Congenital Heart Disease Flashcards
define congenital heart disease
defect in cardiac structure that is present at birth
-may be inherited
-may develop spontaneously due to genetic mutation, toxic, infectious, environmental, drug-related, or nutritional factors
describe the prevalence of congenital heart disease
most common cause of heart disease in young patients!!
<10% of all diagnosed heart disease in dos and cats though
slightly more common in large animals but still pretty rare
when should you expect congenital heart disease?
- breed/family history
- history/clinical signs:
-failure to thrive
-poor exercise tolerance, syncope
-difficulty breathing
-abdominal distension
-sudden death - suggestive PE findings:
-heart murmur!!!
-arrhythmia
-cyanotic MM
-abnormal jugular venous or peripheral arterial pulses
describe innocent/physiologic murmurs in young animals (5)
- sensitive: softer or absent at rest but increases with excitement/exercise
- soft: grade 1-2 /6
- single: no other associated abnormal heart sounds or physical exam abnormalities
- systolic: limited to mid systole
-NEVER CONTINUOUS, DIASTOLIC, or TO and FRO - short-lasting: goes away by 6 months
describe pathologic murmurs in young animals (5)
- can be heard at all times
- loud: grade 3/6 or louder
- associated clinical signs or PE findings:
-cyanosis
-jugular venous distension/pulsation
-exercise intolerance
-difficult breathing
-ascites - can be systolic, diastolic, or continuous
- persists beyond 4-6 months of age
describe normal fetal circulation
- ductus venosus: connects umbilical vein (from mom) to caudal vena cava
- foramen ovale: small opening in septum between RA and LA
- ductus arteriosus: connects pulmonary artery to descending aorta
- respiratory gas exchange: job of maternal lungs
- fetus lungs are collapsed/not fully inflated, so resistance in fetal pulmonary vasculature is HIGH
-resistance in fetal systemic vasculature is LOW
-opposite of post-partum - oxygen RICH blood from placenta enters caudal vena cava via ductus arteriosus
-most is directed across foramen ovale into left atrium
-upper extremities/coronary arteries preferentially receive well oxygenated blood - oxygen-POOR blood enters right atrium via cranial vena cava
-most moves across TV, into RV, and through pulmonary artery
-the majority (80%) then crosses the ductus arteriosus to the descending aorta so that:
–blood is hunted past the non-functional fetal lungs
–poorly oxygenated blood is preferentially delivered back to the placenta to receive more O2
describe normal post-natal cardiovascular changes
- resistance in the pulmonary circulation DECREASES as lungs inflate
- resistance in systemic circulation INCREASES due to loss of placental circulation
- the 3 normal shunts close:
-ductus venosus sphincter constricts
-foramen ovale closes: a passive process where increase in LA pressure shifts the flap, stopping flow
-ductus arteriosus closes: smooth muscle of DA contracts in response to increased O2 tension, loss of placental prostaglandins = constriction
describe normal post-natal cardiovascular pressures
pulmonary artery:
25 syst, 15 diast
aorta:
120 syst
80 diast
RA: 0-5
RV: 25/0
LA: 0-8
LV: 120/0
classify congenital heart lesions by acyanotic vs cyanotic
acyanotic:
-left to right shunts
-obstruction to ventricular flow
-regurgitant valve lesions
cyanotic:
-right to left shunts
describe the most common defects in dogs, cats, horses, calves, and others
dogs: frenchies are the worst
-pulmonary valve stenosis
-PDA
-subaortic stenosis
cats:
-ventricular septal defect
-AV valve dysplasia
foals:
-ventricular septal defect
calves:
-ventricular septal defect
-atrial septal defect
in everyone except dogs: ventricular septal defect most common (ON EXAM!!!)
describe the pathophysiology of left to right shunts
- communication between pulmonary veins, left heart or systemic arterial circulation (LEFT) and systemic venous circulation, right heart, or pulmonary arteries (RIGHT)
- oxygen-rich blood re-circulates repeatedly, leading to volume overload and eccentric hypertrophy (ON EXAM) of structures along affected circuit
- most common L-R shunts: PDA, ventricular and atrial septal defects
describe PDAs
- failure of ductus arteriosus to close normally after birth
- normal closure of DA:
-functional closure in minutes to hours (dogs/cats), 3-4d in horses
-anatomic closure within 1 month
-result: elastic ligamentum arteriosum - uncomplicated PDA: blood shunts left to right
-descending aorta to pulmonary artery during BOTH systole and diastole (continuous)
-shunting leads to volume overload of pulmonary vasculature (arteries and veins) and left heart chambers (result = eccentric hypertrophy)
-if untreated: left sided CHF and pulmonary edema occurs in almost all cases
- uncommonly, blood may shunt right to left (reversed PDA)
-during pulmonary hypertension
describe classic exam findings of PDA (ON EXAM)
- wind blowing through a tunnel/machinery murmur
- grade/intensity: 4-6/6, palpable thrill is common
- location: left heart base
- timing: continuous
-never hear a pause! blood is continuously shunting - hyper kinetic/bounding femoral arterial pulses
-cause: widened pulse pressure due to run off of blood from arterial tree during diastole
describe prognosis and recommendations for PDA
- if untreated, 65% die of heart failure before 1 year of age (dogs)
- prompt surgical closure/occlusion is curative and almost always indicated if defect if left to right shunting
-prognosis is excellent following closure! - additional recommendations:
-screen relatives of affected animals
-do not breed affected animals
-if you hear a continuous heart murmur, do not monitor, REFER!! no exceptions!!
describe ventricular septal defect location
- defect in interventricular septum (IVS) that allows direct communication of the ventricles
-most common congenital heart defect in large animals and cats!! (ON EXAM) - majority located in basilar (upper) portion of IVS (perimembranous)
describe ventricular septal defect pathophysiology
- uncomplicated cases:
-blood flows left to right
-shunting occurs primarily during SYSTOLE, but during diastole, pressures are the exact same
-consequence: pulmonary over-circulation, eccentric hypertrophy (dilation) of left-sided chambers due to volume overload
-if shunt is large, L CHF and pulmonary edema may develop
- volume shunted with each beat depends on:
-size of defect
-pressure difference between the ventricles in systole - rarely, blood shunts right to left
-increase in R sided pressures (pulmonary hypertension)
describe VSD PE findings (ON EXAM)
- grade/intensity: variable, smaller VSD = louder murmur
- location: right heart (apex or base, depending on location of VSD)
- timing: systolic
describe prognosis and recommendations for VSD
- clinical picture/prognosis depends on the size/volume of the shunt/hole
-fortunately, most are small and well-tolerated
-moderate/large shunts may required treatment for CHF - recommended management
-small defects: no intervention
-surgical closure of large defects or minimally invasive occlusion is possible in some cases, but not very widely available
describe lesions causing obstruction/stenosis of ventricular outflow
narrowing/stenosis of ventricular outflow tract increases resistance to blood flow
- proximally:
-ventricle must generate abnormally high pressure to force blood through narrowing
-ventricle responds with pressure-induced CONCENTRIC hypertrophy - distally:
-high velocity, turbulent flow (audible murmur)
-post-stenotic dilation
describe potential consequences of outflow tract stenosis
- congestive herat failure:
-more common with lesions affected RV than LV - sudden cardiac death:
-lethal ventricular arrhythmias due to fibrosis.ischemia - critical stenosis:
-inadequate flow to satisfy body’s demands
-syncope, weakness, lethargy
risk of complications increases with lesion severity!
<30mmHg: no stenosis, normal
30-50mmHg: mild; normal life expectancy
51-80mmHg: moderate, potential for complications if concurrent defects
>80mmHg: severe, greatest risk of symptoms/complications
what 2 lesions can cause obstruction/stenosis of ventricular outflow?
- right ventricular outflow stenosis
- left ventricular outflow stenosis
describe physical exam findings of ventricular outflow stenosis (ON EXAM)
- murmur:
-intensity/grade: variable with severity
-location: left heart base
-timing: systolic - femoral pulses usually normal for RV obstruction, can be reduced in LV obstruction
describe clinical features of stenosis of ventricular outflow
- most apparently asymptomatic for a prolonged period
- with severe stenosis, owner may report:
-exertional fatigue, syncope
-signs of R-sided (pulmonary valve stenosis) or left sided (subaortic stenosis) CHF
-sudden death with no other signsL common with severe subaortic stenosis
describe clinical management of stenosis of ventricular outflow
- B1 adrenergic blockers (atenolol) if moderate or severe
-reduce myocardial oxygen demand and force of contraction, antiarrhythmic - balloon valvuloplasty (catheter-based procedure):
-highly successful for pulmonic, but not subaortic - don’t breed affected dogs!
describe regurgitant valve lesions
- mitral valve dysplasia: left apical systolic murmur
-more common in kittens - tricuspid valve dysplasia: right apical systolic murmurs
-more common in foals and labradors
describe pathophysiology of right to left shunts
- communication between systemic venous circulation, right heart, or pulm arteries (RIGHT) and the pulmonary veins, left heart, or systemic arterial circualtion (LEFT)
- defect allows poorly oxygenated blood to bypass the lungs, desaturating systemic circulation
-visible cyanosis when PaO2 < 40 mmHg, deoxyHgb >5 g/dl
-patients often polycythemic (increase RBCs to compensate for lack of O2) - most common: tetralogy of fallot, eisenmenger’s syndrome (reversed PDA< reversed VSD)
describe Eisenmenger’s syndrome
- reversal of a normally left to right shunting lesion due to increased left sided pressures due to pulmonary hypertension
-when pulmonary vascular resistance > systemic vascular resistance, shunt reverses - may complicate large PDA, VSD, or ASD
- most common example is reversed PDA
describe tetralogy of fallot
- most commonly diagnosed cyanotic heart disease
- malformation of upper ventricular septum leads to 4 abnormalities:
-pulmonary stenosis: restricts normal blood flow from right ventricle to lungs
-right ventricular hypertrophy: purely secondary response
-large ventricular septal defect (VSD): high in the IVS, extends up to the aortic valve
-over-riding aorta (dextroposition): accepts blood from BOTH right and left ventricles
describe clinical features of tetralogy of fallot
- asymptomatic to signs of severe exercise intolerance, syncope, seizures
- PE:
-cyanosis present in 90% at rest, WORSENS with exercise
-most have a pulmonary stenosis murmur: left basilar systolic
-pulses usually normal
describe prognosis and recommendations of tetralogy of fallot
- medical therapy:
-intermittent phlebotomy, exercise restriction
-long term prognosis relatively poor: may survive years with intermittent phlebotomy, many die before 1 year - surgical options are limited:
-definitive: requires cardiac bypass
-pallation: with systemic to pulmonary shunt; reroutes arterial blood through lungs
-modified blalock taussig shunt: subcalvian artery to pulmonary artery conduit
