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RACP Written > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the first thing to change from neonatal to foetal circulation?

A

PFO closure- within minutes

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2
Q

What are the 5 changes seen in transition from neonatal to foetal circulation

A
  1. Umbilical vein closure
  2. PFO closure
  3. Ductus venosus closure (in liver)
  4. DA closure
  5. Umbilical artery closure
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3
Q

What is the valve from RA to RV?

A

Tricuspid

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4
Q

What is the valve from RV to pulmonay artery?

A

pulmonary

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5
Q

What is the valve from LA to LV?

A

mitral

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6
Q

What is the valve from LV to aorta?

A

Aortic valuve

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7
Q

What valves are responsible for S1?

A

Mitral and tricuspid- shut at the end of diastole

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8
Q

What valves are responsible for S2?

A

Pulmonary and aortic closure at end of systolic

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9
Q

What causes FIXED wide splitting of S2?

A

ASD. Think: continuous flow back from LV to RV during diastole meaning there is increased PULMONARY volume.
Also pulmonary stenosis, Ebstein anomaly, total anomalous pulmonary venous return, and right bundle branch block.

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10
Q

What causes narrow splitting of S2?

A

pulmonary hypertension.
Note splitting increasing during inspiration (think filling) and reduces during expiration.

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11
Q

What causes a pansystolic murmur?

A

VSD, mitral regurg and tricuspid regurg

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12
Q

What causes an ejection ssytolic murmur?

A

aortic stenosis, pulmonary stenosis

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13
Q

What are the causes of a diastolic murmur?

A

Aortic regurg, pulmonary regurg, mitral stenosis, tricuspid stenosis

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14
Q

What causes a continous murmur?

A

BT shunt, PDA

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15
Q

Which conditions require endocarditis prophylaxis?

A

Prosthetic heart valve, prev endocarditis, rheumatic heart disease, unrepaired CYANOTIC congenital heart disease and surgical fixation of congenital heart disease within 6 months

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16
Q

What is the incidence of congenital heart disease in the normal population? What does it increase to if there is a previous child with CHD or parent is affected?

A

0.8% in the ppn
Increase to 2-4% if sibling has or parent has

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17
Q

What is the score used for hypermobility in the context of Marfans?

A

Beighton score.
Anything >4 = hypermobile

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18
Q

What layer of the mesoderm forms the heart? And when does the cardiogenic field start developing?

A

Splanchnic mesoderm
Cardiogenic field starts in week 3

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19
Q

What cells contribute to cushion formation in the heart

A

Neural crest cells from the hindbrain

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20
Q

Direction of blood flow in PFO?

A

R to left.
So if right atrial pressures remain high vs lsft, PFO wont close

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21
Q

What medications can keep the ductus arteriosus open

A

Prostaglandin.
Prostaglandin for PATENT ductus arteriosus

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22
Q

Why is splitting normal during inspiration

A

During inspiration, lots of blood being pushed to RV and hence pulmonary artery= longer time to close pulmonary valve. Physiological splitting S2

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23
Q

Generally, what causes S3

A

Fluid overload

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24
Q

Generally, what causes S4

A

Increased pressure

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25
Q

Which valves have 3 leaflet

A

mitral and tricuspid

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26
Q

What percentage of CHD are due to genetic causes

A

20%

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27
Q

What is the most common congenital heart lesion

A

VSD 32%

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28
Q

What % of kids with Trisomy 13 (patau) have CHD and what are the common lesions

A

80%
VSD
PDA
dextrocardia

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29
Q

What % of kids with Trisomy 18 have CHD and what are they?

A

90%
VSD
PDA
PS

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30
Q

What percentage of kids with Downs have CHD? What are the common defects

A

40-50%
VSD/AVSD
Endocardial cusion defects

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31
Q

What % of Turner’s syndrome have CHD and what is the common finding

A

35%
MOST HAVE BICUSPID AORTIC VALVE
- some have coarctation of aorta

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32
Q

What proportion of DiGeorge have CHD and what is the most common defect

A

40%
Conotruncal ie truncus arteriosus

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33
Q

What % of patients with Crit du Chat have heart problems? What are they?

A

This syndrome has cat like cry, low BW, craniofacial dysmorphia. 25% have CHD
anything from VSD, ASD, TOF..

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34
Q

What % of patients with Williams syndrome have CHD? Most common lesion?

A

This is the cocktail personality.
66% have supravalvular aortic stenosis.
Think, very bubbly-, above the rest- supravalvular aortic stenosis

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35
Q

What is the CHD in Alagile and what percentage of kids have it

A

Peripheral pulmonary artery stenosis, 85%

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36
Q

What syndrome has mitten hands and CHD

A

Carpenter syndrome
Think- cant work as a carpenter cos have mitten hands and a bad heart

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37
Q

What % of kids with Carpenter syndrome have CHD

A

50%
1 in 2 carpenters have bad hearts

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38
Q

What proportion of cornealia de lange have CHD

A

30%

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39
Q

CHD in Cornelia de Lange

A

VSD

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40
Q

What is the CHD lesion in EHlers Danlos

A

MV prolapse
Aortic root dilatation

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41
Q

CHD with Pompe’s disease? (GLYCOGEN storage disorder)

A

Hypertrophic cardiomyopathy

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42
Q

What syndrome has cardiac defect and absent thumb/radius

A

Holt-Oram

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43
Q

Which syndrome has pulmonary stenosis, deafness, abnormal genetalia

A

LEOPARD syndrome

Leopards have weird genitals, can’t hear (they move so quietly) and have pulmonary stenosis

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44
Q

What is the CHD in Noonans

A

Pulmonary Stenosis - in 40% if patkients.

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45
Q

Heart defect in Smith-Lemli-Opitz

A

VSD/PDA

SMITH is a man who loves his cholesterol. 7-dehydrocholesterol (7-DHC) reductase issue

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46
Q

Congenital heart defect in Marfans

A

Aortic root dilatation

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47
Q

Name the 5 CYANOTIC congenital heart lesions

A

Use your palm
1. Truncus Arteriosus
2. Transporition of great arteries
3. Tricuspid atresia (3 fingers)
4. Tetralogy of fallot
5. TAPVR

Also hypoplastic left heart

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48
Q

Where does the murmur for TOF come from

A

Pulmonary stenosis.
Large VSD so no VSD murmur.

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49
Q

Name the 4 acyanotic heart lesions

A

VSD, ASD, PDA, Coarctation

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50
Q

What is Eisemenger syndrome

A

Prev L to R shunt
Increasing flow through pulmonary artery
Change in structure/dysfn= turbulent flow and vascular remodelling
Increased pulmonary pressures
Inverted R to L shunt

Treat with prostaglandin to reduce pressure.

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51
Q

What is the most common ASD

A

Ostium Secundum defect

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52
Q

What is heard on auscultation for ASD

A

Widely split second heart sound and can have ejection systolic murmur from increased flow into PA.
Due to prolonged RV emptying

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53
Q

ECG changes associated with ASD

A

RBBB.

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54
Q

What syndrome has AVSD

A

Downs syndrome

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55
Q

What is the name of the defect in AVSD

A

Ostium primum
(secondum most common in jsut normal ASD)

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56
Q

Murmur with VSD

A

Loud, pansystolic murmur.

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57
Q

Complication associated with VSD

A

Aortic valve regurg
due to blood rushing back from LV to RV, valve pulled down and so more floppy

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58
Q

At what age do most small VSDs close

A

Age 4

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59
Q

What is the basic pathophys for TAPVR

A

Essentially problem in pulmonary venous drainage so NO return to LA. PV goes to SVC or IVC and systemic flow from open VSD/ASD.

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60
Q

CXR sign for TAPVR

A

Snowman sign- for RA, RV and PA enlargement

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61
Q

Where does the fluid for a chylothorax come from

A

Chyle from thoracic duct/lymph into the thoracic system

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62
Q

Apart from cardiac surgery, what other things are associated with chylothorax

A

H type TOF
Chest injury
Lymphoma
Lymphangectasia

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63
Q

What is the diet for chylothorax

A

Medium chain trigluceride diet.
High protein, low fat.

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64
Q

What is the indication for surgery for a chylothorax (when chest drain already in)

A

If output >50ml/kg/day

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65
Q

Complications from Chylothorax (2 main)

A

Malnutrition
Agammaglobunaemia and abnormal cell mediated response. T cell more affected.

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66
Q

Possible murmurs with ASD? Think of the flow

A
  1. Increased flow LA–> RA= diastolic murmur LLSE
  2. Increased RV volume so increased flow into the pulmonary artery so ejection systolic CLICK + systolic murmur
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67
Q

ECG for ASD?

A

RBBB

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68
Q

Murmurs in AVSD- think flow

A

Increased LA–> RA: Diastolic murmur
Increased RA volume : Ejection systolic murmur (into pulm artery)
Increased LV -> RV flow = pansystolic murmur

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69
Q

ECG in AVSD- think size of ventricules

A

Severe LAD due to biventricular hypertrophy

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70
Q

Most common VSD

A

Membranous
25-30% of CHD

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71
Q

Murmur with VSD

A

Harsh, pansystolic murmur LLSE. Often heart with a SMALL VSD

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72
Q

Symptoms/presentation of large VSD

A

Usually not cyanotic but
FTT
Poor feeding
Dyspnoea
recurrent chest infections
Tachycardia
Tachypnoeea

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73
Q

As pulmonary pressures increase, what happens to murmur and heart sound in VSD

A

Think: low pulm pressure= reduced pressure in RV so increased backwards flow.
Increasing pressure = reduced flow so murmur more quiet but still loud S2

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74
Q

Complication of VSD

A

Aortic regurg and increased pulmonary pressures

75
Q

What % of VSDs close spontaneously and when

A

80% of muscular VSDs, within 4 years

76
Q

Do prostaglandins work for TAPVR?

A

No.
Because issue with no return to LA and hence LV!

77
Q

What is the one main triggering reason for Eisenmenger

A

Pulmonary HTN

78
Q

How does large PDA lead to Eisengmenger

A

++ flow from aorta to pulmonary artery = increased flow to lungs.
Eventually this causing pulmonary HTN = now R to left shunting = deoxygenated blood to the pierpheries

79
Q

Murmur associated with PDA

A

Machinery continous murmur

80
Q

Treatment for PDA

A

Paracetamol/NSAID/Indomethacin

81
Q

What is the location for 98% of coarctation of aorta?

A

Origin of ductus arteriosus

82
Q

Syndrome commonly associated with coarctation of aorta

A

Turners.
Also remember bicuspid aortic value
Also PHACES

83
Q

Heart changes as a result of a coarct aorta

A

LV hypertrophy

84
Q

Examination findings for coarct aorta

A

Systemic HTN
BP changes UL vs LL
No murmur
lower O2 sats in LL

85
Q

When is mild vs severe coarct generally detected

A

Mild usually later in childhood with leg weakness or incidental HTN

86
Q

Treatment for coarct in neonate

A

Prostaglandin E1 to keep DA open while awaiting surgery.

87
Q

What is a common post-op complication of aortic stenosis

A

Postoperative mesenteric arteritis
Rebound HTN

THink increased blood flow to these organs again= readjustment

88
Q

What are the 4 features to a tetralogy of fallot

A
  1. RVOT (pulmonary stenosis)
  2. VSD
  3. RV hypertrophy
  4. Overriding aorta
89
Q

What is the name of the lesion of aorta overides VSD by 50%?

A

double outlet right ventricle

90
Q

Why does tetralogy of fallot cause cyanosis

A

Essentially:
RVOT causes increased pressure in RV so blood blows (deoxygenated) across the VSD into the LV.
Overiding aorta also means that the aorta is JUST under the VSD so blood from RV essentially flows directly into the aorta.

91
Q

When do Tetralogy of fallot patients start to exhibit signs of cyanosis and why

A

In first few months of life due to increasing RV hypertrophy

92
Q

Pathophys of tet spells

A

Drop in systemic pressures (ie waking) OR increased pulmonary pressures
Crying/upon awakening = drop in systemic BP –> increased deoxy blood in circulation –> drop PaO2–> increased oxygen demand so increased systemic blood flow (of deoxygenated blood) –> cyanosis –> increased resp drive and getting wrose.

93
Q

Treatment of tet spells

A

Keep baby calm
Knee to chest: this kinks femoral artery and increasing systemic pressure.so increased LV pressure which means blood will go THROUGH pulmonary circulation to come to aorta rather than through VSD = improved oxygenation.

94
Q

Why does murmur reduce during tet spells

A

All the flow is via VSD which is large.
Remember the TOF murmur is due to RVOT but in tet spells with drop in systemic BP/high pulmonary pressures, all blood going through VSD into aorta

95
Q

Most common syndrome associated with duodenal atresia

A

Down’s syndrome.
D-duodenal, D - downs

96
Q

CXR for TOF

A

Boot shaped from RV enlargement

97
Q

ECG for TOF

A

RAD, tall peaked p waves

98
Q

Long-term complications to tetralogy of fallot if left unrepaired

A

Cerebral thromboses (from polycythaemia and dehydration), brain abscess, endocarditis

99
Q

What syndrome is associated with a TOF and pulmonary atresia

A

DiGeorge

100
Q

Inheritance of CHD? General and if sibling affected

A

The incidence of congenital heart disease in the normal population is approximately 0.8%, and this incidence increases to 1–4% for a second pregnancy after the birth of a child with congenital heart disease or if a parent is affected.

101
Q

What is doublet outlet RV?

A

Both main vessels priginating from RV with a VSD (flow from LV to RV)

102
Q

What is Ebstein’s anomaly associated with

A

Maternal lithium use in pregnancy. These kids also get WPW

103
Q

Main pathology in Ebsteins

A

Atrialisation of tricuspid valve- WEAK tricuspid valve and RA

104
Q

CXR for Ebsteins

A

wall-wall heart- RVH and LVH

105
Q

What % of d-TGA patients have VSD

A

50%

106
Q

What are risk factors for development of TGA?

A

Maternal diabetes and being male.

107
Q

If there are other cardiac defects ie pulmonary stenosis or R sided aortic arch, what is a syndrome associated with TGA?

A

DiGeorge

108
Q

Pathophys for TGA

A

abnormal arteries. So pulmonary artery from left ventricle and aorta from right ventricle. Issue is the rest remains the same so essentially two SEPARATE circuits which aren’t compatible with life without PDA or VSD etc.

109
Q

Management of TGA?

A

Prostaglandin to keep duct open
Can do atrial septostomy to keep foremen ovale open.

110
Q

What is the procedure called for permanent repair of TGA

A

Arterial switch- done at 2 weeks of age
95% success rate, complications only 2-5%

111
Q

Complications post TGA repair

A

RBBB, arrythmias, heart failure (in adulthood)

112
Q

Main pathology in hypoplastic left heart?

A

NO LV. and as a result, hypoplastic aortic arch

113
Q

in Hypoplastic LH, what are the other heart lesions required to keep the heart working?

A

ASD and PDA

114
Q

What are the three procedures for Hypoplastic left heart, the order of operation and age when they are done?

A

Nor wood at one week
Gleen at 4-6 months
Fontan at 4-5 yo

End result is a two chamber heart

115
Q

What is the main pathology in truncus arteriosus

A

COMBINED aorta and pulmonary artery connected to a VSD. Occurs due a failed truncus septum formation.
4 types.

116
Q

What is specific about heart sounds in truncus arteriosus?

A

SINGLE loud S2

117
Q

Which congenital heart lesions will be present day 1 of life?
(Think of the ones that dont need a PDA)

A

Critical aortic stenosis
Tricuspid or pulmonary atresia
Hypoplastic left heart

118
Q

Which CHD present in days? (think of all the ones that need PDA)

A

TGA
TAPVR
Truncus arteriosus
PDA

119
Q

TGA XR?

A

Egg on a string. Large ventricles trying to make everything work

120
Q

2 viruses associated with foetal endocardial fibroelastosis

A

Mumps and cocksackie
Essentially viral myocarditis leading to endocardial thickening.
COCKsackie - CARDIAL fibroelastosis

121
Q

One maternal cause of foetal HYPERTROPHIC cardiomyopathy?

A

Diabetes

122
Q

What is the most common cause of death in an atheletic adolescent?

A

HYPERTROPHIC CARDIOMYOPATHY
Think atheletic, lots of muscles

123
Q

Syndromic causes of HYPERTROPHIC CDM

A

Noonan syndrome, LEOPARD syndrome, Danon syndrome, Fabry disease, Wolff-Parkinson-White syndrome, Friedreich ataxia, MERRF, MELAS

Pompe’s as well. All the storage disorders.

124
Q

ECG for hypertrophic cardiomyopathy

A

left ventricular enlargement
Some ST and T wave anomalies

125
Q

What is the most common form of cardiomyopathy

A

Dilated CDM

126
Q

What is the most common cause of dilated CDM

A

50% genetic
Usually muscular dystrophies, mitochondrial or fatty acid oxidation defects.

127
Q

Medications leading to dilated CDM

A

DOXORUBICIN

128
Q

Genetic syndromes associated with restrictive CDM

A

Gaucher disease, hemochromatosis, Fabry disease, familial amyloidosis; mucopolysaccharidoses, Noonan syndrome

129
Q

Pathophys of restrictive CDM

A

normal ventricle size, muscle size and contraction but POOR contraction

130
Q

How to differentiate between myocarditis and DCM with onset of new LV dysfn

A

Myocarditis= short onset, raised trop/CRP, normal heart size, lymphocytes on biopsy

DCM= long onset, normal inflamma markers, thin LV, no lymphocytes but scarring ntoed

131
Q

What criteria are used for diagnosis of ARF

A

Jones criteria
Need 2 major and 1 minor OR
1 minor and evidence of prev GAS

132
Q

Major manifestations in ARF criteria?

A

J: Joint (arthritis)
O: Think heart, pancarditis
N: nodules, subcutaneous
E: erythema marginatum
S: sydneham chorea

133
Q

Minor crtieria for ARF

A

FRAPP
Fever
Raised ESRCRP
Arthalgia
Prev RF
Prolonged PR interval.

NOte this is diff for low and high risk ppn

134
Q

First and second most common presenting major criteria for rheumatic fever

A

Arthritis
Pancarditis

135
Q

Classic examination findings for sydenham chorea

A

milkmaid grip on finger squeeze, pronation when arms extended, tongue darting when protruded

136
Q

Treatment for acute ARF

A

10 days Pen V for acute infection.
Monthly Bezathine Penicillin until 21 yo or for 10 years whichever is longer

137
Q

2 of the most common valves involved in RHD

A

mitral and aortic

138
Q

2 most common causes of infective endocarditis in paeds

A

Strep viridans and staph aureus

139
Q

signs of endocarditis (peripheral)

A

Embolic phenomenoa
Roth spots, petechaie, splinter nail bed, haemorrhages, osler’s nodes, janeway lesions

140
Q

Prevention of endocarditis

A

Prophylactic antibiotics for:
1. RHD
2. prosthetic cardiac valves
3. Unrepaired CHD

Cephalexin prior to dental procedures

141
Q

Most common virus assocaited with myocarditis

A

coxsackie

142
Q

Which 2 medications can you not give in SVT in a patient with WPW

A

Verapimil and Digoxin

143
Q

Treatment for atrial flutter in neonates

A

cardioversion

144
Q

Long term therapy for atrial flutter in neonates

A

Digoxin, propranolol, or sotalol for 6-12 mo

145
Q

Which drug binds to and inhibits the sodium/potassium-ATPase (sodium pump) within the plasma membrane of cardiac myocytes.

A

Digoxin

146
Q

What are some antiarrythmics used to manage cardiac arrythmia- just know these vaguely

A

class I agents such as procainamide or propafenone or class III agents such as amiodarone and sotalol

147
Q

In the first week of infancy, are T waves upright or inverted?

A

UPRIGHT in precordial leads

148
Q

When are T waves inverted in paeds

A

Can be until age 8

149
Q

5 causes of peaked T waves

A

Hyperkalemia
Hypercalcaemia
RIGHT ventricular hypertrophy
volume overload
benign early repolarisation

150
Q

5 causes of flat T waves

A

Hypokalemia
Hypocalcaemia
Newborn
hypothyroidism
Digoxin
Peri/myocarditis

151
Q

Hypokalmia ECG changes

A

Flat T waves
U wave
ST depression
Atrial and ventricular ectopics
VF and VT

152
Q

Hyperkalemia ECG changes

A

Peaked T waves
Wide QRS
Increased PR interval

(think of Jen’s dance)

153
Q

Hypocalemia ECG changes

A

Flat or absent T waves
U waves
Prolonged ST and QT

154
Q

ECG changes with hypercalcemia

A

Tall T waves
Reduced QT
Prolonged and depressed ST
Arrythmia

155
Q

AVRT or AVNRT- which is more common in neonates vs childhood

A

AVRT in neonates
AVNRT in childhood

156
Q

Classic features for WPW on ECG

A

Short PR
Delta wave

157
Q

What is WPW associated with

A

Ebstein’s anomaly
(which is also associated with lithium use in pregnancy)

158
Q

Dose for synchronoous cardioversion in kids

A

0.5-2J/kg

159
Q

Which tachycardia ia cardioversion ineffective for

A

junctional ectopic tachycardia

160
Q

Treatment for SVT - first, second line

A

First line: Valsava
If stable-> IV adenosine

If unstable, DC cardioversion

161
Q

Jervell-Lange-Nielsen syndrome

A

What is this syndrome associated with?
Cogenital hearing loss and prolonged QT

Jervell is a QT said Lange, but Jervell couldnt hear as he is deaf.

162
Q

Clinical presentation of long QT syndrome

A

The clinical manifestation of LQTS in children is most often a syncopal episode brought on by exercise, fright, or a sudden startle; some events occur during sleep (LQT3).

163
Q

Treatment for long QT syndrome

A

Propranolol and nadolol may be more effective than atenolol and metoprolol.
Can require pacemaker

164
Q

Which antipsychotics cause prolonged QT

A

haloperidol, risperidone, chlorpromazine

165
Q

Inheritance for Brugada

A

Autosomal dominant

166
Q

Defect in Brugada

A

Cardiac sodium channel genes

‘Think Brugada doesnt like salt’

167
Q

Describe first degree HB

A

Fixed PR prolongation al all atrial impulses–> ventricular beat

168
Q

Describe second degree heart block- Mobitz 1

A

Wenkebach
Progressively longer PR interval and then one missed ventricular contraction (dropped beat)

169
Q

Mobitz II- describe

A

PR prolongation but no progression. Some atrial impulses wont have a ventricular impulse.

170
Q

3rd degree HB? Describe

A

complete dissociation

171
Q

Prevention of CHB in mums with lupus?

A

Commencement of hydroxychloroquiine at 10 weeks

172
Q

What is Holt -Oram syndrome

A

AD
Hypoplastic thumbs and radii, first degree HB

‘Holtaram has no thumbs and heart block’

173
Q

Cardiac problem in PHACES?

A

abberant subclavian origin and coarctation

174
Q

Stelleate iris, long philtrum, prominent lips, supravavular aortic stenosis

A

Williams

175
Q

Category of heart defects in CHARGE

A

conotruncal

176
Q

Gene and chromosome for Charge

A

think 6,7,8
6 letters in charge
CHD 7 gene
Chromosome 8

177
Q

Common cardiac lesion in FASD

A

ASD
A alco , A ASD

178
Q

4 medications that can cause tetralogy of fallot

A

Na valproate
Warfarin
Thalodomide
Oestrogen/progesterone

179
Q

What is the natural pacemaker of the heart?

A

SA node

180
Q

What is the functional unit of a myocyte?

A

Sarcomere

181
Q

How is contraction mediated in the heart

A

Calcium mediated.

181
Q

How is contraction mediated in the heart

A

Calcium mediated.

182
Q

What are the 3 long QT syndromes and a feature of each? Include which one has what ion/channel involved.

A
  1. KCNQ1 – Hannah is bad at swimming, SLOWK (M>F)
  2. KCNH2- 2 startled. FAST potassium channel. (F>M)
  3. SCN5A- Sodium channel and sleep in special care nursery. (causes sleep death)

RACP Written (18 decks)

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