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

Child health- Congenital heart disease Flashcards

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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
what is the function of prostaglandin E2 during pregnancy?
keeps ductus arteriosus open
26
what type of shunt does a PDA cause?
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.
27
what are the complications of a persistant DA?
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
how does a larger PDA present on examination
continuous crescendo- decrescendo machinery murmur heard loudest below the clavicle normal first heart sound, second sound is difficult to hear over the murmur
29
how can a PDA present with symptoms
SOB difficulty feeding poor weight gain LRTI
30
how is PDA managed?
echocardiogram confirms the diagnosis medical closure using indomethacin, ibuprofen or paracetamol attempted in preterm infants- work by inhibiting prostaglandins
31
what are surgical interventions for PDA?
endovascular procedures open surgery
32
what else may need to be managed in PDA?
heart failure diuretics may be used to remove the water
33
what are the types of atrial septal defect
patent foramen ovale (not strictly classified as ASD) Ostium secundum (septum secundum fails to close ostium primum (septum primum fails to close)
34
what are the complications of ASD
stroke in the context of venous thromboembolism atrial fibrillation or atrial flutter pulmonary hypertension and right sided heart failure eisenmenger syndrome
35
when can a DVT cause a stroke rather than a pulmonary embolism?
if there is a history of ASD the clot can bypass the pulmonary circulation and enter the systemic
36
when are ASD detected?
antenatal scans or newborn examinations it may be asymptomatic in childhood and present in adulthood with dyspnoea, heart failure, stroke.
37
what are childhood symptoms of ASD?
SOB Difficulty feeding poor weight gain lower resp tract infections
38
which ASD is linked to migraine with aura?
patent foramen ovale no recommendations for testing or treating patiets with migraine as a potential PFO
39
how is ASD managed
echocardiogram confirms diagnosis paediatric cardiologist manages patients with ASD -active monitoring -percutaneous transvenous catheter closure -open heart surgery
40
which syndromes might VSD be associated with?
turners downs
41
describe the presentation of a VSD
initially symptomless, can present in adulthood can be detected in antenatal scans or newborn baby check
42
what are the typical symptoms of VSD
poor feeding dyspnoea tachypnoea failure to thrive
43
what would a VSD sound like on auscultation
pan systolic murmur heard loudest at the left lower sternal border in the third and fourth intercostal spaces systolic thrill on palpation
44
how is a VSD managed
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
what does VSD increase the risk of
infective endocarditis
46
what would be found on examining a patient with Eisenmengers syndrome
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
which clinical findings can be caused by right to left shunt and chronic hypoxia
cyanosis finger clubbing dyspnoea plethoric complexion
48
what is the definitive treatment for Eisenmengers syndrome
heart-lung transplant
49
which complications need to be managed in Eisenmengers syndrome
SOB- use oxygen pulmonary htn- use sildenafil and bosentan oedema- diuretics arrhythmia polycythaemia- venesection thrombosis - anti coagulation infective endocarditis - antibiotics
50
what is the prognosis of Eisenmenger syndrome
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
where is a coarctation in the aorta usually found
near the ductus arteriosus
52
which genetic condition is coarctation of the aorta particularly associated with?
turners
53
what are signs other than reduced femoral pulses in coarctation of the aorta for infants?
-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
what is the management for coarctation of the aorta?
depends on severity mild may not require surgical intervention severe may require emergency surgery shortly after birth
55
describe hypertrophic obstructive cardiomyopathy
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
what is HOCM associated with
increased risk of heart failure, myocardial infarction, arrythmia and sudden cardiac death
57
is HOCM a genetic conditionq
yes! autosomal dominant resulting from a defect in the genes for the sarcomere proteins
58
what is the prevelance of hocm
1 in 500 people
59
is family history relevant in hocm?
yes, there is usually someone who died suddenly. HOWEVER it can also be a de novo mutation (new)
60
what is the usual presentation of hypertrophic OCM?
most patients asymptomatic non specific presentation of: -SOB -Fatigue -Dizziness -syncope -chest pain -palpitations SEVERE cases may present with symptoms of heart failure
61
what would be found on examination of a patient with HOCM
ejection systolic murmur fourth heart sound thrill at the lower left sternal border
62
how is HOCM diagnosed
echocardiogram or cardiac MRI genetic testing may be considered to establish the affected genes
63
how is HOCM managed?
beta blockers surgical myectomy implantable cardiocerter defibrillator heart transplant
64
what are patients advised to avoid?
intense exercise, heavy lifting and dehydration AVOID ACE inhibitors and nitrates, as they can worsen LVOT obstruction
65
what are possible complications of HOCM
arrhythmia mitral regurgitation heart failure sudden cardiac death

Martha Phase 3a (27 decks)

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