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FRACP Paeds Clinical > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What signs allow you to differentiate the level of a LVOTO?

A

Supravalvular has a suprasternal thrill.

Valvular has a click and a thrill.

Subvalvular has neither.

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2
Q

Which cardiac defects cause increased pulmonary vasculature on chest x-ray?

A
  1. Truncus arteriosis
  2. Total anomalous pulmonary venous drainage
  3. Transposition of the great arteries
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3
Q

Which cardiac defects cause decreased pulmonary vasculature?

A
  1. Pulmonary atresia with intact ventricular septum
  2. Ebsteins anomaly
  3. Tetralogy of Falot
  4. Critical pulmonary stenosis with left to right shunt
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4
Q

What are the causes of a prolonged PR interval?

A
  1. Endocardial cushion defect
  2. Ebsteins anomaly
  3. Acute rheumatic fever
  4. Congenital heart block
  5. Normal variant
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5
Q

What are the causes of a partial RBBB?

A
  1. Ostium primum ASD (with LAD)
  2. Ostium secundum ASD (with RAD)
  3. Ebsteins anomaly (with RAH and delta waves
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6
Q

What causes a complete RBBB?

A
  1. Ventriculotomy (repair of VSD/TOF)
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7
Q

What are causes of left axis deviation?

A
  1. Endocardial cushion defect
  2. Tricuspid atresia
  3. Hypertrophic cardiomyopathy
  4. Inlet VSD
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8
Q

Which cardiac defects cause a wide pulse pressure?

A
  • Aortic regurgitation
  • Patent ductus arteriosis
  • Thyrotoxicosis
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9
Q

What cardiac defects cause narrow pulse pressure?

A
  • Aortic stenosis
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10
Q

What are early complications of Fontan procedure?

A

Low cardiac output/heart failure.

Pleural effusion.

Supravalvular arrhythmias.

Acute liver dysfunction.

Thrombosis.

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11
Q

What are late complications of Fontan procedure?

A

Thrombosis.

Protein losing enteropathy.

Supraventricular arrhythmias.

Hepatomegaly and ascites.

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12
Q

How is severity of AS rated?

A

Doppler pressure gradient (approx. 20% hgher than peak to peak gradient obtained on catherterisation).

  • Mild: Doppler peak gradient <40mmHg
  • Moderate: Doppler peak gradient 40-70mmHg
  • Severe: Doppler peak gradient >70mmHg
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13
Q

Is activity restriction required in AS?

A
  • No limitation in mild AS.
  • No competitive or strenuous sports for >50mmHg - >70mmHg.
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14
Q

What is the natural history of AS?

A
  • Mild disease frequently worsens - calcification of valve leaflets (may eventually requir valve replacement).
  • Progressive AR in discrete subaortic stenosis
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15
Q

What are ECG findings in AS?

A
  • No changes until severe.
  • Develop LVH wth severe disease.
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16
Q

What are the examination findings in AS?

A
  • Narrow pulse pressure, slow rising pulse in severe disease.
  • ESM loudest RUSE.
  • Radiates to the carotids.
  • Suprasternal thrill present.
  • Ejection click mid LSE –> apex in valvular disease.
  • Loudest in expiration.
  • S2 narrow or single in severe.
  • Always listen for associated AR.
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17
Q

How is AS treated?

A

Supravalvular:

  • Widening of stenotic area with diamond shaped patch.

Valvular:

  • In critically unwell infants and neonates - anticongestive measures, PGE1 infusion and balloon valvuloplasty.
  • If balloon valvuloplasty fails or severe AR develops secondary to valvuloplasty:
    • Aortic valve comissurotomy.
    • Aortic valve replacement - mechanical or homograft.

Subvalvular:

  • Excision of membrane.
    • Ross procedure.
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18
Q

Mechanical vs. biologic valve replacement?

A
  • Mechanical valve is durable:
    • Requires lifelong warfarin - bleeding and teratogenecity.
  • Biologic valve:
    • Does not require anticoagulation, lifespan only 10-20 years.
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19
Q

Follow-up post AS surgery.

A
  • Annually as AR develops in 10-30%, membrane recurs in 25-30%.
  • Warfarin for prosthetic valves.
  • Aspirin for biovalves.
  • SBE prophylaxis as indicated.
  • Restriction on strenuous and competitive sports in moderate residual AS or AR.
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20
Q

What are the clinical manifestations of AS?

A
  • Mild to moderate - asymptomatic.
  • Severe - exertional chest pain, syncope, signs of congestive heart failure.
21
Q

What are the recommendations for SBE prophylaxis?

A
  • Recommended only for dental procedures and procedures at the site of established infection.
  • Prosthetic heart valves (mechanical and bio).
  • Rheumatic valvular heart disease.
  • Previous endocarditis.
  • Unrepaired cyanotic CHD (incl. palliative shunts and conduits).
  • Surgical or catheter repair of CHD within 6 months of repair.
22
Q

How is the severity of PS rated?

A

Peak Doppler gradient:

  • Mild: < 35-40mmHg - low to medium pitched.
  • Moderate: 40-70mmHg - harsh, wide split S2, radiation to the back ad axillae, RV heave.
  • Severe: >70mmHg - Long loud murmur, single soft S2, RVF
23
Q

What are differentials for a murmur at the LUSE?

A
  • PS
  • Innocent pulmonary flow murmur.
  • ASD - functional PS.
  • TOF (usually mid to LSE) - long ESM, loud single A2
  • PA stenosis - loudest below L. clavicle, short systolic murmur, radiates widely to back and lungs, RVH only if severe. prominent hilar vessels.
  • CoA - loudest L. interscapular, dec. femoral pulses, upper limb HTN, bicuspid Ao valve (70% - click, thrill, AR), ECG N or LVH.
  • PDA - continuous, loudest below L. clavicle (occasionally systolic).
  • Subvalvular AS
  • Outlet VSD
24
Q

What are the clinical manifestations of PS?

A
  • Mild - symptomatic.
  • Moderate - exertional dyspnoea and easy fatiguability in moderate.
  • Severe - angina, syncope and presyncope, CHF.
25
Q

What is the natural history of PS?

A
26
Q

What are the ECG findings of PS?

A
  • Mild: normal.
  • Moderate: RAD and RVH.
  • Severe: RAH and RVH with strain pattern.
27
Q

How is PS treated?

A
  • Neonates with cyanosis shold be started on PGE1 and balloon valvuloplasty performed.
  • Ballon valvuloplasty is the procedure of choice for PS.
    • Pressure gradient >40mmHg
    • Pressure gradient 30-39mmHg procedure may be reasonable.
    • Symptoms (angina, syncope or pre-syncope) with gradient >30mmHg.
  • Surgical valvulotomy if balloon vavuloplasty unsuccessful, dysplatic valves.
  • Stenosis in main PA requires patch widening.
28
Q

Complications of balloon valvuloplasty in PS.

A
  • PR in 10-40%
  • Pressure gradient from hypertrophied infundibulum - use propanolol to reduce hyperdynamic response.
29
Q

Follow-up of PS post-operatively?

A
  • Periodic ECHO to detect worsening or recurrence of stenosis.
30
Q

Is exercise restriction required in PS?

A

Only in severe disease.

31
Q

What are differentials for LLSE murmur?

A
  • VSD
  • TOF - VSD murmur, RVH
  • TR - PSM, hepatomegaly, RAE if severe. RBBB, RAH
  • AVSD - PSM (similar to VSD), often associated diastolic murmur (functional stenosis of AV valve). Gallop rhythm common, all chambers enlarged. Superior axs.
  • Subvalvular AS - ESM.
  • HOCM - ESM, increases with Valsalva. MR common. Double apex. LVH, deep Q V5, V6.
  • Still’s murmur.
32
Q

How is VSD severity graded?

A
  • Small (<0.5cm): loud =/- thrill with wide radiation ncl. in to back.
  • Moderate (>2:1): may have increased RR and Harrisons sulcus. No overt CHF. Narrowly split with loud P2(pulm. HTN) +/- mitral flow. L. sided dilatation on CXR. LVH on ECG.
  • Severe (>3:1): murmur softer, mitral flow murmur. RV heave. BVH and LAH. CHF and plethora.
33
Q

What are clinical manifestations of VSD?

A
  • Small VSD: asymptomatic with normal growth and development. Grade 2-5/6 regurgitant murmur, loudest at LLSE. Systolic thrill may be palpable at LLSE.
  • Large VSD: delayed growth and development. Recurrent chest infections. CHF and decreased exercise tolerance. Apical diastolic rumble due to functional stenosis of the MV.
  • Pulmonary vascular obstructive disease: cyanosis (Eisenmengers) and decreased level of energy.
34
Q

What is the natural history of VSD?

A
  • Spontaneous closure in 30-40%.
    • Most often trabecular and small.
    • Most often in the first year of life.
  • Large defects tend to become smaller with age.
  • Inlet and infundibular defects do not close spontaneously.
  • CHF develops in infants with large VSD at 6-8 weeks.
  • Pulmonary vascular obstructive disease may begin to develop as early as 6-12m in those with a large defect.
35
Q

What is the management of VSD?

A
  • Treat CHF with diuretics, afterload reducers and sometimes digoxin.
  • No exercise restriction in absence of PHTN.
  • Non-surgical closure for selected muscular VSD.
  • Surgical closure under cardiopulmonary bypass.
  • Qp/Qs >2:1 is an indication for closure.
  • Infants with growth retardation unresponsive to medical therapy should be operated at any age.
  • Large VSD and increasing PVR - operate ASAP.
  • Those that respond to medical therapy - operate 12-18m.
  • Asymptomatic operate 2-4y.
  • Contraindications: PVR/SVR >0.5, PVOD with R-L shunt.
36
Q

Follow-up of VSD repair.

A
  • Review every 1-2 year.
37
Q

Differentials for an apical murmur?

A
  • MR
  • MV prolapse - late systolic murmur, mid-systolic click.
  • AS - ESM and click - sometimes best heard at the apex.
  • HOCM with MR
  • Vibratory/innocent murmur
38
Q

What is the most common cause of MR?

A
  • Rheumatic heart disease (also AR).
  • Fibrosis of leaflets leads to shortening and MR.
39
Q

What are clinical manifestations of MR?

A
  • Usually asymptomatic, may have vague history of fatigue or palpitation.
  • S2 may be widely split due to shortening of LV contraction and early closure of AO valve.
  • Loud S3 is common.
  • Grade 2-4/6 regurgitant systolic murmur at the apex. Transmitted to the axilla.
  • Short low frequency diastolic murmur may be audible at the apex.
  • ECG normal in mild cases. LVH +/- LAH in severe disease.
  • CXR: LV and LA enlargement.
40
Q

Is exercise restriction required in MR?

A

Do not restrict activity in mild cases.

41
Q

How is severity assessed in MR?

A

Degree of LV dilatation directly proportional to severity.

42
Q

Management of MR

A
  • Afterlod reducing medications (ACE -)
  • Anticongestive therapy.
  • Valve repair preferred to replacement in Paeds.
    • Lower mortality and anticoagulation not required.
  • Valve replacement rarely required:
    • Life long anticoagulation
43
Q

Follow-up of MR.

A
  • ECHO every 6-12m before and after intervention.
  • Replacement with mechanical valve - anticoaulate with warfarin and aspirin.
  • Replacement with bio valve - aspirin alone adequate.
44
Q

Causes of AR?

A
  • Sclerosis of the aortic valve.
  • If of rheumatic origin almost always associated with MV involvement.
45
Q

Clinical manifestations of AR.

A
  • Mild: asymptomatic.
  • Severe: reduced exercise tolerance with angina and CHF. Hyperdynamic praecordium, wide pulse pressure, water hammer pulse.
  • High pitched decrescendo diastolic murmur at 3/4 left intercostal space.
  • Louder with sitting forward.
  • The longer the murmur the more severe.
  • Mid-diastolic mitral rumble (Austin Flint) may be present at the apex if AR severe.
46
Q

What are the ECG findings in AR?

A
  • Mild: no change.
  • Severe: LVH +/- LAH
47
Q

Management of AR

A
  • Varying degrees of activity restriction required.
    • Aerobic exercise preferred. Weight lifting etc increases AR.
  • ACE inhibitors reduce dilatation and hypertrophy.
  • CHF: digoxin, diuretics and ACE inhibitor may be temporarily beneficial.
  • Antibiotic prophylaxis.
  • Surgery indicated for those that are symptomatic, LV function <0.5, asymptomatic with progressive LV enlargment.
  • Aortic repair favoured over valve replacement.
  • Mechanical valves - anticoagulation, biovalves - short life span.
  • Ross procedure.
48
Q

Follow-up of AR.

A
  • Every 6-12m with ECHO pre and post-intervention.
  • Anticoagulation for mechanical valves (warfarin and aspirin).
  • Bioprosthesis and no risks - aspirin only.
  • No anticoagulation following Ross procedure.

FRACP Paeds Clinical (9 decks)

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