Cardiology Flashcards
Failure of the palatine processes and the nasal septum to fuse
cleft palate
Failure of the aorticopulmonary septum to spiral during septation
transposition of the great arteries
Acyanotic congenital heart disease causes?
ventricular septal defects (VSD) - most common ~30% atrial septal defect (ASD) patent ductus arteriosus (PDA) coarctation of the aorta aortic valve stenosis
Causes of cyanotic congenital heart disease?
tetralogy of Fallot transposition of the great arteries (TGA) tricuspid atresia
Soft systolic murmur, musical/vibrating tone, best heard at LLSE, may disappear on standing
Still’s murmur (innocent)
Pansystolic murmur at LLSE, may be associated with a thrill, split or loud single S2
Ventricular septal defect
Systolic ejection murmur best heard at ULSE, wide split fixed S2, sometimes associated diastolic flow rumble at LLSE
Atrial septal defect
Continuous machinery murmur at the ULSE, often associated with a thrill
Patent ductus arteriosus
Systolic ejection murmur heard at ULSE and LLSE, thrill palpable at the ULSE, single S2
Tetralogy of Fallot
Pansystolic murmur at LLSE or midsternal border, may have a mid-diastolic murmur at the apex, single S2
Tricuspid atresia
Systolic ejection murmur at LSE, hyperdynamic precordium, single S2
Hypoplastic left heart syndrome
Low-pitched, quiet mid-systolic ejection murmur in axilla or back
Peripheral pulmonary stenosis (innocent)
Systolic ejection murmur at the ULSE with radiation to back, axilla, infraclavicular area, sometimes a “click” is heard, loud S1
Pulmonary stenosis
Systolic ejection murmur at URSE with radiation to carotid arteries, left ventricular heave, and possible thrill
Aortic stenosis
Systolic murmur at LLSE and mid-diastolic murmur at apex, single S2
Transposition of the great arteries
Systolic ejection murmur at ULSE, mid-diastolic flow rumble at LLSE, wide split fixed S2
Total Anomalous Pulmonary Venous Drainage
Systolic murmur, mid-diastolic rumble
Truncus arteriosus
Most common cardiovascular abnormality in William’s syndrome?
Supravalvular aortic stenosis 2nd most common: pulmonary artery stenosis other; Mitral valve regurgitation and prolapse
2nd most common cardiovasc abnormality in William’s syndrome?
Pulmonary artery stenosis 1st most common: Supravalvular aortic stenosis Other: Mitral valve regurgitation and prolapse
CATCH 22?
Cardiac defects Abnormal facial features Thymic aplasia/hypoplasia Cleft palate Hypocalcemia/Hypoparathyroidism 22- Due to 22q11 deletion
ECG changes of hypercalcaemia?
Tall T waves, Reduced QT, Prolonged and depressed ST, Arrhythmia
ECG changes of hyperK?
Tall T waves ST- changes Reduced QT interval Increased PR interval Smaller or absent P waves Widened QRS, broadening to VF
ECG changes of hypoK?
Flat T waves ST depression U wave Atrial and ventricular ectopics VF and VT
ECG changes of hypoCa?
Prolonged QT Prolonged ST Flat or absent T waves U waves
Differences in ECG in children under age 3/4 compared to teenagers?
In neonates, the RV is thicker than the left and the L becomes dominant age 3/4: right ventricular hypertrophy changes include: R axis deviation T-wave inversions in V1, V2, and V3 Dominant R wave in V1
ECG findings in transposition of great arteries?
R axis deviation
CXR findings in transposition of great arteries?
Cardiomegaly, increased pulmonary markings
Definitive treatment of transposition of great arteries?
atrial switch operation (Rastelli procedure)
Mx of transposition of great arteries?
Interim balloon atrial septostomy Definitive: atrial switch operation (Rastelli procedure)
what does ghrelin do?
ghrelin stimulates hunger. It is produced mainly by the P/D1 cells lining the fundus of the stomach and epsilon cells of the pancreas. Ghrelin levels increase before meals and decrease after meals
what does leptin do?
leptin decreases appetite. It is produced by adipose tissue and acts on satiety centres in the hypothalamus and decreases appetite. More adipose tissue -> high leptin levels. Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY)
Most common underlying cause of infective endocarditis in children?
VSD, followed by tetralogy of fallot
Most common IE causative organism in children?
Staphylococcus aureus, followed by Streptococcus viridans
what are Osler’s nodes?
immune complex deposits painful, red, nodes found on hands and feet immunologic signs are 1 /6 minor criteria for Duke’s
What are Janeway lesions?
micro-abscesses: small, non-tender nodes or macules on the palms vascular signs are 1/6 minor criteria for Dukes
Examples of vascular signs of infective endocarditis?
- Major arterial emboli - Septic pulmonary infarct - Mycotic aneurysm - Intracranial haemorrhage - Conjunctival haemorrhage - Janeway lesions
Examples of immunologic signs of infective endocarditis?
- Glomerulonephritis - Osler’s nodes - Roth spots - Rheumatoid factor
Echo findings that constitute major criteria in Duke’s for infective endocarditis?
- Abscess - New partial dehiscence of prosthetic valve - New valvular regurgitation - Oscillating intracardiac mass on valve or supporting structures
Duke’s criteria for IE: major criteria
Characteristic positive blood culture for typical infective endocarditis organisms Characteristic ECHO findings*
Duke’s criteria for IE: minor criteria
- Underlying heart condition - Temp > 38.0° C - Vascular signs** - Immunological signs *** - Positive blood cultures not meeting major criteria - ECHO findings not meeting major criteria
Duke’s criteria for IE: what is diagnostic?
2 major criteria is diagnostic 1 major criteria and 3 minor criteria is diagnostic 5 minor criteria is diagnostic
normal range of HR for a newborn?
110-150
normal range of HR in 2 yo?
85-125
normal range of HR in 4yo?
75 - 115
normal range of HR in >6yo?
60-100
What is the Fontan procedure?
used in children with univentricular hearts. involves diverting the venous blood from the IVC and SVC to the pulmonary arteries without passing through the RV.
most common organism for IE in patients with indwelling lines/ following prosthetic valve surgery?
Staphylococcus epidermidis
what organism for IE is linked with poor dental hygiene or following a dental procedure?
Streptococcus viridans: ie. Streptococcus mitis and Streptococcus sanguinis.
what organism for IE is associated with colorectal cancer?
Strep bovis
Associations of Wolff Parkinson white?
HOCM mitral valve prolapse Ebstein’s anomaly thyrotoxicosis secundum ASD
Management of WPW?
definitive treatment: radiofrequency ablation of the accessory pathway medical therapy: sotalol***, amiodarone, flecainide avoid sotalol if co-existing AF.
Failure of the _______ to develop properly will result in a ventricular septal defect.
endocardial cushions
Starlings law?
- Increase in end diastolic volume will produce larger stroke volume. This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output.
Laplace’s law in cardiac physiology?
explains that the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have impaired systolic function.
Bainbridge reflex?
Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors - normally Increased blood volume will cause increased parasympathetic activity
Who is offered screening by a fetal cardiologist in the antenatal period?
if:
- abnormal four-chamber view on routine/ anomaly scan
- increased nuchal translucency (also increases risk of Down’s)
- Previous child/ FHx of CHD
- Maternal risk: e.g. Phenylketonuria, DM
- Suspected Down’s/ other syndrome
Echodensity on anterior mitral valve papillary muscle found on fetal echocardiogram?
- ie ‘golf valls’
thought to be calcification during development
no importance for CHD
assoc w Down’s Syndrome
no need for echo after delivery
Arrhythmias in fetus in antenatal period:
what investigations are required?
Echo required
- to confirm normal anatomy
- to confirm type of arrhythmia
- fetal ECG is not yet routine
- presence of hydrops is a poor prognostic sign
Arrhythmias in fetus in antenatal period: management of multiple atrial ectopics?
Usually not treated
Arrhythmias in fetus in antenatal period: management of SVT?
Usually with maternal digoxin or flecainide
Arrhythmias in fetus in antenatal period: management of Heart Block?
maternal isoprenaline or salbutamol
Most common Congenital heart defects?
VSD - 30%
Persistent arterial duct - 12%
ASD - 7%
Pulmonary Stenosis - 7%
Which family history increases risk of Congenital heart disease the most?
Mother with CHD
Risk factors of congenital heart disease?
Family history: mother/ father w CHD, siblings with CHD
Presence of other anomaly/ syndrome
Parents w abnormal genotype
Maternal lithium use (ebstein anomaly)
3rd trimester enterovius/ Coxsackievirus -> myocarditis, dilated cardiomyopathy
Maternal SLE (anti-ro/la abs -> complete heart block)
cardiac symptoms to ask in a history?
- heart failure: breathelessness, poor feeding, faltering growth, cold hands/feet
- cyanosis
- neonatal collapse
apart from symptoms of the child, what are important questions in a cardiac history?
- was child born preterm?
- asymptomatic heart murmur found on routine exam?
- syndrome ie. Downs?
- family history of CHD
- did mother have any illnesses/ take any medication during pregnancy?
Examination of child for congenital heart disease:
bedside signs?
dysmorphism
obvious cyanosis or scars
Examination of child for congenital heart disease:
what are some findings suggestive of heart failure?
- thin, malnourished child (faltering growth)
- excessive sweating around the forehead
- tachycardia
- SOB ± subcostal/ intercostal recession
- Poor peripheral perfusion w cold hands/ feet
- large liver
Finding of heart failure in a neonate in up to 7 days of life suggests ?
an emergency
implies a duct dependent lesion
e.g. Hypoplastic left heart/ coarctation
What is the second heart sound composed of?
closure of first the aortic and then the pulmonary valves
What causes fixed splitting of second heart sound?
*Listen at mid-left sternal edge in expiration
ASD
RBBB
What causes a single second heart sound?
Transposition of Great arteries
Pulmonary atresia
Hypoplastic Left Heart Syndrome
What causes a quiet second heart sound?
Pulmonary valve stenosis
Pulmonary artery band
Ejection systolic murmur at ULSE?
Pulmonary stenosis
or
ASD
Ejection systolic murmur at mid/ lower left sternal edge?
possible innocent murmur
Long harsh systolic murmur + cyanosis?
Tetralogy of Fallot
Ejection systolic murmur at URSE?
Aortic stenosis (with carotid thrill)
Pansystolic murmur at lower left sternal edge +/- thrill?
VSD
Continous murmur at any other site (ie lungs, shoulder, head, hind-quarter)?
AV fistula
Continuous murmur infraclavicular + cyanosis + lateral thoracotomy?
BT (Blalock-Taussig Shunt)
- surgical procedure to increase blood flow to lungs ie. shunt from branch of subclavian/ carotid artery to pulmonary art.
- typically to relieve cyanosis while infant is waiting for corrective/ definitive surgery
Median sternotomy + diastolic murmur +/- Pulmonary stenosis murmur
Tetralogy of Fallot, repaired
features of an innocent murmur?
soft (no thrill)
systolic
short (never pansystolic)
asymptomatic
left sternal edge
may change w posture
diastolic murmurs are not innocent
what happens to pulmonary vascular and pulmonary arterial pressure after fetal life?
- pulmonary vascular resistance falls rapidly in the first few breaths, continues until 3 months of age
- pulmonary arterial pressure falls
from fetal life to normal child: what closes?
causes of small arterial pulse volume?
cardiac failure
hypovolaemia
vasoconstriction
causes of large arterial pulse volume?
vasodilation
pyrexia
anaemia
aortic regurg
hyperthyroid
CO2 retention
Pulsus paradoxus?
exaggeration of normal rise and fall of BP with respiration, seen in airway obstruction, such as asthma
Management of SVT in child?
in infants: rate usually >220 bpm
If haemodynamically stable:
vagal manoeuvre + IV adenosine
if shock / difficult access:
repeated synchronous DC shocks without delay if vagal manoeuvre is unsuccessful
Secundum ASD vs Primum ASD (partial AVSD)
Secundum ASD:
middle
- defect in the centre of the atrial septum involving the fossa ovalis
Primum ASD:
lower
- a defect in the lower atrial septum, involving the left AV valve which has three leaflets and tends to leak
Clinical features of ASD:
asymptomatic
80% ASD = secundum, 10% are primum
soft systolic murmur at LSE
Fixed split S2 (difficult to hear)
In primum: apical pansystolic murmur (AV valve regurgitation)
ECG findings in ASD?
Partial RBBB
RVH
In primum: superior axis
CXR findings in ASD?
Increased pulmonary vascular markings
Management of ASD?
secundum vs primum
- Closure at 3-5 years (ideally)
- Secundum: 90% undergo device closure in cath lab
10% undergo surgical closure (too large/ personal preference)
- Primum: all require surgical closure (bc need to repair valve)
A defect at the upper end of the atrial septum, such that the SVC overrides the atrial septum. The right pulmonary veins are usually anomalous and drain directly into the SVC or right atrium adding to the L->R shunt.
Sinus Venosus ASD
Management of Sinus venosus ASD?
Closure at 1- 5 years
All require surgical closure and repair to anomalous pulmonary veins.
5% of ASDs
