Cardiology Flashcards
1
Q
Blue baby
A
- cyanosis occurs when deoxygenated blood enters the systemic circulation
- right to left shunt describes any defect that allows blood to flow from the right side of the heart to the left side of the heart without travelling through the lungs to get oxygenated
2
Q
Blue baby causes
A
- ventricular septal defect
- atrial septal defect
- patent ductus arteriosus
- transposition of the great arteries
- Eisenmenger syndrome
3
Q
Innocent murmurs
A
- also known as flow murmurs
- caused by fast blood flow through various areas of the heart during systole
- soft, short, systolic, symptomless, situation dependent
4
Q
Murmur ix
A
- ECG
- CXR
- echo
5
Q
Pan-systolic murmur
A
- mitral regurgitation heard at the mitral area
- tricuspid regurgitation heard at the tricuspid area
- ventricular septal defect heard at the left lower sternal border
6
Q
Ejection systolic murmur
A
- aortic stenosis heard at the aortic area
- pulmonary stenosis heard at the pulmonary area
- hypertrophic obstructive cardiomyopathy heard at the 4th intercostal space on the left sternal border
7
Q
Splitting of the second heart sound
A
- during inspiration the chest wall and diaphragm pull the lungs open, also pulls the heart open → negative intra-thoracic pressure
- causes right side of the heart to fill faster → increased volume in the RV causes it to take longer for the RV to empty during systole → delay in the pulmonary valve closing
- when the pulmonary valve closes slightly later than the aortic valve, this causes the second heart sound to be ‘split’
8
Q
Atrial septal defect murmur
A
- mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border
- fixed split second heart sound
9
Q
PDA murmur
A
- more significant PDAS cause a normal first heart sound with a continuous crescendo-decrescendo ‘machinery’ murmur that may continue during the second heart sound
- heard at upper left sternal border
10
Q
ToF murmur
A
murmur arises from pulmonary stenosis, given an ejection systolic murmur loudest at the pulmonary area
11
Q
Growth failure
A
Faltering growth refers to less than expected growth over time during the first three years of life when tracked on appropriate growth charts for children of the same age and sex
12
Q
Growth failure risk factors
A
- small for gestational age
- GI problems (reflux, coeliac disease)
- poor carer knowledge
- poor carer-child interaction
- cerebral palsy
- prematurity
13
Q
Growth failure aetiology
A
- inadequate intake
- environmental factors: poor access to healthy food
- social/family factors: household chaos that interferes with regular mealtime routines, child abuse, neglect
- poor appetite: chronic fever, chronic infections, anaemia
- feeding problems: cerebral palsy, neuromuscular disorders, GORD
- catch-up growth: prematurity
14
Q
Growth failure ix
A
- clinical assessment
- FBC
- urinalysis
- serological testing for coeliac disease
15
Q
Growth failure mx
A
- feeding/eating behaviour recommendations
- specialist referral
- hospitalisation
16
Q
Aortic stenosis
A
A narrow aortic valve restricts blood flow from the left ventricle into the aorta
17
Q
Aortic stenosis clinical features
A
- mild aortic stenosis can be completely asymptomatic, picked up through incidental murmur
- symptoms of fatigue, SoB, dizziness
- symptoms typically worse on exertion as outflow from LV cannot keep up with demand
- severe aortic stenosis will present with HF within months of birth
- signs
- ejection systolic murmur heard loudest at the aortic area
- crescendo-decrescendo character and radiates to the carotids
- ejection click just before the murmur
- palpable thrill during systole
- slow rising pulse & narrow pulse pressure
18
Q
Aortic stenosis ix & mx
A
- gold standard investigation = echocardiogram
- regular follow-up under a paediatric cardiologist
- echocardiograms
- ECGs
- exercise testing
- treatment
- percutaneous balloon aortic valvoplasty
- surgical aortic valvotomy
- valve replacement
19
Q
Aortic stenosis complications
A
- left ventricular outflow tract obstruction
- heart failure
- ventricular arrhythmias
- bacterial endocarditis
- sudden death, often on exertion
20
Q
Pulmonary stenosis associations
A
- tetralogy of Fallot
- william syndrome
- noonan syndrome
- congenital rubella syndrome
21
Q
Pulmonary stenosis clinical features
A
- often completely asymptomatic & found by incidental murmur
- fatigue on exertion
- SoB
- dizziness
- fainting
- signs
- ejection systolic murmur heard loudest at the pulmonary area
- palpable thrill
- right ventricular heave due to right ventricular hypertrophy
- raised JVP with giant a waves
22
Q
Pulmonary stenosis mx
A
- gold standard investigation is an echo
- mild → followed up by a cardiologist with a watch and wait
- balloon valvuloplasty via a venous catheter is treatment of choice
- if valvuloplasty is not appropriate/fails open-heart surgery can be performed
23
Q
Atrial septal defects
A
A defect in the septum between the two atria
24
Q
Atrial septal defects pathophysiology
A
- during development, the atria are connected
- two walls grow downwards from the top of the heart & fuse together with the endocardial cushion to separate the atria
- septum primum & septum secondum
- is a small hole in septum secondum = foramen ovale → normally closes at birth
- defects in these two walls leads to ASDs
- septum primum & septum secondum
- ASD leads to a shunt → blood moves from the left atrium to the right atrium due to the pressure differences
- patient doesn’t become cyanotic
- increased flow to the right side of the heart leads to right sided overload & right heart strain → right HF & pulmonary hypertension
- pulmonary hypertension can lead to Eisenmenger syndrome
- pulmonary pressure > systemic pressure
- shunt reverses & blood bypasses the lungs and patient becomes cyanotic
25
Q
Atrial septal defects types
A
- ostium secondum = septum secondum fails to fully close, leaving a hole in the wall
- patent foramen ovale, where the foramen ovale fails to close
- ostium primum, where the septum primum fails to fully close, leaving a hole in the wall → atrioventricular valve defects
26
Q
Atrial septal defects complications
A
- stroke
- AF or atrial flutter
- pulmonary HTN and right HF
- eisenmenger syndrome
27
Q
Atrial septal defects presentation
A
- mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound
- often picked up through antenatal scans or newborn examinations
- asymptomatic
- present in childhood as
- SoB
- difficulty feeding
- poor weight gain
- LRTIs
- presents in adulthood with dyspnoea, HF or stroke
28
Q
Atrial septal defects mx
A
- referral to paediatric cardiologist
- small and asymptomatic = watchful waiting
- can be corrected surgically
- transvenous catheter closure
- open heart surgery
- anticoagulants are used to reduce the risk of clots and stroke in adults
29
Q
Ventricular septal defects
A
A congenital hole in the septum between the two ventricles
- commonly associated with Down’s syndrome and Turner’s syndrome
- acyanotic
30
Q
Ventricular septal defects clinical features
A
- often VSDs are initially symptomless & patients can present in adulthood
- may be picked up on antenatal scans/when a murmur is heard during the newborn baby check
- poor feeding
- dyspnoea
- tachypnoea
- failure to thrive
- examination findings
- pan-systolic murmur more prominently heard at the left lower sternal border in the third & fourth intercostal spaces
- may be systolic thrill on palpation
31
Q
Ventricular septal defects mx
A
- small VSDs with no symptoms/evidence of pulmonary HTN can be watched over time
- can close spontaneously
- can be corrected surgically using transvenous catheter closure via femoral vein/open heart surgery
- increased risk of infective endocarditis
- abx prophylaxis should be considered during surgical procedures
32
Q
ToF
A
Congenital condition where there are four coexisting pathologies:
- ventricular septal defect
- overriding aorta
- pulmonary valve stenosis
- right ventricular hypertrophy
Cyanotic condition
33
Q
ToF risk factors
A
- rubella infection
- increased age of the mother
- alcohol consumption in pregnancy
- diabetic mother
34
Q
ToF ix
A
- echocardiogram
- doppler flow studies - useful in assessing the severity of the abnormality and shunt
- CXR - ‘boot shaped’ heart due to right ventricular thickening
35
Q
ToF clinical features
A
- cyanosis
- clubbing
- poor feeding
- poor weight gain
- ejection systolic murmur heard loudest
- tet spells
- intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode
- happens when pulmonary vascular resistance increases/the systemic resistance decreases
- episodes may be precipitated by waking, physical exertion or crying
- severe spells can lead to reduced consciousness, seizures and potentially death
36
Q
Tet spells treatment options
A
- older children may squat, younger children can be positioned with their knees to their chest
- increases the systemic vascular resistance
- encourages blood to enter the pulmonary vessels
- supplementary oxygen
- beta blockers - relax the right ventricle & improve flow to the pulmonary vessels
- IV fluids - increase pre-load → increasing the volume of blood flowing to the pulmonary vessels
- morphine
- sodium bicarbonate - can buffer any metabolic acidosis
- phenylephrine infusion - increase systemic vascular resistance
37
Q
ToF mx
A
- neonates → prostaglandin infusion can be used to maintain the ductus arteriosus
- total surgical repair by open heart surgery is the definitive treatment
- with this, 90% will live into adulthood
38
Q
TGA
A
A condition where the attachments of the aorta and the pulmonary trunk to the heart are swapped
- right ventricle pumps blood into the aorta
- left ventricle pumps blood into the pulmonary vessels
- baby will be cyanosed
39
Q
TGA clinical features
A
- often diagnosed during pregnancy with antenatal ultrasound scans
- if not detected, it will present with cyanosis at/within a few days of birth
- PDA/ventricular septal defect can initially compensate by allowing blood to mix between the systemic circulation & lungs
- within a few weeks of life, they will develop respiratory distress, tachycardia, poor feeding, poor weight gain & sweating
40
Q
TGA mx
A
- prostaglandin infusion can be used to maintain ductus arteriosus
- balloon septostomy: inserting a catheter into the foramen ovale via the umbilicus & inflating a balloon to create a large atrial septal defect
- definitive management = open heart surgery
- cardiopulmonary bypass machine is used to perform an ‘arterial switch’ procedure within a few days of birth
- VSD/ASD can be corrected at the same time
