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Pediatric Physiology - B. Stevens/Bernstein 2017 > Pediatric Cardiology - Quiz 3 > Flashcards

Pediatric Cardiology - Quiz 3 Flashcards

1
Q

Three main cardiac birth defects

A
  1. bicuspid aortic valve
  2. VSD
  3. ASD: secundum atrial septal defect
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2
Q

In the first week of life, what is the most frequent cause of cardiac cyanosis?

A

Transposition of the great arteries

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3
Q

Most common of the cardiac cyanotic lesions

A

Tetralogy of Fallot (6% of CHD)

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4
Q

What is the best approach to diagnosing a CHD?

A

Sequential systematic analysis of the three major cardiac segments

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5
Q

Three major cardiac segments

A
  1. Atria
  2. Ventricles
  3. Great arteries
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6
Q

Is fetal circulation parallel or in series?

A

Parallel (adults are in series)

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7
Q

In an unborn baby circulation, the RV delivers blood to both pulm and systemic circulation via the __________

A

Ductus arteriosus

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8
Q

In an unborn baby, the LV delivers blood to:

A

Systemic and placental circulation

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9
Q

What allows an unborn baby to survive in utter despite complex lesions?

A

Fetal circulation

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10
Q

What is the pO2 and O2 sat of blood from the placenta?

A

pO2 32-35 mmHg

SpO2 80%

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11
Q

2 directions venous blood can go in fetal circulation

A
  1. umbilical venous blood –> foramen ovale –> LA

2. Abd IVC blood joins the SVC drainage

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12
Q

In an unborn baby, how much blood from the RV passes from the PA via the ductus arteriosus into the descending aorta?

A

> 90%

the rest goes into pulm circulation

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13
Q

In fetal circulation, which ventricle has higher output?

A

RV

450 mL/kg/min

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14
Q

In an unborn baby, which ventricle of the heart has greater thickness?

A

RV

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15
Q

Ratio of RV : LV output

A

1.3 : 1

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16
Q

Changes that occur during transitional circulation

A
  1. Lungs replace gas exchange for the placenta
  2. Spontaneous ventilation –> increased alv O2 concentration
  3. Decreased pulm vasc resistance
  4. increased SVR
  5. rapid drop in systemic venous return to the IVC because umbilical venous flow is removed
  6. RA pressure decreases
  7. LA pressure increases
  8. LA pressure > RA pressure –> foramen ovale closes
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17
Q

How soon after birth does the ductus arteriosus close?

A

10-15 hours

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18
Q

How much does the CO increase after birth:

A

30-80%

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19
Q

What can cause the foramen ovale to reopen after it has closed?

A

increased RA pressure:

  • Crying
  • Pain
  • Hypoxia
  • Hypercarbia
  • Acidosis
  • Lung disease
  • Sepsis
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20
Q

When does anatomic closure of the Foramen ovale occur?

A

3 mo - 1 yr

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21
Q

How does the Foramen Ovale close?

A

Septum primum and septum secundum adhere

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22
Q

How soon does functional closure of the ductus arteriosus occur after birth?

A

72 hrs

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23
Q

How long does anatomic closure of the Ductus Arteriosus take?

A

1-3 mo

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24
Q

2 ways that the ductus arteriosus may be reopened after closure in the case of CHD

A
  1. Prostaglandin E1 infusions - main method

2. Decreases in O2 tension

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25
Q

True or False: Fetal circulation is shunt-dependent.

A

True

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26
Q

What is the pO2 and SpO2 of blood from the IVD and SVC when combined in the RA?

A

pO2 12-14

SpO2 40%

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27
Q

What is the pO2 and SpO2 of the umbilical venous blood when it goes to the ascending aorta, brain, coronary arteries, and upper limbs?

A

pO2 20-22 mmHg

SpO2 65%

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28
Q

What is the pO2 and SpO2 of the blood in the descending aorta?

A

pO2 20-22 mmHg

SpO2 55%

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29
Q

What facilitates O2 uptake from the placenta?

A

Lower P50 of fetal HGB

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30
Q

What causes the ductus arteriosus to close:

A
  1. increased arterial O2 tension
  2. decrease in circulating prostaglandins
  3. bradykinin release from lung expansion
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31
Q

What 2 events cause the separation of the systemic and pulm circulations once a baby is born?

Are these things reversible?

A
  1. closure of foramen ovale
  2. closure of ductus arteriosus

Yes, they are reversible during the first few days of life

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32
Q

Drug used to keep DA open after birth in the case of CHD

A

Alprostadil

it is the fancy name for PGE1

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33
Q

Side effects of Alprostadil

A
  1. Resp depression
  2. Apnea
  3. Fever
  4. Sz
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34
Q

Things that can keep the PDA open (when you want it to be closed)

A
  1. hyperactive precordium
  2. bounding pulses w a wide pulse pressure
  3. hepatomegaly
  4. tachypnea
  5. tachycardia
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35
Q

Potent prostaglandin inhibitor that will close a PDA

A

Indomethacin

36
Q

Blood volumes for:

Premie:
<3 mo:
3-12 mo:
>12 mo

A

Premie: 100-120 mL/kg
<3 mo: 90 mL/kg
3-12 mo: 80 mL/kg
>12 mo: 70 mL/kg

37
Q

True or False: Fetal and postnatal myocardium is structurally and functionally immature w a limited ability to increase CO, compared to an older child.

A

True

38
Q

What can you do to increase CO in an infant?

A

increase HR

increase in preload causes little to no change in CO

39
Q

Why does an infant’s heart have a limited ability to increase SV via the Frank Starling mechanism (Why is it difficult to increase CO via increased afterload?)

A

an infant’s myocardium has fever contractile elements

40
Q

Does an infant’s heart have increased or reduced ventricular compliance? Why?

A

Reduced ventricular compliance

because it has a deficiency of elastic elements

41
Q

What are the implications of the ventricular independence characteristic of a baby’s heart?

A
  1. lower ventricular compliance and equal muscle mass on the R and L ventricles at birth
  2. change in ventricular pressure affects the other ventricule
42
Q

When is LV:RV mass of 2:1 achieved?

A

months after birth

43
Q

True or False: Autonomic innervation of the heart is complete at birth

A

False. It is incomplete

44
Q

True or false: Parasymp innerv of the heart is fully functional at birth.

A

True.

Parasymp slows the heart

45
Q

What is the implication of the immature sympathetic innerv of the heart at birth

A

The baby cannot effectively increase the HR or contractility like an adult can

46
Q 
What does not change in the newborn: 
a. SV
b. slower HR
c. higher BP
D. CO
A

A. Stroke Volume

47
Q

The hallmark of intravasc fluid depletion in neonates and infants is:

A

HoTN w/o tachycardia

48
Q

A concern for paradoxical air embolism may occur in the neonate because of:

A

patent foramen ovale

49
Q

Normal infant vital signs

HR
RR
Premature BP
Neonate BP

A

HR 120-160
RR 30-60
Premature BP 50/25
Neonate BP 70/40

50
Q

How to determine goal for MAP in first few wks of life

A

EGA in weeks

MAP of 42 is good usually

51
Q

Although PVR begins to fall at birth, it doesn’t reach adult levels until ____

A

~ 6 mo old

52
Q

Hypoxia or other presort stimuli can increase pulm vasc resist and lead to R –> L shunting, which can lead to:

A

RV dysfx

53
Q

Environmental factors that can increase pulm vasc resistance

A
  1. Chronic maternal dz
  2. Maternal medication
  3. Drug abuse
  4. Maternal diabetes
  5. ETOH abuse
  6. Lithium
  7. Retinoic acid
  8. Phenytoin
  9. Trimethadione
  10. thalidomine
  11. rubella
  12. SLE
  13. phenylketonuria
54
Q

Volume overload lesions have a _______ shunt and include the following abnormalities:

A

L –> R shunt

  • ASD
  • VSD
  • AVSD
  • PDA
  • Truncus Arteriosus
55
Q

At what 3 levels may L –> R shunts occur?

A
  1. atrial
  2. ventricular
  3. great artery
56
Q

Which side of the heart will be dilated if a shunt is proximal to the mitral valve?

A

R heart

57
Q

Which side of the heart will be dilated if a lesion is distal to the mitral valve?

A

L heart

58
Q

Which side of the heart will be dilated if a pt has an AV septal defect?

A

L heart

59
Q

What is the tx for volume overload lesions?

A
  1. Diuretics
  2. Afterload reduction (ACE inhibitor)
  3. Surgery or trans catheter approach
60
Q

Goal of non-surgical mgmt of volume overload lesions

A

help control pulm overcirculation

61
Q

Opening in the atrial septum permitting free communication of flood b/t the atria
- Seen in 10% of all CHD

A

Atrial Septal Defect

62
Q

Most common type of ASD

A

Secundum ASD

63
Q

What are the 3 major types of ASD?

A
  1. Secundum ASD - at fossa ovalis
  2. Primum ASD - lower in position and is a form of AVSD, MV cleft
  3. Sinus Venous ASD - high in atrial septum, associated w partial anomalous venous return; least common
64
Q

Rare s/s of ASD

A

CHF or other SV symptoms

65
Q

Most common s/s of ASD

A

asymptomatic

  • may have easy fatiguability or mild growth failure
66
Q

Cyanosis does not occur in ASD unless:

A

Pulm HTN is present

67
Q

Clinical S/S of ASD

A
  1. hyperactive precordium
  2. RV heave
  3. Fixed widely split S2
  4. II-III/VI systolic ejection murmur at LSB
  5. mid-diastolic murmur heard over LLSB
68
Q

What causes the systolic and diastolic murmurs of ASD

A

Systolic murmur is caused by increased flow across the pulm valve (NOT BY THE ASD ITSELF)

diastolic murmur - caused by increased flow across tricuspid valve and suggests high flow Qp:Qs is 2:1 (CO pulm: CO systemic)

69
Q

tx for ASD

A

Surgical or Cath lab closure for secundum ASD w a Qp:Qs ratio >2:1 or in children w CHF for significant pulm HTN

Elective closure: b/t ages 2-5 to avoid late complications

70
Q

When is it too late to close an ASD?

A

When pulm HTN w shunt reversal occurs (Eisenmenger syndrome)

71
Q

Is endocarditis ppx required for ASD?

A

Nope!

72
Q

abnormal opening in the ventricular septum which allows free communication b/t L and R ventricles; accounts for 25% of all CHD

A

Ventricular septal defect

73
Q

Most common congenital cardiac anomaly in infants and children

A

Ventricular septal defect

74
Q

4 types of Ventricular Septal Defect

A
  1. Perimembranous
  2. Infundibular (subpulm or supracristal) - involves RV outflow tract
  3. Muscular VSD - can be single or multiple
  4. AVSD - inlet VSD; almost always involves AV valvular abnormalities
75
Q

Most common type of VSD

A

Perimembranous (membranous)

76
Q

Why does a L –> R shunt occur in VSD and what does it lead to?

A
  1. PVR < SVR (not higher pressure in LV)

2. leads to elevated RV and pulm pressures and volume hypertrophy of LA and LV

77
Q

Characteristics of small to mod VSD

A
  • 3-6 mm
  • asymptomatic
  • 50% close spontaneously by age 2
78
Q

Characteristics of mod to large VSD

A
  • almost always symptomatic

- require surgical repair

79
Q

Clinical s/s of VSD

A
  1. II-III/VI harsh holosystolic murmur heard along the LSB, more prominent with small VSD; may be absent w very large VSD
  2. Prominent P2, diastolic murmur
  3. CHF
  4. FTT
  5. Resp infections
  6. exercise intolerance
  7. hyperactive precordium
  8. symptoms develop b/t 1-6 mo
  9. chronic infections
80
Q

tx for small VSD

A
  • no surgical intervention
  • no physical restrictuions
  • reassurance
  • periodic f/u
  • endocarditis ppx
81
Q

tx for symptomatic VSD

A

medical tx initially

  • afterload reducers
  • diuretics
82
Q

Indications for surgical closure of VSD

A
  1. Lg VSD with medically uncontrolled s/s and continued FTT
  2. age 6-12 mo w lg VSD and pulm HTN
  3. age >24 mo w Qp:Qs ratio >2.1
  4. Supracristal VSD of any size, secondary to risk of developing AV insufficiency
83
Q

Results from incomplete fusion of the endocardial cushions, which help to form the lower portion of the atrial septum, the membranous portion of the ventricular septum and the septal leaflets of the tricuspid and mitral valves

A

AVSD

84
Q

What genetic dz is AVSD more commonly seen in?

A

Downs Syndrome (trisomy 21)

85
Q

Would a low premium ASD continuous w a posterior VSD be an AVSD complete form or incomplete form?

A

Complete

86
Q

Would a cleft in both septal leaflets of TV/MV be an AVSD complete form or incomplete form?

A

Complete

87
Q

A patient has diminished/absent femoral pulses and higher BP in the upper extremities than the lower extremities. They also have a pulse discrepancy b/t the R and L arms. What CHD would you suspect?

A

Coarctation of the Aorta

Pediatric Physiology - B. Stevens/Bernstein 2017 (7 decks)

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