Cardiovascular Flashcards
1
Q
S+S of cardiac failure?
A
Sx:
- Breathlessness (particularly on feeding or exertion)
- Sweating
- Poor feeding
- Recurrent chest infections
Signs:
- Poor weight gain or ‘faltering growth’
- Tachypnoea
- Tachycardia
- Heart murmur, gallop rhythm
- Enlarged heart
- Hepatomegaly
- Cool peripheries
2
Q
How does congenital heart disease present? (5)
A
- Antenatal cardiac USS diagnosis
- Heart murmur (most common – most innocent)
- Heart failure
- Shock
- Cyanosis
3
Q
Cardiac examination?
A
- Cyanosis
- Clubbing of fingers or toes
- Pulse – rate, rhythm, volume
- Inspection – distress, precordial bulge, scars, ventricular impulse
- Palpation – thrill (palpable murmur), apex (4th-5th intercostal space, mid-clavicular line), right ventricular heave (lower left sternal edge) shows right ventricular hypertrophy
- Auscultation – heart sounds in four areas (apex, LLSE, ULSE, URSE) and the back. Check for murmurs, loud heart sounds, splitting of heart sounds
- Hepatomegaly
- Lung bases
- Femoral pulses
- Blood pressure
4
Q
Normal pulse rate by age?
A
- <1y = 110-160
- 2-5y = 95-140
- 5-12y = 80-120
- > 12y = 60-100
5
Q
What are the causes of heart failure in
a) Neonates
b) Infants
c) Older children
A
a) Obstructed (duct-dependent) systemic circulation
- Hypoplastic left heart syndrome
- Critical aortic valve stenosis
- Severe coarctation of the aorta
- Interruption of the aortic arch
Infants (high pulmonary blood flow):
- VSD
- AVSD
- Large persistent ductus arteriosus
Older children and adolescents (R–>L heart failure):
- Eisenmenger syndrome (right heart failure only)
- Rheumatic heart disease
- Cardiomyopathy
6
Q
How do you manage a duct-dependent lesion?
A
Prostaglandin infusion until defect fixed to maintain patency
7
Q
How do you manage a R–>L shunt with cardiac failure?
A
- Give diuretics and captopril
- Problem should either resolve or need surgery
8
Q
What are the features of an innocent murmur?
A
- Asymptomatic patient
- Soft blowing murmur
- Systolic murmur only, not diastolic
- Left sternal edge
- Normal heart sounds with no added sounds
- No parasternal thrill
- No radiation
9
Q
What is a venous hum?
A
Harmless murmur in children
Heard above R clavicle over jugular vein
Heard throughout cardiac cycle
Abolished by placing finger on jugular vein
Murmur may disappear on lying or turning head
10
Q
4 conditions with a L–>R shunt?
A
ASD
VSD
AVSD
PDA
11
Q
Most common congenital heart defect?
A
VSD (30%)
12
Q
2 types of ASD?
A
- Secondum ASD (foramen ovale) - 80%
2. Partial AVSD - 20%
13
Q
S+S of ASD?
A
Sx:
- Often asymptomatic
- Recurrent chest infections/wheeze
- Arrhythmias (4th decade onwards)
Signs:
- Ejection systolic murmur
- Best heard at upper L sternal edge (due to increased flow across pulmonary valve because of L–>R shunt)
- Fixed and widely split 2nd heart sound (hard to hear) – due to RV stroke vol being equal in inspiration and expiration
- With partial AVSD apical pansystolic murmur may be heard from AV valve regurgitation
14
Q
CXR and ECG changes in ASD?
A
CXR
- Cardiomegaly
- Enlarged pulmonary arteries
- Increased pulmonary vascular markings
ECG
- Secundum ASD –> partial RBBB (can also occur in normal children) and RAD due to RV enlargement
- Partial AVSD will give a ‘superior’ QRS axis (largely negative in AVF) due to defect being near AV node
15
Q
What is best Ix for ASD?
A
Echo
16
Q
Management of ASD?
A
- Children with large enough defect to cause RV dilation will require treatment
- For secundum ASD this is by cardiac catheterisation with insertion of an occlusion device
- For partial AVSD surgical correction required
- Treatment usually undertaken at 3-5y in order to prevent right HF and arrhythmias in later life
17
Q
How are VSDs classified?
A
Small (80-90%)
- <3mm (smaller than aortic valve)
Large (10-20%)
- >3mm (larger than aortic valve)
18
Q
S+S of small VSD?
A
Sx: asymptomatic
Signs: Loud pansystolic murmur at LLSE
Quiet 2nd sound
19
Q
Ix of small VSD?
A
CXR and ECG = normal
Echo - small VSD with no pulm HTN
20
Q
Management of small VSD
A
These lesions will close spontaneously
21
Q
S+S of large VSD?
A
Sx:
- HF with breathlessness and FTT after 1w old
- Recurrent chest infections
Signs:
- HF –>Tachypnoea, tachycardia and enlarged liver
- Active precordium should be felt (vol overload)
- Soft (large defect) pansystolic murmur heard at LLSE
- Apical mid-diastolic murmur present (due to increased flow across mitral value from blood leaving lungs)
22
Q
What do Ix show in large VSD?
A
CXR
- Cardiomegaly
- Enlarged pulmonary arteries
- Increased pulmonary vascular markings
- Pulmonary oedema
ECG
- Biventricular hypertrophy by 2m of age (upright T wave – pulmonary HTN)
Echo
- Anatomy of defect
- Pulmonary HTN (due to high flow)
23
Q
Management of large VSD?
A
- Treat HF –> diuretics + captopril
- Additional calorie input
- Surgery at 3-6m to prevent Eisenmenger syndrome
24
Q
Clinical features of PDA?
A
- Continuous murmur beneath left clavicle
- Continues into diastole because pressure in pulmonary artery always lower than aorta
- Pulse pressure increased and this → collapsing or bounding pulse
- Sx can be unusual but when duct is large there will be increased pulmonary blood flow with HF and pulmonary HTN
25
Management of PDA?
- Closure recommended to abolish lifelong risk of bacterial endocarditis and pulmonary vascular disease
- Closure is with coil or occlusion device introduced via cardiac catheter at about 1yo
- Occasionally surgical ligation required
26
Which syndrome is AVSD associated with?
Downs
- 15-20% with downs have AVSD
- (45% with Down's have some form of congenital heart disease)
27
Clinical features of aortic stenosis?
Sx:
- Most asymptomatic
- If severe --> reduced exercise tol, chest pain on exertion, syncope
Signs:
- Small vol and slow rising pulse
- Carotid thrill (always)
- Ejection systolic murmur at URSE radiating to neck
- Delayed and soft aortic second sound
- Apical ejection click
28
Management of AS?
Balloon dilatation
- If sx or high resting pressure gradient
- Safe in older children
- Dangerous in neonates
Most children with sig stenosis requiring treatment in first few years of life will eventually require aortic valve replacement
- Early treatment therefore palliative and directed at delaying this for as long as possible
29
S+S of pulmonary stenosis?
Sx:
- Most asymptomatic and diagnosed clinically
- A small number of neonates with critical pulmonary stenosis have duct dependent pulmonary circulation and present in first few days of life with cyanosis
Signs:
- Ejection systolic murmur at ULSE and thrill may be present
- Ejection click may be heard at ULSE
- If severe, prominent RV impulse (heave)
30
Treatment of PS?
Balloon dilatation
31
What could outflow obstruction in well child be due to?
AS
| PS
32
What could outflow obstruction in sick child be due to?
Coarctation
Interruption of aortic arch
Hypoplastic L heart
33
What is coarctation of the aorta?
- Due to arterial duct tissue encircling aorta at point of insertion of duct
- When duct closes, aorta also constricts, causing severe obstruction to LV outflow
- Commonest cause of collapse due to left outflow obstruction
34
S+S of coarctation?
Sx:
- Examination on first day of life usually normal
- Neonates usually present with acute circulatory collapse at 2d of age when duct closes
Signs:
- Sick baby with severe HF
- Absent femoral pulses
- Severe metabolic acidosis
- Murmur may be heard at ULSE
35
Ix for coarctation?
CXR - cardiomegaly from HF and shock
| ECG - normal
36
What are the associations with coarctation?
Bicuspid AV valve
VSD
Turner syndrome
37
Management of coarctation?
Give prostaglandins and HF drugs first
Surgical repair soon after diagnosis
--> Angioplasty with or w/o stenting
- Sometimes open surgery needed
38
What are the duct dependent heart conditions?
```
Coarctation
TGA – Transposition of the great arteries
HLHS – Hypoplastic left heart syndrome
PA – Pulmonary atresia
TA – Tricuspid atresia
Aortic stenosis – if severe
Pulmonary stenosis – if severe
```
39
What is tricuspid atresia?
- Tricuspid valve absent/abnormally developed
- No blood flow RA-->RV
- Must have ASD & VSD to survive
- PDA usually to allow greater pulmonary flow
40
What is pulmonary atresia?
- Pulmonary valve fails to develop
- No outflow from heart to lungs
- No problem in utero
- When born only thing providing O2 to lungs is PDA
- Baby turns blue rapidly
- -> Quick diagnosis
41
Management of duct-dependent lesion?
- Prostaglandin infusion (retain patency)
- This only short term solution
- Formaldehyde should be infiltrated into structure for longer term
42
What is hypoplastic left heart?
- Complete underdevelopment of L side of heart
- Mitral valve small or atretic
- LV diminutive and usually aortic valve atresia
- Ascending aorta v small and almost invariably coarctation
- Must be an ASD to allow returning blood to leave LA and re-circulate
43
Clinical features of hypoplastic left heart?
- May be detected antenatally at USS
- → Allows effective counselling - helps prevent child becoming sick after birth
- If present after birth → sickest of all neonates presenting with duct dependent systemic circulation
- No flow through L side of heart so ductal constriction → profound acidosis and rapid cardiovascular collapse
- Weakness or absence of all peripheral pulses in contrast to weak femoral pulses in coarctation
44
Management of hypoplastic L heart?
Difficult neonatal operation called Norwood procedure
Followed by further operations at 6m and again at 3y
45
What is SVT?
- Most common childhood arrhythmia
| - Presents with rapid heart rate b/w 250-300 bpm
46
Sx of SVT?
- Poor cardiac output and pulm oedema
- Sx of HF in neonate or young infant
- Cause of hydrops fetalis (accumulation of fluid in several separate compartments) and intrauterine death
47
Management of SVT?
Circulatory and respiratory support
- Correct tissue acidosis and give positive pressure ventilation if required
Vagal stimulation manoeuvres
- e.g. carotid sinus massage or ice cold pack to face
- Successful in 80%
IV adenosine = treatment of choice
- Induces AV block after rapid bolus injection
- Terminates tachycardia and hence breaks re-entry circuit that has been set up b/w AV node and accessory pathway
- Given incrementally in increasing doses
Electrical cardioversion with a synchronised DC shock (0.5-2 J/kg body weight)
- If adenosine fails
Maintenancy therapy once sinus rhythm restored
- Flecanide or sotalol
- Treatment stopped at 1y
48
What are the causes of R--> L shunts?
Tetralogy of Fallot
Transposition of the great vessels
Eisenmenger syndrome
49
Key features of tetralogy of fallot?
1 Large VSD
2 Overriding of aorta with respect to ventricular septum (basically this means it receives into from both L and R
ventricles)
3 Sub-pulmonary stenosis causing RV outflow tract
obstruction
4 RV hypertrophy as a result
50
S+S of tetralogy of fallot?
Sx:
- Most diagnosed antenatally or ID of murmur
- Cyanosis
- Breathlessness
- Pallor
Signs:
- Clubbing in older children
- Loud, harsh ejection systolic murmur at L sternal edge from day 1 of life
- With increasing RV outflow obstruction, which is predominantly muscular and below pulmonary valve, murmur will shorten and cyanosis will increase
51
What do Ix show in TOF?
CXR
- Relatively small heart
- RV hypertrophy
- Pulmonary artery bay
ECG
- Normal at birth
- RV hypertrophy later (inverted T waves, no S wave)
52
Management of TOF?
BT shunt
- Early management if v cyanosed
- Increases pulmonary flow by putting tube b/w subclavian and pulmonary aa
Complete correction
- At 6m
- Close VSD
- Releive RV outflow obstruction
Hypercyanotic spells
- Need treatment with Iv propanolol, bicarbonate for acidosis, muscle paralysis and ventilation
- Only if >15mins
53
What is transposition of the great vessels?
- Aorta connected to RV and pulmonary artery connected to LV
- --> Blue blood returned to body and pink blood returned to lungs
- 2 parallel and completely isolated circuits and, unless mixing of blood b/w them → incompatible with life
- Fortunately naturally occurring defects such as VSD and ASD are common
- PDA as well as therapeutic interventions can achieve mixing for short amount of time
54
S+S of transposition of great vessels?
Sx:
- Cyanosis = predominant symptom - can be profound or even life threatening
- Presentation usually on day 2 of life when ductal closure → marked reduction in mixing of desaturated and saturated blood
- Cyanosis less severe and presentation delayed if more mixing of blood for associated abnormalities e.g. ASD
Signs:
- Cyanosis always present
- 2nd heart sound often loud and single
- Usually no murmur, but can be systolic murmur from increased flow or stenosis within LV (pulmonary) outflow tract
55
Ix for transposition of great vessels?
CXR
- Narrow pedicle
- Egg on side
- Increased pulmonary vascular markings
ECG
normal
Echo
Definitive
56
Management of transposition of great vessels?
Immediate = prostaglandin infusion
Balloon atrial septostomy in 20% - makes formaen ovale valve incompetent so mixing allowed
Surgery to switch arteries
- All pts need this
- Performed in first few d of life
57
What cardiac defect associated with Turners?
Coarctation
58
What cardiac defects associated with Noonan's?
Pulmonary stenosis
Hypertrophic cardiomyopathy
Septal defects - ASD/VSD
59
What cardiac defects associated with Marfan's?
Weakened aorta - dissection or aneurysm
| Mitral/tricuspid valve prolapse
60
What causes myocarditis?
Viral / bacterial
- Influenza
- Coxsackie
- Adenovirus
- Polio
- Rubella
- Lyme disease
Inherited
Secondary to metabolic condition
Others:
- Allergies
- Fungus/parasites
- Radiation
- Some drugs
61
S+S myocarditis?
Sx:
- Can be mild at first and difficult to detect or can sometimes appear suddenly
- Include FTT, anxiousness, feeding difficulties, fever, HF, listlessness, low urine output and pale peripheries
- Sx in older children (>2) can include nausea, belly ache, chest pain, cough, fatigue and swelling (legs, feet and face)
- Difficult to diagnose as sx tend to mimic other heart and lung disorders
Signs:
- Rapid heartbeat or abnormal heart sound
- Fluid at lung bases due to pulmonary oedema
- Signs of infection may be present
62
Ix for myocarditis?
CXR:
- Enlargement of the heard borders
Further tests:
- Blood cultures, LFTs, U&E’s, antibody screen, heart biopsy and FBC
Echocardiography:
- Usually the mode of diagnosis
63
Management of myocarditis?
- No cure
- Aim = minimise damage and treat sx until condition resolves
- Treating sx with diuretics and ACE inhibitors and carvedilol (a B-adrenoceptor blocking agent) is important
- Abx, steroids, anti- inflammatory drugs and IV immunoglobulin - protect heart
Usually improves spontaneously, but some children will ultimately require heart transplantation
64
Who is at highest risk of sub-acute bacterial endocarditis? (SBE)
Turbulent blood flow
- VSD
- Coarctation
- PDA
- Prosthetic material
65
Clinical features of SBE?
- Sustained fever
- Anaemia
- Pallor
- Splinter haemorrhages
- Clubbing (late)
- Necrotic skin lesions
- Changing cardiac signs
- Splenomegaly
- Neurological signs of infarcts
- Retinal infarcts
- Arthritis/arthralgia
- Haematuria (microscopic)
--> Raised ESR
66
Diagnosis of SBE?
- Multiple blood cultures before abc
- Echo may show vegetations
- CRP + ESR
67
What is most common pathogen in SBE?
Alpha-haemolytic strep - strep viridans
68
Management of SBE?
High dose penicillin
Aminoglycoside
--> 6w using IV therapy
Surgical removal may be required if incomplete eradication (more common if prosthetic material)
Prophylaxis with good dental hygiene in all with congenital heart disease
