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3a > Paediatrics: Cardiology > Flashcards

Paediatrics: Cardiology Flashcards

1
Q

Fetal Circulation: Where does gas exchange occur?

A

placenta

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2
Q

Fetal circulation: what gets exchanged at the placenta?

A
  • Collect oxygen + nutrients
  • Dispose of waste products (CO2 + lactate)
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3
Q

How many shunts are there in the Fetal circulation ? name them?

A

3
- Ductus venosus
- Foramen ovale
- Ductus arteriosus

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4
Q

Why does blood not go to fetal lungs?

A

Fetal lungs not developed or functional so shunts allow blood to bypass lungs

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5
Q

From where to where does ductus venous shunt? what does it bypass?

A

Umbilical vein => Ductus venosus => Inferior vena cava
- Bypass the liver

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6
Q

If there was no ductus venosus, then where would blood flow?

A

Umbilical vein => portal vein => liver => hepatic vein => inferior vena cava

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7
Q

From where to where does foramen ovale shunt? what does it bypass?

A

Right atrium => foramen ovale => left atrium
- Bypass RV + pulmonary circulation

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8
Q

From where to where does ductus arteriosus shunt? what does it bypass?

A

Pulmonary artery => ductus arteriosus => aorta
- Bypass pulmonary circulation

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9
Q

Fetal circulation: what different ways can blood get from RA to aorta?

A
  • RA => foramen ovale => LA => LV => aorta
  • RA => RV => pulmonary artery => ductus arteriosus => aorta
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10
Q

At birth describe what happens to foramen ovale? explain
what does it become?

A

fist breath expands alveoli in lungs => decrease vascular resistance => decrease pressure in RA => LA pressure > RA pressure => closure of foramen ovale (eventually => fossa ovalis)

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11
Q

What is required to keep ductus arteriosus open? be specific

A

prostaglandins (E1)

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12
Q

At birth describe what happens to ductus arteriosus? explain
What does it become?

A

At birth: increased blood oxygenation => decreased prostaglandin conc => closure of ductus arteriosus (=> ligament arteriosum)

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13
Q

What are congenital heart defects?

A

Group of structural abnormalities of the heart the are present at birth

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14
Q

What physiology would cause a cyanotic CHD? briefly

A

L => R shunt

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15
Q

Give examples of Cyanotic CHD (3)

A
  • Tetralogy of fallot
  • Transposition of the great arteries
  • Tricuspid atresia
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16
Q

give the 2 categories of cyanotic CHD?

A
  • Shunt lesions
  • obstructive lesion
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17
Q

Give examples of shunt lesions? are these cyanotic or not? (3)

A

VSD, ASD, Patent ductus arteriosus
asyanotc but can beomce cyanotic (Eisenmenger syndrome)

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18
Q

how to obstructive CHD affect the heart?

A

narrowing/blockage in heart => increase pressure load => hypertrophy

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19
Q

what are innocent murmurs also known as, are they common?

A

innocent/flow murmurs are common in children

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20
Q

what physiology causes an innocent murmur

A

caused by fast blood flow through hear in systole

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21
Q

What are the typical features of an innocent murmur?

A

SSSSSSSSS
- Soft
- Short
- Systolic
- Symptomless
- Situation dependant

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22
Q

When would you want to investigate a murmur in a child? what signs?

A
  • Loud murmur
  • diastolic
  • louder on standing
  • Other symptoms (failure to thrive, feeding difficulty, cyanosis, sob)
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23
Q

Describe a pan systolic murmur?

A

continue throughout the whole systolic contraction of the heart

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24
Q

What can cause a pnasystolic murmur? (3)

A
  • Mitral regurgitation
  • Tricuspid regurgitation
  • VSD
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25
Q

What can cause an ejection systolic murmur? (4)

A
  • Aortic stenosis
  • Pulmonary stenosis
  • ASD

(- tetralogy of Fallot (due to pulmonary stenosis))

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26
Q

What causes splitting of the second heart sound? During which bit of respiration is it normally heard?

A

Splitting of the second heart sound: normal sound heard on inspiration caused by the negative intrathoracic pressure (generated when chest wall + diaphragm pull lungs open)
- normal on inspiration

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27
Q

What pathology could cause a fixed split second heart sound? describe the murmur associated with this

A

ASD: ejection systolic, crescendo-descrendo murmur, loudest at the upper left sternal border, with fixed split second heart sound (on inspiration + expiration)

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28
Q

what heart murmur would teroatlofy of fallot present with? what is this due to?

A

murmur due to pulmonary stenosis => ejection systolic murmur

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29
Q

What is tetralogy of Fallot?

A

Congenital cardiac condition with 4 co-existing pathologies

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30
Q

what are the 4 pathologies in ToF?

A
  • VSD
  • overriding aorta
  • Pulmonary stenosis
  • Right ventricular hypertrophy

Think of the cowboy riding the aorta, squeezing the pulmonary artery in the boot shaped heart.

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31
Q

Describe the pathophysiology of ToF? of each pathology

A

VSD allos blod to flow through ventricles
- Overriding aorta means ta entrance to aorta (aortic valve) is placed further ro the right than normal => when RV contracts => more (more deoxy blood sent through aorta)
- Stenosis of pulmonary valve => greater resistance against flow of blood form RV => more blood through VSD into aorta => R to L shunt => cyanosis
- Increased strain on RV + pulmonary stenosis => RV hypertrophy

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32
Q

ToF RF? (4)

A
  • Rubella infection
  • Increased maternal age
  • Maternal alcohol use
  • trisomy 21
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33
Q

ToF presentation?

A
  • Mostly picked up antenately, or ejection systolic murmur at NIPE
  • cyanosis, clubbing, poor feeding, poor weight gain
  • tet spells
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34
Q

What are Tet spells?

A

intermittent spells wehre R => L shunt temporarily worsens => cyanotic episode

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35
Q

What causes tet spells ? (physiology)

A

Due to increase in pulmonary vas resistance or decrease in systemic resistance

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36
Q

Features of tet spells? (3)

A
  • Rapid, deep respiration
  • Irritability
  • Increasing cyanosis
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37
Q

Management of ToF? medical and surgical?

A

medical: squatting, prostaglandin infusion, BB, morphine
- Surgical (definitive): total surgical repair by open heart surgery

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38
Q

what is the common CXR finding of ToF

A

boot shaped heart

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39
Q

What is PDA?

A

Patent Ductus Arteriosus
- Failure of closure of the ductus arteriosus

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40
Q

when does normal functional and structural closure of ductus arteriosus occur?

A

Functional: 1-3 days
Structural: 2-3 weeks

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41
Q

PDA RF? (2)

A
  • Prematurity
  • Maternal rubella
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42
Q

what kind of shunt in PDA? describe the pressures briefly ?

A

L => R shunt
- Pressure in aorta > pressure in pulmonary vessels

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43
Q

what does the shunt in PDA cause? describe the steps

A

L to R shunt => increased blood flow through pulmonary circulation => pulmonary hypertension + R sided heart strain => R sided hypertrophy => pulmonary pressure greater than systemic => eisenmengers syndrome => cyanosis

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44
Q

PDA presentation in infants?

A
  • SOB
  • difficulty feeding
  • Poor weight gain
  • Recurrent LRTI
  • murmur
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45
Q

What heard on auscultation of patient with PDA?

A

continuous crevscendo-descrencend machinery murmur during 2nd heart sound

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46
Q

when might PDA first be picked up?

A

murmur on newborn exam

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47
Q

what is the gold standard investigation of PDA?

A

transthoracic echo + doppler (to assess size and character of L=>R shunt)

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48
Q

describe the management of PDA?

A
  • monitor up until 1 yr (unless severe)
  • After 1 yr it is unlikely to close spontaneously so surgery: transcatheter, open heart surgery
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49
Q

What is an atrial septal defect?

A

When the septum between the R + L atria is not formed properly?

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50
Q

what is the most common CHD?

A

VSD
(ASD is second)

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51
Q

describe what forms and makes up the atrial septum? ahem the layers?

A

2 walls grow downward to fuse with endocardial tissue to separate atria
- septum primum + septum secondum

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52
Q

what makes up the foramen ovale?

A

small space formed between septum primum + secondum

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53
Q

what kind of shunt does ASD cause ? cyanotic ?

A

LA => RA shunt (a-cyanotic)

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54
Q

describe what the shunt in ASD can cause?

A

shunt LA to RA => R sided overload + R heart strain => pulmonary hypertension + RHF => Eisenmenger Syndrome (where pulmonary pressure is greater than systemic pressure) => shunt reverse (R=>L) => cyanosis

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55
Q

what are the 3 types of ASD?

A
  • Ostium primum
  • Ostium Secondum
  • PFO (technically not ASD)
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56
Q

what is the most common type of ASD?

A

Ostium Secundum (I think)

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57
Q

Patient presents with DVT that develops a large stroke. What condition should be on your mind? why?

A

ASD
- DVT enters systemic circulation through shunt and goes to brain

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58
Q

What are some complications of ASD?

A
  • Stroke
  • AF
  • Atrial flutter
  • Pulmonary hypertension
  • R sided HF
  • Eisenmenger Syndrome
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59
Q

ASD RF?

A
  • Maternal smoking (1st trimester)
  • Maternal diabetes
  • Maternal rubella
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60
Q

ASD presentation? childhood?

A

vast majority of ASD are asymptomatic
- SOB
- Difficulty feeding
- Poor weight gain
- Recurrent LRTI

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61
Q

ASD presentation? Adulthood?

A
  • Stroke
  • HF
  • Dyspnoea
62
Q

ASD gold standard investigation ?

A

transthoracic echo (gold standard)

63
Q

management for small ASD?

A

Just keep watching it

64
Q

what medical management might you have for ASD? why?

A

anticoags (aspirin, warfarin, NOACs) to reduce stroke risk

65
Q

ASD definitive management?

A

surgical
- transvenous Catheter (via femoral vein) or open heart surgery

66
Q

What is VSD?

A

congenital hold in the septum between the 2 ventricles

67
Q

what is VSD often associated with?

A

underlying genetic condition (downs, turners)

68
Q

what type of shunt in VSD?

A

L to R shunt (acyanotic)

69
Q

what does the shunt in VSD lead to?

A

L to R shunt => R sided overload + RHF + increased flow to pulmonary vessels => pulmonary hypertension => R to L shunt (eisenmengers) => cyanosis

70
Q

VSD RF?

A
  • genetic: Downs, Turners
  • GDM
  • FAS
  • VSD FHx
71
Q

What does septal defect presentation depend on

A

the size of the defect

72
Q

VSD most common presentation

A

asymptomatic

73
Q

VSD presentation in babies?

A
  • Poor feeding
  • SOB
  • failure to thrive
  • Tachypnoea
74
Q

What heart on auscultation of ASD?

A

Ejection systolic murmur
Heard loudest at the upper left-sternal edge
Widely fixed splitting of the second heart sound

75
Q

what heard on auscultation of VSD?

A

pansystollic murmur hear at L lower sternal border

76
Q

What can a pan-systolic murmur indicate? (3)

A
  • VSD
  • MItral regurg
  • Tricuspid regurgitaiton
77
Q

Gold standard investigation for VSD?

A

transthoracic Echo

78
Q

what complications associated with VSD?

A
  • Increased risk of IE
  • Recurrent LRTI
  • Arrhymias
  • Growth failure
  • Congestive HF
79
Q

what medications might you consider in VSD?

A
  • Prophylactic Abx (for IE risk)
  • Dieretic to relieve pulmonary congestion
80
Q

When does Eisenmenger Syndrome occure

A

When blood can flow from R side of heart to L across structural heart lesion
- R=>L shunt means blood bypasses lungs what

81
Q

3 underlying lesion can cause Eisenmenger Syndrome ?

A
  • ASD
  • VSD
  • PDA
82
Q

when does Eisenmenger Syndrome develop ?

A

can develop after 1-2 years with large shunts + adulthood with small

83
Q

what condition makes Eisenmenger develop more quickly?

A

pregnancy so need echo check ups

84
Q

what is cyanosis and what is this due to?

A

blue discolouration of the skin due to low level oxy sats

85
Q

Eisenmenger Syndrome: what is the body’s response to chronic low oxy sats? what does this cause?

A

Increased RBC + haemoglobin production => polycythaemia => high blood viscosity => more prone to blood clots

86
Q

what are some signs of pulmonary hypertension on examination?

A
  • R ventricular heave
  • Raised JVP
  • Peripheral oedema
87
Q

What are some of the signs you might see related to chronic hypoxia on examination?

A
  • Cyanosis
  • Clubbing
  • Dyspnoea
  • Plethoric completion (red complexion related to polycythaemia)
88
Q

Pansystolic murmur: what CHD?

89
Q

Mid systolic crescendo-descrecendo fixed split heart sound: what CHD?

90
Q

Contiunous crescendo-descrendo machiar murmurou during 2nd heart sound: what CHD?

91
Q

How does eisenmengers affect life expectancy ?

A

reduces life expectancy by 20 yrs

92
Q

Eisengmengers management ?

A

heart lung transplant
Prostaglandins?
Oxygen?

93
Q

What is coarctation of the aorta? usually located where?

A

It is a congenital condition where there is narrowing of the aortic arch (usually located around the ductus arteriosus)

94
Q

what genetic condition is coarctation of the aorta often associated with?

A

Turners syndrome

95
Q

Pathophysioloyf of coarctation of the aorta?

A

narrowing of aorta => decreased pressure of blood flowing to arteries distal to narrowing + increased pressure to those proximal (heart _ usually fist 3 branches of aorta

96
Q

Presentation of coarctation of the aorta?

A
  • Weak femoral pulses
  • tachypnoea
  • Increased work of breathing
  • Poor feeding
  • Grey floppy baby
97
Q

what might you find on examination of baby with coarctation of the aorta ?

A

4 limb blood pressure (increased BP in limbs proximal to narrowing + decreased BP distally)

98
Q

management of coarctation of aorta?

A

May live symptom free till adulthood
- If severe emergency surgery
- Prostaglandin

99
Q

why use prostaglandin in critical management of coarctation of aorta?

A

Prostaglandin E keeps ductus arteriosus open while waits for surgery (allows bleed flow through DA into systemic circulation distal to coarctation)

100
Q

What is Congenital Aortic calve stenosis? why bad?

A

Patients born with a narrow aortic valve => restrict blood flow from LV to aorta

101
Q

how many leaflets usually in the aortic valve?

102
Q

what are the leaflets of the aortic valve also known as?

A

aortic sinuses of valsalva

103
Q

how many leaflets might the aortic valves of patients with congenital aortic valve stenosis have?

A

1,2,3 or 4 (compared to the normal 3)

104
Q

how does congenital aortic valve stenosis usually present?

A

asymptomatic (discovered as incidental murmur on routine checkup)if

105
Q

symptomatic, how would congenital aortic stenosis present?

A
  • fatigue
  • SOB
  • dizziness
  • Fainting
    (all worse on exertion)
106
Q

describe the murmur associated with congenital aortic stenosis ? hear loudest where?

A

ejection systolic murmur heard loudest at aortic area
- crescendo-descrenscdo character that radiates to the carotids

107
Q

where is the aortic area (anatomical) ?

A

2nd ICS R sternal border

109
Q

Congenital aortic stenosis complications:

A
  • LV outflow tract obstruction
  • HF
  • Ventricular arrhythmias
  • Sudden death on exertion
110
Q

how may leaflets are there usually in the pulmonary valve?

111
Q

what causes pulmonary valve stenosis?

A

when the 3 leaflets of the pulmonary calve develop abnormally => thicken or fuse

112
Q

pulmonary valve stenosis causes a narrowing from where to where

A

between RV + pulmonary arteries

113
Q

what condition is pulmonary valve stenosis associated with?

114
Q

describe the murmur associated with pulmonary valve stenosis ?

A

ejection systolic murmur heard loudest in pulmonary areaw

115
Q

here is the pulmonary area (anatomical)

A

2nd ICS L sternal border

116
Q

What is ebsteins anomaly ?

A

congenital heart condition where the tricuspid valve is set lower in R heart (towards apex)

117
Q

how does Ebstein’s affect RA + RV ?

A

bigger RA
smaller RV
( because lower tricuspid valve)

118
Q

what septal defect is Ebstein’s anomaly associated with?

119
Q

What is transposition of the Great Arteries ?

A

It is where the attachments of the aorta + pulmonary trunk swap (transpose)

120
Q

in Transposition of the great arteries where to RV and LV pump blood to?

A
  • RV pump blood to aorta
  • LV pump blood to pulmonary vessels
121
Q

why is transposition of the great arteries life threatening?

A

there is no connection between systems circulation + pulmonary circulation => baby will be cyanosed

122
Q

what does immediate survival in transposition of the great arteries depend on?

A

depends on a shunt (PDA, ASD, VSD)
- allows mixing of oxy + deoxy blood

123
Q

egg on string appearance seen on CXR. what condition is this?

A

transposition of the great arteries

124
Q

what is the most common septal defect found in those with Down syndrome ?

125
Q

what CHD is most commonly associated with turners syndrome?

A
  • Coarctation of the aorta
  • Bicuspid aortic valve
126
Q

where is an asd best heard?

A

This murmur is heard in the second intercostal space at the upper left sternal border (pulmonary area)

(same as AVSD)

127
Q

In transposition of the great arteries, what is the acid-base status commonly found in these patients that requires correction? explain

A

Metabolic acidosis

  • Distal organs have a low oxygen supply and thus respire anaerobically producing lactate
128
Q

What is Infective endocarditis ?

A

it is infection of the endothelium (inner surface) of the heart
- Mostly effects the heart valves

129
Q

what are the 3 things in the IE triad ? (things required for IE to happen)

A
  • Endothelial damage
  • Platelet adhesion
  • Microbial adhesion
130
Q

which bit of IE triad do CHDs increase the risk of?

A

structural abnormalities of heart or great vessels => endo damage by sheer stress forces

131
Q

IE RF?

A

Mostly seen in patients with hx of congenital or acquired cardiac disease
- IVDU (quite low is this population group but higher in adults)

132
Q

2 most common causative organisms for IE?

A
  • Staphylococcus aureus
  • Streptococcus viridans
133
Q

IE presentation ?

A

(non-specific)
- Low-grade fever
- malaise
- Fatigue

134
Q

what would be seen on examination for patient with IE?

A
  • New or changing heart murmur
  • Splinter haemorrhages, janeway lesions, oslers nodes, roth spots, finger clubbing, petechiae
135
Q

what investigations for IE?

A
  • Blood cultures (before Abx)
  • Echo (TOE (transoesophageal))
136
Q

what would be seen on echo of IE

A

echo (TOE)
- identify vegetations

137
Q

what score can confirm IE diagnosis?

A

Modified duke criteria: Has major and minor criteria

138
Q

IE management ?

A
  • IV broad spectrum Abx (amoxicillin or ceftrioxone)
  • Surgery: if HF, or large vegetations, or not responding to Abx
139
Q

What is Acute rheumatic fever? associated with what other illness?

A

It is an autoimmune illness that occurs after pharyngitis in some people due to cross reactivity to streptococcus bacteria

140
Q

which system does rheumatic fever affect?

A

Multi system disorder
- affects joints, heart, skin, nervous system

141
Q

which bacteria involved in rheumatic fever? what type of bacteria is this?

A

group A beta-haemolytic strep (e.g. strep pyogenes)

142
Q

rheumatic fever pathophysiology ? describe it

A

type to hypersensitivity reaction
- caused by antibodies created against strep bacteria that also target tissues in body

143
Q

how long after initial infection will symptoms of rheumatic fever present?

A

2-4 weeks following strep infection (e.g. tonsillitis)

144
Q

describe the symptoms rheumatic fever can present with 9think systems)

A
  • Fever
  • Joint: arthritis
  • heart: pericarditis/myocarditis/endocarditis
  • Skin: sub cutaneous nodules, erythema marginatum
  • HS: chorea
145
Q

describe the arthritis associated with rheumatic fever?

A

migratory arthritis affecting the large joints

146
Q

what is used to determine a rheumatic fever diagnosis?

A

Jones criteria (has major - minor criteria)

147
Q

what investigations would you do for rheumatic fever?

A
  • throat swab for bacterial culture
  • ASO antibody titres
  • Echo, ECG, CXR (for heart involvement)
148
Q

rheumatic fever management ?

A
  • the tonsillitis caused by streptococcus should be treated with phenoxymethyl penicillin
  • Clinical features of RF: NSAIDs (joint pain), aspirin and steroids (carditis), prophylactic Abx
149
Q

rheumatic fever complications (3)

A
  • Recurrence of RF
  • Valvular heart disease (mitral stenosis)
  • Chronic HF

3a (43 decks)

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