Cardiology Flashcards
What are some outflow obstruction conditions? Which ones are cyanotic vs non-cyanotic?
Aortic and pulmonary stenosis, aortic coarctation (all non-cyanotic) and hypo plastic left-heart syndrome (cyanotic)
What occurs in aortic and pulmonary stenosis and how does it present?
What are some associations/other abnormalities with AS?
What is the management for it?
The aortic and pulmonary valve leaflets are partially fused together
- > AS often coexistent with coarctation of aorta +/- mitral valve stenosis
- > AS associated with William’s syndrome
Sx:
- > ESM
- > AS = carotid thrill
- > PS = no carotid thrill, harsh heart murmur at left sternal edge, no other symptoms
- > No cyanosis
Mx:
- AS: Balloon valvuloplasty or trans-catheter aortic valve replacement (TAVR)
- PS: Transcatheter balloon dilatation for if moderate-severe
- Endocarditis prophylaxis
How does coarctation of the aorta present?
Narrowing of the aorta - 98% occur distal to L subclavian artery
Sx:
- > Asymptomatic OR
- > ESM
- > Systolic HTN + high BP in arms, lower BP in legs
- > Absent femoral pulses/peripheral pulses
- > ‘Rib notching’ - due to large collateral intercostal arteries forming (CXR)
- > NO cyanosis
- > Often presents after 48h due to PDA closure
How would you Ix and Mx coarctation of the aorta?
Ix:
- > Echo
- > MRA
Mx:
- IF a sick infant - then follow ABC and prostaglandin infusion guidelines
- > If well, surgical repair OR balloon angioplasty +/- stent
note: re-coarctation can occur later
What is hypoplastic left-heart syndrome? How does it present and how is it managed?
Sickest child of all outflow obstruction presentations in a neonate - presents as CYANOTIC
–> V small/absent LV
Mx:
- > 1st = ABCs and prostaglandin infusion
- > 2nd = Blalock-Taussig (BK - artificial PDA) shunt OR Norwood stage 1
- > 3rd = BK shunt removed –> Glenn/Hemi-Fontan –> Fontan or Total cavo-pulmonary connection
How may arrhythmias present in a child? How would you Ix the child?
SVT is the most common childhood arrhythmia
Sx:
- > HR 250-300 bpm –> poor CO, pulmonary oedema
- > Neonates - HF, hydrops fetalis
- > Foetus - IUD
Ix:
- > ECG - narrow complex tachycardia, delta wave in WPW, T wave inversion due to ischaemia
- > Echocardiography
How would you manage SVT in a child?
Mx: need to restore sinus rhythm promptly
- Circulatory and respiratory support - PPV if needed, tissue acidosis corrected
- VAGAL stimulating manoevers + raised legs (ice pack to face, carotid sinus massage) = 80% success
If fails: - IV ADENOSINE = induces AV block and terminates tachycardia
If fails: - DC cardioversion (or chemical: amiodarone/flecainide) + requires maintenance therapy after
- If haemodynamically unstable, attempt vagal manouveres and adenosine as above but don’t delay DC cardioversion
90% children have no further attacks in infancy
–> Catheter ablation is recommended if recurrent/accessory pathway
What is rheumatic fever and how + in who does it present?
What is the criteria required for diagnosis?
What is a complication of it?
Rheumatic fever is caused by GAS (Group A beta-haemolytic streptococcus)
- > Children aged 5-15y
- > Long term damage leads to MITRAL STENOSIS
Sx:
-> Latent interval of 2-6w after pharyngeal infection and then PPE (Polyarthritis, Pericarditis/myo/endo and erythema marginatum - map like outlines)
-> 2-6m later may get Syndenhams chorea (involuntary movements)
-> Diagnosis via JONES criteria where there is evidence of recent strep throat (increased ISO titre/strep Abs or culture) and
2 MAJORS or 1 MAJOR + 2 MINORs of:
MAJOR = CASES (Carditis, arthritis, subcutaneous nodules, erythema marginatum and sydenhams chorea) MINOR = FRAPP (Fever, raised ESR/CRP, Arthralgia, Prolonged PR interval and previous RF)
How is Rheumatic Fever treated? (acute vs long-term)
Mx:
Acute:
- Bed rest + anti-inflammatory agents (high dose ASPIRIN for 1-2 or 6-8w)
- ABx (Penicillin/Amoxicillin) if suspecting persistent infection
- CS if the fever and inflammation doesn’t resolve rapidly
Prophylaxis:
- monthly injections of benzathine penicillin until 10y after last episode/21yo OR lifelong if severe valve disease
- Surgical treatment with valve repair/replacement may be needed
How may infective endocarditis present in a child? What are some risk factors?
RF = any congenital heart defect or abnormality that gives rise to turbulent blood flow e.g. VSD
Sx:
- Fever, anaemia, pallor, petechiae
- Janeway lesions, Osler’s nodes
- Nectrotic skin lesions (infected emboli)
- Clubbing, splinter haemorrhages
- Changing cardiac signs
- Splenomegaly
- Microscopic haematuria
- Neurosigns from cerebral infarct
- Arthritis/arthralgia
How is IE diagnosed and managed?:
- -> Initial blind therapy - native and prosthetic valves
- -> Streptotococci which is penicillin-sensitive or less-sensitive; native and prosthetic valves
- -> Stapylococci; native and prosthetic valve
- -> Other options
Ix:
Dx = multiple blood cultures (before Abx) and Echo to identify vegetations
–> usually caused by Strep. viridans, S. aureus
Mx:
Initial blind therapy for native valves:
- Beta-lactam + low-dose gentamicin
- Low-dose gentamicin + vancomycin - if pen-allergy, severe sepsis or MRSA suspected
- Vancomycin + meropenem - if severe sepsis and RF for Gram-neg infection
Prosthetic valves:
- Vancomycin + rifampicin + low-dose gentamicin
Penicillin-sensitive streptococci
= Benzylpenicillin sodium for 4-6w (6w if prosthetic) or Vancomycin+low dose gentamicin if pen-allergy
If less-sensitive streptococci
= Benzylpenicillin sodium + low-dose gentamicin for 4-6w
Staphylococci:
- Native valve = continue Abx for 4w of Flucloxacillin or Vancomycin+Rifampcin if MRSA/pen-allergy
- Prosthetic = 6w Abx of Flucloxacillin + rifampicin + low-dose gentamicin or replace with Vancomycin if pen-allergy
- Surgical removal of infected prosthetic material
How may a child present with heart failure?
Sx:
- SOB
- Poor feeding, fatigue
- Recurrent chest infections
- Signs = poor weight gain/FTT, increased RR and HR, hepatomegaly, gallop rhythm, signs of venous congestion, enlarged heart, cool peripheries, pallor
What are some causes of HF in paediatric patients?
Neonates: duct dependent, obstructed systemic circulation - hypoplastic LHS - aortic stenosis - severe aortic coarctation - interruption of aortic arch [DO NOT close PDA]
Infants: defect -> high pulmonary flow -> L to R shunt
- persistent VSD, ASD, PDA
Older children: R or L-HF
- Eisenmenger (RHF), rheumatic HD, cardiomyopathy
Other = volume overload (anaemia/sepsis), pressure overload (HTN)
How would you Ix HF?
Ix:
- Basic obs
- CXR
- ECG
- Echo
How would you Mx HF? What are the aims of treatment linking this? [5]
Mx:
Multi faceted with specific aims:
- Reduce preload = diuretics (furosemide) or GTN
- Enhance cardiac contractility = IV dopamine or digoxin/ dobutamine/adrenaline
- Reduce after load = oral ACEi or IV agents e.g. hydralzine
- Improve O2 delivery = B-blockers e.g. carvedilol
- Enhance nutrition + routine daily exercise
- If cyanotic then PROSTAGLANDIN INFUSION
How can congenital heart disease be separated, and examples of these?
What are key Ix required for suspected congenital heart disease?
R–>L shunts (cyanotic)
- Tricuspid atresia
- ToGA
- ToF
- AVSD
- Eisenmenger
L–>R shunts (non-cyanotic)
- ASD
- VSD
- PDA
+ Outflow obstructions, infections etc
Ix:
- -> ECG
- -> CXR
- -> ECHO
When do each of the congenital heart diseases generally present?
Within time of birth:
- Few hours = AVSD, TA, hypo plastic left heart syndrome
- Few days = ToGA (d2), ToF (days-months), large PDA
- Few weeks = aortic stenosis, co-arctation of the aorta
- Few months = any L->R shunt as pulmonary resistance falls
What are features of innocent murmurs? When may they be detected? What are 2 examples?
Think S’s:
- Soft
- aSymptomatic
- Systolic
- Short
- left Sternal edge
- Sitting/standing variation
Can be observed more easily in illness or anaemia (increased CO)
Stills murmur
Venous hum = blowing noise, above clavicles
What are the KEY differentiating features in presentation of:
- Cyanotic
- Non-cyanotic
- Outflow-obstruction in a well child
- Outflow-obstruction + collapse and shock?
Cyanotic
= BLUE baby
Non-cyanotic
= breathless baby
OO in well child
= A or P stenosis
OO with collapse and shock
= Coarctation of aorta
What are ASDs caused by? How do they present?
Either due to:
- -> patent foramen ovale and defect of atrial septum (Secundum) = 80%
- -> defect of AV septum = partial AVSD/primum ASD = 20%
S/S:
- Asymptomatic
- Recurrent chest infections/wheeze
- ESM at ULSE + fixed wide splitting of S2
- Arrhythmias from 40yo
How would you Ix an ASD and what would they show? How would you manage them?
Ix:
- CXR
- ECG - RBBB and RAD in secundum
- ECHO is diagnostic
Mx
- Only required if Sx, RV dilation or Qp:Qs (pul flow 1.5x > systemic)
- usually at 3yo
- Secundum ASD = transcatheter closure - cardiac catherterisation and insertion of occlusive device
- Partial AVSD = open heart surgical correction
How would VSD’s present (think size)?
NOTE: commonest heart defect
Classified by size:
Small <3mm (80-90%)
- Asymptomatic
- LOUD PSM at LLSE
- Soft pulmonary 2nd sound
- E.g. a breathless 3m baby with normal sats, LOUD murmur, poor feeding/tiredness
Large >3mm
- SOB, recurrent infections, hepatomegaly
- HEART FAILURE
- Soft PSM, mid diastolic murmur
- Loud pulmonary 2nd sound
How would you Ix and manage VSDs? What are the aims with the management?
Ix:
- CXR: HF for large VSDs (ABCDE)
- ECG: Large R wave for hypertrophy (>8mm) for large VSDs
- ECHO for Dx
<3mm - higher risk of endocarditis
- Prophylactic amoxicillin
- Self-limiting, close themselves
> 3mm - want to prevent Eisenmenger syndrome
- Calorie input
- Diuretics
- Captopril
- Surgery at 3-6m
How do PDAs present and how may they be managed? Why should they be closed?
PDA = connects pulmonary artery to descending aorta, should close at 1m
- Closed as risk of endocarditis and pulmonary vascular disease
S/S:
- Continuous machine-like murmur/Gibson’s at ULSE
- Heaving apex beat
- Wide pulse pressure
- Bounding, collapsing pulses
- Resp Sx = apnoea, WOB
Mx
- IV Indomethacin (NSAID) to close duct
- Surgical, if medical failed^: surgical ligation or percutaneous catheter
device closure may be used 6m-1yo
If a baby presents with cyanosis, what test can you do? How would you initially manage all babies?
Hyperoxia test
= start 10 minutes 100% oxygen; If SpO2 persistently low, likely congenital cyanotic heart disease (or primary pulmonary pathology) —> Supplemental oxygen to maintain saturations 75-85%
Mx:
- A to E assessment
- Stabilise airway and breathing +/- intubate
- IV or Umbilical line access - crystalloid and adrenaline if needed for hypotension
- PROSTAGLANDIN E1 to maintain duct patency = key to survival
- -> Most infants presenting in 1st week of life are duct dependent
- Regularly check blood glucose
How would tricuspid atresia present? How would you manage it? Can all patients have complete corrective surgery?
Where only LV is effective, RV is too small
S/S
- Cyanosis and SOB very early –> 10 mins of life
- ESM at LSE - must have an ASD/VSD to allow mixing
- Hypoplastic left heart
Mx:
- Prostaglandin E1 and supportive cardio-respiratory support
- 1st, neonates = maintain steady supply of blood to the lungs by BLALOCK-TAUSSIG shunt which connects pulmonary and subclavian arteries
- 2nd, 3-6mo = Glenn, remove shunt and anastomose SVC to PA
- 3rd, 2-5yo = Fontan, connect IVC to PA
- Abx prophylaxis
NO - most cannot, as most cases only have 1 functioning ventricle
How does ToGA present? What would Ix show?
ToGa is when the 2 main vessels out of the heart are switched (PA and aorta)
–> Usually fatal immediately but there are VSD/ASDs/PDA to enable mixing in short term
S/S:
- Cyanosis within a few hours
- Loud S2 but NO murmur
Ix:
- CXR - ‘egg on side’, narrow upper mediastinum
- ECHO
How would you manage ToGA?
Mx:
- Correct body temperature and acidosis/glucose
- Prostaglandin E1
- Balloon atrial septostomy - breaks the flap valve of the foramen ovale and encourages mixing of blood
(+bolus of heparin given before BAS
- Arterial switch surgery in first 2w of life (inc coronary arteries)
What is ToF and how does it present?
Commonest cause of cyanotic heart disease. Has the following 4 features:
- VSD
- Overriding aorta
- Pulmonary stenosis
- RVH
S/S:
- CLUBBING
- Murmur = loud ESM at LLSE due to pulmonary stenosis
- “tet spells’ where child cries, increasing pulmonary resistance, causing R->L shunt and cyanosis
How would you Ix and Mx ToF?
Ix:
- CXR - ‘boot shaped heart due to RVH’
- ECHO
Mx:
- Prostaglandin or alprostadil infusion
- Blalock-taussig shunt to connect subclavian and pulmonary artery
- Surgery from 4mo
Hypercyanotic spells:
- Knee-to-chest position
- Oxygen
- IV morphine, adrenaline and propanolol
- IV fluids and bicarbonate to correct acidosis
- Refer to cardiac centre
What is Eisenmenger’s syndrome? How does it usually present? How may it be managed?
Irreversibly raised pulmonary vascular resistance from chronicle raised pulmonary arterial pressure and flow e.g. large VSD or PDA
- -> R to L shunt formation (cyanotic heart disease)
- -> Occurs ~10-15y later
- -> S/S: blue, cyanotic
Mx = early intervention for pulmonary blood flow, possible heart transplant
