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Paediatrics > Paediatric cardiology > Flashcards

Paediatric cardiology Flashcards

1
Q

What is the primary cardiovascular disorder in children?

A

Congenital heart disease, presents in most children during the first year of life

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2
Q

What is the hyperoxia test?

A

A hyperoxia test is a test that is performed—usually on an infant—to determine whether the patient’s cyanosis is due to lung disease or a problem with blood circulationAlso known as the nitrogen washout test

  • A preductal/ right radial arterial blood gas measurement is obtained after the baby has been breathing 100% oxygen for 15 minutes
  • If the supplementary oxygen does not lead to improved oxygen saturation this suggests the cause is cardiac
  • If the cause of low sats is respiratory, oxygen would lead to increased sats
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3
Q

What can cause a narrow upper mediastinum on chest x-ray?

A

Transposition of the great arteries

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4
Q

How does the ECG look in transposition of the great arteries

A

Normal

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5
Q

What are causes of cyanotic congenital heart disease (blue baby)?

A

Increased pulmonary blood flow

  • Transposition of great arteries
  • Common arterial trunk/ truncus arteriosus
  • Total anomalous pulmonary venous drainage

Decreased pulmonary blood flow

  • Tetralogy of Fallot
  • Severe pulmonary valve stenosis
  • Tricuspid atresia
  • Pulmonary atresia with ventricular septal defect
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6
Q

What is the most common cause of a heart murmur in an asymptomatic child that is growing well?

A

Innocent heart murmur - occur due to increased blood flow in a normal heart

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7
Q

What is rib notching?

A

Occurs in patients with coarctation of the aorta, enlarged arteries erode the chest wall in a bid to bypass the obstruction

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8
Q

Cyanotic vs acyanotic congenital heart disease

A

Right - to - left shunt = CYANOTIC because deoxygenated blood from the right side ends up in the systemic circulation

Left - to - right shunt = ACYANOTIC because there is no cyanosis

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9
Q

During which days of embryogenesis do congenital heart diseases occur?

A

Abnormalities in the structure of the heart that develop between day 20 and 50 of embryogenesis

  • Usually idiopathic but specific types occur secondary to foetal exposure to teratogens, chromosomal abnormalities and other factors
  • Congenital heart disease occurs in 8/1000 births
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10
Q

Shunt direction in acyanotic congenital heart disease?

A

Left to right shunt

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11
Q

Anatomical abnormalities that cause acyanotic heart disease

A
  • Defect in the septum of the heart allows blood to flow from the higher pressure left side to the right side
  • Left to right shunt also occurs in cases of patent ductus arteriosus in which blood flows from the aorta into the pulmonary artery
  • Coarctation of the aorta
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12
Q

Which cardiac lesions are associated with Down’s?

A

Ventricular septal defects and atrioventricular septal defects

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13
Q

What is the most common congenital heart defect?

A

Ventricular septal defect

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14
Q

What is ventricular septal defect?

A

One of the acyanotic heart diseases

  • The most common congenital heart defect
  • Most are small, single defects in the pseudomembranous portion of the ventricular septum
  • The membranous portion of the septum is the upper 1/2 while the lower 2/3 is muscular
  • Asymptomatic at birth, if symptoms develop they can develop after a few weeks - years
  • Systolic murmur can be heard along the L sternal border
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15
Q

Where is a murmur heard in ventricular septal defect?

A

Systolic murmur can be heard along the L sternal border

Think about where the hole is… this is where the sound will be heard

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16
Q

What is an atrial septal defect?

A
  • Typically located in the central septum
  • Usually due to failure of fusion of the septum secundum and septum primum
  • Important to note that the foramen ovale remains patent in 25% of adults
  • Auscultation: fixed split S2 because there is delay in the closure of the pulmonary valve in relation to closure of the aortic valve
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17
Q

What is the murmur heard when a child has atrial septal defect?

A

Widely split, fixed S2 at the upper left sternal border

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18
Q

Atrioventricular septal defect AVSD

A
  • Two types: complete and partial
  • Complete AVSD: defect in the septa also involves the valves and creates one valve between the atria and ventricles instead of two. Allows blood to flow around all 4 chambers of the heart
  • Partial AVSD: defect in the lower part of the atrial septum but no ventricular defect, all valves are usually present but can be defective
  • AVSD is also known as endocardial cushion defect and AV canal defect
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19
Q

Patent ductus arteriosus

A

In utero the PD functions to shunt blood from the pulmonary artery to the aorta

  • Should close soon after birth, if it fails to close blood is shunted through the PDA from the left to the right or from the aorta into the pulmonary arteries as opposed to the other way round as seen in utero
  • Babies can present with normal, pink upper limbs because the subclavian arteries arise before the PDA but cyanotic lower limbs
  • Machine-like murmur heard over the left clavicle
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20
Q

Clinical features of left to right shunt defects

A
  • If small, usually asymptomatic and only detected when a murmur is heard
  • Larger defects cause heart failure - this is because the larger volume of blood flowing through the right side of the heart and lungs causes RV hypertrophy and pulmonary oedema
  • Pulmonary hypertension eventually occurs because the lungs can’t cope with the blood volume
  • When pulmonary hypertension occurs and pulmonary pressure becomes higher than the systemic pressure, the shunt is reversed and becomes right to left. This causes cyanosis because blood doesn’t go to the lungs and is therefore not oxygenated = EISENMENGER’S SYNDROME
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21
Q

Investigations for left-to-right/ cyanotic congenital heart disease

A
  • Left to right shunt may be detected on antenatal foetal anomaly USS at 20 weeks
  • Diagnosis is confirmed by echo
  • Congenital heart disease is not diagnosed using ECG but the results may show complications of left to right shunt esp. RV hypertrophy
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22
Q

Management of congenital heart disease

A
  • Depends on the size of the defect
  • Small lesions monitored every 6-12 months
  • Some small lesions close by themselves
  • Large lesions need repairing surgically before pulmonary hypertension sets in
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23
Q

Medication used in large acyanotic cardiac defects before child goes for surgery

A
  • Diuretics: pulmonary oedema
  • Oxygen: if pulmonary oedema causes hypoxia
  • High calorie formula given by NG tube because feeding ability is impaired and breathing effort is increased
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24
Q

Surgery for acyanotic heart disease

A
  • Repair is done using a patch
  • Valve surgery also required in complete AVSD

PDA closed by cardiac catheterisation occlusion device or ligation

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25
Q

What is obstructive congenital heart disease?

A

Occur when there is a narrowing of the heart valves or vessels leaving the heart

  • Narrowing causes resistance to blood flow so the chamber closest to the obstruction has to overcome higher pressures and as a consequence hypertrophies
26
Q

Types of obstructive congenital heart disease

A

Aortic stenosis: narrowing of aortic outflow tract at various levels:

  1. Valvular level (most common) - the valve itself is narrowed
  2. Supravalvular - above valve
  3. Subvalvular - below valve

The aortic valve is usually narrowed because it is bicuspid instead of tricuspid

Pulmonary stenosis: narrowing of pulmonary outflow tract

Valvular, supravalvular or subvalvular

Coarctation of the aorta: narrowing od descending aorta, typically close to the site of the ductus arteriosus

27
Q

Clinical features of obstructive congenital heart disease

A
  • Mild lesions are usually asymptomatic and only discovered when a murmur is heard
  • Larger lesions associated with heart failure due to ventricular hypertrophy which mean the heart cant pump efficiently
28
Q

Patient has radiofemoral delay - what is this associated with?

A

Coarctation of the aorta

29
Q

Investigations into obstructive congenital heart disease

A
  • Diagnosed by echo
30
Q

Management of obstructive heart disease

A
  • If mild, annual monitoring
  • Severe stenosis requires balloon valvoplasty or open valvotomy
  • Coarctation of aorta is managed surgically - narrowed section is cut out and two ends joined. Recurs in 20% after which a balloon is used to dilate the narrowed section and a mesh to keep it open
31
Q

What is cyanotic congenital heart disease?

A

Occurs either because blood bypasses the lungs because of a right to left shunt (tetralogy of Fallot) or because blood flows through the lungs but not into the systemic circulation

  • Usually cause problems within the first 3-8weeks of life
32
Q

Most common cyanotic heart defect?

A

Tetralogy of Fallot

33
Q

What are the 4 feature of Tetralogy of Fallot?

A
  1. Large membranous ventricular septal defect
  2. Pulmonary stenosis
  3. Overriding aorta
  4. Right ventricular hypertrophy - due to narrowing of the right ventricular outflow tract
34
Q

Why does cyanosis occur in Tetralogy of Fallot?

A

Cyanosis occurs because blood is shunted from the right ventricle to the left ventricle rather than through the narrow pulmonary valve

  • The degree of cyanosis depends on the severity of pulmonary stenosis, so some newborns may be asymptomatic until they cry/ feed etc because this causes spasm of the infundibular septum which exacerbates pulmonary stenosis and worsens cyanosis = tet spells
35
Q

What is transposition of the great arteries?

A

Aorta and pulmonary artery are transposed meaning the aorta comes from the right ventricle and the pulmonary artery from the left ventricle. The systems do not mix unless there is a VSD or a PDA

  • The only way a child can survive with this is if they have a PDA
36
Q

Persistent truncus arteriosus

A
  • Due to failure of neural crest cells to properly migrate to the bulbus cordis
  • Leads to a single vessel coming from the left and right ventricles leading to a large common trunk which eventually lead to the aortic and pulmonary artery but both carry mixed oxygenated and deoxygenated blood
  • The partially oxygenated blood causes cyanosis
37
Q

Total anomalous pulmonary venous return

A
  • Normally the 4 pulmonary veins form close to the lungs and then grow towards the heart to fuse with the left atrium
  • Inn TAPVR the veins fuse at the wrong location and oxygenated blood from the lungs ends up on the wrong side of the heart
  • To reach the body the baby needs to have an atrial septal defect that allows the oxygenated blood from the right side of the heart - the left and then to the body
  • Pulmonary hypertension develops because the right side of the heart is receiving too much blood
38
Q

Tricuspid atresia

A
  • Tricuspid valves is absent or malformed
  • deoxygenated blood returning from the systemic circulation gets trapped in the RA and cant reach the lungs
  • Incompatible with life unless baby has an ASD and a VSD
39
Q

Clinical features of cyanotic heart disease

A
  • Babies with tetralogy of Fallot are usually pink at birth and cyanosis develops during the first weeks of life. A murmur is also heard, boot shaped heart, right axis deviation on ECG
  • Babies with transposition of the great arteries are cyanosed from birth. No murmur, ‘egg on side’ appearance of heart, narrow upper mediastinum, normal ECG
40
Q

Investigations into cyanotic heart disease

A
  • Oxygen saturation in 80s or low 90s
  • Difference between preductal and post ductal saturation - this refers to blood supply in areas of the body that come from pre ductus arteriosus and after so in this test oxygen saturations in the right hand is compared to that of either of the feet
  • 25% of cases are picked up on antenatal scan
41
Q

Management of cyanotic heart disease

A
  • Babies with tetralogy of Fallot tolerate low sats well and can be discharged until surgical correction is carried out at 6-12months
  • Oxygen will not help because the problem is not with oxygenation or the lungs - it is actually avoided in babies with cyanotic congenital heart disease because it can cause the DA to close and it is vital is remains open
  • Babies with transposition of the great arteries need to be started on a prostaglandin infusion to keep the DA open to allow mixing of the pulmonary and systemic circulations - a balloon is used to keep it open until an artery switch procedure is done
42
Q

Most common arrhythmia in children

A

SVT - a paroxysmal rapid heart rate of >220bpm

43
Q

Epidemiology and aetiology of SVT

A
  • SVT presents at any age but most frequently affects those <3months with another peak between age 8-10
  • Caused either by abnormal cardiac conduction at either side of the AV node or due to an accessory pathway connecting the atria and ventricles
44
Q

Clinical features of SVT

A
  • Pallor
  • Tachycardia
  • Tachypnoea
  • Irritability
  • Not feeding
45
Q

Investigations into SVT

A
  • Diagnosis is made following finding a narrow complex tachycardia on ECG
46
Q

Management of SVT

A
  • Priority is to terminate the SVT to prevent complications
  • Vagal stimulation 1st: blow into syringe, cold water on head
  • Adenosine bolus
  • Cardioversion
  • Once SVT is terminated aim is to prevent recurrence
  • Regular antiarrhythmic medication e.g. amiodarone or flecainide prescribed on long term basis
  • Ablation of accessory pathway
47
Q

Which babies are at risk of congenital heart block?

A

Those with mothers with lupus/ other autoimmune conditions/ babies with other congenital heart defects

48
Q

Clinical features and management of heart block in childre

A
  • HR usually <60bpm
  • Most children are asymptomatic with diagnosis made using ECG
  • A minority have Stokes-Adams attacks (pallor associated with collapse)
  • Pacemaker is inserted for 2nd and 3rd degree block
49
Q

Epidemiology and aetiology of infective endocarditis

A
  • Bacteria in blood colonise heart valve
  • Rare in children with normal heart structure
  • Typically occurs in children with congenital cardiac problems because blood flow is often more turbulent and this makes it easier for bacteria to stick to the valves
  • Strep viridians, staph aureus being the most common bacteria
50
Q

Clinical features of infective endocarditis

A
  • Fever, increased inflammatory markers (WCC, CRP, ESR), splenomegaly, positive blood culture
  • Destruction of the valve
  • Embolism and infarcts affect 20-50%
51
Q

Investigations for infective endocarditis

A
  • Echo will show vegetations on heart valves
  • Diagnosis supported by three separate sets of bloods showing growth of bacteria on culture
52
Q

Management of infective endocarditis

A
  • High dose IV antibiotics
  • Cardiac surgery may be needed to remove the vegetations
  • Most recover well but risk of future bouts is increased
53
Q

Kawasaki’s disease

A

Kawasaki disease is a type of vasculitis which is predominately seen in children. Whilst Kawasaki disease is uncommon it is important to recognise as it may cause potentially serious complications, including coronary artery aneurysms.

AKA mucocutaneous LN syndrome

  • Autoimmune disease
  • Cause unknown
  • Results in vasculitis which affects medium and small vessels with coronary arteries being particularly vulnerable
  • Typically affects children <5yrs with a peak incidence around 10 months
54
Q

Clinical features of Kawasaki’s

A

Febrile illness, generally >5 days

Mouth: strawberry tongue, fissured lips

Eyes: conjunctival injection, non purulent

Hands: oedema or erythmea, peeling after 2-3 weeks

While body: diffused rash

LNs: cervical lymphadenopathy, often painful solitary node

Heart: coronary artery aneurysms

55
Q

Most serious complications of Kawasaki’s

A
  • Coronary artery aneurysms are the most serious complication of Kawasaki’s, affecting 25% of untreated children
  • Aseptic meningitis, gall bladder hydrops and infection in multiple organs can also occur
56
Q

Investigations for Kawasaki’s

A
  • Diagnosis made based on clinical features
  • CRP and ESR may be raised
  • All children undergo echo
  • Any child presenting with >5days fever, consider Kawasaki’s
57
Q

Management of Kawasaki’s

A
  • High-dose aspirin
    • Kawasaki disease is one of the few indications for the use of aspirin in children. Due to the risk of Reye’s syndrome aspirin is normally contraindicated in children
  • Intravenous immunoglobulin
  • Echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms

Mortality is low (0.1%)

58
Q

What is Ebstein’s anomaly?

A

Caused by the use of lithium in pregnancy

It occurs when the posterior leaflets of the tricuspid valve are displaced anteriorly towards the apex of the right ventricle

The creates tricuspid regurgitation (pan-systolic murmur) and tricuspid stenosis (mid-diastolic murmur). There is also enlargement of the right atrium.

59
Q

What is acute rheumatic fever?

A

Inflammatory condition affecting heart, joints and neurological system

Epidemiology and aetiology

  • Usually occurs 2 weeks after strep throat
  • Rare in high income countries
  • Most children diagnosed between age 5-15

Investigation:

  • Based on Jones criteria
  • Evidence of recent strep throat + 2 major or one major and one minor criteria from the above table

Management

  • Penicillin to treat infection
  • Analgesia
  • Regular 6-12 month cardiac follow up
  • Secondary penicillin prophylaxis for >5yrs is advised due to risk of recurrence
60
Q

Cardiomyopathy in children

A
  • Usually idiopathic
  • 1/100,000 children
  • 30% cases have a genetic cause
  • Three most common type in children:
  1. Dilated cardiomyopathy: 58% of cases, myocardium is thin and stretched and contracts poorly leading to heart failure
  2. Hypertrophic cardiomyopathy: 30% of cases, myocardium is thickened and stiff and obstructs blood flow through aorta, genetic mutations shown to cause 60% of cases
  3. Restrictive cardiomyopathy: 5% of cases, myocardium stiff and has abnormal relaxation

Clinical features

  • Depend on type and severity
  • Most mild cases have no symptoms
  • Dyspnoea on exercise, chest pain, palpitations and fainting

Investigation

  • Echo
  • Genetic investigations

Management

  • Children with cardiomyopathy require 3-6 month follow up with cardiologist
  • Treatment with beta blockers, calcium channel blockers and anti-arrhythmics
  • Pacemaker to control HR
61
Q

Sudden cardiac death

A

Causes of cardiac arrest in people <35yrs

  • Cardiomyopathy
  • Myocarditis
  • Coronary artery disease
  • Ion channelopathies e.g. long QT
  • Wolff Parkinson white
  • Coronary artery anomalies
  • Kawasaki’s
  • Marfan’s
  • Endocardial fibroelastosis
62
Q

Time of presentation of cyanotic CHD

A

Cyanotic congenital heart disease presenting within the first days of life is TGA

Cyanotic congenital heart disease presenting at 1-2 months of age is TOF

Paediatrics (19 decks)

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