Cardiology Flashcards
What are the shunts in neonatal physiology?
ductus arteriosus ( from pulmonary trunk to descending aorta) ductus venosus (umbilical vein into IVC) foramen ovale (R to L atrium) (placenta)
Changes to physiology after birth
Baby breathes reducing pulmonary vascular resistance** – PVR @ birth is similar to SVR, but PVR steadily drops over 4-8wksweeks, can occur more quickly if O2 given increased systemic vascular resistance** (because placental circulation no longer part of circuit) closure of 3 shunts -PFO (passively closes) - ductus venosus (passive - shortlists after birth, complete closure in 3-7 days) - ductus arteriosus*** —functionally closes <24hrs due to oxygenation and prostaglandins — passively closes/fibroses in 2-3 weeks ** Drs can manipulate this
How common is congenital heart disease?
6-8 per 1000 live births most common congenital defect
What syndromes are associated with CHD?
Down syndrome (trisomy 21)
- 50% risk of CHD
- AVSD (atrioventricular septal defect)
- VSD
Velocardial facial syndrome (VCFS)
- VSD, tetralogy, truncus arteriosus
William Syndrome (7 del) - supra aortic stenosis Turner syndrome - coarctation, bicuspid
CHARGE syndrome
Trisomy 13, 18
Noonan syndrome
Symptoms + signs of CHD?
HISTORY
Cyanosis
Congestive cardiac failure
- tachypnoea +/- increased WOB
- poor feeding/failure to thrive/reduced ET** very important signs
- tachycardia
EXAMINATION
(does the patient look dysmorphic?)
tachycardia/hypoxia/tachypnoea/BP
cyanosis (need SpO2 85% to be visible)
clubbing (late sign, ~12 -18 monts)
pulses (upper + lower body)
hepatomegaly (late)
pericardial overactivity/thrill (late)
murmur
VSD
One of the most common types of CHD
CLASSIFICATION (restrictiveness, location - different behaviour, Mx + prognosis)
Non-restrictive (hole big enough that blood can get through hole)
– potentially worse prognosis if untreated, as increased SVR from higher LV pressures causes damage to pulmonary bed (Eisenmenger syndrome)
- therefore need to close in 1st year of life
- often no murmur
Restrictive ( blood can’t get through) - audible murmur
Muscular VSD (20%)
- likely to close spontaneously
Perimembranous (80%)
- aneurysm formation aortic regurg
Outlet/infundibular/juxta-arterial (8%, 30% in Asians)
- unlikely to close - likely to affect valve esp aortic valve
FEATURES
- MURMUR + CHF (congestion, failure to thrive)*
- PVR raised as neonate, so VSD may not be heard (as not much of a gradient btw PVR/SVR left/right)
- THEREFORE —> more likely to pick up murmur @ 6-8 week mark when PVR reduces
– Bub more likely to be symptomatic as R → L shunt WORSENS (O2 also worsens this as further reduces PVR)
Coactation of aorta
juxta-ductal (abnormal extension of PDA, so it closes + causes CoA) pre-ductal post-ductal PRESENTATION = highly variable - poor feeding - poor weight gain - metabolic collapse - decreased femoral pulses** VERY IMPORTANT SIGN TREATMENT - use prostin, to re-open ductal tissue (temporising) - surgery
Give overview of Tetralogy of Fallot features, findings, Mx
CYANOTIC condition
4 features of ToF
- unrestrictive VSD
- pulmonary stenosis/RVOT
- ( = deoxygenated blood shunts to systemic circulation)
- overriding aorta
- results in RV enlargement -> Eisenmenger
PRESENTATION = variable!
Cyanosis (MOST) w too little pulmonary flow (too much R → L shunt)
Tachypnoea + pulmonary oedema
- but can also have too much pulmonary blood flow if pul stenosis less of a thing, ∴ so manifests as congestive heart failure
Murmur - ejection systolic murmur
“Tet” spells - where baby gets upset, vicious cycle of increasing cyanosis, can be life-threatening*
CXR - R) sided aortic arch, lung field oligaemia (lack of pulmonary blood flow)
Aortic stenosis
Non-cyanotic too little systemic blood flow - presentation depends on severity of stenosis Mx - if unwell, prostin to keep duct open - catheterisation with balloon valvuloplasty - surgery
TGA - transposition of great arteries
CYANOTIC condition pulmonary and aortic arteries switched around with two seperate circulations - condition only survivable if there is mixing btw circulations eg: VSD, PDA, ASD PRESENTATION - cyanosis at birth - metabolic collapse - hyperoxy test = give lots of O2 and see if it makes a difference eg: if CHD, won’t improve, if lung disease then will improve -septostomy - early surgical repair is vital
Recognition and diagnosis
- when do we look for CHD? What can be missed?
Antenatal
only ~30% of lesions are picked up antenatally
Newborn check
PVR still raised, ductus may still be open
= MANY LESIONS WILL BE MISSED
6 week check
PVR should have dropped
Ductus should have closed
= VERY IMPORTANT TIME TO RE-CHECK
PVR decreases (eg: VSD)
- murmurs may change or appear
- there is increased pulmonary flow
Duct closes
- duct dependent PVR ( too little pulmonary flow)
- eg: pulmonary stenosis
- duct dependent SVR ( too little systemic blood flow)
- eg: aortic stenosis
When to be concerned re: CHD in baby + investigations would you order?
murmur characteristics
- Loud murmur
- diastolic murmur (difficult due for fast HR)
- continous murmur
Other signs
- tachypnoea
- hepatomegaly
- decreased pulses
- cyanosis
- abnormal Ix
-
ECG (needs to be paediatric specific)
- include V3r/V4r
- R) side forces prominant
-
bloods
- ABG - hypoxia, low Ca in VCFS
- genetic tests for T21, VCFS
-
CXR (size, position, contour, pul vascularity)
- increased pulmonary vasculature(flow)
- increased heart size
- abnormal cardiac contour
- eg: boot shaped heart where apex of heart lifted up off diaphragm, sign of RV hypertrophy, pul stenosis, ToF)
- eg: dropped egg, thin mediastinum, increased pul blood flow
- eg: cardiomegaly + increased pul markings in unrestrictive VSD
- Echo
- not a routine service, should be in conjunction w paediatric cardiologist
-
ECG (needs to be paediatric specific)
MRI/CT, nuc med, cardiac catheterisation (Dx, HD, interventional)
normal ECG features of neonate
- neonate has RV dominance (QRS progresion in chest leads)
- relative tachycardia
- QRS duration shorter (<70ms)
- QTc long compared w children and adults
all of the above
Types of arrhythmias in neonates + Mx
SVT (AVRT)
rate almost 300 bpm
normal electrical conduction, but also has accessory pathway which creates a short circuit loop
Rx
- vagal manouvres (dunk into ice cold water, gag reflex
- adenosine
- longerterm anti-arrhythmics (sotolol, beta blockers, flecanide
Px - 60 -70% resolve by 12 months, if no further episodes can cease meds
30- 40% require EPS + ablation (~5 yrs old)
atrial flutter
complete heart block
long QT syndrome
abnormal K+ or Na+ channels
- delayed ventricular repolarisation + prolonged QT -> risk of VT + VF
autosomal dominant, 1:2500 people in Aus, up to 10% of SIDS
Ix - if maternal or paternal Hx of LQT -> ECG (neonatal ECG can be physiologically prolonged, recheck in 6 weeks)
Mx - if high suspicion -> beta blockers
