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Neo boards > Cardiology > Flashcards

Cardiology Flashcards

1
Q

O2 sat in chambers of fetal circulation.

Where is O2 sat highest? Lowest?

A
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2
Q
A

PBF ~ 7 - 15% 2nd trimester
30% 3rd trimester (lung growth so increased PBF)
20% around 38 weeks (more O2 so constricts?)

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3
Q
A

66% CO RV vs 33% LV

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4
Q
A

Left - because receiving DV blood flow (from UVC oxygenated blood) primarily without mixing in much “used” deoxygenated blood + little bit of blood from lungs

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5
Q
A

Increase ductus venosus - dilates.

Decrease HR, RR, CO

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6
Q
A

Fetus goes in hibernation mode - relies on maternal thermoregulation, decrease GI absorption, decreased RR, decrease renal tubular absorption

Preferentially sends blood to head, heart, adrenal glands (by dilating ductus venosus to increase blood to RA -> LA via FO). Abd circumference decrease in FGR fetuses (b/c less BF to those organs) and elevated MCA (diastolic flow increased as more BF to brain)

Note-tricuspid valve very sensitive to hypoxemia (therefore, babies with HIE can have TR)

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7
Q
A
  1. Increase PBF via breathing RA (dilates pulm vessels and decrease PVR)
  2. Closure of FO (increase LA pressure due to increase pulm BF and PV return so then closes; also distal SVR will increase LA pressure)
  3. Closure of DA (oxygen exposure of ductal tissue with constrict it, decrease PGE production (detached from placenta) and metabolism (from lung that is working more), decrease bradykinin (helps vasoconstrict)
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8
Q
A

UV constricts - because decrease blood flow
UA constricts - because increase O2 content

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9
Q

How does DCC work?

A
  • continued blood flow from UV to LA/LV so continued preload while 1) lungs are aeration and increasing pulm BF and 2) not an acute drop in SVR so myocardium has time to start to handle a larger blood volume load
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10
Q

What influences ventricular wall stress?

A
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11
Q

Conceptualize Frank Starling curve

A
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12
Q

Frank starling curve - effect of increased and decreased preload

A
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13
Q

Frank starling curve - effect of increased and decreased afterload

A
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14
Q

PS, hypertelorism, downward slanting palpebral fissures, low at ears, short stature, short webbed neck, Percy’s excavation, cryotorchidism, cognitive delays, lymphedema

A

Noonan - most common cause of HOCM kids < 4 although most common cardiac defect with Noonan is PS

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15
Q

1 cyanotic congenital heart disease in infancy/childhood

A

ToF

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16
Q

1 cyanotic CHD in first week of life

A

TGA

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17
Q

describe early formation of cardiac tube

A
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18
Q

early cardiac embryology

A
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19
Q

mediator of cardiac development

A
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20
Q

mediators of septation

A
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21
Q

mediators of L-R differentiation

A
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22
Q

when does cardiac septation occur?

A

8 weeks

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23
Q

heterotaxy - what occurs

A
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24
Q

L atrial isomerism
- describe
- complications

A
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25
Q

R atrial isomerism
- describe
- complications

A
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26
Q

Reverse differential - infant pre ductal is 50% an post-ductal is 70%. Describe the scenario.

A

d-TGA with inadequate atrial or ventricular mixing and elevated PVR or LVOT (eg CoA).

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27
Q

Most common type of VSD. Which VSD types are more likely to close?

A

perimembranous

those with a muscular region (perimembranous or muscular)

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28
Q

Congenital heart disease - XR described as egg on a string

A
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29
Q

Scimitar syndrome X ray

  • describe Scimitar syndrome
  • complications
A

PAVPR (an anomalous pulm vein to RV)

Can develop pphn, can have some R pulm hypoplasia

Other associated anomalies

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30
Q

Snowman appearance on XR (congenital heart defect - cyanotic heart lesion)

A

snowman TAPVR

31
Q

Infant with TEF, vertebral anomalies and hydronephrosis has a cardiac defect. What is the most likely cardiac defect in this scenario.

A

VACTERL
VSD

32
Q

High lying UAC vs low lying UAC - risks and benefits

A

High - less ischemic complications; same rate of HTN
Low - **; same rate of HTN

33
Q

Morphological development of the heart
- what occurs at week 2

A

cardiac development starts at gastrulation (going from 2 to 3 germ layers) and mesodermal cells migrate toward embryonic disk.

34
Q

When does the heart undergo looping? Describe.

A

around 3 - 4 weeks - linear tube begins to bend towards the R side; distinct chambers appear around this time and more looping to get ventricles side by side.

NKX2.5
TBX1

35
Q

When does septation occur?

A

Around 5 weeks.
Septation of atria (primum septum, primum ostium, secundum septum, secundum ostium?)
Septation of ventricles
Septation of truncus

36
Q

EKG changes with D-TGA

A

R axis deviation (R QRS - up in I and down in avF), RVH, may have RAH

NOTE: Varying degrees of AV block extending to complete heart block may be seen in L-transposition of the great arteries

37
Q

EKG changes and murmurs in ToF

A

EKG: RVH (b/c of increased RVP as a result of PS)

38
Q

EKG changes in TA

A

L superior QRS common (0 to -90)
Increased LV forces
Decreased RV forces
RAH with large P wave

38
Q

Adenosine
- mode of action
- indications for use
- adverse effects

A
  • transiently blocks AVN (may need higher dose if on caffeine)
  • SVT
  • hypotension, bronchoconstriction, wheezing
38
Q

Amiodarone
- mode of action
- indications for use
- adverse effects

A
  • K channel blocker -> slows conduction (+also a Na and Ca channel blocker, and B adreno blocker - negative inotropy, chronotropy)
  • SVT that does not respond to adenosine, VT (stable)
  • LFT, PFT, TFT monitoring; Give Ca prior
39
Q

Digoxin
- mode of action
- indications for use
- adverse effects

A
  • Some AV block (helpful w. other agents eg flecainide, sotalol)
  • Use more fetal tachycardias
  • Monitor concentrations, toxic at high levels, NOT in WPW (risk accelerating the antegrade accessory pathway)
39
Q

Flecainide
- mode of action
- indications for use
- adverse effects

A
  • Na channel blocker; min effect on conduction
  • More fetal SVT
  • Monitor levels, worse if renal dysfunction, NO refrigeration (precipitates) and milk ingestion alters absorption
39
Q

Propranalol
- mode of action
- indications for use
- adverse effects

A
  • BB
  • Use if adenosine responsive tachycardia, first line in WPW and FT, possible LT therapy
  • Glucose, BP
40
Q

Sotalol
- mode of action
- indications for use
- adverse effects

A
  • K channel blocker; some BB effect; slows conduction but less effective than amioradone
  • Useful in combo with flecainide in refractory SVT
  • Bradycaria, prolonged QT monitoring, cautiously use in myocardial dysfunction
41
Q

Verapamil
- mode of action
- indications for use
- adverse effects

A
  • Ca channel blocker (slows AV conduction)
  • Contraindicated < 12 mo b/c associations with sudden death
42
Q

Most common cardiac lesion in Turner syndrome

A

L sided lesions eg CoA (30% of Turners have CoA)

Bicuspid aortic valve (If CoA and BV -> sicker, need LT follow)

43
Q

Most common cardiac lesion in Noonan syndrome

A

Pulm valve stenosis (RAS pathway). also HOCM (most “common” cause of HOCM during **)

44
Q

Most common cardiac tri 13

A

Valve dysplasia

45
Q

Brachial arches

A

4 -> R subclavian
6 -> PDA

46
Q

Normal PR newborn

Normal QRS

Normal QTc

A

0.08 - 0.11 s

0.04 - 0.07 s

0.45 s (up until < 6 months)

47
Q
A
48
Q
A
49
Q

Types of shock

A
50
Q

Types of heart block

A
51
Q

Review pressors

A
52
Q

Review pressors

A
53
Q

Review pressors

A
54
Q

Frank starling curve

A
55
Q
A
56
Q
A
57
Q

Causes neonate HTN

A
58
Q

Causes of prolonged QTc

A
59
Q

Recognize torsades

A
60
Q

Management of complete AV block

A
61
Q

reocgnize this EKG

A
62
Q

Management of WPW SVT

A
63
Q
A
64
Q
A

Delta wave
WPW

65
Q
A

prolonged QTc

66
Q
A
67
Q
A
68
Q
A
69
Q
A
70
Q
A

Neo boards (14 decks)

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