Congenital heart disease Flashcards
Congenital heart disease is.. (5)
present at birth.
Malformation of one or more areas of the heart or great vessels.
Or Persistence of normal fetal structure following birth.
Or Valvular abnormalities.
Prevalence 0.46- 0.85%
PDA
persistent ductus arteriosus
Has a very distinct, continuous murmur loudest at the heart base so auscultate! is practically pathognomonic.
Females > males 3:1
Autosomal dominant inheritance (enough for single copy of gene from 1 parent passes it on)
Seen in: maltese, pomeranian, sheltie, english spaniel, corgi, bichon, poodle, yorkie, collie GSD
PDA pathophysiology
– Failure of ductal closure
– Shunting from aorta to pulmonary artery (Left-to-Right).
– Over-circulation of the LA, LV, pulmonary vessels meaning excessive blood volume is being sent through these structures due to the abnormal connection between the aorta and pulmonary artery.
– Long-standing: myocardial failure from volume
overload.
Right-to-left shunting (reversed) PDA: increased
pulmonary vascular resistance -> increased RV
pressure
■ Differential cyanosis
■ UNCOMMON!
Differential cyanosis means the front end is pink, the back end is blue. May present as weak backend.
Right to left shunting is more rare and may not have a murmur at all, it’ll present differently to the usual left to right.
Right-to-left (reversed) PDA occurs when
pulmonary hypertension causes blood to shunt from the pulmonary artery to the aorta, leading to hypoxemia, differential cyanosis (hindlimb cyanosis), and secondary polycythemia.
PDA + R to L PDA
History:
Physical exam:
Diagnosis:
■ History: murmur@vaccination; some with CHF already; precordial thrill.
– R-to-L: stunted growth, pelvic limb weakness.
■ PE: continuous loud murmur, PMI high left heart base.
– R-to-L: differential cyanosis, pelvic limb weakness
■ Diagnosis: continuous murmur nearly pathognomic.
– DDX: aorticopulmonary windows, aberrant bronchoesophageal arteries.
– Echocardiography
PDA management
Management: uncorrected you have a 1 year survival rate of 50%. Corrected, your prognosis is excellent.
When presenting with CHF, prognosis is guarded.
Right to left shunting cannot generally be closed so prognosis is poor.
Tx: surgical correction, catheter intervention
prostaglandin inhibitor that may be given to kids too
NSAIDs
(S)AS
(Sub) aortic stenosis, a congenital heart defect where a fibrous or fibromuscular ridge develops below the aortic valve (subaortic), partially obstructing blood flow from the left ventricle (LV) to the aorta. (Elevated flow velocity, post-stenotic dilation)
Predisposed breeds: Boxer, Gld Retriever, GSD, Newfies: autosomal dominant.
■ Variable severity: asymptomatic with small
murmur, to severely debilitating.
SAS types: (3)
Describe the anatomy-kinetics.
■ Valvular, subvalvular, supravalvular – SubAorticStenosis is the most common.
■ Fibrous band in left ventricular outflow tract.
■ Elevated flow velocity, post-stenotic dilation.
■ LV hypertrophy due to having to work harder to get the blood out.
■ Aortic insufficiency in some.
Diagnosis of SAS.
Physical exam: murmur @vaccination; systolic, PMI left base, cranial thoracic inlet.
*Diastolic component (to-and-fro) if aortic
insufficiency.
DDX: innocent flow murmurs
*Femoral pulses: pulsus tardus et parvus
Echocardiography: morphology of the lesions, severity
“Pulsus tardus et parvus” is a slow-rising (tardus) and weak (parvus) arterial pulse commonly associated with severe aortic stenosis (AS).
SAS severity scaling:
Severity scale:
* Mild <50mmHg
* Moderate 50-80 mmHg
* Severe >80 mmHg
The pressure being measured in the subaortic stenosis (SAS) severity scale is the left ventricular outflow tract (LVOT) pressure gradient, which represents the pressure difference between the left ventricle (LV) and the aorta during systole.
SAS management:
Mild – normal life, but don’t use for breeding
Moderate-severe
*Balloon dilation?
*Beta-blockers
*Risk of bacterial endocarditis
PS heart condition
Pulmonic stenosis
Can be valvular, subvalvular, supravalvular.
Outflow obstruction
RV pressure overload leads to hypertrophy and right-sided heart failure eventually.
High flow velocity resulting in post-stenotic dilation.
PS
Hx:
PE:
Diagnostics:
Hx: murmur @vaccination, some with syncope or
r-CHF.
PE: systolic left base murmur, normal femoral
pulses, jugular distensions, positive hepatojugular reflux.
Diagnostics:
– Radiographs: RV enlargement, post-stenotic dilation
– ECG: right axis deviation
– Echo: RV hypertrophy, valvular lesions, annular hypoplasia, poststenotic dilation.
– Doppler: high velocity across pulmonic valve.
A positive hepatojugular reflux (HJR) occurs when jugular venous distension (JVD) increases persistently during firm pressure on the liver (right upper quadrant) for 10–30 seconds. This indicates right heart dysfunction or volume overload.
What is positive hepatojugular reflux?
A positive hepatojugular reflux (HJR) occurs when jugular venous distension (JVD) increases persistently during firm pressure on the liver (right upper quadrant) for 10–30 seconds. This indicates right heart dysfunction or volume overload.
PS management:
– Balloon valuloplasty (BVP):
Succesful BVP: reduction in class, or reduction 50%.
– Most effective in commissural fusion.
– Severity as with aortic stenosis:
<50, 50-80, >80
– If rCHF, prognosis guarded.
– BVP contraindicated if R2A.
R refers to the right ventricle or right ventricular outflow tract (RVOT).
2A suggests a more severe or challenging form of stenosis where balloon valvuloplasty is contraindicated because the stenosis is often too severe or the anatomy is inappropriate for safe intervention.
This could be due to factors like severe hypertrophy, valve malformation, or vascular anomalies that make balloon dilation ineffective or risky.
VSD
ventricular septal defect: membranous type, defect of septation & muscular type.
■ Left-to-right shunting: volume overload of LA, LV, RV, pulmonary vasculature.
■ Small defects = resistive VSD: louder murmur
■ Large shunting: LV failure from volume overload.
■ Aortic insufficiency: aortic leaflet flails into defect.
■ Eisenmenger’s physiology: R-to-L shunting
Most common congenital heart dz in cats.
Eisenmenger’s physiology occurs as a result of a long-standing left-to-right shunt (due to a congenital heart defect such as (PDA), (ASD), or (VSD)) that eventually causes pulmonary hypertension. Over time, the increased pressure in the lungs (pulmonary artery) causes the shunt to reverse from left-to-right to right-to-left.
VSD
Hx:
PE:
Dx:
History: murmur@vaccination
PE: murmur on right hemithorax
* Can be heard on left base (radiation or
relative PS)
Diagnosis:
* Radiography: chamber dilation, pulmonary
overcirculation
* ECG: may be normal, wide or tall p-waves
* Echo: defect, chamber dilation, hyperkinetic
LV
* Doppler: flow across the septum
VSD management: (5)
– Some close spontaneously.
– Restrictive may not require any treatment.
– Device closure maybe.
– Management of CHF.
– R-to-L shunting: polycytemia needs phlebotomy.
Eisenmenger’s physiology refers to
Eisenmenger’s physiology occurs as a result of a long-standing left-to-right shunt (due to a congenital heart defect such as (PDA), (ASD), or (VSD)) that eventually causes pulmonary hypertension.
Over time, the increased pressure in the lungs (pulmonary artery) causes the shunt to reverse from left-to-right to right-to-left.
ASD
MD
TD
ToF
ASD = atrial septal defect (relatively uncommon in both cats and dogs)
MD = mitral dysplasia
TD = tricuspid dysplasia
ToF = tetralogy of fallot
MD
Hx
PE
Dx
Tx
■ Mitral dysplasia most seen in Bull terriers.
■ Pathophysiology: mitral regurgitation -> volume overloading of LA, LV -> left heart failure.
Hx: systolic murmur (diastolic if stenotic) PMI left apex.
PE: murmur, arrhythmias (Atrial fib., supravent. premat.contraction)
■ Radiography: Left atrial enlargement, Left vent. enlargement, CHF
■ ECG: wide P-waves
■ Echo: LAE, LVE, dysplastic MV
Tx: CHF management
■ Balloon catheterisation?
■ Open-heart surgery?
TD
Tricuspid dysplasia
■ Labrador, Weimaraner, other large breeds. Genetic basis in Labradors.
■ Tricuspid regurgitation, right-sided failure
ToF
Tetralogy of Fallot
■ Uncommon
■ Most common cyanotic heart disease in small animals.
Tetralogy involving: Pulmonic Stenosis, Ventricular Septal Defect, aortic dextroposition, RV hypertrophy due to increased effort to pump blood through the narrowed pulmonary valve.
■ Mosly seen in Gld Retriever, Labrador, Huskies, Toy Poodle.
X-ray: RV Enlargement, hypovascular lungs
Echo: RVH, PS, VSD, Aortic malpositioning
Aortic Dextroposition: The aorta is positioned over the VSD, rather than arising from the left ventricle. This causes the oxygen-poor blood from the right ventricle to be pumped into the aorta.
The majority of congenital heart disease all have…
murmurs so auscultate!
Puppies can have benign murmurs too. Why?
Innocent (physiologic) murmurs are soft, transient, non-pathologic heart murmurs commonly heard in young puppies. They occur due to blood flow turbulence, physiological puppy anemia and typically resolve by 4-6 months of age.
Puppies have physiological anemia.
Some young animals with congenital heart disease can even present in/with… (3)
congestive heart failure
or
syncope
or
more vague, non-cardiac signs such as regurgitation and stunted growth (PRAA).
What to do if you hear a murmur in a young animal?
could be a benign puppy murmur, or not.
options are to do full work-up (echo) or just chest xrays to begin with.
Diagnostic investigations in case of murmur in juvenile animal. (6)
Re-auscultate in 1 month.
Blood biomarkers in puppies not too reliable but exception right to left shunting doesn’t show up in bloods.
Baseline ECG always worth establishing in case arrhythmia or murmur.
X-rays: you may see cardiomegaly, vascular anomalies, megaesophagus. Even if you find nothing at least you’ll have a baseline image ready in case signs progress.
Echocardiography would be ideal to perform.
Advanced imaging next in case surgery planning would be coming.
Are cardiac findings in a juvenile animal a death sentence? (3)
depends on the severity of the defects
depends on if there’s CHF already (mostly left-sided, sometimes right)
some defects can be corrected, some cannot be helped.
Infective endocarditis is
■ Invasion of valvular endothelium by microbes.
■ Mitral and aortic more commonly affected.
– Aortic stenosis predisposes.
– MMVD is not predisposing.
■ Dogs»_space; cats; males > females.
Caused by/predisposed to by: Transient or persistent bacteremia due to
* UTI, prostatitis, discospondylitis, pyoderma, IV catheters, (peridontal Dz).
Usually, Staph.spp., streptococcus spp, e.coli,
Pseudomonas, Enterobacter, Pasteurella, Proteus etc.
60-70% are culture negative - often have received AB already
MSCRAMM =
microbial surface components recognizing adhesive matrix molecules are a group of surface proteins found on various bacteria, particularly pathogens.
These proteins play a crucial role in the ability of bacteria to adhere to host tissues by recognizing and binding to components of the extracellular matrix (ECM), such as collagen, fibronectin, and laminin.
This adhesion is a critical step in the establishment of infections, allowing bacteria to persist and colonize the host such as in endocarditis.
These are crucial to the pathophysiology of endocarditis and other such disease processes.
Pathophysiology of infective endocarditis. (5)
– Non-bacterial thrombotic endocarditis: endothelial damage.
– Colonization of the valve: fibrinogen, fibrin, platelets.
– Valve tissue destruction.
– Embolization – septic or aseptic emboli.
– Hemodynamic. heart failure
Clinical signs of infective endocarditis. (3)
Physical exam findings? (3+)
– Congestive heart failure
– Lameness, lethargy, anorexia, respiratory abnormalities, collapse, neuro signs, hematuria.
– Thromboembolic disease
PE: murmur 90-95%, arrhythmias 40-70%, fever 70%,
joint effusions, lameness, respiratory signs.
Diagnostic approach for infective endocarditis (5)
■ Echocardiography – vegetative lesions on valves
■ Radiography – rule out of concurrent Dz, assessment of heart size, presence of CHF.
■ Blood test – leucocytosis, mature neutrophilia, mild anaemia, azotemia, hypoalbuminemia, elevated liver enzymes.
■ Urinalysis and culture: Urinary exams because if you find cystitis then thats the most likely culprit for the endocarditis.
■ Blood culture – contact the lab, avoid contamination, 3-4 samples, 30-60 minutes apart from different sites, aerobic and anaerobic culture.
Suggested criteria for diagnosis of infective endocarditis in dogs.
Major criteria
Minor criteria
Diagnosis
Infective endocarditis
Ddx:
Ddx:
– MMVD, mitral dysplasia
– Aortic insufficiency – degeneration, stenosis
– Lameness: immune mediated polyarthritis (IMPA); septic or degenerative arthritis
– Fever: many causes
Infective endocarditis
Tx:
Tx:
– Start IV AB Based on culture, or broad spectrum.
– Tx for CHF
– Euthanasia also reasonable.
No to thrombolytics, but maybe could use antithrombotics in some cases but not really cause the thrombi are due to bacterial adhesion not platelet activation or something like that.
Prognosis: depends on agent, severity, affected valve (AoV 3 days, MV 476 days)
