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CRH II > Congenital Heart Disease > Flashcards

Congenital Heart Disease Flashcards

1
Q

define congenital heart disease

A

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

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2
Q

describe the prevalence of congenital heart disease

A

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

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3
Q

when should you expect congenital heart disease?

A
  1. breed/family history
  2. history/clinical signs:
    -failure to thrive
    -poor exercise tolerance, syncope
    -difficulty breathing
    -abdominal distension
    -sudden death
  3. suggestive PE findings:
    -heart murmur!!!
    -arrhythmia
    -cyanotic MM
    -abnormal jugular venous or peripheral arterial pulses
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4
Q

describe innocent/physiologic murmurs in young animals (5)

A
  1. sensitive: softer or absent at rest but increases with excitement/exercise
  2. soft: grade 1-2 /6
  3. single: no other associated abnormal heart sounds or physical exam abnormalities
  4. systolic: limited to mid systole
    -NEVER CONTINUOUS, DIASTOLIC, or TO and FRO
  5. short-lasting: goes away by 6 months
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5
Q

describe pathologic murmurs in young animals (5)

A
  1. can be heard at all times
  2. loud: grade 3/6 or louder
  3. associated clinical signs or PE findings:
    -cyanosis
    -jugular venous distension/pulsation
    -exercise intolerance
    -difficult breathing
    -ascites
  4. can be systolic, diastolic, or continuous
  5. persists beyond 4-6 months of age
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6
Q

describe normal fetal circulation

A
  1. ductus venosus: connects umbilical vein (from mom) to caudal vena cava
  2. foramen ovale: small opening in septum between RA and LA
  3. ductus arteriosus: connects pulmonary artery to descending aorta
  4. respiratory gas exchange: job of maternal lungs
  5. 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
  6. 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
  7. 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
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7
Q

describe normal post-natal cardiovascular changes

A
  1. resistance in the pulmonary circulation DECREASES as lungs inflate
  2. resistance in systemic circulation INCREASES due to loss of placental circulation
  3. 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

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8
Q

describe normal post-natal cardiovascular pressures

A

pulmonary artery:
25 syst, 15 diast

aorta:
120 syst
80 diast

RA: 0-5
RV: 25/0

LA: 0-8
LV: 120/0

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9
Q

classify congenital heart lesions by acyanotic vs cyanotic

A

acyanotic:
-left to right shunts
-obstruction to ventricular flow
-regurgitant valve lesions

cyanotic:
-right to left shunts

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10
Q

describe the most common defects in dogs, cats, horses, calves, and others

A

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!!!)

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11
Q

describe the pathophysiology of left to right shunts

A
  1. communication between pulmonary veins, left heart or systemic arterial circulation (LEFT) and systemic venous circulation, right heart, or pulmonary arteries (RIGHT)
  2. oxygen-rich blood re-circulates repeatedly, leading to volume overload and eccentric hypertrophy (ON EXAM) of structures along affected circuit
  3. most common L-R shunts: PDA, ventricular and atrial septal defects
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12
Q

describe PDAs

A
  1. failure of ductus arteriosus to close normally after birth
  2. 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
  3. 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

  1. uncommonly, blood may shunt right to left (reversed PDA)
    -during pulmonary hypertension
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13
Q

describe classic exam findings of PDA (ON EXAM)

A
  1. wind blowing through a tunnel/machinery murmur
  2. grade/intensity: 4-6/6, palpable thrill is common
  3. location: left heart base
  4. timing: continuous
    -never hear a pause! blood is continuously shunting
  5. hyper kinetic/bounding femoral arterial pulses
    -cause: widened pulse pressure due to run off of blood from arterial tree during diastole
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14
Q

describe prognosis and recommendations for PDA

A
  1. if untreated, 65% die of heart failure before 1 year of age (dogs)
  2. prompt surgical closure/occlusion is curative and almost always indicated if defect if left to right shunting
    -prognosis is excellent following closure!
  3. 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!!
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15
Q

describe ventricular septal defect location

A
  1. defect in interventricular septum (IVS) that allows direct communication of the ventricles
    -most common congenital heart defect in large animals and cats!! (ON EXAM)
  2. majority located in basilar (upper) portion of IVS (perimembranous)
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16
Q

describe ventricular septal defect pathophysiology

A
  1. 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

  1. volume shunted with each beat depends on:
    -size of defect
    -pressure difference between the ventricles in systole
  2. rarely, blood shunts right to left
    -increase in R sided pressures (pulmonary hypertension)
17
Q

describe VSD PE findings (ON EXAM)

A
  1. grade/intensity: variable, smaller VSD = louder murmur
  2. location: right heart (apex or base, depending on location of VSD)
  3. timing: systolic
18
Q

describe prognosis and recommendations for VSD

A
  1. 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
  2. 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
19
Q

describe lesions causing obstruction/stenosis of ventricular outflow

A

narrowing/stenosis of ventricular outflow tract increases resistance to blood flow

  1. proximally:
    -ventricle must generate abnormally high pressure to force blood through narrowing
    -ventricle responds with pressure-induced CONCENTRIC hypertrophy
  2. distally:
    -high velocity, turbulent flow (audible murmur)
    -post-stenotic dilation
20
Q

describe potential consequences of outflow tract stenosis

A
  1. congestive herat failure:
    -more common with lesions affected RV than LV
  2. sudden cardiac death:
    -lethal ventricular arrhythmias due to fibrosis.ischemia
  3. 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

21
Q

what 2 lesions can cause obstruction/stenosis of ventricular outflow?

A
  1. right ventricular outflow stenosis
  2. left ventricular outflow stenosis
22
Q

describe physical exam findings of ventricular outflow stenosis (ON EXAM)

A
  1. murmur:
    -intensity/grade: variable with severity
    -location: left heart base
    -timing: systolic
  2. femoral pulses usually normal for RV obstruction, can be reduced in LV obstruction
23
Q

describe clinical features of stenosis of ventricular outflow

A
  1. most apparently asymptomatic for a prolonged period
  2. 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
24
Q

describe clinical management of stenosis of ventricular outflow

A
  1. B1 adrenergic blockers (atenolol) if moderate or severe
    -reduce myocardial oxygen demand and force of contraction, antiarrhythmic
  2. balloon valvuloplasty (catheter-based procedure):
    -highly successful for pulmonic, but not subaortic
  3. don’t breed affected dogs!
25
Q

describe regurgitant valve lesions

A
  1. mitral valve dysplasia: left apical systolic murmur
    -more common in kittens
  2. tricuspid valve dysplasia: right apical systolic murmurs
    -more common in foals and labradors
26
Q

describe pathophysiology of right to left shunts

A
  1. communication between systemic venous circulation, right heart, or pulm arteries (RIGHT) and the pulmonary veins, left heart, or systemic arterial circualtion (LEFT)
  2. 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)
  3. most common: tetralogy of fallot, eisenmenger’s syndrome (reversed PDA< reversed VSD)
27
Q

describe Eisenmenger’s syndrome

A
  1. 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
  2. may complicate large PDA, VSD, or ASD
  3. most common example is reversed PDA
28
Q

describe tetralogy of fallot

A
  1. most commonly diagnosed cyanotic heart disease
  2. 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

29
Q

describe clinical features of tetralogy of fallot

A
  1. asymptomatic to signs of severe exercise intolerance, syncope, seizures
  2. PE:
    -cyanosis present in 90% at rest, WORSENS with exercise
    -most have a pulmonary stenosis murmur: left basilar systolic
    -pulses usually normal
30
Q

describe prognosis and recommendations of tetralogy of fallot

A
  1. medical therapy:
    -intermittent phlebotomy, exercise restriction
    -long term prognosis relatively poor: may survive years with intermittent phlebotomy, many die before 1 year
  2. 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

CRH II (48 decks)

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