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Paediatrics > Ch 17 - Cardiac disorders > Flashcards

Ch 17 - Cardiac disorders Flashcards

1
Q

Heart disease in children is mostly congenital. The most common congenital abnormalities (account for 80%) can be categorized into 5 groups - name these

A

Left-to-right shunts (breathless)

Right-to-left shunts (blue)

Common mixing (breathless & blue)

Outflow obstruction in well child (asymptomatic with murmur)

Outflow obstruction in sick neonate (collapsed with shock)

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2
Q

Give 3 examples of left-to-right shunts (breathless)

A
  1. VSD
  2. presistent arterial duct (PDA)
  3. ASD
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3
Q

Give 2 examples of right-to-left shunts (blue)

A

tetralogy of fallot

transposition of great arteries

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4
Q

Give 1 example of common mixing defect (blue and breathless)

A

Atrioventricular septal defect (complete)

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5
Q

Give 2 examples of outflow obstruction in a well child

A

Pulmonary stenosis

aortic stenosis

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6
Q

Give an example of outflow obstruction in a sick neonate

A

coarctation of aorta

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7
Q

The most common presentation of congenital heart disease is a heart murmur; give 4 hallmarks of an innoSent ejection mumur

A

aSymptomatic

Soft blowing murmur

Systolic murmur only (not diastolic)

Left Sternal edge

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8
Q

Causes of HF in neonates (4)

A

Hypoplastic left heart syndrome (severely underdeveloped LH - small LV & aorta)

Severe AS

severe aortic coarctation (narrowing at area of ductus arteriosus)

interruption of aortic arch (gap between ascending & descending thoracic aorta - in a sense the complete form of coarctation of aorta)

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9
Q

Causes of HF in infants (3)

A

VSD

ASD

large PDA

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10
Q

causes of HF in older children (3)

A

Eisenmenger syndrome (RH failure only)

rheumatic HD

cardiomyopathy

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11
Q

Features of HF (6)

A

Tachycardia,

tachypnoea

murmur

creps oedema

cool peripheries sacral oedema cardiomegaly hepatomegaly

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12
Q

HF in 1st week of life usually results from LH obstruction e.g. coarctation of aorta. What is the pathophysiology? how would you manage?

A

If very severe coarctation, the only thing that can maintain perfusion is if the ductus arteriosus is open - allowing a R to L shunt “duct dependent circ”.

When this duct closes, the baby rapidly devlopes severe acidosis, collapse & death - unless you restore the ductal patency via PROSTAGLANDIN infusion.

Followed by prompt surgical repair

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13
Q

After 1st week of life progressive HF is probably due to L to R shunt. Explain the pathophysiology (3)

A

L to R shunt (e.g. VSD) results in eventual increase in pulmonary blood flow > pulmonary oedema > dyspnoea

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14
Q

If an L to R shunt is left untreated will develop Eisenmenger syndrome - explain pathophysiology (4)

A

Eventually in response to the L to R shunt, the pulmonary vasc resistance will rise (at about 3 months age) > symptoms will improve but if left untreated will develop Eisenmenger syndrome - which is irreversibly raised pulmonary vascular reistance (resulting from chronically raised pulmonary arterial pressure/flow) this also causes the shunt to become from R to L - and the teenager becomes blue. (requires heart lung trasnplant)

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15
Q

Causes of cyanosis (6) (physical sign that causes bluish discoloration of the skin and is due to lack of oxygenated blood)

A

Cardiac - R to L shunts, common mixing, outflow obstruction

Resp - RDS, meconium aspiration Persistent pulmonary HTN of newborn (pulmonary resistance fails to fall post natally) Septicaemia Inherited metabolic disorders

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16
Q

Name the types of ASDs (2), and where the defects are in these specifically (2)

A

Secundum ASD (80%) - defect in CENTRE of ATRIAL SEPTUM involving foramen ovale

Partial atrioventricular septal defect (pAVSD) - defect of AV septum (both present with similar signs and symptoms)

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17
Q

Partial AVSD is a defect of AV septum and is characterised by: (2)

A

An inter-atrial communication between bottom of atrial septum & AV valves Abnormal AV valves (left AV valve has 3 leaflets & leaks - regurgitates)

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18
Q

Features of ASDs (6)

A

symptoms - usually none,

can get reccurent chest infections,

arrythmias - after 4th decade

Physical signs: Ejection systolic murmur best heard at upper left sternal edge - due to increased flow via pulmonary valve (because of L to R shunt) Fixed & split 2nd heart sound

if partial AVSD will hear an apical pansystolic murmur (due to regurg)

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19
Q

CxR signs of ASDs (3)

A

Cardiomegaly

Larger PAs

increased vascular markings

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20
Q

ECG signs of ASDs (3)

A

Secundum ASD shows partial RBBB + RAD (due to RV hypertrophy)

pAVSD shows superior QRS axis

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21
Q

Management of ASDs (2)

A

treatment only if significant ASD (ie large enough to cause RV dilation)

Secundum ASDs - cardiac catheterization with insertion of an occlusion device pAVSD - require surgery

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22
Q

Murmur of Small VSDs (1)

A

asymptomatic loud pansystolic murmur at lower left sternal edge

quiet pulmonary 2nd sound (p2) (NO PULMONARY htn)

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23
Q

Ix (3) and management (1) of VSDs

A

Ix - CxR & ECG (normal), echo + doppler

Management - spontaneous closure - murmur disappears

prevent bacterial endocarditis via good dental hygiene

24
Q

Large VSDs - same size/larger than aortic valve, features (6)

A

HF + SOB + failure to thrive after 1 week old recurrent chest infections tachycardia tachypnoea

soft pansystolic mumur/ no mumur (implying larger defect)

apical mid-diastolic murmur - from increased blood flow across the mitral valve after the blood has circulated through the lungs

25
Q

Ixs (3) & management (3) of VSD

A

CxR - cardio megaly + large PAs + increased vascular markings + pulmonary oedema ECG - biventricular hypertrophy Echo - pulmonary HTN management - diuretics + ACEis, surgery

26
Q

PDA - definition, associations (3), features (3)

A

Failure of DA closure by 1 month

associations - Down’s, prematurity, female, rubella

features - loud P2, continous mumur at upper left sternal edge, bounding pulse (increased pulse pressure)

27
Q

PDA - Ix (3), management (3)

A

Ix - CXR, ecg - usually normal, echo management - prostaglandin synthetase inhibitors e.g. ibuprofen; occlusion device closure via catheter, surgery

28
Q

Hyperoxia (nitrogen washout test): defintion (1), method (3), management (1)

A

Used to determine heart disease in a CYANOSED infant

give 100% oxygen for 10 min > check right radial PO2, if remains less than 15kPa = congenital cyanotic heart disease (if >20 then not)

managemnet - prostaglandin infusion to maintain ductal patency

29
Q

Tetralogy of fallot - the 4 cardinal features

A

PROV: subPulmonary stenosis (causing RV outflow obstruction) RV hypertrophy (as a result of above) Overriding aorta - with respect to septum large VSD

30
Q

Tetralogy of fallot features (4)

A

Clubbing

hypercyanotic spells - rapid increase in cyanosis, inconsolable crying + SOB + pallor squatting on exercise in infants loud harsh ESM at left sternal edge

31
Q

Tetralogy of fallot Ix (3)

A

CxR - small heart, ‘boot shaped’ because RVH will cause uptilting of apex. pulmonary artery ‘bay’ echo ecg - RVH signs

32
Q

Tetralogy of fallot management (3)

A

surgical VSD closure + RV obstruction relief Blalock-taussig shunt - connects a branch of subclavian artery with PA - allowing more blood to flow to lungs symptomtatic treatment of hypercyanotic episodes - propanol, ventilation, morphine

33
Q

Transposition of great arteries: definition

A

RV connected to aorta & LV connected to PA = deoxygenated blood to body & oxygenated blood to lungs = INCOMPATIBLE with life; unless mixing occurs - which often does (as ppl with this often have other congenitatl defects) e.g. ASD/VSD/PDA

34
Q

Transposition of great arteries: features (2)

A

Consistenly present cyanosis starting from day 2 Loud S2 may have systolic murmur

35
Q

Transposition of great arteries: Ix (3)

A

CxR - narrow upper mediastinum (due to anterposterior relationship of great vessels) ‘egg on side’ appearance ECG - norm Echo

36
Q

Transposition of great arteries: management (3)

A

Prostoglandin infusion

balloon atrial septostomy

arterial switch procedure

37
Q

Complete atrioventricular septal defect (common mixing): features (3), Ix (2), management (2)

A

F - Down’s, cyanosis at birth, SOB

Ix - ECG - superior axis,

Echo - 5 LEAFLET VALVE (in centre of heart)

M - treat HF (diuretics etc.), surgical repair at 3 months

38
Q

Complex congenital heart disease e.g. tricuspid atresia: definition, features (2), management (3)

A

D - basically only LV is effective (small and non functional RV)

F - cyanosis in neonate if duct dependent, SOB

M - Blalock Taussig shunt (increase blood flow to lungs) palliation - ‘hemi-fontan operation’ = connect SVC to RPA ‘fontan operation’ = connect IVC to RPA

39
Q

Outflow obstruction in well child: AS: features (5)

A

ES murmur Slow rising pulse carotid bruits low volume pulse exertional chest pain syncope

40
Q

Outflow obstruction in well child: AS: Ix (2), management (2)

A

CxR - normal/ LVH + post-stenotic ascending aorta dilatation ECG - LVH signs Management - Balloon valvotomy, AV replacement

41
Q

Outflow obstruction in well child: PS: features (3)

A

most asymptomatic if critical stenosis neonates have duct dependent circ & will therefore present in 1st few days of life with cyanosis ESM, prominent RV heave (if severe), ejection click

42
Q

Outflow obstruction in well child: PS: Ix (2) & management (2)

A

CxR - post-stenotic PA dilation ECG - RVH signs (upright T wave in V1) M - trans-catheter balloon dilation

43
Q

Outflow obstruction in well child: Adult type aortic coarctation: definition + features (3)

A

uncommon lesion that is not duct dependent - so presents later as it becomes more severe over yrs

F - asymp, systemic HTN in R arm, ES murmur, collaterals heard wit continuous murmu at the back, radio-femoral delay

44
Q

Outflow obstruction in well child: Adult type aortic coarctation: Ix (CxR 2 signs, ECG)

A

CxR - ‘rib-notching’ due to large intercostal collateral arteries for bypassing obstruction.‘3 sign’ - visible notch in descending aorta at site of coarctation ECG - LVH signs

45
Q

Outflow obstruction in well child: Adult type aortic coarctation: management (2)

A

Stent insertion surgical repair

46
Q

Outflow obstruction in sick neonate: aortic coarctation: features (3), Ix (2), Management (3)

A

F - acute circ collapse at day 2 (as DA closes), absent femoral pulses, severe acidosis

Ix - CxR - cardiomegaly & normal ECG

M - prostaglandin infusion, stent insertion, surgical repair

47
Q

Outflow obstruction in sick neonate: interruption of the aortic arch: defintion, features (4), management (3)

A

D - no connection between proximal aorta & distal to DA - so CO is dependent on R-L shunt

F - VSD is usally present; present with shock, associated with Di George syndrome, absent femoral pulses + left brachial pulse

M - Prostaglandin infusion, VSD closure + Aortic arch repair

48
Q

Outflow obstruction in sick neonate: hypoplastic LH syndrome: definition, features (3), management (2)

A

D - basically underdevelopment of LH - LV small non functional, mitral & aortic valve atresia, aortic coarctation

F - all peripheral pulses absent, collapse, acidosis

M - norwood procedure, hemi-fontan at 6 months, fontan at 3 years

49
Q

SVTs: features (3), ix (1)

A

F - most common childhood arrythmia, HR rapid - 250-300bpm; hydrops fetalis; intrauterine death I

x - ECG - narrow complex tachy 250-300, if WPW syndrome short PR interval + delta wave

50
Q

SVT management: acute (2), maintenance (2)

A

Acute - Vagal manoeuvres - carotid sinus massage IV adenosine - breaks re-entry circuit - terminating SVT DC cardioversion

maintenance - Flecainide; ablation of accessory pathway

51
Q

Congenital complete heart block: defintion, features (3), management (1)

A

D - prevention of development of normal conductive tissue in heart by anti-ro/la abs in maternal serum (these mumus have connective tissue disorders e.g. sjogrens)

F - most asymptomatic for years, syncope, in utero death, HF

M - Endocardial pacemaker implantation

52
Q

long QT syndrome: feature (1), complication (1), associations (3)

A

Feature - sudden LOC during exercise/stress/emotion complication - sudden death from VT if goes unrecognised associations - autsomal dominant inheritance, erythromycin therapy, electrolyte disorders, head injury

53
Q

Syncope: causes (4),

A

Common in teenagers, mostly not cardiac cause neurocardiogenic - prolonged standing, vagal symptoms situational - defacation, coughing, urination, swallowing orthostatic - BP fall > 20 mmHg Ischaemic Arrythmic - Heart block, SVT, VT (increase suspicion of cardiac cause if FH of sudden death, exercise symptoms, palpitations)

54
Q

Rheumatic fever: causes, features (5), Ix (1), management (3)

A

C - S. Pyogenes (5-15yr olds) F - Joints - migrating polyarthralgia, myocarditis, subcutaneous nodules, erythema marginatum, syndenham’s chorea mitral stenosis most common long term damage Ix - ECG - prolonged PR interval M - NSAIDs, steroids, ABs

55
Q

IE: causes (2), features (4), Ix (3), mangement (2), prophylaxis (1)

A

C - S. viridans, enterococcus, S. aureaus F - roth spots, janeway, oslers, splinter haemorrhages, clubbing, splenomagly, haematuria, changing murmur Ix - blood culture, Echo, CRP/ESR M - high dose penicillin, aminoglycoside P - good dental hygiene

Paediatrics (22 decks)

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