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Cardiovascular > Embryology + Congenital + Inherited > Flashcards

Embryology + Congenital + Inherited Flashcards

1
Q

what is the function of the placenta

A 
Fetal homeostasis
Gas exchange
Acid base balance
Nutrient transport to fetus
Waste product transport from fetus
Hormone production
Transport of IgG
produces PGE2 (prostaglandin E2)
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2
Q

describe the lungs in utero

A

fluid filled and unexpanded

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3
Q

what is the role of the pulmonary circulation in utero

A

to supply the lungs with what it needs to grow and develop

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4
Q

what is the role of the liver and gut

A

liver little role in nutrition and waste management

gut not in use

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5
Q

where does the foetal heart pump blood to

A

the placenta via the umbilical arteries

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6
Q

from what arteries do the umbilical arteries arise from

A

illiac arteries

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7
Q

where does blood from the placenta travel to

A

to the foetus via the umbilical vein

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8
Q

where does the oxygenated blood from the placenta return to in the heart and what is its role

A

right side of the heart, to be distributed around the heart to the growing foetus

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9
Q

why is the pulmonary resistance in utero so high

A

as lungs collapsed

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10
Q

what are shunts and why are they needed

A

as pulmonary circulation very high resistance the vessels cant deal with all the blood, shunts are passage ways that allow most of the blood supply to bypass the lungs

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11
Q

what are the 3 shunts in foetal circulation

A

ductus venosus,
foramen ovale,
ductus arteriosus,

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12
Q

what is the role of the ductus venosus

A

connects the umbilical vein to the vena cava, allowing the blood from the placenta to bypass the liver

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13
Q

what is the foramen ovale and what is its role

A

opening in atrial septum connecting RA to LA allowing passage of blood between sides of the circulation

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14
Q

what is the role of the ductus arteriosus

A

connects pulmonary bifurcation to the descending aorta

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15
Q

what is the name of the liver circulation and what is it bypassed by, and why

A

portal circulation
bypassed by ductus venosus
as nutrients from placenta don’t need further processing in liver

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16
Q

why is the mixing of blood facilitated by the foramen ovale so important

A

as allows the best oxygenated blood to enter left atrium then on to LV where it goes to ascending aorta and carotids, supplying the development of the foetus

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17
Q

on which side is the membrane flap of the foramen ovale on

A

left atrium side

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18
Q

how is foetal circulation opposite to adult circulation

A

pressure in right atrium and pulmonary circulation much higher than left side- (because of collapsed lungs) allows blood to flow through foramen ovale

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19
Q

how much of RV output goes to lungs and why

A

7% as pressure do high, rest taken by ductus arteriosus to descending aorta

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20
Q

how is the patency of the ductus arteriosus maintained

A

by circulating prostagladin E2

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21
Q

what happens to the lungs in the first few minutes following birth

A

baby initially low sats (60%)
baby inflates lungs by crying (lung fluid goes into amniotic fluid)
baby goes from blue to pink

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22
Q

what happens to the Pulmonary vascular resistance after birth and how

A

lungs expand, increase in circulating oxygen-

relaxes smooth muscles of lungs = resistance decreases= cardiac output to lungs increases

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23
Q

what happens to systemic vascular resistance after birth

A

cord clamped and cut, placenta gone, resistance to flow in systemic system rises

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24
Q

what do the changes in circulation following birth lead to

A

closure of the foramen ovale and constriction and closure of the ductus arteriosus

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25
Q

what causes the foramen ovale to close

A

fall in P(ulmonary) VR and rise in SVR= increases the LA pressure, making it exceed to RA pressure pushing the membrane flap shut

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26
Q

what causes duct constriction

A 
increased pO2 (only place in body that O2 causes vasoconstriction)
decreased blood flow (decrease pulmonary vascular resistance) 
decreased prostaglandins (placenta removed)
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27
Q

when does the ductus arteriosus close and what does it form

A

functional closure first hours/days
anatomical closure 7-10 days

forms the fibrous ligament- ligamentum arteriosum

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28
Q

what can a patent ductus arteriosus lead to in peterm infants

A

excessive blood in ling circulation and not enough blood in brain and gut

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29
Q

what are the treatment options for a patent ductus arteriosus

A

‘wait and see’, NSAIDs (inhibit prostaglandin production to help constrict the duct),
surgery

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30
Q

what is the treatment for a duct dependant circulation

A

IV prostaglandin E2 can keep duct open until an alternative shunt established/ definitive surgery carried out

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31
Q

when does pulmonary resistance reach a normal level

A

drops after birth until 2-3 months

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32
Q

in what conditions is persistent pulmonary hypertension more common in newborns

A 
sepsis, 
hypoxic ischaemic insult,
meconium aspiration syndrome,
cold stress,
anatomical abnormality (e.g. congenital diaphragmatic hernia)
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33
Q

what physiological failures can cause persistence of pulmonary hypertension in a newborn

A

patent foramen ovale or ductus arteriolus

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34
Q

what are the symptoms of persistent pulmonary hypertension in newborns

A

blue baby, large difference between pre and post ductal oxygen saturation

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35
Q

how is PPHN treated

A

ventilation, oxygenation, high systemic blood pressure, inhaled nitric oxide (will drop vasculature pressure), ECLS (extracorporeal membrane oxygenation (ECMO))

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36
Q

where is pre and post ductal saturation measured

A

pre hands (80%), post feet (60%)

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37
Q

what is congenital heart disease

A

abnormality of the structure of the heart (doesnt include cardiomyopathy or arrhythmias that present later)

“a gross structural abnormality of the heart or intrathoracic great vessels that is actually or potentially of functional significance.”

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38
Q

when do congenital heart diseases present

A

at birth

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39
Q

what is the incidence of congenital heart disease

A

between 1-13 per 1000 live births

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40
Q

what is the spectrum of severity of congenital heart diseases

A

mild, moderate, severe and major

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41
Q

describe mild heart disease

A

asymptomatic- may resolve spontaneously or may progress to moderate of severe in adulthood

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42
Q

describe moderate congenital heart disease

A

require specialist intervention and monitoring in cardiac centre

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43
Q

describe severe congenital heart disease

A

present severely ill/ die in newborn period or early infancy

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44
Q

describe major congenital heart disease

A

requires surgery within the first year of life

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45
Q

give examples of mild Congenital HD and how they can progress

A

Small VSD, PFO / small ASD, small PDA. Bicuspid aortic valve may progress in adulthood to severe AS or AR and need surgery

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46
Q

give examples of moderate congenital HD

A

mild or moderate AS, PS. larger or complex ASD, VSD

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47
Q

give examples of severe congenital heart disease

A

cyanotic lesions, all duct dependant lesions, truncus

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48
Q

how does congenital heart disease present

A

screening: antenatal, newborn baby check

well baby with clinical signs- murmur

unwell baby with- cyanosis, shock, cardiac failure due to low CO

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49
Q

what signs are seen in congenital heart disease when presenting soon after birth

A

cyanosis

50
Q

what signs are seen in congenital heart disease when presenting at the day 1-2 baby check

A

murmurs, abnormal pulses, cyanosis

51
Q

what signs are seen in congenital heart disease when presenting 3-7 days after birth

A

sudden circulatory collapse, shock, cyanosis, sudden death

52
Q

what signs are seen in congenital heart disease when presenting at 4-6 weeks

A

what signs are seen in congenital heart disease when presenting soon after birth

53
Q

what signs are seen in congenital heart disease when presenting at 6-8 weeks

A

incidental finding of murmurs

54
Q

why causes blue baby/ cyanosis

A

any condition that causes deoxygenated blood to bypass the lungs and enter the systemic circulation /

mixed oxygenated and deoxygenated blood enters the systemic circulation from the heart

55
Q

what are the differential diagnosis’ of cyanosis in newborns

A

cardiac disease, respiratory disease, persistent pulmonary hypertension

56
Q

what is the most common cyanotic condition

A

transposition of great arteries

57
Q

why does transposition of the great arteries cause acidosis

A

as babies unable to perform anaerobic metabolism and builds up lactic acod

58
Q

what happens when a duct closes in a baby who has duct dependent circulation

A

collapse, severe cyanosis or pallor, tachypnoea, distress, grunting, rapid deterioration, death

59
Q

what are the clinical signs of duct closure

A

pallor, prolonged CRT, poor or absent pulses, hepatomegaly, crepitations, increased work of breathing, profoundly acidotic

60
Q

how is duct closure treated

A

ABC, prostaglandin E2 to reopen duct, surgery

61
Q

what are the two types of duct dependent conditions

A

duct dependent systemic circulation (physical obstruction to blood getting to left side of the heart)

duct dependent pulmonary circulation (right side of heart)

62
Q

what can cause duct dependent systemic circulation (left side of the heart)

A

hypoplastic left heart,
critical aortic stenosis,
interrupted aortic arch,
critical coarctation of aorta

63
Q

what can cause duct dependent pulmonary circulation (right side)

A

tricuspid atresia,
pulmonary atresia

(complete blockage)

64
Q

describe hypoplastic left heart syndrome

A

underdeveloped left heart- very small LV< mitral valve and ascending aorta= mixed blood in right side, PA and AO. no palpable pulse and increasingly acidotic

65
Q

what does pulmonary atresia result in

A

retrograde filling of PA via ductus arteriosus. No VR output, associated with VSD, circulation to lungs via aorta

66
Q

what can cause a presentation of heart failure

A

large right to left shunts (increased pulmonary load) e.g large VSD

67
Q

when does cardiac failure present in neonates

A

after a few weeks as pulmonary pressure drops

68
Q

what are the clinical signs of heart failure in babies

A 
Failure to thrive
Slow / reduced feeding
Breathlessness (especially when feeding)
Sweatiness
Hepatomegaly
Crepitations
69
Q

when does a VSD murmur develop

A

as pulmonary pressure drops over first weeks

70
Q

why does VSD lead to congestive heart failure

A

as increases pulmonary circulation and work load in right ventricle

71
Q

how is CCF treated in babies

A

diuretics and high calorie formula to help baby grow before surgery

72
Q

what is the long term management for major congenital heart disease

A

surgery, further interventions for developmental problems, hypoxia, further surgery, emotional/ social issues

73
Q

what is a patent ductus arteriosus repaired

A

catheter procedure, in through femoral vein to the heart

74
Q

how is a hypoplastic left heart treated

A

3 stage complex surgery, RV will fail over time, need transplant

75
Q

what mutations can cause inherited cardiac problems

A

on genes that encode cardiac muscle or ion channels of the heart

76
Q

what are the two forms of arrhythmogenic inherited cardiac conditions

A

channelopathies (arrhythmogenesis is related to an ion current imbalance) and cardiomyopathies (arrhythmogenesis related to scar/ electrical barrier formation and subsequent re entry)

77
Q

name two inherited channelopathies

A

congenital long QT syndrome, brugada syndrome, short QT syndrome

78
Q

name two inherited cardiomyopathies

A

hypertrophic cardiomyopathies, arrhythmogenic right ventricular cardiomyopathy (dilated right ventricle that causes arrhythmia), dilated cardiomyopathy

79
Q

how do inherited cardiac conditions present

A

can have no symptoms, heart rhythm, palpitations, fast heart rate, fainting, breathlessness, chest pain, swollen legs, weakness, sudden death

80
Q

how are inherited cardiac conditions diagnosed

A

clinical testing, genetic tests

81
Q

how are the risks of inherited cardiac conditions managed

A

risk management, lifestyle, pharmacological and non pharmacological intervention

82
Q

what electrical activity is mainly affected in a channelopathies

A

depolarisation

83
Q

when should inherited cardiac conditions be considered in patients

A

young people with AF

84
Q

what channel is mostly affected in long QT syndrome

A

potassium channel

85
Q

what does congenital long QT syndrome look like on an ECG

A

polymorphic VT (torsades de pointes)

86
Q

what triggers the polymorphic VT seen in LQTS

A

adrenergic stimulation

87
Q

is LQTS autosomal dominant or recessive

A

can be both- 13 subtypes

88
Q

what is the mechanism behind LQTS

A

less repolarising current and more depolarising current prolongs AP depolarisation

89
Q

what can trigger LQTS

A

exercise, emotional stress, sleep, sudden auditory stimuli, QT prolonging conditions (medications, hypokalaemia)

90
Q

what is the primary presenting complaint of LQTS

A

syncope, sudden cardiac death

91
Q

how is congenital LQTS managed

A

avoidance of stimuli (swimming, breath holding, loud sudden noises), correction of electrolyte adnormalities, avoidance of QT prolonging drugs

92
Q

what creates risk of SCD in LQTS

A

age dependent, gender (pre-teen boys, adult females), increasing QT duration, prior syncope

93
Q

what can be shown on an ECG in brugada syndrome

A

risk of polymorphic VT, VF, AF common, ST elevation, RBBB in V1-3

94
Q

how does brugadas commonly present

A

in young men who go to sleep and dont wake up

95
Q

what types of inheritance pattern does brugadas have

A

autosomal dominant

96
Q

what can trigger VF in brugada

A

rest or sleep, fever, excessive alcohol, large meals

97
Q

what drugs should be avoided in brugada

A

anti-arrhythmic, psycotropics (used in schizophrenia), analgesics, anaesthetics

98
Q

what is catecholaminergic polymorphic ventricular tachycardia

A

channelopathy

99
Q

describe CPVT

A

Adrenergic induced bidirectional and polymorphic VT, SVTs, triggered by emotional stress, physical activity

normal ECG and echo

both autosomal dominant and recessive

100
Q

how is risk managed in CPVT

A

avoidance of strenuous activity, stressful environments

beta blockers and ICD implantation (sometimes flecainide)

101
Q

what are the clinical presentations of hypertrophic cardiomyopathies

A

sudden death, heart failure, angina, atrial fibrillation, asymptomatic

102
Q

how is heart failure in HOCM treated

A

beta blockers, ACE I, diuretics, consider transplantation

103
Q

how is AF or atrial flutter treated

A

oral anticoagulant, antithrombotic, amiodarone to restore sinus rhythm and b blockers, verapamil and diliazem to maintain / catheter ablation

104
Q

what is lamin A/C

A

gene where mutations associated with DCM

105
Q

What is SAD

A

syncope angina dyspnoea

106
Q

what are after depolarisations

A

abnormal depolarisations if cardiac myocytes that interrupt phase 2, 3 or 4 of the cardiac AP in the cardiac conduction system of the heart

can lead to triggered activity

107
Q

what are early depolarisations

A

) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive action potentials before normal repolarization is completed

can result in Torsades de Pointes

108
Q

what is a treatment for DCM

A

ICD- implantable cardiac defibrillator

109
Q

what causes arrhythmogenic right ventricular cardiomyopathy

A

fibro-fatty replacement of cardiomyocytes

110
Q

what adds to the risk of SCD

A 
Family history of premature SCD
Severity of RV and LV function
Frequent non-sustained VT
ECG : QRS prolongation
VT induction on EPS
Male gender
Age of presentation
111
Q

what can help prevent SCD in pre symptomatic patients

A

life style changes, beta blockers, ICDs

112
Q

describe embryonic folding

A

when embryo folds laterally and longitudinally, making the two initial heart tubes fuse, moving them into the midline, and making them start to beat

happens at 18 days

113
Q

what happens when the two primitive heart tubes fuse together

A

form single primordial heart tube situated in the midline of the embryo

114
Q

what is the trunctus arteriosus and what does it form

A

cranial segment of embryonic heart which forms pulmonary and aortic trunks

115
Q

what is heart tube looping

A

when tubular heart forms a c then an s shape which resembles adult heart

116
Q

describe sepation of the heart

A

the formation of atria and ventricles in the embryonic heart from endocardial cushions

117
Q

what is the role of cardinal veins

A

return poorly oxygenated blood from the body if the embryo

118
Q

what is the role of the foramen ovale

A

allows blood to travel from the right to the left atrium (shunt)

119
Q

what is the role of the ductus venosus

A

allows blood from the umbilical vein to bypass the liver into the IVC

120
Q

what is the role of the ductus arteriosus

A

allows blood to pass from the pulmonary trunk into the aorta (blood can bypass the lungs, liver and kidneys whose functions are performed by the placenta)

121
Q

what germ layer is the heart formed from

A

mesoderm

Cardiovascular (34 decks)

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