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Pathophysiology > module 10 congenital heart defects > Flashcards

module 10 congenital heart defects Flashcards

1
Q

circulation in utero

A

fetal pulmonary vascular resistance HIGH
systemic resistance low
placenta is the site of gas exchange

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2
Q

Birth and circulation

A 
gas exchange shifts to lungs
pulmonary resistance decreases
systemic resistance increases 
Closure of foramen ovale: 1st month
Closure of ductus arteriosis: 10-21 days
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3
Q

foramen ovale

A

opening between RA and LA

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4
Q

ductus arteriosus

A

connects pulmonary artery and aorta

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5
Q

congenital heart defects

A

may be attributed to
- maternal rubella during first trimester
- exposure to cardiac teratogens
- genetic influences
result in 2 primary pathologic processes
- shunting of blood through abnml pathways
- obstruction of blood flow d/t narrowing

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6
Q

shunting of blood

A 
left to right: acyanotic
-> inc. workload on R. side of heart 
-> RV hypertrophy 
-> inc. Right sided pressure 
--- possible switching to a right to left shunt 
right to left: cyanotic
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7
Q

obstructive

A

stenosis or atresia: failure of valves to develop

coarctation of aorta: narrowing

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8
Q

acyanotic congenital defects

A

desorders that result in left to right shunting

  • atrial septal defect
  • ventricular septal defect
  • patent ductus arteriosus
  • coarctation of the aorta
  • pulmonary and aortic stenosis or atresia
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9
Q

ASD atrial septal defect

A 
foramen ovale did not close
-> inc. pulmonary blood flow
-> inc. right side hypertrophy
small defects may be asymptomatic for years
long term: 
- pulmonary HTN
- RV hypertrophy
- possible reversal of shunt to a right to left pattern
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10
Q

VSD ventricular septal defect

A

commonly associated w/ other cardiac defects
initially left to right w/ inc. pulmonary flow
-> RV hypertrophy -> reversal of shunt
systolic murmur

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11
Q

PDA patent ductus arteriosis

A 
ductus arteriosis does not close 
nml closure 1-2 days after birth 
-blood from aorta -> pulmonary artery 
- can close spontaneously 
-- prostaglandin inhibitors can induce closure 
- harsh systolic murmur
- systolic thrill 
- can lead to pulmonary hyperTN -> RSHF -> reversal of shunt
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12
Q

COA coarctation of the aorta

A

narrowing of the aorta
rarely happens by self
males > females 3-4x
can occur anywhere in aorta but usually close to ductus arteriosus
- preductal: more severe
-> lower blood flow maintained by ductus arteriosus -> RSHF
- postductal: less severe
Upper extremity: Inc. BP
Lower extremity: Dec. BP and weak pulses
systolic murmur
ventricular hypertrophy

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13
Q

pulmonary stenosis/atresia

A

No communication between RV and lungs

  • blood must go through septal opening then through ductus arterisosus
  • RV hypoplasia
  • ASD large
  • mild-severe: depends on narrowing of pulmonic valve
  • RV hypertrophy secondary to high afterload caused by narrow opening
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14
Q

Aortic stenosis/ atresia

A 
rare
not compatible with life 
correctable with good prognosis
Inc. LV afterload r/t small opening 
systolic murmur
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15
Q

cyanotic congenital defects

A

result in right to left shunting

  • Tetralogy of Fallot
  • transposition of great arteries
  • truncus arteriosus
  • tricuspid atresia
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16
Q

Tetralogy of Fallot

A

4 characteristic abnormalities
- overriding aorta: above VSD
- VSD
- RV hypertrophy
- Pulmonary stenosis
Enlarged heart r/t extensive RV hypertrophy
Aorta receives unoxygenated blood and oxygenated blood

17
Q

transposition of great arteries

A

aorta arises from RV, and pulmonary artery from LV.

  • 2 separate non-communicating circulations
  • unless there are septal defects for mixing
    • not compatible with life
18
Q

truncus arteriosus

A

pulmonary artery and aorta do not separate

  • > one large vessel
  • Large VSD
  • Single valve over both ventricles
  • amount of blood entering pulmonary vs systemic circulation depends on vascular resistance.
  • inc. pulmonary blood flow -> pulm. HTN -> RV hypertrophy -> inc. pulm resistant -> cyanosis as blood enters systemic circulation instead of pulmonary
19
Q

tricuspid atresia

A

absence of tricuspid valve, underdevelopment of RV, and septal defect
- blood bypasses RV
patent ductus arteriosus needed to perfuse lungs
- cyanosis at birth

20
Q

Kawasaki disease

A

mucocutaneous lymph node syndrome

  • acute self-limiting systemic vasculitis that may result in cardiac sequelae
  • immune system attacks arteries
    • endothelial cells attacked -> exposed underlying tissue
  • inc. risk of thrombus -> ischemia
  • weak artery walls -> aneurysm
  • fibrin in walls -> thick vessel walls -> dec. function
  • 5 y/o or younger
  • males > females
21
Q

s/s of kawasaki disease

A 
conjunctivitis 
rash 
adenopathy
strawberry tongue: top layer sluffs off
hand and feet swelling/ rash
5 or more days of high fever 
"CRASH burn"
22
Q

systemic HTN in peds

A 
often have underlying disease
- renal disease
- COA
- adrenal tumors
- space occupying lesions of cranium 
defined by SBP and DBP >95th percentile for age and gender on 3 occasions

Pathophysiology (80 decks)

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