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Peadiatrics > Cardiovascular Disorders > Flashcards

Cardiovascular Disorders Flashcards

1
Q

What is the most common form of structural malformations

A

Congenital heart disease

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2
Q

Causes of Chd

A

Genetic chromosomal - 8%
Teratogens
Idiopathic (most common)

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3
Q

Egs of teratogens causing CHD? Cause what?

A 
Congenital rubella (eg PDA, pulmonary stenosis) 
Alcohol (ASD, VSD)
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4
Q

Chromosomal disorders causing CHD ? Eg?

A

Downs - AVSD
Turners - aortic stenosis, coarctation
Williams - supra valvular AS
Chromosome 22 deletions

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5
Q

What are the two types of CHD ? Why?

A

Acyanotic (L–>R shunts)

Cyanosis (R->L shunts)

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6
Q

Egs of L->r shunts

A 
VSD -30%, PDA -12%, ASD -7%.
Outflow obstruction (pulmonary (7%) / aortic (5%) stenosis, coarctation 5%)
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7
Q

Egs of R->L shunts

A

Tetralogy of fallot 5%

Transposition of the great arteries 5%

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8
Q

Outline the fetal circulation.
Placenta ->?
Pressure highest?
What causes change in pressures

A

Placenta delivers oxygenated blood to R atrium
Blood is unable to flow through lungs -> R side pressure Highest.
Blood flows through ductus arteriosus and foramen ovale.
Birth lungs expand -> decreased R sided pressure (smaller than left)

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9
Q

How does CHD present

A 
Antenatal uss diagnosis 
Heart murmur 
Cyanosis
Shock (low cardiac output) 
Cardiac failure
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10
Q

What are the two types of ASD

A

Ostium secundum defect (80%)

Partial AVSD + ostium primum defect

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11
Q

Where does an ostium secundum defect occur ? Who is it more common in?

A

High in atrial septum involving foramen ovale

2x more common in girls

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12
Q

Where is a partial AVSD ? What 2 things characterise it

A

Defect in atrioventricular septum
1- inter atrial communication between bottom end of atrial septum and atrioventricular valves (primium ASD)
2 - abnormal AV valves (typically mitral regurgitation )

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13
Q

Clinical features of ASD

A

Abnormal right ventricular impulse
Widely split and fixed second heart sound (s2)
Tricuspid flow murmur -> rumbling mid diastole murmur at LEFT STERNAL EDGE
Pulmonary flow murmur -> soft ejection systolic murmur in PULMONARY AREA

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14
Q

Symptoms of ASD

A

None - common
Recurrent chest infections / wheeze
Heart failure
Arrythmias - 4th decade onwards

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15
Q

Investigations for ASD ? What is seen?

A

CXR - cardiomegally, enlarged pulmonary arteries and increased pulmonary vascular markings (all NON SPECIFIC)
ECG - right ventricular hyper trophy (R AXIS DEVIATION), partial right bundle beach block (MaRRoW)
Echo - diagnostic without cardiac catheterisation

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16
Q

Management of ASD ? Aim ? What age ?

A

Surgical to prevent heard failure and arrythmias

3-5 best

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17
Q

What is the surgery for secundum ASD

A

Cardiac catheterisation with insertion of occlusive device

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18
Q

Surgical management of partial AVSD

A

Open surgical correction required

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19
Q

What 2 factors alter the prognosis of VSD

A

Size of defect and its position in septum

Development of changes due to L->R shunting

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20
Q

What changes occur in eisenmenger syndrome?

A

Increased blood to lungs -> arteries become stuff and narrow -> pressure becomes so great the shunt reverses. R->L
DANGEROUS

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21
Q

Symptoms of small

A

Asymtomatic

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22
Q

Signs of small VSD

A

Pan systolic murmur (sometimes palpable thrill) at the lower left sternal edge

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23
Q

Investigations for small VSD

A

CXR and ECG - normal

Echo - can demonstrate haemodynamic effects using Doppler echocardiography

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24
Q

Treatment of small VSD

A

Most close spontaneously - followed with ECG and murmur

While VSD present - endocarditis prophylaxis before dental extractions and gold dental hygiene

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25
Q

How big are large VSDs

A

Same size or bigger than aortic valve

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26
Q

Symptoms of large VSDs

A

Heart failure and failure to thrive after 1 week old

Recurrent chest infections

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27
Q

Signs of large VSDs

A

Acute precordium
Harsh pan systolic murmur loudest in 3rd/4th IC space (may be soft or absent if v big)
Loud pulmonary s2 (due to increased pulmonary arterial diastolic pressure)
Tachycardia, tachypneaand hepatomegally from heart failure

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28
Q

Investigations for large VSDs and what’s seen

A

CXR - cardiomegally, enlarged pulmonary markings and arteries, pulmonary oedema
ECG - biventricular hyper trophy by 2/12, pulmonary hypertension (tall T waves in V1)
Echo - demonstrates anatomy and can elicit haemodynamic effects and pulmonary HTN severity

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29
Q

Management of large VSD

A

Initial - management for heart failure and pulmonary hypertension.
Followed by surgery in cardiopulmonary bypass

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30
Q

What is done in infants with large VSD ? Why?

A

Pulmonary artery banding (band around PA to reduce flow / pressure)
Allows respite until child has grown enough to withstand definitive correction

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31
Q

When is a PDA physiological

A

Preterm infants

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32
Q

Where does the ductus come from ? What does it do!

A

Demand of 6 aortic arch.

Joins pulmonary artery and aorta (just after origin of left subclavian )

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33
Q

When does the PDA usually close

A

In first week of life

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34
Q

Clinical features of PDA

A

Continuous murmur beneath left clavicle
Increased pulse pressure (bounding pulse )
+ symtoms if duct is large (heart failure and breathlessness)

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35
Q

Investigations for PDA

A

CXR / ECG - usually normal

Echo - with Doppler

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36
Q

Management of PDA

A

High risk of bacterial endocarditis if left patent -> prostaglandin inhibitors (eg ibuprofen) in premature babies.
Surgery - if large at 1-3/12 if small at 1 year (in cardiac catheter lab)

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37
Q

Surgical methods in PDA

A

Division

Ligation or transvenous umbrella occlusion

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38
Q

Types of pulmonary stenosis

A

Valvular (90%), subvalvular (infundibular) or supra valvular

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39
Q

Which type of pulmonary stenosis occurs in tetralogy of fallot

A

Infundibular (with large VSD)

40
Q

Symtoms of pulmonary stenosis

A

Most are asymtomatic

41
Q

Signs of pulmonary stenosis

A

Ejection systolic murmur best heard at UPPER LEFT STERNAL EDGE (+thrill) accompanied by ‘ejection click’ in same area.
Widely spit s2 with a soft or absent p2

42
Q

Investigations for pulmonary stenosis

A

CXR - normal (may have post stenotic dilatation)

ECG - evidence of R ventricular hyper trophy (UPRIGHT T WAVE IN V1)

43
Q

Treatment of pulmonary stenosis

A

Trans catheter balloon dilatation

44
Q

Types of coarctation ? Which is worse? Who gets more

A 
Pre ductal (sick child)  - interruption of aortic arch 
post ductal (asymtomatic ) 
Males 2x more
45
Q

Features of pre ductal coarctation

A

Sick neonate with absent femoral pulses.

While ductus arteriosus is open the RV maintains cardiac output but after it closes -> HEART FAILURE

46
Q

Treatment of pre ductal coarctation

A

Prostaglandin infusion to maintain ductal patency then transfer to cardiac surgery

47
Q

Symtoms of post ductal coarctation

A

Usually asymtomatic - may get leg pains or headaches

48
Q

Signs of post ductal coarctation

A

Hypertension in the right arm, radio femoral delay / absent femoral pulses
Opening click over aortic area (due to associated bicuspid aortic valve)
Sometimes ejection systolic murmur audible at L INTERSCAPULAR AREA

49
Q

Investigations for post ductal coarctation

A

CXR - rib notching (due to development of large collaterals intercostal arteries running under ribs posteriorly (teens and adults))
- 3 sign (visible notch in descending aorta at site of coarctation)

ECG - LVH -> inverted T in v6, deep S in v2 and tall R in v6

50
Q

Treatment of post ductal coarctation

A

Stenting by cardiac catheterisation

Surgical repair in severe cases

51
Q

What needs to be determined in cyanosis

A

If it is peripheral (any cause eg sick, cold)

Or CENTRAL blueness of tongue and buccal mucosa which is associated with decrease in arterial oxygen tension

52
Q

How do you clinically detect central cyanosis

A

Only possible if conc is >5g/dl (therefore less pronounced if child is anaemic)

53
Q

Differentials for newborn with respiratory distress

A

Cardiac disorders - cyanotic CHDs
Respiratory disorders - surfactant deficiency, meconium aspiration, pulmonary hypoplasia …)
Persistent pulmonary hypertension of the newborn (PPHN)
Infection - septicaemia, group b strep…
Polycythaemia

54
Q

Give the two main mechanisms for cyanosis in CHD

A

1- decreased pulmonary blood flow with shunting of deoxygenated blood from R->L (eg tetralogy of fallot)

2- abnormal mixing of systemic and pulmonary venous return usually associated with an increased pulmonary flow (eg transposition of the great arteries)

55
Q

Diagnosis of CHD without echocardiography

A

Hyperoxia (nitrogen washout) test

(Measure arterial blood gas on air - then on 100% O2 ->
if lungs are healthy then will be no effect on ABG (R->L shunt likely)
If increased due to lung problem as O2 augments lungs ability)

56
Q

What is the most common cause of cyanotic CHD

A

Tetralogy of fallot

57
Q

What are the 4 features of tetralogy of fallot

A

Large VSD
Right ventricular outflow obstruction (50%infundibular stenosis,10%pulmonary valve stenosis, 30% both)
Aorta overriding ventricular septum
Right ventricular hyper trophy

58
Q

Presentation of tetralogy of fallot

A

Cyanosis in first 1-2/12

Hyper cyanotic spells (due to infundibular spasm) and squatting on exercise

59
Q

Physical signs of tetralogy of fallot

A

Cyanosis with /out clubbing
Loud and single s2 (A2 without p2)
Loud EJECTION SYSTOLIC MURMUR loudest at 3rd L ICS)

60
Q

Tetralogy investigations and results (3 on X-ray)

A

CXR - usually normal. If child is older small heart (possibly with uptilted apex ‘boat sloped) due to RVH. Pulmonary artery ‘bay’ - con cavity on L heart border where convex shaped main pulm artery and RV outflow are normally profiled. Oligaemic blood flow (decreased pulm vascular markings.

ECG - Normal at birth. Then RVH & RIGHT AXIS DEVIATION (upright T wave in v1 and pure R wave (no S wave) )

61
Q

Tetralogy hyper cyanotic spells management and reasons

A

Morphine - relieves pain and abolishes hyperpnea
Sodium bicarbonate IV - correct acidosis
Propranolol - cause peripheral vasoconstriction and relieve infundibular spasm

62
Q

When is surgical treatment for tetralogy done ? What is done

A

BT SHUNT - between subclavian and pulm arteries (increased pulm blood flow
Patch closure of VSD and widening of R ventricular outflow tract

63
Q

Who gets more TGA (transposition of great arteries)

A

Males 3x

64
Q

What happens in a complete ‘D’ transposition?

What coexists

A

Aorta arises anteriorly from RV
Pulm artery arises posteriorly from LV

Defects that allow mixing of 2 circulations (ASD VSD PDA)

65
Q

Features of TGA ? What is it unresponsive to ?

A

Severe cyanosis - often in first 1-2days of life

  • usually when ductus closes which decreases mixing of systemic and pulm circulation
  • arterial hypoxaemia often profound (1-3kPa PaO2) & unresponsive to O2 inhalation
66
Q

Physical signs of TGA

A

Cyanosis always
Clubbing (if child presents after 1year)
Second heart sound is single and loud ( may be a murmur of VSD or PDA if septum is not intact)

67
Q

Investigations for TGA and results

A

CXR - classically narrow upper mediastinum with an ‘egg on side’ appearance of cardiac show (due to anterior posterior relationship of great vessels and the hypertrophic RV

ECG - usually normal

68
Q

What is given to sick cyanosed newborn with TGA

A

Prostaglandin E1 (PGE1) infusion to reopen ductus arteriosus

69
Q

Management of TGA ?

How is a definitive repair completed

A

Pge1 infusion
Emergency cardiac catheterisation and therapeutic balloon atrial septosomy (rashkind procedure)

Repair with an arterial switch procedure in first few weeks of life

70
Q

What is a septosomy

A

a small hole is created between the atria

71
Q

What’s often heard during febrile illness / anaemia and why

A

Innocent murmurs due to increased cardiac output

72
Q

Hallmarks of innocent murmurs

A

Asymtomatic
No parasternal thrill / radiation
No diastolic component
Localised to L sternal edge

73
Q

2 egs of innocent murmurs

A

Soft blowing systolic - firm right pulmonary outflow in the 2nd L ICS )

Short buzzing murmur - from L side of heart due to aortic blood blow I’m 4th L ICS )

74
Q

What is rheumatic fever

A

Sequela of group A B haemolytic strep infection (usually tonsilopharyngitis) caused by abnormal immune response in 1%

75
Q

Leading cause of valvular disease

A

Rheumatic fever

76
Q

When after infection does rheumatic fever develop

A

2-6/52

77
Q

What are the features of rheumatic fever

A 
Polyarthriris, fever and malaise 
Pan carditis (30%)
78
Q

What is the arthritis like in rheumatic fever

A

Fleeting lasting 1-52 in individual joints and commonly affects large eg knees and ankles

79
Q

What are the types of pancarditis in rheumatic fever

A

Pericarditis (friction rub and pericardial effusion) -> endocarditis which commonly affects L sided valves leading to murmurs eg. Mitral incompetence

Myocarditis - can lead to heart failure

80
Q

What is a rare later effect of rheumatic fever

A

Sydenham’s chorea

6/12 later with emotional liability and chorea

81
Q

How is the diagnosis of rheumatic fever made

A

Duckett-Jones criteria (2 major or 1M and 2m)

82
Q

Treatment for rheumatic fever?

Acute? Severe? recurrent ?

A

Acute - bed rest and aspirin to relieve fever and arthritis
Steroids for sever carditis
Diuretics and ACEi for heart failure
Recurrent - prophylactic penicillin

83
Q

When should children get prophylactic Abx

A

All with CHD (bar secundum ASD ) before any dental procedure / surgical treatment

84
Q

When should you always ?endocarditis

A

Child with fever and significant heart murmur

85
Q

Features of endocarditis

A

Bacteraemia (fever, malaise)
Valvulitis (HF, murmurs)
Immunological changes (gomerulonephritis)
Embolic changes (CNS abscess, sprinter haemorrhages )

86
Q

Most common cause of endocarditis

A

Streptococcus viridans

87
Q

Diagnosis of endocarditis

A

Blood cultures

Cross sectional Echo

88
Q

Treatment of endocarditis

A

4-6 weeks high dose IV Abx +/- surgical removal of infected prostheses

89
Q

Acute vs chronic features of myocarditis

A

Acute - cv collapse

Chronic - gradual onset congestive cardiac failure

90
Q

Myocarditis treatment

A

Supportive - most recover but some have dilated cardiomyopathy

91
Q

Infections associated with myocarditis

A

Coxsackie, rubella,

92
Q

Normal arrythmia in children ? Why?

A

Sinus arrythmia - detectable change in HR with respiration (increase during inspiration and decrease during expiration)

93
Q

What is the most common peadiatric arrythmia ? What is it ?

A

Supraventricular tachycardia - HR of 250-300

94
Q

Features of supraventricular tachycardia

A

Most asymtomatic but some develop cardiac failure (and present with decreased feeding, sweating, irritability, sob)
Older children may describe palpitations

95
Q

Diagnosis of supraventricular tachycardia

A

ECG shows narrow complex tachycardia with some p waves discernible after QRS due to retrograde action of atria via accessory pathway

When in sinus rhythm - decreased PR interval

96
Q

What’s seen in wolf Parkinson white ECG

A

D wave and decreased PR interval

97
Q

Treatment for supraventricular tachycardia

A

Vagal stimulation - cold water to face, carotid sinus massage, valsalva manoeuvre

IV ADENOSINE (if fails -> DC cardioversion (shock them) )

Peadiatrics (14 decks)

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