Paeds cardiology Flashcards
continuous blowing noise heard just below the clavicles
venous hum
Low-pitched sound heard at the lower left sternal edge
stills murmur
features of innocent murmurs
Soft
Short
Systolic
Symptomless
Situation dependent, particularly if the murmur gets quieter with standing or only appears when the child is unwell or feverish
ddx for Pan systolic murmur
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
ddx for ejection systolic murmur
Aortic stenosis
Pulmonary stenosis (+ tetralogy of fallot)
ASD
Hypertrophic obstructive cardiomyopathy
coarctation and bicuspid aortic valve (both in turners)
when can splitting of the second heart sound be normal
can be normal with inspiration
Fixed splitting of second heart sound indicates?
ASD
Causes of PDA
- genetic
- maternal rubella
- prematurity
Pulse character in PDA
large volume, bounding, collapsing pulse
continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound, making the second heart sound difficult to hear
PDA
Diagnostic investigation heart murmurs
echocardiogram
Management isolated PDA
indomethacin or ibruprofen if symptomatic
may choose to monitor and do trans-catheter or surgical closure if still present at 1 year
What do you do to keep PDA open
prostaglandin E1
ddx for diastolic murmurs
early diastolic:
- aortic regurg
- pulmonary regurg
mid diastolic:
- mitral stenosis
Most common ASD
Ostium secondum
Complications ASD
Stroke in the context of venous thromboembolism (see below)
Atrial fibrillation or atrial flutter
Pulmonary hypertension and right sided heart failure
Eisenmenger syndrome
mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound
ASD
Management ASD
ASDs can be corrected surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery.
Anticoagulants (such as aspirin, warfarin and NOACs) are used to reduce the risk of clots and stroke in adults.
What is ebsteins anomaly
tricuspid valve is set lower in the right side of the heart (towards the apex), causing a bigger right atrium and a smaller right ventricle. This leads to poor flow from the right atrium to the right ventricle, and therefore poor flow to the pulmonary vessels. It is often associated with a right to left shunt across the atria via an atrial septal defect.
ECG wolff-parkinson white
short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway*
right axis deviation if left-sided accessory pathway*
Evidence of heart failure (e.g. oedema)
Gallop rhythm heard on auscultation characterised by the addition of the third and fourth heart sounds
Cyanosis
ebstein’s anomaly
what can ebstein’s anomaly cause
wolff-parkinson white
Management ebsteins anomaly
Medical management includes treating arrhythmias and heart failure. Prophylactic antibiotics may be used to prevent infective endocarditis. Definitive management is by surgical correction of the underlying defect.
Causes ebsteins anomaly
lithium use in pregnancy
ECG ASD caused by ostium secundum
RBBB with RAD
ECG ASD caused by Ostium primum
RBBB with LAD, prolonged PR interval
Causes VSD
congenital VSDs are often association with chromosomal disorders:
Down’s syndrome
Edward’s syndrome
Patau syndrome
cri-du-chat syndrome
congenital infections
acquired causes
post-myocardial infarction
failure to thrive, pan systolic murmur left lower sternal border. There may be a systolic thrill on palpation.
VSD. louder in smaller defects
Management VSD
- w&w
- surgical closure: trans-catheter or open heart
- antibiotic prophylaxis
Cardiac assocations downs syndrome
- endocardial cushion defect (most common, 40%, also known as atrioventricular septal canal defects)
ventricular septal defect (c. 30%)
secundum atrial septal defect (c. 10%)
tetralogy of Fallot (c. 5%)
isolated patent ductus arteriosus (c. 5%)
Examination findings pulmonary hypertension
Right ventricular heave: the right ventricle contracts forcefully against increased pressure in the lungs
Loud P2: loud second heart sound due to forceful shutting of the pulmonary valve
Raised JVP
Peripheral oedema
Complications VSD
- aortic regurg
- eisenmengers
- pulmonary hypertension
- infective endocarditis
associations coarctation
more common in males Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
features of coarctation
weak femoral pulses
radio-femoral delay
ejection/mid systolic murmur heard at left infraclavicular space radiating to interscapular area
apical click from the aortic valve
management coarctation
- prostaglandin E to keep PDA open
- Surgery
Options for management congenital aortic stenosis
Limit exercise, regular follow ups and ECG
Percutaneous balloon aortic valvoplasty
Surgical aortic valvotomy
Valve replacement
Associations congenital pulmonary stenosis
Tetralogy of Fallot
William syndrome
Noonan syndrome
Congenital rubella syndrome
Complications congenital aortic stenosis
Left ventricular outflow tract obstruction
Heart failure
Ventricular arrhythmia
Bacterial endocarditis
Sudden death, often on exertion
Management pulmonary stenosis
w&w
balloon valvuloplasty via a venous catheter
4 things in tetralogy of fallot?
PROVE
Pulmonary stenosis
Right ventricular hypertrophy
Overriding of the aorta
VSD
Ejection systolic murmur
Risk factors for ToF
RAID
Rubella infection
Alcohol consumption in pregnancy
Increased age of the mother (over 40 years)
Diabetic mother
“boot shaped” heart
right ventricular hypertrophy - ToF sign
Pathophysiology tet spells
Physically exertion –> generating a lot of carbon dioxide –> vasodilaton –> systemic vasodilation and therefore reduces the systemic vascular resistance –> Blood flow will choose the path of least resistance, so blood will be pumped from the right ventricle to the aorta rather than the pulmonary vessels, bypassing the lungs
can also occur with increased pulmonary vascular resistance
Presentation tet spells
precipitated by waking, physical exertion or crying. The child will become irritable, cyanotic and short of breath. Severe spells can lead to reduced consciousness, seizures and potentially death.
Management tet spell
- position with knees to chest to increase systemic vascular resistance
- O2
- beta bockers to decrease pulmonary vascular resistance
- IV fluids can increase pre-load
Morphine can decrease respiratory drive, resulting in more effective breathing.
Sodium bicarbonate can buffer any metabolic acidosis that occurs.
Phenylephrine infusion can increase systemic vascular resistance.
In what conditions may you want to keep PDA open?
- coarctation
- tetralogy of fallot
- transposition of the great arteries
Management ToF
- Prostaglandin E1 infusion
- open heart surgery
Management transposition of the GA
- prostaglandin E1
- Balloon septostomy
- Open heart surgery
When does ToF present?
presents at around 1-2 months, although may not be picked up until the baby is 6 months old
most common cause infective endocarditis
Staphylococcus aureus
pathogen infective endocarditis after dental procedure
Streptococcus viridans
pathogen infective endocarditis up to 2 months after valve replacement
coagulase-negative Staphylococci such as Staphylococcus epidermidis
non infective causes endocarditis
systemic lupus erythematosus (Libman-Sacks)
malignancy: marantic endocarditis
inheritance Hypertrophic obstructive cardiomyopathy
autosomal dominant
Management hypertrophic obstructive cardiomyopathy
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
Pathophysiology hypertrophic obstructive cardiomyopathy
Usually due to a mutation in the gene encoding β-myosin heavy chain protein
Echo findings hypertrophic obstructive cardiomyopathy
Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
ECG pericarditis
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
Management pericarditis
NSAIDs
Colchicine
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericarditis
cyanotic CHDs
Tetralogy of fallot
Transposition of great vessels (TGA)
Tricuspid abnormalities eg ebsteins
Tricuspid atresia
Total anomalous pulmonary venous return
Truncus arteriosus
Most common cardiac abnormality in turners
bicuspid aortic valve (ejection systolic murmur)
Murmurs ebsteins anomaly
tricuspid regurgitation (pan-systolic murmur) and tricuspid stenosis (mid-diastolic murmur)
gallop rhythm, fixed splittng of second heart sound if ASD
murmur grades
One- Very faint. Heard by an expert in optimum conditions
Two - Heard by a non-expert in optimum conditions
Three- Easily audible, no thrill
Four- A loud murmur, with a thrill
Five -Very loud, often heard over a wide area, with thrill
Six - Extremely loud, heard without a stethoscope
management SVT
ABCDE
Cardioversion:
- syncronised eg defib
- adenosine
- amiadarone before 3rd shock
with appropriate sedation
+ analgesia (e.g. IM/intranasal
ketamine if delay in IV access)
examples of vagal manourvres SVT
Vagal maneuvers – For infants, apply bag containing ice water to the face above the nose and mouth for 15 to 30 seconds. Do not obstruct ventilation. In older children, bearing down or blowing into an occluded straw for 15 to 20 seconds provides vagal stimulation.
define SVT in children
Infant > 220 min-1
Child > 180 min-1
Abrupt onset
Another name for wolff-parkinson white syndrome
AV reciprocating/bundle of kent
re-entry point is an accessory pathway
pathophysiology SVT
Early depolarisation –> shortened PR interval and narrow QRScomplex
what is considered a narrow QRS?
<0.12 seconds
