CV Flashcards
What are the PC of Cardiac Failure?
Symptoms
- SOB particularly on feeding or exertion
- Sweating
- Poor feeding
- Recurrent chest infections
Signs - primarily of LHF
- FTT ie poor weight gain or growth
- Tachypnoea (remember they cannot increase tidal vol so this is best way to get more O2)
- Tachycardia (they cannot increase SV so to increase CO they must increase HR)
- heart murmur, S3 (gallop rhythm)
- Enlarged heart
- Hepatomegaly
- Cool peripheries
what distinguishes a pathological and an innocent murmur?
An innocent murmur: soft blowing murmur, asymptomatic, L sternal edge, systolic murmur, no signs. With no radiation or parasternal thrill.
what are the features of a venous hum?
continuous murmur, “machinery hum” heard during diastole and systole. best heard above the clavicle (it results from turbulence in the jugular v). It does not radiate. It can be reduced/ abolished by changing head positions, lying child on back.
What is the initial management of cardiac failure?
Ix: ECG, CXR, Echo.
Medical management to stabilize child:
Diuretics + Captopril
Nutrition- High E formula through NGT if req bc of difficulty feeding
O2 support if required.
if Duct dependent lesion, use PGE1 to maintain Patent DA.
depending on cause - may req surgical repair. If PDA, Indomethacin usually causes closure.
what is the ddx for cardiac failure?
Neonates - obstruction of LH outflow + reliance on Ductal circulation for R to L shunt of blood. 1. Coarctation of the Aorta (severe) 2. Critical Aortic valve stenosis 3. Hypoplastic L Heart 4. SVT Infants: L to R shunt increases as pulmonary resistance falls, increasing pulmonary blood flow, leading oedema + breathlessness. 1. VSD 2. AVSD 3. Large PDA 4. SVT Older children + adolescents: R to L shunt due to chronic pulmonary HT increasing vascular resistance. 1. Eisenmenger's Syndrome 2. Cardiomyopathy
a neonate presents with breathlessness, what are your ddx?
L to R shunts:
VSD (most common- remember 3 components meeting)
persistent Ductus Arteriosus
ASD
ie oxygenated blood is leaving the arterial circulation and entering into pulmonary circulation and therefore less oxygen is being delivered to the body.
What are the presenting features of ASD? Is it rare or common? Where would you best hear this murmur?
Baby is pink, may be Breathless but often asymptomatic until later life (arrhythmia). FO site of lesion.
recurrent chest infections/ wheeze
Relatively common
Best heard at Upper LSE, fixed splitting of S2, murmur is ejection systolic due to flow of extra blood across pulmonary valve. Insertion of cardiac occlusion device. S
what syndromes carry a risk of cardiac abnormalities?
Down’s syndrome
Mostly associated with AVSD and VSD. almost 40% incidence.
Turner’s- co-arctation of the aorta
Noonan’s - ASD, hypertrophic cardiomyopathy, pulmonary valve stenosis
Marfann’s- dilatation of the aorta – may lead to dissection.
William’s - Aortic Stenosis
Kawasaki’s - Coronary a aneurysm.
what are the features of VSD? How common is it? How is it managed? What are the consequences of VSD?
Most Common CHD. Most common CHD in Trisomy 21.
Small defect- Pink baby, asymptomatic. (loud pan systolic murmur- small defect), quiet P2. All small resolve spontaneously w/o tx.
Large defect-Thin, Breathless, signs of HF- hepatomegaly, tachypnoea, tachycardia, loud P2 due to increased pulmonary artery P, heaves + thrills, Faltering growth, recurrent chest infections. May be pansystolic LLSE but may be silent if v big. Loud P2 due to increased Pulmonary P.
murmur often undetectable at birth.
To manage HF BEFORE Surgery, diuretics + captopril + high E feeds. If HF/ affecting feeding + growth, surgical intervention required.
Complication- Eisenmenger Syndrome. Due to prolonged pulmonary HT –> damage pulm capillary bed + thickened pulm a wall, increasing resistance to flow–> shunt flow decreases over time until it reverses and blood flows R->L and teenager is BLUE. RHF + death results in 40s-50s. Irreversible. Req heart + lung transplant.
when an infant presents with cyanosis, what is occurring?
deoxygenated blood is entering the arterial circulation.
This occurs in three primary conditions:
transposition of the great vessels ie deoxygenated blood in R heart is entering aorta.
AVSD (breathless + blue)
Tetralogy of fallot:
1. pulmonary stenosis (increases P)
2. VSD but due to increased P in pulmonary artery, pushes deoxygenated blood to L heart (R L shunt)
3. RV hypertrophy bc heart pumping vs higher P in PA.
4. Aorta overriding VSD bc larger of 2 vessels (remember PA and Aorta are divisions of singular vessel embryol)
what might be the cause of an asymptomatic murmurs?
pulmonary stenosis
aortic stenosis
venous hum
small VSD
what is tetralogy of fallot? What are hyper cyanotic spells?
- pulmonary artery stenosis
- VSD
- overriding aorta
- RV hypertrophy.
Hypercyanosis: rapidly increasing cyanosis, with irritability/ inconsolable crying bc of severe hypoxia and
breathlessness and pallor because of tissue acidosis
Ejection systolic murmur at LSE. Cyanosis.
what is coarctation of the aorta?
arterial duct tissue encircling the aorta
just at the point of insertion of the duct therefore when D shuts, severe outflow obstruction.
How is an ASD identified on ECG, CXR, Echo? How is it managed?
CXR: cardiomegaly, increased pulmonary markings
ECG: R axis deviation due to RVHypertrophy (due to increased blood in R ventricle). RBBB is common.
If large enough to cause RVHypertrophy, requires closure via cardiac catheterization with occlusion device to prevent future arrhythmias/ HF when child aged 3-5.
what is the anatomy of AVSD?
It is pathonomonic for Trisomy 21, v rare in other babies. A complete AVSD is a defect in the middle of the heart with the presence of a 5 leaflet common valve between the atria and ventricles and stretches across entire atrioventricular junction and leaks. This is a huge defect and therefore pulmonary HT results.
