Cardiovascular Flashcards
S+S of cardiac failure?
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
How does congenital heart disease present? (5)
- Antenatal cardiac USS diagnosis
- Heart murmur (most common – most innocent)
- Heart failure
- Shock
- Cyanosis
Cardiac examination?
- 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
Normal pulse rate by age?
- <1y = 110-160
- 2-5y = 95-140
- 5-12y = 80-120
- > 12y = 60-100
What are the causes of heart failure in
a) Neonates
b) Infants
c) Older children
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
How do you manage a duct-dependent lesion?
Prostaglandin infusion until defect fixed to maintain patency
How do you manage a R–>L shunt with cardiac failure?
- Give diuretics and captopril
- Problem should either resolve or need surgery
What are the features of an innocent murmur?
- 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
What is a venous hum?
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
4 conditions with a L–>R shunt?
ASD
VSD
AVSD
PDA
Most common congenital heart defect?
VSD (30%)
2 types of ASD?
- Secondum ASD (foramen ovale) - 80%
2. Partial AVSD - 20%
S+S of ASD?
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
CXR and ECG changes in ASD?
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
What is best Ix for ASD?
Echo
Management of ASD?
- 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
How are VSDs classified?
Small (80-90%)
- <3mm (smaller than aortic valve)
Large (10-20%)
- >3mm (larger than aortic valve)
S+S of small VSD?
Sx: asymptomatic
Signs: Loud pansystolic murmur at LLSE
Quiet 2nd sound
Ix of small VSD?
CXR and ECG = normal
Echo - small VSD with no pulm HTN
Management of small VSD
These lesions will close spontaneously
S+S of large VSD?
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)
What do Ix show in large VSD?
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)
Management of large VSD?
- Treat HF –> diuretics + captopril
- Additional calorie input
- Surgery at 3-6m to prevent Eisenmenger syndrome
Clinical features of PDA?
- 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
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
Which syndrome is AVSD associated with?
Downs
- 15-20% with downs have AVSD
- (45% with Down’s have some form of congenital heart disease)
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
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
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)
Treatment of PS?
Balloon dilatation
What could outflow obstruction in well child be due to?
AS
PS
What could outflow obstruction in sick child be due to?
Coarctation
Interruption of aortic arch
Hypoplastic L heart
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
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
Ix for coarctation?
CXR - cardiomegaly from HF and shock
ECG - normal
What are the associations with coarctation?
Bicuspid AV valve
VSD
Turner syndrome
Management of coarctation?
Give prostaglandins and HF drugs first
Surgical repair soon after diagnosis
–> Angioplasty with or w/o stenting
- Sometimes open surgery needed
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
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
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
Management of duct-dependent lesion?
- Prostaglandin infusion (retain patency)
- This only short term solution
- Formaldehyde should be infiltrated into structure for longer term
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
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
Management of hypoplastic L heart?
Difficult neonatal operation called Norwood procedure
Followed by further operations at 6m and again at 3y
What is SVT?
- Most common childhood arrhythmia
- Presents with rapid heart rate b/w 250-300 bpm
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
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
What are the causes of R–> L shunts?
Tetralogy of Fallot
Transposition of the great vessels
Eisenmenger syndrome
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
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
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)
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
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
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
Ix for transposition of great vessels?
CXR
- Narrow pedicle
- Egg on side
- Increased pulmonary vascular markings
ECG
normal
Echo
Definitive
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
What cardiac defect associated with Turners?
Coarctation
What cardiac defects associated with Noonan’s?
Pulmonary stenosis
Hypertrophic cardiomyopathy
Septal defects - ASD/VSD
What cardiac defects associated with Marfan’s?
Weakened aorta - dissection or aneurysm
Mitral/tricuspid valve prolapse
What causes myocarditis?
Viral / bacterial
- Influenza
- Coxsackie
- Adenovirus
- Polio
- Rubella
- Lyme disease
Inherited
Secondary to metabolic condition
Others:
- Allergies
- Fungus/parasites
- Radiation
- Some drugs
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
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
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
Who is at highest risk of sub-acute bacterial endocarditis? (SBE)
Turbulent blood flow
- VSD
- Coarctation
- PDA
- Prosthetic material
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
Diagnosis of SBE?
- Multiple blood cultures before abc
- Echo may show vegetations
- CRP + ESR
What is most common pathogen in SBE?
Alpha-haemolytic strep - strep viridans
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
