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FRACP exam paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

When can you hear a loud P2?

A

Pulmonary hypertension

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2
Q

What is normal splitting of the second heart sound?

A

Splitting of A2 and P2 in INSPIRATION

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3
Q

When is normal splitting heard?

A

Children and young adults

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4
Q

What is wide mobile splitting of the second heart sound?

A

Wide splitting of A2 and P2 heard in BOTH inspiration and expiration, inspiration >expiration

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5
Q

When is wide mobile splitting of the second heart sound heard?

A

Pulmonary stenosis
Pulmonary hypertension
RBBB

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6
Q

What is reversed splitting of the second heart sound?

A

Wide splitting of A2 and P2 during EXPIRATION

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7
Q

When is paradoxical splitting of the second heart sound heard?

A

Aortic stenosis
LBBB
HOCM

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8
Q

What is wide fixed splitting of the second heart sound?

A

Wide splitting of A2 and P2 heard in BOTH inspiration and expiration, inspiration = expiration

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9
Q

When is wide fixed splitting of the second heart sound heard?

A

ASD

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10
Q

What is S3?

A

Heard after S2 in ventricular relaxation
Due to rapid ventricular filling
Can be normal OR pathological
1. Normal in children, athletes, pregnancy
2. Increased LV stroke volume- AR, MR
3. Restrictive ventricular filling - constrictive pericarditis, restrictive cardiomyopathy
4. Ischaemic heart disease

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11
Q

What is S4?

A 
Heard before S1 in atrial contraction, before ventricular contraction
Always pathological
Due to forceful atrial contraction
Seen in:
HOCM
Long-standing HTN
IHD
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12
Q

What is an ejection click?

A

An extra SYSTOLIC sound.
A high pitched sound heard just after S1 - indicates maximal opening of aortic and pulmonary valve.
Heard in:
Biscuspid valve
Flexible stenotic aortic or pulmonary valve
Pulmonary dilatation
Dilated aorta

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13
Q

What is an opening snap?

A

An extra DIASTOLIC sound
Heard just after S2
Best heard in the apex
Heard in mitral stenosis- sound as the mitral leaflets suddenly dome into the LV during early diastole

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14
Q

What cardiac surgery gives a Left thoracotomy with a normal brachial pulse?

A

PDA ligation
Pulmonary artery banding
Non-cardiac

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15
Q

What cardiac surgery gives a Left thoracotomy scar with a normal or reduced brachial pulse?

A

Blalock-Taussig shunt

Co-arctation repair (left subclavian flap)

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16
Q

What cardiac surgery gives a Right thoracotomy scar wit a normal brachial pulse?

A

Right Blalock-Taussig shunt

Non-cardiac

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17
Q

What cardiac surgery gives a median sternotomy scar?

A

Any corrective cardiac surgery. Brachial artery will be normal

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18
Q

What is the normal axis shown by the anterior leads?

A

Lead I - upright (R)
Lead II- upright (R)
Lead III- equivocal

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19
Q

What is the LAD axis shown by the anterior leads?

A

Lead I - upright (R)
Lead II- equivocal
Lead III -downward (S)

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20
Q

What is the RAD axis shown by the anterior leads?

A

Lead I- downward/equivocal
Lead II- upright (R)
Lead III- upright (R)

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21
Q

What is the superior axis shown by the anterior leads?

A

S >R wave in AvF

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22
Q

How do you know if you are truly in sinus rhythm?

A

P wave reflects that it is originating from the RA (SA node)
Upright P wave in lead I (therefore originating from R) and moving left)
and in AvF (therefore moving from top to bottom)

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23
Q

What are features of an ASD on ECG and auscultation?

A

Murmur R) upper sternal edge
Mild RAD
May have partial RBBB

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24
Q

What are features of an ASD on ECG and other IX

A 
ESM murmur R) upper sternal edge
Fixed split of second heart sound
RV lift
Normal pulses
Normal Axis or RAD
May have partial RBBB
Plethora on CXR
Cardiomegaly on CXR
Prominent PA on CXR
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25
Q

What are anterior leads on an ECG?

A

V3, V4

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26
Q

What are the inferior leads on an ECG?

A

II, III, AvF

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27
Q

What are the lateral leads on an ECG?

A

I, AvL, V5, V6

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28
Q

What are the septal leads on an ECG?

A

V1, V2

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29
Q

What ECG changes do you see in L-TGA

A

Deep Q wave V1

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30
Q

What are normal Q waves?

A

Q waves present in I,II,III, AvF, V5, V6

and up to 7mm in II and III

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31
Q

What are pathological Q-waves in children?

A

Broad AND deep

Present in V1 (indicate L-TGA, single ventricle, severe RVH or inferior MI

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32
Q

What features suggest a Still’s murmur?

A

2-3/6 vibratory murmur ULSE + LLSE
Normal pulses
Normal ECG
Disappears or becomes quieter on sitting up and extending the neck

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33
Q

What are the ULN of S waves in V1 and the R waves in V6 according to age? (looking for RVH)

A 
S waves in V1
birth- 20mm
6m- 25mm
1yr- 12mm
10y-25mm
R waves in V6
Birth- 13mm
6m- 25mm
1yr-25mm
10y-30mm
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34
Q

What ECG and other changes do you get with a VSD without pulmonary HTN?

A

Normal ECG or LVH
Loud pansystolic murmur, may have a parasternal thrill
Normal pulses
CXR may be normal or have cardiomegaly if LVH

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35
Q

What ECG and sx do you get with a VSD WITH pulmonary HTN?

A

RVH on ECG
Loud pansystolic murmur with parasternal thrill
Loud P2 (increased flow through pulmonary valve)
+/-mid-diastolic murmur APICAL murmur if large VSD due to increased flow coming back through the lungs through mitral valve
CXR- cardiomegaly, increased pulmonary vascular markings

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36
Q

What ECG changes and Sx do you get with Eisenmeger syndrome?

A 
Pansystolic murmur
Cyanosis, fatigue, dyspnoea, haemoptysis
Right ventricular heave
Loud P2
RVH on ECG 
Tall and spiked P waves
CXR- Cardiomegaly, prominent pulmonary artery with peripheral tapering of pulmonary vessels
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37
Q

What ECG changes do you expect in LVH

A

Tall R wave in V1
Deep S wave in V5/V6
LAD

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38
Q

What are the ULN of R waves in V1 and the S waves in V6 according to age? (looking for LVH)

A 
R wave in V1
birth- 20mm
6m- 17mm
1yr- 16mm
10yr-12mm
S wave in V6
birth-15mm
6m- 10mm
1yr-7mm
10y-5mm
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39
Q

What do you see on ECG in biventricular hypertrophy?

A

Big R wave in V1
Big R and S waves in V5/6
May have big R/S waves in V3-V4

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40
Q

What ECG changes do you see in RVH?

A

RAD
Upright T wave in V1
Tall R wave in V1
Deep S wave in V6

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41
Q

When is an upright T wave in V1 pathological?

A

when upright from the age of D4 to around 4 years old

Sign of RVH

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42
Q

What causes cyanosis and RVH?

A
  1. Tetralogy of fallot (right to left shunt due to outflow obstruction)
  2. Severe pulmonary stenosis and an ASD
  3. Severe pulmonary stenosis and a VSD
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43
Q

When can an inverted T wave be pathological?

A

In severe RVH due to “strain”

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44
Q

What changes on ECG do you see in RAH?

A

Tall, peaked P waves (>3mm).in lead II and V1

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45
Q

What causes RAH and RVH on ECG?

A

Total anomalous venous pulmonary drainage

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46
Q

What changes on ECG do you see with LAH?

A

Bifid P wave ( P mitrale) and prolonged (>2.5 small sq or 0.1s) in Lead II
In V1 have bifid with 1st half upright (representing RA) and 2nd half inverted and larger (representing LA)

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47
Q

What changes on ECG do you see with combined atrial hypertrophy?

A

Lead II- Bifid wave with first half tall and peaked and second half rounded
V1- Bifid wave with equiphasic waves. First half upright, second half inverted

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48
Q

What causes RAH?

A 
Ebsteins anomaly
Pulmonary stenosis
Tricuspid regurg
Tricuspid stenosis (rare)
Pulmonary stenosis
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49
Q

What causes LAH

A

Mitral regurg
Large VSD
Mitral stenosis (rheumatic heart disease)
Severe untreated LVH

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50
Q

What changes do you see in ASD primum

A

LAD (conduction of bundle has shifted)
IRBBB
ESM over pulmonary area
Plethoric on CXR +/- cardiomegaly

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51
Q

ECG changes in ASD secundum

A

May have LAD
RBBB (conduction abnormalities)
Abnormalities in the right precordial leads (i.e. V3R or V4R) –> rSr or rsR
(resulting from dilation and hypertrophy of the right ventricular outflow tract caused by volume overload of the right heart.)

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52
Q

LAD

A 
LVH with overload i.e.Large VSD
ASD primum (AVCD)
TA
L-TGA
LBBB (rare. broad complex)
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53
Q

What can cause an elevated ST segment in children?

A

Myocarditis, pericarditis, severe LVH

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54
Q

What are normal ST elevation levels

A

Up to 1mm in most leads

Up to 2mm in V2-V4

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55
Q

What congenital heart disease cause issues during fetal life causing fetal loss or hydrops?

A

Valvular regurgitation

  • Developed heart (esp TR)
  • In complete atrial ventricular canal defec
  • In Truncus arteriosus (MR/TR)
  • Arrythmia (complete block (bradycardia) or atrial arrhythmia (tachycardia)
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56
Q

What CHD may present with a critically ill child in the first 24 hours of life? (usually not breathless)

A

Severe vulvular regurgitation (might be born in
- especially ebstein’s anomaly (bad TR and large atria with pulmonary hypoplasia) and absent pulmonary valve syndrome –> only if severe, otherwise sats about 85% and looks ok
Obstructed TAVPD
“early” duct dependent presentation (if PDA closes)

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57
Q

What CHD present with a critically ill child after the first 24 hours of life? (severe cyanosis)

A
  1. Dependent on a PDA for PULMONARY blood flow
    - Severe cyanosis when duct closes
    e.g. critical PS, pulmonary atresia, single ventricle with PS or PA

2.Dependent on PDA for SYSTEMIC blood flow
 -Low cardiac output when duct closes
e.g critical AS, critical coarctation, HLHS

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58
Q

What CHD present with an ill child after the first 24 hours of life- 2weeks? (severe cyanosis)

A
  1. Dependent on a PDA for PULMONARY blood flow
    - Severe cyanosis when duct closes
    e.g. critical PS, pulmonary atresia, single ventricle with PS or PA
  2. Dependent on PDA for SYSTEMIC blood flow
     -Low cardiac output when duct closes
    e.g critical AS, critical coarctation, HLHS
  3. Dependent on PDA for mixing
    • Cyanosis when duct closes
    • TGA
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59
Q

What is Ebstein’s anomaly?

A

Leaflets of Tricuspid are displaced downward and posteriorly = big RA + very small non-functioning RV
= big dilated RA of the heart (=big heart on CXR) and can cause pulmonary hypoplasia

Cyanosis since birth
Extreme cardiomegaly on CXR with oligaemia and also RA enlargement
LAD and LVH with possible delta waves (WPW) on ECG

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60
Q

What causes a very big heart +/- pulmonary hypoplasia on CXR?

A

Ebstein’s anomaly

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61
Q

What can cause a slightly enlarged heart with respiratory distress and pneumonia (DDX respiratory)

A

TAVPD with venous obstruction (confluence is)obstructed)

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62
Q

What is TAVPD?

A

Veins form behind the heart but don’t join to the heart

  • either come in behind and join the anomanent (supracardiac- present more like an ASD)
  • or come down and joining IVC (infra diaghragmatic) - most likely to be obstructed

Small left atrium
Left to Right shunt across PFO/ASD

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63
Q

What gives a “snowman” cardiac silhouette on CXR?

A

SUPRACARDIAC TAVPD
SVC is big
Veins come in behind up and join the anomanent

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64
Q

What tests do you do to investigate a child you suspect has CHD?

A 
Investigations
• CXR, ECG
• Hyperoxia test (pO2 >150mmHg very unlikely with cyanotic heart
disease)
• Echocardiogram when indicated
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65
Q

DO you hear a murmur in a child with TGA?

A

No

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66
Q

What is TGA?

A

Due to abnormal development of the fetal heart during the first 8 weeks of pregnancy, Swappage of the large vessels of the heart (function as 2 separate pumps)
M>F
Blue, looking well, maybe slightly breathless
CXR- lung fields look ok or plethoric (pooling and stasis of blood)
Don’t respond to oxygen–> so echo

67
Q

What cyanotic (Duct dependent lesions) present with oligaemic (more black as decreased blood flow) on CXR?

A

Pulmonary stenosis

pulmonary atresia

68
Q

What cyanotic (Duct dependent lesions) present with plethora (increased blood flow) on CXR and a narrow mediastinum on CXR?

A

TGA

position of pulmonary artery is Posterior anterior

69
Q

What cyanotic (Duct dependent lesions) present with congestion (pooling blood flow) on CXR?

A

TVAPD

70
Q

How do you treat TGA?

A
  1. Start prostin to keep ductus open

2. Introduce balloon to enlarge atrial sepum

71
Q

What cardiac causes heart failure (breathless, poor feeding) between 2-6 weeks (due to decreasing pulmonary vascular resistance)

A 
VSD with coarctation (occurs the earliest - at 2 weeks)
Large VSD
PDA
CAVC
Truncus
TOF with pulmonary atresia
Single ventricle with no PS
72
Q

What CHD causes cardiac failure in babies between 2-6 weeks with plethora on CXR, left atrial enlargement,
a slightly big heart that may be a bit globular in shape?

A

Large VSD

73
Q

What can cause hyperinflation on CXR in a child with CHD?

A

Congestive heart failure

74
Q

What can CHD can present with a right aortic arch?

A

TOF

75
Q

What happens in TOF with pulmonary atresia?

A

No main pulmonary artery supply

Blood supply comes from primitive collaterals branching from the aorta (blood then moves through the PDA)

76
Q

What are symptoms of CHF in infants

A
  • Tachypnoeic
  • Poor feeding
  • Poor growth
  • Tachycardia
  • Diaphoresis
  • Hepatomegaly
77
Q

What lesions do you need to pick up earlier because they are high pressure which can cause pressure overload (requires repair as can cause pulmonary HTN)

A

Large VSD

Truncus arteriosus

78
Q

What lesions cause pressure load on the heart?

A

Large VSD

Truncus arteriosus

79
Q

What lesions cause volume load on the heart?

A

ASD

80
Q

What kinds of asymptomatic murmurs are there?

A 
“Functional” commonest (Still's)
ASD
Mild PS
Mild AS (ejection click)
Coarctation, PDA (NOT heard at time of delivery), etc
81
Q

When is a heart murmur more likely to be associated with CHD?

A

<12 months of age
Have features of congestive heart failure

On Cardiovascular examination have-
loud murmur
loud second heart sound
abnormal brachial and/or femoral pulses

82
Q

What are important points in children aged 18months- 5 years with a heart murmur?

A 
-New murmurs are unlikely to be related
to important CHD
- A delay in diagnosis of ASD or minor aortic or pulmonary
-Valve anomalies is rarely of any
consequence
-Most can wait until 3+‐ 5 years of age
for a further assessment
83
Q

What is the most common cause of murmurs (other than Still’s - extra flow across pulmonary valve) in children > 3 years old?

A

ASD
May present with hyper-dynamic precordium (can feel the RV)
Widely split second sound
Systolic flow murmur

84
Q

What types of ASD are there?

A 
secundum ASD (middle of septum)
sinus venous ASD (often fairly high up)
Primum ASD (low down- close to AV valve) - may be associated with MR
85
Q

What type of ASD is associated with anomalus pulmonary drainage?

A

Sinus venous ASD

86
Q

What are the features of Coarctation?

A

• Murmur heard posteriorly between scapula
• Diminished femoral pulses
May have have radio-femoral delay
• Hypertension
• Association with bicuspid aortic valve (can give dilated aortic root)

87
Q

What is a venous hum?

A

Innocent murmur
Continuous murmur
Accentuated in diastole
Varies with posture, head movement (turning head to the side)

88
Q

What does the colour Doppler mean?

A

Blue- going away
Red- coming towards
Direction of flow and velocity (brighter = speeding up)

89
Q

What is the Bernoulli equation?

A

From Velocity to Pressure Change
Used to calculate pressure change i.e across a valve (in an echo)

The (simplified) Bernoulli Equation
 Pressure = 4 x (distal velocity2 ‐ proximal velocity2)
• The proximal velocity only matters if its elevated
(eg coarctation)

• The (very simplified) Bernoulli Equation
 Pressure = 4 x distal velocity2

90
Q

What are the normal pressures in the chambers of the heart?

A

add here

91
Q

How do you calculate fractional shortening?

A

FS = (EDD-ESD)/EDD

92
Q

How do you calculate ejection fraction?

A

EF = (EDV-ESV) / EDV

93
Q

What is fractional shortening?

A

Fractional shortening (FS) is the fraction of any diastolic dimension that is lost in systole.
Faster to calculate than EF. one dimensional
Normal is 30%
If >30% possible hyperdynamic
If <30% dysfunction

94
Q

What is ejection fraction?

A

The amount, or percentage, of blood that is pumped (or ejected) out of the ventricles with each contraction.
3 dimensional, takes longer. Increase risk of inaccurancy
Normal approx. 60%

95
Q

What is Fick’s principle for calculating the ratio of systemic flow and pulmonary flow to determine if there is a shunt?

A

Systemic flow = QS
Pulmonary flow = QP
In a normal heart the QS=QP, therefore the ratio is 1

QP/QS= (aortic oxygen saturation - mixed venous saturation)/ (pulmonary venous saturation - pulmonary arterial saturation)

QP/QS= (Aosat - Mvsat)/(Pvsat - PAsat)

96
Q

How do you calculate pulmonary vascular resistance?

A

Using an adapted equation which is related to Poiseuilles equation (R = 8ln/πr^4)

PVR (measured in um2)
MAOP (mmhg) = mean pulmonary arterial wedge pressure. This measures the pressure of the left atria
Cardiac output (measured in l/min)

PVR = (MABP- MAOP)/Cardiac output

97
Q

What is Poiseuilles equation?

A

is a physical law that gives the pressure drop in an incompressible and Newtonian fluid in laminar flow flowing through a long cylindrical pipe of constant cross section.
It can be used to look in respiratory and cardiology to look at resistance in a tube (i.e bronchioles, alveoli, or blood vessels)

R = 8ln/πr^4 (l=length, n=viscosity, r = radius)

98
Q

What are the normal and abnormal ratios of pulmonary blood flow to systemic blood flow (QP/QS)?

A

Ratio 1 = normal heart
>1 = left to right shunt
<1 = right to left shunt

99
Q

What are the normal values of oxygen saturations in the heart and surrounding vessels?

A

RA-75% LA-95%
RV - 75% LV - 95%
PA-75% AO-95%

100
Q

What are the normal values of pressures in the heart and surrounding vessels?

A

RA- <10mmhg LA- <10mmhg
RV- 25/5mmhg LV- 100/5mmhg
PA- 25/10 (mean 15mmhg) AO- 100/60 (varies)

101
Q

Why is it important to treat cardiac lesions in children with Trisomy 21?

A

Because they have a much earlier onset of pulmonary vascular obstructive disease (when you get severe and irreversible pHTN)

102
Q

What is the risk of mortality of cardiac catheterisation?

A

0.13%

103
Q

What are the risks of dilating a stenotic aortic valve?

A

If over do it can cause Aortic regurgitation
Can damage the mitral valve
Can cause arrhythmia

104
Q

How does atrial balloon valvuloplasty work when treating TGA?

A

Via cardiac catheterisation
First keep PDA open with Prostin
Introduce balloon into atria –> push through the septum primumm to tear a hole and create a permanent flap

105
Q

Why does pulmonary balloon vavuloplasty not work/not work as well in Noonan’s syndrome?

A

In Noonan’s syndrome there is often a DYSPLASTIC valve as well as pulmonary stenosis. This means you usually have to repair the valve and widen the annular ring instead

106
Q

What syndrome can present with pulmonary stenosis, aortic stenosis, LVH and the endocrine condition of hypercalcemia?

A

William’s syndrome

107
Q

What is peripheral pulmonary stenosis and what is the nature of the murmur?

A

An innocent murmur which occurs after 48hrs of life and occurs in early infancy.
Sound is due to turbulent flow of the pulmonary arteries as vascular resistance decreases.
Grade 1-2 Mid ejection systolic murmur heard loudest LUSE with radiation to the axilla or to the back.

108
Q

What murmur do you hear in Triscuspid atresia and when?

A

Hear it at birth
Baby has poor apgars usually
Blowing murmur heard maximally at LLSE

109
Q

What does a PDA sound like?

A

Heard at the upper left sternal edge
Continuous murmur
Crescendo-decrescendo
Present at birth until ductus closes

110
Q

What is an AVSD?

A

AKA complete AV canal defect or endocardial cushion defect
Associated with Down’s syndrome
Heart failure occurs one to two months after birth
Recurrent pneumonia
If no surgical intervention,most die by two to three years
Pulmonary vascular disease develops as early as six-12 months of age
Down syndrome makes infant particularly prone to pulmonary vascular disease

111
Q

What is the Rx of AVSD?

A

Medical management:

Start digoxin, diuretics, captopril if signs of CHF
Antibiotics and supportive measures for pneumonia and infection
Antibiotic prophylaxis for SBE

Surgical management:

Complete AVSD = surgery (to correct sturctural haemodynamic derangement)
Most infants are unresponsive to medical management +/- elevated pulmonary vascular resistance
Repair between three to eight months.
Earlier for Down syndrome

Procedures:

Curative: closure of primum ASD &inlet VSD, and reconstruction of left AV valves under cardiopulmonary bypass. OR
Palliation with pulmonary arterial banding is reserved for the subset of patients who are either too small or have other associated lesions that make early corrective surgery too risky

112
Q

What changes on ECG do you see in AVSD?

A

LAD
Mean frontal QRS is in superior position
Biventricular hypertrophy (by 2 months of age)
Q wave lead I and AVL
RSR V1 (RBBB)
May have tall P waves (Right atrial hypertrophy)
Prolonged PR

113
Q

What murmurs do you hear with AVSD

A

Same as ostium secundum (region of fossa ovalis, and most common defect):
May have mild left precordial bulge
May have R) ventricular systolic left at parasternal border
Sometimes pulmonary systolic click
Wide and split fixed heart sound (from increased pulmonary flow)

In addition to:
Apical mid-diastolic low rumbling murmur LLSE or apex due to flow through AV valves
May have harsh apical pansystolic murmur at the apex which radiates to the axilla (mitral valve insufficiency)

114
Q

What is preload?

A

The end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand

115
Q

What is afterload?

A

Afterload is the pressure against which the heart must work to eject blood during systole (systolic pressure). The lower the afterload, the more blood the heart will eject with each contraction. Like contractility, changes in afterload will raise or lower the Starling curve relating stroke volume index to LAP.

116
Q

What is the main thing which affects cardiac output in exercise?

A

HR

CO = HR x SV

117
Q

What are the DDx for S2?

A

Single S2 suggests pulmonary or aortic atresia or severe stenosis, truncus arteriosus, transposition of the great arteries or ToF

118
Q

What would you see in TOF with mild LVOTO?

A

Acyanotic lesion - pink well perfused child
Single S2
Loud, harsh LLSE murmur, radiates widely = increased flow pulmonary valve

ECG- The ECG demonstrates right axis deviation (negative deflection lead I, positive deflection aVF) and right ventricular hypertrophy (tall R wave R1 with upright T waves, deep S V6, positive T wave in V4R). These changes are consistent with ToF.

CXR- may or may not have increased pulmonary vascular markings.
Typical boot shape EXCEPT may not be seen in early ToF with mild RVOTO as RV hypertrophy may be minimal.

119
Q

What are the signs, sx and ECG changes for acute pericarditis?

A

Causes are mainly viral

  • Cocsackie virus, enteroviruses
  • Staph, TB
  • Oncological, rheumatic fever

Signs and sx

  • acute inspiratory chest pain, better on sitting up and forward
  • Acute collapse from pericardial effusion
  • soft muffled HS, pericardial friction rub
  • Fever

ECG
ST elevation widespread and convex upwards
T wave inversion

Rx: Ibuprofen, drainage of large effusion (or can cause constrictive pericarditis with depressed voltages

120
Q

What shows the ‘egg on side’ shape on a CXR in a neonate with CHD?

A
  • TGA

- Narrow vascular pedicle (the aorta is in front of the PA)

121
Q

What shows the ‘Boot’ shape on a CXR in a neonate with CHD?

A
  • TOF with pulmonary atresia

- Pulmonary artery bay because of absent pulmonary artery

122
Q

What shows the ‘snowman IN a snow storm’ shape on a CXR in a neonate with CHD?

A

Head of snowman is made of superior mediastinal shadow formed by SVC on right side, vertical vein on left side and left brachicephalic vein superiorly. Body of snowman is the heart.

Snowstorm is in reference to pulmonary plethora

  • Obstructed TAPVD
  • Small heart with pulmonary venous congestion
123
Q

What shows the ‘snowman’s sign’ shape on a CXR in an infant with CHD?

A
  • TAPVD without obstruction

- Visible ascending vein in left upper border

124
Q

What shows a wall to wall heart on a CXR in a neonate with CHD?

A
  • Ebstein anomaly

- Massive cardiomegaly with RA dilatation

125
Q

In what condition in an older child do you have Cardiomegaly with increased vascular markings on CXR?

A

ASD

126
Q

In what condition in an older child do you have a small heart and pulmonary oligaemia on CXR?

A
  • Eisenmenger syndrome

- Possibly secondary to VSD or AVSD

127
Q

What shows a Globular heart on CXR

A
  • Pericardial effusions
  • Pericarditis with effusion
  • Dilated cardiomyopathy
128
Q

What CHD is associated with oligaemic lung fields?

A

Caused by reduced pulmonary blood flow

  • TOF
  • Ebstein’s anomaly
  • PPHTN
129
Q

What CHD is associated with plethoric lung fields?

A

Left to Right shunts

especially VSD and AVSD

130
Q

What ECG changes do you see in Pulmonary stenosis

A

Normal axis
R) ventricular hypertrophy
In critical PS will have RAH

131
Q

What ECG changes do you see in Severe aortic stenosis?

A

LVH
Peaked T-waves

No murmur if critical and will be cyanosed with RHF

132
Q

What ECG changes do you see in Tricuspid atresia

A

Superior axis
LVH

  • Duct dependent. No murmur usually
  • Boot shaped heart on CXR
  • SEVERE cyanosis at birth
133
Q

What ECG changes do you see in Truncus arteriosus?

A

LVH or Biventricular hypertrophy

134
Q

What happens critical aortic stenosis in a neonate?

A

RVH

Right to left shunt once the ductus closes through the foramen ovale. SO slightly low sats (approx 90%)

135
Q

What ECG and CXR changes do you see in Ebstein’s anomaly?

A

LAD
LVH
Short PR and delta waves (wpw)
R–> L shunt through the foramen ovale = ++volume left side
RA hypertrophy due to small R) ventricle and increased pressure for R –> L shunt
Mixing of deoxy and oxy via the PDA = sats ~85%

CXR:
Pulmonary oligaemia
Cardiomegaly
Enlarged RA

Is a DUCT DEPENDENT lesion (cyanosis in first week of life)

136
Q

What ECG changes do you see in TOF?

A

RVH, RAD

Boot shaped heart on CXR

137
Q

What are the type 1 antiarrythmics and how are they useful in children/neonates?

A

1a- procainamide, quinadine
1c- flecanide

MOA:

138
Q

What are the type II antiarrythmics?

A

ADD HERE

139
Q

What are the type III antiarrythmics?

A

Sotalol and Amiodarone
- Sotalol used in conjunction with digoxin as an IV infusion to help with atrial tachycardia
-Amiodarone
ADD HERE

140
Q

Antimicrobial prophylaxis is now recommended for

prevention of bacterial endocarditis in which cardiac conditions?

A

• Cardiac Conditions for which Endocarditis Prophylaxis is
Recommended
• Prosthetic Heart Valves (Bio or Mechanical)
• Rheumatic Heart Disease
• Previous Endocarditis
• Unrepaired Cyanotic Congenital Heart Disease i.e TOF (includes
palliative shunts and conduits)
• Surgical or Catheter Repair of Congenital Heart Disease within
6 months of repair procedure

141
Q

What ECG changes do you see in WPW?

A

• ECG at rest: short PR interval, delta waves (most obvious leads II, III, avF and
V4) = Wolff Parkinson White syndrome.
• ECG during palpitations: Regular, broad complex tachycardia at ~280 bpm, this
would be difficult to distinguish from VT.

142
Q

WPW is capable of both initiating and maintaining which type of tachycardia?

A

Antidromic atrio-ventricular re-entrant tachycardia.

• Antidromic atrioventricular re-entrant tachycardia (regular, broad complex tachycardia, impulses transmitted via the accessory pathway, with retrograde conduction via the AV node, much less common than orthodromic)

143
Q

What is Orthodromic (narrow complex) atrioventricular re-entrant tachycardia?

A

Regular, narrowcomplex tachycardia, as impulses are transmitted in the normal atria toventricle route via the AV node)
More common than Antidromic

Need to have a re-entrant tachycardia which requires accessory pathway for initiation and maintenance such as WPW

144
Q

What is Antidromic (broad complex) atrioventricular re-entrant tachycardia

A

regular, broad complex tachycardia, impulses transmitted via the accessory pathway, with retrograde conduction via the AV node, much less common than orthodromic

145
Q

What re-entrant tachycardias do not need an accessory pathway for initiation and maintenance?

A
  • Atrioventricular nodal re-entrant tachycardia
  • Atrial fibrillation
  • Atrial flutter
  • Ventricular tachycardia
  • Ventricular fibrillation
146
Q

What is the most likely aetiology of the progressive fatigue (and reduced exercise tolerance) in a child with doubly committed (supracristal, conal) ventricular septal defect?

A

Aortic regurgitation

• Supracristal VSD is the least common type of VSD (~5% of all VSDs) and is located adjacent to the
pulmonary and aortic valves
• A supracristal VSD can be complicated by PROLAPSE of an AORTIC LEAFLET into the defect, resulting in
aortic insufficiency; eventually occurs in 50-95% of patients
• RV outflow tract obstruction can also occur
• Left-to-right shunting of blood through the defect is believed to progressively pull aortic valve tissue
(especially the right coronary cusp) through a Venturi effect

147
Q

What is a superior axis?

A 
AKA extreme axis deviation (right)
Rare
QRS -90 to 180
Negative in both aVF and I
Causes:
Severe blocks
Severe Ventricular hypertrophy

Funnily enough seen in Noonan’s not for causes above but possibly due to counterclockwise rotation of the heart and the disturbed conduction system in some patients (RBBB)

148
Q

What is an important diagnostic marker of kids with possible Noonan’s syndrome?

A

Superior axis deviation (aka extreme axis deviation)
Found in 60% in children with Noonan’s AND cardiac abnormalities (most common being pulmonary stenosis, hypertrophic cardiomyopathy and interventricular communication)

149
Q

Fontan procedure

A

ADD

150
Q

Cardiac procedures

A

ADD

151
Q

Lateral MI in infants

A

ADD

152
Q

Coronary artery fistulae

A

Coronary artery fistulae account for 50% of congenital coronary artery abnormalities.

-They involve a direct communication between a coronary artery and either a chamber of the heart (coronary-cameral fistula) or a segment of the systemic or pulmonary circulation (coronary arteriovenous fistula), bypassing the intervening myocardial capillary bed.

  • Small fistulae do not cause any haemodynamic compromise and are asymptomatic.
  • The haemodynamic consequence of larger fistulae depends on the chamber or vessel in which the fistula drains into.
  • 90% terminate into the right side of the heart. Fistulae that drain into the systemic veins or RA mimics an ASD.
  • Those that drain into the pulmonary arteries have a physiology similar to a PDA, those into the LA produce a volume load into the LA mimicking MR and those that drain into the LV have a physiology similar to aortic valve regurgitation.
  • Large fistulae that drain into low pressure systems may cause coronary artery steal with myocardial ischaemia of the distal arterial bed. As flow through this low pressure system increases over time, aneurysmal dilation of the proximal vessel may evolve.

The majority of children with these fistulae are asymptomatic and are incidentally discovered on auscultation or during investigation of other lesions by echocardiogram or angiogram.

-The murmur is continuous, similar to a PDA, but is heard lower down on the sternal border and often peaks in mid-to-late diastole. Less commonly these lesions may present with angina, cardiac failure, endocarditis or arrhythmias

153
Q

Murmurs at birth

A
  • coronary artery fistulae (50% of cases). Usually asymptomatic
  • patent foramen ovale is not associated with any abnormal clinical signs and is asymptomatic unless complicated by paradoxical embolism
  • Pulmonary atresia (usually with a VSD) presents with cyanosis, a single S2 and typically a systolic murmur loudest at the left lower sternal border
  • Tetralogy of Fallot with absent pulmonary valve is a very rare disorder often detected prenatally. Signs and symptoms at birth include respiratory distress, variable degrees of cyanosis, a single second heart sound and a characteristic “to-and-fro” systolic and diastolic murmur best heard in the pulmonary area. This murmur is not continuous, as there is a short pause between the diastolic and systolic components.
  • ADD
154
Q

Perimembranous VSD and ECG changes

A

-Only get ECG changes if large, usually with significant shunting. Would expect LVH, RVH, LA enlargement

155
Q

PDA and ECG changes

A

If ECG changes present, would be of LVH, sometimes biventricular hypertrophy (only if big PDA which would only occur in babies)

156
Q

Pulmonary valve stenosis and ECG changes

A

ECG changes are of right axis deviation and RVH for the most part

In critical pulmonary stenosis - RAH and RVH

157
Q

Sub aortic stenosis and ECG changes

A

Gives you LVH on ECG with prominent Q in precordial leads (V1-V6)

158
Q

Long QT

A

The upper limit of normality is 0.45 secs up to six months of age and 0.44 secs in older children.
(shouldn’t be over 0.46 in boys, 0.47 in girls)

Causes of prOlOnged QT:
HypOkalemia
HypOcalcemia
ROmanO-ward syndrome
ErythrOmycin
Hypothermia
PhaeOchrOmOcytOma
HypOmagnesemia
Others:
◾Jervell-Lange-Nielsen syndrome
◾Cisapride
◾CNS/Head injury
◾Adrenal insufficiency
◾Quinidine
159
Q

Estimating Co using ficks principle

A

O2 consumption (ml/min)/ Ao sats- venous sats (ml/l)

= CO (L/min)

160
Q

TOF and ECG

A

RVH and RAD (+ boot shaped heart)

161
Q

Ebsteins anomaly and ECG

A

LAD, LVH
Possible delta waves (WPW)

Extreme cardiomegaly on CXR + oligaemia and large RA
Mild cyanosis (sats about 85%) at birth
162
Q

Diastolic murmurs

A

Early - pulmonary or aortic regurg

Mid- Mitral stenosis, tricuspid stenosis, severe mitral regurg causing ‘functional’ mitral stenosis

Late- complete heart block

163
Q

Tricuspid valve stenosis and ECG

A

RSR V1
RAH (p pulmonale)

mid diastolic murmur
Cor pulmonale with hepatomegaly and neck vein distension but not breathless therefore RV not involved

164
Q

Tet spell

A

Cyanotic spells
Occurs in TOF

Hypercyanotic episodes are characterised by:
◾paroxysms of tachypnoea
◾prolonged crying
◾intense cyanosis
◾decreased intensity of the murmur of pulmonic stenosis (ejection systolic) due to greater obstruction

FRACP exam paediatrics (25 decks)

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