250 Congenital Heart Disease Flashcards

1
Q

What is pulmonic regurgitation

A
  • primary congenital regurgitation is uncommon resulting from abnormal development of valve leaflets or dilation of pulmonary annulus
  • Causes right ventricular overload and eccentric hypertrophy
  • Hear variable systolic and diastolic murmurs at the left heart base
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2
Q

What is aortic regurgitation

A
  • isolated congenital aortic regurgitation is rare, an is more often recognised as complication of other disorders.
  • mild to moderate AR reported in dogs with bicuspid or quadricuspid
  • Will cause hyperkinetic pulses from higher stroke volume and reduced diastolic pressure owing to diastolic runoff of aortic blood back into the LV
  • eccentric or mixed hypertrophy of the LV develops.
  • severe AR -> causes LSCHF
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3
Q

What is the consequence of AV valve dysplasia?

A

1) mitral or tricuspid valve regurgitation
2) inflow obstruction (mitral or tricuspid valve stenosis)
3) dynamic obstruction of LVOT via inappropriate systolic displacement of the mitral valve into the LVOT

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4
Q

What is the pathogensis of AVD?

A
  • TVD has a genetic basis in some breeds. Lab retrievers have an autosomal dominant mutation with incomplete penetrance mapped to chromosome 9
  • wide spectrum of morphologic abnormalities: shortening, rolling, notching, and thickening f valve leaflets; incomplete separation valve components; elongation shortening, fusion, thickened cordage tendinae; atrophy, hypertrophy, malpasitioning of papillary and chordate tendinae
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5
Q

What is the pathophysiology of AV valve malformations?

A
  • produces volume overload and manifests as atrial dilation and eccentric hypertrophy of affected ventricles.
  • severe AV stenosis limits cardiac output so hypotension, syncope, or collapse can occur
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6
Q

How is AVD managed/treated?

A
  • surgical replacement of dysplastic AV valve successfully accomplished in dogs with mitral or tricuspid
  • balloon valvuloplasty for valve stenosis
  • meds for heart failure: diuretics, ACE inhibitors, and pimobendan
  • Significant LVOT obstruction secondary to SAM of mitral valve, regardless of presence or absence of clinical signs is treated with beta blockers to alleviate the obstruction.
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7
Q

What is pulmonic stenosis?

A
  • Valvular lesion consist of varying degrees of valve thickening, leaflet fusion, and hypoplasia of valve annulus
  • valve leaflets are thickened, misshapen or fused.
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8
Q

What is the pathophysiology of PS?

A
  • Obstruction to RV outflow increases resistance to ejection causing proportional increase ventricular systolic pressure
  • RV Concentric hypertrophy occurs to normalise wall stress
  • During systole blood ejected from RV accelerates at is traverses the obstructive office. Blood flow increases in main pulmonary artery as turbulent blood decelerates and expends some of its kinetic energy against the vessel wall.
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9
Q

What breeds is PS common in?

A
Beagles
Samoyed
Chihauhuas
English bulldogs
Miniature schanuzers
Cocker spaniels
Boykin spaniels
Labradors
Mastif
Chow chow
Newfoundland’s
Basset hounds
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10
Q

What are common physical exam findings of PS?

A
  • systolic ejection murmur heard over left heart base that radiates dorsally.
  • holosystolic murmur of tricuspid regurgitation noted over right hemithorax
  • large amplitude jugular pulses result from a giant wave caused by atrial contraction into stiff RV or from cv waves indicating significant tricuspid regurgitation.
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11
Q

What is subvalvular aortic stenosis (SAS)?

A
  • common congenital cardiac malformation in large breed dogs
  • result from fixed ring or ring of fibrous tissues in LVOT just below aortic valve
  • difficult to diagnose and to treat
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12
Q

What is the pathology and pathogensis of SAS?

A
  • Newfoundland breeding studies show autosomal dominant abnormality in PICALM gene
  • autosomal recessive mode of inheritance in Dogue de Bordeaux

Grade 1 = small white slightly raised nodules on endocarditis surface of ventricular septum below aortic valve
Grade 2= narrow ridge of whitish thickened endocardium
Grade 3= fibrous bad, ridge, or collar completely encircling LVOT below aortic valve.

In some dogs there findings diverge from description
In cats long tunnel like obstructions can occur

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13
Q

What is the pathophysiology of SAS?

A
  • obstruction to LV outflow causes an increase in LV systolic pressure and concentric hypertrophy.
  • high velocity and turbulent flow across stenosis area produces systolic ejection murmur and contributes to poststenotic dilation involving ascending aorta, aortic arch, and brachiocephalic artery.
  • Jet lesions predisposes to infective endocarditis
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14
Q

What are the clinical findings?

A

Congenital SAS Common in Newfoundland’s, boxers, Rottweilers, golden retrievers, and GSD
Valvular AS common in bull terriers

  • Asymptomatic dogs have soft ejection murmur, that is easily confused with innocent or functional heart murmur
  • severely affected dogs present with exertion all fatigue, syncope, or left sided congestive heart failure.
  • severe SAS has systolic murmur that becomes louder and later peaking to holosystolic when obstruction is more severe.
  • retrospective study showed out of 96 dogs, 21 dies suddenly during first 3 years of life.
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15
Q

What is the management/treatment of mild SAS?

A
  • prophylactic AB’s during periods of anticipated bacteruria (i.e. dental, surgery)
  • open resection of obstructing lesions during cardiopulmonary bypass clearly offers best opportunity to reduce systolic pressure gradient
  • balloon valvuloplasty of SAS as alternative to surgery or lifelong medical therapy. - can reduce severity by 50% in dogs and not shown to improve survival time when compared to medical therapy (atenolol)
  • balloon dilation is more challenging than valvuloplasty
  • prevent vigorous exercise, administer betaadrenergic receptor blockers (atenolol) to reduce max heart rate, decrease myocardial consumption, and increase time for diastolic coronary artery flow (prevent is he is and development of arrhythmias)
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16
Q

What is Tetralogy of Fallot?

A
  • the defining features of ToF is RV obstruction, secondary RV hypertrophy, a large perimembranous VSD, and rightward positioned aorta (dextroaorta)
17
Q

What is the pathogenesis and pathophysiology of ToF?

A
  • likely related to ventrocranial deviation of ventricular outlet septum
  • predominant components are severe subvalvular RVOT obstruction and VSD -> results in desaturated blood shunt from right heart through septal defect to mix with oxygenated blood from the LV.

-> the desaturated blood from RV to systemic circulation causes arterial hypothermia, decreased hemoglobin o2 saturation, cyanosis, and secondary erythrocytosis.

18
Q

What are the clinical findings of ToF?

A
  • common in keeshond, English bulldog, and now recognised in cats
  • murmur of ToF is produced by high-velocity, turbulent blood flow through obstructed RVOT
  • Exercise or excitement may induce or enhance detection of peripheral cyanosis by accentuating right-to-left stunting
19
Q

How is ToF managed?

A

History and survival times of dogs and cats is not well characterised-It can be tolerated for years

  • limited exercise capacity.
  • sudden death is common due to hypoxemia+ hyperviscosity+ or cardiac arrhythmia.
  • surgical option is to close VSD and remove or bypass stenosis, but surgery is rarely performed in animals
  • The stenosis should not be completely relieved if VSD cannot be closed as loss of RV pressure results in marked left-to-right shunting with subsequent left-sided CHF
  • maintain hydration
  • periodic phlebotomy to keep PCV 64%-68%
  • some children with ToF benefit from nonspecific beta blockade and propranolol to reduce hyper dynamic contraction of RV that increases outflow obstruction
20
Q

Apart from ASD list other atrial malformations.

A

Cor triatriatum sinister (CTS) =
Cor triatriatum dexter - most often reported and occurs mostly in dogs
Supravalvular mitral ring = mitral stenosis characterised by obstructive membrane between mitral valve and LA
Double outlet right atrium = characterised by extreme leftward eviction of ventral atrial septum with insertion of the membrane dorsolateral in to the mitral valve

Cor triatrium = partitioning of left (sinister) or right (dexter) atrium into two chambers creating three atria

21
Q

Apart from VSD what are other rare disorders of the ventricles?

A
  • A condition where RV myocardium is absent and replaced its fibrous tissues and fat (like Uhl’s disease), and reported in cats and one dog.
  • Endocardial fibroelastosis (EFE) = believed to be familial in Burmese and Siamese cats. Secondary endocardial thickening associated with chronic LV dilation. Usually early development of left sided heart failure or biventricular failure before 6 months age.