Cardiology Flashcards
Congenital heart disease, blue baby, murmurs, cyanotic spells, HF, arrhythmias, Kawasaki disease
Circulatory changes at birth
LA pressure low in fetes cos they don’t breathe; RA pressure high as receives systemic/placental flow. Blood goes through foramen ovale from RA-LA, then into LV then upper body
First breath: resistance to pulmonary flow drops, blood to lungs, LAP increases + RAP decrease - foramen ovale closes, ductus arteriosus (PA to aorta) closest n hours-days
Causes of congenital heart disease
Maternal disorders-rubella (PS, PDA), SLE (complete heart block), DM
Maternal drugs-warfarin (PS, PDA), fetal alcohol syndrome (ASD, VSD, TOF)
Chromosomal abnormalities-T21 (AVSD, VSD, other trisomies, Turner syndrome (AS, CoA), chromosome 22q11.2 deletion (ToF, aortic arch abnormalities), Noonan syndrome (hypertrophic cardiomyopathy, ASD, PS)
Blue baby
Cyanosis + resp distress (RR>60). Causes include cyanotic CHD, RDS, meconium aspiration, persistent pulmonary HTN of the newborn (failure of pulmonary vascular bed to fall after birth), infection, inborn error of metabolism, nitrates in drinking water causing methaemoglobinaemia (Hb less able to carry O2, highest risk <3m)
Acrocyanosis: common in healthy, peripheral cyanosis around mouth + extremities cos of benign vasomotor changes-vasoconstriction. can last up to 48h
Child with murmur
Innocent ejection murmur: v v common. Soft blowing murmur, Systolic, aSymptomatic, left Sternal edge; normal HS with no added sounds, no thrill, no radiation. May occur in states of raised CO e.g. fever, anaemia
Pathological murmur: may not be present at birth as pulmonary vascular resistance still high
- Aortic stenosis: asymptomatic unless severe causing reduced exercise/CP on exertion/syncope. Always causes carotid thrill; is an ejection systolic murmur @ upper RSE radiates to neck, apical ejection click
- Pulmonary stenosis: most asymptomatic, ejection systolic murmur @ upper LSE, may have thrill/ejection click/RV heave
- CoA: asymptomatic but can cause systemic HTN, ejection systolic murmur @ upper sternal edge, radio-femoral delay (blood bypasses obstruction via chest wall collaterals so leg pulses delayed)
Cyanotic spells
Peripheral: cold, unwell, polycythaemia
Central: less pronounced if child anaemic as can only be seen if Hb>50
If persists but child otherwise well suggests structural disease
Hypercyanotic spells-imp to recognise as can lead to MI/stroke/death. CF are rapid cyanosis, irritability/inconsolable due to hypoxia, pallor, v short murmur. Usually self-limiting then they sleep. If >15 min they need sedation + analgesia, IV propranolol/alpha agonist to vasoconstriction, IV fluids, bicarb if acidotic
Heart failure
Causes:
- Neonates: obstructed systemic circulation. E.g. severe CoA, hypo plastic left heart syndrome, critical AS, interruption of aortic arch. First week usually left heart obstruction (so need to keep DA open!), after first week usually L-R shunts
- Infants: VSD, AVSD, large PDA
- Older children: Eisenmenger syndrome (RHF when L-R shunt reverses after years), rheumatic, cardiomyopathy
CF:
- Sx: breathless esp feeds/exertion, sweating, recurrent chest infection
- Signs: poor weight gain, tachypnoea/cardia, murmur, gallop rhythm, cardiomegaly, hepatomegaly, cool peripheries; sins of RHF like oedema/ascites are rare in developed countries
Patent ductus arteriosus
When it doesn’t close by 1m, so still link from PA to descending aorta (if persists in preterm infant isn’t CHD until after 1m past EDD)
CF: continuous murmur below left clavicle, continues in diastole, increased pulse pressure (collapsing/bounding)
M: close it around 1y to reduce risk of pulmonary vascular disease/endocarditis
Atrial septal defect
No murmur caused by the ASD, but can get PS murmur because of increased flow through PV (ejection systolic @ upper LSE)
Secundum ASD is commonest type
CF: usually none, may get recurrent chest infection/wheeze, may p/w arrhythmia in an adult
M: may need catheterisation to occlude it if it is large enough to cause RV dilatation
Ventricular septal defect
Small: asymptomatic, loud pan systolic murmur @ lower LSE, normal ECG/CXR, close spontaneously
Larger: cause HF + recurrent chest infections, soft pan systolic or absence of murmur. Ix-cardiomegaly, enlarged pulmonary arteries, pulmonary oedema. M- treat HF with diuretics + captopril, surgery when a few months old
Ebstein’s anomaly
Low insertion of tricuspid valve causing large atrium + small ventricle
A/w tricuspid incompetence (pansystolic murmur, giant V waves in JVP) and WPW syndrome
Can be caused by exposure to lithium in-utero
Tetralogy of Fallot
Large VSD + overriding aorta (wrt ventricles) + sub-pulmonary stenosis (causes RV outflow obstruction) + RVH (as a result!)
Usually early diagnosis or antenatal, classic signs used to be severe cyanosis + hyper cyanotic spells + squatting on exercise, loud harsh ejection systolic murmur, with increasing obstruction murmur shortens
CXR: may have boot shaped heart (lifted apex cos of RVH)
M: surgical around 6m to close VSD + relieve RV obstruction
Transposition of the great arteries
Aorta connected to RV, PA connected to LV, so blue blood to body + pink blood to lungs
Incompatible with life, but often there is another anomaly like ASD meaning some mixing of the systems so they can live until surgery. Give prostaglandin infusion to maintain DA patency, balloon atrial septostomy (tear atrial septum to allow mixing), surgery to sort the anatomy out
Eisenmenger syndrome
When a large L-R shunt isn’t treated early - shunt decreases as resistance increases - over time shunt reverses - blue teenager, they will die in of RHF in their 30-40s, transplantation only cure once this stage reaches
Atrioventricular septal defect
A/w DS. Leads to pulmonary HTN, cyanosis/HF in early neonatal, no murmur, medical management surgery 3-6m
Tricuspid atresia
Only the LV is effective as the RV is small + non-functional, LA has mixed pulm+systemic circ. Surgeries for palliation, usually can’t fully correct
