Cardiology Flashcards

1
Q

What are the clinical signs of aortic stenosis?

A
  • Slow rising, low volume pulse
  • Narrow pulse pressure
  • Apex beat is sustained in stenosis (HP: heaving pressure-loaded)
  • Thrill in aortic area (R sternal edge, second intercostal space)
  • Auscultation - crescendo-decrescendo ejection systolic murmur (ESM) heard loudest in aortic area during expiration and radiating to the carotids
  • If severe would hear a soft and delayed A2 due to immobile leaflets and prolonged LV emptying, delayed (not loud) ESM, fourth heart sound (S4)
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2
Q

What would you find if there was evidence of complications from AS?

A
  • Endocarditis: splinters, Osler’s nodes (finger pulp), Janeway lesions (palms), Roth spots (retina), temperature, splenomegaly and haematuria
  • Left ventricular dysfunction: dyspnoea, displaced apex and bibasal crackles
  • Conduction problems: acute (endocarditis), chronic (calcified aortic valve node)
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3
Q

Name some DDx of Aortic Stenosis

A
  • HOCM
  • VSD
  • Aortic sclerosis: normal pulse character and no radiation of murmur
  • Aortic flow: high output clinical states e.g. pregnancy or anaemia
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4
Q

What are the causes of aortic stenosis?

A
  • Congenital: Bicuspid aortic valve
  • Acquired: Age (senile degeneration and calcification), Streptococcal (Rheumatic)
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5
Q

What conditions are associated with Aortic Stenosis?

A
  • Coarctation of the aorta
  • Bicuspid aortic valve
  • Angiodysplasia
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6
Q

What mortality is associated with different symptoms of aortic stenosis?

A
  • Angina - 5 years
  • Syncope - 3 years
  • Breathlessness - 2 years
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7
Q

What investigations would you request in someone with suspected AS?

A
  • ECG: LVH on voltage criteria, conduction defect (prolonged PR interval)
  • CXR: often normal; calcified valve
  • Echo: mean gradient >40mmHg and aortic valve area of <1.0cm2 if severe
  • Catheter: invasive transvalvular gradient and coronary angiography (coronary artery disease often co-exists)
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8
Q

How would you manage a patient with confirmed AS?

A

Asymptomatic:
- None specific, good dental health
- Regular review: symptoms and echo to assess gradient and LV function

Symptomatic:
- Surgical - aortic valve replacement +/- CABG. Operative mortality is 3-5% depending on the patient’s EuroScore

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9
Q

What are Duke’s criteria for infective endocarditis?

A

Major:
- Typical organism in 2x blood cultures
- Echo: abscess, large vegetation, dehiscence
Minor:
- Pyrexia >38
- Echo suggestive
- Predisposed e.g. prosthetic valve
- Embolic phenomena
- Vasculitis phenomena (raised ESR, CRP)
- Atypical organism on blood culture

You would diagnosis IE if patient had 2x major, 1 major and 2 minor, or 5 minor criteria.

Having associated HF or heart block or being resistant to antibiotics are an indication for urgent surgery

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10
Q

Who receives antibiotic prophylaxis for IE?

A
  • Those with prosthetic valves, previous endocarditis, cardiac transplants with valvulopathy and certain types of congenital heart disease
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11
Q

What are the clinical signs of AR?

A
  • Collapsing pulse (waterhammer pulse) reflecting a wide pulse pressure (e.g. 180/45)
  • Apex beat is hyperkinetic and displaced laterally (TV: thrusting volume-loaded)
  • Thrill in aortic area
  • Auscultation: early diastolic murmur (EDM) heard loudest at the lower L sternal edge with the patient sat forward in expiration. There may be an aortic flow murmur and a mid-diastolic murmur (Austin-Flint murmur) due to regurgitant flow impeding mitral opening. In severe AR there may be ‘free flow’ regurgitation and the EDM may be silent.
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12
Q

What signs indicate severe AR?

A
  • Collapsing pulse
  • Third heart sound (S3)
  • Pulmonary oedema
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13
Q

What signs are associated with AR?

A
  • Corrigan’s sign: visible vigorous neck pulsation
  • Quinke’s sign: nail bed capillary pulsation
  • De Musset’s sign: head nodding
  • Duroziez’s sign: diastolic murmur proximal to femoral artery compression
  • Traube’s sign: ‘pistol shot’ sound over the femoral arteries
  • Lighthouse sign - flushing and paling of forehead
  • Muller’s sign - uvula pulsation
  • Rosenbach’s sign - hepatic pulsation
  • Gerhardt’s sign - splenic pulsation (if enlarged)
  • Landolfi’s sign - change in pupil size synchronous with cardiac cycle
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14
Q

What are the causes of AR?

A

Congenital:
- Bicuspid aortic valve
Peri-membranous VSD
Acquired:
- Due to valve leaflet: endocarditis (acute) or rheumatic fever and drugs such as pergolide, slimming agents (chronic)
- Due to aortic root: dissection type A or trauma (acute) or due to dilatation secondary to Marfan’s or HTN or due to aortitis secondary to syphilis, ank spond or vasculitis (chronic)

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15
Q

Name some other causes of a collapsing pulse

A
  • Pregnancy
  • Patent ductus arteriosus
  • Paget’s Disease
  • Anaemia
  • Thyrotoxicosis
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16
Q

What investigations would you request in someone with suspected AR?

A
  • ECG: lateral T wave inversion
  • CXR: cardiomegaly, widened mediastinum and pulmonary oedema
    -TTE/TOE: to look for cause of AR such as intimal dissection flap or vegetation and also to check severity of AR by looking at LVEF and dimensions, root size and jet width
  • Cardiac catheterisation: grade severity aortogram and check coronary patency
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17
Q

How would you manage a patient with AR?

A

Medical:
- ACEi and ARBs (reducing afterload)
- Regular review: symptoms and Echo: LVEF, LV size and degree of AR
Surgical:
- Replace aortic valve when symptomatic dyspnoea and reduced exercise tolerance (NYHA >II) AND/OR wide pulse pressure >100mmHg, ECG changes on ETT, Echo: LV enlargement >5.5cm systolic diameter or EF >50%
- Ideally the valve should be replaced before there is any evidence of LVSD.

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18
Q

What is the prognosis of patients with AR?

A
  • If asymptomatic with EF >50% then have a 1% mortality at 5 years
  • If symptomatic and all 3 criteria present - 65% mortality at 3 years
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19
Q

What are the clinical signs of Mitral Stenosis?

A
  • Malar flush
  • Irregular pulse if AF is present
  • Tapping apex (palpable first heart sound)
  • L parasternal heave if pulmonary HTN is present or enlarged LA
  • Auscultation reveals a loud first heart sound. There is also an opening snap of mobile mitral leaflets opening followed by a mid-diastolic murmur, which is best heard at the apex in the L lateral position in expiration with the bell. Pre-systolic accentuation of MDM if the patient is in sinus rhythm. If severe then the opening snap occurs nearer A2 and the MDM is longer.
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20
Q

What complications can arise as a result of Mitral Stenosis?

A
  • Pulmonary Hypertension: functional tricuspid regurgitation, right ventricular heave and loud P2
  • LVF: pulmonary oedema
  • RVF: pedal oedema
  • Endocarditis
  • Embolic complications - stroke is high risk if mitral stenosis and AF
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21
Q

What are the causes of MS?

A

Congenital (rare)
Acquired:
- Rheumatic (commonest)
- Senile degeneration
- Large mitral leaflet vegetation from endocarditis (mitral ‘plop’ and late diastolic murmur)

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22
Q

What are the DDx of Mitral Stenosis?

A
  • L atrial myxoma
  • Austin-Flint Murmur
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23
Q

What investigations would you request in someone with suspected Mitral Stenosis?

A
  • ECG: p-mitrale (broad, bifid), and AF
  • CXR: enlarged L atrium (splayed of carina), calcified valve, pulmonary oedema
  • TTE/TOE: valve area (<1.0cm2 is severe), cusp mobility, calcification and L atrial thrombus, right ventricular failure
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24
Q

How would you manage a patient with confirmed Mitral Stenosis?

A
  • Medical: +AF - rate control and oral anti-coagulants, diuretics
  • Mitral valvuloplasty: if pliable, non-calcified with minimal regurgitation and no L atrial thrombus
  • Surgery: closed mitral valvotomy (without opening the heart) or open valvotomy (requiring cardiopulmonary bypass) or valve replacement
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25
Q

What is the prognosis of someone with Mitral Stenosis?

A
  • Latent asymptomatic phase - 15-20 years
  • NHYA >II - 50% mortality at 5 years
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26
Q

What is Rheumatic Fever?

A

Rheumatic fever occurs when there is an immunological cross-reactivity between Group A Beta-Haemolytic streptococcal infection e.g. Strep pyogenes and valve tissue

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27
Q

What are the Duckett-Jones diagnostic criteria?

A

Used for Rheumatic Fever

Require proven beta-haemolytic strep infection diagnosed by throat swab, rapid antigen detection test (RADT), anti-streptolysin O titre (ASOT) or clinic scarlet fever plus 2 major or 1 major and 2 minor criteria.

Major:
- Joint involvement (polyarthritis)
- O - myocarditis
- Nodules, subcutaneous
- Erythema marginatum
- Sydenham’s chorea

Minor:
- CRP elevated
- Arthalgia
- Fever
- Elevated ESR
- Prolonged PR interval
- Anamnesis of Rheumatic fever
- Leukocytosis

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28
Q

How would you treat Rheumatic Fever?

A
  • Rest, high-dose aspirin and penicillin
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29
Q

What prophylactic treatment is given in Rheumatic Fever?

A
  • Primary prevention: Pen V (or Clindamycin) for 10 days
  • Secondary prevention: Pen V for about 5-10 years
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30
Q

What are the clinical signs associated with MR?

A
  • Scars: lateral thoracotomy (valvotomy)
  • Pulse: AF, small volume
  • Apex: displaced and volume loaded
  • Palpation: thrill at apex
  • Auscultation: pan-systolic murmur (PSM) heard loudest at the apex radiating to the axilla. Loudest in expiration. Wide splitting of A2P2 due to the early closure of A2 because the LV empties sooner. S3 indicates rapid ventricular filling from LA, and excludes significant MS.
  • Pulmonary oedema
  • Potentially signs of endocarditis if this is the cause
  • LVF and AF (late sign)
  • Other murmurs such as ASD
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31
Q

What are the causes of MR?

A

Congenital: association between cleft mitral valve and primum ASD
Acquired:
- Related to valve leaflets:
— Acute:
——–Bacterial endocarditis
— Chronic:
——–Myomatous degeneration (prolapse)
——–Rheumatic fever
——–CTD
——–Fibrosis (fenfluramine/pergolide)
- Valve Annulus:
— Chronic:
——–Dilated L ventricle (functional MR)
——–Calcification
- Related to Chordae/Papillae:
— Acute:
——–Rupture
— Chronic:
——–Infiltration e.g. Amyloid
——–Fibrosis (post-MI, trauma)

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32
Q

How would you investigate a patient with suspected MR?

A
  • ECG: p-mitrale, AF and previous infarction (Q waves)
  • CXR: cardiomegaly, enlargement of the L atrium and pulmonary oedema
  • TTE/TOE: to assess severity by size/density of MR jet and to check for LV dilatation and reduced EF and to look for cause e.g prolapse, vegetations, ruptured papillae, fibrotic restriction and infarction
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33
Q

How would you manage a patient with confirmed MR?

A

Medical:
- Anticoagulation for AF and embolic complications
- Diuretic, beta-blocker and ACEi
Percutaneous:
- mitral clip device for palliation in inoperative cases of mitral valve prolapse
Surgical:
- Valve repair (preferable) with annuloplasty ring or replacement
- Aim to operate when symptomatic, prior to severe LV dilatation and dysfunction

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34
Q

What is the prognosis of a patient with MR?

A
  • Often asymptomatic for >10 years
  • Symptomatic - 25% mortality at 5 years
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35
Q

Who tends to get mitral valve prolapse and how may it present? What are the associated risks?

A
  • It is common (5%), especially in young, tall women
  • Associated with CTD e.g. Marfan’s syndrome and HOCM
  • Often asymptomatic, but may present with chest pain, syncope and palpitations
  • Small risk of emboli and endocarditis
  • Auscultation - mid-systolic ejection click. Pan-systolic murmur that gets louder up to A2. Murmur is accentuated by standing from a squatting position or during the straining phase of the Valsalva maneouvre, which reduces the flow of blood through the heart.
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36
Q

What are the clinical signs associated with TR?

A
  • Raised JVP with giant CV waves
  • Thrill at L sternal edge
  • Auscultation: pan-systolic murmur (PSM) heard loudest at the tricuspid area (lower L sternal edge) in inspiration. Reverse split second heart sound due to rapid RV emptying. Right ventricular rapid filling gives an S3
  • Pulsatile liver, ascites and peripheral oedema
  • Endocarditis from IV drug abuse: look for needle marks
  • Pulmonary HTN: RV heave and loud P2
  • Other valve lesions: rheumatic mitral stenosis
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37
Q

What are the causes of TR?

A

Congential:
- Ebstein’s anomaly (atrialisation of the R ventricle and TR)

Acquired:
- IE (acute)
- Functional (commonest) - chronic
- Rheumatic fever - chronic
- Carcinoid syndrome - chronic

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38
Q

What investigations would you carry out in a patient with suspected TR?

A
  • ECG: p-pulmonale (large, peaked) and RVH
  • CXR: double R heart border (enlarged R atrium)
  • TTE: TR jet, RV dilatation
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39
Q

How would you manage a patient with confirmed TR?

A

Medical:
- Diuretics, beta-blockers, ACEi and support stockings for oedema
Surgical:
- Valve repair/annuloplasty if medical treatment fails

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40
Q

What are the clinical signs of Pulmonary Stenosis?

A
  • Raised JVP with giant A waves
  • L parasternal heave
  • Thrill in the pulmonary area
  • Auscultation: ESM heard loudest in the pulmonary area on inspiration. Widely split second heart sounds due to delay in RV emptying. If severe would have inaudible P2 and longer murmur duration obscuring A2.
  • RVF: ascites and peripheral oedema
  • Tetralogy of Fallot: PS, VSD, over-riding aorta and RVH (sternotomy scar)
  • Noonan’s syndrome: phenotypically like Turner’s syndrome but male sex
  • Other murmurs: functional TR and VSD
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41
Q

What investigations would you request in a patient with suspected Pulmonary Stenosis?

A
  • ECG: p-pulmonale, RVH and RBBB
  • CXR: oligaemic lung fields and large R atrium
  • TTE: to look at severity (pressure gradient), RV function and associated cardiac lesions
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42
Q

How would you manage a patient with Pulmonary Stenosis?

A
  • Pulmonary valvotomy - if gradient >70mmHg or there is RV failure
  • Percutaneous pulmonary valve implantation (PPVI)
  • Surgical repair/replacement
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43
Q

What is carcinoid syndrome, how does it present and how is it treated?

A
  • Gut primary with liver mets secreting 5-HT into the blood stream
  • Toilet symptoms: diarrhoea, wheeze and flushing
  • Secreted mediators cause R sided heart valve fibrosis resulting in tricuspid regurgitation and/or pulmonary stenosis
  • Rarely a bronchogenic primary tumour or a R-to-L shunt can release 5-HT into the systemic circulation and cause L-sided valve scarring.
  • Treatment: Octreotide or surgical resection
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44
Q

What are the clinical signs of prosthetic heart valves: aortic and mitral?

A
  • Audible prosthetic clicks (metal) on approach and scars on inspection
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45
Q

Which scars are associated with which conditions?

A
  • Midline sternotomy scar: CABG, AVR, MVR
  • Lateral thoracotomy: MVR, mitral valvotomy, coarctation repair, BT shunt
  • Subclavicular: Pacemaker, AICD
  • Anticubital fossa: angiography
  • Should also look in the wrist and groins for angiography scars/bruising and legs for saphenous vein harvest used in bypass grafts.
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46
Q

What is heard on auscultation of an aortic valve replacement?

A

Metal prosthetic closing click is heard instead of A2. There may be an opening clock and Ejection systolic flow murmur. A bioprosthetic valve often has normal heart sounds.

Abnormal findings would include AR and decreased intensity of the closing click (clot or vegetation)

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47
Q

What is heard on auscultation of a mitral valve replacement?

A

Metal prosthetic closing click is heard instead of S1. An opening click may be heard in early diastole followed by a low frequency diastolic rumble.

Abnormal findings would include MR and decreased intensity of the closing click.

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48
Q

What are the late complications associated with prosthetic valves?

A
  • Thromboembolus: 1-2% per annum despite warfarin
  • Bleeding: fatal 0.6%, major 3%, minor 7% per annum on warfarin
  • Bioprosthetic dysfunction and LVF: usually within 10 years, can be treated percutaneously (valve-in-valve)
  • Haemolysis: mechanical red blood cell destruction against the metal valve
  • IE : early IE (<2 months post-op) can be due to Staph epidermidis from skin. Late IE is often due to Strep viridans by haematogenous spread. A second valve replacement is usually required to treat this complication. Mortality of prosthetic valve endocarditis approaches 60%
  • AF: particularly in MV replacement
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48
Q

What are the pros and cons of metal vs porcine valve?

A

Metal Valve:
- Durable
- Requires warfarin
- Used in those who are young and on warfarin e.g. for AF

Porcine Valve:
- Doesn’t require warfarin
- Less durable
- Used in the elderly and those at risk of haemorrhage

Operative mortality is 3-5%

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49
Q

What are the clinical signs of an implantable device?

A
  • Incisional scar in the infraclavicular position (may be abdominal)
  • Palpation demonstrates a PPM
  • Signs of HF: raised JVP, Bibasal crackles and pedal oedema
  • Medic alert bracelet
  • Local infection: hot, tender, red, fluctuant, erosion
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50
Q

When are ICDs inserted?

A

Primary Prevention:
MI >4 weeks ago (NYHA no worse than class III):
- LVEF <35% and non-sustained VT and positive EP study or
- LVEF <30% and QRSd >/= 120ms
Familial condition with high risk SCD:
- LQTS, ARVD, Brugada, HCM, complex congenital heart disease

Secondary Prevention (without other treatable cause):
- Cardiac arrest due to VT/VF
- Haemodynamically compromising VT or
- VT with LVEF <35% (not NYHA IV)

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51
Q

What are the clinical signs of pericardial disease?

A
  • Predominantly R sided HF: Raised JVP (dominant brief y-descent due to rapid early ventricular filling and rise in diastolic pressure, rapid dominant y-descent due to high RA pressures and an early rise in RV diastolic pressure due to poor pericardial compliance)
  • Kussmaul sign: paradoxical increase in JVP on inspiration (may need to sit patient at 90 degrees rather than 45 degrees to observe the JVP meniscus)
  • Pulsus paradoxus: >10mmHg drop in systolic pressure in inspiration
  • Auscultation: pericardial knock - high-pitched snap (audible, early S3 due to rapid ventricular filling into a stiff pericardial sac)
  • Ascites, hepatomegaly (congestion) and bilateral peripheral oedema
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52
Q

When should CRT be considered?

A
  • LVEF <35%
  • NYHA II-IV on optimal medical therapy
  • Sinus rhythm and QRSd >150ms (if LBBB may be >120ms)
53
Q

What are the causes of pericardial disease?

A
  • TB: cervical lymphadenopathy
  • Trauma (or surgery): sternotomy scar, post-MI
  • Tumour
  • Therapy (radio): radiotherapy tattoos, thoracotomy scar
  • Connective Tissue Disease: Rheumatoid hands, SLE signs
54
Q

What investigations would you order in a patient with suspected pericardial disease?

A
  • CXR: pericardial calcfication, old TB, sternotomy wires
  • Echo: high acoustic signal from pericardium, septal bounce, reduced mitral flow velocity during inspiration
  • Cath lab: dip and plateau of diastolic wave form: square root sign. Equalisation of LV and RV diastolic pressures
  • CT: thickened pericardium
55
Q

What is the pathophysiological of pericardial disease?

A

Thickened, fibrous capsule reduces ventricular filling and ‘insulates’ the heart from intrathoracic pressure changes during respiration leading to ventricular interdependence - filling of one ventricle reduces the size and filling of the other

56
Q

How would you treat pericardial disease>

A
  • Medical: diuretics and fluid resuscitation
  • Surgical: pericardial stripping
57
Q

Describe the jugular venous pressure waves

A

a: atrial systole
c: closure of tricuspid valve
x: movement of atrioventricular ring during ventricular systole
v: filling of the atrium
y: opening of the tricuspid valve

58
Q

Outline PDA

A
  • Condition in which the ductus arteriosus fails to close after birth
  • Connection occurs between the pulmonary trunk and the descending aorta usual just distal to the origin of the L subclavian artery
  • PDA often occurs with other abnormalities
  • Higher incidence in females and premature babies, those for which maternal rubella has occurred in the first trimester and those associated with fetal alcohol syndrome
  • Indomethacin used to close ductus in premature babies
  • Open surgery is standard treatment
59
Q

Why are R sided murmurs heard better on inspiration

A

Due to inspiration increasing venous return and flow across the valves.

60
Q

What are the features of PDA?

A
  • L subclavicular thrill
  • Enlarged L heart and apical heave
  • Continuous ‘machinery’ murmur
  • Wide pulse pressure
  • Bounding pulse
  • Signs of Pulmonary HTN and Eisenmenger’s syndrome
61
Q

What are the DDx for PDA?

A
  • Fallot’s tetralogy
  • AV fistula (coronary, systemic, pulmonary)
62
Q

How would you investigate a patient with suspected PDA?

A
  • Echo
  • CXR: may show enlargement in pulmonary vasculature, left ventricle and atrium
  • ECG: may be signs of LVH
63
Q

How do you manage a patient with a PDA?

A
  • Indomethacin closes the duct in 90% of babies but is ineffective in babies born to term
  • IV prostaglandin E1 (PGE1) may reverse the natural closure (this is useful when PDA is associated with coarctation or hypoplastic L heart syndrome and in complete transposition of the great vessels because it will help to maintain flow between the systemic and pulmonary circulations)
  • The standard treatment for PDA is open surgery
  • Endovascular closure of PDA is carried out by passing a catheter through a vessel into the artery. The ductus is measured before and occlusion device is introduced.
64
Q

What are the clinical signs of ASD?

A
  • Raised JVP
  • Pulmonary area thrill
  • Auscultation - fixed split second heart sounds that do not change with respiration. Pulmonary ejection systolic and mid-diastolic flow murmurs with large L->R shunts
  • Pulm HTN: RV heave and loud P2 and cyanosis and clubbing (Eisenmenger’s: R->L shunt)
  • Congestive Heart Failure
65
Q

What are the different types of ASD?

A
  • Ostium primum - associated with AVSD and cleft mitral valve - seen in Down’s Syndrome
  • Ostium Secundum (commonest)
66
Q

What complications can arise as a result of ASD?

A
  • Paradoxical embolus
  • Atrial arrhythmias
  • RV dilatation
67
Q

What investigations would you request in a patient with suspected ASD?

A
  • ECG: RBBB and LAD (primum) and RAD (secundum), AF
  • CXR: small aortic knuckle, pulmonary plethora and double heart border (enlarged RA)
    -TTE/TOE: site, size and shunt calculation, amenability to closure
  • R heart catheter shunt calculation (not always necessary)
68
Q

What in the history would make you consider VSD?

A
  • Stroke
  • Dyspnoea and SOBOE
  • IE
  • Eisenmenger’s
69
Q

What would you find on examination of a patient with VSD

A
  • Normal pulse
  • Normal palpation - rarely a thrill or apex displacement
  • Pansystolic murmur heard a L lower sternal edge and apex
  • If evidence of Pulm HTN then also RV heave, loud P2, ?TR ?PR
70
Q

What are the causes of VSD?

A
  • Congenital: Turner’s syndrome, Down’s syndrome, as part of Tetralogy of Fallot, or sporadic
  • Post-MI
71
Q

What Ix would help diagnose VSD?

A
  • ECG: may show L or R ventricular hypertrophy
  • CXR: may show enlarged pulmonary arteries
  • Echo and cardiac catheterisation - would confirm anatomical abnormalities, pressures and O2 sats
72
Q

What complications can arise as a result of VSD?

A
  • CCF
  • Pulmonary HTN and Eisenmenger’s
  • IE
  • AR - R coronary cusp collapse in 5%
  • Infundibular Stenosis - RHF as a result of RV causing outflow obstruction
73
Q

What are the indications for closure of a VSD?

A
  • If significant pulmonary pressures before Eisenmengers
  • Volume overload and failure
  • Recurrent endocarditis
  • Acute septal rupture
  • If associated AR
74
Q

What types of VSD are there?

A
  • Membranous septum (‘infracristal’) - the commonest site, just behind the medial papillary muscle of the tricuspid valve which may oppose it and help it to close spontaneously.
  • Muscular Septum - variable site and may be multiple (acquired VSD after septal infarction is usually the Swiss cheese type)
  • Infundibular (‘supracristal’) - a high VSD just beneath the pulmonary valve and below the R coronary cusp of the aortic valve; the latter may be inadequately supported and prolapse causing AR.
  • Posterior (Atrioventricular defect) - a paratricuspid defect
75
Q

What are the signs of ASD on examination?

A
  • RV Heave due to increased pressure in atrium
  • ESM in Pulmonary valve area due to L to R shunting
  • Normal Apex
  • Fixed splitting of S2 because of delayed pulmonary valve closure
  • May be Eisenmenger’s: clubbing, central cyanosis, RV heave
76
Q

What complications can arise as a result of ASD?

A
  • Arrhythmias
  • Stroke - systemic emboli
  • Pulmonary HTN
77
Q

What are the causes of ASD?

A
  • Congenital syndromes such as Down’s
78
Q

What types of ASD are there?

A
  • Ostium secundum - most common.
  • Ostium primum - less common and usually presents in childhood with associated mitral regurgitation. Seen in Down’s syndrome
79
Q

What investigations would be useful if suspecting ASD?

A
  • ECG: RBBB and LAD (primum) and RBBB and RAD (secundum), AF
  • CXR: small aortic knuckle, pulmonary plethora and double-heart-border (enlarged RA)
  • TTE/TOE - site/size and shunt calculation; amenability to closure
  • R heart catheter shunt calculation (not always necessary)
80
Q

What are the contraindications to ASD closure?

A
  • Severe pulmonary hypertension and Eisenmenger’s syndrome
81
Q

What different types of closure are there for ASDs?

A
  • Percutaneous closure device - secundum ASD only, no L atrial appendage thrombus or anomalous pulmonary venous drainage, adequate rim to anchor device
  • Surgical patch repair
82
Q

What is tetralogy of Fallot?

A
  • VSD
  • Pulmonary Stenosis
  • Overriding aorta
  • Right ventricular hypertrophy
83
Q

Describe Blalock-Taussig (BT Shunts)

A
  • Partially corrects the Fallot’s abnormality by anastomising the subclavian artery to the pulmonary artery
  • Absent radial pulse and scar
84
Q

What are the causes of an absent radial pulse?

A
  • Blalock-Taussig Shunt
  • Acute: embolism, aortic dissection, trauma
  • Chronic: atherosclerosis, coarctation, Takayasu’s arteritis (‘pulseless disease’)
85
Q

Describe coarctation of the aorta

A
  • A congenital narrowing of the aortic arch that is usually distal to the L subclavian artery
86
Q

What are the clinical signs of coarctation of the aorta?

A
  • HTN in R +/- L arm (coarctation usually occurs between L common carotid and L subclavian arteries)
  • Prominent upper body pulses, absent/weak femoral pulses, radio-femoral delay
  • Heaving pressure loaded apex
  • Auscultation: continuous murmur from the coarctation and collaterals radiating through to the back. There is a loud A2. There may be murmurs from associated lesions
87
Q

What associations are there with coarctation of the aorta?

A
  • Cardiac: VSD, bicuspid aortic valve and PDA
  • Non-cardiac: Turner’s syndrome and Berry aneurysms
88
Q

What investigations would you request in a patient with suspected coarctation of the aorta?

A
  • ECG: LVH and RBBB
  • CXR: rib notching, double aortic knuckle (post-stenotic dilatation)
89
Q

How would you manage a patient with suspected coarctation of the aorta?

A
  • Percutaneous: endovascular aortic repair (EVAR)
  • Surgical: Dacron patch aortoplasty
  • Long-term anti hypertensive therapy
  • Long-term follow-up/surveillance with MRA: to rule out late aneurysms and recoarcation
90
Q

What is a patent ductus arteriosus?

A
  • A continuity between the aorta and pulmonary trunk with L to R shunt.
  • A risk factor for PDA is rubella
91
Q

What are the clinical signs of PDA?

A
  • Collapsing pulse
  • Thrill in the second intercostal space
  • Thrusting apex beat
  • Auscultation: loud continous ‘machinery murmur’ loudest below the L clavicle in systole
92
Q

What complications are associated with PDA?

A
  • Eisenmenger’s syndrome
  • Endocarditis
93
Q

How is a PDA managed?

A

Closed surgically or percutaneously.

94
Q

What are the causes of Eisenmenger’s syndrome?

A
  • Large VSD
  • ASD
  • PDA
  • Fallot’s
95
Q

What complications can arise as a result of Eisenmenger’s syndrome?

A
  • Haemoptysis
  • RV failure
  • CVA
  • Sudden death
  • Brain abscess
  • Bleeding or thrombosis
  • Paradoxical embolism
  • IE
  • Hyperuricaemia with tophaceous gout
96
Q

What complications can arise following repair of a coarctation?

A
  • Aortic valve disease from co-existent bicuspid valve
  • Aneurysm at site of repair (can be mycotic)
  • Aneurysm rupture
  • Recoarctation
  • Aortic dissection later in life
97
Q

What conditions are also associated with coarctation of the aorta?

A
  • Turner’s syndrome - neck webbing, wide spaced nipples, short, valgus elbow
  • Marfan’s - tall, arachnodactyly, high arched palate
  • Bicuspid aortic valve - listen for murmur or look for repair/artificial valve
98
Q

What are the complications of artificial valves?

A
  • Acute thrombosis - massive output failure
  • Acute dehiscence - massive CCF
  • Acute endocarditis post-op - S.aureus/epidermidis
  • SABE - strep viridans as normal
  • Haemolysis
  • Embolic phenomena
  • Bleeding from warfarin
  • Leakage - chronic CCF
99
Q

What causes of anaemia may be from a heart valve?

A
  • Haemolytic anaemia
  • From IE
  • Bleeding from anticoagulation
100
Q

What features in the history may suggest HOCM?

A
  • Asymptomatic
  • SOBOE
  • Chest pain
  • Syncope
  • Dizziness and palpitations
  • FHx of sudden death
101
Q

What would you find on examination of a patient with HOCM?

A
  • Bifid carotid pulse (jerky pulse)
  • JVP a wave
  • Double apical impulse (palpable atrial and ventricular contraction)
  • PSM at apex from mitral regurgitation (mitral valve prolapse)
  • ESM at L sternal edge increased by valsalva and standing, decreased by squatting
  • 4th heart sound due to blood hitting a hypertrophied and stiff ventricle during atrial systole.
  • May be features of Friedrich’s ataxia or myotonic dystrophy
102
Q

What investigations would you request in a patient with suspected HOCM?

A
  • ECG: LVH with strain (deep T-wave inversion across the precordial leads)
  • CXR: often normal
  • TTE: MR SAM ASH (mitral regurgitation, systolic anterior motion of the anterior mitral leaflet and Asymmetric Septal Hypertrophy
  • Cardiac MR: identifies apical HCM more reliably than TTE
  • Cardiac catheterisation: gradient accentuated by a ventricular ectopic or pharmacological stress, identification of septals
  • Genetic tests: sarcomeric proteins mutation
103
Q

How would you manage a patient with HOCM?

A
  • Asymptomatic: avoid strenuous exercise, dehydration and vasodilators
  • Symptomatic and LVOT gradient >30mmHg: beta-blockers, PPM, alcohol septal ablation, surgical myomectomy
  • Rhythm-disturbance/high risk for SCD: ICD
  • Refractory: cardiac transplant
  • Genetic counselling for first degree relatives (autosomal dominant inheritance)
104
Q

What are the poor prognostic factors related to HOCM?

A
  • Young age at diagnosis
  • Syncope
  • FHx of sudden death
  • Septal thickness >3cm
105
Q

What examination findings would you expect in a patient with dextrocardia?

A
  • Impalpable apex on L, palpable on R
  • HS louder on R side
  • Liver and stomach bubble - R or L?
  • Bronchiectasis
  • Finger clubbing
106
Q

How would you investigate a patient with suspected dextrocardia?

A
  • CXR - confirm diagnosis or situs inversus
  • Echo - any associated structural defect
107
Q

What conditions are associated with dextrocardia?

A
  • Kartagener’s syndrome - situs inversus, bronchiectasis and sinusitis
  • Asplenia
  • Turner’s syndrome
  • Cardiac malformations
108
Q

What cardiac conditions can be seen in Down’s Syndrome?

A
  • AVSDs
  • ASD
  • VSD
  • Tetralogy of Fallot
109
Q

What is dilated cardiomyopathy?

A
  • Dilated ventricle in the absence of ischaemic heart disease or abnormal loading (HTN or valvular heart disease) and causes systolic dysfunction.
  • Causes include alcohol, genetic disorders (Duchenne’s, myotonic dystrophy), nutritional deficiencies (eg thiamine), inflammatory causes (infection, toxic, eosinophilic) and drugs (e.g. anthracyclines)
110
Q

What are the causes of culture negative IE?

A
  • Antibiotic use (most common)
  • HACEK organisms (difficult to culture)
  • Organisms that tend never to culture including Coxiella burnetti (Q fever), Bartonella (trench fever, louse borne) and some fungi and yeasts (Candida, aspergillus, Histoplasma, cryptococcus)
111
Q

How does restrictive cardiomyopathy present?

A
  • With R sided heart failure (cachexia, hepatomegaly, raised JVP, ascites and oedema)
112
Q

What is the most common cause of restrictive cardiomyopathy?

A
  • Cardiac amyloidosis
113
Q

What are the causes of restrictive cardiomyopathy?

A

Myocardial causes:
- Idiopathic
- Scleroderma
- Amyloid
- Sarcoid
- Haemochromotosis
- Glycogen storage disorders
- Guacher’s disease

Endomyocardial causes:
- Endomyocardial fibrosis
- Hyper-eosinophilic syndromes (including Loffler’s)
- Carcinoid
- Malignancy
- Radiotherapy
- Toxin related

114
Q

What are the DDx of restrictive cardiomyopathy?

A
  • Constrictive pericarditis
  • Other forms of cardiomyopathy
  • Pericardial effusion
  • Cardiac tamponade
  • PE
  • PTX
  • Chronic pericarditis
115
Q

What are some of the ECG features of Mitral Stenosis?

A
  • P Pulmonale if pulmonary HTN (tall and peaked in II and upright in V1 if severe)
  • AF
  • RAD
  • R ventricular hypertrophy in pulmonary HTN
116
Q

List some CXR features in Mitral Stenosis?

A
  • Enlarged L atrium
  • Widened carinal angle
  • Kerley B lines (indicating a L atrial pressure >20mmHg)
  • Alveolar oedema
  • Pulmonary haemosiderosis (haemosiderin containing macrophages in the airways)
117
Q

What might Echo be used to assess in mitral stenosis

A
  • Transvalvular gradient
  • Mitral valve area: 1.5-2.2cm2 mild stenosis, 1.0-1.5cm2 in moderate stenosis and <1cm2 in severe stenosis
  • Rigidity and nature of valve disease
  • Cardiac chamber dimensions
  • Pulmonary artery pressure
  • Presence of any associated mitral regurgitation
118
Q

What is the place of cardiac catheterisation?

A
  • Can provide more accurate assessment of pulmonary artery and heart chamber pressures
  • Can be used to measure both pressure gradients and flow rate across the valve.
119
Q

List some ECG features of Mitral Regurgitation

A
  • L atrial enlargement (P mitrale)
  • AF if L atrium enlarged
  • L ventricular hypertrophy (often coexists with dilatation)
120
Q

List some CXR features that might show MR

A
  • L atrial and L ventricular enlargement
  • Signs of L ventricular failure
121
Q

Why might patients with aortic stenosis develop angina?

A

May be due to:
- Outflow obstruction impairing coronary sinus filling
- Squeezing coronary arteries by hypertrophied muscle
- Increased myocardial demand from hypertrophied muscle

122
Q

What anaemia associations are there with AS?

A
  • Angiodysplasia
  • Microangiopathic haemolytic anaemia
123
Q

List some causes of L ventricular outflow obstruction.

A
  • AS
  • HOCM
  • Discrete congenital subvalvular aortic stenosis
  • Supravalvular aortic stenosis (uncommon, congenital)
124
Q

What features can be seen on ECG in AS?

A
  • LVH
  • ST segment depression and T-wave inversion (L ventricular strain) in leads I and aVL and in anterolateral precordial leads
125
Q

What might a CXR show in AS?

A

Essentially normal unless a calcified valve can be seen

126
Q

Which drugs should be used with caution or avoided in AS?

A
  • Excessive diuretics - as diastolic dysfunction is common and adequate preload is needed to maintain cardiac output.
  • Although evidence is limited, drugs that reduce afterload or preload (e.g. ACEis, ARBs and nitrates) should be avoided with increasing severity. A reduction in afterload will increase the gradient across the valve. Heart responds by increasing cardiac output but cannot do this if preload is compromised.
127
Q

What ECG findings might you see in AR?

A
  • Left ventricular strain
128
Q

What CXR features may be seen in AR?

A
  • LV enlargement
  • Prominent aorta
129
Q

What treatments may be considered for AR?

A

Surgery is the definitive treatment to halt volume overload. Aim is to replace before significant LVSD. Criteria for considering surgery are symptoms, LVEF <50%, LV end systolic dimension of >50mm or LV end diastolic dimension of >70mm.

130
Q

What are the causes of Mitral Valve prolapse?

A
  • Marfan’s syndrome
  • Rheumatic heart disease
  • An ostium secundum ASD
  • Ehlers Danlos syndrome
  • Ebstein’s anomaly
  • Systemic Lupus Erythematosus