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Case 13 - Heart Murmur > Valve disease > Flashcards

Valve disease Flashcards

1
Q

How can aortic stenosis present congenitally and as acquired?

A

Congenital

  • Subaortic e.g. membrane, fibromuscular ring
  • Valvular e.g. bicuspid valve
  • Supravalvular e.g. Williams syndrome - narrowing of aorta just above the valve

Acquired

  • Age-related degenerative calcific
  • Rheumatic
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2
Q

What does AS cause and what are the symptoms?

A

Causes increased after-load, failure to increase CO during exertion, progressive LV hypertrophy (increased myocardial oxygen requirement), decreased systemic and coronary flow (decreased myocardial oxygen delivery)

Clinical presentation is exertional breathlessness, chest pain and dizziness
Usually insidious onset, sudden death

LV sustains increased CO until severe/critical so asymptomatic until this stage

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3
Q

What are physical findings and investigations in AS?

A
  • Slow rising, low volume pulse
  • BP - narrow pulse pressure
  • Heaving apex beat (LVH)
  • Ejection systolic murmur
    (harsh ‘seagull’ in severe AS, aortic area/left sterna edge, radiates to carotids, loudst in expiration, may be very quiet in critical AS, quiet aortic component of S2)

Investigations - ECG for LV hypertrophy with strain and CXR for cardiomegaly (LVH) and pulomnary oedema

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4
Q

How would you quantify AS on echo?

A
  • Use doppler
  • Measure pressure difference (peak gradient) between LV outflow tract and aorta

calculation of pressure gradient is by modified Bernoulli equation:
Difference in pressure = 4(v2 squared - v1 squared)

Where v1<1.5 it is 4v2 squared

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5
Q

How do you get LV systolic pressure from pressure difference and how do you meure AS severity?

A

To get LV systolic pressure add onto sytolic BP so if 120 and pressure difference is 64 then LV systolic pressure would actually be 184mmHg

Mild <35mmHg
Mod 36-64
Severe >65

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6
Q

How would you manage AS?

A
  • 1-5 yearly follow-up with echo
  • Avoid vasodilators
  • Consider intervention if symptomatic - severe
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7
Q

What are two main options in an intervention?

A

Surgical aortic valve replacement (general anaethetic, mortality risk, stroke.MI/bleeding risk)

Transcatheter aortic valve implant/replacement (TAVI/TAVR) - biological tissue valve, percutaneous or transapical approach

TAVI is minimally invasive but new technique so ? longevity
Indicated in very elderly, major co-morbities, risk of surgery prohibitive

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8
Q

Aortic regurgitation - how can this be caused?

A

Abnormal valve cusps

  • Rheumatic disease
  • Bicuspid valve
  • Degenerative
  • Consequences of endocarditis

Aortic disease

  • HTN
  • Aortoannular ectasia
  • Marfan’s and other connective tissue diseases
  • Dissection

Traumatic

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9
Q

What is pathophysiology of AR?

A
  • Diastolic reflux of blood back into LV
  • Volume overload
  • Can cause Lv dilatation
  • Better tolerated than pressure load chronically

Clinically presentation as breathless on exertion, orthopnoea, ankle swelling potentially

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10
Q

Physical findings in AR?

A
  • Collapsing pulse
  • Wide pulse pressure
  • Displaced apex beat
  • Early systolic murmur
    High pitched
    Left sternal edge/aortic area
    Loudest in expiration whilst sitting forward
    Often shorter when AR severe, longer when less severe

ECG and CXR investiations

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11
Q

Management of AR

A
  • Annual follow up with echo
  • Strict BP control to minimise aortic dilatation
  • Consider surgery if symptomatic or left ventricle dilating
  • Surgical AVR
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12
Q

How is mitral stenosis caused and what is pathophysiology?

A

Rehumatic fever or congenital

  • Causes obstruction of normal transmitral flow (mainly positive), increased LA pressure to maintain flow (dilated LA)
  • Increased pulmonary venous pressure - pulmonary congetion
    Secondary right heart failure, tricuspid regurgitation
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13
Q

Rheumatic MS - how does this present?

A

Onset of symptoms 4th-5th decade, exertional breathlessness, HF symptoms, AF

Physical findings
- AF (irregularly irregular pulse)
- Tapping apex beat
- Low pitched rumbling apical MDM
- Mid-diastolic murmur
Low pitched, apex, louder in left lateral position, louder after exertion, absence of silence

Investigations - ECG and CXR

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14
Q

MS management?

A
  • Annual follow up with echo
  • AF - increased rates poorly tolerated - BB/digoxin
  • Anticoagulation
  • If severe and symptomatic - consider intervention
    (percutaneous balloon valvuloplasty, surgical valve replacement)

Balloon mitral valvuloplasty is first choice if valve is suitable, symptom relied, no general anaesthesia, catheter-based treatment via femoral vein, trans-septal puncture

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15
Q

Mitral regurgitation - what causes it?

A

Can be caused by leaflets, chordae, papillary muscles, annulus

Caused by rheumatics, degenerative, congenital, ischaemic or infective (endocarditis)

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16
Q

Clinical presentation of MR

A

Breathless on exertion, HF symptoms (orthopnoea, oedema)

Prognosis worsens with symptoms and Lv dilatation or systolic dyfunction

17
Q

What are physical findings of MR and what investigations needed?

A
  • May be in AF - irregularly irregular pulse
  • May have displaced apex beat
  • Pan systolic murmur (blowing, apex, radiates to axilla, volume relates to severity)

Investigations - ECG (AF) and CXR (cardiomegaly, pulmonary oedema)

18
Q

What is mitral valve prolapse murmur?

A
  • Can sound like typical mitral regurgitation murmur
  • Late systolic
  • Apex
  • Radiates to axilla
19
Q

MR management?

A
  • Annual follow up with echo
  • Intervention if breathless and severe MR and/or LV dilatation - mitral valve repair (valve reconstruction and annuloplasty so minimally invasive), mitral valve replacement, mitraclip (emerging procedure/patients not fit for open surgery), TMVR - trancatheter MV replacement - as per TAVI
20
Q

Tricuspid regurgitation causes and physical findings

A

Causes - rheumatic, secondary to right heart dilatation, secondary to pulmonary HTN

Phyisically

  • Right ventricular heave (secondary to primary cause)
  • Pan systolic murmur - left sternal edge, less harsh than ventricular septal defect, loudest in inspiration
21
Q

TR management

A
  • Largely management of underlying condition - pulmonary embolism, chronic lung disease
  • Rarely valve surgery (repair/replacement)
  • Biological valve if possible - risk of thrombosis - low velocity flow
22
Q

Tricuspid stenosis

A

Rare, rheumatic cause
Mid-diastolic mumrur - low pitched, left sternal edge, louder in inspiration
Annual echo, avoid surgery, biological valve if possible

23
Q

Pulmonary regurgitation

A

Largely in congenital heart disease
Right ventricular heave, early disastolic murmur (high pitched, pulmonary area/left sternal edge, loudest in inspiration, accentuated sitting forward

24
Q

Pulmonary stenosis

A

Right ventricular heave

Ejection systolic murmur - harsh, pulmonary area, loudest in inspiration, sitting forward may accentuate

25
Q

Selection of valve replacement

A

Mechanical prosthesis or bioprosthesis

Mech - longevity and lower risk of needing repeat surgery but anticoagulation mandatory and no option for percutaneous intervention in future

Bio - no AC required, option of PCI later but less longevity and higher risk of needing repeat surgery

26
Q

What are the post-op complications of valve replacement?

A
  • Infective endocarditis
  • valve thrombosis
  • Regurgitation
  • Stenosis

Case 13 - Heart Murmur (5 decks)

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