congenital heart defects Flashcards

1
Q

L→R shunts

A

VSD (most common CHD)
ASD
PDA

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2
Q

symptoms of L→R shunts

A

late cyanosis “blue kids”
less dangerous in short term, less severe, more common than R→L shunt
asymptomatic until exercise: SOB, cyanosis

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3
Q

R→L shunts

A
5 T's
Truncus arteriosus (1 vessel)
Transposition of great vessels (2 vessels switched)
Tricuspid atresia (3 = Tri)
Tetrology of Fallot (4 defects = Tetra) (most common cause of early childhood cyanosis)
Total anomalous pulmonary venous return (TAPVR) (5 letters)
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4
Q

symptoms of R→L shunts

A

early cyanosis “blue babies”: deoxy blood into systemic circulation, bypass lungs
diagnosed prenatally or immediately after birth
require urgent surgical correction or PDA maintenance

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5
Q

harsh holosystolic murmur

A

VSD

when ventricles contract: LV → RV

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6
Q

loud S1

wide, fixed S2

A

ASD

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7
Q

continuous, machine-like murmur in LUSB

A

PDA

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8
Q

VSD presentation

A

asymptomatic at birth
most resolve (esp first 6 mo)
may manifest weeks after birth or remain asymptomatic in life
larger lesion require surgery: LV overload → heart failure
harsh holosytolic mumur

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9
Q

cause of VSD

A

interventricular septum defect

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10
Q

cause of ASD

A
septum are missing tissue (not unfused septum primum + septum secundum causing PFA)
foramen ovale (of septum secundum) and foramen secundum (of septum primum) overlap
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11
Q

ASD presentation

A

asymptomatic
larger lesion: RVH → heart failure
loud S1, wide, fixed split S2

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12
Q

PDA presentation

A

late cyanosis in lower extremities

continous machine-like murmur

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13
Q

cause of PDA

A

higher pressure in aorta → lower pressure in pulmonary trunk (↓ lung resistance with first breath)
progressive RVH and/or LVH → heart failure

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14
Q

name this condition:
longstanding, uncorrected L→R shunt (VSD, ASD, PDA) → ↑pulmonary blood flow → ↑pulmonary circulation pressure → progressive pulmonary HTN→ RVH →now R→L shunt → late cyanosis, clubbing, SOB

A

Eisenmenger syndrome

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15
Q

↑ blood pressure in upper extremities, ↓ blood pressure + weak, delayed pulses in lower extremities
other associations:
notching of ribs: intercostal arteries dilated along inferior edge = collateral circulation
aortic regurgitation: abnormal valve or ↑afterload damages valve→ regurgitation → heart failure

A

coarctation of aorta

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16
Q

conditions that require maintenance of ductus arteriosus with PGE2

A

infantile coarctation of aorta (narrowed aorta proximal to DA)
transposition of great vessels (need PGE2 to allow oxygenated left sided blood into aorta → systemic circulation until surgery, otherwise die in first few months)

17
Q

cause of persistent truncus arteriosus

A

failure of neural crest cells to cause aorticopulmonary septum to divide the ascending aorta and pulmonary trunk
usually have VSD too - mixes blood

18
Q

presentation of truncus arteriosus

A

infant with cyanosis, respiratory distress, heart failure

VSD: RV blood mixes with LV blood → leaves for systemic circulation

19
Q

cause of transposition of great vessels

A

RV →aorta and LV → pulmonary trunk
aorticopulmonary septum doesn’t spiral
separation of systemic + pulmonary circulation
need shunt to allow mixing of blood (otherwise not compatible with life): VSD, ASD, PDA, patent foramen ovale

20
Q

cause of tricuspid atresia

A
absence of tricuspid valve (no RA to RV opening) → hypolastic RV
need ASD (deoxy RA blood → LA) AND VSD (LA → LV → RV → oxygenate blood) to be compatible with life
21
Q

cause of total anomalous pulmonary venous return (TAPVR)

A

pulmonary veins drain into right-heart circulation (SVC or coronary sinus) → RA
closed loop → no deoxygenated blood going into LA → aorta
need R→L shunt to maintain CO (ASD, PDA)

22
Q

cause of tetralogy of fallot

A

displacement of infundibular septum
IHOP
1) Interventricular septal defect = VSD
2) Hypertrophy - RVH (push against stenoic valve)
3) Overriding aorta (sits over VSD)
4) Pulmonic valve stenosis (RV outflow obstruction)

23
Q

boot shaped heart on xray, think

A

kid: RVH due to tetralogy of fallot
adult: RVH due to COPD or primary pulmonary HTN

24
Q

effect of squatting in tetralogy of fallot

A

↑ systemic vascular resistance → ↑afterload → R→L shunt becomes L→R shunt → VSD allows deoxy blood to be forced to R side into lungs for oxygenation→ improves cyanosis

25
Q

presentation of tetralogy of fallot

A
most time: L→R shunt across VSD (acyanotic, RV pushes harder to get across pulmonic stenosis)
some times (crying, feeding, ↑ activity): R → L shunt across VSD (cyanotic)
26
Q

CHD associated with preexisting maternal diabetes

A

transposition of great vessels

27
Q

CHD associated with maternal lithium use

A

Ebstein anomaly

28
Q

CHD associated with alcohol use

A

TOF, VSD, ASD, PDA

29
Q

CHD associated with DiGeorge syndrome (22q11 syndrome)

A

truncus ateriosus

TOF

30
Q

CHD associated with Down Syndrome

A

endocardial cushion defect: ASD or VSD

31
Q

CHD associated with congenital rubella

A

pulmonary artery stenosis

PDA

32
Q

CHD associated with Turner Syndrome

A

bicuspid aortic valve

infantile coarctation of aorta

33
Q

CHD associated with Marfan Syndrome

A

thoracic aortic aneurysm and dissection

aortic regurgitation

34
Q

what is name for this condition:
tricuspid leaflets displaced into RV → hypoplastic RV
tricuspid regurgitation or stenosis

A

ebstein anomaly

35
Q

complication of ebstein anomaly

A

dilated RA → risk for SVT or WPW

36
Q

widely split S2 + tricuspid regurgitation

A

ebstein anomaly

37
Q

cause of patent foramen ovale

A

unfused septum primum + septum secundum after birth

can lead to paradoxical emboli (venous thromboembolus enters arterial circulation)

38
Q

complication of patent foramen ovale or ASD

A

can lead to paradoxical emboli (venous thromboembolus enters arterial circulation)

39
Q

what type of CHD would ↑afterload (squat or knees to chest in infant) be beneficial

A
R→L shunt:
TOF
transposition of great vessels
truncus arteriosus
eisenmenger syndrome with VSD, ASD, or PDA