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Neo Board Review > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Percentage of fetal CO received by placenta

A

45%

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2
Q

Percentage of fetal CO received by lungs

A

7-35%
Less earlier in gestation (7-15% in second trimester)
In third trimester there’s increases pulm vessel growth and PBF ~35%

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3
Q

DA remains patent in utero due to?

A

Prostaglandins E2
Prostacyclin I2
Thromboxane A2

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4
Q

PDA closure after birth - mechanism

A

Higher O2 concentration within ductal tissue
Lower E type prostaglandins because you lose placental production and the increased PBF (lungs metabolize PG)
Bradykinin from lungs at birth further constricts the DA

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5
Q

Cardiac out =

A

CO = HR x SV

CO = SBP/total peripheral vascular resistance

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6
Q

Factors affecting CO

A
  1. Preload (degree of stretch at end of diastole)
  2. Afterload (tension/stress in ventricular wall during ejection)
  3. Contractility (force and velocity of contraction)
  4. HR (regulated by parasympathetic and sympathetic NS as well as hormonal system)

Afterload does not impact CO as much as preload because it does not alter the CO until the BP reaches a critical level

Neonates more dependent on HR than SV

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7
Q

What increases preload

A

Increased blood volume
Increased venous tone
Increased ventricular compliance
Increased atrial contraction
Decreased intrathoracic pressure

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8
Q

Ventricular wall stress =

A

Ventricular wall stress = (ventricular pressure x ventricular radius) / wall thickness

And wall stress is afterload

So increased vascular resistance distally -> increased proximal pressure -> increased wall stress aka afterload
So ventricular dilation -> increased radius -> increased wall stress aka afterload
So hypertrophied wall -> increased wall thickness -> decreased wall stress aka afterload

Afterload corresponds directly with end systolic volume (increased afterload means more blood left after he thin and increased in end systolic volume)

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9
Q

Stroke work =

A

Stroke work = mean arterial pressure x SV

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10
Q

Frank starling principle

A

Increased LV diastolic filling -> cardiac muscle stretch -> greater force of contraction -> increased stroke volume

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11
Q

O2 consumption =

A

O2 consumption = delivered - returned
= (BF x O2 arterial content) - (BF x O2 venous content)

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12
Q

Qp/Qs =

A

Qp/Qs = (1 / [pulm vein O2 sat - pulm artery O2 sat]) / (1 / [aortic O2 sat - mixed venous O2 sat])

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13
Q

PVR =

A

Resistance of flow as it passes through the lungs
PVR = (mean PA pressure - mean LAP) / PBF

change is pressure across a circulation divided by flow through that circulation

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14
Q

SVR =

A

SVR = (mean aortic P - mean RAP) / SBF
Resistance of flow as it passes through the body

change is pressure across a circulation divided by flow through that circulation

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15
Q

Cyanosis

A

Absolute amount of unbound (reduced) Hb NOT O2 saturation
Anemia can decrease clinical detection of cyanosis
Observed clinically if >3-5g of reduced Hb per dL of capillary blood

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16
Q

O2 saturation =

A

O2 saturation = HbO2 / (HbO2 + Hb)
Hb is reduced or unbound
HbO2 is saturated with O2

So it’s the percentage of bound / total

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17
Q

Specific cardiac lesions:
Right radial paO2 (pre ductal) 100mmHg
Umbilical arterial paO2 (post ductal) 45mmHg

A

Critical preductal CoA with PDA and increased PVR

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18
Q

Specific cardiac lesions:
Right radial paO2 (pre ductal) 45mmHg
Umbilical arterial paO2 (post ductal) 80mmHg

A

DTGA with intact ventricular septum and PDA with 1 of the following:
- PH
- Interrupted aortic arch
- Preductal coarctation of the aorta

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19
Q

Specific cardiac lesions:
Right radial paO2 (pre ductal) 75mmHg
Umbilical arterial paO2 (post ductal) 50mmHg

A

Pulmonary hypertension with right to left shunting across PDA

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20
Q

Specific cardiac lesions:
Umbilical arterial paO2 (post ductal) 65mmHg
Umbilical venous pO2 (high line) 95mmHg

A

Infradiaphragmatic TAPVR (usually obstructive)

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21
Q

Localization of murmurs
URSB
LLSB
ULSB
Apex

A

URSB - AS
ULSB - PDA, PS, ASD
LLSB - VSD, TR
Apex - MR, IHSS

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22
Q

Medication for pulmonary hypertension

A

Nitric oxide
Sildenafil (phosphodiesterase 5 inhibitor)
Bosentan
Iloprost

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23
Q

Nitric oxide mechanism

A

Endothelium derived molecule that relaxes vascular tone
NO formed from L arginine by NOS in endothelial cells lining blood vessel walls
Diffused to vascular smooth muscle and activates guanylyl cyclase which increased cGMP (from GTP) which decreases vascular tone
INO selectively vasodilates the blood vessels that are ventilated - improving VQ matching

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24
Q

Risk of another child with CHD

A

2-5% if one child with CHD
5-10% if 2 children with CHD
Recurrence risk

If mom with CHD the child 2-18% risk
If father with CHD the child with 1-3% risk

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25
Q

Cyanosis heart disease

A

5 Ts DO and ESP

Truncus arteriosus
TGA
TA
TOF
TAPVR

DORV

Ebstein anomaly
Single ventricle
Pulmonary atresia

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26
Q

dTGA repair and common complications

A

Repair at 1 week of age
Fairly common to develop main or branch PA stenosis
Fairly common to develop aortic insufficiency

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27
Q

TOF repair timing and common complications

A

Repair of TOF at 3-6 months
Fairly common for stenosis of pulmonary valve or RV-PA conduit
Most patients have RBBB on EKG
Fairly common for pulmonary valve regurgitation

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28
Q

Tricuspid atresia repair

A

Shunt at 1 week
Glenn at 3-6 months
Fontan at 2-4 years

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29
Q

Pulmonary atresia repair timing

A

PA with VSD repair with shunt at 1 week or conduit at 1 week and vsd closure at 3-6 months

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30
Q

Truncus arteriosus a/c what syndrome

A

DiGeorge syndrome

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31
Q

Truncus arteriosus repair timing and common complications

A

Truncus repair at 1-2 weeks of age with RV to PA conduit and VSD patch
Fairly common complications: consist stenosis and pulmonary hypertension

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32
Q

TAPVR repair timing and complications

A

Obstructive TAPVR is emergent surgery
Nonobstructive TAPVR surgery less than 6 months
Can get pulmonary being obstruction, atrial arrhythmias and PH

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33
Q

DORV timing of repair

A

DORV repair at 3-6 months with VSD closure and if TGA then it’ll be a RV to PA conduit across the VSD

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34
Q

VSD repair timing

A

VSD repair 6-12 months although some small ones spontaneously close

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35
Q

ASD timing of repair

A

2-4 years of age for ASD repair with patch or device

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36
Q

Complete AV canal repair timing and complications

A

Complete AV canal repair 4-8 months
Fairly common complications include residual ASD and VSD, TVR (which may result in atrial arrhythmia), MVR, ventricular arrhythmia

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37
Q

PAPVR associations with other defects

A

Right PVs draining into SVC a/c sinus venous
Right PVs draining into IVC a/c scimitar syndrome
Or right PVs can drain directly into RA

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38
Q

PAPVR repair timing

A

PAPVR repaired 2-4 years of age

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39
Q

Syndrome a/c coarctation of Ao and other defects seen with CoA

A

30% of turner syndrome have CoA
>50% also with bicuspid AV and increased risk of VSD

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40
Q

Syndrome a/c supravalvar AS

A

Supravalvar AS a/c Williams syndrome

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41
Q

Neonatal and fetal heart

A

Decreased heart compliance
Less ability to augment cardiac output with stroke volume
Sensitive to afterload
Less contractile elements and immature sarcoplasmic reticulum
Sensitive to calcium as an ionotrope
Less fluid or preload responsive because of less compliance

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42
Q

Presentation and types cardiac tumors

A

Asymptomatic, hydrops, fetal arrhythmia

Rhabdomyoma (m/c) usually multiple - risk of TS, can regress, surgery required of obstruction of flow

Fibroma - single and fibrous, usually do not regress

Myxoma - majority are found in adulthood

Sarcoma - very rare

Teratoma - typically intrapericardial

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43
Q

EKG right atrial enlargement

A

Peaked P-wave > 3 mm ( > 3 tiny squares) in any lead

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44
Q

EKG left atrial enlargement

A

Increase P-wave duration (>0.2-0.23 sec) in any lead. May have biphasic P-wave.

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45
Q

EKG Q wave abnormalities

A

Small Q waves <5mm fine in II III avF V5 V6

Abnormal:
No Q in V5 V6 = L TGA, single ventricle, L BBB
Deep Q left leads = LVH, BiVH, myocarditis, RCM
Deep wide Q = infarction, HCM
Deep Q in I avL V4 V5 V6 = ALCAPA

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46
Q

Normal QRS axis

A

In neonate 100 to 150°

47
Q

Normal P-wave axis

A

Normally upright in lead 1 and aVF normal P axis 0 to 90°

48
Q

Normal T-wave axis

A

Normally upright in inferior and lateral leads

49
Q

Fetal SVT characteristics management, in utero, and postnatal management

A

Accounts for 70 to 80% of tachyarrhythmias. Presents between 28 and 32 weeks gestational age. Hydrops is dependent on duration of tachycardia not degree of SVT.

First line treatment is digoxin. Second line treatment. If the fetus is not sick is flecainide, but the mortality is 10 to 15% sotalol can also be tried but mortality is 30% and not as effective.

Other second line agent, if the fetus is sick, is amiodarone, usually given after 1 to 2 doses of digoxin. There are maternal complications with this.

Postnatal management includes monitoring of complications from antiarrhythmics, such as hyper bilirubinemia, anemia from BM Suppression, and greater risk of NEC. Infants remain on antiarrhythmics for six months generally 

50
Q

Fetal atrial flutter presentation and treatments

A

Atrial flutter Accounts for 20 to 30% of tachyarrhythmias.

Presents later in pregnancy then SVT in hydrops is less common 

Digoxin is first line.  sotalol, is safe and works in 80% of atrial flutter and the treatment of choice for refractory atrial flutter. Amiodarone is not effective. 

51
Q

What is associated with premature atrial contraction?

A

Hypokalemia, hypoglycemia, hypercalcemia, drugs, hypoxemia Central line irritation of right atrium

52
Q

Premature beats

A

Premature atrial contractions are typically benign and treat underlying cause

Premature junctional contraction generally do not require treatment

Premature ventricular contractions - if asymptomatic and isolated PVCs with normal cardiac anatomy - do not usually need treatment

53
Q

Underlying causes of PVCs

A

Digoxin toxicity
Infection
Ca/K/Mag abnormalities
Hypoxemia
Acidosis
CHD
Excess aminophylline/caffeine
Myocarditis

54
Q

Ddx for wide QRS

A

SVT with BBB
AV Re-entry tachycardia/antidromic
Vtach

55
Q

QTc

A

Corrected QT = QT(seconds) / square root of previous RR interval (seconds)

Normal is <0.45 sec if <6 months

56
Q

EKG findings with hypercalcemia

A

Shortened QT interval

57
Q

EKG findings with hypocalcemia

A

Prolonged QT interval

58
Q

EKG findings with hyperkalemia

A

> 6 tall peaked T wave, shortened QT interval, depressed ST segment
7.5 prolonged PR interval, widened QRS complex, flattened P wave
9 absent p wave, sinusoidal QRS wave, asystole and v fib can occur

59
Q

EKG findings with hypokalemia

A

<2.5 slightly widened QRS complex, depressed ST segment, biphasic T wave attributable to visible U wave
~1.0 prominent u wave, flat T wave, if sustained may develop prolonged PR and sinoatrial block

60
Q

Screen for what with Truncus arteriosus?

A

Screen for digeorge - look for thymus and check calcium’s

61
Q

Alpha 1 receptors

A

Location: arterial and venous smooth muscle, Cardiac myocytes
Action: sm muscle contraction by increasing calcium entry; increase contractility; gluconeogenesis; decrease insulin release

62
Q

Alpha 2 receptors

A

Location: sympathetic nerves, CNS
Action: blocks NE release, inhibits sympathetic output; vascular smooth muscle relaxation

63
Q

Beta 1 receptors

A

Location: sinoatrial node, atrial and ventricular muscle, conduction cells
Action: increases HR, increased conduction velocity, increases contractility, increases renin secretion

64
Q

Beta 2 receptors

A

Location: arterial and venous smooth muscle, bronchial smooth muscle
Action: smooth muscle relaxation, bronchial relaxation, increases HR and contractility, decreased intestinal motility and tone, induces glycogenolysis, increases insulin secretion

65
Q

What can PGE1 make worse

A

Tapvr obstructive
Hlhs with intact or restrictive atrial septum
TGA with restrictive atrial septum
Mitral valve atresia with restricted pfo

66
Q

Carpenter syndrome a/c

A

PDA, VSD, PS, ASD, TOF, TGA

67
Q

Cat eye syndrome a/c

A

TAPVR, persistent left SVC

68
Q

CHARGE syndrome a/c

A

TOF DORV VAD ASD PDA right sided aortic arch (50-70%)

69
Q

Cornelia de Lange syndrome a/c

A

VSD most common

70
Q

Cri du chat a/c

A

Variable

71
Q

DiGeorge syndrome a/c

A

Aortic arch abnormalities (right sided aortic arch, interrupted aorta, Truncus arteriosus), TOF, PA

72
Q

Ehlers Danlos syndrome a/c

A

Aortic root dilation, MVP

73
Q

Ellis van creveld syndrome a/c

A

50%
Common atrium

74
Q

Glycogen storage IIa (pompe) a/c

A

Hypertrophic cardiomyopathy

75
Q

Goldenhar syndrome a/c

A

VSD > PDA > TOF > CoA

76
Q

Holt Oram syndrome a/c

A

ASD most common

77
Q

Homocystinuria a/c

A

Arterial and venous thrombosis, medial degeneration of the aorta and elastic arteries

78
Q

Hurler syndrome a/c

A

Thickened valves (especially mitral), CAD, HCM

79
Q

Klinefelter a/c

A

TOF, MVP

80
Q

Klippel feil sequence a/c

A

VSD

81
Q

Marfan syndrome a/c

A

Dilated aorta and aortic root, aortic aneurysm, MVP

82
Q

Meckel gruber syndrome a/c

A

ASD, VSD, PDA, CoA, PS

83
Q

Noonan syndrome a/c

A

Dysplastic or thickened pulmonary valve, LVH, ASD VSD PDA, branch stenosis of pulmonary arteries

84
Q

Rubenstein Taybi syndrome a/c

A

PDA VSD ASD

85
Q

TAR syndrome a/c

A

TOF ASD

86
Q

Trisomy 13 a/c

A

80-90% with VSD or PDA

87
Q

Trisomy 18 a/c

A

VSD PDA PS CoA TOF polyvalvular disease

88
Q

Trisomy 21 a/c

A

Complete AVC > VSD > PDA, also ASD and TOF

89
Q

Turner syndrome 44, X a/c

A

Bicuspid aortic valve (30%), CoA (10%), aortic stenosis, MVP, aortic dissection, hypertension later in life

90
Q

VACTERL association a/c

A

VSD > TOF, CoA

91
Q

Williams syndrome a/c

A

Supravalvar subaortic stenosis > peripheral pulmonary artery stenosis, PS

92
Q

Rubella a/c

A

PDA, peripheral pulmonic stenosis, PS, AS, TOF, myocarditis

93
Q

Maternal diabetes a/c risk of infant CHD

A

DTGA, VSD, CoA, ventricular hypertrophy
Greater risk if insulin dependent prior to pregnancy.

94
Q

AS a/c which syndromes

A

Turner
Jacobsen
Loeys Dietz
Kabuki

95
Q

Shones syndrome

A

Small L sided structures, supravalvar mitral ring, parachute MV, subaortic stenosis, coarct, not quite LV apex

96
Q

Supravalvar PS a/c

A

Noonan, holt oram, leopard

97
Q

PPHN due to

A

Failure of 1 of 3 mechanisms
1. Abnormal lung parenchyma (MAS, RDS, PNA)
2. Hypoplastic vasculature (like CDH)
3. Remodeled pulm vasculature (idiopathic)

98
Q

Trisomy 13 CHD

A

ASD
PDA
VSD

99
Q

Trisomy 18 CHD

A

ASD
ECD
PDA
TOF
VSD

100
Q

Trisomy 21 CHD

A

ECD
VSD
ASD

101
Q

CHARGE CHD

A

TOF
ECD
Ao arch anomalies

102
Q

Deletion 22q11 CHD

A

IAA
TOF
VSD
Truncus

103
Q

Holt Oram CHD

A

ASD
VSD
COA

104
Q

Kartagener CHD

A

Dextocardia

105
Q

Loeys Dietz CHD

A

Aortic dilation
MVP

106
Q

Marfan CHD

A

Aortic dilation
MVP
TVP
pulm artery dilation

107
Q

Neuorfibromatosis CHD

A

PS
Aortic dilation
MVP
HCM

108
Q

Noonan CHD

A

PS
HCM

109
Q

Smith Lemli Opitz CHD

A

TAPVR
AV Canal

110
Q

TAR CHD

A

ASD
TOF

111
Q

Turner CHD

A

AS (BAV)
COA
HLHS

112
Q

Williams CHD

A

Supravalvar AS
PPS

113
Q

Alagille CHD

A

TOF
hypoplastic or stenotic pulm arteries

114
Q

Maternal DM CHD

A

VSD
TGA
TOF
DORV
HCM
BVH

Neo Board Review (12 decks)

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