Valvular disease Flashcards
Valvular anatomy
Left sided valves: aortic and mitral
Right sided valves: pulmonary and tricuspid
What are the two types of aortic valve disease?
- Aortic valve stenosis
- Aortic valve regurgitation
Discuss aortic valve stenosis
Occurs when the aortic valve orifice is narrowed and obstructs forward blood flow through the valve during systole
Orifice area: normal = 3-4cm2
Stenosis: symptoms occur when valve <1.5cm2
Cause: mechanical stress over time causes fibrosis and calcification (especially if aortic valve is bicuspid because mechanical stress is divided over 2 leaflets not 3)
Consequences of aortic valve stenosis:
Left ventricle is under stress because it has to work harder to force the valve open - opens with a clicking noise in later disease
- LV hypertrophies as a result
Blood is forced through a narrow opening causing turbulence: MURMUR, gets quieter as contraction subsides = CRESCENDO DECRESCENDO MURMUR
BURRRRR DUB
- Less blood gets to the body putting the patient at risk of HF
- Syncope: less blood reaches brain
- Chest pain/ angina: less blood reaches myocardium
- Microangiopathic anaemia: RBCs destroyed when forced through small opening
Epidemiology of aortic stenosis
50% cases due to bicuspid aortic valve
2% >65yrs, 4% >85yrs
Markers of aortic stenosis:
- Clinical: slow rising pulse, narrow pulse pressure, LV heave at apex, thrill, soft S2
- Echo: <1.5cm2 valve area, thoracic echo showing LV hypertrophy due to increased afterload
- ECG: LV hypertophy shown by massive R waves in left sided chest leads (V4-V6)
Symptoms of arotic stenosis:
- Dyspnoea, fatigue: LV hypertrophy and stiffening, less blood able to get out of heart
- Angina: poor blood flow to myocardium + many patients also have ischaemic heart disease
- Presyncope or syncope: stenosis limits cardiac output so poor brain perfusion
- HF symptoms: systolic HF indicates irreversible change
Management of aortic valve stenosis: valve replacement
Where does aortic valve stenosis murmur radiate to?
Carotids
SYSTOLIC EJECTION MURMUR
Listen for the aortic stenosis murmur at the right upper sternal border
Sounds: ejection click as valve opens, crescendo-decrescendo murmur as blood rushes through small area, sounds radiates to carotids as turbulent flow,
Discuss aortic valve regurgitation
This occurs when an incompetent valve allows blood to leak back into the left ventricle during diastole
*Usually chronic and therefore allows for remodelling but can occur acutely following endocarditis or aortic dissection - acute causes leave no time to compensate and therefore cardiogenic shock can occur*
Causes:
50% cases due to aortic root dilatation: valves cannot reach each other so blood leaks back into ventricle
Infective endocarditis
Rheumatic fever
Diseases that predispose to aortic regurgitation:
- Aneurysm or dissection: dirupts aortic root
- Connective tissue diseases: Marfan’s, EDS, osteogenesis imperfecta
- Inflammatory diseases: RA, ankylosing spondylitis, large artery vasculitis
Consequences of aortic valve regurgitation:
- Blood leaks back into LV meaning there is an increased end diastolic volume in the LV >> as a result stroke volume increases as stretch increases >> higher stoke volume = higher systolic BP
- Eventually compensation can no longer occur and LV fails
- Pulse pressure is wide because diastolic BP decreases while systolic BP increases: this causes bounding pulses
Clinical features of aortic regurgitation
- Long latent period while LV compensates
- Dyspnoea
- Orthopnoea
- Paroxysmal noctural dyspnoea
- Angina because there is reduced volume of blood and pressure in the aortic root
Murmur: best heard on left sternal edge with patient leaning forwards on expiration, heard during early diastole in a decrescendo pattern
Examination findings in aortic regurgitation:
- Decreases diastolic BP
- Laterally displaced apex due to LV hypertophy
- Murmur at left sternal edge when patient sits forward on expiration: the longer the murmur the worse the regurgitation
Investigations:
- 2D echo to measure aortic root and LV dimensions
- Doppler to assess volume of regurg jet
Management: valve replacement, ACEi to cause vasodilation and thus cause less blood to return to hear - reduced strain while waiting for replacement
*Avoid using b-blockers because they prolong diastole and therefore make situation worse by allowing more time for blod to leak back*
Where would we listen for aortic valve disease?
Right 2nd intercostal: aortic stenosis
Left 3rd intercostal with patient sat forwards on expiration: aortic regurgitation
What are the 3 types of mitral valve disease?
- Mitral stenosis
- Mitral regurgitation
- Mitral prolapse
Discuss mitral valve stenosis
Slowly progressive disease with a long latent period lasting decades - becomes apparent when orifice area is <2cm2
Causes of mitral valve stenosis:
Most common cause = rheumatic heart disease so not common in high income countries
*Rheumatic disease causes mitral valve leaflets to fuse together*
Congenital heart disease
Mitral valve calcification
Previous infective endocarditis
Pathology of mitral valve stenosis:
- Blood struggles to get into the LV from the LA so some blood stays in LA
- Valve makes a snapping sound when it opens followed by a rumble as blood rushes through small oepning
- Constant increased pressure and volume in LA means blood back up into pulmonary circulation causing pulmonary congestion, oedema and dyspnoea
- Pulmonary congestion means RV has to work harder to get blood into lungs so right sided HF occurs
- Increased stretch in the atria makes AF more likely
Clinical features:
- Dyspnoea: pulmonary congestion and oedema
- Cough
- Fatigue
- Paroxysmal nocturnal dyspnoea
- Orthopnoea
- Palpitations
Signs:
Malar flush occurs due to co2 retention causing vasodilation
1st heart sound: palpable and loud
MURMUR: mid-diastolic murmur, low pitched rumbling character, does not radiate, best heart with bell over apex during expiration
Most patients will have AF due to atrial dilation
Diagnosis:
- ECG: P wave mitrale: a bifid wave caused by LA enlargement
- CXR: pulmonary congestion and oedema
- Echo: LA dilatation, thickening, calcification, leaflet fusion, reduced orifice area
- Doppler: increased blood flow velocity during diastole
Management:
Asymptomatic/ mild: monitor
Manage AF to reduce risk of VTE
Surgery if severe - balloon valvuloplasty
Poor prognosis if patient has pulmonary artery HTN
What should always be looked for if a patient is diagnosed with mitral valve stenosis?
AF
Mitral valve stenosis means LA becomes stretched as higher pressures are needed to force blood into LV through small opening
Discuss mitral valve regurgitation
Leading cause is mitral valve prolapse where the leaflets of the valve of the chordae teniniae weaken = MYXOMATOUS DEGENRATION
This leads to an increased leaflet area and elongation of the chordae tendiniae, cord can rupture (usually the posterior ones) which allows the posterior valve to fold up into the atrium
Types of mitral valve regurgitation:
- Primary: occurs as a result of disease directly affecting the mitral valves or structures supporting the valves
- Secondary: secondary to LV dilatation which stretches the valve apparatus and distorts it, also if there is an MI in the RCA the posteromedial papillary muscle can rupture
Epidemiology: non-significant regurg is common, significant regurg affects 1-2%
Causes:
Primary: infective endocarditis, rheumatic heart disease, mitral valve prolapse, congenital disease
Secondary: LV dilatation
Pathology:
- Both the LA and LV experience volume overload and hypertophy leading to LV failure and pulmonary HTN
Clinical features:
- Asymptomatic for years
- Lethargy and fatigue: poor LV function
- Dyspnoea, cough, orthopnoea, PND: pulmonary oedema due to back flow from LA
- Palpitations: AF due to LA stretching
Signs of mitral regurgitation: laterally displaced apex due to LV hypertophy, pansystolic murmur (loudest at apex and radiates to axilla best heard on expiration), pulmonary HTN
Diagnosis: Usually follows identification of pansystolic murmur at the apex
- ECG shows P mitrale and AF, CXR shows pulmonary oedema and enlarged LA, echo shows increased LA and LV size
Discuss mitral valve prolapse
Occurs if one or both mitral valve leaflets prolapse back into the LA
AKA Barlow’s valve
Most common valve abnormality, affecting 5% population
Clinical features:
- Atypical chest pain, palpitations and anxiety
- Characteristic mid systolic click is hear as the valve apparatus becomes tense during systole, followed by a late systolic murmur if mitral regurg is present
- If mitral regurg is not present, the mid-systolic click may be the only clinical sign
Management:
- Asymptomatic: reassure and monitor
- Medication: b-blockers for palpitations, anxiety and atypical chest pain
Which valve disease is most commonly associated with anxiety, depression and atypical chest pain that does not respond to GTN
Mitral valve prolapse
What is P mitrale?
P-mitrale occurs when the depolarisation of the right atrium and left atrium are both visible in the P wave
This is seen as a notch in the P wave and occurs when the left atrium is markedly enlarged, such as in mitral valve stenosis
Discuss endocarditis
Endocarditis = inflamed inner layer of the heart
Most common cause is microbial infection (infective endocarditis
Types of endocarditis:
Non infective: damage occurs to endocardium which exposes collagen and tissue factor, platelets and fibrin get stuck and form blood clots
- Can occur in hypercoagulable states e.g. pancreatic ca.
- Also associated with SLE where valvular masses can be seen on echo = Libman Sacks endocarditis
- This type rarely results in valve destruction
Infective: occurs when pathogens find their way into the endocardium either from a wound, dental abscess or surgical procedure
- Most commonly affects the left sided valves - mitral most commonly followed by aortic
- Bacteria attach to valves, colonise and attract fibrin which promotes clot formation >> known as vegetations or lumps of crud
- Vegetations are usually found on the underside of the valve but can occur on either side
Microbes responsible:
Oral streptococci: 50% cases (most commom) - prev. called viridians - classic picture is older patient following dental work
Staph aureus: 25% cases, particulary bad because causes large vegetations on tricuspid valve and can destroy valve
Staph epidermis: clasically attracted to prosthetic valves because it forms a biofilm allowing it to stick to the valve
HACEK organisms: gram negative bacteria part of normal mouth flora, cause 10% cases
Right sided endocarditis classically occurs in IVDUs because bacteria is injected into venous system which returns to RA
Clinical features of infective endocarditis
- Insidious course: typical of streptococcus, acute course typical of staphylococcus
- Typical symptoms of infection
- Tachycardia, pyrexia, new or evolving murmur, signs of valve dysfunction
- Vegetations embolise: left sided go to systemic circulation right sided go to lungs and cause PE
Diagnosis:
- Duke criteria requires 2 x major, 1 x major + 3 minor or 5 minor criteria for a diagnosis
Major criteria: Two + cultures showing typical organism, echo showing vegetation, new valvular regurg murmur
Minor critera: temperature >38, predisposing factors, vascular phenomena e.g. stroke, cultres showing atypical infection
Investigations for infective endocarditis
- 3 blood cultures from different sites taken 30 mins apart
- CRP, WCC, ESR
- Serum albumin commonly decreases
- Echo
- Aortic valve endocarditis can affect AV node conduction
- All should have dental assessment
Management
- Blind antibiotic therapy - usually a combination of 3 antibiotics
- Once organism identified regimen altered
- 6 weeks of antibiotics, usually at leat 4 weeks IV
Signs of infective endocarditis on examination
Septic signs: fever, rigors, night sweats
Cardiac lesions: new murmur or change in murmur, aortic root abscesses cause prolonged PR interval
Immune complex deposition: causes vasculitis indicated by microscopic haematuria, AKI, glomerulonephritis, splinter haemorrhages, Osler’s nodes (ouch, painful) abd Janeway lesions (just red, not painful)
Osler’s nodes are on the tip of the finger or toes and painful. Janeway lesions occur on palm and soles and are non-painful
