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Cardiology Flashcards

1
Q

From what embryologic structure does the heart form?

A

Mesoderm

First system to function in utero

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2
Q

What embryologic structures form the tube of the heart structure and when?

A

Two sheets of mesodermal angiogenic cells (Day 15) –>
Upper sheet enlarges to encircle other sheet (Day 17)–>
Beating initiated in upper tube (Day 20)

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3
Q

How and when does the heart tube structure form ventricles?

A

Tube bends to the right (D-loop) (Day 21)–>
Chambers form (Day 22)–>
Ventricles migrate to side-by-side (Day 28)

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4
Q

How and when does cardiac septation occur?

A

Atrial septum: grows within atria and forms 2 septum (Day 34)

Ventricular septum: Cells near inferior single ventricle grow upward to form septum (Day 38-46)

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5
Q

When is cardiac structure complete?

A

7-8 weeks

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6
Q

Describe the position of the atria relative to the viscera

A

1st letter:
S- solitus

I - inversus

A- ambiguous

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7
Q

Describe the position of the ventricle:

A

2nd letter:
D-loop: right ventricle on right side

L-loop: mirror image

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8
Q

Describe the position of the great arteries:

A

3rd letter:
S- solitus (aorta to right and posterior of pulmonary artery)

I- inversus/mirror image

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9
Q

What are the cardiac designations for:

  • Normal
  • TGA (Right and left)
  • Situs inversus totalis
A

Normal: SDS

D-TGA: SDD (right)

L-TGA: SLL (left)

Situs inversus: ILI

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10
Q

When do cardiac defects occur during embryogenesis?

A

Most by 8 weeks

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11
Q

Cardiac morphogenesis- when does it occur and why?

A

Can occur progressively throughout pregnancy

Occurs due to acquired conditions or decreased blood flow

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12
Q

Where is most blood volume in the fetal heart?

A

Right ventricle

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13
Q

Where is the smallest blood volume in the fetal heart?

A

Right atrium

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14
Q

What percentage of fetal blood volume shunts through the PDA?

A

60%

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15
Q

What percentage of fetal blood flow goes to the lungs?

A

10%

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16
Q

What percentage of fetal blood volume is each of the 4 heart chambers?

A

Right atrium (20-25%)–>

Left atrium (27%)–>

Left ventricle (34%)–>

Right ventricle (65-70%)

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17
Q

Blood from the upper body drains to the ____ ventricle which then supplies the _____ body

A

Right

Lower

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18
Q

Blood from the lower body and placenta drain to the_____ then 1/3 cross the PFO to ___________ and 2/3 supplies the upper body

A

IVC

Cerebral and coronary arteries

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19
Q

The ______ ventricle supplies the majority of cardiac output in the fetus

A

Right

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20
Q

The highest oxygen content in the fetus is in the __________

A

Umbilical veins (70%)

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21
Q

Cardiac output equals

A

Systemic blood pressure/
Total peripheral vascular resistance

OR

HR X Stroke volume

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22
Q

Heart rate or stroke volume have a bigger impact on cardiac output?

A

Heart rate

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23
Q

What 3 things keep the ductus arteriosus open in utero?

A

Prostaglandin 2
Prostacyclin
Thromboxane A2

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24
Q

What medication maintains an open doctor’s arteriosus?

A

Prostaglandin 1

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25
Q

The lowest oxygenation content in the fetus is in the

A

Umbilical artery

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26
Q

Fetal hemoglobin contributes to lower pO2 tolerance by

A

Higher oxygen affinity
Low p50
Left shift in oxyhemoglobin curve (easier to release O2)
Increased hemoglobin levels for increased O2 carrying capacity
Anaerobic metabolism

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27
Q

Calculation of cardiac output:

A

HR X SV

OR

SBP/TPVR

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28
Q

Right ventricle stroke work is roughly equal to _____ left ventricle stroke work

A

1/6

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29
Q

An increased cardiac contraction resulting from increased preload/stretch is described by the

A

Frank Starling principle

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30
Q

Cardiac contractility is increased by

A

Catecholamines

Thyroid hormone

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31
Q

Pulmonary: systemic shunt calculation:

A

sO2 (ao) - sO2 (SVC)/

sO2 (LA or Pulm v) - sO2 (PA)

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32
Q

Pulmonary vascular resistance calculation:

A

P PA- P LA/

P blood flow

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33
Q

Systemic vascular resistance calculation

A

P Ao - P RA/

Sys blood flow

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34
Q

Cyanosis is visible if hemoglobin decreases by

A

3 to 5 g reduced Hgb

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35
Q

What causes differential cyanosis and what is it?

A

Critical coarctation with PDA and increased PVR

Right to shunting causing cyanosis in the lower body more than the upper body

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36
Q

What is reverse differential cyanosis?

A 
Upper body more cyanotic than lower body
Due to TGA with intact septum, associated with pulmonary hypertension, 
interrupted aortic arch, 
or coarctation of the aorta,
          and PDA
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37
Q

PaO2s associated with critical preductal coarctation of the aorta with PDA and increased PVR are

A

Right radial paO2 = 250. ^^^^^

Umbilical artery paO2 = 45. vvvvv

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38
Q

PaO2s associated with TGA with intact ventricular septum, PDA and (PHTN, interrupted aortic arch, or preductal CoA) are

A

Right radial paO2 = 50

Umbilical artery paO2 = 250

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39
Q

PaO2s associated with infradiaphragmatic TAPVR are

A

Umbilical artery paO2 = 90

Umbilical venous paO2 = 250

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40
Q

S1 heart sound represent

A

Closure of mitral and tricuspid valves

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41
Q

A widely split s1 can represent

A

Right bundle branch block

Ebstein’s anomaly

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42
Q

S2 represents

A

Closure of the aortic valve in pulmonary valve

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43
Q

A widely split S2 can represent

A

ASD

PAPVR

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44
Q

A single S2 can represent

A

Pulmonary hypertension

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45
Q

VSD murmur is characterized by

A

Holostystolic murmur beginning with S1 and continuing to S2

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46
Q

A crescendo ejection murmur can represent

A

Stenotic aortic or pulmonic valves

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47
Q

Valvular regurgitation sounds like a

A

Blowing murmur

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48
Q

Diastolic murmurs are _____ and can represent ________

A

Always pathologic

Aortic regurgitation
Pulmonic regurgitation

Tricuspid or mitral stenosis

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49
Q

Continuous murmurs occur with

A 
PDA 
AV fistula 
Venous hum 
Collateral vessels 
Truncus arteriosus 
Aortopulmonary window
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50
Q

Narrow pulse pressure occurs with

A

Pericardial tamponade
Aortic stenosis
Intravascular depletion

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51
Q

Wide pulse pressure occurs with

A 
PDA
Thyrotoxicosis
AV fistula
Aortic regurgitation
Truncus arteriosus
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52
Q

Mean blood pressure is calculated as

A

Diastolic blood pressure + 1/3 ( systolic blood pressure - diastolic blood pressure)

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53
Q

Tachycardia in early compensated shock is due to

A

Catecholamine release

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54
Q

In neonates the most common type of shock is

A

Hypovolemic shock

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55
Q

Kerley B lines indicate

A

Congestive heart failure, linear densities in lungs due to interstitial edema

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56
Q

Recurrence of congenital heart disease in a subsequent sibling is

A

2-5%

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57
Q

Risk of congenital heart disease in a child to a mother with Congenital heart disease is
If the father had CHD

A

~7%

~2%

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58
Q

Most inheritable type of congenital heart defects are

A

Left-sided obstructive lesions

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59
Q

The most common CHD is ______ at ____ percentage

A

VSD

16%

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60
Q

Most common cyanotic heart disease presenting in the first week of life is _____ at the _____ percentages

A

TGA

5-10%

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61
Q

Cyanotic heart disease most likely to present in the first week of life and cause mortality is

A

HLHS

2%

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62
Q

Most common cyanotic heart disease beyond infancy is

A

TOF

8-10%

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63
Q

Name the cyanotic heart disease listed in the 5T/DO/ESP

A 
Truncus arteriosus
Transposition of the great arteries
Tricuspid atresia
Tetralogy of Fallot
TAPVR
DORV
Ebstein's anomaly
Single ventricle
Pulmonary atresia
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64
Q

CHF related to congenital heart defects tend to be ______ type of defects

A

Obstructive

HLHS with restrictive atrial defect
Severe TR or PR
Large systemic aortovenous fistula
Obstructed TAPVR
TGA
Ebstein's anomaly
Critical AS or PS
Preductal CoA
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65
Q

TGA is more common in

A

Males

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66
Q

About 50% of TGA will also be associated with a

A

VSD

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67
Q

The more common form of TGA has the aortic valve positioned

A

Interior, inferior, and to the right of the pulmonary valve

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68
Q

LTGA is also known as

A

Congenitally corrected TGA

Aortic valve is anterior and left of the pulmonary valve

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69
Q

Which type of TGA is most likely to have severe cyanosis at birth?

A

D-TGA

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70
Q

Which congenital heart defect has the appearance of egg on a string on x-ray and no murmur?

A

TGA

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71
Q

EKG in TGA tends to show

A

Right QRS axis
Right ventricular hypertrophy
Right atrial hypertrophy

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72
Q

Immediate management of TGA includes

A

PGE1
Rashkind (balloon septostomy)
Treat CHF

Arterial switch (Jatene) and VSD/PS repairs at older age

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73
Q

25% of tetralogy of fallot have

A

Right aortic arch

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74
Q

Four abnormalities associated with tetralogy of fallot are

A

VSD
RVOT
RVH
OAo

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75
Q

What distinguishes a pink tet from a blue tet?

A

Severity of right ventricular outflow tract obstruction

Decreased pulmonary blood flow, decrease pulmonary veins return to left atrium

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76
Q

How does increased pulmonary vascular resistance and decreased systemic vascular resistance lead to a tet spell?

A

Changes in pulmonary and systemic resistance lead to increase right to left shunting which causes decreased pulmonary blood flow–>
Decreased blood flow through the pulmonary arteries decreases the PO2 causing acidosis and increased carbon dioxide

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77
Q

What methods counteract a tet spell?

A 
Knees to chest
Morphine
Bicarb
Vasoconstrictors
Propranolol or esmolol
Fluid bolus
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78
Q

Surgical management of TOF involves

A

Blalock Taussig shunt

VSD closure and RVOT obstruction repair

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79
Q

Survival with pulmonary atresia is dependent on the presence of

A

ASD or PFO with PDA

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80
Q

RVH occurs in pulmonary Atresia due to

A

RVOT

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81
Q

EKG for pulmonary Atresia will show

A

Normal QRS
LVH» RVH
RAH 70%

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82
Q

In addition to PGE, PA is treated with

A

Angiography to determine anatomy

BT shunt +/-RVOT reconstruction (if not RV dependent)

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83
Q

Truncus arteriosus is associated with

A

DiGeorge syndrome

TA’GD

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84
Q

Truncus arteriosus increases the risk of

A

Right aortic arch

Interrupted aortic arch

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85
Q

What other defect is always associated with the truncus archeriosis?

A

VSD

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86
Q

Which type of TA is most common and has the main pulmonary artery branch from the truncus then split?

A

Type 1, 50-70%

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87
Q

What is the difference between type 2 and 3 truncus arteriosus?

A

Type 2 PA branches posteriorly

Type 3 PA branches laterally, least common type

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88
Q

Truncus arteriosus is marked clinically by

A 
Cyanosis
CHF
Wide pulse pressure
Bounding pulses
Pansystolic murmur
Single S2
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89
Q

Truncus arteriosus is associated with right aortic arch ____%

A

50%

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90
Q

Surgical repair plan for truncus arteriosus is

A

Early, complete repair

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91
Q

Tricuspid Atresia without a _____ has a worse severity.

A

VSD- poor RV development, ductal dependent

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92
Q

30% of tricuspid Atresia also have

A

Great arteries transposed

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93
Q

Clinical findings in tricuspid Atresia are

A 
Severe cyanosis
CHF
Systolic murmur and single S2
\+/- Pulmonary vascular markings if PBF
Left superior QRS
LV>>RV
Arterial hypertrophy
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94
Q

Following PGE1, surgical plan for tricuspid Atresia is

A

Rashkind (balloon septostomy)

PA banding if ++ PBF

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95
Q

The Congenital heart defect associated with maternal lithium use

A

Ebstein’s anomaly

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96
Q

A heart defect with an enlarged right atrium, displaced tricuspid valve, small right ventricle, and 80% with an ASD is

A

Ebstein’s anomaly

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97
Q

20% of ebstein’s anomaly have this arrhythmia

A

WPW

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98
Q

The high mortality of ebstein’s anomaly is attempted treatment with:

A

PGE1
Treat CHF
Airway stabilization
If severe symptoms, surgical intervention

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99
Q

A non-cardiac complication of ebstein’s anomaly is

A

Airway compromise due to dramatic cardiomegaly

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100
Q

Asplenia or polysplenia are increased in which congenital heart defect?

A

Single ventricle

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101
Q

Single ventricle usually looks like

A

Single left ventricle with left transposition (Aorta comes off small leftward RV)
Absent ventricular septum (complete mixing)

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102
Q

Symptoms of single ventricle dependent on:

A

PBF-

  • Increased: CHF, mild cyanosis, enlarged heart/PVM
  • Decreased: mod-severe cyanosis, mild CHF, normal heart size/PVM
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103
Q

Surgical treatments for single ventricle are

A

CHF-> PA banding

Palliative -> Glenn procedure
Definitive -> Fontan procedure

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104
Q

TAPVR is defined as

A

Pulmonary veins drain to RA

PV can be supracardiac, cardiac, or infracardiac

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105
Q

PV draining to coronary sinus in TAPVR is

A

Cardiac

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106
Q

PV draining to portal vein or IVC in TAPVR is

A

Infracardiac

*Most likely to be obstructive

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107
Q

The TAPVR type with the worst severity is

A

Infracardiac/obstructive

Surgical repair urgently

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108
Q

Treating TAPVR with PGE1 can cause

A

worsened pulmonary congestion/edema

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109
Q

If the aorta and pulmonary artery both come from the RV, this is ________.

The other anomalies associated with DORV are

A

Double outlet right ventricle

VSD
Great arteries can be side by side or transposed, +/- PS

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110
Q

Clinical presentation in DORV is dependent on

A

Size/type of VSD
+/- PS
EKG: RVH

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111
Q

Arrhythmia associated with DORV is

A

First degree heart block

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112
Q

What kind of surgical repair is indicated for DORV?

A

Depends on severity of VSD and PS

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113
Q

What is the most common cause of CHF after the 2nd week of life?

A

VSD

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114
Q

Most common type of VSD is

A

Perimembranous (70%)

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115
Q

Inlet and outlet VSD’s each make up ____% of all VSD’s.

A

~7%

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116
Q

Describe the presentation of a mod -large VSD

A

Clinically silent for 2-3 days, then CHF, poor feeding, respiratory distress, then harsh holostystolic murmur

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117
Q

Definitive surgery for VSD is indicated when

A

Significant left to right shunt (2:1)
Severe CHF
Poor growth
Increased pulmonary artery pressure

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118
Q

Second most common cardiac defect is

A

ASD (6-11%)

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119
Q

ASD is more common in

A

Females

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120
Q

RV overload occurs in ASD because

A

Left to right shunting due to increased RV&raquo_space; LV compliance

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121
Q

In contrast to VSD, EKG in ASD shows

A

RVH, RAD

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122
Q

Surgery in ASD is

A

At 2-5 years, definitive closure if RV overload

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123
Q

Molecules that prompt PDA closure

A

PGFa, acetylcholine, bradykinin, oxygen

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124
Q

Physiology of a PDA mimics a

A

VSD

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125
Q

A continuous or systolic machinery murmur suggests a

A

PDA

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126
Q

Complete AV canal defect is associated with

A

Trisomy 21

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127
Q

Associated defects with AV canal defects are

A

PDA and TOF (10%)

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128
Q

Primum ASD, inlet VSD, and common AV valve is a

A

Complete AV canal defect

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129
Q

Complete and partial AV canal defects are differentiated by

A

Partial:
+/- cleft in MV
No VSD
Normal TV

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130
Q

Symptoms in AV canal defects are

A

Dependent on ASD/VSD contributions

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131
Q

AV canal murmur is

A

Systolic due to VSD

+/- apical diastolic murmur, +/- gallop

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132
Q

Surgical correction of AV canal defect involves

A

ASD/VSD closure

AV valve separation

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133
Q

Partial anomalous pulmonary venous return is

A

One or more PV drain into RA

RIGHT»> LEFT (2:1)

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134
Q

In PAPVR, left pulmonary veins most often drain

A

To the innominate vein

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135
Q

Clinically PAPVR mimics

A

ASD

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136
Q

Pulmonary congestion in PAPVR is dependent on

A

Number of anomalous veins
ASD qualities
PVR

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137
Q

Similar to ASD, PAPVR clinically has

A

ASD murmur
RVH, RAE
increased PVM
EKG: RVH, RV conduction delay

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138
Q

Does PAPVR need surgical correction?

A

Only for clinically significant left to right shunt

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139
Q

Obstructive cardiac lesions are

A

Coarctation of the aorta
Pulmonic stenosis
Aortic stenosis
Infracardiac TAPVR

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140
Q

Coarctation of the Aorta of associated with

A

Turners syndrome (30% of Turner’s patients)

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141
Q

Cardiac defects associated with CoA

A

Bicuspid aortic valve

VSD

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142
Q

The form of CoA with the worst severity is

A

Preductal

Presents after birth
Differential cyanosis
Shock following PDA closure
Associated with other defects

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143
Q

The CoA most likely to have collateral vessels:

A

Juxtaductal and postductal

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144
Q

Rib notching in CoA is a sign of

A

Collateral vessels

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145
Q

Juxta- and post- ductal CoA commonly presents with

A

Hypertension or BP gradient

146
Q

CoA murmur is

A

Systolic rejection at left interscapular area

+/- AR bicuspid valve murmur

147
Q

CoA surgery involves

A

End to end anastomosis
+/- balloon angioplasty

Surgery often followed by hypertension

148
Q

Pulmonic stenosis and aortic stenosis are each approximately ___% of CHD

A

5%

149
Q

_________ stenosis is more common in males.

A

Aortic (4:1)

150
Q

Williams syndrome is associated with ________ stenosis

A

Both pulmonic and aortic stenosis, supravalvular

151
Q

Subvalvular pulmonic stenosis is associated with ______

A

TOF

152
Q

Bicuspid aortic valve is associated with ______ ________ stenosis

A

Valvular aortic stenosis

153
Q

Valvular positioning of pulmonic and aortic stenosis can result in

A

Post-stenotic dilation

154
Q

If mild, both pulmonic and aortic stenosis present

A 
Asymptomatic
No cyanosis
Election click
Split S2
Normal heart size
155
Q

Severe pulmonic and aortic stenosis both require

A

PGE1

balloon valvuloplasty

156
Q

Pulmonic stenosis murmur

A

ULSB Systolic ejection with radiation to back

Grade proportional to stenosis

157
Q

Aortic stenosis murmur

A

URSB, left midsternal systolic ejection murmur, radiation to LLSB
Grade is INDEPENDENT of degree of stenosis
Increased stenosis–> 2nd R intercostal thrill

158
Q 
Aortic valve regurgitation:
Phys
Presentation
CXR/EKG
Management
A

Incr preload/SV-> aorta dilation
Wide pulse pressure, bounding pulses. Early diastolic murmur.
LVE, dilated Aorta. ST depression, T wave inversion
Treat CHF, valve repair

159
Q 
Mitral valve regurgitation
Phys
Presentation
CXR/EKG
Management
A

LA/LV overload–> hypertrophy
Systolic blowing & diastolic murmurs at apex
Increased LV
Treat CHF, valvuloplasty vs MV replacement

160
Q 
Tricuspid valve regurgitation
Phys
Presentation
CXR/EKG
Management
A 
RA/RV overload
RV dysfunction+/- cyanosis if R-L
Systolic blowing murmur, diastolic murmur at LLSB
Hepatic congestion
RAH
Conservative, surgery only if necessary
161
Q

HLHS is most common in

A

Males

162
Q

The second most common CHD with cyanosis in the guest week of life is

A

HLHS

163
Q

Aortic or mitral valve atresia/stenosis, hypoplastic LV and aortic arch hypoplasia is

A

HLHS

164
Q

Patients with HLHS shows symptoms when

A

The PDA closes–>

CHF, metabolic acidosis, shock

165
Q

HLHS EKG/CXR show

A

+PVM, cardiomegaly, RVH, RAD

166
Q

Management of HLHS

A

PGE1, inotropes->
balloon septostomy –>
Norwood—>
heart transplant if needed

167
Q

Hypertrophic cardiomyopathy is associated with

A

Pompe
Hurler
Noonan
IDM

168
Q

Dilated cardiomyopathy is associated with

A

Myocarditis
Carnitine deficiency
Abnormal perfusion
Post-arrhythmia

169
Q

Cardiac dysfunction in dilated cardiomyopathy is due to

A

Decreased ventricular function due to overstretch/dilation of LA/LV

170
Q

Cardiomyopathy with CHF and MR murmur is

A

Dilated cardiomyopathy

171
Q

The least common form of cardiomyopathy is

A

Restrictive

172
Q

Marked arterial»ventricular dilation with abnormal ventricular filling is

A

Restrictive cardiomyopathy

173
Q

EKG in HCM shows

A

LVH, ST and T wave changes

Possible arrhythmia

174
Q

If obstructive, HCM should be treated with

A

Preload
Myomectomy
Avoid digoxin, inotropes

175
Q

An S4 gallop is seen in

A

Dilated cardiomyopathy

176
Q

EKG In dilated cardiomyopathy shows

A

Increased LV, ST and T wave changes
Q waves
possible arrhythmia

177
Q

Dilated cardiomyopathy should be treated with

A

Vasodilators
Treat CHF
Possible anticoagulation
Possible heart transplant

178
Q

Restrictive cardiomyopathy can mimic

A

Pulmonary hypertension

179
Q

Persistent pulmonary overcirculation, pulmonary vasculature remodeling, increased PVR and RA/RV enlargement are due to

A

Eisenmengers complex- progression of untreated CHD

180
Q

Treatment of eisenmengers complex includes

A

Nifedipine
Prostacyclin
Nitric oxide
Lung transplant

181
Q

Acquired pulmonary vasoconstriction leading to RVH and RV dysfunction that results from severe lung disease is

A

Cor pulmonale

182
Q

Although irreversible, Cor pulmonale is treated with

A

Addressing underlying disease, diuretics, pulmonary vasodilators, oxygen

183
Q

Pulsus paradoxus from rapid fluid accumulation is

A

Pericardial effusion–> cardiac tamponade

184
Q

Pericardial effusion can be caused by

A

Pericarditis
Severe anemia/CHF
Post cardiac surgery
CVL leakage

185
Q

Treatment of pericardial effusion

A

Pericardiocentesis

Treat underlying disease

186
Q

Left coronary artery originating from pulmonary artery is

A

Anomalous origin of the LCA from the PA (ALCAPA)

187
Q

4 stages of ALCAPA are marked by

A

1- elevated PVR, adequate perfusion

2- decreased PVR and ALCA flow, increased dependence on collaterals

3- asymptomatic phase, collaterals maintaining perfusion

4- decrease PVR-> decrease collateral flow to ALCA (pulmonary-coronary steal)–> LV ischemia, LAD infarction, pulmonary congestion

188
Q

Clinical presentation of ALCAPA is

A 
Onset 2-3 months
Respiratory distress
Feeding intolerance
FTT
Transient ischemia: pallor, paroxysmal crying, diaphoresis
189
Q

When ALCAPA reaches stage 4 (CHF), EKG shows

A

Deep Q waves (I, aVL, v4, v5, v6)

ST elevations v4-6

190
Q

Diagnosis and treatment of ALCAPA include

A

EKG (showing infarction)
Echo with Doppler
Cardiac Cath if echo non-confirmatory (incr Pulm:syst blood flow)
ALCA anastamosis to aorta

191
Q

Prognosis of ALCAPA is

A

Dependent on early intervention before significant myocardial injury
May require transplant
High mortality of undiagnosed

192
Q

In general, in utero cardiac tumors can cause

A

Hydrops
Fetal arrhythmia

Can be asymptomatic

193
Q

The most common cardiac tumor is

A

Rhabdomyoma

194
Q

Qualities and treatment of rhabdomyomas

A

Usually multiple
Commonly involve ventricle and septum
Associated with tuberous sclerosis
Surgery if outflow obstruction

195
Q

A well circumscribed, fibrous single cardiac tumor is

A

Fibroma

Most in LV

196
Q

A cardiac tumor found in adulthood in the LA that can cause inflow obstruction

A

Myxoma

197
Q

A rare cardiac tumor of cardiac myocytes is

A

Sarcoma

198
Q

An intrapericardial tumor that can cause pericardial effusion is

A

Teratoma

199
Q

The cardiac malformations associated with asplenia are

A

Always severe

200
Q

Bilateral ______ sidedness is associated with asplenia.

A

Right

201
Q

Bilateral left sidedness and less severe cardiac malformations are associated with

A

Polysplenia

202
Q

TAPVR, bilateral SVC, AVC, TGA, PS/PA, single ventricle, dextrocardia are associated with both asplenia and polysplenia, but ________ are associated specifically with asplenia.

A

Aorta/IVC juxtaposition (100%)

203
Q

Non cardiac sequelae of asplenia are

A 
2 right lungs, gallbladders
Malrotation
Howell-Jolly & Heinz bodies
Strep pneumo
Cyanosis

Poor prognosis

204
Q

Non cardiac sequelae of polysplenia are

A

2 left lungs
Biliary atresia
Malrotation
Cyanosis

Poor prognosis

205
Q

Fibromuscular septum divining the LA to two compartments is

A

Cor triatriatum

206
Q

Cor triatriatum presents

A 
Decreased peripheral pulses
Tachypnea
FTT
pulmonary edema
Loud P2
Increased PVM
EKG: RAD, RVH
207
Q

Treatment of Cor triatriatum

A

Treat pulmonary edema

Surgery if necessary

208
Q

Cyanide heart disease more prone to pulmonary over circulation are

A

TAPVR
HLHS
TGA/VSD
Truncus arteriosus

209
Q

Chest x-ray finding of a boot shaped heart is concerning for

A

Tetralogy of Fallot

210
Q

Chest x-ray finding of an egg on a string is concerning for

A

D-TGA

211
Q

Chest x-ray finding of a snowman shaped heart is concerning for

A

TAPVR, supracardiac

212
Q

Chest x-ray finding of an extremely large heart with decreased pulmonary markings is

A

Ebstein’s anomaly

213
Q

Chest x-ray findings of a small heart with increased pulmonary markings is

A

Obstructive TAPVR

214
Q

Chest x-ray findings concerning for right aortic arch with increased pulmonary markings is

A

Truncus arteriosus

215
Q

Chest x-ray findings concerning for right aortic arch with decreased pulmonary markings is

A

Tetralogy of Fallot

216
Q

QTc calculation

A

QT/ √RR interval

217
Q

In infants over 6 months, normal QT is

A

<0.45s

218
Q

RV hypertrophy on EKG is

A

V1: increased R, persistent upright T, increased R/S ratio, possible Q wave

219
Q

LV hypertrophy on EKG is

A

V6: increased R, Q wave (+v5), peaked T waves, increased R/S ratio

220
Q

Neonates <1 months and those with TOF have an EKG axis

A

+90- +/- 180°

221
Q

Infants with tricuspid Atresia or AV canal have an EKG axis

A

0- -90°

222
Q

Infants older than 1 month or with PA with intact septum have any EKG axis

A

0- +90°

223
Q

Upright T wave in V1 after 72h suggests

A

RVH

224
Q

Normally, p wave is ______° and QRS/T are ________°

A

0-90°

100-150°

225
Q

Arrhythmia affect ___% of fetuses

A

1-2%

226
Q

Fetal magnetocardiography (FMCG) increases into about arrhythmias with

A

Observation of QRS and QT interval, beat variability, and presence of T waves

227
Q

Most tachyarrhythmias are

A

SVT (70-80%)

228
Q

SVT typically presents at _____ weeks

A

28-32

229
Q

Factors that determine perversion to groups in SVT

A

Prematurity and duration of SVT

230
Q

Top 3 treatments for fetal SVT:

A

Digoxin

Amiodarone

Procainamide/flecainide/sotalol

231
Q

Side effect of procainamide for fetal SVT

A

Can induce contractions

232
Q

Flecainide and sotalol are limited to 2nd line treatment for SVT due to increased

A

Mortality

7-15% flecainide
30% sotalol

233
Q

For tachyarrhythmias, a treatment that works in SVT but not Atrial flutter is

A

Amiodarone

234
Q

Both tachyarrhythmias are associated with an increased risk of

A

Necrotizing enterocolitis

235
Q

Cardiac change associated with maternal thyrotoxicosis

A

Sinus tachycardia

236
Q

AV block is associated with ______ and presents at ___ weeks

A

Maternal SSA/SSB antibodies

Any gestational age

237
Q

AV block with maternal antibodies is at risk for

A 
Needing cardiac pacing at birth
Cardiomyopathy b(30%)
238
Q

AV block with a poorer prognosis has

A

No maternal antibodies
Additional cardiac defects
Higher risk for hydrops/CHF/demise
+/- a-/poly- splenia

239
Q

There is an increased risk of SVT in the first month of life if the fetus has

A

Fetal ectopy

240
Q

PACs are associated with

A

Hyperthyroidism
CHD
Cardiomyopathy
Central line misplacement

241
Q

PVC’s can be caused by

A 
Digoxin toxicity
Infection
Electrolyte abnormalities
Hypoxemia
Acidosis
CHD
Aminophylline/caffeine
Myocarditis
242
Q

Premature junctional contractions

A

Lack p waves with normal QRS

243
Q

WPW, atrial flutter, atrial fibrillation, SVT, and ventricular tachycardia are examples of ______, the most common type of tachyarrhythmia.

A

Reentrant tachycardia

244
Q

Reentrant tachycardia can be treated with

A

DC cardioversion

245
Q

Junctional ectopic tachycardia, ectopic atrial tachycardia and ventricular tachycardia are _______ tachyarrhythmia.

A

Abnormal automatic focus

Typically refractory to DC conversion

246
Q

Abnormal p waves with atrial ectopic focus and rapid rate is

A

Ectopic atrial tachycardia

Treated with beta blocker/antiarrhythmic

247
Q

Junctional ectopic tachycardia happens most often _______ with EKG __________

A

Post operatively

Ventricular rate faster than atrial rate

248
Q

Junctional ectopic tachycardia happens most often _______ with EKG __________

A

Post operatively

Ventricular rate faster than atrial rate

249
Q

Junctional ectopic tachycardia is treated with

A

Normalize electrolytes
Limit inotropes
Arterial pacing+/- amiodarone, procainamide

250
Q

Adenosine or ice given to an infant with atrial flutter causes

A

Allowed HR that can reveal sawtooth pattern

251
Q

Atrial flutter is treated with

A

Digoxin

DC synchronized cardioversion/esophageal pacing if unstable

252
Q

Atrial rate of 360+ bpm is __________ and treated with _____________

A

Atrial fibrillation

DC defibrillation, digoxin

253
Q

Tachycardia with a wide QRS should be assumed to be

A

Ventricular tachycardia

254
Q

Ventricular tachycardia is usually treated with

A

Lidocaine

If unstable, DC cardioversion

255
Q

Causes of ventricular tachycardia

A 
CHD
Electrolyte abnormalities
Hypoxemia
Myocarditis
Cardiac tumors
Digoxin toxicity
Prolonged QT
Cardiomyopathy
256
Q

Rapid irregular rate with abnormal QRS

A

Ventricular fibrillation

257
Q

Causes of ventricular fibrillation

A 
CHD
Prolonged hypoxia
Hyperkalemia
Myocarditis
Medications
Cardiomyopathy
Tumors
258
Q

Prolonged PR is a

A

First degree AV block

259
Q

Increasing PR interval leading to a dropped atrial impulse is

A

second degree AV block
Mobitz I
Wenckebach

260
Q

Abrupt missing atrial beat without change in PR interval is

A

Second degree AV block

Mobitz II

261
Q

Dissociated AV construction with independent ventricular and atrial rates

A

Complete AV block
Third degree AV block

Associated with LTGA, AVC, lupus

262
Q

Outcome of compete heart block

A

Poor prognosis of HR <55, prolonged QT, wife QRS, ventricular dysfunction

pacing required if symptomatic

263
Q

RBBB is associated with

A

Ebstein’s anomaly

264
Q

Prolonged QT interval is ______ and can lead to _______

A

> 0.45s

Ventricular tachycardia, SIDS

265
Q

Treatment for prolonged QT is

A

Propranolol

Pacing if necessary

266
Q

SA node injury after cardiac surgery is

A

Sick sinus syndrome

Can be associated with atrial flutter/fibrillation

267
Q

Cardioversion dosing

A

0.25-0.5j/kg

Max dosing 2j/kg

268
Q

Defibrillation dosing

A

1-2 J/Kg

Max dosing 4j/kg

269
Q

A prolonged QRS with slurring is

A

WPW

270
Q

WPW is associated with

A

form of SVT
Ebstein’s anomaly
L-TGA

271
Q

WPW is treated similarly to

A

SVT

If stable, vagal maneuvers, adenosine, digoxin, propranolol

If unstable, synchronized DC cardioversion

272
Q

Verapamil is contraindicated in infants less than 12 months due to

A

Increased risk of sudden death

273
Q

EKG changes in hypercalcemia are

A

Shortened QT interval

274
Q

EKG changes in hypocalcemia are

A

Prolonged QT interval

275
Q

EKG changes in hyperkalemia

A

Peaked T wave, short QT, depressed ST–>

Prolonged PR, wide QRS, flat P wave–>

Absent P, sinusoidal QRS, systole/ventricular fibrillation

276
Q

EKG changes in hypokalemia

A

Wide QRS, depressed ST, biphasic T-> u wave

–> Flat T, prominent U, prolonged PR, sinoatrial block

277
Q

Shortening fraction calculation

A

LV diastolic dimension- LV systolic dimension/
LV diastolic dimension

X 100

278
Q

On echo, AVC is best viewed

A

By apical view

279
Q

On echo, ASD is best viewed

A

by subcostal view

280
Q

Aortic arch is best seen on echo by

A

Suprasternal notch view

281
Q

Left heart and valves are best seen on echo by

A

Parasternal view

282
Q

Optimal timing of fetal echo is

A

18-32w

Transvaginal can be fine as early as 10 weeks

283
Q

CHD difficult to visualize on fetal echo are

A

CoA,
Minor valve anomalies
VSD
ASD

284
Q

Cardiac A1 receptors are located ______ and cause _______

A

Vascular smooth muscle
Cardiac myocytes

Increase contractility
Vasoconstriction

285
Q

Cardiac a2 receptors are located ________ and cause _________

A

CNS
Sympathetic nerves

Block NE release
Inhibits sympathetic response
Vascular smooth muscle relaxation

286
Q

Cardiac B1 receptors are located _____ and cause ________

A

Sinoatrial node
Cardiac muscle
Conduction cells

Increased HR (SA node)
Increased contractility
287
Q

Mechanism of action of no milrinone/amrinone is

A

Phosphodiesterase inhibitor

Leads to accumulation of cAMP

288
Q

Effects of phosphodiesterase inhibitors are

A

Chronic inotropy
Decreases SVR
Some pulmonary vasodilation

289
Q

cAMP accumulation by phosphodiesterease inhibitors causes

A

Inhibited cAMP breakdown leading to increased calcium cellular entry, increased contractility, relaxation of vascular smooth muscle

290
Q

Mechanism of action of digoxin is

A

Inhibits sodium potassium ATPase pump

Increases calcium influx

291
Q

What are the clinical effects of digoxin

A

Negative chronotropic
Inotropy
Decreased SVR

292
Q

N/K ATPase pump inhibition by digoxin causes

A

Decreased afterload

Anti-arrhythmic via decreased AV conduction

293
Q

Digoxin toxicity can cause

A 
GI symptoms
Bradycardia
Prolonged PR
AV block
Hyperkalemia, hypercalcemia
294
Q

Mechanism of action of dobutamine

A

Acts on beta 1&raquo_space;> beta 2 receptors

295
Q

Clinical effects of dobutamine are

A

Chronotropy
Inotropy
Decreased SVR

296
Q

Dobutamine acts as a

A

Synthetic catecholamine

297
Q

Limited effects on afterload make dobutamine useful in settings of

A

Cardiogenic shock and myocardial dysfunction

298
Q

Mechanism of action of dopamine

A

Endogenous catecholamine
Inhibits N/K ATPase and Na/H pump
Epinephrine and norepinephrine precursor
Promotes endogenous release of norepinephrine

299
Q

Clinical effects of dopamine

A

++ Chronotrope
Inotropy
Dose dependent SVR increase

300
Q

Clinical benefits of dopamine are

A

LOW DOSE: Renal vasculature dilation

MODERATE DOSE: B1 and dopaminergic receptors -> inotropy, ^HR

HIGH DOSE: B1 and A1

301
Q

Mechanism of epinephrine

A

Potent vasopressor

B1, B2&raquo_space; a

302
Q

Clinically effects of epinephrine

A

Strong Chronotropy
Inotropy
Dose dependent SVR increase
Can improve coronary artery perfusion

303
Q

Epinephrine adverse effects include

A

Hypokalemia
Local tissue ischemia
Renal vascular ischemia
Severe hypertension

304
Q

Mechanism of isoproterenol

A

Synthetic catecholamine

B only

305
Q

Clinical effects of isoproterenol

A

+++++ Chronotropy
–> useful for complete heart block

Inotropy
Decreased SVR
Not helpful in shock

306
Q

Effects of nitroprusside

A

Decreased SVR
Vasodilator
Increases intracranial pressure
Can cause cyanide toxicity, tissue necrosis

307
Q

Mechanism of norepinephrine

A

A> B1 > B2

Chronotropy, inotropy
Increases SVR

308
Q

Adverse effects of norepinephrine

A 
Second line to epinephrine
Profound vasoconstriction
Renal vasoconstriction
Hypocalcemia
Hypoglycemia
309
Q

Mechanism of indomethacin

A

Cyclooxygenase inhibitor
Blocks prostaglandin synthesis
60-80% successful PDA closure, 30% relapse

310
Q

Mechanism of prostaglandin

A

Vasodilator, maintains PDA

311
Q

6-15% of patients receiving prostaglandin will have

A

Apnea

312
Q

PGE1 relatively contraindicated in

A

Obstructive TAPVR
HLHS with intact septum
TGA, restrictive septum
Mitral valve Atresia

313
Q

Endocarditis prophylaxis is indicated for

A 
Unrepaired CCHD
Repaired CCHD with prosthetic material 6 months post-op
Incompletely repaired CCHD
Cardiac transplant
Prosthetic valve
Prior bacterial endocarditis
Rheumatic heart disease
HCM
MV prolapse+ regurg
314
Q

Fetal valvuloplasty is offered to prevent HLHS for patients with:

A

Critical AS <26 weeks without progression to LV hypoplasia

315
Q

Fetal valvuloplasty is offered to prevent hypoplastic right ventricle to patients with

A

PA with intact ventricular septum

316
Q

Fetal ASD creation is offered to palliate HLHS to patients with

A

HLHS with intact septum
Or
TGA with intact septum

317
Q

The rashkind procedure is a ________ and is used in

A

Septostomy

D-TGA
Severe MS
HLHS with inadequate mixing

318
Q

The Blalock-taussig procedure creates _________ and is used for

A

Shunt between subclavian artery and ipsilateral pulmonary artery
Increases PBF

TA, PA, TOF with severe PS

319
Q

The Glenn procedure creates _________ and is used for

A

Connection between SVC and PA to increase PBF without RV

TA
Single ventricle with severe PS

320
Q

Mustard, Senning, Rastelli and Jatene are all procedures used for treating

A

D-TGA

321
Q

The mustard procedure creates

A

An intraatrial baffle after atrial septum removed

SVC/IVC -> LA -> LV -> PA

322
Q

Senning procedure differs from the Mustard

A

Because the baffle is made using atrial septum and RA wall instead of pericardium

323
Q

The Rastelli procedure

A

Patches the VSD to decrease deoxygenated blood mixing into aorta.

Used in d-TGA with VSD and PS

324
Q

The procedure to switch the arteries position in d-TGA is the

A

Jatene procedure

325
Q

The procedure to reroute the SVC and IVC to the PA is

A

Fontan

Used in tricuspid Atresia and single ventricle

326
Q

The 3 stages of the Norwood to repair HLHS are

A

1- septostomy, MPA division, hypoplastic aorta repair, shunt to increase PBF

2- Bidirectional Glenn, shunt removed, SVC connected to PA

3- Modified Fontan (SVC/IVC to PA)

327
Q

Syndromes with a >50% likelihood of CHD

A

C- Carpenter and CHARGE

E- Ellis van Creveld

H- Holt-Oram

N- Noonan

T- Tri 13, 18, 21

V- VACTERL

W- Williams

328
Q

Most common CHD in carpenter syndrome

A

VSD, ASD

329
Q

Most common CHD in cat eye syndrome

A

TAPVR

330
Q

Most common CHD in CHARGE

A

TOF

331
Q

Most common CHD in Cornelia-de-Lange

A

VSD

332
Q

Most common CHD in cri du chat

A

Varies

333
Q

Most common CHD in DiGeorge

A

Aortic arch (Truncus arteriosus)

334
Q

Most common CHD in Ehler-Danlos

A

Aortic root dilation, MV prolapse

335
Q

Most common CHD in Ellis van Creveld

A

Common atrium

336
Q

Most common CHD in glycogen storage diseases 2a (Pompe)

A

HCM

337
Q

Most common CHD in Goldenhar

A

VSD, PDA, TOF

338
Q

Most common CHD in Holt-Oram

A

ASD

339
Q

Most common CHD in homocysteinuria

A

Arterial/venous thromboses

340
Q

Most common CHD in Hurler

A

Thickened valves
CAD
HCM

341
Q

Most common CHD in Klinefelter

A

TOF

MV prolapse

342
Q

Most common CHD in Klippel-Feil

A

VSD

343
Q

Most common CHD in Marfan

A

Aortic dilation
Aneurysm
MV prolapse

344
Q

Most common CHD in Meckel-Gruber

A

ASD, VSD

345
Q

Most common CHD in Noonan

A

Dysplastic pulmonary valve

LVH, HCM

346
Q

Most common CHD in Rubenstein -Taybi

A

VSD, ASD

347
Q

Most common CHD in TAR (thrombocytopenia, absent radius)

A

TOF

ASD

348
Q

Most common CHD in trisomy 13

A

VSD/PDA (80-90%)

50% with other anomalies

349
Q

Most common CHD in trisomy 18

A

VSD, PDA, PS, CoA

350
Q

Most common CHD in trisomy 21

A

Complete AVC
VSD
PDA

351
Q

Most common CHD in Turner

A

Bicuspid aortic valve
CoA
AS

352
Q

Most common CHD in VACTERL

A

VSD

TOF/CoA

353
Q

Most common CHD in Williams

A

Supravalvular subaortic stenosis

354
Q

Infectious causes of myocarditis are

A

Coxsackie B

Parvovirus B19

Rubella

355
Q

CHD due to rubella are

A

AS
PS
TOF

356
Q

Maternal medications that can cause VSD are

A 
Ethanol
Hydantoin
Phenytoin
Trimethadione
Valproic acid
357
Q

Maternal medications that can cause ASD are

A 
Ethanol
Hydantoin
Phenytoin
Trimethadione
Valproic acid
358
Q

Maternal medications that can increase risk of HLHS

A

Retinoic acid

Trimethadione

359
Q

Maternal medications that increase risk of pulmonary hypertension

A

Aspirin

SSRI

360
Q

Thalidomide can cause

A

Conotruncal malformations

361
Q

The medication that can cause TGA is

A

Retinoic acid

362
Q

_____ % of mother’s of an infant with complete heart block have lupus

A

30-60%

Neo Boards (15 decks)

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