Cardiology Flashcards

1
Q

What is the most common cardiological problem / presenting feature in children?

A

A MURMUR

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2
Q

Are most murmurs concerning?

A

Most murmurs are completely innocent

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3
Q

What percentage of children will have an innocent murmur at some point during their childhood?

A

30%

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4
Q

What are some features that will make a murmur reassuring?

A

THE S FACTORS

  • Systolic (commonly ejection systolic) - no diastolic murmur present
  • Soft, blowing murmur
  • aSymptomatic patient
  • Left sternal edge

***these are all factors that would reassure you to a murmur being innocent

Extra re-assuring factors:

  • Normal heart sounds with no added sounds
  • No parasternal thrill
  • No radiation
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5
Q

What are some causes of innocent murmurs?

A

Mostly the murmurs are idiopathic and we don’t identify a cause. Organic causes include:

  • FEBRILE ILLNESS
  • ANAEMIA

***theory behind these aetiologies is just that they increase CO so theoretically any pathology that increases CO could cause murmur

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6
Q

What should you do if you hear a murmur? Next step…

A

Even if convinced murmur is innocent then document your findings and discuss them with parents - reassure them that it is very unlikely to mean the child has anything wrong with their heart
If there are ANY concerning features or parents / you are concerned for any reason then refer to PAEDIATRIC CARDIOLOGY (paeds cons with special interest)

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7
Q

How do we investigate murmurs to rule out pathology?

A

ECG
CXR
Echocardiogram - gold standard

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8
Q

What are the four cardinal features of TOF?

A

Overridng aorta
VSD
Pulmonary stenosis
RVH

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9
Q

How is TOF identified?

A

Nowadays usually antenatally or following identification of a murmur in the first 2/12
If not there might be severe CYANOSIS in the first few days of life

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10
Q

What symptomatic features of TOF can you see?

A

Severe CYANOSIS, breathlessness, pallor caused by exercise/crying and relieved by squatting

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11
Q

What might you find o/e in TOF?

A

Might find soft murmur during tet spell
May have clubbing
LOUD, HARSH EJECTION SYSTOLIC MURMUR at Left sternal edge

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12
Q

What investigations should you do if suspecting TOF?

A

CXR, Echo and ECG

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13
Q

What changes might you see on a CXR in TOF?

A

BOOT SHAPE (uplifted apex due to RVH) and pulmonary artery ‘BAY’ - concavity at L border due to pulmonary stenosis

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14
Q

How should a tet spell be managed?

A
oxygen 
sedation and pain relief (morphine)
IV propanolol - perisperhal vasoconstrictor
IV fluids 
Bicarbonate to correct acidosis
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15
Q

When will definitive surgery for TOF be offered and what will it involve?

A

At 6 months and will involve closure of the VSD and relieving of the right ventricular outflow tract

A surgery can be offered in the neonatal period as well in severe cases - SHUNT between the subclavian and pulmonary arteries to improve blood flow to the lungs

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16
Q

What is transposition of the great arteries (TGA)?

A

When the pulmonary artery connects to the LV and the aorta to the RV forming two closed circulations
INCOMPATIBLE WITH LIFE UNLESS there is a defect that stays open (VSD)

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17
Q

How and when does TGA present?

A

Profound cyanosis

Usually presents around day 2 of life as the DA starts to close and there is reduction in blood mixing

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18
Q

What clinical signs might we be able to hear on TGA?

A

Second heart sound often loud and single

Usually no murmur but might be one associated with increased pressure through pulmonary artery

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19
Q

What three investigations should be done for TGA?

A

CXR, Echo and ECG

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20
Q

What will the CXR show in TGA?

A

Egg on its side

There might also be some signs of pulmonary oedema due to the increased pressures through the pulmonary system

21
Q

What is the initial management for TGA and what is the definitive management?

A

Initial management is to preserve blood mixing and so PROSTAGLANDINS are given to keep the DA patent
Sometimes a BALLOON ATRIAL SEPTOSOTOMY may be needed - rupture the foramen oval to improve blood mixing

The definitive treatment - an operation to switch the arteries then ideally occurs in the second week of life

22
Q

What are the two types of atrial septal defect?

A

Primum / AVSD

Secundum (80%)

23
Q

What structure does a secundum ASD involve?

A

The foramen ovale

24
Q

What structure does a primum ASD involve?

A

The atrio-ventricular junction
There is inter-atrial communication between the bottom half of the atrial septum and involved of the atrioventricular valves
The valves themselves are also commonly abnormal with the left valve often having three leaflets

25
Q

How are atrial septal defects detected clinically?

A
Often ASx (sometimes chest infections, or arrhythmias) 
Detected when a murmur is heard on routine examination
26
Q

What will the murmur with a ASD sound like?

A

Ejection systolic and at the upper left sternal edge (due to increased flow across the pulmonary valve due to L-R shunt)
Fixed and widely split second heart sound

27
Q

What condition are AVSDs commonly associated with?

A

Down Syndrome

28
Q

How do we managed ASDs?

A

Secundum ASDs can be treated with cardiac catheterisation

For primum AVSDs surgical intervention is often needed Usually treated around 3-5yo

29
Q

What is the most common congenital cardiac defect?

A

VSDs - 30% of all cases of cardiac abnormalities

30
Q

How do we describe VSDs?

A

According to their size (Small or large)

Small <3mm, large >3mm

31
Q

What are some of the clinical features and clinical signs of VSDs?

A

Asymptomatic

Loud panysystolic murmur at LLSE

32
Q

Do small or large VSDs produce louder murmurs?

A

Small - more resistance

33
Q

How do we investigate small VSDs?

A

CXR, Echo and ECG

CXR and ECG both normal

34
Q

How do we managed small VSDs?

A

Watch and wait - usually they will close spontaneously but arrange regular follow up

35
Q

How will large VSDs present clinically?

A

Acute breathlessness due to pulmonary oedema due to the failure of the heart and increase pulmonary blood flow

Failure to thrive after 1 week old

Recurrent chest infections

36
Q

What are some clinical signs in large VSDs?

A

Tachypnoea, tachycardia, enlarged liver due to heart failure

37
Q

What murmur will be heard in large VSDs?

A

A very soft one or no murmur at all

?apical mid-diastolic murmur as there is increased blood flow over the mitral valve due to increased pulmonary blood flow

38
Q

What investigations should be done in large VSDs?

A

CXR, Echo and ECG

39
Q

What will a chest radiograph show in large VSDs?

A

Cardiomegaly, enlarged pulmonary arteries and increase pulmonary vascular markings, pulmonary oedema

40
Q

How should large VSDs be managed?

A

Drug therapy for heart failure - DIURETICS AND CAPTOPRIL(ACE-i used in HF)

41
Q

What is a potential complication of large VSDs?

A

Persistent L-R shunt could lead to EISENMENGER SYNDROME

42
Q

When is corrective surgery offered in large VSDs?

A

3-6 months

43
Q

What structures does the ductus arteriosus connect in the foetus?

A

The pulmonary artery to the aorta to bypass pulmonary circulations (pulmonary circulations very high pressure in the unborn baby)

44
Q

What changes happen at birth that lead to the closure of the DA?

A

The baby takes its first breath and pulmonary vascular resistance plummets and the direction of the shunt changes enabling it to close

45
Q

How long does the DA have to remain patent for before we class it as pathological?

A

1 month (corrected gestational age - so prems have longer)

46
Q

How are children with PDAs usually identified?

A

With persistent murmurs under the L clavicle (heard in both systole and diastole)
Symptoms are unusual but might be to do with heart failure

47
Q

What are some characteristics of a PDA murmur?

A

MACHINE-HUM MURMUR

48
Q

What happens to the pulse in children with PDA?

A

Becomes collapsing or bounding due to increase in pulse pressure

49
Q

How is PDA managed? What complications could there be if it is not treated?

A

Coil or occlusion device via cardiac catheterisation at around 1 year of age

Lifelong risk of infective endocarditis if it is not corrected