AORTIC REGURGITATION
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Presentation
Acute AR ® features of heart failure
§ Sudden dyspnoea
§ Chest pain
§ Bibasal crackles
§ Raised JVP
Chronic AR ® may be asymptomatic for decades
§ Palpitations
§ Angina
§ Dyspnoea
§ Collapsing water hammer pulse, wide pulse pressure
§ Bounding carotid pulse
§ Chest signs ® displaced apex, ejection diastolic murmur, soft S1 and S2, absent 2nd heart sound
AR Murmur ® decrescendo diastolic murmur, systolic ejection murmur. Best heard leaning forward with breath held in
expiration.
Eponymous signs
§ De Musset’s ® head nodding with heart beat
§ Quincke’s ® pulsation of nail beds
§ Traube’s ® pistol shot femorals
§ Duroziez’s ® to and fro murmur heard when stethoscope compresses femoral vessels
§ Muller’s ® pulsation of uvula
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Pathophysiology
Aortic regurgitation (AR) results from an incompetent aortic valve, causing regurgitant flow of blood in diastole.
§ Usually presents during 4th and 6th decades of life, affecting males 3x more than women
§ Causes can be due to either primary disease of aortic valve leaflets or dilation of the aortic root
§ Aortic valve leaflets
o Rheumatic heart disease ® autoimmune condition following Streptococcal (Group A) infection
§ Chronic disease leads to fibrosis and typically a stenotic valve, but regurgitant valves may develop
o Congenital ® bicuspid, quadcuspid valve
o Degenerative ® calcification (most common cause)
o Endocarditis ® inflammation of endocardium, usually due to infection
§ Results in acute disease
§ Vegetations may cause flailing of valve leaflets
§ Infective causes include: Streptococcus viridans, Staphylococcus aureus, Enterococci.
§ Aortic root
o Connective tissue disorder ® Marfan’s syndrome, EDS
o Aortitis ® inflammation of aortic root
§ May be associated with chronic inflammatory conditions e.g. RA, ankylosing spondylitis
§ May occur in Takayasu arteritis also
o Aortic dissection ® in Stanford A dissections, secondary to impaired leaflet coaptation or prolapse
§ Causes acute disease regurgitation
§ Medical emergency
§ Aortic regurgitation may develop acutely or chronically
o Acute ® medical emergency
§ Ac acute rise in left atrial pressure ® pulmonary oedema and cardiogenic shock
§ Valvular incompetence occurs rapidly, no time for compensatory changes to develop
§ Regurgitation of blood during diastole ® increase in left ventricular EDV and pressure
§ This causes the following effects:
• Reduced coronary flow ® coronaries fill mostly during diastole, regurgitant flow at this time
reduces filling, causing angina or myocardial ischaemia
• Increased end-diastolic pressure ® causes increased pulmonary pressures with resulting
pulmonary oedema and dyspnoea and severly, cardiogenic shock
-----------------------------------------------------------------------------------------------------------------------------------------------------
Presentation
Acute AR ® features of heart failure
§ Sudden dyspnoea
§ Chest pain
§ Bibasal crackles
§ Raised JVP
Chronic AR ® may be asymptomatic for decades
§ Palpitations
§ Angina
§ Dyspnoea
§ Collapsing water hammer pulse, wide pulse pressure
§ Bounding carotid pulse
§ Chest signs ® displaced apex, ejection diastolic murmur, soft S1 and S2, absent 2nd heart sound
AR Murmur ® decrescendo diastolic murmur, systolic ejection murmur. Best heard leaning forward with breath held in
expiration.
Eponymous signs
§ De Musset’s ® head nodding with heart beat
§ Quincke’s ® pulsation of nail beds
§ Traube’s ® pistol shot femorals
§ Duroziez’s ® to and fro murmur heard when stethoscope compresses femoral vessels
§ Muller’s ® pulsation of uvula
-----------------------------------------------------------------------------------------------------------------------------------------------------
Pathophysiology
Aortic regurgitation (AR) results from an incompetent aortic valve, causing regurgitant flow of blood in diastole.
§ Usually presents during 4th and 6th decades of life, affecting males 3x more than women
§ Causes can be due to either primary disease of aortic valve leaflets or dilation of the aortic root
§ Aortic valve leaflets
o Rheumatic heart disease ® autoimmune condition following Streptococcal (Group A) infection
§ Chronic disease leads to fibrosis and typically a stenotic valve, but regurgitant valves may develop
o Congenital ® bicuspid, quadcuspid valve
o Degenerative ® calcification (most common cause)
o Endocarditis ® inflammation of endocardium, usually due to infection
§ Results in acute disease
§ Vegetations may cause flailing of valve leaflets
§ Infective causes include: Streptococcus viridans, Staphylococcus aureus, Enterococci.
§ Aortic root
o Connective tissue disorder ® Marfan’s syndrome, EDS
o Aortitis ® inflammation of aortic root
§ May be associated with chronic inflammatory conditions e.g. RA, ankylosing spondylitis
§ May occur in Takayasu arteritis also
o Aortic dissection ® in Stanford A dissections, secondary to impaired leaflet coaptation or prolapse
§ Causes acute disease regurgitation
§ Medical emergency
§ Aortic regurgitation may develop acutely or chronically
o Acute ® medical emergency
§ Ac acute rise in left atrial pressure ® pulmonary oedema and cardiogenic shock
§ Valvular incompetence occurs rapidly, no time for compensatory changes to develop
§ Regurgitation of blood during diastole ® increase in left ventricular EDV and pressure
§ This causes the following effects:
• Reduced coronary flow ® coronaries fill mostly during diastole, regurgitant flow at this time
reduces filling, causing angina or myocardial ischaemia
• Increased end-diastolic pressure ® causes increased pulmonary pressures with resulting
pulmonary oedema and dyspnoea and severly, cardiogenic shock
