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Cardiovascular Flashcards

1
Q

S+S of cardiac failure?

A

Sx:

  • Breathlessness (particularly on feeding or exertion)
  • Sweating
  • Poor feeding
  • Recurrent chest infections 


Signs:

  • Poor weight gain or ‘faltering growth’
  • Tachypnoea
  • Tachycardia
  • Heart murmur, gallop rhythm
  • Enlarged heart
  • Hepatomegaly
  • Cool peripheries
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2
Q

How does congenital heart disease present? (5)

A
  • Antenatal cardiac USS diagnosis
  • Heart murmur (most common – most innocent)
  • Heart failure
  • Shock
  • Cyanosis
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3
Q

Cardiac examination?

A
  • Cyanosis
  • Clubbing of fingers or toes
  • Pulse – rate, rhythm, volume
  • Inspection – distress, precordial bulge, scars, ventricular impulse
  • Palpation – thrill (palpable murmur), apex (4th-5th intercostal 
space, mid-clavicular line), right ventricular heave (lower left sternal 
edge) shows right ventricular hypertrophy
  • Auscultation – heart sounds in four areas (apex, LLSE, ULSE, URSE) 
and the back. Check for murmurs, loud heart sounds, splitting of 
heart sounds
  • Hepatomegaly
  • Lung bases
  • Femoral pulses
  • Blood pressure
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4
Q

Normal pulse rate by age?

A
  • <1y = 110-160
  • 2-5y = 95-140
  • 5-12y = 80-120
  • > 12y = 60-100
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5
Q

What are the causes of heart failure in

a) Neonates
b) Infants
c) Older children

A

a) Obstructed (duct-dependent) systemic circulation
- Hypoplastic left heart syndrome
- Critical aortic valve stenosis
- Severe coarctation of the aorta
- Interruption of the aortic arch

Infants (high pulmonary blood flow):

  • VSD
  • AVSD
  • Large 
persistent ductus arteriosus

Older children and adolescents (R–>L heart failure):

  • Eisenmenger syndrome (right heart failure only)
  • Rheumatic heart disease
  • Cardiomyopathy
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6
Q

How do you manage a duct-dependent lesion?

A

Prostaglandin infusion until defect fixed to maintain patency

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7
Q

How do you manage a R–>L shunt with cardiac failure?

A
  • Give diuretics and captopril

- Problem should either resolve or need surgery

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8
Q

What are the features of an innocent murmur?

A
  • Asymptomatic patient
  • Soft blowing murmur
  • Systolic murmur only, not diastolic
  • Left sternal edge
  • Normal heart sounds with no added sounds
  • No parasternal thrill
  • No radiation
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9
Q

What is a venous hum?

A

Harmless murmur in children
Heard above R clavicle over jugular vein
Heard throughout cardiac cycle
Abolished by placing finger on jugular vein
Murmur may disappear on lying or turning head

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10
Q

4 conditions with a L–>R shunt?

A

ASD
VSD
AVSD
PDA

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11
Q

Most common congenital heart defect?

A

VSD (30%)

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12
Q

2 types of ASD?

A
  1. Secondum ASD (foramen ovale) - 80%

2. Partial AVSD - 20%

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13
Q

S+S of ASD?

A

Sx:

  • Often asymptomatic
  • Recurrent chest infections/wheeze
  • Arrhythmias (4th decade onwards)

Signs:

  • Ejection systolic murmur
  • Best heard at upper L sternal edge (due to increased flow across pulmonary valve because of L–>R shunt)
  • Fixed and widely split 2nd heart sound (hard to hear) – due to RV stroke vol being equal in inspiration and expiration
  • With partial AVSD apical pansystolic murmur may be heard from AV valve regurgitation
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14
Q

CXR and ECG changes in ASD?

A

CXR

  • Cardiomegaly
  • Enlarged pulmonary arteries
  • Increased pulmonary vascular markings

ECG

  • Secundum ASD –> partial RBBB (can also occur in normal children) and RAD due to RV enlargement
  • Partial AVSD will give a ‘superior’ QRS axis (largely negative in AVF) due to defect being near AV node
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15
Q

What is best Ix for ASD?

A

Echo

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16
Q

Management of ASD?

A
  • Children with large enough defect to cause RV dilation will require treatment
  • For secundum ASD this is by cardiac catheterisation with insertion of an occlusion device
  • For partial AVSD surgical correction required
  • Treatment usually undertaken at 3-5y in order to prevent right HF and arrhythmias in later life
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17
Q

How are VSDs classified?

A

Small (80-90%)
- <3mm (smaller than aortic valve)

Large (10-20%)
- >3mm (larger than aortic valve)

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18
Q

S+S of small VSD?

A

Sx: asymptomatic

Signs: Loud pansystolic murmur at LLSE
Quiet 2nd sound

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19
Q

Ix of small VSD?

A

CXR and ECG = normal

Echo - small VSD with no pulm HTN

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20
Q

Management of small VSD

A

These lesions will close spontaneously

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21
Q

S+S of large VSD?

A

Sx:

  • HF with breathlessness and FTT after 1w old
  • Recurrent chest infections

Signs:

  • HF –>Tachypnoea, tachycardia and enlarged liver
  • Active precordium should be felt (vol overload)
  • Soft (large defect) pansystolic murmur heard at LLSE
  • Apical mid-diastolic murmur present (due to increased flow across mitral value from blood leaving lungs)
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22
Q

What do Ix show in large VSD?

A

CXR

  • Cardiomegaly
  • Enlarged pulmonary arteries
  • Increased pulmonary vascular markings
  • Pulmonary oedema

ECG
- Biventricular hypertrophy by 2m of age (upright T wave – pulmonary HTN)

Echo

  • Anatomy of defect
  • Pulmonary HTN (due to high flow)
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23
Q

Management of large VSD?

A
  • Treat HF –> diuretics + captopril
  • Additional calorie input
  • Surgery at 3-6m to prevent Eisenmenger syndrome
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24
Q

Clinical features of PDA?

A
  • Continuous murmur beneath left clavicle
  • Continues into diastole because pressure in pulmonary artery always lower than aorta
  • Pulse pressure increased and this → collapsing or bounding pulse
  • Sx can be unusual but when duct is large there will be increased pulmonary blood flow with HF and pulmonary HTN
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25
Q

Management of PDA?

A
  • Closure recommended to abolish lifelong risk of bacterial endocarditis and pulmonary vascular disease
  • Closure is with coil or occlusion device introduced via cardiac catheter at about 1yo
  • Occasionally surgical ligation required
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26
Q

Which syndrome is AVSD associated with?

A

Downs

  • 15-20% with downs have AVSD
  • (45% with Down’s have some form of congenital heart disease)
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27
Q

Clinical features of aortic stenosis?

A

Sx:

  • Most asymptomatic
  • If severe –> reduced exercise tol, chest pain on exertion, syncope

Signs:

  • Small vol and slow rising pulse
  • Carotid thrill (always)
  • Ejection systolic murmur at URSE radiating to neck
  • Delayed and soft aortic second sound
  • Apical ejection click
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28
Q

Management of AS?

A

Balloon dilatation

  • If sx or high resting pressure gradient
  • Safe in older children
  • Dangerous in neonates

Most children with sig stenosis requiring treatment in first few years of life will eventually require aortic valve replacement
- Early treatment therefore palliative and directed at delaying this for as long as possible

29
Q

S+S of pulmonary stenosis?

A

Sx:

  • Most asymptomatic and diagnosed clinically
  • A small number of neonates with critical pulmonary stenosis have duct dependent pulmonary circulation and present in first few days of life with cyanosis

Signs:

  • Ejection systolic murmur at ULSE and thrill may be present
  • Ejection click may be heard at ULSE
  • If severe, prominent RV impulse (heave)
30
Q

Treatment of PS?

A

Balloon dilatation

31
Q

What could outflow obstruction in well child be due to?

A

AS

PS

32
Q

What could outflow obstruction in sick child be due to?

A

Coarctation
Interruption of aortic arch
Hypoplastic L heart

33
Q

What is coarctation of the aorta?

A
  • Due to arterial duct tissue encircling aorta at point of insertion of duct
  • When duct closes, aorta also constricts, causing severe obstruction to LV outflow
  • Commonest cause of collapse due to left outflow obstruction
34
Q

S+S of coarctation?

A

Sx:

  • Examination on first day of life usually normal
  • Neonates usually present with acute circulatory collapse at 2d of age when duct closes

Signs:

  • Sick baby with severe HF
  • Absent femoral pulses
  • Severe metabolic acidosis
  • Murmur may be heard at ULSE
35
Q

Ix for coarctation?

A

CXR - cardiomegaly from HF and shock

ECG - normal

36
Q

What are the associations with coarctation?

A

Bicuspid AV valve
VSD
Turner syndrome

37
Q

Management of coarctation?

A

Give prostaglandins and HF drugs first
Surgical repair soon after diagnosis
–> Angioplasty with or w/o stenting
- Sometimes open surgery needed

38
Q

What are the duct dependent heart conditions?

A 
Coarctation
TGA – Transposition of the great arteries 
HLHS – Hypoplastic left heart syndrome 
PA – Pulmonary atresia

TA – Tricuspid atresia
Aortic stenosis – if severe 
Pulmonary stenosis – if severe
39
Q

What is tricuspid atresia?

A
  • Tricuspid valve absent/abnormally developed
  • No blood flow RA–>RV
  • Must have ASD & VSD to survive
  • PDA usually to allow greater pulmonary flow
40
Q

What is pulmonary atresia?

A
  • Pulmonary valve fails to develop
  • No outflow from heart to lungs
  • No problem in utero
  • When born only thing providing O2 to lungs is PDA
  • Baby turns blue rapidly
  • -> Quick diagnosis
41
Q

Management of duct-dependent lesion?

A
  • Prostaglandin infusion (retain patency)
  • This only short term solution
  • Formaldehyde should be infiltrated into structure for longer term
42
Q

What is hypoplastic left heart?

A
  • Complete underdevelopment of L side of heart
  • Mitral valve small or atretic
  • LV diminutive and usually aortic valve atresia
  • Ascending aorta v small and almost invariably coarctation
  • Must be an ASD to allow returning blood to leave LA and re-circulate
43
Q

Clinical features of hypoplastic left heart?

A
  • May be detected antenatally at USS
  • → Allows effective counselling - helps prevent child becoming sick after birth
  • If present after birth → sickest of all neonates presenting with duct dependent systemic circulation
  • No flow through L side of heart so ductal constriction → profound acidosis and rapid cardiovascular collapse
  • Weakness or absence of all peripheral pulses in contrast to weak femoral pulses in coarctation
44
Q

Management of hypoplastic L heart?

A

Difficult neonatal operation called Norwood procedure

Followed by further operations at 6m and again at 3y

45
Q

What is SVT?

A
  • Most common childhood arrhythmia

- Presents with rapid heart rate b/w 250-300 bpm

46
Q

Sx of SVT?

A
  • Poor cardiac output and pulm oedema
  • Sx of HF in neonate or young infant
  • Cause of hydrops fetalis (accumulation of fluid in several separate compartments) and intrauterine death
47
Q

Management of SVT?

A

Circulatory and respiratory support
- Correct tissue acidosis and give positive pressure ventilation if required

Vagal stimulation manoeuvres

  • e.g. carotid sinus massage or ice cold pack to face
  • Successful in 80%

IV adenosine = treatment of choice

  • Induces AV block after rapid bolus injection
  • Terminates tachycardia and hence breaks re-entry circuit that has been set up b/w AV node and accessory pathway
  • Given incrementally in increasing doses

Electrical cardioversion with a synchronised DC shock (0.5-2 J/kg body weight)
- If adenosine fails

Maintenancy therapy once sinus rhythm restored

  • Flecanide or sotalol
  • Treatment stopped at 1y
48
Q

What are the causes of R–> L shunts?

A

Tetralogy of Fallot
Transposition of the great vessels
Eisenmenger syndrome

49
Q

Key features of tetralogy of fallot?

A

1 Large VSD
2 Overriding of aorta with respect to ventricular septum (basically this means it receives into from both L and R 
ventricles)
3 Sub-pulmonary stenosis causing RV outflow tract 
obstruction
4 RV hypertrophy as a result

50
Q

S+S of tetralogy of fallot?

A

Sx:

  • Most diagnosed antenatally or ID of murmur
  • Cyanosis
  • Breathlessness
  • Pallor

Signs:

  • Clubbing in older children
  • Loud, harsh ejection systolic murmur at L sternal edge from day 1 of life
  • With increasing RV outflow obstruction, which is predominantly muscular and below pulmonary valve, murmur will shorten and cyanosis will increase
51
Q

What do Ix show in TOF?

A

CXR

  • Relatively small heart
  • RV hypertrophy
  • Pulmonary artery bay

ECG

  • Normal at birth
  • RV hypertrophy later (inverted T waves, no S wave)
52
Q

Management of TOF?

A

BT shunt

  • Early management if v cyanosed
  • Increases pulmonary flow by putting tube b/w subclavian and pulmonary aa

Complete correction

  • At 6m
  • Close VSD
  • Releive RV outflow obstruction

Hypercyanotic spells

  • Need treatment with Iv propanolol, bicarbonate for acidosis, muscle paralysis and ventilation
  • Only if >15mins
53
Q

What is transposition of the great vessels?

A
  • Aorta connected to RV and pulmonary artery connected to LV
  • –> Blue blood returned to body and pink blood returned to lungs
  • 2 parallel and completely isolated circuits and, unless mixing of blood b/w them → incompatible with life
  • Fortunately naturally occurring defects such as VSD and ASD are common
  • PDA as well as therapeutic interventions can achieve mixing for short amount of time
54
Q

S+S of transposition of great vessels?

A

Sx:

  • Cyanosis = predominant symptom - can be profound or even life threatening
  • Presentation usually on day 2 of life when ductal closure → marked reduction in mixing of desaturated and saturated blood
  • Cyanosis less severe and presentation delayed if more mixing of blood for associated abnormalities e.g. ASD

Signs:

  • Cyanosis always present
  • 2nd heart sound often loud and single
  • Usually no murmur, but can be systolic murmur from increased flow or stenosis within LV (pulmonary) outflow tract
55
Q

Ix for transposition of great vessels?

A

CXR

  • Narrow pedicle
  • Egg on side
  • Increased pulmonary vascular markings

ECG
normal

Echo
Definitive

56
Q

Management of transposition of great vessels?

A

Immediate = prostaglandin infusion

Balloon atrial septostomy in 20% - makes formaen ovale valve incompetent so mixing allowed

Surgery to switch arteries

  • All pts need this
  • Performed in first few d of life
57
Q

What cardiac defect associated with Turners?

A

Coarctation

58
Q

What cardiac defects associated with Noonan’s?

A

Pulmonary stenosis
Hypertrophic cardiomyopathy
Septal defects - ASD/VSD

59
Q

What cardiac defects associated with Marfan’s?

A

Weakened aorta - dissection or aneurysm

Mitral/tricuspid valve prolapse

60
Q

What causes myocarditis?

A

Viral / bacterial

  • Influenza
  • Coxsackie
  • Adenovirus
  • Polio
  • Rubella
  • Lyme disease

Inherited

Secondary to metabolic condition

Others:

  • Allergies
  • Fungus/parasites
  • Radiation
  • Some drugs
61
Q

S+S myocarditis?

A

Sx:

  • Can be mild at first and difficult to detect or can sometimes appear suddenly
  • Include FTT, anxiousness, feeding difficulties, fever, HF, listlessness, low urine output and pale peripheries
  • Sx in older children (>2) can include nausea, belly ache, chest pain, cough, fatigue and swelling (legs, feet and face)
  • Difficult to diagnose as sx tend to mimic other heart and lung disorders

Signs:

  • Rapid heartbeat or abnormal heart sound
  • Fluid at lung bases due to pulmonary oedema
  • Signs of infection may be present
62
Q

Ix for myocarditis?

A

CXR:
- Enlargement of the heard borders

Further tests:
- Blood cultures, LFTs, U&E’s, antibody screen, heart biopsy and FBC

Echocardiography:
- Usually the mode of diagnosis

63
Q

Management of myocarditis?

A
  • No cure
  • Aim = minimise damage and treat sx until condition resolves
  • Treating sx with diuretics and ACE inhibitors and carvedilol (a B-adrenoceptor blocking agent) is important
  • Abx, steroids, anti- inflammatory drugs and IV immunoglobulin - protect heart

Usually improves spontaneously, but some children will ultimately require heart transplantation

64
Q

Who is at highest risk of sub-acute bacterial endocarditis? (SBE)

A

Turbulent blood flow

  • VSD
  • Coarctation
  • PDA
  • Prosthetic material
65
Q

Clinical features of SBE?

A
  • Sustained fever
  • Anaemia
  • Pallor
  • Splinter haemorrhages
  • Clubbing (late)
  • Necrotic skin lesions
  • Changing cardiac signs
  • Splenomegaly
  • Neurological signs of infarcts
  • Retinal infarcts
  • Arthritis/arthralgia
  • Haematuria (microscopic)

–> Raised ESR

66
Q

Diagnosis of SBE?

A
  • Multiple blood cultures before abc
  • Echo may show vegetations
  • CRP + ESR
67
Q

What is most common pathogen in SBE?

A

Alpha-haemolytic strep - strep viridans

68
Q

Management of SBE?

A

High dose penicillin
Aminoglycoside
–> 6w using IV therapy

Surgical removal may be required if incomplete eradication (more common if prosthetic material)

Prophylaxis with good dental hygiene in all with congenital heart disease

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