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1
Q

Mechanisms of hydrocortisone to increase BP

A

Vasoconstriction
* decreased NOS
* decreased prostaglandin
* decreases catecholamine metabolism
* upregulates angiotensin-II receptors

Contractility:
* Increases Ca++
* increase adrenergic receptors

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2
Q

Factors that promote closure of the PDA

A

Functional closure
1. increase PaO2
2. Decrease BP in ductus arteriosus (fall in PVR)
3. Decrease PGE2
4. Decreased PGE2 receptors

Structural closure:
1. oxygen-mediated constriction: tissue hypoxia ductal media
2. Hypoxia induced GF (VEGF, TGF-beta)

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3
Q

Types of SVT

A

Orthodromic MCC
Antidromic tachycardia
AV nodal re-entry tachycardia

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4
Q

Antidromic tachycardia

A
  1. p wave axis superior, inverted in II/avF, wide QRS with WPW
  2. less common
  3. Pathway: down accessory/antidromic, returns back to atria backwards
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5
Q

AV nodal re-entry tachycardia

A
  1. p wave not visible- atria/ventricle depolarize SAME TIME
  2. less common
  3. slow and fast pathways
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6
Q

Antiarrhythmic drug classes and where they work on phases

A

I: active depolarization (Na block)

II and III: sustained depolarization phase (beta- and K-block)

IV: repolarization (Ca-block)
*Do not use Ca-channel blockers (verapimil) in neonates

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7
Q

Orthodromic tachycardia pathway

A

down AV node, up accessory/orthodromic pathway
(p wave after QRS)

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8
Q

MCC SVT

A

Orthodromic tachycardia

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9
Q

Orthodromic tachycardia EKG

A

p wave AFTER QRS, narrow QRS, +/- WPW

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10
Q

Antidromic tachycardia pathway

A

down accessory/antidromic, returns back to atria backwards

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11
Q

Antidromic tachycardia EKG

A
  • p wave axis superior
  • inverted in II/avF
  • wide QRS with WPW
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12
Q

AV nodal re-entry tachycardia EKG

A

p wave not visible- atria/ventricle depolarize AT SAME TIME

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13
Q

Pulmonary artery sling compresses?

A

As the left pulmonary artery courses to supply the left lung, it compresses the distal trachea and right mainstem bronchus.

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14
Q

postnatal EKG timing of in utero first degree block

A

at 1 year of age if transient

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15
Q

MC association with truncus?

A

right aortic arch

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16
Q

what is the first system to function in utero?

A

CV system

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17
Q

what trilaminar layer does heart arise from?

A

mesoderm

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18
Q

what are the developmental stages of heart formation

A
  1. tube formation
  2. looping
  3. septation
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19
Q

when is heart formation complete?

A

7-8 weeks

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20
Q

steps in tube formation

A

ED 15: two flat sheets mesodermal angiogenic cells
ED 17: upper sheet expands and forms tube encircling other sheet; straightens out
ED 20: beats start in upper tube

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21
Q

steps in looping

A

ED 21: linear tube bends towards right
ED 22: distinct chambers appear
ED28: further looping until ventricles side to side

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22
Q

steps in septation

A

ED 34: atrial septation
ED 38-46: ventricle septation

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23
Q

{__,__,__}

A

{atrial situs = S, I or A ,
looping = D or L
great arteries = S or I}

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24
Q

{S, D, S}

A

normal

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25
Q

{S, D, D}

A

dTGA

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26
Q

{S, L, L}

A

l - TGA

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27
Q

{I, L, I)

A

situs inversus totalis

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28
Q

fetal improved tolerance for low pO2

A
  1. HbF high O2 affinity
  2. increased Hb concentration
  3. decreased O2 consumption
  4. increased anaerobic metabolism
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29
Q

fetal compensation for hypoxemia

A
  1. blood flow preferentially to heart, brain adrenals
  2. dilation of DV; better oxygenated blood shunted to LA
  3. suppressed respiration, bradycardia, decreased CO
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30
Q

CO =

A

= HR * SV

= systemic BP/total peripheral vascular resistence

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31
Q

ventricular wall stress =

A

= ventricular P x ventricular radius / wall thickness

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32
Q

which impacts CO more? preload or afterload?

A

preload bc afterload does not effect until a critical BP level is reached

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33
Q

SV =

A

= EDV - ESV

EDV = volume in LV at end of filling
ESC = volume in LV at end of ejection

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34
Q

how to increase EDV

A

increase preload or increase ventricular compliance/stretch

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35
Q

how to decrease ESV

A

increase contractility
decrease afterload

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36
Q

stroke work =

A

= MAP x SV

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37
Q

how does RV and LV stroke work compare?

A

RV 1/6 of LV

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38
Q

Qp/Qs> 1; what kind of shunt?

A

L > R
large is > 2

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39
Q

Qp/Qs < 1; what kind of shunt?

A

R > L
large of < 0.7

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40
Q

O2 consumption =

A

= amount O2 delivered by heart - O2 returning to heart

= blood flow x O2 arterial - blood flow x O2 venous

  • O2 content = O2 Hb + O2 dissolved *
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41
Q

Qp/Qs =

A

= PBF/SBF
= {aorta O2 sat - mixed venous O2 saturation} / {LA or pulm vein O2 sat - pulmonary artery O2 saturation}

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42
Q

PVR =

A

= {Mean PA pressure - Mean LAP} / PBF

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43
Q

SVR =

A

= {Mean aortic P - Mean RAP} / SBF

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44
Q

R ~

A

{8 x viscosity x L} / pi x r^4

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45
Q

what reduction in Hgb is needed to see cyanosis?

A

3-5 g or reduced Hb/dl of capillary blood

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46
Q

preductal 100mmHg; post ductal 45 mmHg

A

CoA with PDA + PVR

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47
Q

preductal 45 mmHg; postductal 80mmHg

A

TGA + intact septum + PDA
+ PPHN or iAoA or preductal CoA

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48
Q

preductal 75 mmHg; 50 mmHg postductal

A

PPHN + R>L across PDA

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49
Q

65 mmHg postductal; 95mmHg venous

A

infradiaphragmatic TAPVR (obstructive)

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50
Q

hyperoxia test

A

paO2< 100 without CO2 retention = CHD
paO2 100-200 mixing lesion
paO2 > 250; CHD unlikely

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51
Q

S1 and S2

A

S1 = MV or TV
S2 = AV or PV

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52
Q

widely split S1

A

RBBB or Ebstein

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53
Q

widely split, fixed S2

A

volume overload (ASD, PAPVR)

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54
Q

single S2

A

PPHN, one semilunar valve (PA, AA, HLHS, TA)
P2 not heard in TGA, ToF or severe PS

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55
Q

paradoxically split S2

A

AV follows PV if LV ejection delayed in severe AS

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56
Q

what size should BP cuff be?

A

width = 2/3 - 3/4 circumference of extremity

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57
Q

how does A line transducer position effect reading

A

too low - elevates BP
too high - lowers BP

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58
Q

Mean BP =

A

= DBP + 1/3 (SBP + DBP)

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59
Q

what structural causes of CHF present at birth

A

HLHS + restrictve AS
severe TR or PR
large AV fistula

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60
Q

what structural causes of CHF present at DOL1

A

obstructive TAPVR
TGA
severe Ebsteins

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61
Q

what structural causes of CHF present at week 1-4

A

critical AS or PS
preductal CoA

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62
Q

NO MoA

A

normally made by L-arginine by NOS in endothelial cells

  1. activates guanylyl cyclase
  2. converts GTP to cGMP
  3. vascular smooth muscle relaxation and decreased vascular tone

remaining goes to blood, binds Hb and becomes oxidized to NO2 or NO3 which are inactive (no systemic hypotension)

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63
Q

what percent of those with CHD have other anomalies?

A

25%

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64
Q

recurrence risk of CHD

A

1 child: 2-5%
2 children: 5-10%
mother: 6.7%
father: 1.5 -3%

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65
Q

MC cyanotic CHD beyond infancy

A

TOF

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66
Q

MC cyanotic CHD presenting in 1st week

A
  1. TGA
  2. HLHS
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67
Q

MCC of mortality in 1st week

A

HLHS

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68
Q

where is the aortic valve in L TGA

A
  • anterior and left of PV
  • in dTGA: anterior and right
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69
Q

EKG findings on dTGA and LTGA

A

dTGA = right QRS (90-160), RVH

LTGA = absence of Q waves in I, V5, V6, may have AV block

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70
Q

what percent of TOF have right AoA?

A

25%

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71
Q

the VSD in TOF is mostly what type?

A

perimembranous

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72
Q

during the Tet spell, what happens to the murmur?

A

decreases intensity because of decreased flow across PV and more across VSD

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73
Q

management of Tet spell

A
  • knee to chest
  • morphine: break agitation
  • HCO3: correct acidosis and decrease respiratory drive
  • vasoconstrictors: increase SVR
    oxygen to decrease PVR
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74
Q

QRS in pulmonary atresia and tricuspid atresia

A

TA = superior
PA = normal

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75
Q

truncus types

A

I (50-70%) = MPA from truncus then splits
II (30-50%) = each PA comes off posteriorly from truncus
III (10%) = each PA comes off laterally from truncus

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76
Q

EKG in Ebsteins

A

RBBB, RAE
WPW in 20%
occasional 1st deg AV block

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77
Q

TAPVR types

A

supracardiac = PV to vertical vein to innominate, azygous or SVC

cardiac = PV to RA directly or indirectly via coronary sinus to RA

infracardiac = PV cross diaphragm and drain into portal vein or hepativ vein or IVC

mixed

78
Q

heart size in chest XR in obstructed vs nonobstructed TAPVR

A

obstructed = small or normal bc decreased blood flow to heart

nonobstructed = increased, snowman

79
Q

Most common cause of CHF after second week

A

VSD

80
Q

distribution of types of VSD

A

70% perimembranous
25% muscular
5-7% supracristal, conal, subpulmonary
5-8% posterior and inferior to perimembranous

81
Q

timing of functional and anatomic closure of PDA

A

functional 90% by 48 hours
anatomic 2-4 weeks

82
Q

constrictors of PDA

A

PGFa
acetylcholine
bradykinin
oxygen

83
Q

dilators of PDA

A

PGE1
PGI2 (prostacyclin)
hypoxemia
acidosis

84
Q

PS vs AS which is more successfully treated with balloon?

A

PS

85
Q

ALCAPA

A

left main coronary from PA

  1. elevated PVR, adequate perfusion of ALCAPA
  2. decreased PVR, not enough blood flow; rely on collaterals
  3. asymptomatic reliance on collaterals
  4. as PVR continues to drop, less into collaterals –> myocardial ischemia (anterolateral distribution)
86
Q

egg on a string

A

d TGA

87
Q

snowman

A

supracardiac TAPVR

88
Q

extremely large heart with decreased PBF

A

ebsteins

89
Q

small heart with increased PBF

A

obstructive TAPVR

90
Q

peaked P wave

A

RAE (especially lead II)

91
Q

increased P wave duration

A

LAE

92
Q

absent Q wave in v5 and v6

A

L TGA, single ventricle, L BBB

93
Q

deep Q wave in left leads

A

LVH, biventricular hypertrophy
myocarditis
restrictive cardiomyopathy

94
Q

deep and wide Q wave

A

infarction
hypertrophic cardiomyopathy

95
Q

deep Q waves in I, aVL, V4, V5 and v6

A

ALCAPA

96
Q

R QRS deviation

A

neonates until 1 month
TOF

97
Q

when do you see normal QRS in infants

A

after 1 month age
PA with intact septum

98
Q

L superior QRS

A

TA
AVC

99
Q

EKG leads corresponding to part of heart

A
100
Q

EKG with corresponding locations

A
101
Q

which presents later in pregnancy flutter or SVT?

A

atrial flutter

102
Q

which is more likely associated with hydrops; flutter or SVT?

A

SVT

103
Q

treatment of SVT in utero

A
  1. digoxin
  2. if sick amiodarone or if less ill flecainide
104
Q

treatment of flutter in utero

A
  1. digoxin
  2. sotalol

NOT amiodarone

105
Q

treatment of EAT

A

betablocker if severe and prolonged

does not response to cardioversion or adenosine

106
Q

treatment of MAT

A

amiodarone

does not response to cardioversion or adenosine

107
Q

treatment of JET

A

normalize electrolytes
minimize inotropes
atrial pacing
amio
procainamide
+/- cooling

108
Q

neonatal treatment of atrial flutter

A

stable: block atrial (digoxin) and ventricular rates

unstable: DC synchronized cardioversion or esophageal pacing

109
Q

neonatal treatment of atrial fibrillation

A

DC defibrillation
digoxin to slow rate

110
Q

treatment of orthodromic tachycardia

A

vagal
adenosine

111
Q

treatment of antidromic tachycardia

A

vagal
adenosine

112
Q

treatment of AVnRT

A

vagal and adenosine

113
Q

differences between orthodromic, antidromic and AVnRT

A

orthodromic - MC; down AV node up accessory; p wave retrograde

antidromic - down accessory and returns backwards to atria, may have delta wave

AVnRT - p wave may not be visible bc atria and ventricle depolarize same time; down slow path; up fast path

114
Q

treatment of Vtach

A

stable - amiodarone, lidocaine or beta blocker
unstable - DC cardioversion

115
Q

treatment of Vfib

A

DC defibrillation, lidocaine, amiodarone

116
Q

MoA adenosine

A

blocks AV node
dc SVT
unmask atrial flutter

117
Q

MoA amiodarone

A

K+ channel blocker

118
Q

MoA digoxin

A

AV block

119
Q

MoA flecainide

A

Na channel block

120
Q

MoA propanalol

A

beta blocker

121
Q

flecainide toxicity

A

renal, levels increase when NPO
milk affects absorption

122
Q

which med should you not put in fridge because it precipitates

A

flecainide

123
Q

MoA sotalol

A

K + channel blocker
less effective than amiodarone
some beta block

124
Q

MoA verapamil

A

CCB - slows AV node conduction

125
Q

which med causes sudden death if used < 12 months

A

verapamil

126
Q

WPW aspects

A
  1. prolonged QRS
  2. shortened PR
  3. slurring QRS = delta wave
127
Q

WPW a.w

A

ebstein
ltga
but also in structurally normal hearts

128
Q

what causes WPW

A

secondary to electrical pathway between atrium and ventricle bypassing AV node; SVT

129
Q

first deg AV block

A

PR prolongation

130
Q

treatment of first deg AV block

A

not needed

131
Q

second deg AV block type 1

A

wenckebach
increasing PR until drop

132
Q

treatment of second deg AV block type 1

A

not needed

133
Q

second deg AV block type II

A

dropped beats; no change in PR interval

134
Q

treatment of second deg AV block type II

A

pacemaker

135
Q

third deg AV block

A

dissociation of A and V rates

136
Q

third deg AV block a/w

A

LTGA, AVC
lupus
cardiac surgery

137
Q

treatment of AV block

A

asymptomatic - no treatment
symptomatic or poor risk factors - pacemaker

138
Q

RBBB on EKG

A

right axis deviation
rSR’, prolonged QRS
slurring of S in I, v5 and V6

139
Q

RBBB a/w

A

Ebstein
cardiac surgery

140
Q

LBBB on EKG

A

left axis deviation
prolonged QRS
loss of Q waves in I, V5, V6
wide S in V1 and V2

141
Q

QTc =

A

= QT / sqrt(RR interval)

142
Q

causes of prolonged QT

A

hypocalcemia
myocarditis
long QT syndrome

143
Q

what is first line treatment of prolonged QT

A

propanolol; then pacemaker

144
Q

what is sick sinus syndrome

A

SA node injury after surgery
slow irregular sinus rate a/w a.flutter and a.fib

145
Q

when should you use infant size pads in cardioversion/defibrillation?

A

until 1 year of age or 10 kg

146
Q

cardioversion dose

A

0.25-0.5 J/kg
max 2 J/kg

147
Q

defibrillation dose

A

1-2J/kg with max 4 J/kg

148
Q

hypo and hypercalcemia on EKG

A

hypercalcemia = shortened QRS
hypocalcemia = prolonged

149
Q

hyperkalemia by dose

A

> 6 tall peak T, short QT, depressed ST

> 7.5 prolonged PR, wide QRS, flat P

> 9 absent P, sinusoidal QRS, asystole and afibrillation

150
Q

hypokalemia by dose

A

< 2.5 wide QRS, depressed ST, biphasic T + visible U wave

< 1 prominent U wave, flat T wave, prolonged PR and SA block

151
Q

what is M mode on echo used for?

A
  1. size of chambers, ventricular wall thickness
  2. LV function
  3. valve movement and septal wall motion
  4. pericardial fluid
152
Q

shortening fraction % =

A

{LV diastolic dimension - LV systolic dimension}/LV diastolic dimension x 100

normal = 28-40%

153
Q

parasternal view good for:

A

long axis = left side (MV, AV, LV, LA, ascending aorta)l relationship to interventricular septum

short axis: PDA, semilunar valves, MV, papillary muscles, PA, RVOT, coronaries, LV

154
Q

apical view good for:

A

AVC; all 4 chambers

155
Q

subcostal view good for:

A

ASD

156
Q

suprasternal view good for:

A

aortic arch

157
Q

timing of fetal echo methods

A

transabdominal 18-32
transvaginal as early as 10 weeks

158
Q

a1 location and effect

A

arterial and venous smooth muscles and cardiomyocytes

Vasoconstriction, increases contractility
gluconeogenesis decreases insulin release

159
Q

a2 location and effect

A

sympathetic, CNS

blocks NE release, inhibits sympathetic output
vascular smooth muscle relaxation

160
Q

b1

A

SA node, atrial and ventricular muscle
conduction cells

increase HR, conduction velocity, contractility, renin release

161
Q

B2

A

arterial and venous smooth muscles, bronchial smooth muscles

smooth muscle relaxation
bronchial relaxation
increases HR and contractility
decreases intestinal motility and tone
induces glycogenolysis
increases insulin secretion

162
Q

MoA milrinone

A

phosphodiesterase 3 inhibitor - inhibits cAMP breakdown

163
Q

MoA digoxin

A

inhibits NaK ATPase leading to Ca influx

164
Q

BT shunt

A

R subclavian to RPA

165
Q

Fontan

A

SVC and IVC to PA

166
Q

Glenn

A

SVC to PA

167
Q

Norwood stage I

A
  1. AS
  2. divide MP; DKS proximal PA to ascending aorta
  3. reconstruction of hypoplastic aorta
  4. BT shunt or Sano
168
Q

Norwood stage II

A

bidirectional Glenn; decrease volume overload on RV; remove shunt + SVC to PA

169
Q

Norwood stage III

A

modified Fontan
both SVC and IVC to PAs

170
Q

Rashkind

A

BAS

171
Q

Rastelli

A

patch VSD + Sano

for dTGA with VSD + PS or DORV

172
Q

primary myocardial substrate used by heart

A

fatty acids

173
Q

mediator of normal pulmonary vascular transition at birth

A

NO

174
Q

MC gene in long QT

A

KCNQ1

175
Q

preferred treatment in hypertrophic cardiomyopathy

A

propanalol or other betablocker like esmolol

176
Q

primary target of CCHD

A

HLHS

177
Q

ALDH1A2

A

retinoic acid production enzyme
a/w TOF

178
Q

major pathway of energy production in hypoxia-ischemia conditions

A

lactate dehydrogenase

179
Q

WPW first line treatment

A

propanolol

180
Q

the reaction involved in FaO by neonatal cardiomyocytes is catalyzed by

A

carnitine palmitoyl transferase

181
Q

what causes widely split S2 in ASD

A

delayed RV depolarization with little change in venous return to RA with inspiration

182
Q

when do endocardial cushions come together to form intracardiac septum?

A

week 8

183
Q

MoA dobutamine

A

b1 agonist > B2, a1

184
Q

MoA dopamine

A

inhibits NaK ATPase and Na/H pump
dopaminergic then beta some alpha at high dose

185
Q

MoA epi

A

beta 1 and 2 > alpha

186
Q

MoA isopreterenol

A

B1 and B2

187
Q

MoA nitroprusside

A

decrease SVR

188
Q

MoA NE

A

a1 > a2 > b1 > b2

189
Q

MCC hypertrophic cardiomyopathy

A

Noonan

190
Q

ductus comes from what arch?

A

L 6th aortic arch

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