Cardiology Flashcards
How does a paediatric ECG differ from adult?
Marked sinus arrhythmia (HR varies dramatically with breathing, increases on inspiration)
Right axis deviation in newborn (marked RV hypertrophy as RV pumps against high-resistance collapsed lung in-utero), V4R (additional lead) often placed in right 5th intercostal space (midclavicular) to capture the right ventricle. V1 (looking directly at right ventricle) and V2-3 often have dominant R wave.
Possible partial RBBB (normal QRS complex plus RSR pattern in V1)
T wave inversion: normal in V1-3 (& possibly V4)
Q waves: normal in inferior (AVF, II, II) and left pre-cordial leads (V5-V6)
What is normal cardiac axis?
1w– 1m +110 (+30 to 180) 1m – 3m +70 (+10 to +125) 3m – 3yrs +60 (+10 to +110) Over 3 years +60 (+20 to +120) Adult +50 (-30 to +105)
What is corrected QT interval?
start of Q wave > end of T wave
<6 months: <0.49 seconds
>6 months: <0.44 seconds
What commonly causes tachycardia?
Sinus tachy: physiological processes altering sympathetic tone e.g. excessive activity, crying / being upset, stress.
May also be caused by secondary problem e.g. fever, infection, hyperthyroidism, anaemia or problems causing high metabolic rate. Rarely due to primary cardiac cause (but more likely if particularly high, or an isolated finding).
What commonly causes bradycardia?
Usually physiological (particularly athletes and during sleep).
Other causes: Drugs e.g. beta blockers Cushing’s reflex (bradycardia, hypertension, reduced consciousness & irregular respiration – sign of raised ICP) Shock / sepsis Heart block
What is SVT?
Narrow complex tachycardia originating at or above AV node (narrow complexes and no P waves)
Most common tachyarrhythmia in paediatrics
Most common cause: re-entry mechanism anywhere along the AV junction. Generally children will have an anatomic abnormality / variant such as an accessory conduction pathway or abnormal division of an existing conduction pathway (e.g. Bundle of Kent in Wolff-Parkinson White syndrome).
How does SVT present?
Varies with age & severity of condition, typically palpitations although some may present in HF or cardiorespiratory arrest
Infant
Palpitations: HR >220, irritable, inconsolable crying / quiet, pallor
HF: SOB (especially when feeding), initially poor weight gain, oedema / weight gain, enlarged liver
Child
Palpitations: Pallor, HR >180, irritable, complaining of chest pain / fluttering heart, nausea
Heart Failure: SOB, initially poor weight gain, oedema / weight gain, enlarged liver
How should SVT be investigated?
Hx if stable (or from caregiver) – can indicate diagnosis and guide / focus further Ix
ECG: narrow complex tachycardia, rate generally >220 for infant and >180 for older child, no discernible P waves and no rate variability.
CXR: useful indicator of HF (plethoric lungs), may also exclude pulmonary causes of SOB (e.g. consolidation, pneumothorax, pleural effusion)
Blood gas: degree of systemic compromise (lactate, CO2 and base excess) – electrolyte levels (K+, Ca2+) often available from blood gas machine
Blood glucose: any unwell child as hyper or hypo can cause or worsen many presentations
Haem / biochem: anaemia, infection or dehydration may exacerbate tachycardia, electrolyte imbalances (K+, Mg, Ca2+) or thyroid dysfunction may also trigger arrhythmia – must specifically request Mg (not in normal electrolyte workup)
Echo: underlying structural abnormalities
How can SVT be differentiated from sinus tachycardia ?(often difficult)
SVT: • Sudden onset • No rate variation • Very fast rate (>220 infant, >180 older child) • Not responsive to fluid bolus • No P waves visualised on ECG reading
How should SVT be managed?
If Stable: initially attempt vagal manoeuvres (vary depending on age). Must attach to heart monitor so cardioversion can be captured and sent to local tertiary unit.
Infant: ice immersion (wrap infant & immerse face in ice bath for ~10s) – stimulates the diving reflex (another variation: place bag of crushed ice on face for 15-30s)
Child: Valsalva manoeuvre blow into empty 10mL syringe
If Unstable: more acutely compromised or initial vagal manoeuvres do not work: ADENOSINE or DC-cardioversion may be needed.
Complications of SVT?
In acute setting: cardiovascular compromise, insufficient cardiac output, shock & ultimately death.
Vagal manoeuvres & adenosine can cause asystole so should be done under careful monitoring, with full resuscitation facilities available.
Following resolution of SVT: further ECG abnormalities may be detected e.g. Wolff-Parkinson-White syndrome (slurred R wave i.e. delta wave across all leads). Delta wave is caused by an accessory conduction system bypassing AV node, shortening PR interval and making patient prone to episodes of re-entry tachycardia.
Prognosis / long term management of SVT?
In general, single episode carries good prognosis (particularly with uncomplicated presentation).
May also have recurrent episodes: in long-term (particularly if frequent episodes) prophylactic measures should be considered (paediatric cardiologist). Initially: advice regarding vagal manoeuvres and when to summon help. May also start anti-arrhythmics, although longer term medicines carry side effects. Medications are stopped after having an ablation (radiofrequency ablation of accessory pathway can be done in adolescence & renders the pathway non-functional).
What is VT?
Broad complex tachycardia (electrical activity originates within ventricles, resulting in slower conduction than via the bundle of His & Purkinje fibres).
Short asymptomatic runs are possible, but typically presents in very compromised tachycardic, hypotensive patient who may go on to have a cardiac arrest.
How is VT managed?
If pulseless: CPR, cardiac defibrillation & possibly adrenaline / amiodarone
If pulse & in shock: synchronised DC cardioversion
If pulse & not in shock: amiodarone
Review frequently and look for reversible causes of arrhythmia in their histories, examinations and biochemical evaluations. Ix similar to that for SVT.
Complications and prognosis of VT?
Sudden death (therefore any suggestion on ECG > immediate evaluation by senior clinician) – high risk of cardiac arrest & further deterioration to VF
Prognosis: highly dependent on aetiology & clinical situations, short asymptomatic runs could go unnoticed over lifetime, but may also be first noted at cardiac arrest
What are the most common forms of congenital heart disease?
Incidence: ~1% or 8 in 1000 livebirths
- VSD
- PDA
- Pulmonary stenosis
- ASD
- Coarctation of aorta
- TOF
- Aortic stenosis
- TGA
How does congenital heart disease usually present? How is it diagnosed?
Cyanosis, shock or HF.
Increasingly diagnosed antenatally and some centre routinely check SaO₂ in newborns, increasing early diagnosis of cyanotic congenital heart disease.
Ix: ECG, CXR, echocardiogram & cardiac catheterisation.
Most major congenital defects increase right heart impulse (palpate the sternal border).
Broadly speaking, what are causes of congenital heart disease?
Chromosomal (Down’s – AVSD, ASD, VSD, Turner’s – coarctation of aorta, AS, Williams – AS, peripheral pulmonary stenosis, Noonan – pulmonary stenosis),
Infection (rubella)
Maternal disease (diabetes, SLE – congenital heart block)
Drugs in pregnancy (alcohol, anticonvulsants)
May also present later in life due to underlying multisystem disorder e.g. Marfan’s & Ehlers-Danlos syndrome.
Why can detecting congenital heart disease based on cyanosis be difficult?
Peripheral cyanosis common in normal infants
Central cyanosis may be seen on vigorous crying
Mild desaturation (85-95% SaO₂) in infants is often clinically undetectable
Check gums & tongue for duskiness or lack of pinkness!
Blue baby: cyanosis can also be caused by respiratory, neurological & haematological conditions!
What can cause cyanotic congenital heart disease?
TOF
Transposition of great arteries (TGA)
Truncus arteriosus
Total Anomalous Pulmonary Venous Drainage (TAPVD)
Hypoplastic Left Heart Syndrome (HLH)
Tricuspid Atresia
Complete atrioventricular septal defect (AVSD)
What is Tetralogy of Fallot?
Most common congenital cyanotic heart disease, 4 features:
Infundibular pulmonary stenosis: causes ‘right outflow tract obstruction’ - difficult for RV to pump enough blood to lungs for oxygenation
Right ventricular hypertrophy (secondary to RV exertion)
Ventricular Septal Defect: deoxygenated blood from RV (operating at a higher than normal pressure due to the outflow tract obstruction)
Overriding Aorta: abnormal insertion of aorta, opens directly over VSD so left & right ventricles both pump into it
How is TOF diagnosed?
Often picked up on routine antenatal scanning – allows better preparation at birth and if possible delivery at a specialist cardiac unit.
ECG: right axis deviation & right ventricular hypertrophy (dominant R wave V1-4R)
CXR: boot-shaped heart from right ventricular hypertrophy and oligemic lung fields due to pulmonary stenosis
ECHO for definitive diagnosis
How does TOF present?
If presenting postnatally, dependent on degree of outflow tract obstruction (i.e. severity of pulmonary stenosis).
If PS critical: cardiovascular compromise + cyanosis soon after birth.
If moderate: likely detected during secondary evaluation of heart murmur found on NIPE (due to the PS - systolic murmur heard best over the ULSE). May also present with hypercyanotic spells – moments of acute right ventricular outflow tract obstruction brought on by agitation or exertion, where child appears cyanotic + compromised.
If mild obstruction: presentation may coincide with HF.
How is TOF managed? Complications of management?
Acutely unwell: prostaglandin infusion (bypassing pulmonary stenosis) + referral (tertiary unit for urgent surgery).
Hypercyanotic Spells: knees-to-chest position increases systemic vascular resistance, reducing right > left flow through VSD, increasing flow through pulmonary artery. High flow oxygen & morphine (act as pulmonary vasodilator + systemic vasoconstrictor). If conservative measures fail > IV morphine or beta-blockers.
All require surgical repair (close VSD + widen ventricular outflow tract). Previously, would have a Blalock-Taussig shunt between subclavian + pulmonary arteries (palliative – similar effect to PDA) before definitive surgical repair.
Complications: thrombosis & infection. Standard practice: complete surgical repair in first year, but if baby too small or compromised, may have temporary shunt first. Future surgery may be required if develops pulmonary regurgitation (complication of widening the ventricular outflow tract).
What is the prognosis of TOF?
Simple forms of disease with early surgery: excellent long-term outcomes (small risk of life-threatening ventricular arrhythmias remain).
Without surgery: mortality increases with age – TOF associated with pulmonary atresia has worst prognosis.
What is TGA? How is it diagnosed?
Most common cyanotic heart disease to present in the neonatal period > cyanosis + circulatory compromise.
Aorta attaches to RV, PA attaches to LV. 2 separate circuits: oxygenated blood LA > LV > lungs & deoxygenated blood pumped RA > RV > body.
Incompatible with life unless further defects permit shunting across heart (allows oxygenated blood into systemic circulation).
Normal ECG. CXR shows cardiac outline of egg on side + increased pulmonary vascular markings.
