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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
Cyanosis heart disease
5 Ts DO and ESP Truncus arteriosus TGA TA TOF TAPVR DORV Ebstein anomaly Single ventricle Pulmonary atresia
26
dTGA repair and common complications
Repair at 1 week of age Fairly common to develop main or branch PA stenosis Fairly common to develop aortic insufficiency
27
TOF repair timing and common complications
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
28
Tricuspid atresia repair
Shunt at 1 week Glenn at 3-6 months Fontan at 2-4 years
29
Pulmonary atresia repair timing
PA with VSD repair with shunt at 1 week or conduit at 1 week and vsd closure at 3-6 months
30
Truncus arteriosus a/c what syndrome
DiGeorge syndrome
31
Truncus arteriosus repair timing and common complications
Truncus repair at 1-2 weeks of age with RV to PA conduit and VSD patch Fairly common complications: consist stenosis and pulmonary hypertension
32
TAPVR repair timing and complications
Obstructive TAPVR is emergent surgery Nonobstructive TAPVR surgery less than 6 months Can get pulmonary being obstruction, atrial arrhythmias and PH
33
DORV timing of repair
DORV repair at 3-6 months with VSD closure and if TGA then it’ll be a RV to PA conduit across the VSD
34
VSD repair timing
VSD repair 6-12 months although some small ones spontaneously close
35
ASD timing of repair
2-4 years of age for ASD repair with patch or device
36
Complete AV canal repair timing and complications
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
37
PAPVR associations with other defects
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
38
PAPVR repair timing
PAPVR repaired 2-4 years of age
39
Syndrome a/c coarctation of Ao and other defects seen with CoA
30% of turner syndrome have CoA >50% also with bicuspid AV and increased risk of VSD
40
Syndrome a/c supravalvar AS
Supravalvar AS a/c Williams syndrome
41
Neonatal and fetal heart
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
42
Presentation and types cardiac tumors
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
43
EKG right atrial enlargement
Peaked P-wave > 3 mm ( > 3 tiny squares) in any lead
44
EKG left atrial enlargement
Increase P-wave duration (>0.2-0.23 sec) in any lead. May have biphasic P-wave.
45
EKG Q wave abnormalities
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
46
Normal QRS axis
In neonate 100 to 150°
47
Normal P-wave axis
Normally upright in lead 1 and aVF normal P axis 0 to 90°
48
Normal T-wave axis
Normally upright in inferior and lateral leads
49
Fetal SVT characteristics management, in utero, and postnatal management
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
Fetal atrial flutter presentation and treatments
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
What is associated with premature atrial contraction?
Hypokalemia, hypoglycemia, hypercalcemia, drugs, hypoxemia Central line irritation of right atrium
52
Premature beats
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
Underlying causes of PVCs
Digoxin toxicity Infection Ca/K/Mag abnormalities Hypoxemia Acidosis CHD Excess aminophylline/caffeine Myocarditis
54
Ddx for wide QRS
SVT with BBB AV Re-entry tachycardia/antidromic Vtach
55
QTc
Corrected QT = QT(seconds) / square root of previous RR interval (seconds) Normal is <0.45 sec if <6 months
56
EKG findings with hypercalcemia
Shortened QT interval
57
EKG findings with hypocalcemia
Prolonged QT interval
58
EKG findings with hyperkalemia
>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
EKG findings with hypokalemia
<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
Screen for what with Truncus arteriosus?
Screen for digeorge - look for thymus and check calcium’s
61
Alpha 1 receptors
Location: arterial and venous smooth muscle, Cardiac myocytes Action: sm muscle contraction by increasing calcium entry; increase contractility; gluconeogenesis; decrease insulin release
62
Alpha 2 receptors
Location: sympathetic nerves, CNS Action: blocks NE release, inhibits sympathetic output; vascular smooth muscle relaxation
63
Beta 1 receptors
Location: sinoatrial node, atrial and ventricular muscle, conduction cells Action: increases HR, increased conduction velocity, increases contractility, increases renin secretion
64
Beta 2 receptors
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
What can PGE1 make worse
Tapvr obstructive Hlhs with intact or restrictive atrial septum TGA with restrictive atrial septum Mitral valve atresia with restricted pfo
66
Carpenter syndrome a/c
PDA, VSD, PS, ASD, TOF, TGA
67
Cat eye syndrome a/c
TAPVR, persistent left SVC
68
CHARGE syndrome a/c
TOF DORV VAD ASD PDA right sided aortic arch (50-70%)
69
Cornelia de Lange syndrome a/c
VSD most common
70
Cri du chat a/c
Variable
71
DiGeorge syndrome a/c
Aortic arch abnormalities (right sided aortic arch, interrupted aorta, Truncus arteriosus), TOF, PA
72
Ehlers Danlos syndrome a/c
Aortic root dilation, MVP
73
Ellis van creveld syndrome a/c
50% Common atrium
74
Glycogen storage IIa (pompe) a/c
Hypertrophic cardiomyopathy
75
Goldenhar syndrome a/c
VSD > PDA > TOF > CoA
76
Holt Oram syndrome a/c
ASD most common
77
Homocystinuria a/c
Arterial and venous thrombosis, medial degeneration of the aorta and elastic arteries
78
Hurler syndrome a/c
Thickened valves (especially mitral), CAD, HCM
79
Klinefelter a/c
TOF, MVP
80
Klippel feil sequence a/c
VSD
81
Marfan syndrome a/c
Dilated aorta and aortic root, aortic aneurysm, MVP
82
Meckel gruber syndrome a/c
ASD, VSD, PDA, CoA, PS
83
Noonan syndrome a/c
Dysplastic or thickened pulmonary valve, LVH, ASD VSD PDA, branch stenosis of pulmonary arteries
84
Rubenstein Taybi syndrome a/c
PDA VSD ASD
85
TAR syndrome a/c
TOF ASD
86
Trisomy 13 a/c
80-90% with VSD or PDA
87
Trisomy 18 a/c
VSD PDA PS CoA TOF polyvalvular disease
88
Trisomy 21 a/c
Complete AVC > VSD > PDA, also ASD and TOF
89
Turner syndrome 44, X a/c
Bicuspid aortic valve (30%), CoA (10%), aortic stenosis, MVP, aortic dissection, hypertension later in life
90
VACTERL association a/c
VSD > TOF, CoA
91
Williams syndrome a/c
Supravalvar subaortic stenosis > peripheral pulmonary artery stenosis, PS
92
Rubella a/c
PDA, peripheral pulmonic stenosis, PS, AS, TOF, myocarditis
93
Maternal diabetes a/c risk of infant CHD
DTGA, VSD, CoA, ventricular hypertrophy Greater risk if insulin dependent prior to pregnancy.
94
AS a/c which syndromes
Turner Jacobsen Loeys Dietz Kabuki
95
Shones syndrome
Small L sided structures, supravalvar mitral ring, parachute MV, subaortic stenosis, coarct, not quite LV apex
96
Supravalvar PS a/c
Noonan, holt oram, leopard
97
PPHN due to
Failure of 1 of 3 mechanisms 1. Abnormal lung parenchyma (MAS, RDS, PNA) 2. Hypoplastic vasculature (like CDH) 3. Remodeled pulm vasculature (idiopathic)
98
Trisomy 13 CHD
ASD PDA VSD
99
Trisomy 18 CHD
ASD ECD PDA TOF VSD
100
Trisomy 21 CHD
ECD VSD ASD
101
CHARGE CHD
TOF ECD Ao arch anomalies
102
Deletion 22q11 CHD
IAA TOF VSD Truncus
103
Holt Oram CHD
ASD VSD COA
104
Kartagener CHD
Dextocardia
105
Loeys Dietz CHD
Aortic dilation MVP
106
Marfan CHD
Aortic dilation MVP TVP pulm artery dilation
107
Neuorfibromatosis CHD
PS Aortic dilation MVP HCM
108
Noonan CHD
PS HCM
109
Smith Lemli Opitz CHD
TAPVR AV Canal
110
TAR CHD
ASD TOF
111
Turner CHD
AS (BAV) COA HLHS
112
Williams CHD
Supravalvar AS PPS
113
Alagille CHD
TOF hypoplastic or stenotic pulm arteries
114
Maternal DM CHD
VSD TGA TOF DORV HCM BVH

Neo Board Review (12 decks)

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