Congenital Heart Disease Flashcards Preview

D&T 3: Exam 1 > Congenital Heart Disease > Flashcards

Flashcards in Congenital Heart Disease Deck (21)
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1
Q

Heart Folding

A

Right (d-looping) causes the atrium and sinus venosus to migrate cranially; neural crest cells by this point have participated in Aorticopulmonary septation and helped form the primitive aortic arches

(Roughly week 4)

2
Q

What forms the borders of the AVC?

A

Cardiac jelly, fusion of superior and inferior endocardial cushions

=»Endocardial cells then differentiate to form the fibrous portion of the valves

3
Q

3 origins of the membranous part of the IVS

A

Right bulbar ridge, left bulbar ridge, and the av septum (endocardial cushions)

4
Q

By what day does the heart have 4 chambers

A

50

5
Q

1st aortic arch =»

A

Maxillary and external carotid arteries

6
Q

Third aortic arch =»

A

Common carotid artery

7
Q

Fourth aortic arch =»

A

Left= aortic arch; right=subclavian

8
Q

Sixth aortic arch =»

A

Right= RPA/LPA; Left= Ductus arteriosus

9
Q

Pulmonary Vein development

A

Lung buds from the embryonic foregut incorporate a common vein to the left atrium at week 8 and separate into two distinct veins by week 12

10
Q

What does the sinus venosus become?

A

The smooth part of the RA

11
Q

Atrial Septal Defect

A

Leads to right atrial enlargement, right ventricular enlargement, and increased pulmonary flow

Clinical: Soft systolic ejection mumur at the left upper sternal border, fixed split S2, and prominent RV impulse

CXR may show cardiomegaly; echo is gold standard

Tx: May close spontaneously or can close w/ cardiac catheterization procedure

12
Q

Ventricular Septal Defect

A

Most common congenital heart disease

Blood flows from LV to RV causing increased pulmonary flow, some LV enlargement, and LA enlargement

Signs:Presents at ***4-8 weeks w/ tachypnea, diaphoresis, failure to thrive

PE: Hyperdynamic precordium, holosystolic mumur at lower left sternum, possible mid-diastolic rumble at the apex w/ large defects

Tx: Surgery

13
Q

PDA

A

Common in preemies; decreased pulmonary resistance at birth causes L=>R shunting increasing return and leading to LA and LVL enlargement

Signs: Tachypnea, diaphoresis

PE: Harsh, machine-like murmur at the upper left sternal border, tachypnea

PDA: Indomethacin, cardiac catheterization procedure

14
Q

Atrioventricular Septal Defect

A

Partial defect is similar to ASD, complete defect has combination of ASD and VSD (severe)

Clinical: Partial =» asymptomatic; Complete =» CHF signs

PE: Partial- Fixed S2 impulse, systolic ejection murmur at upper left sternal border
Complete-Loud S2, hyperdynamic precordium, murmur at lower-left sternum

Tx: Partial- Observation, elective surgery when older
Complete- Management of CHF, surgery at 3-6months

15
Q

Aortic coarction

A

Commonly seen in Turner’s Syndrome (XO); causes a rise in EDV leading to increased LV and LA pressures and pulmonary edema

***HTN in upper extremities; hypotension in lower extremities

PE: CHF signs once ductus arteriosus closes; possibly mild HTN in older children

Tx: PGE1 to maintain ductus arteriosus, inotropy support, correction of metabolic acidosis

16
Q

Hypoplastic Left Heart Syndrome

A

Self-described; causes a dominant right heart and causes things light aortic atresia/stenosis alongside mitral atresia/stenosis depending on the size of the LV

-While Ductus arteriosus is open, some blood from the pulmonary artery will enter systemic circulation

PE: Shock once PDA closes but mild cyanosis before that; usually seen prenatally

-Dyspnea, single loud S2

Tx: PGE1, inotropy help, hypoventilation to manage pulmonary resistance
-Eventual severe surgery is performed connecting the IVC to the pulmonary artery (FYI)

17
Q

Tetrology of Fallot

A

PROVe

-Initially a L=>R shunt due to V, hypertrophy of RV and increased pulmonary stenosis eventually changes it to R=>L shunt

PE: Normal S2, cyanosis, harsh systolic ejection murder on left sternal border that radiates to the back

*HYPERCYANOTIC EPISODES: acute increase in R=>L shunting that causes cyanosis, irritability, lethargy, hyperpnea
=»Put baby in knee-chest position to decrease VR and increase SVR (goal is to improve pulmonary flow)
-Also give IV fluids (increased pulmonary flow), morphine, phenylephrine, BB

***Boot-shaped heart on CXR

Tx: Surgery

18
Q

Tricuspid atresia

A

Pts. have interatrial communication, hypoplastic right ventricle, and a VSD
-Systemic venous return mixes w/ pulmonary return in LA, all pulmonary flow must go across the VSD and degree of cyanosis depends on this flow

PE: Neonatal (early) cyanosis, normal S2, left ventricular impulse

Tx: PGE1, surgery

19
Q

Transposition of the Great Vessels

A

Assoc. w/ patent foramen ovale, VSD, and aortic coarction; degree of mixing of blood determines cyanosis

PE: Neonatal cyanosis, may be a murmur

Tx: PGE1, surgery

20
Q

Truncus Arteriosis

A

Assoc. w/ 22q.11 deletion; pulmonary blood flow depends on resistance

PE: CHF, mild cyanosis, holosystolic murmur from VSD
***ONLY DISORDER TO HAVE A DIASTOLYLIC MURMUR TOO (from truncal regurgitation)

21
Q

Total Anomalous Pulmonary Venous Return

A

Assoc. w/ hetortaxy syndrome; Pulmonary arteries connect back to the RA; systemic flow depends on patent foramen ovale or ASD

PE: Unobstructed-Asymptomatic initially, then feeding problems, tachypnea, failure to thrive, widely split S2, systolic murmur
Obstructed- Severe respiratory distress and cyanosis on 1st day of life, normal cardiac signs

-Snowman sign on CXR, echo

Tx: Unobstructed- Medical therapy then surgery
Obstructed- SURGICAL EMERGENCY; stabilize (inotropics, PGE1, mecahnical ventilation) and surgery