Congenital Heart diseases Flashcards
(41 cards)
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!!
