Pediatric Cardiology - Quiz 3 Flashcards
1
Q
Three main cardiac birth defects
A
- bicuspid aortic valve
- VSD
- ASD: secundum atrial septal defect
2
Q
In the first week of life, what is the most frequent cause of cardiac cyanosis?
A
Transposition of the great arteries
3
Q
Most common of the cardiac cyanotic lesions
A
Tetralogy of Fallot (6% of CHD)
4
Q
What is the best approach to diagnosing a CHD?
A
Sequential systematic analysis of the three major cardiac segments
5
Q
Three major cardiac segments
A
- Atria
- Ventricles
- Great arteries
6
Q
Is fetal circulation parallel or in series?
A
Parallel (adults are in series)
7
Q
In an unborn baby circulation, the RV delivers blood to both pulm and systemic circulation via the __________
A
Ductus arteriosus
8
Q
In an unborn baby, the LV delivers blood to:
A
Systemic and placental circulation
9
Q
What allows an unborn baby to survive in utter despite complex lesions?
A
Fetal circulation
10
Q
What is the pO2 and O2 sat of blood from the placenta?
A
pO2 32-35 mmHg
SpO2 80%
11
Q
2 directions venous blood can go in fetal circulation
A
- umbilical venous blood –> foramen ovale –> LA
2. Abd IVC blood joins the SVC drainage
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
13
Q
In fetal circulation, which ventricle has higher output?
A
RV
450 mL/kg/min
14
Q
In an unborn baby, which ventricle of the heart has greater thickness?
A
RV
15
Q
Ratio of RV : LV output
A
1.3 : 1
16
Q
Changes that occur during transitional circulation
A
- Lungs replace gas exchange for the placenta
- Spontaneous ventilation –> increased alv O2 concentration
- Decreased pulm vasc resistance
- increased SVR
- rapid drop in systemic venous return to the IVC because umbilical venous flow is removed
- RA pressure decreases
- LA pressure increases
- LA pressure > RA pressure –> foramen ovale closes
17
Q
How soon after birth does the ductus arteriosus close?
A
10-15 hours
18
Q
How much does the CO increase after birth:
A
30-80%
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
20
Q
When does anatomic closure of the Foramen ovale occur?
A
3 mo - 1 yr
21
Q
How does the Foramen Ovale close?
A
Septum primum and septum secundum adhere
22
Q
How soon does functional closure of the ductus arteriosus occur after birth?
A
72 hrs
23
Q
How long does anatomic closure of the Ductus Arteriosus take?
A
1-3 mo
24
Q
2 ways that the ductus arteriosus may be reopened after closure in the case of CHD
A
- Prostaglandin E1 infusions - main method
2. Decreases in O2 tension
25
True or False: Fetal circulation is shunt-dependent.
True
26
What is the pO2 and SpO2 of blood from the IVD and SVC when combined in the RA?
pO2 12-14
SpO2 40%
27
What is the pO2 and SpO2 of the umbilical venous blood when it goes to the ascending aorta, brain, coronary arteries, and upper limbs?
pO2 20-22 mmHg
SpO2 65%
28
What is the pO2 and SpO2 of the blood in the descending aorta?
pO2 20-22 mmHg
SpO2 55%
29
What facilitates O2 uptake from the placenta?
Lower P50 of fetal HGB
30
What causes the ductus arteriosus to close:
1. increased arterial O2 tension
2. decrease in circulating prostaglandins
3. bradykinin release from lung expansion
31
What 2 events cause the separation of the systemic and pulm circulations once a baby is born?
Are these things reversible?
1. closure of foramen ovale
2. closure of ductus arteriosus
Yes, they are reversible during the first few days of life
32
Drug used to keep DA open after birth in the case of CHD
Alprostadil
| it is the fancy name for PGE1
33
Side effects of Alprostadil
1. Resp depression
2. Apnea
3. Fever
4. Sz
34
Things that can keep the PDA open (when you want it to be closed)
1. hyperactive precordium
2. bounding pulses w a wide pulse pressure
3. hepatomegaly
4. tachypnea
5. tachycardia
35
Potent prostaglandin inhibitor that will close a PDA
Indomethacin
36
Blood volumes for:
Premie:
<3 mo:
3-12 mo:
>12 mo
Premie: 100-120 mL/kg
<3 mo: 90 mL/kg
3-12 mo: 80 mL/kg
>12 mo: 70 mL/kg
37
True or False: Fetal and postnatal myocardium is structurally and functionally immature w a limited ability to increase CO, compared to an older child.
True
38
What can you do to increase CO in an infant?
increase HR
| increase in preload causes little to no change in CO
39
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?)
an infant's myocardium has fever contractile elements
40
Does an infant's heart have increased or reduced ventricular compliance? Why?
Reduced ventricular compliance
| because it has a deficiency of elastic elements
41
What are the implications of the ventricular independence characteristic of a baby's heart?
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
When is LV:RV mass of 2:1 achieved?
months after birth
43
True or False: Autonomic innervation of the heart is complete at birth
False. It is incomplete
44
True or false: Parasymp innerv of the heart is fully functional at birth.
True.
Parasymp slows the heart
45
What is the implication of the immature sympathetic innerv of the heart at birth
The baby cannot effectively increase the HR or contractility like an adult can
46
```
What does not change in the newborn:
a. SV
b. slower HR
c. higher BP
D. CO
```
A. Stroke Volume
47
The hallmark of intravasc fluid depletion in neonates and infants is:
HoTN w/o tachycardia
48
A concern for paradoxical air embolism may occur in the neonate because of:
patent foramen ovale
49
Normal infant vital signs
HR
RR
Premature BP
Neonate BP
HR 120-160
RR 30-60
Premature BP 50/25
Neonate BP 70/40
50
How to determine goal for MAP in first few wks of life
EGA in weeks
| MAP of 42 is good usually
51
Although PVR begins to fall at birth, it doesn't reach adult levels until ____
~ 6 mo old
52
Hypoxia or other presort stimuli can increase pulm vasc resist and lead to R --> L shunting, which can lead to:
RV dysfx
53
Environmental factors that can increase pulm vasc resistance
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
Volume overload lesions have a _______ shunt and include the following abnormalities:
L --> R shunt
- ASD
- VSD
- AVSD
- PDA
- Truncus Arteriosus
55
At what 3 levels may L --> R shunts occur?
1. atrial
2. ventricular
3. great artery
56
Which side of the heart will be dilated if a shunt is proximal to the mitral valve?
R heart
57
Which side of the heart will be dilated if a lesion is distal to the mitral valve?
L heart
58
Which side of the heart will be dilated if a pt has an AV septal defect?
L heart
59
What is the tx for volume overload lesions?
1. Diuretics
2. Afterload reduction (ACE inhibitor)
3. Surgery or trans catheter approach
60
Goal of non-surgical mgmt of volume overload lesions
help control pulm overcirculation
61
Opening in the atrial septum permitting free communication of flood b/t the atria
- Seen in 10% of all CHD
Atrial Septal Defect
62
Most common type of ASD
Secundum ASD
63
What are the 3 major types of ASD?
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
Rare s/s of ASD
CHF or other SV symptoms
65
Most common s/s of ASD
asymptomatic
- may have easy fatiguability or mild growth failure
66
Cyanosis does not occur in ASD unless:
Pulm HTN is present
67
Clinical S/S of ASD
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
What causes the systolic and diastolic murmurs of ASD
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
tx for ASD
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
When is it too late to close an ASD?
When pulm HTN w shunt reversal occurs (Eisenmenger syndrome)
71
Is endocarditis ppx required for ASD?
Nope!
72
abnormal opening in the ventricular septum which allows free communication b/t L and R ventricles; accounts for 25% of all CHD
Ventricular septal defect
73
Most common congenital cardiac anomaly in infants and children
Ventricular septal defect
74
4 types of Ventricular Septal Defect
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
Most common type of VSD
Perimembranous (membranous)
76
Why does a L --> R shunt occur in VSD and what does it lead to?
1. PVR < SVR (not higher pressure in LV)
| 2. leads to elevated RV and pulm pressures and volume hypertrophy of LA and LV
77
Characteristics of small to mod VSD
- 3-6 mm
- asymptomatic
- 50% close spontaneously by age 2
78
Characteristics of mod to large VSD
- almost always symptomatic
| - require surgical repair
79
Clinical s/s of VSD
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
tx for small VSD
- no surgical intervention
- no physical restrictuions
- reassurance
- periodic f/u
- endocarditis ppx
81
tx for symptomatic VSD
medical tx initially
- afterload reducers
- diuretics
82
Indications for surgical closure of VSD
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
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
AVSD
84
What genetic dz is AVSD more commonly seen in?
Downs Syndrome (trisomy 21)
85
Would a low premium ASD continuous w a posterior VSD be an AVSD complete form or incomplete form?
Complete
86
Would a cleft in both septal leaflets of TV/MV be an AVSD complete form or incomplete form?
Complete
87
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?
Coarctation of the Aorta
