Cardiovascular Flashcards
In ~30% children you may hear an innoSent murmur, what are the 4 hallmarks of innoSent murmurs? and other features?
:)
-aSymptomatic
-Soft blowing murmur
-Systolic murmur only
-left Sternal edge
There should be normal heart sounds w/ no added sounds, no parasternal thrill and no radiation :)
Why are innocent/flow murmurs sometimes heard in children during a febrile illness/anaemia?
Increased CO (so examine child after such illnesses are corrected)
What can help you differentiating innocent from pathological murmurs in children?
- referral to paediatric cardiologist for exho
- CXR
- ECG
Why may newborns with potential shunts e.g. PDA, VSD have no murmur/symptoms at birth? When may they become apparent?
- as at birth pulmonary vascular resistance is still high
- several weeks of age when pul. vasc. resistance falls
Where could a “VSD” be present? Anywhere in the ..
- ventricular septum
- perimembranous region (next to tricuspid valve)
- muscular area
How are VSDs categorised? What mm?
-By size: “small” is smaller than the aortic valve in diameter (up to ~3mm)
“large” are the same size or bigger than the aortic valve
Describe signs of a small VSD:
- asymptomatic
- signs: loud pansystolic murmur at lower left sternal edge, quiet pulmonary second sound (p2)
What investigations would you do/see for a small VSD:
- CXR will be normal
- ECG will be normal
- Echo: allows visualisation of defect, doppler to assess haemodynamics
- No pulmonary HT
Small VSDs management:
- close spontaneously, confirm by ECG/normal echo at follow up
- while present, prevent bact. endocarditis by maintaining good dental hygeine
Name some symptoms of large VSDs:
- heart failure, breathlessness & faltering growth after 1 week old
- recurrent chest infections
Name some signs of large VSDs:
- tachypnoea, tachycardia, hepatomegaly from HF
- active precordium
- soft pansystolic murmur/no murmur
- apical and mid-diastolic murmur (from increased flow across mitral valve after the blood has circulated through lungs)
- loud p2 from raised pulmonary arterial pressure
Large VSD CXR findings:
- cardiomegaly
- enlarged pulmonary arteries
- increased pulmonary vascular markings
- pulmonary oedema
What ECG and Echo findings may be present in a large VSD?
- ECG: biventricular hypertrophy by 2months olg
- Echo: can visualise defect size and doppler for flow which is high flow so pulmonary HT also present
What is the management of large VSDs?
- Diuretics + captopril for the HF
- additional calorie input
- surgery ~3-6months to manage HF and faltering growth and to prevent permanent lung damage from pulmonary HT and high blood flow
What is the most common congenital cause of cyanotic heart disease? What direction is the shunt?
Tetralogy of Fallot
Right to Left
What are the 4 clinical features of the tetralogy of Fallot?
- large VSD
- overriding of aorta w respect to the ventricular septum
- subpulmonary stenosis causing RV outflow obstruction
- RV hypertrophy as a result
How is Tetralogy of Fallot often recognised?
- antenatally
- following murmur identification in first months of life +/- cyanosis
Although rare in developed countries, classic T of F: severe cyanosis, squatting on exercise and especially hypercyanotic spells are important to recognise as these spells can lead to__ if untreated
- MI
- CVA
- death
What characterises a hypercyanotic spell in Tetralogy of Fallot? Often associated with_?
NB: a very short murmur can be auscultated during a spell.
-rapid increase in cyanosis often associated with irritability/inconsolable crying because of severe hypoxia, breathlessness & pallor because of tissue acidosis.
**A clinical sign of Tetralogy of Fallot: is finger and toe __ in older children. Describe the murmur present and how it changes?
- clubbing
- loud harsh ejection systolic at left sternal edge from birth
- with increasing RV outflow tract obstruction (from muscle) below the pulmonary valve, the murmur will shorten and cyanosis will increase
What will a CXR show in a child with Tetralogy of Fallot?
-small heart +/- uptilted apex (due to RV hypertrophy)
-pulmonary artery ‘bay’-a concavity on the L heart boarder where the convex PA and RV outflow tract would normally be.
+/- right sided aortic arch
What may an ECG/Echo show for Tetralogy of Fallot?
ECG: normal at birth, more RV hypertrophy with age
Echo: cardinal features but need cardiac catheter to detail coronary artery anatomy
Tetralogy of Fallot management is initially medical w surgery ~6months of age, what does the surgery aim to do and how?
- close the VSD
- relieve the RV outflow obstruction (can be with an artificial patch that extends across the pulmonary valve)
In very cyanosed neonates with tetralogy of fallot, what can be done to increase pulmonary blood flow and how? (between which arteries or using a __)
-shunt via surgical placement of tube between subclavian and pulmonary artery or via balloon dilatation of the RV outflow tract.
Hypercyanotic spells in TofF are often self-limited followed by sleep, if prolonged >15mins, what prompt treatments should be given and why: (name 3+)
- sedation and pain relief e.g. morphine
- IV propranolol or a-agonist, for peripheral v.constriction and to relieve subpulmonary muscular obstruction that is causing reduced pulmonary flow
- IV fluid
- bicarbonate to correct acidosis
- muscle paralysis and artificial ventilation to reduce metabolic o2 demand
Give 3 causes of cyanosis in a new-born with resp distress (>60breaths/min)
- cyanotic congenital heart disease
- persistent pulmonary HT of new-born
- infection e.g. GBAHS
- inborn errors of metabolism
- respiratory disorders such as:..
- resp distress syndrome
- -meconium aspiration
- -pulmonary hypoplasia
Give 3 examples of left to right shunts in newborns? Presents w breathlessness or can be asymptomatic..
- ASD
- VSD
- PDA
Give 2 examples of right to left shunts in newborns? Presents w blue baby
TETRALOGY OF FALLOT
TRANSPOSITION OF THE GREAT ARTERIES
Name 1 condition that will cause outflow obstruction in a child but is asymptomatic/well and 1 outflow obstruction cause that will –> sick neonate:
- well: aortic or pulmonary stenosis
- sick: coarctation, HLHS (hypoplastic left heart syndrome)
What is the anatomical difference between these ASDs (both L->R)
- secundum ASD (80%)
- primum ASD aka partial AV SD
- secundum: defect in centre of atrial septum involving foramen ovale
- primum/partial = AV septum defect either interatrial communication between atrial septum and AV valves or the valves are abnormal and regurgitant
ASDs mostly are asymptomatic or -> recurrent chest infections, what signs may you notice on auscultating the chest?
- ejection systolic murmur loudest on upper L sternal edge (due to shunt -> more flow across pulmonary valve)
- fixed, widely split 2nd heart sound (as RV SV is equal in both inspiration and expiration)
- if AV valve regurg in partial AVSD -> apical pansystolic murmur
What ECG change may you see in an ASD (secundum ASD)
- partial RBBB common
- right axis deviation (as RV enlarges)
Children with ASDs -> RV enlargement require rx. What is the rx for:
- secundum ASDs
- partial AVSDs
- secundum: cardiac catheterisation + insert an occlusion device
- partial AVSD: surgical correction
suggest 2 locations of a VSD
- anywhere in ventricular septum
- perimembranous area
- muscular area
Small VSDs are asymptomatic (<3mm) what signs may you notice on chest auscultation?
NB: CXR, ECG, no pulmonary HT will be normal
- loud pansystolic murmur at L sternal edge (louder murmur = smaller defect)
- quiet pulmonary 2nd sound (P2)
Small VSDs management?
- none
- close spontaneously
- murmur will disappear as closes
Large VSDs = > size of aortic valve
- symptoms
- signs
- murmur
- loud P2 why
- sx: HF, breathlessness, faltering growth from week1 and recurrent chest infections
- signs: tachyC, tachyP, hepatomegaly, active precordim
- murmur: soft pansystolic murmur or none (massive defect), apical mid-diastolic murmur (increased flow across mitral valve
- loud P2 from raised pulmonary arterial pressure
What will you see on CXR and ECG with a large VSD
CXR: cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings, pulmonary oedema
-ECG: biventricular hypertrophy
How are large VSDs managed?
- drug therapy for HF w diuretics +/-catopril
- additional calorie input
- surgery by 6months to manage HF and growth and prevent permanent lung damage from p HT
- surgery on large VSDs is done by 6months to prevent permanent lung damage
- why does this damage happen
- what is it called in adults
- persistent pulmonary hypertension irreversibly damages the pulmonary capillary vascular bed
- Eisenmenger Syndrome
Persistent ductus arteriosus..flow of blood from aorta to pulmonary artery (L->R), what are clinical fts?
- continuous murmur beneath left clavicle
- increased pulse pressure -> collapsing/bounding pulse
- heart failure and pulmonary hypertension due to increased pulmonary blood flow
How is PDA managed
- closure to reduce lifelong risk of bacterial endocarditis and pulmonary vasc disease
- close with coil/occlusion device, introduce by cardiac catheter at ~1yr
- or surgical ligation
R -> L shunts like ToF and TGA present w cyanosis in first week, what is the hyperoxia nitrogen washout test used for?
- to identify if theres heart disease in a cyanosed neonate
- put infant in 100% O2 for 10mins, if radial PaO2 on ABG is still low can diagnose cyanotic congenital heart disease
State 2 principles in the management of the cyanosed neonate:
- ABC
- Prostaglandin infusion (maintains ductal patency-child may be duct dependent)
- watch for SEs of the infusion e.g. apnoea, seizures, vasodilation and hhpotension
Tof the great arteries: RV connects to aorta -> body, LV connects to pulmonary artery -> lungs, not compatible with life but along with VSDs/ASDs/PDA can achieve mixing.. name some clinical features:
- cyanosis (profound, life threatening)
- presents ~day 2 (as ductal closure-> marked decrease in mixing)
- loud, single second heart sound
What are the classic findings on chest XR of baby with transposition of the great arteries?
- narrow upper mediastinum
- ‘egg on side’ appearance of cardiac shadow
- increased pulmonary vascular markings
State 3 principles of the management of T of great Arteries:
- improve mixing in cyanosed neonate
- maintain patent DA with prostaglandin infusion
- balloon atrial septostomy can be life-saving (allows systemic and pulmonary venous blood to mix in atrium)
- all require surgery (arterial switch procedure + CAs are switched to new aorta)
Eisenmenger Syndrome is…
- high pulmonary blood flow (due to large L->R shunt) -> thick walled pulmonary arteries
- more resistance to flow
- in early teens, shunt REVERSES & teenager becomes blue
- progressive, adult will die in R HF in 40s/50s
Common mixing in a child will present
- blue and
- breathless
- Suggest a cause of this?
- complete atrio-ventricular septal defect (AVSD)
- complex congenital heart disease e.g. tricuspid atresia
complete AVSD
- commonly seen in children w …
- what is it?
- due to the large defect what develops
- w Down’s syndrome
- defect in middle of heart with a single 5-leaflet vale between atria and ventricles
- often leaks
- due to large -> pulmonary hypertension
Give 2 features of a complete AVSD:
e.g. how presents antenatally, at birth, at ~3weeks, how is lesion detected?
-present on antenatal US screening
-cyanosis at birth/ HF by 3 weeks of life
-no murmur heard, lesion detected on routine ECHO (for Down’s babies)
-always superior axis on ECG
-
Management for complete AVSD?
as for large VSDs
- manage HF medically
- surgical repair by 6months
What is tricuspid atresia (a form of complex congenital heart disease)
-how does it present?
- only LV is effective (RV is small and non-functional)
- ‘common mixing’ in LA
- presents with cyanosis and breathlessness in neonatal period
AS, PS and coarctation of aorta -> outflow obstruction in a child,
will they be well or not?
Well child
Name 2 clinical fts/signs on exam of aortic stenosis in a chlid?
e.g. describe the murmur, pulse, carotids, heart sounds..?
- asymptomatic murmur +/- reduced exercise tolerance, syncope
- ejection systolic murmur, maximal at upper R sternal edge, radiates to neck
- apical ejection click
- small volume, slow rising pulse
- carotid thrill
- delayed and soft aortic second sound
How is outflow obstruction caused by aortic stenosis in a child managed?
- regular assessment and ECHOs
- balloon valvotomy for those w sx on exertion/high resting P across valve
- balloon dilatation in older children is safe
- eventually will probs need aortic valve replacement
Pulmonary Stenosis (PS) = valve leaflets partly fused together (restricted exit from RV) -give 3 features/signs
- most asymptomatic (if duct-dependent will -> cyanosis in first days =critical)
- ejection systolic murmur, loudest at upper L sternal edge
- +/- thrill
- ejection click at upper L sternal edge
- when severe -> prominent RV heave
Treatment of choice for sx children/ high pressure in pulmonary stenosis is:
-transcatheter balloon dilatation
Adult-type coarctation of aorta =uncommon, gradually becomes more severe over yrs.
- give 3 clinical fts:
e. g. murmurs? BP? radio-fem delay-why?
- asymptomatic
- systemic HT in the RIGHT arm
- Ejection Systolic Murmur at upper L sternal edge
- Continuous murmur at the back
- Radio-Femoral Delay (as blood bypasses the obstruction via collateral vessels in the chest wall hence pulse in legs is delayed)
Adult-type coarctation of aorta, CXR and ECG findings, name 2
- CXR: rib notching due to large collateral intercostal arteries running under ribs posteriorly to bypass
- 3 sign on CXR (visible notch in descending aorta at site of coarctation)
Adult-type coarctation of aorta is assessed with ____, when severe what management may be needed?
- ECHO
- stent inserted in cardiac cath lab
- or surgical repair
Coarctation of aorta, interruption of aortic arch and hypoplastic left heart syndrome are outflow obstruction causes in a well or unwell child? Present how?
- UNWELL
- present sick with HF and shock in neonatal period
Coarctation of aorta, interruption of aortic arch and hypoplastic left heart syndrome all -> outflow obstruction in SICK child, principle of management =
- resuscitate (ABC)
- prostaglandin infusion ASAP
- refer to cardiac centre for early surgical intervention
Interruption of aortic arch
- what is it?
- association with which chromosome abnormality?
- what is also often present that will be repaired during surgery?
- no connection between proximal aorta and distal so CO depends on R-> L shunt via DA
- associated w: DiGeorge Syndrome= chromosome 22q11.2 microdeletion.. no thymus, hypoCa2+, palate defects..)
- VSD often present too
The Norwood procedure neonatal operation is done for the sickest duct-dependent outflow obstruction cause? What am i describing? How do neonates present as ductal closure occurs?
- Hypoplastic Left Heart Syndrome
- underdeveloped L heart (small Mitral valve, tiny LV, v small ascending aorta often + coarctation)
- present w profound acidosis, rapid CV collapse, no peripheral pulses
