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Pediatrics > Congential heart defects > Flashcards

Congential heart defects Flashcards

1
Q

Atrial septal defect

A

left to right shunt d/t a hole in the septum leading to a high pressure symptoms

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2
Q

What are the symptoms of HF in general?

A

Small = asymptomatic
Over time = CHF

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3
Q

s/s of atrial septal defect

A

Fixed, split S2 and pulmonic ejection murmur (louder with age)
Infants and children :Respiratory infections, Failure to thrive
Adults (before 40): Palpitations, exercise intolerance, dyspnea, fatigue

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4
Q

growth of septum primum

A

septum primum leads to sotrium primum and then we have osteum secundum

septic secundum

this leads to the foramen ovale

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5
Q

What is the function of foramen ovale

A

allows blood to flow from LA to RA

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6
Q

What is the ostium secondum defect

A

defect where the foramen ovale

MC of the ASD

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7
Q

What is ostium primum common of?

A

down syndrome

because this happens earlier in development

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8
Q

Why do you get a split S2 ASD?

A

Some of the blood goes from the RA to the LA allowing it to close slightly before (2 sounds)

turbulence leads to a murmur

pulmonic systolic murmur increases with time

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9
Q

How wo diagnose ASD

A

ECHO

also right heart cath

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10
Q

what would you see on cxr of ASD?

A

Right heart dilation because of the shunt allowing it to have to pump harder

  • Prominent pulmonary vascularity
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11
Q

What do you see for increased concentration in for ASD?

A

RA
RV
pulmonary artery

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12
Q

Treatment of ASD

A

wait and watch for small lesions <8 mm

try not to rush the surgery and let them grow unless hemodynamic

surgery at 1-3 yo

if you wait too long you will get reverse flow and worse prognosis

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13
Q

What is ventricular septal defect?

A

VSD

Right heart failure d/t blood flow leading from LV to RV

Heart failure
▸ Pulmonary HTN
▸ Arrhythmias
▸ Stroke

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14
Q

How does the septum grow

A

from bottom to top

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15
Q

How does the top and bottom septum differ?

A

Upper is more membranous
Lower is more muscular (more concerning)

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16
Q

What is the MC VSD?

A

Membranous - upper septum (most common but less concerning)

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17
Q

What is an inlet VSD?

A
  • in the posterior portion of the V septum beneath the TV
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18
Q

Why is VSD typically a-cyanotic?

A

left to right shunt

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19
Q

When do you likely not need treatment for VSD?

A

< 6 mm

if greater than this, then surgery after 2

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20
Q

What happens if there is too big of a LV -> RV shunt

A

pulmonary HTN, which can eventually lead to a right to left shunt instead (cyanosis and dyspnea)

want to get surgery done before this

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21
Q

VSD murmur

A

holosystolic murmur (bigger than ASD because of ventricular)

poor feeding
failure to thrive
CHF
worsening tachypnea
hepatomegaly

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22
Q

when is congenital heart defects most likely to lead to death

A

birth up to a month

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23
Q

VSD diagnostic

A

Echo (1st choice)
MRI
CXR might show LAE

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24
Q

What do you do if echo is undiagnostic for VSD? When would you also get this no matter what?

A

Cardio cath

always order if pulmonary HTN

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25
Q

Treatment of VSD

A

small VSD close on it’s own
Lasix if CHF
higher calories because they will have tachypnea (concentrate the formula!)
surgery after 2 years old

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26
Q

what are the 2 surgeries of VSD

A

Patch closure over ventricular septaI defect (preferred treatment)

Transcatheter closure : Mesh to close VSD (higher risk)

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27
Q

When would you do surgery <2 yo

A

VSD > 8 mm
unstable
pulmonary HTN
Aortic insufficiency
LA/LV dilation

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28
Q

What is patent ductus arteriorsis and why is it concerning?

A

Can actually be useful to survive

often have other problems though

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29
Q

What does the PDA connect

A

Persistence of the normal fetal vessel that joins the PA to the Aorta.

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30
Q

When does the PDA normally close?

A

Normally w/in the first week of life

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31
Q

MC and 2nd MC heart defect

A

VSD MC
PDA 2nd MC

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32
Q

What is the RF of PDA

A

Higher incident in preterm infants weighing​ <1500 grams and infants born at higher altitudes >10,000 feet
Females > Males (2:1)​

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33
Q

PDA physiology

A

Blood goes to aorta and bypasses the

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34
Q

2 Pathognomic for PDA

A

holosystolic machine-like murmur

also differential cyanosis (upper extremities are normal because blood first goes to UE but feet are blue because the blood is not oxygenated d/t bypass)

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35
Q

s/s of PDA

A

Depend on size of PDA
Smaller
Usually asymptomatic
Neonates: holosystolic “machine-line” murmur on auscultation Infants, children, adults: continuous murmur
Moderate
Exercise intolerance
Continuous murmur
Wide systemic pulse pressure
Displaced ventricular apex
Larger
Infants: leads to heart failure
Children: shortness of breath, fatigability, Eisenmenger syndrome

some of the oxygenated blood goes back to the lungs

do not see cyanosis until deoxygenated blood goes from aorta to the extremeties

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36
Q

Dx of PDA

A

Echo
EKG shows Left ventricular hypertrophy, left atrial enlargement

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37
Q

When do you see murmur of PDA

A

increased O2 demand

38
Q

treatment of small PDA

A

monitor

39
Q

treatment of PDA if you wanna close it?

A

protoglandan inhibitor
Symptomatic moderate/large PDA During heart failure : Digoxin, furosemide

monitor

40
Q

If prostoglandin inhibitor fails to close, what is required?

A

surgery

41
Q

pulmonary stenosis 3 scenarios

A

Stenosis of the valve itself ​
Most Common - valve has 3 leaflets and they are either thickened or fused ​

Thickened muscle below valve​ Stenosis of the pulmonary artery below valve​

42
Q

Microangiopathic hemolytic anemia

A

pathgonomic for PULMONARY STENOSIS meaning that there is mechanical damage

43
Q

what are the s/s of pulmonary stensosis

A

Systolic ejection murmur at the LUSB which increases withinspiration​

opening click

44
Q

diagnosis of pulmonic stenosis

A

ECHO:
EKG shoes RVH d/t trying to push against it

45
Q

treatment of pulmonary stenosis

A

valvoplasty or surgery if unsuccessful

46
Q

Coarctation of aorta

A

Part of the aortic arch (usually the proximal descending aorta)is narrower than usual causing blockage of normal blood flowto the body, backing blood flow into the left ventricle. Thiscauses the muscles to work harder to get the blood out of theheart​

47
Q

Coarctation of aorta MC population

A

females w/ Turner syndrome

48
Q

What is the aortic valve of coarctation?

A

Coarctation of aorta

49
Q

What is coarctation pathophys 2 types

A

narrowing leading to not enough O2 in systemic circulation

50
Q

What helps Coartcation of aorta?

A

If you have PDA so that there can actually be more blood flow into systemic circulation (even though it is deoxygenated)

also leads to RAAS system

51
Q

BP of coartaction?

A

UE have higher BP (above coarctation) but LE have lower BP

difference of more than 20 BP is most likely this

52
Q

Adult coarctation

A

PDA closes
increased BP upstream
increased brain aneursym
increased risk of aortic dissection

LE is opposite: pale, decreased BP

53
Q

S/s of adult coarctation

A
54
Q

what might be the only way that coarctation presents? What should you do?

A

no femoral pulse

ORDER AN ECHO

need to measure pressure on the right side

55
Q

What is the presentation of coarctation of the aorta?

A

Secondary hypertension
Severe heart failure, shock if/when PDA closes
Other symptoms may more apparent with age
Chest pain, cold extremities, claudication on exertion
Left ventricular impulse palpable, sustained
Pulsations felt in intercostal spaces

56
Q

What does a CXR show of coarctation of aorta?

A

Rib notching: 3-sign (narrowed aorta resembles notch of number 3 due to prestenotic of aortic arch & postenotic of descending aorta dilatation)

pathognonimic!

57
Q

Treatment of coarctation of aorta

A

Prostoglandin in order to keep PDA so that there is an increase of flow the LE

eventually surgery

58
Q

coarctation prognosis

A

Survival through the neonatal period without developing heart failure tend todo well throughout childhood and adolescence​
Infective endocarditis is rare before adolescence, but can occur in bothrepaired and unrepaired coarctation​
correction after age 5yrsare at increased risk for HTN and myocardialdysfunction​​

59
Q

What is mandatory for coarctation if they do athletic activities?

A

Exercise testing is mandatory for these children prior to their participationin athletic activities​

60
Q

What happens with aortic stenosis?

A

ventricle has to work hard to pump the blood, leading to a delay in the opening - leading to a click

murmur will increase with time, leading to cresendo-decresendo murmur

61
Q

what ventricle is hypertrophic with aortic stenosis?

A

left

62
Q

when do you order a cath for aortic stenosis?

A

60​ - 80 mmHg

63
Q

what is the treatment of aortic stensosi

A

similar to pulmonic stenosis

balloon valve (ross procedure)

64
Q

What is the prognosis of aortic stenosis

A

pretty good

severe obstruction can lead to arrythmia (cannot clear for sports)

65
Q

What is worrying of cyanosis? What typically causes this?

A

MUCOUS MEMBRANES

Presence > 3 g/dl deoxy HgB correlates with 80-85% SpO2

66
Q

Why can anemia make it hard to tell if there is cyanosis?

A

Less blood cells making it harder to visualize because of less concentration

67
Q

What is hyperoxia test?

A

Give 100% O2 and if no improvement, then it is cardio!

other etiologies (sepsis, ect) will improve

68
Q

hyperoxia test and what to do if cardio

A

O2 stat increases to 100% = lung disease

O2 stat to 75% = cardio orgin

cardio origin = prostoglandins

69
Q

What are the 5 Ts of cuanotic heart disease?

A

Truncus Arteriosus
TGA (d-Transposition of the great arteries)
Tricupsid Atresia
Tetralogy of Fallot
Total anomalous pulmonary venous return

70
Q

What is the MC cyanotic heart defect?

A

tetralogy of fallot

71
Q

tetraology of fallot

A

Pulmonary stenosis

Large VSD

Overriding Aorta

Right Ventricular Hypertrophy

72
Q

Pulmonic stenosis in tetraology of fallot

A

narrowing of RV outlet causing decrease BF to the pulmonary artery causing thickening of the ventricular wall

makes it harder for deoxy blood to get to to pulmonary circulation

73
Q

what is pathognomic for tetralogy of fallot?

A

Boot shape cxr

74
Q

what is a tet spell?

A

patient might look ok, but there is HYPERcyanotic epsiodes with increased demands

anything that increases O2 demand or decreases SVR

Pathognomic!

fever, exercise, agitation

can be life threatening if untreated!

74
Q

How to stop an acute tet spell

A

increase venous return by squatting or flexing the knees, which will reverse the right to left shunt (because the veins squeeze, backing to the left side of the heart).

calm the baby to stop crying (to decrease the O2 demand)
hydration
meds

75
Q

What are the meds for a tet spell

A

Morphine (relaxes)
Bicarbonate (to correct metabolic stenosis, dilating pulmonary pressure)
Phenylephrine to increase SVR
BB to decrease dynamic RVOT obstruction

76
Q

Long term management of tet spell

A

SURGICAL REPAIR

77
Q

Transposition of great arteries heart defect?

A

Aorta comes off RV (instead of LV)
PA comes off LV

critical!

deoxygenated blood comes to the RA, RV, then aorta to the body (never to the lungs)

78
Q

D-transpostion of great arteries

A

Oxygenated blood goes from pulmonary artery to the lungs and never goes to the body

parallel circuit

focus on this one

79
Q

What is the L type?

A

switch of the ventricles, not the arteries

not as sick, not going to die

leads to HF over time

80
Q

D-transpostion of great arteries shunts that help

A

PDA or VSD

81
Q

MC patient population for transposition of great arteries?

A

Males > females

3:1

NEED to treat immediately

82
Q

RF of mom having kid with transposition of great artery

A

Diabetes
Rubella
Poor nutrition
Consumption of alcohol
> 40 years old

83
Q

If pulse ox is higher in lower extremetiy than upper extremetiy, what is there?

A

transposition of great artery

start prostoglandin to keep the PFO open

84
Q

Classic triad of CXR of transposition of great arteries

A

“egg on a string” narrowed mediastinum (near the trachea)
Lung congestion
Cardiomegaly

85
Q

treatment of transposition of great arteries

A

prostoglandins while waiting for helicpoter to ICU

86
Q

What is hypoplastic left heart syndrome?

A

Underdeveloped left ventricle, ascending aorta

  • Aortic/mitral valves may also be affected, narrow, or absent (atresia)

If untreated: left-sided heart failure >cardiogenic shock > death

no blood is leaving left side to go to the rest of the body because of narrowing

need PDA or ASD

87
Q

s/s of hypoplastic heart

A

same as cyanotic heart failure

88
Q

treatment of all cyanotic heart defects

A

prostoglandins to maintain PDA

3 step surgery

89
Q

can hypoplastic heart kids play in sports?

A

NO

only one that is completely restricted

90
Q

6 common innocent murmurs in childhood

A

Newborn murmur (1st days or hours)
Peripheral pulmonary stenosis
Still’s murmur
Pulmonary ejection murmur
venous hum
carotid bruit

if soft, not as worried.

91
Q

what is pathognomic for still murmur

A

Loud when supine; disappears with inspiration or sitting
Loud with anemia and fever

Pediatrics (7 decks)

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