Summary
paediatric summary
- Module
- Medicine
- Institution
- Queens University Belfast (QUB)
Summary of 150 pages for the course Medicine at QUB (paediatric summary)
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Paediatrics,Cardiology
Important Presenting Symptoms and Signs in Cardiology
You should be able to list the 3-4 commonest causes of these symptoms/signs at various ages and be able to
differentiate these (by features and investigations):
• Tachycardia
• Murmurs
• Cyanosis
• Heart failure
The Spectrum of Clinical Conditions in Cardiology
You should be able to describe - aetiology, presentation, natural history, signs, diagnosis and basic
management of an infant/toddler/older child with:
• Congenital heart disease - describe anatomical and physiological basis for pathology and physical
signs
• Heart failure
• Innocent versus pathological asymptomatic murmurs
• SBE
• Rheumatic fever
• Kawasaki syndrome
• Cardiomyopathy
Practical skills
You should be able to list the 3-4 commonest causes of these symptoms/signs at various ages and be able to
differentiate these (by features and investigations):
• Cardiovascular examination
• Blood pressure measurement
• Recognise heart sounds/murmurs
• Recognise signs of heart failure
Congenital heart disease – commonest form of congenital abnormality
Foetal circulation
Blood needs to go via placenta to collect oxygen and nutrients and dispose of waste products i.e. CO2 and
lactate via mother, foetal lungs not fully developed so blood does not pass through pulmonary circulation –
shunts allow blood to bypass lungs
1. Ductus venosus connects umbilical vein to IVC bypassing liver
2. Foramen ovale connects RA→LA bypassing right ventricle and pulmonary circulation
3. Ductus arteriosus connects pulmonary artery with aorta bypassing pulmonary circulation
,At birth
• First breath expands the alveoli decreasing pulmonary vascular resistance, this causes fall in pressure in
right atrium, left atrial pressure > right atrial pressure squashing the atrial septum causing functional
closure of foramen ovale, structurally shuts after few weeks becomes fossa ovalis
• Prostaglandins require to keep ductus arteriosus open, increased blood oxygenation causes drop in PG
causing closure, becomes ligamentum arteriosum
• Immediately after birth ductus venosus stops functioning because umbilical cord is clamped, no flow in
umbilical veins, structurally closes few days later becoming ligamentum venosum
• Persistent fetal circulation/persistent pulmonary HTN of newborn – deoxy blood passing from
pulmonary arterty to aorta, deeply cyanosed, ill at birth, Rx: drop pressure within pulmonary arteries
with oxygen, dilators i.e. NO
Congenital heart disease
• Structural CHD
• Congenital rhythm disease (120-160bpm: normal)
o Too fast
▪ Can occur due to temperature, infection
o Too slow
▪ Can occur due to extrinsic vagal stimulus
• Genetic conditions associated:
o Trisomy’s i.e. 21, 13 (Patau’s), 18 (Edwards)
o Monosomy 45 XO (Turner) – typically left heart problems i.e. bicuspid aortic valve and aortic
coarctation
o Noonan’s syndrome, 22q11 deletion (DiGeorge)
• Abnormal connections, holes or obstructions, either cyanotic or acyanotic
o Cyanotic (R→L)
▪ Blue babies
▪ 5T’s: TGA, tetralogy of Fallot, TAPVD, truncus arteriosus, tricuspid atresia
o Acyanotic (L→R)
▪ Breathless babies
▪ VSD, ASD, PDA, PS, AS, Coarctation, HLHS
▪ Rx:
• Diuretics e.g. furosemide/spironolactone (keep K high)
• Vasodilators e.g. captopril
• Consider inotropes if poor ventricular function
• ? digoxin sometimes
Innocent murmurs (flow murmurs)
Common in children, due to fast blood flow through heart during systole, Ivx are normal (ECG, CXR, echo)
Typical features (5S)
• Soft
• Short
• Systolic
• Symptomless
• Situation dependant – quiet with standing or only appears when unwell/feverish
Often don’t require investigations, features prompting:
• Murmur louder than 2/6 (i.e. thrill heard)
• Diastolic murmurs
• Louder on standing
• Other symptoms i.e. failure to thrive, feeding difficulty, cyanosis, SOB
, • Pan-systolic murmurs
• Mitral regurgitation heard at mitral area (5th ICS, MCL)
• Tricuspid regurgitation heard at tricuspid area (5th ICS, left sternal border)
• Ventricular septal defect heard at left lower sternal border
• Ejection-systolic murmurs
• Aortic stenosis heard at aortic area (2nd ICS, right sternal border)
• Pulmonary stenosis heard at pulmonary area (2nd ICS, left sternal border)
• Hypertrophic obstructive cardiomyopathy heard at 4th ICS, left sternal border
• Splitting of second heart sound
• During inspiration there is negative intra-thoracic pressure (chest wall and diaphragm pull lungs
open), causes right side of heart to fill faster pulling blood from venous system
• Increased volume in RV, takes longer to empty during systole causing delay in pulmonary valve closing
• When pulmonary valve closes slightly later than aortic valve – 2nd heart sound sounds “split”
• Atrial septal defect
• Mid-systolic, crescendo-decrescendo murmur loudest at upper left sternal border, fixed split-second
heart sound
• Splitting of 2nd heart sound can be normal with inspiration but “fixed split” means it does not change
with inspiration/expiration
• Occurs as blood flowing from left atrium into right atrium across ASD increasing the volume of blood
that RV has to empty before pulmonary valve can close, doesn’t vary with respiration
• Patent ductus arteriosus
• Significant PDAs cause normal first heart sound with continuous crescendo-decrescendo “machinery”
murmur that may continue during second heart sound, making second sound difficult to hear
• Small PDAs may not cause abnormal sounds
• Tetralogy of Fallot
• From pulmonary stenosis giving ejection systolic murmur, loudest at pulmonary area
• Cyanotic heart disease
• Deoxygenated blood enters systemic system, blood bypasses pulmonary circulation, occurs across
right→left shunt, causes;
o Ventricular septal defect (VSD)
o Atrial septal defect (ASD)
o Patent ductus arteriosus (PDA)
o Transposition of great arteries (TGA)
• Pts with VSD, ASD, PDA usually not cyanotic as pressure in left side of heart is greater than right side,
blood flows from high-low pressure preventing R→L shunting. If pulmonary pressure increases
beyond systemic pressure blood will flow across the defect causing cyanosis – Eisenmenger syndrome
• Pts with TGA always cyanosed because right side pumps blood directly into aorta and systemic
circulation
Patent ductus arteriosus – failure to close, normally stops functioning 1-3days, closes completely 2-3wks,
unclear why, ? genetics or maternal infections i.e. rubella, prematurity key RF
• Picked up during new-born examination, SOB, difficulty feeding, poor weight gain, LRTI
• Significant PDAs cause normal first heart sound with continuous crescendo-decrescendo “machinery”
murmur that may continue during second heart sound, making second sound difficult to hear
• Small PDA can be asymptomatic, no function problems, close spontaneously, may present in
adulthood with signs of heart failure
• Pressure in aorta > pulmonary vessels, left → right shunt, causes pulmonary HTN leading to right
sided heart strain, right ventricle struggles to contract against increased resistance
• Pulmonary HTN and right sided HF cause right ventricular hypertrophy, increased blood flowing
through pulmonary vessels returning to left side of heart causes left ventricular hypertrophy
• Confirmed by echocardiogram, doppler flow during can assess size of shunt, hypertrophy can be seen
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