MITRAL REGURGITATION
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Presentation
§ Palpitations
§ Displaced apex beat
§ Systolic thrill (severe)
§ Auscultation ® S1 soft (due to incomplete closure), additional heart sound S3 may be heard (rapid filling of dilated
ventricle)
§ Heart failure ® bi-basal crackles, peripheral oedema (chronic), flash pulmonary oedema (acute), shock and
breathlessness (acute), dyspnoea and orthopnea (chronic)
Murmur ® pansystolic.
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Pathophysiology
Refers to incompetence of the mitral valve that may occur due to abnormalities of valve leaflets, subvalvular apparatus or
left ventricle.
§ Blood leaks back through the valve during ventricular systole
§ Primary MR ® pathology affects valve components e.g. degenerative disease
§ Secondary MR ® as a result of changes to left ventricular geometry
o Results in distortion of subvalvular apparatus and valve leaflets
o E.g. dilated and ischaemic cardiomyopathies.
§ Mitral valve ® bicuspid valve sitting between left atrium and ventricle
o 2 valve leaflets – anterior, posterior
o Posterior leaflet divided by indentations into three scallops (P1, P2, P3)
o The corresponding areas on the anterior leaflet may also be divided to reflect the posterior scallops (A1, A2,
A3)
o Normal cross sectional area of mitral valve orifice = 4-6 cm2
o Each leaflet attached to chordae tendinae
§ Chronic MR
o Primary ® degenerative valve disease, infective endocarditis, rheumatic heart disease, congenital abnormality,
medications (ergotamine, bromocriptine, pergolide)
o Secondary ® ischaemic MR may result in this following an MI, which leads to LV remodelling and
dysfunction impairing the valves ability to close, other causes include cardiomyopathy
o MR results in backflow of blood during ventricular systole from the LV into the LA
o This reduces the ejection fraction (EF) as part is flowing backwards and raises atrial pressure
o In chronic MR there is gradual worsening of regurgitant fraction that initially allows for compensatory
mechanisms to occur
o Eventually failure results ® due to decompensation
o Compensated state ® LV and LA dilate
§ Compliant, dilated LV undergoes eccentric hypertrophy, can maintain larger SV and EF
§ Compliant and dilated LA prevents rises in atrial and pulmonary pressures
o Decompensated state
§ Eventually changes cannot maintain normal function
§ Remodelling becomes more pathological
§ Heart failure, EF falls and pulmonary pressures rise
§ Acute MR
o Typically results from primary forms
o Can occur following MI with secondary papillary muscle rupture and valvular incompetence
o Non-ischaemic forms include ruptured chordae tendinae and valvular disease 2nd to infective endocarditis and
rheumatic heart disease
o Changes occur fast without time for adaptation or remodelling to occur
o New regurgitation causes increased pressure within an on-compliant LA
o Lack of compliance is reflected in rise in pulmonary pressure (pulmonary circulation)
o Pulmonary hypertension may cause pulmonary oedema to develop
o EF falls as blood is ejected back across regurgitant valve instead of forward through aortic valve
o Tachycardic response may help compensate for reduced EF
o Not sufficient ® cardiogenic shock can occur.
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Presentation
§ Palpitations
§ Displaced apex beat
§ Systolic thrill (severe)
§ Auscultation ® S1 soft (due to incomplete closure), additional heart sound S3 may be heard (rapid filling of dilated
ventricle)
§ Heart failure ® bi-basal crackles, peripheral oedema (chronic), flash pulmonary oedema (acute), shock and
breathlessness (acute), dyspnoea and orthopnea (chronic)
Murmur ® pansystolic.
-----------------------------------------------------------------------------------------------------------------------------------------------------
Pathophysiology
Refers to incompetence of the mitral valve that may occur due to abnormalities of valve leaflets, subvalvular apparatus or
left ventricle.
§ Blood leaks back through the valve during ventricular systole
§ Primary MR ® pathology affects valve components e.g. degenerative disease
§ Secondary MR ® as a result of changes to left ventricular geometry
o Results in distortion of subvalvular apparatus and valve leaflets
o E.g. dilated and ischaemic cardiomyopathies.
§ Mitral valve ® bicuspid valve sitting between left atrium and ventricle
o 2 valve leaflets – anterior, posterior
o Posterior leaflet divided by indentations into three scallops (P1, P2, P3)
o The corresponding areas on the anterior leaflet may also be divided to reflect the posterior scallops (A1, A2,
A3)
o Normal cross sectional area of mitral valve orifice = 4-6 cm2
o Each leaflet attached to chordae tendinae
§ Chronic MR
o Primary ® degenerative valve disease, infective endocarditis, rheumatic heart disease, congenital abnormality,
medications (ergotamine, bromocriptine, pergolide)
o Secondary ® ischaemic MR may result in this following an MI, which leads to LV remodelling and
dysfunction impairing the valves ability to close, other causes include cardiomyopathy
o MR results in backflow of blood during ventricular systole from the LV into the LA
o This reduces the ejection fraction (EF) as part is flowing backwards and raises atrial pressure
o In chronic MR there is gradual worsening of regurgitant fraction that initially allows for compensatory
mechanisms to occur
o Eventually failure results ® due to decompensation
o Compensated state ® LV and LA dilate
§ Compliant, dilated LV undergoes eccentric hypertrophy, can maintain larger SV and EF
§ Compliant and dilated LA prevents rises in atrial and pulmonary pressures
o Decompensated state
§ Eventually changes cannot maintain normal function
§ Remodelling becomes more pathological
§ Heart failure, EF falls and pulmonary pressures rise
§ Acute MR
o Typically results from primary forms
o Can occur following MI with secondary papillary muscle rupture and valvular incompetence
o Non-ischaemic forms include ruptured chordae tendinae and valvular disease 2nd to infective endocarditis and
rheumatic heart disease
o Changes occur fast without time for adaptation or remodelling to occur
o New regurgitation causes increased pressure within an on-compliant LA
o Lack of compliance is reflected in rise in pulmonary pressure (pulmonary circulation)
o Pulmonary hypertension may cause pulmonary oedema to develop
o EF falls as blood is ejected back across regurgitant valve instead of forward through aortic valve
o Tachycardic response may help compensate for reduced EF
o Not sufficient ® cardiogenic shock can occur.
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