R PDA
due to erythrocytosis differential cytosis may be very apparent from front to back (not only pink in front but bright red!!)
in a 6-8 week old dog with a PDA what do you have to realize about murmur
“silent at 6-8 weeks”
that this is switchover time and the machinery murmur you might have heard at 2-4 weeks may not be there any more because pressure have sort of equalized at the moment
”>8 weeks murmur”
So make sure listen at later age also!
“listen carefully above base of heart for murmur”
since it typically won’t be as pronounced
what are pulses going to be like in L-R PDA
R-L PDA
Bounding
Can be normal
what is signalment for PDA
min/toy poodle - polygenetic trait (F3:M1)
GSD
Collies
CS of PDA
incidental finding at first vx
CHF <16mos age
Cats < few weeks
L-R machinery murmur w/ palpable thrill, water hammer pulses
R-L maybe murmur, differential cyanosis, split S2
How Dx PDA
Radiography: L or R enlarge (< 2.5-3 rib spaces; dorsally displaced trachea, L Atrial lump), lung vessels (ck cranial lobe ABV pattern; V will be wider than A due to back daming of blood from L heart), pulmonary edema in perihilar area (cotton wool appearence)
U/S: definitive dx can see PDA & flow
Angiography: can see PDA w/ contrast medium
EKG: not much, maybe L/R atrial/ventricular enlarge
Tx for L-R PDA
Sx Plan A: tie close
Branham sign: reflex bradycardia due to incr pressure post repair, have atropine on board
PU/PD common post sx while body readjusts to decr volume blood needed (RAAS system was activated to compensate for PDA)
Sx Plan B:
embolization coils & Amplatz occluders
Tx for R-L PDA
Sx: NONE due to incr. resistance in pulm. vasculature developed as compensation when L-R PDA (what created R-L PDA in first place)
Medical: diuretics & ACE inhibitors to slow down CHF.
Px for L-R PDA
R-L PDA
Prevention
excellent
poor: manange erythrocytosis w/ blood removal, hydroxurea (chemotherapeutic) or sildenafil (pulm arteriodilator)
Dont breed!
Aortic stenosis
fibrocartilage in the aortas outflow tract, mostly occurs below the valves but can occur at or above them!
SAS (subaortic stenosis) most common
born normal but by 3-8 wks fibrocart begins to appear
Seen in Newfies (found a gene!), Boxers, Retrievers, Rotties
Greatest risk of death by ? with SAS?
arrhythmias (VPDs, Vtach, Vfib), sudden death
rarely die from CHF!
What can be giveaway that it is SAS on auscultation, pulses, palpation
Since SAS causes pressure overload, weak pulses felt but, can auscultate murmur over heart base loudest, palpate ventricular “heave” against chest wall & radiating murmur to carotids & R hemithorax & femoral arteries
It’s not a problem of heart failure its heart overworking!
The two big Ddx for a continuous or machinery murmur?
#1 PDA
#2 SAS
How to Dx SAS?
Radiographs: concentric hypertrophy so enlargement seen? NOT generally! But may be able to see post stenotic dilation
U/S: best modality to see in!
Tx for SAS
empirical/pallitive
if dog has CS, arrhythmias, S-T depression, flow >4m/s (65mm Hg), trying to prevent progression/death
Tx with ß-blockers to improve diastolic function, lidocaine/mexiletine, sotalol for arrhythmias
If CHF present: standard tx: Furosemide & ACE inhibitors
BEWARE HYPOTENSION
Px of SAS
Progressive, if Boxer or Neufie doesn’t have murmur by 4mos then 88% chance will be ok when he gets to 1 yr.
All SAS 20% mort <3yrs
Severe SAS 70% mort <3yrs
predisposed to bacterial endocarditis⇒CHF
Whats up with Pulmonic stenosis?
less common than SAS!
can be valvular, subvalvular or supravalbular but…
Pulmonary valvular dysplasia most common
can be compounded by a thickened, hypoplastic annulus also!
AND!: Dynamic outflow obstruction!!
What things go wrong with PAS just like SAS?
Signalment for PAS?
CS?
Bulldog, beagles, Chi, Spaniel etc., often normal for long periods
Incidental mumur at 1st vx→ CS occur after (3-5) years, exercise intol, weaknes, syncope, sudden death (arrhythmias), RCHF if tricuspid dysplasia
Does NOT progress as in SAS!
PE: systolic murmur @ heart base
Radiographic signs of PAS
R enlargement (incr sternal contact)
pulmonary trunk dilation :lateral= bump at 10:30, vd bump at 2
decr visualization of pulmonary vessels!
infundibular hypertrophy & dynamic outflow obstruction w/ angiography
Tx for PAS
Px for PAS
Balloon valvuloplasty wipes out valves & widens stenotic area if no hyperplastic annulus,
* Will only work to wipe out valves if hyperplastic annulus present due to strength of connective tissue in it!
Px w/o hyperplastic annulus 90% live for 6 mos-1 year & w/ = 60% improve & 50% live 6 mos
Patchgraft vavuloplasty: if hyperplastic annulus is present!
If a Single R coronary artery type R2A is present then Right ventricle to pulmonary trunk conduit is placed.
Px for PAS
mild = normal lives
mod/severe = 35% show severe signs→3 yrs⇒ arrythmias/CHF
Sx: good to excellent
Ventral Septal Defect
failure of septal development “hole in heart”
signalment of VSD
Cats
Bulldogs
Keeshonds
What type of flow does VSD have and what problem does it cause
Blood flows from L - R and into PA which travels back into L heart causing volume overload (eccentric hypertrophy)
Larger defect ⇒ less murmur
Smaller defect ⇒ greater murmur!
Right side murmur!!
What is seen on xrays with VSD
Since blood is shunting L-R & volume overload there will be incr. pulmonary vessels due to backup of flow into L side, enlarged L atrium
Definite Dx = U/s
Tx of VSD
Px?
Sx:
Small → none may close on own
Lg → close defect
Med:
vasodilators (hydralazine)
Px: mild-mod = good
R-L shunting = POOR
Tetralogy of Fallot
Overriding Aorta
Pulmonic Stenosis
Ventricular Septal Defect
Enlarged R Ventrical
“Blue babies”
CS of ToF
whole body cyanosis
depends on severity of Pulm stenosis & VSD
syncope/exer. intolerance
incr. PCV. erythrocytosis/hyperviscosity (remember decr. murmur!) due to decr. oxygenated blood to kidneys
Radiographs: R-L enlarged RH, decr pulmonary vessels
Tx for ToF
Sx: subclavian to pulm. artery, anastamosis of PA to Aorta
Med: ß-blockers for RH stiffness, decr. blood viscosity
Vasodilators Contraindicated in R-L shunting!!!!!
Atrial Septal Defect
Defect between L & R atria
causes volume overload & L-R shunt
relative pulmonic stenosis due to extra volume reaching RV. Causes murmur
_Ddx: aortic or pulmonic stenosis! Watch with Boxers (_since Aortic stenosis is common & poor px vx ASD with better px.)
AV valve insufficiency
valve or muscle dysplasia
common in cats! & lg breed dogs (labs)
causes regurgitation & volume overload
common in young (vs. endocardiosis in old)
Tx: ?
Inherited Ventricular Arrhythmias in Young GSDs
@ 3mos start having VPDs, VT, sudden death
can worsen until 9mos, ⇒ after 18 mos ok
Tx: Sotalol + mexilitine until 18 mos
Sotalol alone makes worse, mexilitine alone no effect
