Valvular heart disease - mitral stenosis Flashcards
4 valves
atrio ventricular valves - move blood from atria to ventricles
* mitral / bicuspid (LAV) = 2 cusps (only 1 anterior cusp, others have 2)
* tricuspid (RAV) = 3 cusps
these AV valves are attached to chordae tendinae
semi lunar valves - move blood from the ventricles to the lungs + body
* aortic (between LV and aorta) = 3 cusps
* pulmonary (between RV and pulmonary artery) = 3 cusps
first heart sound caused by
mitral / bicuspid = LAV
tricuspid = RAV
second heart sound caused by
SL valves
aortic
pulmonary
valve defects can either be
valve doesn’t open
- obstructed bloodflow
- STENOSIS
valve doesn’t close
- back leakage
- REGURGITATION
mitral stenosis
structural anomoly of the mitral valve
resulting in a narrow valve opening
so obstructed blood flow across the mitral valve
reduces blood flow from the LA to the LV
aetiology - main cause
due to rheumatic heart disease
following PREVIOUS RHEUMATIC FEVER
(from an infection with group A b-haemolytic streptococcus, common in LIC)
rheumatic fever causes
fusion of the mitral valve (2 cusps)
so harder for blood to flow from LA to LV
other causes of mitral stenosis
- congenital
- AI diseases - SLE, RA
- prosthetic valves
- mitral annular calcification - if extensive, more commonly in elderly pt and those with ESRD
- carcinoid tumours metastasizing to the lungs or primary bronchial carcinoid (carcinoid/endocardial fibroelastosis)
- mucopolysaccharides
- Lutembacher’s syndrome (combo of acquired mitral stenosis + atrial septal defect)
peak incidence in
women
LIC - more common epidemic for rheumatic fever
pathophysiology
INCREASES LA PRESSURE
* blood backflows into the lungs, can’t be ejected
* increases pulmonary capillary pressure
* causing pulmonary oedema and pulmonary hypertension (and dysponea - trouble breathing)
* causes backward HF and RV hypertrophy
OBSTRUCTS BLOODFLOW INTO THE LV
* limited diastolic filling of the LV
* decreased SV (end-diastolic LV volume)
* decreased CO
* forward HF
LA DILATION
* rhythm can deteriorate to AF w/ tachycardia - increases risk of thrombus formation and stroke
* can compress oesophagus and cause dysphagia
symptoms
so symptoms begin when <2cm
normal mitral valve opening is 4-6cm
PULMONARY HYPERTENSION causes:
* worsening dysponea (+ due to pulmonary oedema)
* haemoptysis (cough productive of bloody, frothy sputum if ruptured thin-walled, dilated bronchial veins)
* RHS HF w/ weakness, fatigue, abominal or lower limb swelling
INCREASED LA PRESSURE causes:
* AF causes palpitations and eventually systemic emboli
* hoarseness (compresses RLN)
* dysphagia (compresses oesophagus)
* bronchial obstruction
OTHERS:
* fatigue
* palpitations
* chest pain
* systemic emboli
* IE (rare)
* RHS HF
* PND (paroxysmal nocturnal dysponea)
* orthopnea
* haemoptysis
signs
FACE
* malar flush = bilateral, cyanotic or dusky pink discolouration over the upper cheeks (due to reduced CO w/ arteriovenous anastomoses and vascular stasis)
PULSE
* small volume pulse
* starts as ** regular** (sinus rhythm) but deteriorates into irregularly irregular (AF)
JUGULAR VEINS
* RHS HF can cause JV distension
* pulmonary hypertension/tricuspid stenosis so a-wave is present, until AF occurs
PALPATION
* palpable S1 as a tapping, non-displaced apex beat
* RV heave
* extra sustained parasternal impulse due to RV hypertrophy = tapping impulse parasternally on LHS due to palpable 1st heart sound combined w/ LV backward displacement produced by an enlarging RV
AUSCULTATION
* loud S1 if mitral valve is flexible (not if calcified)
* opening snap heard after S2 as valve opens with force of increased LA pressure
* then a low-pitched, rumbling MID-DIASTOLIC murmur (heard with bell of stethoscope at apex beat (5th left IS midclavicular line) best heard when pt lies on LHS in expiration
* if pt has sinus rhythm, murmur is louder at the end of diastole due to atrial contraction (pre-systolic accentuation)
* pulmonary hypertension can cause pulmonary valve regurgitation which causes an early diastolic murmur in the pulmonary area (Graham Steell murmur)
if more severe mitral stenosis
- increased length of mid-diastolic murmur
- opening snap becomes closer to S2
complications
- condition progresses to valve thickening
- cusp fusion
- calcium deposition
- a severely narrowed (stenotic) valve orifice
- progressive immobility of the valve cusps
diagnosis
ECHO = TTE (transthoracic echocardiography)
- shows LA size and degree of thickening, calcification and mobility of the mitral leaflets
- CROSS SECTIONAL AREA OF MITRAL VALVE <1CM
- provides enough information for routine management
can also use TOE (trans-oesophageal echocardiography)
- shows LA thrombus
- carries out detailed assessment before considering surgical or percutaneous intervention
- before PMC/after an embolic episode/if TTE provides insufficient information
other investigations
- CXR
- ECG
- use Wilkins score - echocardiograph assessment of the mitral valve (leaflet mobility, valve thickening, valve calcification and subvalvular apparatus)
CXR findings for mitral stenosis
- LA enlargement (straightening of the LHS heart border and double shadow on RHS heart border - so both borders of right and left atria)
- later severity - might see calcified mitral valve on penetrated or lateral view
- intersitital oedema
- pulmonary oedema, vascular congestion and enlarged main pulmonary arteries maybe seen
ECG findings for mitral stenosis
- can be normal, showing sinus rhythm
- with a bifid p wave due to delayed LA activation
- AF usually present - irregularly irregular rhythm, no p waves, and wavy baseline (not proper isoelectric)
- progressive right axis deviation due to RV hypertrophy
- maybe tall R waves in lead V1 due to RV hypertrophy
management for early symptoms of mitral stenosis eg. mild dysponea
first manage AF = RATE CONTROL
ANTI-COAGULATION to prevent atrial thrombus and systemic embolisation
* warfarin for moderate/severe MS
* DOACs for milder MS
DIURETICS to reduce preload and pulmonary venous congestion
management for severe mitral stenosis,
surgically manage AF
- balloon valvuloplasty (if flexible, non-calcified valve)
- open mitral valvotomy
- mitral valve replacement
managing asymptomatic pt
- monitor with regular echos
(don’t recommend percutaneous and surgical management)
managing symptomatic pt
- percutaneous mitral balloon valvotomy
- mitral valve surgery (commissurotomy) or replacement
trans-septal balloon valvotomy
- a catheter is introduced into RA via the femoral vein in the cath lab
- interatrial septum is then punctured and the catheter is advanced into the LA and across the mitral valve
- balloon is passed over the catheter to lie across the mitral valve and then inflated briefly to split the valve commissures
RISK of mitral regurgitation - needs valve replacement later
INDICATED in flexible valves, minimal mitral regurgitation
CONTRAINDICATED in heavy calcified mitral valves, severe mitral regurgitation or thrombus in the LA
(TOE done prior to balloon valvotomy to exclude LA thrombus)
closed valvotomy
fused cusps are forced apart by a dilator introduced through the apex of LV and guided into position by surgeon’s finger inserted via the LA appendage
INDICATED in mobile, non-calcified and non-regurgitant mitral valves
GOOD PROGNOSIS for >10years but valve cusps can re-fuse and may need another operation
DOESN’T NEED cardiopulmonary bypass
open valvotomy
cusps are dissected apart under direct vision
NEEDS cardiopulmonary bypass
PREFER OPEN over closed - reduces chance of causing mitral regurgitation
mitral valve replacement
using artificial valves to treat mitral stenosis
- if mitral regurgitation is also present
- if calcified stenotic valve that can’t be re-opened without causing regurgitation,
- if there is severe mitral stenosis and thrombus in the LA depsite anticoagulation
GOOD PROGNOSIS for >20years
NEED ANTICOAGULANTS to prevent thrombus forming, which might embolize or obstruct the valve
