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Cardiology > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

History and examination findings mitral stenosis

A

History

  • Dyspnoea, orthopnoea, PND, haemoptysis (ruptured bronchial veins), ascites, oedema, fatigue (PHTN)

Examination

  • General → tachypnoea, mitral facies, peripheral cyanosis (severe)
  • Pulse & BP → normal/reduced in volume, AF due to LA enlargement
  • JVP → normal, prominent a wave if PHTN, loss of a wave in AF
  • Palpation → tapping quality apex beat (palpable S1), RV heave (parasternal impulse), palpable P2 if PHTN present, rarely diastolic thrill (lie on left side)
  • Auscultation → loud S1, loud P2, opening snap, low pitched rumbling diastolic murmur (left lateral position), late diastolic accentuation of murmus may occur in sinus rhythm - best heard left lateral, after exercise
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2
Q

Causes of mitral stenosis

A
  1. Rheumatic (F>M)
  2. Severe mitral annular calcification (sometimes associated with hypercalcaemia and hyperparathyroidism → rare)
  3. After mitral valve repair for mitral regurgitation
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3
Q

Clinical signs of severity in mitral stenosis

A
  • Small pulse pressure
  • Early opening snap (raised left atrial pressure)
  • Length of mid-diastolic rumbling murmur (persists as long as there is a gradient)
  • Diastolic thrill at apex (rare)
  • Presence of pulmonary hypertension
    • Prominent a wave in JVP (if patient in sinus rhythm)
    • Right ventricular impulse
    • Loud P2, palpable P2
    • Pulmonary regurgitation
    • Tricuspic regurgitation
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4
Q

Results of investigations in mitral stenosis

A

ECG:

  • P mitrale (broad bifid p wave)
  • Atrial fibrillation (sign of chronicity)
  • Right ventricular systolic overload
  • Right axis deviation (severe)

CXR

  • Mitral valve calcification
  • Large left atrium - double left atrial shadow, displaced left main bronchus, big left atrial appendage
  • Signs of pulmonary hypertension - large central pulmonary arteries, pruned peripheral arterial tree
  • Signs of cardiac failure

If investigations suggest LV dilatation in presence of mitral stenosis murmur consider

  • Associated mitral regurgitation
  • Associated aortic valve disease
  • Associated hypertension
  • Associated IHD

ECHO

  • Posterior mitral valve leaflet maintains anterior position in diastole
  • Valve area 4-6cm normal, <1cm severe
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5
Q

Indications for surgery in mitral stenosis

A
  • Exertional dyspnoea and falling valve area (when valve area falls to about 1cm) with signs of increasing right heart heart pressures
  • Should be performed before pulmonary oedema or major haemoptysis occurs
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6
Q

Contraindications to percutaneous mitral balloon valvotomy in mitral stenosis (i.e. indications for surgery)

A
  1. Mitral valve area >1.5cm
  2. Left atrial thrombus
  3. Moderate to severe MR
  4. Severe or bicommisural calcification
  5. Absence of commiserate fusion
  6. Severe concomitant aortic valve disease, or severe combined tricuspid regurgitation and stenosis
  7. Comcomitant CAD requiring bypass surgery
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7
Q

History and examination findings in mitral regurgitation

A

History

Dyspnoea (increased left atrial pressure), fatigue (decreased CO)

Examination

General → tachypnoea

Pulse → normal, or sharp upstroke due to rapid LV decompression, AF common

Palpation → displaced apex, diffuse, hyperdynamic, occasional pansystolic thrill. Parasternal impulse (LA enlargement behind RV) (LA often larger in MR than MS)

Auscultation → soft or absent S1, LV S3, pansystolic, holosystolic murmur at apex radiating to axilla (regurg jet posterior → axilla, anteriorly → sternum. Findings may be increased with handgrip. Can also get diastolic flow murmur

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8
Q

Signs of severe chronic mitral regurgitation

A
  • Small volume pulse (very severe)
  • Loud s3
  • Soft S1
  • Early A2
  • Signs of pulmonary hypertension
  • Signs of LV failure
  • Enlarged left ventricle
  • Early diastolic rumble
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9
Q

Causes of chronic mitral regurgitation

A
  1. Mitral valve prolapse
  2. Degenerative - associated with aging
  3. Rheumatic (M>F) - MR rarely the only murmur present
  4. Papillary muscle dysfunction (LV failure or ischaemia)
  5. Cardiomyopathy - hypertrophic, dilated, restrictive
  6. CTD - Marfan’s, RA, anklyosing spondylitis
  7. Congenital → endocardial cushion defect (primum ASD, cleft mitral leaflet), parachute valve, corrected transposition
  8. Secondary/Functional MR → heart failure, ischaemic or non-ischaemic
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10
Q

Results of investigations in mitral regurgitation

A

ECG

P mitrale, AF, left ventricular diastolic overload, RAD

CXR

Large left atrium, increased LV size, mitral annular calcification, pulmonary hypertension (much less common)

ECHO

Thickened leaflets (rheumatic), prolapsing leaflets, LA size, LV size and function, Doppler detection of regurgitant jet, estimation of RV systolic pressure from TR jet, other abnormalities → aortic valve disease from rheumatic carditis, ASD A/W MV prolapse, calcification of mitral annulus, stress echo → failure of EF to increase during exercise

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11
Q

Features and causes of acute mitral regurgitation

A

Features

Present with pulmonary oedema and collapse

Murmur may be softer and lower pitched than chronic MR, short and decrescendo

Causes

Myocardial infarction

Infective endocarditis

Trauma/surgery

Spontaneous rupture of a mycomatous cord (sometimes during exercise)

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12
Q

Features of mitral valve prolapse

A
  • Auscultation → midsystolic click followed by a middle or late systolic murmur that extends to the second heart sounds. Blowing quality. occur earlier and become louder with Valsalva and with standing. Softer with squatting and handgrip

Causes

Myxomatous degeneration of the mitral valve tissue - v common, women (but more likely to progress to significant MR in men), severity increases with age

May be associated with ASD (secundum), HCOM, Marfan’s

Complications

MR, Infective endocarditis

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13
Q

Indications and options for surgery mitral regurgitation

A

Chronic → Class III, IV symptoms or asymptomatic patients with left ventricular dysfunction (LVEF ≤60%)

Acute → haemodynamic collapse

Options

MV replacement or repair → repair is the recommended technique when results are expected to be durable

Mitraclip (transcatheter edge-edge MV repair) → if high surgical risk, favourable anatomy, and life expectancy > 1 year

Secondary MR

Guideline directed medical therapy for heart failure

Surgical repair/replacement not shown to reduce hospitalisation or death

Mitraclip (transcatheter edge-edge repair) → reduces hospitalisation for HF and all-cause mortality compared to GDMT alone

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14
Q

Features of aortic stenosis

A

History

Exertional chest pain, dyspnoea, syncope

Examination

Pulse → Plateau or anacrotic pulse late peaking and small volume

Palpation → hyperdynamic apex beat, may be slightly displaced. Systolic thrill at base

Auscultation → narrow split or reverse S2 (delayed LV ejection), harsh midsystolic ejection murmur loudest over aorta and extending into carotids → loudest sitting up in full expiration. ejection click in congenital AS

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15
Q

Features of severe aortic stenosis

A
  • ECHO - Valve area <1cm, jet velocuty >4m/sec, mean gradient >40mmHg
  • Plateau pulse
  • Carotid pulse reduced in volume
  • Thrill in aortic area
  • Soft of absent S2
  • LVF
  • Pressure loaded apex beat
  • Length, harshness and lateness of the peak of the systolic murmur
  • S4
  • Paradoxical splitting of the second heart sound
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16
Q

Causes of aortic stenosis

A
  1. Degenerative calcific AS - elderly
  2. Congenital bicuspid valve (<65)
  3. Rheumatic
  4. Radiation
  5. William’s syndrome (supravalvular AS)
  6. HOCM (subvalvular AS)
17
Q

Notes on low-flow, low gradient aortic stenosis

A
  • High velocity and gradient depends on normal flow of blood → patients with low flow (LV dysfunction, altered haemodynamics) will have lower gradients
  • Aortic valve area will be <1
  • Conventional LFLG AS - reduced LVEF (<50%) and stroke volume (<35ml)
  • Paradoxical LFLG AS - preserved LVEF and reduced stroke volume
18
Q

Results of investigations in aortic stenosis

A
  • ECG → LVH
  • CXR:
    • LVH, Valve calcification

ECHO

Doppler estimation of gradient

Calcification of valve area

Valve cusp mobility

LVH

Left ventricular dysfunction

19
Q

Management of aortic stenosis

A
  • 5 year survival in severe, inoperable AS = 5%
    • HF → 2 years survival, syncope 3 years, angina 5 years
  • Treat when symptomatic. Or asymptomatic with severe AS and LVEF < 55% without another cause, or symptoms on exercise testing, or fall in BP ≥20mmHg during exercise testing
    • If not meeting above criteria → consider itnervention if very severe AS (gradient ≥ 60mmHg), severe valve calcification, markedly high BNP
  • Surgical replacement vs TAVI
    • Low risk patients → reduced death, stroke and mortality in TAVI group, other studies almost identical outcomes between groups
    • Intermediate risk group → no significant difference in death or stroke between groups
    • Generally - younger, lower risk = SAVR, older, higher risk = TAVI
  • Valve-in-valve TAVI
    • Considered in those with degeneration of a previous bioprosthetic aortic valve instead of re-do surgery → lower risk of death, stroke, pacemaker, hospitalisation.
    • Risk of coronary obstruction → needs to be assessed carefully on CT

Mechanical or tissue

Tissue offered to patients over 65 or to younger patients who wish to avoid warfarin. Life expectancy of tissue valve = 15 years. TAVR are also tissue valves.

20
Q

Complications of TAVI

A
  1. Incomplete valve deployment
  2. Paravalvular leak
  3. Mitral regurgitation
  4. Valve position/migration
  5. Aortic root injury /dissection
  6. Pericardial effusion
21
Q

Features of aortic regurgitation

A

History

(Late stage) → exertional dyspnoea, fatigue, palpitations and angina

Examination

Appearances or Marfan’s, ank spond, Argyll Robertson pupils

Pulse → collapseing (water hammer), wide pulse pressure. Biferens pulse (beat twice) - severe AR or combined AS/AR, Hill’s sign → increased BP >20mmHg in the legs compared to arms

Neck → Corrigan’s sign (prominent carotid pulsations)

Palpation → apex beat displaced and hyperkinetic, diastollic thrill at LSE

Ausculation → soft A2, decrescendo high pitched diastolic murmur, often systolic ejection murmur (concomitant AS), Austin-Flint murmur → low pitched, rumbling mid-diastolic murmur and presystolic murmur at apex (mitral valve leaflet shudders from regurg jet)

22
Q

Signs of severe aortic regurgitation

A
  1. Collapsing pulse, wide pulse pressure
  2. Long decrescendo diastolic murmur
  3. Left ventricular S3
  4. Soft A2
  5. Austin Flint murmur
  6. Signs of LVF
23
Q

Causes of aortic regurgitation

A

Congenital/leaflet abnormalities

Bicuspid, unicuspid. VSD

Acquired leaflet abnormalities

Senile calcification, infective endocarditis, rheumatic heart disease, radiation

Congenital/genetic aortic root abnormalities

Ehlers-Danlos, Marfan syndrome, osteogenesis imperfecta

Acquired aortic root abnormalities

Idiopathic aortic root dilatation, systemic hypertension, autoimmune → SLE, ank spond, Reiter’s, aortitis → syphilis, Takayasu’s, aortic dissection, trauma

24
Q

Results of investigations in aortic regurgitation

A

ECG → left ventricular hypertrophy

CXR → left ventricular dilatation, aortic root dilatation or aneurysm, valve calcification

ECHO → left ventricular dimensions and function, Doppler estimation of size or regurg jet, vegetations, aortic root dimensions, valve cusp thickening or prolapse (associated AS)

25
Q

Indications for treatment and management or aortic regurgitation

A
  • Symptoms → dyspnoea, exertion
  • Worsening LV function
  • Progerssive LV dilatation on serial ECHOs - LV end-systolic dimension >5.5cm

Treatment → aortic valve replacement

26
Q

Notes on acute aortic regurgitation

A
  • Causes → aortic dissection and endocarditis
  • Common clinical and ECHO clues are missing
    • Short diastolic murmur
    • Non-dilated left ventricle
  • Can be life threatening
  • Treatment → aortic valve replacement.
  • Avoid bradycardia
  • Intra-aortic balloon pump contraindicated
27
Q

Features of tricuspid regurgitation

A

Examination

  • JVP → large V waves, elevated if RV failure
  • Palpation → parasternal impulse
  • Auscultation → pansystolic murmur maximal at lower end of sternum, increases on inspiration, diagnosis can be made on peripheral signs alone
  • Abdomen → pulsatile, large, tender liver, ascites, oedema, plerual effusions
  • Legs → dilated, pulsatile veins
28
Q

Causes of tricuspid regurgitation

A
  • Functional (RV failure) → 80% cases
  • Rheumatic - rarely seen alone
  • Infective endocarditis (right sided endocarditis in IVDU)
  • Tricuspid valve prolapse (rare)
  • RV papillary muscle infarction
  • Trauma (steering wheel injury to sternum)
  • Congenital (Ebstein’s anomaly)
  • Pacemaker or defiibrillator lead
29
Q

Results of investigations in tricuspid regurgitation

A
  • CXR → RV enlargement, biventricular enlargement (if secondary to HF).
    • Box shaped heart in Ebstein’s anomaly, narrow cardiac base
  • ECHO → allows measurement of regurg jet and estimation of RVSP
30
Q

Notes on surgery for tricuspid regurgitation

A

Usually in conjunction with left sided valve surgery - isolated TV surgery outcomes not ideal - particularly not good if RV dysfunction or pulmonary hypertension

31
Q

Bernoulli Equation

A
  • Change in pressure across an orifice is proportional to the square of the velocivty of the fluid flowing through the orifice
  • Used to estimate pulmonary artery pressure
    • Velocty of TR jet if proportional to RVSP
    • RVSP = 4(TR velocity)2 + right atrial pressure
32
Q

Features of tricuspid stenosis

A

Very rare

  • JVP → Raised, giant a waves with a slow y descent
  • Auscultation → diastolic murmur at left sternal edge accentuated by inspiration. Very similar to MS except area of maximal intensity and effect of inspiration. TR and MS often present. No signs of pulmonary hypertension.
  • Abdomen → presystolic pulsation of liver

Causes

Rheumatic heart disease

33
Q

Features of pulmonary stenosis

A
  • Peripheral cyanosis if severe
  • Pulse → normal or reduced if CO low
  • JVP → giant a waves due to RA hypertrophy, JVP may be elevated
  • Palpation → parasternal impulse, thrill over pulmonary arteries
  • Ausculation → ejection click possible, harsh ejection systolic murmur, heard best in pulmonary area and with inspiration. RV S4 may be present, not well heard over carotid arteries
  • Abdomen → presystolic pulsation of liver
34
Q

Features of severe pulmonary stenosis

A
  • Ejection systolic murmur peaking late in systole
  • Absence of an ejection click
  • Presence S4
  • Signs of RVF
35
Q

Causes of pulmonary stenosis

A
  • Congenital
  • Carcinoid syndrome
36
Q

Features and causes of pulmonary regurgitation

A

Uncommon

  • Auscultation → decrescendo diastolic murmur, high pitched, audible at left sternal edge, typically increases on inspiration.
    • Called Graham Steel murmur when it occurs secondary to pulmonary artery dilatation in pulmonary hypertension

Causes

Pulmonary hypertension

Infective endocarditis

Following balloon valvotomy for pulmonary stenosis or surgery for pulmonary atresia

Congenital absence of pulmonary valve

37
Q

Notes on mixed valve disease

A
  • Usually one dominant pathology
  • More commonly seen with rheumatic and radiation valve disease, and failing bioprosthetic valves
  • Concomitant severe AS and MR common → surgical vs transcatheter approach different
    • In surgical replacement AV often needs MV done at same time → difficulty weaning off bypass. TAVI patients better tolerate MR and might get away with not fixing.
38
Q

Clinical manifestations and diagnosis of acute rheumatic fever

A
  • Sequela that occurs 2-4 weeks following Group A streptococcal pharyngitis (S. Pyogenes)
  • Clinical manifestations
    • Five major
      • Arthritis → migratory polyarthritis involving large joints (60-80%). Good response to NSAIDs,
      • Carditis and valvulitis - 50-80%. Left sided valves, MR most common
      • CNS → Sydenham’s chorea
      • Subcutaneous nodules
      • Erythema marginatum
    • 4 minor
      • Arthralgia
      • Fever
      • Elevated acute phase reactants
      • Prolonged PR on ECG

Diagnosis of an initial episode

  • 2 major or 1 major + 2 minor features
  • Do not need history of streptococcal throat infection - can look for evidence of prior GAS infection with throat culture, streptococcal antigen test or ASO titre
39
Q

Late sequelae of acute rheumatic fever

A

Rheumatic heart disease

  • Usually 10-20 years after original illness
  • Most common cause of acquired valve disease in the world
  • Mitral > aortic. MR most common finding → can progess to mitral stenosis

Jaccoud arthropathy

  • Benign, chronic arthropathy → loosening and lengthening of periarticular structures and tendons in hands and feet
  • Painless, correctable with manipulation and do not cause functional impairment
  • Not associated with active inflammation

Cardiology (9 decks)

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