Cardiology Flashcards

1
Q

What are some outflow obstruction conditions? Which ones are cyanotic vs non-cyanotic?

A

Aortic and pulmonary stenosis, aortic coarctation (all non-cyanotic) and hypo plastic left-heart syndrome (cyanotic)

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2
Q

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?

A

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
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3
Q

How does coarctation of the aorta present?

A

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
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4
Q

How would you Ix and Mx coarctation of the aorta?

A

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

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5
Q

What is hypoplastic left-heart syndrome? How does it present and how is it managed?

A

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
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6
Q

How may arrhythmias present in a child? How would you Ix the child?

A

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
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7
Q

How would you manage SVT in a child?

A

Mx: need to restore sinus rhythm promptly

  1. Circulatory and respiratory support - PPV if needed, tissue acidosis corrected
  2. VAGAL stimulating manoevers + raised legs (ice pack to face, carotid sinus massage) = 80% success
    If fails:
  3. IV ADENOSINE = induces AV block and terminates tachycardia
    If fails:
  4. 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

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8
Q

What is rheumatic fever and how + in who does it present?

What is the criteria required for diagnosis?

What is a complication of it?

A

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)
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9
Q

How is Rheumatic Fever treated? (acute vs long-term)

A

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
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10
Q

How may infective endocarditis present in a child? What are some risk factors?

A

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
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11
Q

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
A

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
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12
Q

How may a child present with heart failure?

A

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
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13
Q

What are some causes of HF in paediatric patients?

A
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)

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14
Q

How would you Ix HF?

A

Ix:

  • Basic obs
  • CXR
  • ECG
  • Echo
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15
Q

How would you Mx HF? What are the aims of treatment linking this? [5]

A

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
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16
Q

How can congenital heart disease be separated, and examples of these?

What are key Ix required for suspected congenital heart disease?

A

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
17
Q

When do each of the congenital heart diseases generally present?

A

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
18
Q

What are features of innocent murmurs? When may they be detected? What are 2 examples?

A

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

19
Q

What are the KEY differentiating features in presentation of:

  • Cyanotic
  • Non-cyanotic
  • Outflow-obstruction in a well child
  • Outflow-obstruction + collapse and shock?
A

Cyanotic
= BLUE baby

Non-cyanotic
= breathless baby

OO in well child
= A or P stenosis

OO with collapse and shock
= Coarctation of aorta

20
Q

What are ASDs caused by? How do they present?

A

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
21
Q

How would you Ix an ASD and what would they show? How would you manage them?

A

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
22
Q

How would VSD’s present (think size)?

A

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
23
Q

How would you Ix and manage VSDs? What are the aims with the management?

A

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
24
Q

How do PDAs present and how may they be managed? Why should they be closed?

A

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

25
Q

If a baby presents with cyanosis, what test can you do? How would you initially manage all babies?

A

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
26
Q

How would tricuspid atresia present? How would you manage it? Can all patients have complete corrective surgery?

A

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

27
Q

How does ToGA present? What would Ix show?

A

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
28
Q

How would you manage ToGA?

A

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)

29
Q

What is ToF and how does it present?

A

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
30
Q

How would you Ix and Mx ToF?

A

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
31
Q

What is Eisenmenger’s syndrome? How does it usually present? How may it be managed?

A

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