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Martha Phase 3a > Child health- Congenital heart disease > Flashcards

Child health- Congenital heart disease Flashcards

1
Q

describe transposition of the great arteries

A

the aorta and pulmonary artery are transposed, so the aorta is supplying the right atrium and the PA is supplying left atrium

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2
Q

how would Transposition of the Great Arteries be diagnosed

A

echocardiogram

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3
Q

what are the four aspects of the tetralogy of Fallot

A

Stenotic pulmonary valve
Ventricular septal defect
Overriding Aorta
Right ventricular hypertrophy

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4
Q

what does Spells refer to in ToF?

A

physiological stress causes cyanosis of the patient, causing them to have a ‘blue spell’

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5
Q

how are spells treated in ToF?

A

using morphine to relax the infundibulum muscle

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6
Q

what is the main risk of ToF

A

acidosis

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7
Q

describe hypoplastic left heart syndrome

A

life limiting condition, often detected antenatally, in which the left ventricle is underdeveloped, causing poor systemic blood flow.

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8
Q

which conditions are acyanotic heart diseases?

A

Atrial septal defect
ventricular septal defect
persistent ductus arteriosus

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9
Q

describe ASD and VSD

A

hole between either the atria or ventricles

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10
Q

where is the most common location for a hole in ASD

A

where the FO was previously. failure to close

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11
Q

what are the risks of ASD and VSD

A

heart failure, more common in VSD.

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12
Q

when would a loud murmur be heard?

A

in smaller VSD as there is more turbulent blood flow

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13
Q

how does heart failure present in children

A

right sided more common: hepatic oedema

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14
Q

how is the ductus arteriosus kept open?

A

prostaglandins eg. PGE1

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15
Q

how is the ductus arteriosus closed?

A

prostaglandin inhibitors

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16
Q

describe coarctation of the aorta

A

there is a narrowing of the aorta, often presents with a child collapsing around day 3-5 after birth (the closing of the ductus arteriosus reduces the compensation)

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17
Q

how is the coarctation of the aorta detected

A

in the new baby examination, femoral pulses will be different.

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18
Q

what treatment is given if a coarctation is detected

A

prostaglandins, stent in the aorta.

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19
Q

describe aortic stenosis

A
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20
Q

describe pulmonary stenosis

A
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21
Q

which conditions are cyanotic heart diseases

A

tetralogy of fallot

transposition of the great arties

total anomalous pulmonary venous return

hypoplastic left heart syndrome

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22
Q

describe eisenmenger syndrome

A

when there is a right to left shunt eg ASD, VSD, PDA the pressure in the left should be greater to avoid blood coming into the left side of the heart.

Eisenmenger’s is when the right sided pressure increases to bypass this affect, allowing for cyanosis.

pulmonary pressure is greater than systemic pressure- allows right to left movement.

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23
Q

which population more commonly have Patent DA?

A

premature babies

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24
Q

where is prostaglandin E2 produced?

A

in the placenta

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25
Q

what is the function of prostaglandin E2 during pregnancy?

A

keeps ductus arteriosus open

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26
Q

what type of shunt does a PDA cause?

A

pressure in the aorta is higher than the pulomonary vessels so blood flows from aorta to pulmonary artery.

this is a left to right shunt.

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27
Q

what are the complications of a persistant DA?

A

additional blood creates more pressure in pulmonary vessels

causes strain on right ventricle.

pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy

there is an increased volume of blood returning from the lungs to the left side of the heart- this causes left ventricular hypertrophy

28
Q

how does a larger PDA present on examination

A

continuous crescendo- decrescendo machinery murmur

heard loudest below the clavicle

normal first heart sound, second sound is difficult to hear over the murmur

29
Q

how can a PDA present with symptoms

A

SOB

difficulty feeding
poor weight gain

LRTI

30
Q

how is PDA managed?

A

echocardiogram confirms the diagnosis

medical closure using indomethacin, ibuprofen or paracetamol attempted in preterm infants- work by inhibiting prostaglandins

31
Q

what are surgical interventions for PDA?

A

endovascular procedures

open surgery

32
Q

what else may need to be managed in PDA?

A

heart failure

diuretics may be used to remove the water

33
Q

what are the types of atrial septal defect

A

patent foramen ovale (not strictly classified as ASD)

Ostium secundum (septum secundum fails to close

ostium primum (septum primum fails to close)

34
Q

what are the complications of ASD

A

stroke in the context of venous thromboembolism

atrial fibrillation or atrial flutter

pulmonary hypertension and right sided heart failure

eisenmenger syndrome

35
Q

when can a DVT cause a stroke rather than a pulmonary embolism?

A

if there is a history of ASD

the clot can bypass the pulmonary circulation and enter the systemic

36
Q

when are ASD detected?

A

antenatal scans or newborn examinations

it may be asymptomatic in childhood and present in adulthood with dyspnoea, heart failure, stroke.

37
Q

what are childhood symptoms of ASD?

A

SOB

Difficulty feeding

poor weight gain

lower resp tract infections

38
Q

which ASD is linked to migraine with aura?

A

patent foramen ovale

no recommendations for testing or treating patiets with migraine as a potential PFO

39
Q

how is ASD managed

A

echocardiogram confirms diagnosis

paediatric cardiologist manages patients with ASD
-active monitoring
-percutaneous transvenous catheter closure
-open heart surgery

40
Q

which syndromes might VSD be associated with?

A

turners
downs

41
Q

describe the presentation of a VSD

A

initially symptomless, can present in adulthood

can be detected in antenatal scans or newborn baby check

42
Q

what are the typical symptoms of VSD

A

poor feeding

dyspnoea

tachypnoea

failure to thrive

43
Q

what would a VSD sound like on auscultation

A

pan systolic murmur

heard loudest at the left lower sternal border in the third and fourth intercostal spaces

systolic thrill on palpation

44
Q

how is a VSD managed

A

echocardiogram confirms the diagnosis

A paediatric cardiologist will manage patients with a VSD. Management options include:

-Active monitoring (small defects may -close on their own)
-Percutaneous transvenous catheter closure (via the femoral vein)
-Open-heart surgery

45
Q

what does VSD increase the risk of

A

infective endocarditis

46
Q

what would be found on examining a patient with Eisenmengers syndrome

A

signs of pulmonary hypertension
-right ventricular heave

  • loud P2 (forceful closing of pulmonary valve)
  • raised JVP

-peripheral oedema

murmurs relating to the underlying septal defect (ASD,VSD, PDA)

47
Q

which clinical findings can be caused by right to left shunt and chronic hypoxia

A

cyanosis

finger clubbing

dyspnoea

plethoric complexion

48
Q

what is the definitive treatment for Eisenmengers syndrome

A

heart-lung transplant

49
Q

which complications need to be managed in Eisenmengers syndrome

A

SOB- use oxygen

pulmonary htn- use sildenafil and bosentan

oedema- diuretics

arrhythmia

polycythaemia- venesection

thrombosis - anti coagulation

infective endocarditis - antibiotics

50
Q

what is the prognosis of Eisenmenger syndrome

A

reduces life expectancy by around 20 years compared with healthy individuals

main causes of death- heart failure, infection, thromboembolism and haemorrhage

mortality up to 50% in pregnancy

51
Q

where is a coarctation in the aorta usually found

A

near the ductus arteriosus

52
Q

which genetic condition is coarctation of the aorta particularly associated with?

A

turners

53
Q

what are signs other than reduced femoral pulses in coarctation of the aorta for infants?

A

-Raised respiratory rate
-Increased work of breathing
-Poor feeding
-Heart failure
-Shock

Additional signs may develop over time:

Left ventricular heave due to left ventricular hypertrophy
Underdeveloped left arm where there is reduced flow to the left subclavian artery
Underdevelopment of the legs

54
Q

what is the management for coarctation of the aorta?

A

depends on severity

mild may not require surgical intervention

severe may require emergency surgery shortly after birth

55
Q

describe hypertrophic obstructive cardiomyopathy

A

thickening of the left ventricle muscle, especially the ventricular septum

thickening reduces space in the ventricle, blocking blood flow to the aorta
known as left ventricular outflow tract obstruction

56
Q

what is HOCM associated with

A

increased risk of heart failure, myocardial infarction, arrythmia and sudden cardiac death

57
Q

is HOCM a genetic conditionq

A

yes!

autosomal dominant resulting from a defect in the genes for the sarcomere proteins

58
Q

what is the prevelance of hocm

A

1 in 500 people

59
Q

is family history relevant in hocm?

A

yes, there is usually someone who died suddenly.

HOWEVER it can also be a de novo mutation (new)

60
Q

what is the usual presentation of hypertrophic OCM?

A

most patients asymptomatic

non specific presentation of:
-SOB
-Fatigue
-Dizziness
-syncope
-chest pain
-palpitations

SEVERE cases may present with symptoms of heart failure

61
Q

what would be found on examination of a patient with HOCM

A

ejection systolic murmur

fourth heart sound

thrill at the lower left sternal border

62
Q

how is HOCM diagnosed

A

echocardiogram or cardiac MRI

genetic testing may be considered to establish the affected genes

63
Q

how is HOCM managed?

A

beta blockers
surgical myectomy
implantable cardiocerter defibrillator
heart transplant

64
Q

what are patients advised to avoid?

A

intense exercise, heavy lifting and dehydration

AVOID ACE inhibitors and nitrates, as they can worsen LVOT obstruction

65
Q

what are possible complications of HOCM

A

arrhythmia
mitral regurgitation
heart failure
sudden cardiac death

Martha Phase 3a (27 decks)

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