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PACES 2024 > Station 3: Cardiology > Flashcards

Station 3: Cardiology Flashcards

1
Q

Murmur of Mitral Stenosis?

A

Mid diastolic murmur heard loudest over apex in the left lateral position
- low pitched rumbling
- auscultated with bell
- loudest on expiration

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2
Q

how to grade intensity of murmur?

A
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3
Q

Heart sounds in mitral stenosis?

A

Loud S1 with opening snap

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4
Q

Apex beat in mitral stenosis?

A

Tapping apex beat

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5
Q

Complications to always mention in examination of any valvular murmur?

A
  • LV Failure: bibasal crepitations
  • Pulmonary hypertension: Loud P2, parasternal heave, functional TR, functional PR (Graham steel murmur)
  • RV failure: Raised JVP, pedal oedema
  • any stigmata of IE
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6
Q

Pulse in Mitral stenosis?

A

usually in AF

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7
Q

signs that suggest severe mitral stenosis?

A

Soft S1 - indicates immobile valve cusps
Early opening snap - increased LA pressure
Longer murmur
Graham steel murmur of pulmonary regurgitation

Presence of Pulmonary HTN/ LVF

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8
Q

ECG in mitral stenosis?

A

ECG: AF, P mitrale (L Atrial hypertrophy, P pulmonale (R atrial hypertrophy in Pulmonary HTN)

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9
Q

Ix in valvular murmurs?

A

Ix to diagnose, assess severity and complications

ECG, CXR, Echo, Coros

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10
Q

CXR in Mitral stenosis?

A

LA dilatation: splaying of the carina (increase of the tracheal bifurcation angle to over 90 degrees)

Pulmonary congestion: upper lobe diversion, dilated pulmonary trunks, kerly B lines, perihilar infiltrates

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11
Q

Echocardiogram in mitral stenosis?

A

Severe: mitral valve < 1cm2
Transvalvular gradient > 10mmHg

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12
Q

Murmur of mitral regurgitation?

A

pan systolic murmur
- best heard over the apex
- loudest on expiration
- radiation to axilla (anterior leaflet), can radiate to carotid for posterior leaflet

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13
Q

heart sounds in mitral regurgitation?

A

Soft S1
S3

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14
Q

Apex beat in mitral regurgitation?

A

Displaced and thrusting

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15
Q

Pulse in mitral regurgitation?

A

Usually AF
May get a jerky pulse

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16
Q

Signs suggesting severe mitral regurgitation?

A

Soft S1
S3
Displaced thrusting apex
AF
presence of LVF

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17
Q

ECG findings in mitral regurgitation?

A

AF (wont have p waves)

if in sinus:
p mitrale (LAH)
p pulmonale (RAH in pulmonary HTN)

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18
Q

CXR in mitral regurgitation?

A

look for
LA dilatation: splaying of carina

Pulmonary congestion

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19
Q

Echo for mitral regurgitation

A

do echo with doppler for regurgitation

Severe
EF < 60%
LVESD > 45mm

can also look for cause, complications e.g IE

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20
Q

Murmur of aortic stenosis?

A

Ejection systolic murmur
- heard loudest over aortic region
- louder on expiration
- radiation to carotids

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21
Q

heart sounds in aortic stenosis?

A

Soft and delayed S2
Paradoxical split of S2
S4

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22
Q

apex beat in aortic stenosis?

A

Heaving, not displaced

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23
Q

pulse in aortic stenosis?

A

low volume, slow rising pulse

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24
Q

clinical signs that suggest severe aortic stenosis?

A

low volume slow rising pulse
heaving apex
soft S2, paradoxical splitting of S2, S4
early ejection click
long murmur, late peak
thrill
complications of LVF/pulm HTN

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25
Q

ECG in Aortic stenosis?

A

LVH, LBBB
1st degree heart block

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26
Q

cxr in Aortic stenosis?

A

cardiomegaly,
pulmonary congestion
calcified aortic valve

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27
Q

echo findings of severe aortic stenosis?

A

Valve area < 1 cm2 (if less than 0.7 cm2 = critical)

Transvalvular gradient:
> 50 mmHg
if > 80 mmHg = critical

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28
Q

murmur in aortic regurgitation?

A

early diastolic murmur
- loudest in the lower left sternal edge
- loudest in expiration
- with patient leaning forward

may be associated with austin-flint murmur:
aortic regurgitant jet impinging on the anterior mitral valve leaflet leading to functional mitral stenosis

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29
Q

what is an austin flint murmur?

A

aortic regurgitant jet impinging on the anterior mitral valve leaflet leading to functional mitral stenosis

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30
Q

what is graham steel murmur?

A

functional murmur of pulmonary regurgitation due to high pulmonary arterial pressures

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31
Q

heart sounds in aortic regurgitation?

A

S1S2

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32
Q

apex beat in aortic regurgitation?

A

displaced, thrusting

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33
Q

pulse character in aortic regurgitation?

A

collapsing pulse

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34
Q

peripheral signs in aortic regurgitation?

A

quicke’s (nail)
corrigans (carotids)
mullers (uvula)
de mussets (head)
duroziez’s (bruit heard over femoral artery with light compression)
traubes (pistol shot over femorals)

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35
Q

signs of severe aortic regurgitation?

A

wide pulse pressure
long murmur
S3
Austin flint murmur (AR jet causing functional MS)
LVF

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36
Q

ecg in aortic regurgitation?

A

T wave inversions in lateral leads
LVH

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37
Q

CXR in aortic regurgitation?

A

dilated pulmonary trunk

LV enlargement, cardiomegaly
prominent aortic root with valvular calcification

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38
Q

Echo findings in aortic regurgitation?

A

severe:
Aortic root > 55mm
LVESD > 55 mm
EF < 55%

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39
Q

IE Prophylaxis in patients with valvular stenosis/ regurgitation?

A

good dental hygiene
no need for antibiotic prophylaxis if no previous IE

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40
Q

Medical management of mitral stenosis/ mitral regurgitation?

A

treat CVRF
regular follow up with echo

manage AF: rate and rhythm control, anticoagulation

Cardiac failure: diuretics
ACEi, BB, Spironolactone and digoxin as with HF guidelines

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41
Q

Surgical management of mitral stenosis?
indications

A

1) symptomatic + severe

Asymptomatic + severe with:
1) high thromboembolic risk:
> history of systemic embolism
> new onset or pAF
> dense spontaneous contrast in LA

2) high risk haemodynamic compromise
> PASP >50mmHg at rest
> desire for pregnancy
> need for major non cardiac surgery

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42
Q

surgical options for mitral stenosis?

A
  1. Percutaneous balloon mitral commisurotomy (PBMC) generally preferred over valve replacement
  2. valvuloplasty
  3. valve replacement
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43
Q

DDx of mitral stenosis (mid diastolic murmur)

A

Atrial myxoma
LV thrombus
Austin flint murmur secondary to aortic regurgitation

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44
Q

causes of mitral stenosis?

A

rheumatic heart disease (>90%)

Others
Degenerative - mitral annular calcification
Radiation associated valve disease
IE
LA myxoma
congenital parachute valves

rare: carcinoid syndrome, connective tissue diseases (SLE, RA)

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45
Q

indications for surgical management of mitral regurgitation?

A
  1. Symptomatic severe

or asymptomatic but severe and
2. EF <= 60%
3. LV end systolic diameter >= 40 mm
4. new onset AF,
5. PASP (pulmonary arterial systolic pressure) >50mmHg

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46
Q

DDx of Mitral regurgitation (PSM)?

A

VSD
Tricuspid regurgitation

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47
Q

Causes of mitral regurgitation?

A

ischaemic heart disease
- dilated cardiomyopathy
- chordae tendinae rupture or dysfunction post MI

mitral valve prolapse
rheumatic heart disease
infective endocarditis
connective tissue diseases: Marfans, Ehlers Danlos, Ankylosing spondylitis
Autoimmune: SLE
Previous valvotomy for MS

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48
Q

medical management of aortic stenosis?

A

treat CVRF
regular follow up with echo

statins
ACEi
Advise patient to watch for symptoms

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49
Q

indications for surgical management of aortic stenosis?

A

1) symptomatic, severe
2) Asymptomatic:
Area < 0.6
Hypotension with exercise
VT
LV Systolic dysfunction
LVH > 15 mm
3) moderate AS but going for surgery

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50
Q

Ddx of Aortic stenosis (ESM)?

A

Aortic sclerosis
HOCM
Supravalvular aortic stenosis
Aortic flow murmur

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51
Q

causes of aortic stenosis?

A

denenerative calcification
congenital bicuspid valves
rheumatic heart disease

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52
Q

what is aortic sclerosis?

A

thickening/ calcification of the aortic valves without outflow obstruction

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53
Q

medical management of aortic regurgitation

A

treat CVRF
regular follow up with echo

Medications to manage HF as per HF guidelines

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54
Q

indications for surgical management of aortic regurgitation?

A

Acute

Or

symptomatic + severe

Or
Asymptomatic + severe +
1) LVEF <= 50%
2) LV ESD > 50 mm
3) going for other cardiac surgery eg CABG

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55
Q

DDx of aortic regurgitation (EDM)

A

Pulmonary regurgitation

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56
Q

causes of aortic regurgitation?

A

Most commonly:
Degenerative calcific
Bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis

———
acute:
aortic dissection
infective endocarditis
ruptured sinus of valsava
trauma

chronic
Most common:
- valvular: degenerative calcific, rheumatic heart disease, congenital bicuspid valve (assoc with CoA)
- aortic ring dilatation: aortitis (syphilis), marfans, connective tissue disease eg RA, AS

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57
Q

how to complete examination in aortic regurgitation?

A

examine for underlying aetiology e.g. connective tissue diseases (marfans, ehler danlos), ankylosing spondylitis

BP: wide pulse pressure

other signs of aortic regurgitation

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58
Q

murmur of ASD

A

fixed splitting of S2 (delayed closure of PV)
ESM at upper left sternal edge (increased flow across PV)

+/- PSM at LLSE (functional TR from RV volume overload)
+/- Mid diastolic murmur at apex (Acquired MS ~Lutembacher’s syndrome)

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59
Q

heart sounds in ASD?

A

Loud P2
fixed splitting of S2

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60
Q

apex beat in ASD/ VSD?

A

displaced, thrusting

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61
Q

peripheral clinical signs in ASD/ VSD?

A

central cyanosis, clubbing

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62
Q

Murmur in VSD?

A

harsh pan systolic murmur
lower left sternal edge

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63
Q

heart sounds in VSD?

A

Loud P2

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64
Q

Complications of ASD/ VSD?

A

pulmonary hypertension
displaced apex (LVF)

Eisenmengers syndrome:
eventually developing cyanotic right to left shunt

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65
Q

ECG of ASD/ VSD?

A

LVH
Biventricular hypertrophy
Left atrial hypertrophy/ enlargement

if pulm HTN present: RVH, p pulmonale

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66
Q

CXR of ASD/ VSD?

A

Cardiomegaly
pulmonary congestion

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67
Q

Echo findings in ASD/VSD?

A
  • to confirm diagnosis
  • localise, determine size and direction of shunt

LV and RV hypertrophy
PASP

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68
Q

Coronary catheterization for ASD/VSD?

A

can see severity and direction of shunt

to check for reversibility for pulmonary hypertension with vasodilator therapy

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69
Q

treatment of ASD/ VSD?

A

small defects: reassurance

larger defects with pulmonary hypertension:
- duretics for CCF
- treatement for pulmonary HTN
- VSD closure if no contraindication (VSD closure can be done if pHTN is reversible)

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70
Q

Causes of VSD?

A

congenital:
- syndromes: Down, Edwards

Acquired:
- ischaemia
- iatrogenic

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71
Q

murmur of HOCM?

A

ESM loudest at LLSE
- accentuated by standing or valsalva (Decreased venous return worsens LTOT obstruction)

+/- PSM apex radiating to axilla (may have mitral regurgitation due to systolic anterior motion of the mitral valve and significant LV outflow gradients)

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72
Q

apex beat in HOCM?

A

double apical impulse
(presystolic atrial contraction)

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73
Q

pulse character in HOCM?

A

jerky bifid pulse (pulsus bisferiens)

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74
Q

complications of HOCM?

A

syncope
angina
arrhythmias
cardiac arrest

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75
Q

ECG findings in HOCM?

A

25% normal

LVH
deep TWI anterior lateral leads
Deep Q infero- lateral leads

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76
Q

Echo findings in HOCM?

A

asymmetrical septal hypertrophy
SAM (Systolic anterior motion) of the anterior MV leaflet
Diastolic dysfunction

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77
Q

treatment of asymptomatic HOCM?

A

education and genetic counselling
- screen family (1st degree relatives) with ECG and echo
- lifestyle advice: avoid strenuous exercise

asymptomatic: just clinical observation and follow ups with echo

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78
Q

medical therapy of HOCM?

A

aimed at symptom relief:
e.g SOB, lethargy, syncope, angina attributable to LVOT obstruction

1) beta blockers

2nd line: verapamil, diltiazem (non-dihydropyridine CCBs)

3) BB + disopyramide

tx complications of CCF, AF
prevention of sudden death: amiodarone, dual chamber pacing

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79
Q

options for septal reduction surgery in HOCM?

A

surgical myectomy, septal ablation with alcohol

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80
Q

what therapies to avoid in hocm?

A

therapies that may increase LVOT obstruction
through peripheral vasodilation, intravascular volume depletion, or increasing myocardial contractility

e.g CCB (nifedipine, amlodipine), nitroglycerin, ACEi/ARB, digoxin

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81
Q

murmur finding in coarctation of aorta?

A

ESM aortic region radiates to thoracic spine

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82
Q

apex beat in coarctation of aorta?

A

heaving, undisplaced

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83
Q

peripheral clinical signs of coarctation of aorta?

A

radial radial delay (between brachiocephalic and left subclavian)

radial femoral delay (stenosis distal to left subclavian)

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84
Q

complications of coarctation of aorta?

A

hypertension
hypoplasia of lower limbs
LVF
endocarditis

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85
Q

ecg findings in coarctation of aorta?

A

LVH
p mitrale (LA hypertrophy)

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86
Q

CXR of coarctation of aorta?

A

rib notching
cardiomegaly
pulmonary congestion
prominent aortic knuckle
3 sign: upper bulge due to dilatation of left subclavian artery and lower bulge formed by post stenotic dilatation of aorta

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87
Q

echo findings in coarctation of aorta?

A

assess aorta
LV function
outflow tract pressure gradient
screen for other cardiac defects

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88
Q

cardiac catheterization in coarctation of aorta?

A

confirm diagnosis, measure peak gradients across the defect

demonstrate deficit/ presence of collaterals

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89
Q

treatment of coarctation of aorta?

A

surgery:
- resection
- patch aortoplasty
- left subclavian flap angioplasty

catheter based intervention:
- balloon angioplasty
- stent insertion

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90
Q

midline sternotomy scars?

A

CABG
prosthetic Valve replacement
Valve repair/ annuloplasty
surgery for congenital cyanotic heart disease
cardiac transplant

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91
Q

Lateral thoracotomy scar?

A

Mitral valvotomy (think of MS complicated by MR)
BT shunt (Tetralogy of Fallot)
Coarctation of aorta repair
PDA ligation

respiratory:
lobectomy, pneumonectomy, wedge resection, bullectomy
lung volume reduction surgery
lung transplant

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92
Q

Cyanosis +/- clubbing?

A

cyanotic heart disease: ToF
Eisenmenger’s
IE
Severe pulmonary hypertension

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93
Q

prominent neck pulsations?

A

aortic regurgitation
tricuspid regurgitation (dilated CMP, carcinoid, IE, congenital TR in ebsteins anomaly)

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94
Q

parasternal heave/ palpable P2?

A

pulmonary hypertension -> could be 2’ cardiac (MS/MR/AR) or lung pathology (cor pulmonale)

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95
Q

heart murmurs due to congenital heart disease?

A

ASD
VSD
PDA
Coarctation
PS
PR

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96
Q

presentation of cardiovascular examination

A
  1. chest signs
  2. pulmonary hypertension
  3. CCF
  4. pulse
  5. signs of IE
  6. rheumatological signs
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97
Q

what causes third heart sound?

A

rapid filling of the LV from the large volume of blood from the LA occuring in early diastole

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98
Q

what congenital conditions can be associated with Mitral regurgitation?

A

corrected transposition of great arteries (TGA)
partial AV canal
Ostium primum atrial defect (cleft mitral valve)

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99
Q

why may pulse be jerky in mitral regurgitation?

A

pulse is sharp and abbreviated due to lack of sustained forward stroke volume with a reduced systolic ejection time because of regurgitant leak into the LA

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100
Q

how do you differentiate an MDM from severe MR vs MS?

A
  • MS has opening snap
  • severe MR associated w S3
  • MS murmur is longer
  • MS has loud S1
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101
Q

how do you differentiate between MR and TR murmur?

A
  • MR louder on expiration, TR louder on inspiration
  • Radiation towards axilla (MR), towards right of sternum (TR)
  • JVP: normal in MR, giant V waves with pulsatile liver in TR
  • apex beat: MR (displaced), TR (not displaced)
  • pulse: jerky (MR), normal (TR)
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102
Q

how to differentiate between MR and VSD murmur?

A

loudest at apex (MR), LLSE (VSD)
high pitched murmur (MR), harsh/low pitched (VSD)
S1: Soft (MR), normal (VSD)

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103
Q

how does respiration affect murmurs?

A

murmurs on the right louder on inspiration due to increased venous return and blood flow to right side of the heart

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104
Q

how does valsalva manouevre affect murmurs?

A

valsalva decreases preload

straining phase:
reduced systemic return, reduced filling of right and left heart chambers, SV and BP drops

most murmurs become softer and shorter except for

1) HOCM - murmur louder as LV volume reduced
2) MVP - murmur longer and louder

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105
Q

how does squatting affect murmurs?

A

squatting increases venous return and systemic arterial resistance

most murmurs are louder

HOCM: systolic murmur softer, outflow obstruction is reduced as LV size increases

MVP: click occurs later and murmur shorter as LV size increased

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106
Q

how does standing affect murmurs?

A

most murmurs softer

except
HOCM - louder
MVP- louder and longer

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107
Q

how do isometric exercises affect murmurs?

A

increases afterload

AS- softer murmur due to reduction of pressure gradient across the valve
HOCM - softer
MVP: shorter murmur, later click

MR, AR, VSD louder

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108
Q

how to diagnose IE?

A

dukes criteria
- 2 major, 1 major + 3 minor, or 5 minor

Major:
- + blood c/s with typical organism (need at least 2 or more positive cs), typical organism (strep viridans, bovis, enterococcis, staph aureus, HACEK)
- endocardial involvement with positive echo for vegetations/abscess/valve perforation/dehiscence or new valvular regurgitation

minor:
- predisposing heart condition
- fever
- vascular phenomenon
- immunologic phenomenon (GN, roth spots, osler nodes)
- positive c/s not satisfying major criteria
- positive echo not satisfying major criteria

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109
Q

Surgical Treatment of IE?
indications

A
  • heart failure
  • failure of medical therapy
  • valvular complications e.g. valvular abscess, valvular obstruction, rupture into the pericardium, septal formation, fistula
  • fungal endocarditis
  • prosthetic valves esp if unstable or early (< 60 days) or cause by S aureus
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110
Q

failure of medical therapy in IE?

A

1) presence of fever and inflammatory syndrome after 1 wk of appropriate and adequate abx
2) presence of mobile vegetation > 10 mm with 1 major embolism after 1 wk of abx
3) presence of mobile vegetation > 15 mm after 1 wk of abx

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111
Q

when and how would u initiate prophylaxis against IE?

A

High risk patients + Orodental procedures

prosthetic valves (mechanical + bioprosthetic), prev IE, congenital cyanotic heart disease (unrepaired cyanotic or repaired with shunt), ventricular assist device, cardiac transplant

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112
Q

prophylactic antibiotics against IE for orodental procedures

A

to prevent streptococcal IE from oral -dental sources

amoxicillin / ampicillin / cefazolin, ceftriaxone

if pen allergic: azithromycin/ cephlexin/ doxycycline, cefazolin/ ceftriaxone

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113
Q

what causes an opening snap?

A

opening of a stenosed mitral valve and indicates that leaflets are pliable

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114
Q

why is the first heart sound loud in mitral stenosis?

A

mitral valve is held open during diastole by transmitral gradient
- valve suddenly slammed shut during ventricular contraction

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115
Q

Management of rheumatic fever?

A

primary prevention:
IM Ben Pen or 10 days of Pen V

Secondary prevention: patients w history of Rheumatic fever should receive prophylaxis
IM Pen G once/ month or Pen V daily

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116
Q

what is ortner’s syndrome?

A

Hoarseness of voice from compression of the left recurrent laryngeal never from an enlarged left atrium

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117
Q

what is Lutembacher’s syndrome?

A

association of MS with ASD

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118
Q

what is the normal cross sectional area of the mitral valve?

A

4-6 cm2

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119
Q

what is a significantly stenosed mitral valve?

A

< 1 cm2 and > 10mmHg gradient across the valve

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120
Q

what conditions to satisfy to qualify for balloon commissurotomy/ valvuloplasty for mitral stenosis?

A
  • no LA thrombus
  • minimal calcification
  • no or mild MR
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121
Q

in which trimester does pregnancy result in symptomatic MS?

A

2nd trimester due to increase in blood volume

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122
Q

what causes a mid systolic click?

A

inability of the papillary muscles or the chordae tendinae to tether the mitral valves in the late stages of systole -> the prolapsing of the valve leaflet into the LA and sudden tensing of the mitral valve apparatus causes the mid systolic click

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123
Q

causes of mitral valve prolapse?

A

myxomatous degeneration of the mitral valve tissue

associated with
- ASD
- Cardiomyopathy
- Myocarditis

systemic conditions:
marfans
ehlers danlos
osteogenesis imperfecta
PCKD
SLE

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124
Q

what maneouvres accentuate mitral valve prolapse?

A

standing up, valsalva manouevre

-> these decrease preload, and cardiac volume
-> further impairing the papillary muscles from maintaining tension on the leaflets
-> systolic click occurs earlier with a longer duration of the systolic murmur

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125
Q

how may patients with mitral valve prolapse present?

A

asymptomatic

or

symptomatic: palpitations, anxiety, atypical chest pain, light headedness

complications of mitral regurgitation:
CCF, IE, arrhythmias, embolic phenomenon

sudden death

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126
Q

ix of mitral valve prolapse?

A

to confirm diagnosis and look for complications of mitral regurgitation

127
Q

management of mitral valve prolapse?

A

education and reassurance

medical:
- may need antibiotic prophylaxis if MVP associated with MR
- palpitations: Beta blockers
- tx underlying cause of associations
- tx complications: AF, CCF, IE

surgery: indications as per Mitral regurgitation

128
Q

causes of mixed mitral valve disease (ie. stenosis and regurgitation)

A

rheumatic heart disease

MS with valvotomy done that has been complicated by MR

129
Q

what is the significance of a third heart sound in mixed mitral valve disease?

A

presence of S3 implies no significant MS

130
Q

what are the frequencies of valvular involvement in rheumatic heart disease?

A

MV - 80%
AV - 50%
Mixed MV and AV - 20%
TV - 10%
PV - 1%

131
Q

Causes of a collapsing pulse?

A

Aortic regurgitation
PDA
ruptured aneurysm of the aortic sinus
active paget’s
high fever
severe anaemia
pregnancy

132
Q

BP in aortic regurgitation?

A
  • wide pulse pressure
  • severe hypertension
  • UL and LL discrepancy with systolic in LL > UL = Hill’s sign
133
Q

How to differentiate austin flint murmur from mitral stenosis?

A

opening snap
loud S1
tapping apex beat, which is not displaced

134
Q

Prognosis of aortic regurgitation?

A

4% develop symptoms, CCF or both annually

135
Q

how to differentiate between ESM in Aortic stenosis and HOCM?

A

HOCM - volume increases with valsalva and with standing
- decreases with squatting

136
Q

what does a normal pulse volume in AS mean?

A

transvalvular gradient < 50 mmHg

137
Q

what does a palpable systolic thrill imply in aortic stenosis?

A

transvalvular gradient > 40 mmHg

138
Q

what does the second heart sound indicate about the aortic stenosis?

A

soft S2 means poorly mobile and stenotic valve

S2 normally created by closure of aortic then pulmonary valve. if closure of aortic valve is delayed enough, it may close after pulmonary, creating paradoxical splitting of S2

normal S2 implies insignificant stenosis

139
Q

what is the Gallavardin phenomenon?

A

systolic murmur in Aortic stenosis may radiate towards the apex, which may be confused with a MR murmur

140
Q

how may haemolytic anaemia result from aortic stenosis?

A

MAHA from severely calcified aortic valve

141
Q

why may patients get syncope in aortic stenosis?

A
  • cardiac arrhythmias
  • peripheral vasodilation e.g. post exercise without concomitant increase in cardiac output
  • transient electromechanical dissociation
142
Q

young patient with AS murmur but normal aortic valve?

A

supravalvular stenosis
- can be isolated or assoc w Williams syndrome

subvalvular stenosis

143
Q

williams syndrome

A

inherited auto dominant disorder

elfin facies
hypertension
mental impairment
cardiac lesions: supravalvular stenosis, pulmonary stenosis

144
Q

what is a wide/ narrow pulse pressure?

A

normal - 40 mmHg
Wide > 60
Narrow < 25

145
Q

causes of a mixed aortic valvular lesion?

A

rheumatic heart disease
bicuspid aortic valve

146
Q

on detecting central cyanosis and clubbing, what to examine?

A
  • differential cyanosis and clubbing (ULs/ LLs/ unilateral LL)
  • look for weak L radial pulse (BT shunt)
  • shunt scar (BT shunt)

auscultation:
- Eisenmenger: ASD/VSD/PDA, no PS. pulm HTN
- Tetralogy of Fallot: PS murmur, no pulm HTN but has RVH

147
Q

how to differentiate between ASD / VSD / PDA in terms of heart sounds

A

ASD: fixed splitting S2
VSD: single S2
PDA: reversed spitting S2

148
Q

How to differentiate Tetralogy of Fallot vs Eisenmenger’s syndrome?

A

ToF has PS murmur with a systolic thrill and a soft P2

ToF has no pulmonary hypertension

149
Q

Characteristic findings of a patent ductus arteriosus?

A

collapsing pulse
continuous “machinery” murmur heard best just below the left clavicle and radiates to the back
-> murmur heard louder during systole > diastole

150
Q

DDx of continuous murmur?

A

Collapsing pulse:
- PDA
- MR with AR
- VSD with AR

No collapsing pulse:
- BT shunt
- Venous hum (right of sternum, children, disappears when lying flat or right JVP occluded)

151
Q

What is Tetralogy of Fallot?

A

congenital heart condition comprising of:
VSD
RVH
Overriding aorta
RV outflow obstruction: Pulmonary stenosis

152
Q

indications for anticoagulation in ASD?

A
  • AF
  • evidence of bidirectional shunting to prevent strokes from paradoxical emboli
153
Q

indications for surgical closure of ASD?

A
  • early childhood: closure recommended at 5-10 years of age to prevent complications
  • large ASDs or pulmonary to systemic flow ratio > 2

*closure prevents pulm HTN and right HF but does not alter incidence of AF

154
Q

types of ASD?

A
  1. ostium secundum type (90%): foramen ovale defect with no valvular involvement
    > most are asymptomatic
    > if small< 2 cm, normal life expectancy with no symptoms
    > larger defects may present in 20s/30s with dyspnoea/fatigue
  2. ostium primum type (10%): anterior and inferior aspect with involvement of mitral and tricuspid valves
  3. sinus venosus type: defect in the septum just below the entrance of SVC
155
Q

how do patients present with ASD?

A
  • asymptomatic

or

symptomatic:
fatigue
dyspnoea
right HF
AF from atrial dilation
recurrent pulmonary infections
IE
paradoxical emboli

+ in ostium primum defects: syncope (Heart block)

156
Q

ASD murmur + MR/TR or VSD murmur?

A

ostium primum type ASD which can involve mitral and tricuspid valves

157
Q

ASD + mitral Mid diastolic murmur?

A

Lutembacher’s syndrome, possible iatrogenic ASD due to previous mitral valvulotomy

158
Q

ASD + tricuspid Mid diastolic murmur + pulmonary ESM

A

increased flow of blood through the pulmonary and tricuspid valve due to left to right shunting of blood via the ASD

159
Q

Why may S2 be split normally?

A

can happen physiologically during inspiration because the increase in venous return results in prolonged right heart emptying, thus a delay in P2

160
Q

wide splitting of S2 in ASD?

A

RV continuously overloaded because of L>R shunt, producing a widely split S2 with delayed P2

161
Q

how to differentiate between a flow murmur through the pulmonary valve vs a PS murmur?

A

PS murmur is associated with soft delayed P2 that varies with respiration

162
Q

what is holt-oram syndrome?

A

ASD secundum type
Hypoplastic thumb with accessory phalanx
hypoplastic radius
autosomal dominant

163
Q

where do collaterals arise in coarctation of aorta?

A
  • internal mammary to external iliac
  • spinal and intercostal arterires to descending aorta (notching on CXR)
164
Q

what cardiac conditions are associated with aortic coarctation?

A

bicuspid aortic valves (50%)
patent ductus arteriosus
VSD

165
Q

what other conditions cause rib notching?

A

BT shunt
subclavian artery obstruction
SVC syndrome
neurofibromatosis
AV malformation of lung and chest wall

166
Q

ECG in patent ductus arteriosus?

A

normal in small defects

LVH, RVH, p mitrale
Pulmonary hypertension: Right axis deviation, p pulmonale

167
Q

CXR in patent ductus arteriosus?

A
  • cardiomegaly, LA and LVH
  • pulmonary plethora initially
  • pulmonary hypertension later with prominent pulmonary trunks, rapid tapering of the peripheral pulmonary arteries and oligaemic lung fields
  • CCF
168
Q

management of patent ductus arteriosus?

A

conservative management:
- prostaglandin inhibitors (IV indomethacin, ibuprofen) in neonates
- diuretics for congestive symptoms

surgical management: percutaneous device or open surgery
-> usually considered if there LV overload or RV pressure overload

169
Q

what is a patent ductus arteriosus?

A
  • part of fetal circulation, maintained by prostaglandin E
  • connection between pulmonary artery to the aorta distal to the origin of left subclavian artery
  • usually functionally closes by 15h of life
170
Q

complications of patent ductus arteriosus?

A

LV dysfunction
pulmonary HTN/ eisenmengers
ductal aneurysm and calcification/ rupture

171
Q

causes of PDA?

A

prematurity
low birth weight
maternal use of prostaglandin antagonists like NSAIDs
maternal alcoholism, phenytoin use, rubella

172
Q

indications for surgical closure of VSD?

A

evidence of pulmonary hypertension or CCF
Right to left flow ratio > 2
recurrent IE
cx by Aortic regurgitation
Acquired cause e.g. rupture of septum from MI

173
Q

contraindication for surgical management of VSD?

A

development of eisenmengers

174
Q

causes of VSD?

A

congenital: maternal diabetes, alcoholism, syndromes including down’s, edwards, patau’s, di george’s

acquired: post MI, trauma/iatrogenic (complication of alcohol septal ablation, RV pacing with septal puncture)

175
Q

what conditions in which VSD is a part of?

A
  • Tetralogy of Fallot
  • Truncus arteriosus
  • AV canal defects
  • DORV (double outlet RV)
176
Q

How do you differentiate an isolated VSD with one that is associated with Tetralogy of Fallot?

A
  • Clubbing and central cyanosis (VSD with Eisenmengers)
  • Pulmonary thrill, Pulmonary stenosis murmur
177
Q

how do you differentiate VSD from HOCM?

A

ESM rather than PSM in HOCM
Apex not displaced, double apical impulse
Jerky pulse

178
Q

Complications of VSD?

A

Paradoxical embolism
Pulm HTN/ Eisenmenger’s
IE
Ventricular arrhythmias

179
Q

Ix in HOCM?

A

the usual ECG, CXR, Echo

Treadmill exercise test for symptoms/ BP response/ inducible arrhythmia/ myocardial ischaemia

Holter for arrhythmias

Right/left heart catheterisation: prior to alcohol septal ablation to assess coronary anatomy, for endomyocardial biopsy

180
Q

markers of severe HOCM on echocardiogram?

A

septal thickness > 18mm
outflow tract gradient > 40 mmHg at rest

181
Q

treatment in HOCM

A

aimed at symptom relief and prevention of sudden cardiac death

182
Q

pathophysiology of HOCM?

A
  • autosomal dominant
  • asymmetrical myocardial hypertrophy often involving interventricular septum leading to outflow tract obstruction
  • obstruction can be caused by asymmetrical septal hypertrophy and systolic anterior motion of mitral valve
183
Q

why is there a prominent ‘a’ wave in JVP for HOCM?

A

forceful atrial contraction against a non compliant RV

184
Q

why is there a double apical impulse in HOCM?

A
  • presence of LV heave with a prominent presystolic pulse caused by atrial contraction

DDx LV aneurysm

185
Q

what is the Brockenbrough-Braunwauld-Morrow sign?

A

reduced pulse pressure in the post extrasystolic beat occuring in HOCM and AS

186
Q

causes of HOCM?

A
  • familial
  • idiopathic
  • Friedrich’s Ataxia
187
Q

complications of HOCM?

A

Angina
arrythmia: AF, VT, sudden death
heart failure
MR
IE

188
Q

how would you predict poor outcome in HOCM?

A
  • family history of sudden death
  • history of syncope, cardiac arrest
  • drop in BP during exercise
  • holter monitoring with non sustained VT
  • echo findings: LV thickness > 30 mm
  • Particular genetic mutations e.g. myosin binding protein C and troponin T
189
Q

what dynamic manouevres increase HOCM murmur?

A

valsalva,
standing

190
Q

conditions associated with HOCM?

A

Friedrich’s ataxia
Fabry’s disease
WPW syndrome
Hereditary lentiginosis

191
Q

types of metallic valve prosthesis?

A

bileaflet or single leaflet tilting disc
ball and cage (phasing out)

192
Q

Anticoagulation INR target for different valve replacements?

A

Aortic valve: 2-3
Mitral valve: 2.5-3.5
Ball and cage (highest thrombogenic risk): 3.5-4.5

193
Q

complications of a metallic prosthetic valve?

A
  • valve leakage
  • haemolytic anaemia
  • IE
  • Thromboembolism
  • complications of anticoagulation
194
Q

Bridging anticoagulation for dental procedures for patients taking warfarin for metallic valve replacement?

A

depends on thrombogenic risk

usually can omit warfarin for 2-3 days if low thrombogenic risk, restart after procedure

if high thrombogenic risk: admit, monitor INR. start IV unfractionated heparin when INR below target range. Omit heparin before procedure. restart heparin and warfarin after bleeding has stopped

195
Q

prosthetic valves in pregnancy: option of anticoagulation?

A

don’t use warfarin. use clexane

196
Q

upper limbs findings in Marfan’s syndrome?

A

overall tall with disproportionately long limbs compared to trunk

arachnodactyly, hyperextensible joints: thumb sign
collapsing pulse (AR)
reduced extension of elbows

197
Q

facial findings in Marfan’s syndrome?

A

long head
high arched palate
iridodonesis
myopia
superolateral lens dislocation
blue sclera

198
Q

chest findings in marfans syndrome

A

pectus excavatum or carinatum
thoractomy scar (hx of repair of aortic aneurysm)
no gynaecomastia

199
Q

features to look for in Marfans syndrome pt when standing up?

A

kyphoscoliosis
pes planus
hyperextended knees
abdomen: inguinal or femoral hernia/ hernia scars

200
Q

cardiovascular / respiratory examination in Marfan’s

A

Mitral valve prolapse, Aortic regurgitation murmur

Pneumothorax: scars suggestive of chest tube or pleurodesis

201
Q

neuro examination in marfans syndrome

A

can examine LL for weakness/numbness secondary to dural ectasia

202
Q

DDx for patient with tall stature?

A
  • Marfan’ syndrome
  • Homocystinuria
  • MEN 2b: Marfanoid habitus
  • Klinefelter’s syndrome
203
Q

features of homocystinuria?

A

autosomal recessive inborn error of metabolism of amino acid

malar flush, mental retardation, inferomedial lens dislocation

cx epilepsy, IHD, DVT, osteoporosis

diagnosis: presence of homocystine in urine via cyanide-nitroprusside test

204
Q

what is marfan’s syndrome?

A

inherited autosomal dominant connective tissue disease

affects skeletal system, cardiovascular system with ocular abnormalities

205
Q

mode of transmission in marfans syndrome?

A

autosomal dominant
chromosome 15q21
fibrillin gene defect

206
Q

how is marfan’s syndrome diagnosed?

A

based on ghent criteria, taking into account:
family history
molecular studies
6 organ systems: skeletal, skin, eyes, CVS, pulmonary, dura (dura ectasia)

207
Q

ocular features of marfan’s syndrome

A

small spherical lens
cataracts
lens subluxation
glaucoma
hypoplasia of dilator papillae, therefore difficulty with pupillary dilatation
myopia
retinal detachment

208
Q

ix of marfans syndrome?

A

molecular studies
annual echo to monitor aortic diameter (normal < 40 mm) and MV function
ophthalmic examination

209
Q

mx of marfan’s syndrome?

A
  • education and psychological counselling
  • annual cardiology review: beta blockade to slow rate of aortic root dilatation, aortic root graft if Aortic root > 50 mm, IE prophylaxis
  • Eye review
210
Q

prognosis of Marfan’s syndrome?

A

death due to cardiovascular complications
- aortic dissection
- CCF 2’ Aortic regurgitation

life span ~mid 40s

211
Q

complications of pregnancy in marfan’s syndrome?

A

early premature abortion
death from aortic dissection (safe if aortic root < 40 mm)

212
Q

how would you counsel patient about marfans syndrome

A
  • affected individuals can transmit the condition to 50% of their offspring
  • emphasize variability of the disease, as an affected child may be more or less affected than the parent
213
Q

How do you assess hypermobility?

A

beightons’ 9 point scale
if 4 or more > joint laxity

214
Q

causes of hypermobile joints?

A
  • marfans syndrome
  • ehlers danlos syndrome
  • osteogenesis imperfecta
  • benign joint hypermobility syndrome (majority)
215
Q

causes of blue sclera?

A

marfans syndrome
ehlers danlos syndrome
Osteogenesis imperfecta
pseudoxanthoma elasticum
chronic steroid intake

216
Q

Men 2B?

A

phaeochromocytoma, medullary thyroid cancer, marfanoid, mucosal neuromas

217
Q

When to start medications in patient with newly diagnosed HTN?

A

If stage 2: always offer

If stage 1:

218
Q

Overall role of medications in valve disease?

A
  1. Treating symptoms/ complications of valve disease.
  2. Secondary prevention of cardiovascular risk factors.
  3. Palliation where intervention is not possible.
219
Q

Management of acute rheumatic fever

A

• Early IV antibiotics benzylpenicillin G or ceftriaxone. Follow on doses of 4- weekly IM benzylpenicillin
or oral penicillin V should be continued daily for up to 10 years or into adulthood after an episode of
ARF to reduce the risk of late complication with rheumatic heart disease.

• Acute carditis: oral prednisolone (1mg/ kg daily) to a maximum of 80 mg daily.
• Acute arthritis responds to high- dose aspirin

220
Q

Indication for surgical management of mitral valve prolapse

A

Surgical indication is when the left ventricle has dilated to an
end- systolic diameter of >4 cm.

Gold standard treatment for MVP with severe MR is by open surgical
repair

221
Q

Indications for surgery in native valve IE:

A
  • Heart failure with acute AR or MR
  • Annular or aortic root abscess (prolongation of PR interval on ECG)
  • Large (>10 mm) mobile vegetation or recurrent embolism
  • Fungal infection on culture
  • Persistent infection >10 days after starting antibiotics
    (fever, bacteraemia, leucocytosis)
222
Q

Indication for surgery in prosthetic valve IE?

A
  • heart failure
  • Annular or aortic root abscess (prolongation of PR
    interval on ECG)
  • Large (>10 mm) mobile vegetation or recurrent embolism
  • Staphylococcus aureus or fungal infection on culture
  • Persistent fever >10 days after starting antibiotics
  • Early PV IE ≤2 months after surgery
  • Prosthetic valvular dehiscence or dysfunction
223
Q

Concept of antibiotic regime for IE?

A

Aminoglycosides (e.g. gentamicin) synergize with cell wall inhibitors (e.g. benzylpenicillin) for bactericidal activity.

224
Q

Duration of abx in native valve vs prosthetic valve IE?

A

Prosthetic valve- at least 6 wks

Native valve- usually 4-6 wks

225
Q

recommendations for antibiotic prophylaxis in dental procedures?

A

European guidance:

  1. Prosthetic cardiac valves, including transcatheter-implanted prostheses and homografts.
  2. Prosthetic material used for heart valve repair, such as annuloplasty rings, chords or clips.
  3. Previous IE
  4. Unrepaired cyanotic congenital heart defect or repaired congenital heart defect, with residual shunts or valvular regurgitation at the site adjacent to the site of a prosthetic patch or prosthetic device.
  5. Cardiac transplant with valve regurgitation due to a structurally abnormal valve.

Good oral, dental and skin hygiene is recommended by all guidelines.

226
Q

Surveillance of family members of pt with HOCM?

A

First degree relatives of patients with HCM, should undergo lifelong surveillance (due to delayed age-
related penetrance), beginning in adolescence

227
Q

Risk factors for sudden cardiac death in patients with HOCM?

A

Non sustained VT on Holter monitoring (≥3 ventricular beats at >120 bpm, lasting <30 seconds is non- sustained VT)

Abnormal BP response to exercise:
Exercise testing: BP not
increasing by >25 mmHg

Septal thickness >30mm

FHx of 1st degree relative w sudden cardiac death <45yo

Hx of syncope

Resting LVOT gradient >30 mmHg

228
Q

Most sensitive ix for HOCM

A

Cardiac mri

Sensitivity for anatomical diagnosis approaches 100%

229
Q

Indication for ICD implantation in HOCM?

A

The presence of ≥2 risk factors for SCD is an indication for ICD implantation.

Or
If previous cardiac arrest

230
Q

treatment of myocarditis?

A

exclude reversible cuases:
angio to exclude coronary obstruction

inpatient monitoring during acute phase of inflammation

management of heart failure as per standard heart failure guidelines

endomyocardial biopsy if LV function not improving:
transvenous sampling through RV endocardium, immunohistochemistry of biopsy sample

immunosuppressant drugs (rarely needed)- guided by biopsy findings. e.g steroids, azathioprine, IFN-B

231
Q

NYHA (New York Heart Association) Functional classification of Heart Failure severity?

A

NYHA I - IV

I: no limitation of physical activity
II: Slight limitation
III: Marked limitation
IV: inability to carry out any physical activity without discomfort

232
Q

utility of ECG as investigation in heart failure?

A

tachyarrhythmia: may reflext the cause/ complication of heart failure

LVH/ HCM

Q waves: prev transmural infarction

conduction disease
heart block, LBBB -> may indicate benefit for biventricular pacing (cardiac resynchronisation therapy)

233
Q

utility of natriuretic peptides e.g BNP, NT-pro BNP in heart failure?

A

natriuretic peptides are non specific but very sensitive, so a normal level virtually excludes heart failure

234
Q

utility of echo in heart failure?

A

diagnosis and classification; HFrEF vs HFpEF

severity (EF)

Aetiology e.g. severe AS, RWMA

alternative diagnosis e.g. pulm HTN

235
Q

blood inx in chronic HF?

A

FBC - anaemia
RP - renal function, guides use of diuretics and K sparing agents e.g. ACEi, spironolactone
CVRF: lipid panel, Hba1c
TFTs

236
Q

management of heart failure?

A
  1. lifestyle modifications:
    graded exercise training, alcohol/smoking cessation, diet and nutrition, weight loss
  2. medical:
    HF -targeted treatment
    treat HTN/ DM/ HLD
  3. coros:
    PCI or bypass may be indicated where imaging demonstrates “viability” in the context of blocked coronary arteries
  4. Cardiac resyndchronisation therapy/ ICD
  5. ventricular assist devices as a “bridge to transplant”
  6. heart transplant in carefully selected patients
237
Q

mx in HFrEF

A

ACEi or ARB
+
BB

+ spironolactone

or hydralazine and nitrate (if ACEi/ARB not tolerated)

consider ivabradine if on max tolerated dose of BB and HR > 70/75

238
Q

indications for cardiac resynchronisation thearpy +/- ICD in heart failure

A

ICD, CRT, CRT-D (With defibrillator) and CRT-P (with pacing) are recommended for HR pts who have LV dysfunction and a LVEF </= 35%

239
Q

indications for ICD insertion?

A

primary arrhythmia prevention: in selected patients with family cardiac conditions w a high risk of sudden cardiac death
- brugada/ Long QT syndrome/ HOCM/ ARVD

or in selected patients who have undergone surgical repair of congenital heart disease

secondary prevention: sustained VF arrest
symptomatic sustained VT with heamodynamic compromise

240
Q

Management of pericarditis

A

Treat cause and hospitalise if poor
prognostic signs/ non- idiopathic

High dose: aspirin/NSAIDs for 1-2/ 52 (use aspirin post- AMI)

± colchicine: recurrent or pain >2/ 52 0.5 mg BD for 3– 6 months
(side effects: GI upset, neutropenia)

± steroids if pain despite above: 0.5 mg/ kg/ day for 2– 4/ 52.

Emerging therapy:
IVIG and interleukin- 1B antagonists of possible benefit in refractory cases.

241
Q

Poor prognostic factors in pericarditis

A

Normally good prognosis unless:

fever < 38°C
subacute onset
low BP
immunosuppressed
effusion >2 cm
myopericarditis
JVP elevated
history of anticoagulants.

242
Q

Management of pericardial effusion

A

Treat specific cause (60%
associated with known
disease)

but when cause
unclear: trial aspirin/ NSAIDs
For 1-2 weeks (± colchicine
± steroids [if recurrent/
prolonged]) (until <30 mL/
24 hours)

Consider pericardial window
or pericardectomy if recurrent.

Emerging therapy
intrapericardial therapies (triamcinolone) to reduce steroid usage.

243
Q

Utility of cardiac CT and cardiac MRI in constrictive pericarditis?

A

Cardiac CT and cardiac MRI: to
look for evidence of myocardial
atrophy and fibrosis, respectively (both adverse prognostic signs).

244
Q

Prognosis in constrictive pericarditis?

A

Poor, unless indication for
surgery noted early (long- term
survival similar to general
population).

Prognosis considerably worse
in presence of myocardial
fibrosis or atrophy or adhesions

245
Q

Management of constrictive pericarditis

A

Pericardectomy (unless
extensive myocardial fibrosis/
atrophy, severe disease +
NYHA IV).

Mortality 6– 12% in patients
suitable for surgery.

Symptomatic management
(diuretics, digoxin, β-
blockers) for congestion or arrhythmias, pre- operatively.

Cardiac CT used prior to
surgery to detect myocardial
fibrosis or atrophy pre- op.

246
Q

Bifasicular block

A

Bifascicular block: RBBB and either left anterior or left posterior hemiblock (therefore two fascicles);
LBBB (due to involvement of both fascicles).

247
Q

Trifascicular block

A

Trifascicular block: first degree heart block and RBBB, and either left anterior or left posterior
hemiblock.

248
Q

Ix of bradycardia

A

◆
ECG

◆
Ambulatory ECG: intermittent bradycardia.

◆
Echocardiography: for structural heart disease.

◆
Exercise testing: for chronotropic response if chronotropic incompetence suspected.

249
Q

Management of bradycardia

A

If asymptomatic treatment may not be necessary

◆ IV atropine ± isoprenaline if symptomatic.

◆ Treat reversible causes (e.g. metabolic abnormality or stop offending drug).

◆ Consider pacemaker insertion.

250
Q

Indications for pacing in sinus node disease

A

When symptoms clearly linked to bradycardia.

251
Q

Indications for pacing in AV block?

A

Mobitz type II second degree AV block and CHB even if asymptomatic.

Mobitz type I second degree AV block if symptoms.

First degree AV block if PR interval 300 ms and significant symptoms. Post- AV node ablation (e.g. atrial fibrillation with poor rate control).

252
Q

Indications for pacing in LVOT obstruction eg HOCM

A

If contraindication to alcohol septal ablation and no indication for ICD.

253
Q

causes of AF/ atrial flutter

A

•Valvular heart disease: Especially mitral stenosis, also mitral regurgitation (both dilate left atrium).
• Non-valvular heart disease: IHD, HTN, myocarditis, pericarditis, cardiomyopathy, WPW, dilated left atrium.
• Lung disease: Pulmonary emboli, lung malignancy, COPD, severe pneumonia.
• Other: Thyrotoxicosis, alcohol abuse, cocaine abuse, caffeine excess.

254
Q

Causes of non cyanotic congenital cardiac disease?

A

Left to right shunts: usually result from anatomical defects with higher left- sided pressures (the commonest
congential lesions):

• VSD (32% of cardiac abnormalities).
• ASD (8%).
• PDA (7%).
• Anomalous pulmonary venous drainage (1%).

255
Q

Risk factors for congenital cardiac abnormalities?

A
  • maternal rubella during pregnancy -> PDA, pulmonary stenosis
  • alcohol -> VSD, ASD
  • maternal age: risk of chromosomal abnormalities increases with age
  • maternal DM: Double outlet right ventricle. Truncus arteriosus (an undivided artery arising from both ventricles). Transposition of the great arteries. VSD. Hypoplastic left heart syndrome.
  • prescription drugs E.g. NSAIDs have been implicated in risk of septal and arterial defects.
256
Q

Cyanotic cardiac conditions?

A

Cyanosis results when overall oxygenation is so poor that circulating deoxygenated blood >5 g/ dL.

◆ Pulmonary stenosis (with right to left shunting) (7% of cardiac abnormalities).
◆ Tetralogy of Fallot (5%)
◆ Transposition of the great arteries (4%)
◆ Truncus arteriosus (1%): common arterial trunk (receives and mixes deoxygenated and oxygenated blood).
◆ Single ventricle (free mixing of deoxygenated and oxygenated blood)

  • Ebstein anomaly
  • Subsequent eisenmenger’s syndrome
257
Q

Complications of cyanosis

A

Complications of cynanosis result from a combination of chronic hypoxaemia and secondary erythrocytosis:

• Increased red cell turnover, consequent iron deficiency.
• Hyperviscosity with risk of stroke, thromboembolism and thrombocytopenia.
• Increased urate and risk of renal stones.
• Clubbing and acne.
• Risk of cerebral abcesses.

258
Q

why does inspiration affect right sided murmurs?

A

inspiration causes increase in venous return to the right heart -> resulting in greater flow across the pulmonic valve

259
Q

Role of echo in patent ductus arteriosus?

A

echo is diagnostic

+ also evalute for LV overload
+ estimate PASP, pulmonary artery size and RV dilatation

260
Q

Ix of patent ductus arteriosus apart from usual ECG, CXR, echo?

A

cardiac MR/CT

invasive assessment such as right cardiac catheterization is indicated when there is evidence of raised PASP for further evaluation of pulmonary / RV pressures as well as calculation of pulmonary and systemic vascular resistance

261
Q

indications for closure of PDA?

A

left ventricular overload

pulmonary hypertension but with pulmonary artery pressures <2/3 systemic pressure or pulmonary vascular resistance <2/3 that of systemic vascular resistance

262
Q

follow up after closure of PDA?

A

no residual shunt/ normal LV function/ normal pulmonary artery pressure: do not require follow up beyond 6 months

LV dysfunction or residual pulmonary hypertension shoould be followed up with evelauation and at a grown up congenital cardiac disease centre

263
Q

complications of Eisenmenger’s syndrome

A

RV failure
paradoxical emboli
IE
Haemoptysis
Hypoxaemia

264
Q

posterior thoracotomy scar in a young patient with congenital cardiac disease?

A

could be pulmonary artery banding to reduce blood flow to pulmonary system to reduce risk of developing pHTN

265
Q

most common complication following a tetralogy of fallot surgical repair?

A

pulmonary regurgitation

-> which may eventually lead to RV dilatation and functional tricuspid regurgitation

266
Q

corrective repair of tetralogy of fallot in childhood comprises of…?

A

1) closure of VSD with synthetic dacron patch
2) relief of RV outflow obstruction: resecting outflow tract obstruction, widening the pulmonary outflow tract with a patch

267
Q

how to address complication of pulmonary regurgitation following repair of Tetralogy of Fallot surgery?

A

pulmonary valve replacement
or percutaneous pulmonary valve

268
Q

posterior-lateral thoracotomy scar with an ipsilateral absent or weak radial pulse?

A

BT shunt

269
Q

what is the blalock taussig shunt used for

A

The procedure involves connecting a branch of the subclavian artery or carotid artery to the pulmonary artery.

In modern practice, this procedure is temporarily used to direct blood flow to the lungs and relieve cyanosis while the infant is waiting for corrective or definitive surgery when their heart is larger.

  • temporary procedure for cyanotic congenital heart disease
270
Q

some reasons for posterior thoractomy scar?

A

pneumonectomy or lobectomy
repair of cooarctation of aorta
BT shunt (usually assoc with weaker pulse on one side)

271
Q

echo showing biatrial dilatation, normal or mildly reduced left ventricular (LV) and right ventricular ejection fraction, and nondilated ventricles with hypertrophy

A

restrictive cardiomyopathy

-> diastolic dysfunction due to restricted filling of the ventricles

272
Q

treatment for restrictive cardiomyopathy?

A

treatment of underlying cause if any secondary cause (e.g. disease modifiying treatment for amyloidosis)

Treatment for RCM centers on relieving congestion with loop diuretics.

Heart transplant maybe considered for select patients.

273
Q

treatment of constrictive pericarditis?

A

surgical management with stripping of the pericardium

274
Q

causes of restrictive cardiomyopathy?

A

primary:
primary myocardial fibrosis
loeffler’s eosinophilic endocarditis

secondary or infiltrative causes:
amyloidosis (impt to rmb to exclude multiple myeloma)
systemic sclerosis
sarcoidosis
haemochromatosis (iron overload- can also be due to recurrent blood transfusions)
drug causes (rare): hydroxychloroquine

275
Q

indications of anticoagulation in mitral valve disease (mitral stenosis)?

A

atrial fibrillation (paroxysmal, persistent, or permanent), thromboembolic events, and the presence of left atrial thrombus

276
Q

Which dental procedures require antibiotic prophylaxis against IE?

A

procedures that involve
- manipulation of gingival (gum) tissue - manipulation of periapical region (area around the roots) of teeth, e.g. root canal, scaling
- perforation of the oral mucosa. e.g. implant surgery, oral biopsies

277
Q

What manoeuvres increase the intensity of mitral regurgitation murmur?

A

Squatting or leg raise
- both increase venous return

278
Q

What manoeuvres decrease the intensity of mitral regurgitation murmur?

A

Standing or Valsalva
- decreased venous return

279
Q

signs of mitral valve prolapse

A

mid systolic click
mid to late systolic murmur
normal S1
loudest at apex, in left lateral position

posterior valve prolapse: murmur radiates to sternum
anterior valve prolapse: murmur radiates towards back

280
Q

Auscultation findings of Tricuspid Regurgitation?

A

Pansystolic murmur loudest at LLSE
- radiates to LRSE
- accentuated by inspiration

281
Q

peripheral findigns of tricuspid regurgitation?

A

raised JVP with giant V waves
pulsatile liver
Loud P2, suggestive of pulmonary hypertension
pedal oedema

282
Q

signs of severe tricuspid regurgitation?

A

giant V wave
signs of R heart failure

283
Q

Causes of tricuspid regurgitation?

A

primary:

Congenital: Ebsteins anomaly
Acquired:
- Rheumatic heart disease
- IE
- Carcinoid syndrome
- PPM-related

Secondary (functional TR):
- pulmonary hypertension
- RV disease
- RV volume overload e.g. shunts
- RA dilatation e.g. AF

284
Q

indications for surgical management of tricuspid regurgitation?

A

Primary TR:
- symptomatic severe isolated primary TR without severe RV dysfunction

Secondary TR:
- severe secondary TR undergoing left sided valve surgery regardless of symptoms

285
Q

pathophysiology of HOCM?

A

autosomal dominant inheritance with variable penetrance

presence of increased LV wall thickness in the absence of other cardiac, systemic or metabolic disease capable or producing the magnitude of LVH

result of genetic mutation in the cardiac sarcomere genes

286
Q

causes of HOCM?

A

familial: sarcomeric gene mutation (40-60%)
Unknown (25-30%)
Others (5-10%):
Friedreich’s ataxia, Mitochondrial disease, Anderson-Fabry, Amyloidosis

287
Q

when to consider surgical management of HOCM?

A

if refractory symptoms despite medical therapy

288
Q

heart sounds in HOCM?

A

may have S4

289
Q

signs of severe ASD?

A

symptoms
signs of RV overload, pulmonary HTN: parasternal heave, loud P2, functional TR

290
Q

Types of ASD?

A
  1. Ostium secundum (80%): location in region of fossa ovalis
  2. Ostium primum (15%): failure of septum primum to fuse with endocardial cushion.
    - AV valves are typically malformed -> various degrees of regurgitation
  3. Sinus venosus defect: absence of normal tissue between right pulmonary vein(s) to right atrium
  4. Unrooted coronary sinus: separation of coronary sinus from left atrium can be partially or completely missing
291
Q

indications for surgical management of ASD?

A

RV Volume overload and no Pulmonary arterial hypertension, regardless of symptoms

*remember that ASD closure is contraindicated in Eisenmenger physiology and severe PAH

292
Q

technique for ASD closure?

A

device closure is preferred for secundum ASD, when technically suitable

293
Q

Types of VSD?

A

4 types:

  1. Membranous (80%): located in membranous septum
  2. Muscular (15-20%): completely surrounded by muscle
  3. Outlet (5%): located below the semilunar valves in the conal or outlet septum
    - assoc with aortic regurg due to prolapse of aortic cusp
  4. Inlet (<1%): immediately inferior to the AV valve apparatus
    - typically in Down syndrome
294
Q

signs of severity of VSD?

A
  • softer murmur (intensity of murmur reduces with larger defect- lower pressure gradient)
  • parasternal heave, loud P2
  • Cyanosis
295
Q

indication for closure of VSD?

A

LV volume overload and no PAH, regardless of symptoms

  • VSD closure is contraindicated in Eisenmenger physiology and severe PAH
296
Q

peripheral findings in PDA?

A

differential clubbing and cyanosis ie. of the toes but not fingers

due to the right-to-left shunt across the PDA, deoxygenated blood from the right ventricle is preferentially directed into the aorta distal to the left subclavian artery and into the lower extremities

297
Q

what is a patent ductus arteriosus?

A

persistent communciation between proximal left pulmonary artery and descending aorta just distal to the left subclavian artery

298
Q

Indication for closure of PDA

A

LV volume overload and no PAH, regardless of symptoms

  • PDA closure is contraindicated in Eisenmenger’s
299
Q

technique for closure of PDA?

A

device closure is preferred over surgery, when technically suitable

300
Q

what happens to the murmur in PDA when eisenmenger’s develops?

A

continuous machinery murmur disappears when shunt reversal occurs

-> may be left with soft systolic component

301
Q

What is eisenmenger syndrome?

A

congenital heart disease with large systemic to pulmonary shunt which in turn induces severe pulmonary vascular disease and PAH, resulting in reversal of shunt and central cyanosis

302
Q

Findings in a patient with Eisenmenger syndrome?

A

Central cyanosis and clubbing
JVP: prominent A wave in PDA with a R->L shunt

RV heave
Palpable, loud P2
PSM at LLSE (functional TR)

303
Q

management of eisenmenger syndrome?

A
  • supplemental O2 therapy
  • iron supplement if iron deficient
  • pulmonary vasodilator therapy
  • Oral anticoagulation may be considered in pulmonary artery thrombosis in the absence of significant haemoptysis
304
Q

What to counsel patients on avoiding if they have eisenmenger syndrome?

A

pregnancy is contraindicated
closing of primary cardiac defect is contraindicated

305
Q

what pulmonary vasodilator therapy may be used in eisenmenger syndrome?

A
  • endothelin receptor antagonist e.g. Bonsentan
  • Phosphodiesterase type 5 inhibitors
  • Prostacyclin analogues
  • Prostacyclin receptor agonist
306
Q

what are some haematological issues that may arise in eisenmenger syndrome?

A

patients are at risk of both bleeding and thrombosis

  • abnormalities in platelets (thrombocytopenia), coagulation pathways
  • Use of anticoagulation is controversial
307
Q

infraclavicular scar with implanted device?

A

cardiac implantable electronic device:
PPM (permanent pacemaker)
ICD (Implantable cardioverter-defibrillator)
CRT-D or CRT-P (cardiac resynchronization therapy with defibrillator or pacemaker)

308
Q

factors affecting choice for metallic vs bioprosthetic valve replacement?

A

shared decision making with patient
- patient’s preference
- age of patient (older favours bioprosthetic, >65 as rough cut off)
- any existing indication for anticoagulation e.g. AF

309
Q

presentation of prosthetic valve replacement should include?

A
  1. metallic vs bioprosthetic valve replacement
  2. which valve (most common mitral and aortic)
  3. function of valve
  4. complications
  5. aetiology of valvular pathology
310
Q

findings of metallic mitral valve replacement?

A

Metallic click in S1
soft opening snap

311
Q

findings of metallic aortic valve replacement?

A

metallic click in S2
soft opening snap
usually has systolic flow murmur across AVR (not in MVR as LV pressure is much higher)

312
Q

what to comment on for function of valve in a valve replacement?

A
  • any valvular regurgitation
  • presence of heart failure
313
Q

complications of valve replacement?

A

presence of over-anticoagulation
- bruises/ ecchymosis/ gum bleeding

presence of haemolysis
- anaemia, jaundice

presence of infective endocarditis

314
Q

what cyanotic congenital heart disease may BT shunt be used for?

A

tetralogy of fallot
pulmonary atresia
tricuspid atresia
hypoplastic left heart syndrome

PACES 2024 (14 decks)

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