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.
What are the findings on auscultation, CXR and ECG of VSD?
Auscultation: pansystolic murmur heard best at LLSE. (louder-smaller defect)
CXR: If large, increased pulmonary markings and cardiomegaly, increased pulmonary arteries.
ECG: If large, R axis deviation due to RVH, but if 2m or later, see biventricular hypertrophy.
What is Eisenmenger’s Syndrome?
Pulmonary vascular Disease.
Prolonged Pulmonary HT damaging pulmonary capillary vasculature + thickened pulm a wall which increases resistance to flow.
VSD shunt flow decreases over time (L–>R) until it reverses and blood flows R->L and teenager is BLUE. RHF + death results in 40s-50s. Irreversible.
Requires heart transplantation.
what are the common types of duct dependent lesions?
Transposition of the great vessels
Coarctation of the Aorta
Hypoplastic Left Heart Syndrome
how does hypoplastic left heart syndrome present? how is it managed?
Early onset cyanosis, breathlessness
v sick child.
There is no flow through the left side of the
heart, so ductal constriction leads to profound acidosis
and rapid cardiovascular collapse. There is weakness
or absence of all peripheral pulses.
What is PDA? How does it present?
persistent ductus arteriosus 1 month after expected date of delivery (therefore if born pre-term this must be adjusted for) due to a defective constrictor mechanism. In a pre-term infant this results from pre-maturity rather than CHD. Remember that in fetalhood, the DA provides R–> L shunt for blood. Once born however, it provides a L–>R shunt for blood as the pulmonary resistance drops following birth.
continuous murmur below L clavicle. It radiates to the back. Murmur is constant bc pressure in Pulm A is always lower than in the Aorta.
PP increased causing collapsing pulse. ie diff between SBP and DBP bc of a decrease in the diastolic pressure
Symptoms not common unless large in which case presents with HF and Pulm HT.
How is PDA managed?
Closure surgically helpful to reduce chance of bacterial endocarditis and pulm HT. Closure via cardiac catheterization and occlusive device.
what are the cardiac associations with Turner’s syndrome?
co-arctation of the aorta, aortic valve stenosis
which conditions are duct dependent?
TGA TOF if critical stenosis AS + PS coarctation of aorta Hypoplastic L heart
what is Eisenmenger’s syndrome?
HF continues, pulmonary blood flow continues to be high due to L to R flow. Pulmonary HT ensues. Due to HT, increased pulmonary vascular resistance to reduce blood flow eventually causing R to L flow of blood so teenager becomes blue. Only option is heart + lung transplant.
what are your ddx for cyanosis + resp distress in a newborn?
CHD (TOF, TGA, AVSD)
RDS, Meconium Aspiration, pulmonary hypoplasia
Sepsis - GBS
inborn errors of metabolism
how would Coarctation of the aorta present?
Once DA closing SICK BABY Increased CRT Pale, mottled skin diff feeding. Poor brachial pulses Impalpable femoral pulses severe metabolic acidosis Tachypnoea
what are the L to R shunts? How do they appear on ECG/ CXR?
ASD VSD PDA ASD: Cardiomegaly, increased pulmonary vascular markings, enlarged pulmonary arteries. R axis deviation due to RVH. Partial RBB. Small VSD: normal on both Large VSD: Cardiomegaly, increased pulmonary vascular markings, enlarged pulmonary arteries, Pulmonary oedema. Biventricular Hypertrophy. PDA small: normal PDA large: Same as Large VSD
What are the R to L shunts? How do they present?
How are they managed?
TGA: No murmur TOF: Loud murmur ULSE, Hypercyanotic spells. Finger clubbing in older kids Cyanosis, Low O2 sats <94 or Collapsed These children have DD lesions. Acute management: ABCDE PGE1 infusion
TOF- surgical repair
TGA- surgical balloon atrial septostomy
Which defects make a child present as blue + breathless?
Complex CHD
AVSD
Common mixing of blood therefore low O2 sats in peripheral circulation and low 02 blood reaching peripheries.
What is SVT? How does it present? How do you acutely manage?
Commonest arrhyhmia in kids.
Narrow complex regular tachycardia
HR: 180 children, >220 infants.
Children – palpitations (90%), chest pain / discomfort,
dizziness, dyspnea, syncope
Infants- pallor, tachypnoea, poor feeding, irritable,
ABCDE
High flow O2
CRT, BP, pulse etc
peripheral pulses weak + CRT delayed.
Vagal manouver, blow up balloon, dunk babies (diving reflex)
Adenosine Bolus
DC shock
Long term, use flecainide or sotalol (1 year).