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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
What is the natural history of PS?
26
What are the ECG findings of PS?
* Mild: normal. * Moderate: RAD and RVH. * Severe: RAH and RVH with strain pattern.
27
How is PS treated?
* 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
Complications of balloon valvuloplasty in PS.
* PR in 10-40% * Pressure gradient from hypertrophied infundibulum - use propanolol to reduce hyperdynamic response.
29
Follow-up of PS post-operatively?
* Periodic ECHO to detect worsening or recurrence of stenosis.
30
Is exercise restriction required in PS?
Only in severe disease.
31
What are differentials for LLSE murmur?
* 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
How is VSD severity graded?
* 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
What are clinical manifestations of VSD?
* 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
What is the natural history of VSD?
* 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
What is the management of VSD?
* 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
Follow-up of VSD repair.
* Review every 1-2 year.
37
Differentials for an apical murmur?
* 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
What is the most common cause of MR?
* Rheumatic heart disease (also AR). * Fibrosis of leaflets leads to shortening and MR.
39
What are clinical manifestations of MR?
* 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
Is exercise restriction required in MR?
Do not restrict activity in mild cases.
41
How is severity assessed in MR?
Degree of LV dilatation directly proportional to severity.
42
Management of MR
* 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
Follow-up of MR.
* 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
Causes of AR?
* Sclerosis of the aortic valve. * If of rheumatic origin almost always associated with MV involvement.
45
Clinical manifestations of AR.
* 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
What are the ECG findings in AR?
* Mild: no change. * Severe: LVH +/- LAH
47
Management of AR
* 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
Follow-up of AR.
* 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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