Valvular Disease Flashcards

1
Q

Pathophysiology of Mitral Stenosis (and complications it can lead to)

A

(1. ) Stenosed MV results in narrowing of orifice so reduced blood flow from LA to LV, preventing normal diastolic filling.
(2. ) High atrial pressure and blood flow though a stenosed valve makes snap sound (S1) in early diastole. This is the stenosed valves opening.
(3. ) It is then followed by a diastolic rumbling as blood is forced through a smaller opening (diastolic murmur).
(4. ) Elevated volume & pressures causes LA enlargement and pulmonary congestion.
(5. ) Pulmonary HTN = RV has to work harder, can lead to RVH + RSHF + rupture bronchial vessels (haemoptysis).
(6. ) Dilation of LA can cause AF
(7. ) Right and left ventricles can’t contract properly anymore which can create stagnant blood -> Risk of thrombosis formation

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2
Q

Aetiology of Mitral Stenosis (3).

A

Structural abnormality of mitral valve

  • Rheumatic heart disease (most common)
  • Infective Endocarditis
  • Mitral annular calcification
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3
Q

Symptoms of Mitral Stenosis (7.)

A
  1. Can be asymptomatic for years and then present with a gradual decrease in activity.
  2. Breathing problems: SoB on exertion, exercise intolerance, orthopnoea, paroxysmal nocturnal dyspnoea
  3. Fatigue due to low CO
  4. Palpitations/AF
  5. RSHF Sx: Ascites, oedema, hepatomegaly
  6. Haemopytsis: indicates pulmonary HTN or acute pulmonary oedema
  7. Thromboembolism: Indicates atrial stasis and AF
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4
Q

Physical signs (including auscultation) of Mitral Stenosis (4).

A
  1. Malar flush (plum-red discolouration) on the cheeks.
    - Reduced CO with CO2 retention and its vasodilatory
  2. Raised jugular venous pressure
    - Due to pulmonary HTN and RVH
  3. Signs of RSHF
    - hepatomegaly, ascites, peripheral oedema
  4. Auscultation
    - Mid-Diastolic murmur
    - Loud early diastolic opening S1 snap
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5
Q

Describe mid-diastolic murmur in MS

A
  • Low pitched diastolic rumble (due to turbulent flow) of blood flow through a stenosed valve
  • Heard best when pt lying on the left side in held expiration at the apex
  • NOTE: intensity does not correlate with severity
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6
Q

Why may you hear a loud S1 snap in early diastole in MS?

A
  • Inc atrial pressure means mitral valve ‘snap’ open.
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7
Q

Investigation of Mitral Stenosis

A
  1. Doppler ECHO(TTE, TOE)
    - GOLD STANDARD
    - Assess severity, mobility, gradient of MS.
    - Evaluates pulmonary artery pressures, LA size
  2. ECG
    - May show AF
    - bifid P-waves due to LAH
    - tall R waves due to RVH.
  3. CXR
    - May show LA enlargement, pulmonary congestion, calcified MV
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8
Q

Treatment and management of MS

A

Medical Management

  1. Anticoagulants - AF, reduce thrombosis risk
  2. B-blockers or CCB, Digoxin - slows HR, allows for filling
  3. Diuretics - pulmonary congestions

Surgical Management: If symptomatic, severe MS, pulmonary HTN.

  1. PMC/PMBV [1st line]
    - CI = LA thrombus, mitral regurgitation, severe or bicommisural calcification.
  2. Mitral Valve replacement
  3. Mitral Commissurotomy (valvulotomy)
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9
Q

Complications of MS?

A

Dilated LA

  • Pulmonary HTN
  • RSHF
  • AF
  • Thromboemoblic events
  • Rheumatic fever
  • Infective endocarditis
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10
Q

Pathophysiology of Mitral Regurgitation

A

(1.) MVR is the backflow of blood from LV into LA due to mitral valves failing to close properly

(2. ) During systole, blood flows back into LA (inc preload) and this falls back into the LV again (inc SV)
- ->Inc blood volume in LA = increased preload delivered to LV
- –> Inc stroke volume of LV = volume overload in LV
- -> Volume overload in both LA and LV

(3. ) Compensatory mechanisms in response to this: LA enlargement + LVH
(4. ) Progressive LA dilation causes pulmonary HTN, which could lead to RV dysfunction
(5. ) Compensatory mechanisms are not sustainable and progressive volume overload leads to progressive heart failure

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11
Q

Aetiology of Mitral Regurgitation (4)

A
  1. Damage to valve cusps and chordae: Rheumatic heart disease, endocarditis, MI, Ischaemic or infarction of the paillary muscle
  2. Dilation of LV and mitral valve orifice
  3. Mitral Valve prolapse: ‘floppy’ valve associated w/ Marfan + Ehlers-Danlos Syndrome.
  4. Mitral valve surgery, prosthetic mitral valve dysfunction
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12
Q

Symptoms of Mitral Regurgitation

A

Acute MR
- Pulmonary oedema

Chronic MR

  • May be asymptomatic
  • Breathlessness
  • Fatigue
  • Oedema, ascites
  • Palpitations
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13
Q

What may you hear on auscultation in a pt with Mitral Regurgitation?

A
  1. Pansystolic murmur
    - Pansystolic = persisting throughout systole
    - Mid-frequency murmur starts at S1 and extends to S2
    - This is the regurgitation of blood from LV into LA
  2. Soft S1: Valves do not close properly
  3. S3: Inc and rapid flow of blood into LV
  4. Displaced apex beat: Cardiomegaly
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14
Q

Investigations of Mitral Regurgitation

A

(1. ) Doppler TOE
- Confirm the diagnosis and assess severity
- Estimation of LA, LV size and function. Valve structure assessment.

(2. ) ECG
- may show AF as a result of LA dilation
- broad P-wave indicates LA enlargement

(3. ) CXR
- LA and LV enlargement, pulmonary congestion

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15
Q

Treatment and Management of Mitral Regurgitation

A

(1. ) ECHO and regular review
- Mild = 2-3y, Moderate = 1-2y, Severe = 6-12m

(2. ) Diuretics and vasodilators - moderate MR
(3. ) Digoxin and anticoagulant - if AF is present
(4. ) ACEi or ARBs should be given - if systemic HTN is present

(5. ) Valve Repair/Replacement indicated if:
(a. ) Acute, Severe MR
(b. ) Worsening Sx - e.g. progressive cardiomegaly, deteriorating LV function
(c. ) Sx at rest or exercise
(d. ) Asymptomatic with EF <60%
(e. ) If new onset of AF/raised pulmonary artery pressure

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16
Q

Pathophysiology of Aortic Stenosis

A

(1. ) Aortic valves become narrowed and stiff due fibrosis and calcification.
(2. ) This inc pressure gradient across aortic valves and LV has to work harder to eject blood –> becomes LVH
(3. ) Compensatory mechanism is not sustainable and LV’s function declines: reduced CO, reduced tissue perfusion
(4. ) Angina may be experienced w/o coexisting CAD due to a fixed outflow obstruction (stenosed valve) so heart is unable to meet inc demands required on exercise.

17
Q

RF of Aortic Stenosis

A
  • Age
  • Degenerative calcification (most common)
  • Rheumatic heart disease
  • Congenital aortic stenosis
  • Congenital bicuspid valve
18
Q

Symptoms of Aortic Stenosis (3)

A

Mild-moderate AS = asymptomatic

Severe develops ~10-20yrs:

(1. ) Angina, Dyspnoea
- Inc demand of hypertrophied LV working against outflow obstruction

(2. ) Syncope (fainting, passing out)
- Usually on exertion where CO fails to meet rise in demand, leading to fall in BP

(3.) Sudden death

Note: Pts with severe AS may not have symptoms due to sedentary lifetyle

19
Q

Clinical signs (inc murmurs) of Aortic Stenosis (4)

A

(1.) Slow rising carotid pulse (pulses tradus and parvus) when measuring pulse over carotid artery.

(2. ) Soft/absent S2
- Aortic valve not closing

(3. ) S4 gallop
- indicates LVH in severe AS

(4. ) Ejection systolic murmur
- crescendo-decrescendo character

20
Q

Investigations for Aortic Stenosis

A

(1. ) ECHO and Doppler
- Assesses presence and severity of AS
- Allows for imaging of valve, orifice, LV.

(2. ) ECG: LVH, LBBB
(3. ) CXR: May show enlarged LV, dilated ascending aorta

(4. ) Exercise Testing- monitor BP, ECG
- may be used in asymptomatic AS pts to unmask symptoms

21
Q

Treatment and Management of Aortic Stenosis

A

Surgical interventions

  • Indicated in: Severe asymptomatic & symptomatic AS, Elderly
    (1. ) Valve replacement [1st line]
    (2. ) TAVI: If pt not medically fit for surgery/valve-replacement
    (3. ) Balloon Valvuloplasty: For Congenital AS

Medical Interventions

(1. ) Anticoagulants - If AF present
(2. ) ACEi, diuretics - ease symptoms of HF h/e CI in severe AS

Regular Review and Doppler Echo

(1. ) Moderate-Severe AS = 1-2y
(2. ) Older pts w/heavily calcified valves = 3-6m
(3. ) Asymptomatic AS with good prognosis should be reviewed too.

22
Q

Pathophysiology of Aortic Regurgitation

A
  1. AR arises due to valve leaflets or primary aortic root disease, that cause mal-coaptation of the aortic valves leaflets so they do not close properly.
  2. This causes a backflow of blood from aorta to LV during diastole.
  3. As ventricle relaxes, even before mitral valve opens, blood is entering LV from aorta thus inc EDV (preload).
  4. Increase in volume combined with pressure causes LVH (compensatory mechanism) which ultimately leads to HF. Resulting in declined LV function.
  5. Inc LV mass means inc myocardial oxygen requirements. This with reduce coronary perfusion pressure causes myocardial ischemia and exertional chest pain.
23
Q

Aetiology of

Aortic regurgitation

A

(1. ) Aortic root dilation
- vessel itself dilates, makes it hard for valves to close all the way, letting some blood flow backwards
- Causes: Marfan’s syndrome, aneurysm, aortic dissection, syphyllis

(2. ) Congenital bicuspid valve (the most common congenital cause).
(3. ) Rheumatic disease.
(4. ) Infective endocarditis.
(5. ) Trauma

24
Q

Symptoms of Aortic Regurgitation

A

Mild/moderate AR

  • Asymptomatic
  • Palpitations, due to inc contractility

Severe AR (LSHF)

  • Angina
  • Dyspnoea, Exertional, orthopnea, paroxysmal nocturnal dyspnea
25
Q

Examination of Aortic Regurgitation

A

(1. ) Wide pulse pressure
- ‘Wide’ difference between systolic and diastolic pressure
- Low Diastolic BP - as larger volumes of blood are regurgitated during diastole so aortic diastolic pressures drop significantly
- High systolic BP - due to hypertrophied LV to maintain cardiac output

(2. ) Murmurs
- Austin flint murmur: Low pitched diastolic rumbling - best heard at apex.
- Displaced apex beat (volume overload)

(3. ) Eponymous signs of aortic regurgitation
- Corrigan sign, ‘water hammer’ - rapid/forceful then collapsing carotid pulsations
- Duroziez sign - double intermittent mumur heard over femoral artery
- De Musset sign - head nodding with each pulse
- Quincke sign - Capillary pulsation in nail beds

26
Q

Investigations of Aortic Regurgitation (4)

A

(1. ) Doppler ECHO
- Evaluation of aortic valve and aortic root with measurement of LV dimensions and function

(2.) ECG: Initially normal, later: LVH, T-wave inversion

(3. ) Cardiac Catherisation
- Assess severity of regurgitation
- Determine if dilation is present
- Screen for coexisting CAD

(4.) CXR, MRI: Assess enlarged cardiac silhouette and aortic root enlargement

27
Q

Treatment and Management of Aortic Regurgitations

A
  1. Systemic HTN control with ACEi
  2. Monitor and ECHO
    - mild-moderate = every 2y
    - severe AR = every 6-12m
    - report development of angina, breathlessness
  3. Aortic Valve Replacement indicated in:
    - Acute and Severe AR
    - Symptomatic
    - Asymptomatic if EF drops below 50% or LV becomes dilated
28
Q

What is it Infective Endocarditis?

A

(1. ) Infection of heart valves or other endothelial lines structures within the heart (such as septal defects, pacemaker leads, surgical patches etc)
(2. ) Commonly caused by staph or strep, but can be other organisms
(3. ) FEVER + NEW MURMUR = ENDOCARDITIS unless proven otherwise

29
Q

RF/Incidences of Infective Endocarditis?

A

In pts with normal valves: skin breaches, renal failure, immunosuppression, DM

Abnormal Valves

  • Prosthetic valves or valve disease
  • IVDU (develop endocarditis on right side of heart)
  • Introducing infectious material into blood stream or directly onto heart during surgery

RF

  • Congenital heart disease
  • Hx of IE
  • Elderly
  • Male
30
Q

Aetiology of Infective Endocarditis?

A
  • Bacteraemia
  • Staph.aureus: most common, prosthetic vales, IVDU
  • Steph.viridans, Strep.Bous
  • P.aeruginosa
  • HACEK (oropharyngeal commensal gram -ve)
  • Fungi
  • Enterococci
31
Q

When would IE be suspected? (8)

A

(1. ) New regurgitant heart murmur
(2. ) Embolic event of unknown origin
(3. ) Sepsis of unknown origin (especially if associated with IE causative organism)
(4. ) Septic signs = Fever, rigors, night sweats, malaise, weight loss, anaemia
(5. ) Intracardiac prosthetic material (e.g. prosthetic valve, pacemaker, implantable defrbillator)
(6. ) Hx of IE
(7. ) Previous valvular or congenital heart disease
(8. ) Other predispositions of IE (e.g. immunocompromised)

32
Q

Examination/Signs of IE (6)

A
  1. Fever
  2. Heart murmurs - common aortic regurgitation murmur
  3. Petechiae: clusters of spots on skin
  4. Splinter haemorrhages underneath nail
  5. Osler’s nodes: small tender red-to-purple nodules on pulp of digits
  6. Roth’s spots: retinal haemorrhages
  7. Janeway’s lesions: irregular painless erythematous macules on finger, palms, sole
33
Q

Diagnosis of IE

A
  • Diagnosis is made using Modified Dukes Criteria
34
Q

Investigations of IE (5)

A
  1. Blood tests + cultures: raised CRP shows sign of infection although non-specific
  2. CXR - Cardiomegaly, pulmonary oedema
  3. ECGs - Any conduction defects?
  4. ECHO TTE: detection of vegetation
  5. CT - Look for emboli in spleen, brain etc
35
Q

Treatment and Management of IE (4)

A

(1. ) IV Antibiotics (1st line)
- blind therapy = Ampicillin, flucloxacillin, gentamicin (gram +ve) OR vancomycin, gentamicin (penicillin allergy) OR meropenem, vancomycin (gram -ve)

(2.) Treatment of complications e.g. emboli, arrhythmia, HF etc

(3. ) Cardiac surgery, when to operate:
- To remove infectious device
- Infection cannot be cured with antibiotics
- Complications such as aortic root abscess, severe valve damage
- Remove large vegetations before they embolise

(4. ) Consider IE prophylaxis in high risk pts (prosthetic valves, previous IE, complex congenital disease)
- Antibiotic should cover IE organisms