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MBBS IV - Junior Clerkship WCS > JC05 - Valvular heart disease > Flashcards

JC05 - Valvular heart disease Flashcards

1
Q

Pathophysiology of acute and chronic rheumatic fever

A

Acute: molecular mimicry

  • Delayed immune response to infection with certain strains of Group A Strep
  • Cross-reactiveness targeting cardiac proteins (anti-M)
  • Result: inflammation in ALL layers: endocardium, myocardium and pericardium

Chronic:
- Repeated ARF attacks over decades → progressive fibrosis and fusion of heart valves

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2
Q

S/S of acute rheumatic fever

A
  • Preceded by Strep throat 2-3m weeks before
  • Fever, anorexia, lethargy
  • Pancarditis: SOB, Palpitation, Angina, Murmurs
  • Associated: Arthritis, Skin (subcutaneous nodules), Sydenham’s chorea
  • Valvular involvement: Commonly Mitral (MS > MS+MR > MR) and Aortic
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3
Q

Type of murmur associated with acute rheumatic fever

A

Transient MR/AR murmur, MDM at apex (Carey-Coombs murmur)

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4
Q

Name of diagnostic criteria for rheumatic fever

A

Jone’s criteria

2 major manifestation or 1 major + 2 minor + evidence of preceding streptococcus infection

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5
Q

Investigation and treatment of acute rheumatic fever

A

Ix:
□ Throat swab (rarely positive) and serology for ↑ASO titres
□ ESR/CRP
□ Echocardiogram: MR ± AR, MVP, pericardial effusion

Tx:
Acute: single dose IM benzylpenicillin

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6
Q

Heart valves affected by rheumatic fever

A 
Site: 
MV alone (most common)

AV+MV, AV alone

TV (rare)

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7
Q

Pathophysiology of IE

A

Endothelial damage → attract platelet/fibrin deposits → protects vs host defense
→ favours colonization by blood-borne organisms

Fibrin/platelet accumulation → growth of vegetation → obstruction/embolism

Infection destroy adjacent tissues → abscess formation

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8
Q

Risk factors of IE

A 
Prior rheumatic HD (30%)
Normal valves (40%)
IVDU (10%)
Congenital defects (10%)
Prosthetic heart valve (10%)
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9
Q

Complications of IE

A

□ Systemic infection due to continuous bacteraemia
□ Valvular heart disease due to vegetation formation
□ Septic embolization due to dislodging of vegetation materials
□ Immune complex deposition due to systemic inflammatory response

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10
Q

Groups of pathogens that cause IE

A

S. aureus: most common

Viridans strep: 2nd most common cause (eg. S. sanguis, S. mutans)

Group A/B streptococci, i.e. S. pyogenes and agalactiae

Group D streptococci, i.e. Enterococcus, S. bovis

HACEK: group of slow-growing fastidious G- bacilli

Others:

  • Animal contact: Coxiella burnetti (Q fever), Brucella
  • Fungal (IV line, immunocompromised)
  • Coagulase -ve staphylococcus (prosthetic valve)
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11
Q

Primary sources of bacteria that cause IE

A

S. aureus - skin/ skin infection/ IVDU

Viridans strep. - Oropharyngeal commensal, dental procedure, brushing

Group D strep. - GI/ GU tract diseases [classically a/w colonic ulcerative lesions, eg. CA colon, ulcerative colitis]

HACEK - oropharynx

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12
Q

Antibiotics sensitivity of causative bacteria of IE

A

S. aureus: variable, often penicillin-resistant

Viridans strep, Group A/B strep - Penicillin

Group D strep:

  • S. bovis: penicillin
  • Enterococcus: penicillin-resistant, need aminoglycoside

Staphylococcus/ HACEK: variable, often penicillin-resistant

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13
Q

Causes of negative blood culture for IE

A

Culture-negative endocarditis:

  1. Inadequate technique
  2. Prior antibiotics
  3. Fastidious organisms (require prolonged culture) e.g. Mycoplasma, HACEK
  4. Fungal (mainlining addicts, immunocompromised)

May take additional 3 cultures in these cases

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14
Q

Causes of Non-bacterial thrombotic endocarditis

A

Deposition of sterile thrombus on valve leaflets

Causes: 
metastatic malignancy (marantic, esp mucin-producing adenocarcinoma), 
thrombophilia, 
SLE
Libman-Sacks endocarditis
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15
Q

S/S of systemic infection complication in IE

A

S/S:

  • Persistent fever
  • Chills and rigors
  • General malaise
  • weight loss
  • Pallor
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16
Q

S/S of Cardiac involvement in IE

A

S/S

  • Chest pain
  • S/S of heart failure
  • Changing murmurs (esp regurgitation murmurs)
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17
Q

S/S, associated conditions for Septic embolism due to IE

A

Conditions:

  • Stroke
  • Brain abscess
  • Cold limbs
  • Splenic/renal/visceral infarcts/abscesses

S/S:

  • Skin petechiae
  • Roth spots
  • Janeway lesions
  • Splinter haemorrhage
  • Splenomegaly
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18
Q

S/S, associated conditions for systemic immune deposition due to IE

A

associated conditions:

  • Arthralgia/myalgia
  • Tenosynovitis
  • Glomerulonephritis

P/E:

  • Arthritis
  • Uraemia
  • Vascular phenomena
  • Osler’s nodes
  • Finger clubbing
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19
Q

Sample collection method for microbiological workup of IE

A

3 venous cultures taken at different sites, separated by ≥0.5h + 3 cultures if initially negative (esp if prior Abx)

Microbiological diagnosis:
>2 of 3 venous blood cultures(taken at different sites and separated by at least 0.5h) showingpersistent bacteraemia of typical organisms:

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20
Q

Imaging modalities for IE

Indications for each approach

A

Trans-thoracic echo - first line for screening

Trans-esophageal echo - see vegetation, cardiac complications, first line for prosthetic valve

  • Indications:
    (1) Prosthetic valve/ intracardiac device (difficult to visualize)
    (2) TTE non-diagnostic or –ve but high clinical suspicion
    (3) TTE +ve but high risk for complications
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21
Q

First-line investigations for IE

A

Blood culture

Echocardiogram

Blood: leukocytosis, ESR, CRP

Urine: proteinuria, haematuria, pyuria, RBC casts

ECG: AV block or conduction delays

CXR: HF, cardiomegaly, septic pulmonary emboli

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22
Q

Clinical diagnostic criteria for IE

A

Duke’s criteria: Pathologic + Clinical criteria:
Diagnosis made when one of following is met

□ Pathologic criteria:
→ Micro-organisms demonstrated in a vegetation
→ IE confirmed by histology

□ Clinical criteria:
→ Definite IE = 2 major OR 1 major + 3 minor OR 5 minor
→ Possible IE = 1 major + 1 minor OR 3 minor

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23
Q

List all major criteria in Duke’s criteria for IE

A

1) Positive blood culture: demonstrate persistent bacteria
→ Typical organisms grown in 2 separate blood C/ST or >12h apart
→ Skin contaminants grown in 3 or majority of ≥4 separate C/ST (with 1st and last drawn ≥1h apart)
→ Coxiella burnetii: single +ve C/ST or phase I IgG titre >1:800

2) Evidence of endocardial involvement:
→ Echo: vegetation, abscesses or prosthetic valve dehiscence
→ New valvular regurgitation

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24
Q

List all minor criteria in Duke’s criteria for IE

A

□ Predisposition: VHD/cardiac conditions or IVDU

□ Fever ≥38.0oC

□ Vascular phenomena, eg. embolism, septic PE, mycotic aneurysm, Janeway lesion, conjunctival haemorrhage

□ Immunological phenomena, eg. GN, Osler’s nodes, Roth spots, ↑RF

□ Suggestive blood cultures: organism grown but does not meet major criterion or serologic evidence
of active infection with organism consistent with IE

25
Q

Main mechanisms of heart valve defect and effect on heart chambers

A

Valvular stenosis (cannot open properly):
 Hypertrophy of the proximal chamber (e.g. aortic stenosis - left ventricular hypertrophy)
 Dilatation occurs as the chamber fails (e.g. mitral stenosis - left atrial enlargement)

Valvular regurgitation (cannot close properly):
 Dilatation of the chambers on either side of the valve (e.g. mitral regurgitation - left atrium and left ventricle enlarged)
26
Q

S/S of valvular heart disease

A
  1. Left heart failure - progressive exertional dyspnea (SOB)
  2. Right heart failure (progressive to involve right heart) - ankle oedema, hepatic pain (hepatic congestion)
  3. Myocardial ischaemia - chest pain
  4. Atrial fibrillation etc. - palpitations
  5. Low output - easy fatigability
  6. Complications:
    a) Thromboembolism (esp atrial fibrillation)
    b) Infective endocarditis
    c) Problems during pregnancy (higher demand of cardiac output)
27
Q

First-line investigations for valvular heart diseases

A
  1. ECG: chamber enlargement, atrial fibrillation
  2. CXR
  3. Echocardiogram*
  4. Exercise testing: objective assessment of functional capacity
  5. Cardiac catheterization (to assess status before valvular surgery):
    a) Associated coronary artery disease
    b) Pressure gradient
    c) Inject contrast to assess regurgitant lesions
28
Q

Outline tests done on Echocardiogram in assessment of valvular heart diseases

A

Echocardiogram* (accurate, noninvasive):
 Valvular architecture
 Chamber size
 Chamber function
 Doppler: assess valvular gradient/regurgitation
 Low dose dobutamine (β-adrenergic receptor stimulant) to assess ischaemia and contractile reserve

29
Q

Symptoms of IE

A

Systemic:
Fever (FUO), chills, rigor
Septic emboli: Stroke, Cold limb (PAD), Renal symptoms

Cardiac:
Heart failure: Chest pain, dyspnea, palpitations

Immunological reaction: 
 Arthralgia
 Myalgia
 Tenosynovitis
 Glomerulonephritis
30
Q

Signs of IE

A 
Systemic: 
 Fever, secondary sinus tachycardia (increase 10bpm/oC)
 Pallor
 Weight loss
 Splenomegaly
Intravascular lesions: 
 Changing murmurs
 Splinter haemorrhages
 Osler’s nodes
 Janeway lesions (unpainful)
 Signs of heart failure (bilateral basal crackles)
 Petechiae
 Roth spots
Immunological reaction: 
 Arthritis
 Uraemia
 Vascular phenomena
 Finger clubbing
31
Q

First- line investigations for IE

A

Systemic:

  • CBC: Anaemia, Leucocytosis (PMN)
  • Inflammatory: Raised ESR
  • Microbiology: Blood culture with C/ST, Sepsis workup (swab oral cavity, nasopharynx, vagina etc.)

Intravascular lesions:

  • RBC in urine, albumin negative (acute nephritic syndrome)
  • CXR
  • Echocardiogram
  • Arteriography
  • Liver-spleen scans
  • Fundoscopy
Immunological reactions: 
 Proteinuria, casts
 Polyclonal Ig
 High rheumatoid factor
 Low complements, immune complexes
32
Q

First-line management options for IE

A
  1. Eradicate source of infection
  2. Bactericidal agents:
    - Streptococcus: penicillin + gentamicin
    - Penicillin-resistant or allergic: vancomycin
    - Methicillin-resistant Staphylococcus: vancomycin
  3. IV high dose antibiotics (4-6 weeks)
  4. Surgery and complications management:
    i) Large emboli/ hemodynamically unstable
    ii) Prosthetic valve endocarditis
    iii) Fungal endocarditis
33
Q

Methods to monitor treatment for IE

A
  1. Physical signs; body weight
  2. Urine testing
  3. Renal function and blood counts (ESR may take weeks to decrease, drug level)
  4. Echocardiogram
  5. Fever may take 1-2 week to decrease
34
Q

Antibiotics prophylaxis for IE

  • type of antibiotics
  • typical indications for prophylaxis
  • Reasons for revision of IE prophylaxis guidelines
A

2g amoxicillin

Procedures:
 All dental procedures that involve manipulation of gingival tissues or periapical region of teeth or perforation of oral mucosa only
 Procedures on respiratory tract or infected skin, skin structures, or musculoskeletal tissue
 Not recommended for GU or GI tract procedures (e.g. no need for OGD, colonoscopy)

Reasons for revision of guidelines:

  1. IE is much more likely to result from frequent exposure to random bacteremias associated with daily activities
  2. Prophylaxis may prevent an exceedingly small number of cases of IE
  3. The risk of antibiotic-associated adverse events exceeds the benefit
  4. Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia
35
Q

Cardiac conditions associated with poor prognosis in IE

A
  1. Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
  2. Previous IE
  3. Congenital heart diseases:
    - Unrepaired cyanotic CHD
    - Acute infection within 6 months of complete prosthetic repair
    - Prosthetic defect in repaired CHD
  4. Cardiac transplantation recipients who develop cardiac valvulopathy
36
Q

Mitral stenosis

Etiologies

A

95% chronic rheumatic heart disease

5% congenital malformation of mitral valve

Rare:
 Mitral annular calcification
 Anorectic drugs
 Carcinoid syndrome
 SLE
 Infective endocarditis
37
Q

Mitral stenosis

Hemodynamic changes

A

Obstruction to LV inflow

Increase LA pressure (blood accumulates in left atrium)

Increase pulmonary venous pressure and thickness of pulmonary vascular beds

pulmonary arterial hypertension (second stenosis)

right heart failure

38
Q

Mitral stenosis

Symptoms

A
  1. Respiratory symptoms: SOB on exertion, paroxysmal nocturnal dyspnea
  2. Chronic RV failure: congestive cardiac failure
  3. Atrial fibrillation
  4. Systemic embolization caused by blood stasis in LA
39
Q

Mitral stenosis

Signs

A 
Malar flush (LA pressure increased + pulmonary hypertension)
Pulse volume: small, irregular if in AF
Venous:
 Loss of a wave in AF
 Increase JVP if RHF
Precordium:
 Parasternal heave / tapping apex
 Loud S1
 Opening snap
 Mid-diastolic rumble
 May be enhanced with exercise, lying on the left side

Signs of complications:
 Pulmonary oedema (basal crepitation in lungs)
 Embolisation – peripheral vessels (reduced pulses), stroke

40
Q

Mitral stenosis

Causes of acute decompensation
First-line investigations

A

Acute decompensation:

  1. Atrial fibrillation
  2. Chest infection
  3. Pregnancy (high intravascular volume)

Investigations:
CXR: Left atrial enlargement, Pulmonary edema, Kerley’s A and B lines
ECG: bifid P wave, AF, RVH
Echo: thickened and dome-like LA
Cardiac catheterization (for associated CAD)

41
Q

Mitral stenosis

Medical and surgical treatment options

A

Medical:

  1. Diuretics for congestion symptoms
  2. Digoxin, beta-blocker, CCB if Atrial fibrillation
  3. Anticoagulation if high risk of stroke
  4. Antibiotic prophylaxis against infective endocarditis

Surgical:

  1. Valvuloplasty (balloon) if no calcification or MR
  2. Mitral valvotomy (closed or open)
  3. MVR (mitral valve replacement) if calcified or destroyed: Mechanical with lifelong warfarin or Bioprosthetics
42
Q

Mitral stenosis

Prognosis
Major causes of mortality

A

Time lapse from rheumatic fever to symptoms = 16 years
Untreated, symptomatic MS: 10 years survival at 50%
Concurrent pulmonary hypertension: median survival < 3 years

Major causes of mortality:
  Progressive heart failure (60-70%)
 Systemic embolism (20-30%)
 Pulmonary embolism (10%)
 Infection (1-5%)
43
Q

Mitral regurgitation

Etiologies

A
  1. Rheumatic
  2. Mitral valvular prolapse: a/w secundum ASD, Turner’s syndrome, PDA, Wolff- Parkinson-White syndrome
  3. Ruptured chordae tendinae:
     Degenerative or collagen disease e.g. Marfan syndrome
     Infective e.g. IE
     Active rheumatic heart disease
  4. Ischaemia/ myocardial infarction- papillary muscle dysfunction
  5. Left ventricular dilatation - enlarged MV ring
44
Q

Mitral regurgitation

Haemodynamic changes

A

High LA pressure only during systole

Volume overload of LV can lead to LV enlargement and failure

  • asymptomatic if cardiac hypertrophy with reduced LV function
  • Functional MR with poor LV function and refractory HF
45
Q

Mitral regurgitation

Symptoms and signs
Complications

A

Symptoms: can be asymptomatic

  • Exercise limitation
  • Heart failure/ acute LV failure
  • Atypical chest pain and palpitations

Signs:
 LV dilatation
 S1 not increased, S2 obscured by murmur, S3 usual
 Pansystolic murmur best heard at apex radiating to axilla
 For mitral valvular prolapse: Mid systolic click(s), Late systolic murmur (accentuated by standing)

Complications:

  1. Progressive severe MR
  2. Emboli
  3. Atrial fibrillation
46
Q

Mitral regurgitation

First line investigations

A

CXR:
left atrial and ventricular enlargement
Pulmonary oedema
Kerley’s A and B lines

Echocardiogram:
MVP, LV dilatation

Cardiac catheterization for asso. CAD

47
Q

Mitral regurgitation

Medical and surgical management options

A

Medical: Anticoagulants for symptomatic heart failure, treat underlying cause

Surgical: Mitral valve replacement or mitral valve repair

48
Q

Aortic stenosis

Etiologies

A

Etiologies by age:
Commonest = Degeneration and calcification (>75 years old)

60-75: Calcified bicuspid valve

<60: Rheumatic heart disease, Congenital valvular defect (unicuspidal/ bicuspid valve)

49
Q

Aortic stenosis

Hemodynamic changes

A

AV cannot open properly in systole

blood accumulates in LV

compensatory LVH

Progressive LV dysfunction, reduced ejection fraction and eventual LV dilatation, HF

50
Q

Aortic stenosis

S/S
Tx

A

Symptoms:

  1. Exertional dyspnoea
  2. Angina pectoris (e.g. during exercise)
  3. Congestive cardiac failure
  4. Syncope or sudden death

Signs:
 Slow rising pulse
 LVH (heaving apex)
 Weak A2 (if calcified & severely stenotic)
 Thrill + murmur at aortic area (ejection systolic murmur), radiating to neck

Tx:
Aortic valvular replacement

51
Q

Define severe Aortic stenosis

A

AV area <1cm2 and/or mean pressure gradient > 50mmHg

52
Q

Aortic regurgitation

Etiologies

A
  1. Degeneration
  2. Rheumatic heart disease
  3. Seronegative rheumatoid syndrome – ankylosing spondylitis, Reiter’s syndrome, psoriatic arthropathy
  4. Infective endocarditis
  5. Syphilis (syphilitic heart disease): Dilatation of aortic valvular ring and aortitis, calcification of aorta
  6. Congenital – Marfan syndrome, congenital bicuspid valve
  7. Traumatic – aortic dissection, rupture sinus of Valsalva, external trauma
53
Q

Aortic regurgitation

Haemodynamics changes

A

Increase End-diastolic volume in LV

LV dilatation (not hypertrophy) to increase stroke volume 
Early mitral valve closure and heart failure if LV function worsens

More blood goes to LV instead of coronary arteries during diastolic phase

54
Q

Aortic regurgitation

S/S

A

More blood goes to LV instead of coronary arteries during diastolic phase

Symptoms

  1. Exertional dyspnoea
  2. Angina pectoris (e.g. during exercise)
  3. Congestive cardiac failure
  4. Syncope or sudden death

Signs:

  1. Collapsing pulse (if pulse pressure >50mmHg)
  2. LV dilatation (displaced apex)
  3. Early blowing diastolic murmur following S2 (lower sternal border, exaggerated when lean forward in full expiration)
55
Q

Eponyms/ special signs of aortic regurgitation

A
  1. Corrigan’s pulse (rapid upstroke and collapse of the carotid artery)
  2. De Musset’s head bobbing sign
  3. Austin-Flint murmur – diastolic murmur across MV
  4. Duroziez sign – to and fro murmur over femoral arteries
  5. Quincke’s pulse – capillary pulsation in finger tips or mucous membranes
  6. Tranle’s sign – pistol shot murmur
56
Q

Tricuspid regurgitation

Etiologies

A 
Etiologies: 
Right heart failure/ functional TR (90%): due to left-sided heart disease
Infective endocarditis
Rheumatic
Infiltrative
57
Q

Tricuspid regurgitation

Symptoms and signs
Tx

A 
S/S:
Right heart failure, cardiac cirrhosis
Systolic S wave (giant v wave in JVP
RV heave
Pansystolic murmur over lower sternal border (increase with inspiration)
Pulsatile liver

Tx:
Bed rest
Diuretics + spironolactone
Valvuloplasty

57
Q

Tricuspid regurgitation

Symptoms and signs
Tx

A 
S/S:
Right heart failure, cardiac cirrhosis
Systolic S wave (giant v wave in JVP
RV heave
Pansystolic murmur over lower sternal border (increase with inspiration)
Pulsatile liver

Tx:
Bed rest
Diuretics + spironolactone
Valvuloplasty

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