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MBBS 3: Pediatrics > Common Cardiac Diseases > Flashcards

Common Cardiac Diseases Flashcards

1
Q

What are septal defects?

A

hole in the heart - a gap between the:
1. 2 atria (atrioseptal defect)
2. 2 ventricles (ventriculoseptal defect)
3. at endocardial cushion (where all 4 meet)

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2
Q

What are vessel abnormalities?

A
  1. transposition of the great arteries
  2. coarctation of the aorta
  3. pulmonary stenosis
  4. patent ductus arteriosus
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3
Q

What are valve abnormalities?

A
  1. tricuspid atresia
  2. aortic stenosis
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4
Q

Major structural abnormalities?

A
  1. Fallot’s tetralogy
  2. hypoplastic left heart
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5
Q

Failure of transition?

A
  1. patent ductus arteriosus
  2. persistent foetal circulation
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6
Q

Which congenital structural lesions produce stenosis?

A
  1. Transposition of the great arteries
  2. Tetralogy of Fallot
  3. Critical pulmonary stenosis
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7
Q

What is meant by “duct-dependant” heart disease?

A
  • Some structural abnormalities of the heart are incompatible with life outside the womb once the ductus arteriosus closes.
  • This event is often delayed compared to normal, but inevitably the baby will collapse within the first 2-3 weeks of life
    Note: Giving oxygen may precipitate/ accelerate duct closure
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8
Q

Acyanotic congenital heart diseases?

A
  1. pre-ductal coarctation of the aorta
  2. ventricular septal defect
  3. atrial septal defect
  4. atrioventircular septal defect
  5. patent ductus arteriosus
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9
Q

What are the 4 components of Tetralogy of Fallot?

A
  1. Pulmonary Stenosis
  2. Right ventricular hypertrophy
  3. ‘Perimembranous’ VSD
  4. Overriding Aorta
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10
Q

Incidence of TOF?

A

Usually presents in infancy/early childhood

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11
Q

Physical signs of TOF?

A
  1. persistent cyanosis
    - the child may be noted to be dusky from early life, gradually increasing over time
  2. an ejection systolic murmur corresponding to the pulmonary stenosis
  3. Polycythaemia occurs
  4. hyper-cyanotic spells, which may be the presenting feature
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12
Q

CXR of TOF?

A

shows boot shaped heart

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13
Q

Diagnosis of TOF?

A

echocardiogram

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14
Q

Treatment of TOF?

A
  1. definitive treatment - surgical
  2. medical management
    - Antibiotic prophylaxis
    - Anticoagulation
    - Treatment of Cyanotic Spells
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15
Q

What are hyper-cyanotic spells in TOF?

A

severe episodes of severe cyanosis due to decreased pulmonary blood flow secondary to increased right ventricular outflow tract obstruction
- Right ventricular outflow obstruction tends to get worse over time, and acute episodes of “pulmonary infundibular spasm” occur.

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16
Q

Precipitation of tet spells?

A

Spells precipitated by activity e.g. feeding, playing
- and may last minutes and then resolve, or progress

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17
Q

Signs of hyper-cyanotic spells in TOF?

A
  1. deepening cyanosis
  2. agitation
  3. tachypnoea
  4. pallor
  5. ultimately floppiness and loss of consciousness
    - with which brain damage may occur
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18
Q

Treatment of cyanotic spells?

A
  1. Put the child in a squatting or knee-chest position
    – to increase systemic vascular resistance and promote systemic venous return to the heart
  2. Give oxygen
    - to decrease peripheral pulmonary vasoconstriction
  3. Analgesia (e.g. morphine)
    - to decrease release of catecholamines thereby decrease heart rate (increasing filling time) and relaxation of the infundibular spasm
  4. i.v. fluid bolus
    - to improve right ventricular preload
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19
Q

Congenital lesions which may give heart failure?

A
  1. VSD
  2. ASD
  3. PDA
  4. Coarctation of the aorta
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20
Q

What is ventricular septal defect?

A

A connection between the 2 ventricles causing left to right blood flow
- Commonest cause of heart failure in infancy
Note: A large ventricular septal defect does not produce a murmur in the newborn period because the initially high pulmonary vascular resistance results in minimal shunting across the defect

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21
Q

What does a VSD sound like?

A

The bigger the hole, the quieter the murmur
Note: Harsh pansystolic murmur loudest at left lower sternal edge

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22
Q

Treatment of VSD?

A
  1. treat heart failure
  2. antibiotic prophylaxis
    - 60% will close spontaneously. some never close and require surgery
23
Q

What is an atrial septal defect?

A

Connection between the 2 atria, causing left to right blood flow, and an overloaded right side of the heart

24
Q

Clinical features of an ASD?

A

most children will be asymptomatic

25
Q

Describe the murmur of a ASD?

A

Murmur is one of increased blood flow through the pulmonary valve
i.e. ejection systolic murmur loudest in pulmonary area

26
Q

Chest x-ray of an ASD?

A

big heart, large pulmonary artery, pulmonary plethora, small aorta

27
Q

Treatment and management of ASD?

A
  1. treatment
    - surgery
  2. management
    - treat heart failure
    - antibiotic prophylaxis
28
Q

What is patent ductus arteriosus?

A

failure to close ductus arteriosus after birth
- mostly premature infants

29
Q

Consequence of a PDA?

A

‘Reversed’ flow (compared to in utero) means blood in aorta diverted to pulmonary circulation

30
Q

Describe the murmur of a PDA?

A

machinery murmur below left clavicle

31
Q

What is coarctation of the aorta?

A

a narrowing at a specific point in the aorta
- Usually before the point at which the ductus arteriosus joins

32
Q

When does coarctation of the aorta present and why?

A

presents when the ductus arteriosus closes with collapsed baby and heart failure
- because the ductus arteriosus has now closed

33
Q

Clinical features of COA?

A
  1. May have reduced or absent femoral pulses
  2. Systolic murmur
34
Q

Treatment and management of coarctation of the aorta?

A
  1. treatment
    - surgery
  2. management
    - Treat heart failure
    Antibiotic prophylaxis
    Note: many survive into adult life without knowing they have a coarctation
35
Q

Acquired causes of heart failure?

A
  1. rheumatic heart disease
  2. cardiomyopathy
  3. myocarditis
  4. bacterial endocarditis
36
Q

What is the cause of rheumatic heart disease?

A

Episode (or episodes) of acute rheumatic fever leading to endocardium inflammation
- Mainly affects the mitral and aortic valves

37
Q

How does RHD affect the valves?

A

Inflammation settles with scarring, fibrosis and deformity of the valve, which may lead to heart failure over time

38
Q

Describe mitral regurgitation as a consequence of RHD?

A
  1. During systole, blood goes ‘backwards’ through the incompetent valve from the left ventricle to the left atrium and pulmonary veins
  2. This reduces cardiac output and eventually leads to pulmonary oedema
  3. The left ventricle hypertrophies to compensate
39
Q

Symptoms of mitral regurgitation secondary to RHD?

A
  1. Symptoms may take a long time to develop
  2. Patient is easily fatigued and breathless as heart failure develops
40
Q

What is cardiomyopathy?

A

weakened heart muscle, commonly with dilatation
- May be idiopathic or related to underlying metabolic or connective tissue disorders

41
Q

What is myocarditis?

A

inflammatory process of heart muscle, commonly following viral illness

42
Q

Clinical features of cardiomyopathy and myocarditis?

A
  1. Characterised by a poorly-contracting, large ‘flabby’ heart with heart failure
  2. Present at any age with heart failure, poor perfusion, and often a mitral regurgitation murmur
    - difficult to distinguish
43
Q

What is bacterial endocarditis?

A
  • Occurs in children with congenital or acquired heart defects which cause turbulent blood flow e.g. across a valve
  • Bacterial ‘vegetations’ form on damaged endothelium and shed infective emboli
  • It is part of the differential of fever in a child with cardiac signs
44
Q

Phenomenon of shed off infective emboli?

A

Janeway lesions, splinter hemorrhages, roth spots

45
Q

Clinical features of BE?

A
  1. acute onset: with fever, prostration and heart failure
  2. insidious onset: with fever, fatigue, loss of appetite, joint pains
46
Q

What is seen on examination of BE?

A

variable heart murmur, petechial rash, splinter haemorrhages, Oslers nodes, clubbing, subconjunctival haemorrhages, splenomegaly, neurology

47
Q

What is antibiotic prophylaxis?

A
  1. Used to prevent infective endocarditis.
  2. The risk is highest in those lesions producing a high velocity turbulent blood flow
    - Antibiotics should be given to children with these heart lesions when they have any form of surgery/minor op/ dental procedure
48
Q

3 treatments of heart failure?

A
  1. Reduce the amount of blood that the heart has to pump
  2. make the heart pump harder
  3. supportive therapy
49
Q

Treatment of heart failure: reduce amount of work?

A
  1. Diuretics
    - Frusemide (1-3mg/kg/day)
    - Spironolactone (1-3mg/kg.day)
  2. Vasodilators (reduce amount f work)
    - captopril
    Note: Captopril can cause hypotension particularly in patients with ventricular dysfunction. Measure BP before introducing captopril
50
Q

Treatment of heart failure: make heart pump harder?

A
  1. Digoxin: (10-30ug/kg/day)
  2. Inotropes: noradrenaline and adrenaline given on ICU/HDU
51
Q

Supportive therapy of heart failure?

A
  1. Feeding
    - Tube feeding is helpful in babies if there are feeding difficulties
    - Dietary advice e.g. low salt
  2. Nursing
    - Nurse in a sitting position
51
Q

Why might children with untreated VSD’s or ASD’s eventually turn blue?

A

Eisenmenger’s syndrome

52
Q

What is Eisenmenger’s syndrome?

A
  • Untreated ASD/ VSD’s cause a chronic increase in pulmonary blood flow.
  • Irreversible damage to the pulmonary vasculature occurs causing pulmonary hypertension
  • Eventually, flow across the VSD/ASD reverses (R-L), the child becomes cyanosed, polycythaemic etc : It is now to late to fix the septal defect

MBBS 3: Pediatrics (41 decks)

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