Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infant Transport Team > Neonatal Cardiology > Flashcards

Neonatal Cardiology Flashcards

CHD and perfusion

1
Q

General Approach to CHD

A
  1. pre/post ductal saturations
  2. Hyperoxia test
  3. CXR
  4. PEG1
  5. Consider need for intuabtion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Neonates who get PGE1

A

TOF
DTGA
Tricuspid atresia
Truncus arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Neonates who would get worse with PGE1

A

TAPVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

TOF relies on

A

VSD and PDA

Relies on VSD and PDA because of the RVOT obstruction that can happen (Tea spell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Left sided obstructive lesions

A
  1. Hypoplastic left heart
  2. Coarctation of the aorta
  3. critical aortic stenosis
  4. HOCM with SAM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Right sided obstructive lesions

A

TOF
Pulmonary atresia
(pulmonary stenosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Parallel Circulation

A

D-TGA
TAPVC
Truncus Arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

BP gradient

A

difference between arms and legs suggestive of LV dysfunction or service coarctation of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does respiratory distress in cyanotic CHD present

A

Often no increased WOB, but hypoxemic from right to left shunt. Textbook answer is resting tachypnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Definition of cyanosis

A

3-5g/DL of dexoygenated hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why do we perform a hyperoxia test?

A

To help distinguish cardiac and pulmonary causes of cyanosis. A hyperoxia test will not increase oxygenation greatly in CHD, but will improve in parenchymal lung disease.

can be useful in the setting without TnECHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the physiologic bases of the hyperoxia test

A

If the child has parnchymal lung disease, saturations will increase with administration of oxygen. If the child has a cardiac shunt with right to left physiology, the hyperoxia test will not provide a sufficient increase in saturations.

In cyanotic CHD due to Right to left shunting, blood in the pulmonary veins are fully saturated with oxygen in ambient air.

Administration of higher concentration of FiO2 increases the amount of dissolved oxygen but has MINIMAL effect on oxygen tension levels because there is no effect on the deoxygenated blood that is shunting the systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What will happen to patients with parenchymal pulmonary disease with an hyperoxia test

A

supplemental oxygen will increase SpO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Formal Hyperoxia testing (using ABGs)

A

Testing is performed by measuring the PaO2 in the right radial artery (preductal) before and after administration of 100% fio2 for 10 minutes

PaO2 >150 suggests hyperoxia test suggests pulmonary disease. An increase <150suggests CHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

informal hypoxia testing

A

an increase in the oxygen saturations <10 percent with admin of 100% fio2 suggests a pulmonary cause of cyanosis

delta of > 10 = CHD/PPHN
delta of <10 = parnchymeal lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Four characteristics of TOF

A
  1. PS
  2. RV hypertrophy
  3. over-ride of the aorta
  4. VSD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why are TOF babies cyanotic

A

If the RV obstruction or increase in PVR is significant enough to increase resistance, it will be easier for blood to cross the VSD from the RV into the LV and go out into the aorta, which becomes the path of least resistance

the right to left shunt across the VSD results in a large volume of desaturated blood entering the systemic circulation, causing cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TOF/Tet spell treatment plan

A
  1. calm baby (decrease PVR)
  2. oxygen (pulmonary vasodilator and systemic vasoconstrictor)
  3. knees to chest (increase SVR by pressing on the femoral arteries)
  4. Prostaglandin (to maintain ductal potency and pulmonary flow pending on surgical repair)
  5. Morphine
  6. Betablocker and phenylphrine (BB to relax RVOT and phenyl to increase SVR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

d-TGA relies on:

A

PDA/PFO or VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe d-tga in one sentence

A

discordant lesion in which the aorta arises from the RV and the pulmonary artery arises from the LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why does DTGA lead to cyanosis

A
  1. deoxygenated systemic venous blood goes into the RA/RV and back into the systemic circulation via the aorta
  2. oxygenated pulmonary venous blood to the left atrium and back to the lungs via the LV and pulmonary artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

whats the importance of the PDA in DTGA

A

it allows oxygenated rich blood in the LV go through the pulmonary artery and through the PDA which connects in to the aorta, which them provides systemic oxygenation (not a lot but some)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

d-TGA mgmt/tx:

A
  1. prostaglandin to keep DA patent.
  2. balloon atrial septostomy
  3. material switch operations (ASO) is standard for surgical repair for DTGA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

define Truncus arteriosus

A

there is a common arterial trunk. the lack of wall development also impairs the creation of separate aortic and pulmonary valves, resulting in the single truncal valve associated with TA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Physiology of Truncus arterisosus

A

main concern is developing HF 2nd to left tor right shunting.

in the new born, with TA, PVR is initially high, with relatively little left tor right shunting at birth. The amount of flow into the pulmonary arteries is relatively normal and is almost equal to the systemic cardiac output.

over the first several weeks of life, the PVR drops and left to right shunting increases to the point of heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Truncus arteriosus

mgmt

A
  1. Alprostadil (PGE1)
  2. diuretic therapy
  3. inotropy
  4. angiotensin blockade
  5. NIPPV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tricuspid Atresia definition

A

is a cyanotic CHD lesion that is characterized by congenital agenesis or absence of the TV resilient in NO direct communication between right atrium and RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

In Tricuspid atresia the exit of blood from the RA is

A

through the PFO or ASD. this obligatory right to left shunt is necessary for survival as it allows deoxygenated systemic blood to enter the LA and subsequently the LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Tricuspid atresia mgmt

A
  1. Alprostadil (PGE1) to maintain an adequate patent ductus arteriosus
  2. intubation, mech vent, inotropic support prn
  3. surgical mgmt - the goal of staged single ventricle palliation is to ensure adequate pulmonary and systemic BF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is total anomalous pulmonary venous connection- TAPVC

A
  • The TAPVC is a cyanotic CHD in which all four pulmonary veins fail to make their normal connection into the left atrium

the result is drainage of all pulmonary venous return into the systemic venous circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Physiology of TAPVC

A
  1. venous mixing
    - the entire oxygenated pulmonary venous return mixes with deoxygenated blood from the systemic venous system
    - because both the RA and RV receive so much volume, they dilate and fail
  2. Pulmonary venous congestion
    - in partially obstructed forms of TAPVC there is significant obstruction of the pulmonary venous return to the heart. pulmonary venous pressures rises and the high pressure is transmitted back to the lung vasculature resulting in progressive interstitial and alveolar edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

obstructed TAPVC

A

generally present as critical ill and will die without immediate surgical correction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

unobstructed TAPVC physiology and when does it present with cyanosis

A

unobstructed lesions may only have subtle cyanosis immediately after birth. after the immediate new born period symptoms are related to pulmonary edema. overtime this results in RV hypertrophy and failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

mgmt of TAPVC

A
  1. supplemental oxygen
  2. mech vent
  3. inotropic support
  4. dont give alprostadil
  5. needs ecmo for refractory shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

d-TGA relise on

A

PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Tricuspid Atresia relies on

A

PFO/ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Truncus arteriosus relies on

A

VSD/PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

TOF cxr

A

boot shaped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

dTGA cxr

A

Egg on a string

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

TAPVC CXR

A

pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how much more does Fetal Hgb retain oxygen than that of an adult

A

1.34 (adult) 1.37 fetal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MAP should equal

A

GA, but pressure doesn’t equal flow. still have to look at SBP/DBP readings and correlate clinically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Factors contributing to Low systolic BP

A 
low pulmonary BF
impaired filling
structural/rhtyhm
myocardial injury
failed adapation
vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Common causes of low diastolic BP

A

vasodilation

hypovolemia

45
Q

common causes of preterm hemodynamic instability

A
  • failed adaption to transition
  • PDA
  • Sepsis/NEC
  • Low pulmonary BF (PPHN, high mean airway pressures)

Cardiogenic Shock

  • congenital heart
  • PPHN

Hypovolemic Shock

  • Hemorrhagic (
  • Non-hemorrhagic (insensible losses)

Obstructive
-tension pneumothorax

Distributive
-Sepsis

46
Q

Common causes of HD instability in the term infant

A
  • HIE –> Acidotic environment
  • Pulmonary HTN (RV failure)
  • sepsis
  • CHD
47
Q

Hydrocortison is useful in neonates because

A

the neonate doesn’t have the endogenous ability to secrete cortisol the same as an adult is able to

48
Q

Dobutamine dose

A

2-10mcg/kg/min usually for anytime you want inotropy. Dont have to worry as much about the vasodilator effects that you do with adults, but its still there

49
Q

cardiogenic shock inotropes in neonate

A

dobutamine and then maybe milirone for inotropy.

50
Q

distributive shock warm pressor choice

A

levophed, vasopressin, dopamine, epi

51
Q

distributive cold shock pressors

A

dobutamine, epi

52
Q

indicators of poor CVS health

A
  • tachycardia
  • systolic hypotension
  • diastolic hypotension
  • increased CRT
  • Pallor/cyanosis
  • deceased LOC
  • Decreased UO
  • Elevated lactate
  • metabolic acidosis
  • low scvo2
53
Q

distributive shock causes in neonates

A
  • sepsis
  • sepsis
  • sepsis
  • NEC
  • iatrogenic
  • hydrops
  • liver failure
  • adrenal insufficiency
54
Q

Functional and anatomical clousure of the PDA occurs when

A

Functional : first few hours of life (10-15)

Anatomical: 2-3 weeks after delivery

55
Q

proper placement of a UVC is through the

A

ductus venous. If it goes into the portal veins it could cause a hematoma.

56
Q

if the DV fails to close after birth, it is deemed a

A

patent ductus venosus, and thus an intrahepatic portosystemic shunt (PSS).

57
Q

Describe why the preductual sat is > than the post ductal sat with failure to transition

A

The RV pumps deoxygenated blood up the pulmonary trunk, into the PDA and into the systemic circulation - which is typically after the first one or two branches off the aorta. The LA receives oxygenated blood from the pulmonary circulation, which goes into the LV which pumps it though the aorta and out of the first branch of the aorta to the right hand (preductual) providing it with oxygenated hemoglobin.

58
Q

Non-cyanotic cardiac conditions

A

ASD
VSD
PDA
Obstruction to flow: PS, AS, Coarc

59
Q

How are ASD’s treated

A

Often with interventionists, not often surgery anymore

60
Q

Which way does BF in VSD/ASD typically

A

left to right (non-cyanotic)

61
Q

When do PDAs typically close in term babies 👶 (anatomically)

A

2-5 days of life

62
Q

When do tet spells typically develop

A

4-6months of age

63
Q

Clinical signs of coarc

A
  • deminishing/abscent femoral pulses
  • BP gradient in arms
  • 90% have systolic HTN of upper extremities
  • pulse discrepancies of R and L arm
64
Q

Adverse effects of PGE

A

Cutaneous Flush
Hyperthermia
Apnea
Hypotension

65
Q

How does PGE improves oxygenation

A

Improved oxygenation comes not only from reestablishment of PDA but also from pulmonary vasodilation which reduces PVR and promotes pulmonary BF

66
Q

When doing a 4 limb BP what are the main things to look for and be suspicious of

A
  1. SBP
    - be suspicious with a difference >10mmHg
    - be very, very suspicious with >20mmHg
67
Q

What are cyanotic CHD

A

Lesions that allow circulation of deoxygenated blood in the systemic circulation via intracardiac or extracardiac shunting

68
Q

What are ductal-dependent lesions

A

Lesions which are dependent upon a PDA to supply the pulmonary or systemic BF, or to allow mixing between parallel circulations

69
Q

Whats the importance of a PDA in right heart obstructions

A

The PDA is necessary to supply BF to the lungs

70
Q

In critical left heart lesions, whats the importance of a PDA

A

The PDA supplies systemic circulation

71
Q

Whats the importance of a PDA in parallel circulation

A

The PDA allows bidirectional flow, allowing for mixing between oxygenated and deoxygenated circuits

72
Q

RF for CHD

A
  • Prematurity
  • Family hx
  • Genetic syndromes and extra cardiac abnormalities
  • Maternal Factors (GDM, connective tissue disorders)
  • Fertliity treatment
  • in utero infection
73
Q

Closure of PDA in the first few days of life can precipitate profound cyanosis…. how??

A

In patients with critically obstructive right heart lesions (PS, pulmonary atresia w/ VSD) pulmonary blood flow is supplied retrograde from the aorta via the PDA (kinda like coronary vessels).

Therefore, progressively severe cyanosis occurs as the ductus closes and BF to the lungs decreases.

74
Q

How does closing of the PDA cause cyanosis and cardiogenic shock in the context of LEFT cardiac lesions

A

Post-ductal saturations will be lower because of right to left shunting through the PDA. However, upon closure of the ductus, systemic circulation is compromised, resulting in cardiogenic shock and cyanosis.

75
Q

Why do patients with parallel circulation depend upon a PDA

A

They relain on an PDA and ASD/VSD for mixing of oxygenated and deoxygenated blood. With closure in the absence of an adequate ASD profound cyanosis occurs.

76
Q

What is differential cyanosis

A

In differential cyanosis, the preductal sat is > post-ductal sat. The upper extremities are pink and perfused and the lower half is cyanotic.

This can occur with PPHN, COA, interrupted arch, or critical aortic stenosis. In these lesions, the flow of deoxygenated blood through the PDA supplies the lower half of the body and oxygenated blood from the left heart supplies the upper body via the vessels proximal to the PDA.

77
Q

In critical RIGHT HEART obstruction, the PDA is necessary to supply the

A

Lungs

78
Q

In critical left heart obstruction the PDA is dependent to supply

A

the systemic circulation.

79
Q

In parallel circulation, the PDA provides

A

Bidirectional flow that allows mixing between oxygenated and deoxygenated circuits.

80
Q

Infants with these lesions may present with cardiogenic shock as the ductus arterosis closes and systemic perfusion decrease

A

Left heart issues.

  • hypolastic left heart syndrome
  • critical aortic valve stenosis
  • critical coractation of the aorta
  • interrupted aorta
81
Q

Whats differenital cyanosis

A

Differenital cyanosis is when the upper half of the body is pink and the lower is cyanotic
This can occur in patients with COA or PPHN

In these lesions, deoxygenated blood from the PDA supply the lower half of the body and the upper is supplied from oxygenated rich blood that flows through the first two branches of the aorta before it mixes with the PDA deoxygenated blood.

82
Q

What is reversed differential cyanosis

A

Is a rare finding that may occur in patients with TGA associated with COA or PPHN

In these infants, oxygenation is higher in the lower extremities than the upper extremities. As most oxygenated blood flow is pumped by the LV out to the pulmonary artery and this across the PDA.

83
Q

How high should the SBP go up after eGA 23 weeks

A

2mmHg q week

84
Q

For each week beyond eGA SBP should increase by 2mmHg and MAP continues with GA while DBP continues to be _____

A

half of SBP

85
Q

What should the SBP/DBP and MAP of a 23 weeker be

A

SBP 30/15 with MAP of 23

86
Q

What should the SBP/DBP and MAP be of a 28 weeker

A

MAP 28

SBP 38/19

87
Q

What should the SBP/DBP and MAP be for a 30 weeker

A

MAP 30

44/22

88
Q

What should the MAP/SBP/DBP of a 38 weeker be

A

MAP 38

68/34

89
Q

Common causes of HD instability for low pulmonary BF

A

RV dysfunction
Might Mean airway pressure
PPHN

90
Q

Common causes of HD instability for impaired filling

A

HOCM w SAM
Tamponade
T. Pneumo

91
Q

Common causes of HD instability for structural/Rhythm

A

CHD

SVT/VT

92
Q

Common causes of HD instability in the setting of vasoconstriction

A

Cold septic shock
Exogenous
Vasopressors

93
Q

What does the SBP tell you

A

Force exerted on the vessel wall during systole

94
Q

What does diastolic pressure tell you

A

Resting pressure of blood on the vessel

95
Q

What does MAP tell you

A

Time-weighted average of pressure valves in large systemic arteries during cardiac cycle

96
Q

What is Denervation Hypersensitivity

A

The finding that myocardial adrenoreceptors show a pattern of “denervation hypersensitivity” in which small concentrations achieve maximal stimulation.

As
gestational age increase, more innervation occurs.

97
Q

HD significant PDA results in

A

Progressive volume of the LV output being diverted from systemic to pulmonary circulation.

98
Q

What creates a HD significant PDA

A

Though ductal size is a contributing factor, a primary determinant of flow between systems is the difference in pressure between the chambers of either side.

99
Q

Therapeutic goals in neonates with oxygenation failure and compromised HD include:

A

Reduction of PVR and augmentation of RV systolic function.

100
Q

Describe RV failure in the setting of PPHN

A

PPHN is a failure of normal decline in PVR after birth. Low PBF leads to poor left heart filling and therefore low LVO despite normal LV systolic performance

The RV is exposed to high afterload which contributes to wall stress and is associated with increased myocardial oxygen demand which is not met by supply due to changes in RCA flow

High RV systolic pressure reduces RCA systolic flow and low systolic systemic BP leads to a decline in RCA diastolic flow

This leads to RV myocardial ischemia which causes progressive RV dilation and dysfunction and may further reduce PBF.

101
Q

Approach to diastolic hypotension in neonate

A

initial therapy is crystalloid (10-20ml/kg to max 60ml/klg) followed by early pressor such dopamine

102
Q

The three shunts of fetal circulation

A

ductus venous
forman ovale
ductus arteriosus

103
Q

What are the two right to left shunts of fetal circulation

A

FO

DA

104
Q

When does the DV functionally start to close?

A

closes soon after clamping and structurally over days to weeks

105
Q

How does the FO close?

A

Oxygen is a pulmonary vasodilator, which decrease PVR. Which increases pulmonary BF, which means more return to the LA from the pulmonary arteries, which increase LA pressure > RA pressure so the FO flap closes

106
Q

During transition, the PVR _______ to or at below _____ and the ____ to left shunting decreases

A

During transition, the PVR decreases to or at below SVR and the right to left shunting decreases

107
Q

What happens when you clamp the cord

A

Clamping the cord causes SVR to increase, your left atrial pressure goes up and the FO closes
Then a breath takes place which decreases PVR more and then DA slowly closes

108
Q

How long can it take for SVD babies to obtain full FRC at 30ml/kg?

A

2-3 hours

109
Q

How long can it take C-section babies to obtain full FRC at 30ml/kg?

A

5-6 hours

Infant Transport Team (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions