AR

Aortic regurgitation
Highlights
Summary Overview
Basics
Definition Epidemiology Aetiology Pathophysiology Classification
Prevention
Primary Secondary
Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history
Treatment
Details Step-by-step Guidelines Evidence
Follow Up
Recommendations Complications Prognosis
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History & exam

Key factors
presence of risk factors diastolic murmur
Other diagnostic factors

dyspnoea fatigue weakness orthopnoea paroxysmal nocturnal dyspnoea pallor mottled extremities rapid and faint peripheral pulse jugular venous distension basal lung crepitations altered mental status urine output <30 mL/hour soft S1 soft or absent A2 collapsing (water hammer or Corrigan's) pulse cyanosis tachypnoea displaced, hyperdynamic apical impulse chest pain pink frothy sputum wheeze (cardiac asthma) additional heart sounds arrhythmias ejection systolic flow murmur Austin Flint murmur systolic thrill Hill's sign bisferiens pulse de Musset's sign Muller's sign Traube's sign Quincke's sign Duroziez's sign Mayen's sign
Lighthouse sign Becker's sign Landolfi's sign Rosenbach's sign Gerhardt's sign Lincoln's sign Sherman's sign palmar click syncope History & exam details
Diagnostic tests
1st tests to order
ECG CXR echocardiogram M-mode and 2-dimensional imaging colour flow Doppler pulsed wave Doppler continuous wave Doppler
Tests to consider
radionuclide angiography MRI exercise stress testing cardiac catheterisation Diagnostic tests details
Treatment details
Acute
acute AR inotropes + vasodilators + urgent aortic valve replacement
Ongoing
mild to moderate chronic AR o asymptomatic with normal left ventricular function reassurance
symptomatic or left ventricular dysfunction investigation and treatment of alternative underlying cause severe chronic AR: asymptomatic with ejection fraction >50%
o o o o o
compensated disease reassurance transitional disease: negative exercise test reassurance transitional disease: positive exercise test vasodilator therapy decompensated disease: surgical candidate aortic valve replacement decompensated disease: non-surgical candidate vasodilator or ACE inhibitor therapy severe chronic AR: asymptomatic with ejection fraction 50%
o o
surgical candidate aortic valve replacement non-surgical candidate vasodilator or ACE inhibitor therapy severe chronic AR: symptomatic
o o o
surgical candidate aortic valve replacement vasodilator therapy non-surgical candidate vasodilator therapy Treatment details
Summary
The diastolic leakage of blood from the aorta into the left ventricle (LV). Chronic aortic regurgitation (AR) may be asymptomatic for years until overt symptoms of congestive heart failure develop. Initial symptoms can include palpitations and uncomfortable awareness of the pounding heart when lying on the left side. Acute AR is a medical emergency, presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock. May also present as myocardial ischaemia or aortic root dissection. Echocardiography is the best non-invasive test to diagnose and grade the severity of AR.
Vasodilator therapy improves haemodynamics and delays the need for aortic valve replacement/repair (AVR) in asymptomatic patients with chronic severe AR.
AVR is indicated in symptomatic patients or those with LV ejection fraction <50%, and asymptomatic patients with severe AR if LV end-diastolic volume is >75 mm or LV end-systolic volume is > 55mm.
Other related conditions

Infective endocarditis Mitral regurgitation Marfan's syndrome Chronic congestive heart failure Aortic stenosis Aortic dissection Rheumatic fever
Definition
Aortic regurgitation (AR) is the diastolic leakage of blood from the aorta into the left ventricle. It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root. It can remain asymptomatic for decades before patients present with irreversible myocardial damage.
Epidemiology
AR is not as common as aortic stenosis and mitral regurgitation. One US study showed a prevalence of 13% in men and 8.5% in women with most being trace or mild; a prevalence of 15.6% was reported in AfricanAmericans. [2] Prevalence increases with age in both genders.[3] Of asymptomatic people >55 years of age, 13% have moderate or severe echocardiographic AR with a total prevalence of 29% (including mild AR). [4] A prospective multicentre epidemiological study of healthy young adults aged 23 to 35 years revealed a prevalence of AR of 1.3%. There was no difference in the prevalence on the basis of gender or race. [5]
Aetiology
AR can be caused by primary disease of the aortic valve leaflets or dilation of the aortic root. In developing countries rheumatic heart disease is the most common cause, but congenital bicuspid aortic valve and aortic root dilation account for most of the cases in developed countries. Causes of aortic root dilation include Marfan's syndrome, related connective tissue diseases, and aortitis secondary to syphilis, Behcet's, Takayasu's, Reiter's syndrome, or
ankylosing spondylitis. Endocarditis can lead to rupture of leaflets or even paravalvular leaks. Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of blood. [6] Aortic root dissection is a cause of acute AR. AR may develop acutely (acute AR) or over a period of many years in progressively increasing severity (chronic AR). An analysis of the causes of AR in patients >20 years of age undergoing isolated aortic valve replacement/repair (AVR) found non-valvular causes accounted for 54% of cases and valvular causes for 46%. Acute AR was responsible for only 18% of AVR, and, of these, 56% resulted from active infective endocarditis and 44% from aortic dissection. Aortic enlargement from unclear aetiology was the most common cause of chronic AR, accounting for 34% of the total, followed by bicuspid congenital malformation (22% of total). Older patients most commonly had an unclear aetiology. [7] The role of systemic hypertension in aortic root dilation leading to AR is a frequent source of debate. Aortic root diameter at the supra-aortic ridge, which is the site of commissural attachment, is significantly greater in hypertensive patients than in age and gender-matched normotensive
patients. [8]
Causes of AR
Pathophysiology
AR can present acutely or over decades. Acute AR is a medical emergency with high mortality and results in an acute rise in left atrial pressure, pulmonary oedema, and cardiogenic shock. During acute AR: End-diastolic pressure in the left ventricle rises sharply .
The heart tries to compensate by increasing the heart rate and increasing the contractility (Starling's law) to keep up with the increased preload, but this is insufficient to maintain the normal stroke volume and fails. Chronic progressive AR results in:
Both left ventricular volume and pressure overload. An increase in left ventricular volume and pressure causes an increase in wall tension. According to Laplace's law, wall tension is directly proportional to the product of cavity pressure and radius, and inversely proportional to wall thickness.
To compensate for the increased wall tension, the heart wall undergoes hypertrophy. Both concentric and eccentric hypertrophy can occur but most are eccentric. Eccentric hypertrophy, in which sarcomeres are laid down in series, results from volume overload; concentric hypertrophy, in which sarcomeres replicate in parallel, results from pressure overload from increased systolic pressure to normalise the end-systolic stress. [9]
Systolic hypertension occurs secondary to increased stroke volume, which combines both regurgitant and forwards stroke volume.
The volume overload, which is directly related to the severity of the leak, results in an increase in left ventricular end-diastolic volume.
End-diastolic pressure remains normal due to an increase in ventricular compliance resulting from increased cavity size. In chronic AR, most patients remain asymptomatic for decades, as the left ventricle maintains forwards stroke volume with compensatory chamber enlargement and hypertrophy. Eventually, the left ventricular systolic dysfunction supervenes and left ventricular end-diastolic pressure rises resulting in symptomatic congestive heart failure. Timing AVR before irreversible myocardial dysfunction develops is of critical importance.
Classification
Acute aortic regurgitation: clinically accepted criteria A medical emergency where the left heart rapidly decompensates due to its inability to handle a sudden increase in end-diastolic volume. Most commonly it results from aortic dissection or endocarditis and, in rare cases, trauma. Chronic aortic regurgitation: clinically accepted criteria Chronic regurgitation has a prolonged course over a period of months to years. The left ventricle is able to compensate for volume overload initially but
then decompensates with the appearance of clinical symptoms of congestive heart failure.
Primary prevention
Streptococcal throat infection should be treated with antibiotics to avoid the development of rheumatic fever. High blood pressure should be controlled to prevent damage to the aortic root. Intravenous drug abuse should be avoided. Good dental hygiene should be maintained.
Secondary prevention
Antibiotic prophylaxis is recommended for patients with prosthetic valves during surgical or dental procedures to prevent endocarditis. [34]
History & examination

Key diagnostic factorshide all
presence of risk factors (common)
Risk factors include bicuspid aortic valve, rheumatic fever, endocarditis, Marfan's syndrome and related connective tissue disease, and aortitis.
diastolic murmur (common)
The absence of diastolic murmur significantly reduces the likelihood of AR. [17] The severity of the AR correlates well with the duration of murmur, instead of the intensity of murmur. In mild AR the murmur is early diastolic, and increases in duration to holodiastolic in severe AR.
A diastolic murmur may be absent in acute AR. Other diagnostic factorshide all dyspnoea (common)
Caused by pulmonary oedema in acute AR, or progressive left ventricular dysfunction in chronic severe AR.
fatigue (common) Symptom of chronic AR due to progressive left ventricular dysfunction. weakness (common) Symptom of chronic AR due to progressive left ventricular dysfunction. orthopnoea (common) Symptom of chronic AR due to progressive left ventricular dysfunction. paroxysmal nocturnal dyspnoea (common) Symptom of chronic AR due to progressive left ventricular dysfunction. pallor (common) Sign of cardiogenic shock. mottled extremities (common)
Sign of cardiogenic shock.
rapid and faint peripheral pulse (common) Sign of cardiogenic shock. jugular venous distension (common) Sign of cardiogenic shock and CHF. basal lung crepitations (common) Sign of pulmonary oedema. altered mental status (common) Sign of cardiogenic shock. urine output <30 mL/hour (common) Sign of cardiogenic shock. soft S1 (common)
May be soft due to early coaptation of the mitral valve leaflets from increased end-diastolic pressure.
soft or absent A2 (common) Caused by inadequate closure of aortic valve in severe AR collapsing (water hammer or Corrigan's) pulse (common)
Arterial pulse shows rapid rise and a quick collapse resulting in widened pulse pressure >50 mmHg.
cyanosis (common) Sign of acute AR. tachypnoea (common) Sign of acute AR with pulmonary oedema. displaced, hyperdynamic apical impulse (common) Present on chronic AR with left ventricular enlargement. chest pain (uncommon)
Most common in chronic AR, although can be presenting symptom in acute AR. Acute severe central crushing pain may indicate myocardial ischaemia, or, if referred to the back, aortic dissection.
pink frothy sputum (uncommon) Sign of pulmonary oedema. wheeze (cardiac asthma) (uncommon) Sign of pulmonary oedema. additional heart sounds (uncommon) Left ventricular dysfunction can result in S3 gallop or occasionally S4 due to LVH. arrhythmias (uncommon) May be present in acute severe AR or chronic AR. ejection systolic flow murmur (uncommon)
Sometimes associated with moderate to severe AR. The murmur occurs after S1 due to the flow of increased stroke volume across a non-stenotic aortic valve. It is an early peaking, crescendodecrescendo systolic sound, best heard at second right intercostal space, and can be differentiated from an aortic stenosis murmur by the absence of an ejection click.
Austin Flint murmur (uncommon)
A soft, rumbling, mid to late diastolic murmur heard best at the apex. It is produced by the abutment of an aortic regurgitant jet against the left ventricular endocardium. [16] An Austin Flint murmur is distinguished from the murmur of mitral stenosis by the absence of an opening snap and loud S1. It is a specific finding for severe AR.
systolic thrill (uncommon) May be palpable over the base of the heart or suprasternal notch due to increased stroke volume. Hill's sign (uncommon)
Systolic pressure over popliteal artery exceeds brachial systolic blood pressure by >60 mmHg. Peripheral haemodynamic sign associated with a bounding pulse and systolic hypertension of chronic severe AR.
bisferiens pulse (uncommon) Double systolic arterial impulse. de Musset's sign (uncommon)
Patient's head may bob in time with each heart beat. Peripheral haemodynamic sign associated with a bounding pulse and systolic hypertension of chronic severe AR.
Muller's sign (uncommon) Pulsations of the uvula. Traube's sign (uncommon)
Pistol shot sounds over the femoral artery with compression. Peripheral haemodynamic sign associated with a bounding pulse and systolic hypertension of chronic severe AR.
Quincke's sign (uncommon)
Subungual or lip capillary pulsations due to the large stroke volume. Peripheral haemodynamic sign associated with a bounding pulse and systolic hypertension of chronic severe AR.
Duroziez's sign (uncommon)
Systolic and diastolic murmurs heard over the femoral artery when compressed proximally and distally, respectively. Peripheral haemodynamic sign associated with a bounding pulse and systolic hypertension of chronic severe AR.
Mayen's sign (uncommon) Diastolic drop of blood pressure >15 mmHg with arm raised. Lighthouse sign (uncommon) Blanching and flushing of forehead. Becker's sign (uncommon) Pulsations of retinal vessels. Landolfi's sign (uncommon) Alternating constriction and dilation of pupil. Rosenbach's sign (uncommon) Systolic pulsations of liver. Gerhardt's sign (uncommon) Pulsatile spleen. Lincoln's sign (uncommon)
Pulsatile popliteal artery. Sherman's sign (uncommon) Dorsalis pedis pulse is unexpectedly prominent in age >75 years. palmar click (uncommon) Palpable systolic flushing of palms. syncope (uncommon)
Risk
Rare presentation. factorshide all
Strong bicuspid aortic valve
This congenital abnormality accounts for most of the cases of AR in developed countries. Some pathological abnormalities of bicuspid aortic root occur, which lead to proximal aortic dilation and worsening of aortic regurgitation. [7] [10]
rheumatic fever One of the most common causes of AR in developing countries. endocarditis
Can lead to rupture of leaflets or even paravalvular leaks. Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of blood. [6]
Marfan's syndrome and related connective tissue disease aortitis
80% of Marfan's patients present at an early age with a diastolic murmur. [11] Disorders such as Marfan's syndrome often lead to progressive dilation of aortic root resulting in AR. Inflammation of the aorta secondary to systemic diseases such as syphilis, Behcet's, Takayasu's, Reiter's syndrome, and ankylosing spondylitis results in weakening of the aortic root and dilation. [12]
Weak systemic hypertension Can lead to aortic root dilation and inadequate closure of aortic valve leaflets. [8] older age
Older patients are more prone to develop aortic regurgitation along with aortic sclerosis. [4]
Diagnostic tests
1st tests to orderhide all
Test
ECG Provides only supportive evidence. Echocardiography is required to confirm the presence of AR.
Chronic severe AR: may demonstrate non-specific ST-T wave changes, LVH with left axis deviation due to comp LV conduction delays may be seen. Acute AR: may reveal some non-specific ST-T wave changes and sinus tachycardia or arrhythmias; evidence of myocardial ischaemia may also be present. Conduction abnormalities can also be seen in active infective endocarditis resulting from paravalvular abscess. CXR
left ventricular (LV) chamber enlargement, or isolated premature ventricular contraction. In later stages of LV dys
Chronic AR may produce cardiomegaly in the leftwards and inferior direction due to compensatory eccentric hyp aortic root dilation.
from increased end-diastolic volume. The aortic knob is typically prominent in severe hypertensive patients and t
In chronic severe AR, the aortic root sometimes progressively enlarges due to increased stroke volume and incre combined atrial stenosis and AR. echocardiogram
systolic blood pressure; calcification of the aortic valve is uncommon in pure AR but can be seen in patients with
The preferred method for non-invasive detection and evaluation of the severity and aetiology of aortic regurgitatio
M-mode and 2-dimensional imaging assessing aortic root dilation, and monitoring the left ventricular response to volume overload.View image leaflet from the regurgitant aortic jet, and hyperdynamic interventricular septal motion.
Helps indirectly assess AR. Two-dimensional echocardiography is very important in evaluating the valvular anato
Possible findings include premature closure of the mitral valve (severe/acute AR), diastolic fluttering of the anteri
colour flow Doppler proximal jet widthView image to left ventricular outflow tractView image and ratio of cross-sectional area of jet to also be used.View image [18]
One of the most specific and sensitive techniques used to judge the severity of the regurgitant flow by using the r
ventricular outflow tract. Vena contracta, which is the narrowest region of regurgitant jet just below the aortic valv
The length of the jet column in the ventricle was previously used but is no longer considered a measure of severi Parasternal views are preferred over the apical view because of better axial resolution.
pulsed wave Doppler
As AR gets worse, a greater degree of flow reversal occurs and holodiastolic flow reversal indicates severe AR; p
wave Doppler can quantitate this effect by assessing the regurgitant stroke volume and effective regurgitant orific The diastolic flow reversal is measured in the descending aorta from a suprasternal probe position.View
image Regurgitant stroke volume can be calculated by subtracting forwards stroke volume, which can be determ calculated from this. regurgitant stroke volume by jet velocity time integral of the AR assessed by continuous wave Doppler. [18] continuous wave Doppler
mitral valve, from total stroke volume (aortic valve). Both regurgitant stroke volume and regurgitant fraction can b
Effective regurgitant orifice area is another measure to assess the severity of AR, and can be calculated by divid
As aortic regurgitation gets worse, left ventricular diastolic pressure rapidly increases and aortic diastolic pressur of the assessment of AR severity.View image
falls, resulting in shorter pressure half-time or steeper slope of velocity deceleration. These measures can be use
Tests to considerhide all

Test
radionuclide angiography A useful non-invasive, accurate method of evaluating AR in patients with sub-optimal echocardiogram. Serial measurements can be helpful in early detection of systolic dysfunction. [19]
MRI
Provides accurate assessment of ventricular diameters and volumes both in systole and diastole. It also allows a
measurement of regurgitant volume and orifice size. MRI is the most accurate non-invasive technique for assess and AR severity in patients with an inconclusive echocardiogram. exercise stress testing symptoms and chronic AR. [1] cardiac catheterisation Used to evaluate coronary anatomy in patients with high risk for CAD and who will be undergoing aortic valve replacement/repair. Men aged >35 years, premenopausal women aged >35 years with risk factors for CAD, and postmenopausal women should undergo coronary angiography. Although echocardiogram accurately evaluates
but is seldom used due to its high cost. MRI can be used for initial and serial evaluation of left ventricular function
Not used as a diagnostic test, but can be used to assess the symptomatic response in patients with history of eq
severity of AR, if the results are inconclusive or discordant with clinical findings, cardiac catheterisation should be
performed to assess the severity of AR and LV function. [1] With the help of aortic root angiography, the severity and aortic root size can be assessed.
Last upda
Differential diagnosis
Condition Differentiating signs/symptoms Differentiating tests
Mitral regurgitation (MR)
Distinguishing signs are right ventricular heave, soft S1, split S2, and aloud P2. The classical murmur of MR is pansystolic at the apex radiating to the axilla.
CXR: pulmonary oedema, enlarged left atrium and left ventr calcification.
ECG: can present with atrial fibrillation.
Echocardiography: for MR it is used to assess left ventricula
Mitral stenosis
Distinguishing features are a malar flush, low volume pulse, a tapping and undisplaced apex beat, and loud S1 with an opening snap.
CXR: pulmonary oedema, enlarged left atrium, and mitral va
ECG: can present with atrial fibrillation. RVH may also be pr Echocardiography: diagnostic for mitral stenosis.
The murmur is a rumbling middiastolic one, which can be distinguished from the Austin Flint murmur sometimes heard in severe AR by the absence of the opening snap and loud S1.
Aortic stenosis
Presentation includes dyspnoea, dizziness, fainting, and congestive cardiac failure.
CXR: LVH, calcified aortic valve.
ECG: P-mitrale, LVH with strain pattern, left bundle branch b block.
Echocardiography: diagnostic for aortic stenosis.
Characteristic signs are a slow rising pulse, heaving but undisplaced apex bear, left ventricular heave, and an ejection systolic murmur that radiates towards the carotids and can have an ejection click. This can be distinguished from the ejection systolic murmur that is sometimes heard with moderate or severe AR by absence of an ejection click and no radiation towards the carotids.
Pulmonary regurgitation
Diamond-shaped diastolic murmur best heard in the second and third left intercostal spaces. The murmur increases with inspiration,
CXR: may show dilation of main pulmonary artery with right ECG: right ventricular hypertrophy is usually present. Echocardiography: diagnostic for pulmonary regurgitation.
and P2 is loud in the presence of pulmonary artery hypertension.
Step-by-step diagnostic approach

AR is usually detected on clinical examination with a diastolic murmur, or incidentally during echocardiographical evaluation for other causes. ECG, CXR, and echocardiogram are routinely performed for all patients with features of AR.
Acute AR: clinical presentation

The patient can present with sudden onset of pulmonary oedema and hypotension or in cardiogenic shock. Patients may also present with signs and symptoms of myocardial ischaemia or aortic root dissection. When valvular regurgitation is acute, many of the characteristic findings of chronic AR are absent and the severity of the problem may be underestimated. For example, during the physical examination, no increase in left ventricular (LV) size may be detected and the diastolic murmur may be short and/or soft due to diastolic pressure equilibrium between aorta and ventricle occurring before the end of diastole. An apical diastolic rumble may be present. Pulse pressure may not be increased due to reduced systolic pressure. [1] Signs and symptoms of pulmonary oedema Dyspnoea Pink frothy sputum Pale and sweaty Basal lung crepitations Wheeze (cardiac asthma). Signs and symptoms of cardiogenic shock Pale and/or cyanotic, cool to touch with mottled extremities Evidence of hypoperfusion with altered mental status and decreased urine output Rapid and faint peripheral pulses Jugular venous distension Third and fourth heart sounds may be present
Arrhythmias Dyspnoea. Mycardial ischaemia, due to decreased perfusion pressure in acute severe AR, classically presents with central crushing chest pain radiating to the jaw or left arm. Aortic root dissection classically presents with chest pain radiating to the back.
Acute AR: investigation and imaging

ECG Determines any arrhythmias and the rate of tachycardia. It will also rule out or diagnose myocardial ischaemia or infarction. CXR May not show cardiomegaly, which is a characteristic finding for chronic AR. There may be evidence of pulmonary oedema with bilateral basal shadowing, pleural effusions at costophrenic angles, and fluid in the lung fissures. Trans-thoracic echocardiogram One of the best non-invasive diagnostic tests to evaluate the valvular diseases. [13] Confirms the presence and severity of the valvular regurgitation, assesses LV size (which is usually normal) and systolic function, and determines a cause. Trans-oesophageal echocardiogram Performed if aortic root dissection is suspected: classically, patients have chest pain that radiates to the back . [1]
Chronic AR: clinical symptoms

Patients have a protracted course and remain asymptomatic for decades. LV systolic dysfunction often precedes the development of symptoms. Patients may remain asymptomatic with normal exercise tolerance even with chronic severe AR due to LV compensation. Initial symptoms may include uncomfortable awareness of the pounding heart when lying on the left side, due to closer contact of the enlarged LV with the chest wall. [9] Palpitations occur frequently, secondary to premature ventricular contractions. These symptoms may persist for years before exercise intolerance occurs. With progressive systolic dysfunction, patients will complain of typical symptoms of CHF including fatigue, weakness, orthopnoea, and paroxysmal nocturnal dyspnoea.
Uncommonly, patients may complain of angina without CAD at rest or with exercise. Myocardial ischaemia can result in interstitial fibrosis, which further deteriorates LV systolic function. Syncope and sudden cardiac death are rare.
Chronic AR: clinical signs

Pulse Arterial pulse shows rapid rise and a quick collapse (Corrigan's pulse or water hammer pulse) resulting in widened pulse pressure >50 mmHg. There are multiple eponymous peripheral haemodynamic signs associated with a bounding pulse and systolic hypertension of chronic severe AR. The sensitivity and specificity of these signs in diagnosing AR is low and should be used only as supportive evidence. [14] Apical impulse volume. Murmurs The murmur of AR is a high-pitched early diastolic, decrescendo blowing sound, which is heard best with the diaphragm of the stethoscope just after A2. [15] The murmur is usually soft and can be accentuated with the patient sitting up, leaning forwards, and holding his or her breath at the end of expiration. The murmur due to valvular cause is best heard at the third and fourth intercostal space at the left sternal border. Regurgitation due to aortic dilation resulting from dissection or aneurysm is best heard at the second to third right intercostal space. Manoeuvres that increase arterial pressure, such as squatting, accentuate the murmur, whilst inhalation of amyl nitrate or Valsalva, which lower arterial pressure, decreases the intensity of the murmur. Moderate to severe AR is sometimes associated with an ejection systolic flow murmur after S1 due to the flow of increased stroke volume across a non-stenotic aortic valve. The murmur is an early peaking, crescendo-decrescendo systolic sound, best heard at the second right intercostal space, and can be differentiated from an aortic stenosis murmur by the absence of an ejection click. Another murmur that is often associated with severe AR is the Austin Flint murmur. It is a soft, rumbling, mid to late diastolic murmur heard best at the apex. It is produced by the abutment of an aortic regurgitant jet against the LV endocardium. [16] An Austin Flint murmur is distinguished from the murmur of mitral stenosis by the absence of an opening snap and loud S1. Heart sounds Diffuse, hyperdynamic, and shifted inferiorly and leftwards. A systolic thrill may be palpable over the base of the heart or suprasternal notch due to increased stroke
Chronic AR is also associated with changes in heart sounds. S1 may be due to early coaptation of the mitral valve leaflets from increased end-diastolic pressure. With increasing severity of AR, end-diastolic pressure can rise steeply above left atrial pressure causing even diastolic closure of the mitral valve.
LV dysfunction can result in S3 gallop or occasionally S4 due to LVH. Inadequate closure of aortic valve in severe AR may cause a soft A2 or even absent A2.
Chronic AR: imaging and investigations

Physical signs are not specific enough to judge the severity of the AR. Echocardiography should be performed for evaluation of symptomatic and asymptomatic chronic AR. If the echocardiogram is of insufficient quality, radionuclide angiography or MRI can be ordered to evaluate the valvular abnormality. ECG CXR Cardiomegaly is a characteristic finding in chronic AR. Echocardiogram For asymptomatic patients with chronic AR, the diagnosis can be established using a good-quality echocardiogram, and no further diagnostic testing is required. [1] This test allows visualisation of the origin of the regurgitant jet and its width, and detection of the cause of aortic valve pathology. A trans-thoracic echocardiogram is usually adequate, but a trans-oesophageal echocardiogram can be used if the quality of the trans-thoracic echocardiogram is inadequate. [1] Two-dimensional echocardiography helps in evaluating the valvular anatomy and the impact of volume overload on the ventricular size and function. M-mode imaging indirectly assesses the AR by detecting premature closure of the mitral valve and diastolic fluttering of the anterior mitral leaflet from the regurgitant aortic jet. Doppler echocardiography is the most specific technique used for detecting the severity of regurgitation. Several indices are used to assess severity. Colour flow Doppler provides visualisation of the origin of the regurgitant jet and its width. There are several pulsed and continuous wave Doppler methods that give clues to the severity of AR. These include colour flow, pulsed wave, and continuous wave Doppler. Exercise testing In chronic severe AR, if the patient's physical activity is minimal or symptoms are equivocal, exercise testing is helpful to assess the functional status and symptomatic response. [1] Cardiac catheterisation, angiography, or MRI Normal early in the disease but shows left axis deviation in chronic aortic regurgitation supporting LV volume overload. May also show signs of conduction abnormalities. [1]
In asymptomatic patients with chronic AR, if the quality of the echocardiogram is inadequate to assess LV function, radionuclide angiography or MRI can be used. [1] In cases of acute AR, right and left heart catheterisation shows severe elevations of LV end-diastolic pressure and pulmonary capillary wedge pressure (PCWP) due to sudden volume overloading of a normal sized LV. LV end-diastrolic pressure is often much higher than PCWP because of early closure of the mitral valve.
Angiography is also used to evaluate coronary anatomy in patients with high risk for CAD and who will be undergoing aortic valve replacement/repair. In this setting, men aged >35 years, premenopausal women aged >35 years with risk factors for CAD, and postmenopausal women should undergo coronary angiography.
Click to view diagnostic guideline references.
Diagnostic criteria
Classification of the severity of aortic regurgitation in adults (ACC/AHA practice guidelines for the management of patients with valvular heart disease) [1]
Mild AR
Angiographic grade: 1+ Colour Doppler jet width: central jet, width <25% of left ventricular outflow tract (LVOT) Doppler vena contracta width (cm): <0.3 Regurgitant volume (mL/beat): <30 Regurgitant fraction (%): <30 Regurgitant orifice area (cm^2): <0.10.
Moderate AR
Angiographic grade: 2+ Colour Doppler jet width: greater than mild but no signs of severe AR Doppler vena contracta width (cm): 0.3-0.6 Regurgitant volume (mL/ beat): 30-59 Regurgitant fraction (%): 30-49
Regurgitant orifice area (cm^2): 0.10-0.29.
Severe AR
Angiographic grade: 3-4+ Colour Doppler jet width: central jet, width >65% of LVOT Doppler vena contracta width (cm): >0.6 Regurgitant volume (mL/beat): 60 Regurgitant fraction (%): 50 Regurgitant orifice area (cm^2): 0.30 Left ventricular size: increased.
Stages of chronic aortic regurgitation assessed by echocardiogram and cardiac catheterisation

Different criteria have been developed to diagnose patients based on Doppler echocardiographic and cardiac catheterisation measurements, to help time the surgery and ensure the benefits outweigh the perioperative risk (mortality 4%) and long-term complications of prosthetic valve. [20] [21] [1] Compensated
Ejection fraction >55% Fractional shortening >32% End-diastolic diameter <60 mm End-systolic diameter <45 mm End-diastolic volume <120 mL/m^2 End-systolic volume <50 mL/m^2
Transitional
Ejection fraction 51% to 55% Fractional shortening 30% to 31%
End-diastolic diameter 60-70 mm End-systolic diameter 45-50 mm End-diastolic volume 130-160 mL/m^2 End-systolic volume 50-60 mL/m^2
Decompensated
Ejection fraction 50% Fractional shortening <29% End-diastolic diameter >75 mm End-systolic diameter > 55 mm End-diastolic volume >170 mL/m^2 End-systolic volume >60 mL/m^2
Case history #1
A 55-year-old white man presents with weakness, palpitations, and dyspnoea on exertion. On physical examination, his blood pressure is 148/50 mmHg with a bounding pulse and an early diastolic murmur over the left sternal border. He denies any history of drug abuse, rheumatic fever, or connective tissue disorder. The patient is taking hydrochlorothiazide for high blood pressure. Echocardiography reveals a left ventricular ejection fraction (LVEF) of 55%, left ventricular end-diastolic diameter of 70 mm, and end-systolic diameter of 50 mm.
Case history #2
A 31-year-old black man presents to clinic for the first time for a routine physical examination. He denies any complaints. On physical examination the only abnormality is a systolic murmur best heard over the second right intercostal space and an early diastolic murmur best heard over the third left sternal border. LVEF is 55% to 60% with mild LVH. Left ventricular endsystolic diameter is 45 mm and aortic root diameter is 3.5 cm.
Other presentations
In acute AR, patients can present with sudden onset of pulmonary oedema and hypotension or in cardiogenic shock. Patients may also present with signs and symptoms of myocardial ischaemia or aortic root dissection. Due to the acute nature of the aortic regurgitation, there may be no increase in left ventricular size, and the diastolic murmur may be short and/or soft due to diastolic pressure equilibrium between aorta and ventricle occurring before the end of diastole. An apical diastolic rumble may be present. Pulse pressure may not be increased due to reduced systolic pressure. [1]
Treatment Options
Treatment Patient group acute AR line 1st Treatmenthide all
inotropes + vasodilators + urgent aortic valve replacement
Acute AR is a surgical emergency. Haemodynamic support with inotropic agents (dopamine and dobutamine) and vasodilators may be necessary for stabilisation before surgery.
Aortic valve replacement or repair should be performed as soon as possible. Prosthetic valve patients are at high risk for thromboembolism and need antithrombotic therapy. The risk of bleeding must be weighed against the benefit of anticoagulation.
Intravenous infusion rates >10 micrograms/kg/min may lead to cyanide toxicity with nitroprusside. Primary Options dopamine : 2-5 micrograms/kg/min intravenously initially, titrate to effect, maximum 20 micrograms/kg/min or dobutamine : 0.5 micrograms/kg/min intravenously initially, titrate to effect, maximum 20 micrograms/kg/min -- AND -nitroprusside : 0.3 to 0.5 micrograms/kg/min intravenously, titrate to effect, maximum 10 micrograms/kg/min -- AND -aortic valve replacement
Acute
Treatment Patient group mild to moderate chronic AR line Treatmenthide all
Acute
Treatment Patient group asymptomatic with normal left ventricular function line 1st Treatmenthide all
reassurance
Patients with normal left ventricular function (ejection
Acute
Treatment Patient group line Treatmenthide all
fraction >50%) do not require treatment and can be reassured. The outcome in these patients with no
Acute
therapy is excellent.
Acute
Treatment Patient group symptomatic or left ventricular line 1st Treatmenthide all
investigation and treatment of alternative underlying cause
Acute
Treatment Patient group dysfunction line Treatmenthide all
Medical therapy and surgery are not recommended,
Acute
as an alternative cause is likely. Patient should be
Acute
investigated for alternative causes for the symptoms
Acute
of left ventricular dysfunction: for example,
Acute
hypertension, CAD, or a cardiomyopathy.
Acute
Treatment Patient group severe chronic AR: asymptomatic with ejection line Treatmenthide all
Acute
Treatment Patient group fraction >50% line Treatmenthide all
Acute
Treatment Patient group compensated disease line 1st Treatmenthide all
reassurance
Patients with normal left ventricular (LV) function
Acute
(ejection fraction >50%) and no LV dilation as indicated by normal end-diastolic and end-systolic
Acute
diameters have compensated disease. No treatment is required in these patients.
Acute
Treatment Patient group transitional disease: negative exercise test line 1st Treatmenthide all
reassurance
Acute
(ejection fraction >50%) and either end-diastolic diameter 60-70 mm or end-systolic diameter 45-50
Acute
mm have transitional disease.
Acute
These patients require an exercise tolerance test. If the results are normal, no treatment is required.
Acute
Treatment Patient group transitional disease: positive exercise test line 1st Treatmenthide all
vasodilator therapy
Acute
(ejection fraction >50%) and either end-diastolic diameter 60-70 mm or end-systolic diameter 45-50
Acute
mm have transitional disease.
Acute
These patients require an exercise tolerance test. If there is an abnormal haemodynamic response to an
Acute
exercise test, vasodilator therapy is recommended. Vasodilators include hydralazine and nifedipine.
Acute
Primary Options
Acute
nifedipine : 30-60 mg orally (extended-release) once daily
Acute
OR
Acute
hydralazine : 10-25 mg orally 2 to 4 times daily
Acute
initially, titrate according to response, maximum 300
Acute
mg/day
Acute
Treatment Patient group decompensated disease: surgical candidate line 1st Treatmenthide all
aortic valve replacement
Patients with normal left ventricular (LV) function but
Acute
an end-diastolic diameter >70 mm or an end-systolic diameter >50 mm have decompensated disease.
Acute
These patients require surgery.
Acute
Aortic valve replacement with a mechanical or a biological valve has a low rate of requiring
Acute
reoperation. This durability comes at the expense of valve-related complications such as
Acute
thromboembolism, anticoagulant-related bleeding, and infective endocarditis.
Acute
Prosthetic valve patients are at high risk for thromboembolism and need antithrombotic therapy.
Acute
The risk of bleeding must be weighed against the benefit of anticoagulation.
Acute
Treatment Patient group decompensated disease: nonline 1st Treatmenthide all
vasodilator or ACE inhibitor therapy
Acute
Treatment Patient group surgical candidate line Treatmenthide all
Patients with normal left ventricular (LV) function but
Acute
an end-diastolic diameter >70 mm or an end-systolic
Acute
diameter >50 mm have decompensated disease.
Acute
Surgery is contraindicated in patients with severe
Acute
comorbidities. Severe LV dysfunction is not a
Acute
contraindication. If contraindications to surgery are
Acute
present, these patients can be managed with medical
Acute
therapy.
Acute
Vasodilator therapy may be considered for long-term
Acute
treatment in stable patients (class IIb). [1] Long-term
Acute
studies on the effects of vasodilators on
Acute
haemodynamics have shown inconsistent
Acute
results. [26] [27] [28] [29] [30]There are no
Acute
recommendations on the preference of vasodilators.
Acute
Primary Options nifedipine : 30-60 mg orally (extended-release) once
Acute
Treatment Patient group severe chronic AR: asymptomatic with ejection line Treatmenthide all
Acute
Treatment Patient group fraction 50% line Treatmenthide all
Acute
Treatment Patient group surgical candidate line 1st Treatmenthide all
Patients with an ejection fraction 50% have
Acute
decompensated disease and require surgery.
Acute
Aortic valve replacement with a mechanical or a biological valve has a low rate of requiring
Acute
reoperation. This durability comes at the expense of valve-related complications such as
Acute
thromboembolism, anticoagulant-related bleeding, and infective endocarditis.
Acute
Acute
Acute
Treatment Patient group non-surgical candidate line 1st Treatmenthide all
vasodilator or ACE inhibitor therapy
Acute
Patients with an ejection fraction 50% have
Acute
decompensated disease.
Acute
Acute
comorbidities. Severe LV dysfunction is not a
Acute
contraindication. If contraindications to surgery are
Acute
present, these patients can be managed with medical
Acute
therapy.
Acute
Vasodilator therapy may be considered for long-term
Acute
treatment in stable patients (class IIb). [1] Long-term
Acute
studies on the effects of vasodilators on
Acute
haemodynamics have shown inconsistent
Acute
results. [26] [27] [28] [29] [30]There are no
Acute
recommendations on the preference of vasodilators.
Acute
Primary Options nifedipine : 30-60 mg orally (extended-release) once
Acute
Treatment Patient group severe chronic AR: symptomatic line Treatmenthide all
Acute
Treatment Patient group surgical candidate line 1st Treatmenthide all
Indicated for all symptomatic patients regardless of
Acute
left ventricular function or dilation. Aortic valve replacement with a mechanical or a biological valve
Acute
has a low rate of reoperation. This durability comes at the expense of valve-related complications such
Acute
as thromboembolism, anticoagulant-related bleeding, and infective endocarditis.
Acute
Acute
Acute
adjunct [?]
vasodilator therapy
Using vasodilator therapy should be considered while
Acute
awaiting surgery.
Acute
Primary Options
Acute
Acute
OR
Acute
Acute
Acute
mg/day
Acute
Treatment Patient group non-surgical candidate line 1st Treatmenthide all
vasodilator therapy
Acute
comorbidities. Severe LV dysfunction is not a contraindication. If contraindications to surgery are
Acute
present, these patients can be managed with medical therapy.
Acute
Using vasodilator therapy should be considered in symptomatic patients who have contraindications to
Acute
surgery.
Acute
Primary Options
Acute
Acute
OR
Acute
Acute
Acute
mg/day
Acute
Ongoing
Last updat
Treatment approach
Acute AR is an emergency requiring urgent surgical intervention. Chronic AR has a protracted course and the patient may remain asymptomatic for decades. Many of those who have mild or moderate AR remain stable and may never require any corrective surgery. Surgery should be performed as soon as possible in patients with chronic AR who develop haemodynamic instability or CHF. The treatment of chronic AR depends on 5 factors:
Whether the regurgitation is mild, moderate, or severe Whether the patient is asymptomatic or symptomatic Whether the patient has normal left ventricular (LV) function or LV dysfunction Whether the patient has LV dilation Whether the patient is a surgical candidate.
Assessment of disease severity

Mitral regurgitation is classified as mild, moderate, or severe based on defined echocardiographic, Doppler, and angiographic features. [1] Mild AR
Angiographic grade: 1+ Colour Doppler jet width: central jet, width <25% of left ventricular outflow tract (LVOT) Doppler vena contracta width (cm): <0.3 Regurgitant volume (mL/beat): <30 Regurgitant fraction (%): <30 Regurgitant orifice area (cm^2): <0.10.
Moderate AR
Angiographic grade: 2+
Colour Doppler jet width: greater than mild but no signs of severe AR Doppler vena contracta width (cm): 0.3-0.6 Regurgitant volume (mL/ beat): 30-59 Regurgitant fraction (%): 30-49 Regurgitant orifice area (cm^2): 0.10-0.29.
Severe AR
Angiographic grade: 3-4+ Colour Doppler jet width: central jet, width >65% of LVOT Doppler vena contracta width (cm): >0.6 Regurgitant volume (mL/beat): 60 Regurgitant fraction (%): 50 Regurgitant orifice area (cm^2): 0.30 Left ventricular size: increased.
Acute AR
Acute AR is a surgical emergency. Patients require assessment and management of the airway, with intubation if necessary. Positive inotopic agents (e.g., dopamine and dobutamine and a vasodilator) and a vasodilator (e.g., sodium nitroprusside) are recommended for haemodynamic support. The definitive management is with urgent surgery, especially for patients with AR resulting from infective endocarditis and aortic root dissection. [1]
Mild to moderate chronic AR

Patients with mild to moderate disease who are asymptomatic with normal LV function do not require treatment and can be reassured; the outcome in these patients is excellent . In patients with this degree of AR severity, symptoms or LV dysfunction, if present, are unlikely to be due to AR. An alternative underlying cause such as hypertension, CAD, or a cardiomyopathy is more likely and should be investigated and treated.
Severe chronic AR
Patients who are asymptomatic are managed according to the stage of their disease, which is reflected by the presence and severity of LV function, measured by the ejection fraction (EF), and LV dilation, measured by the end-diastolic (EDD) and end-systolic (ESD) diameters.
Compensated disease: if LV function is normal (EF >50%) and there is no LV dilation (EDD <60 mm or ESD <45 mm), no treatment is required and the patient can be reassured. Transitional disease: if LV function is normal but LV dilation in the range EDD 60-70 or ESD 45-50 mm is present, an exercise tolerance test should be performed. If the exercise test is normal, no treatment is required. However, if an abnormal haemodynamic response occurs, vasodilator therapy (hydralazine or nifedipine) is recommended. [B Evidence] Decompensated disease: surgery is required in patients with normal LV function but an EDD >70 or ESD >50 mm or with abnormal LV function (EF 50%). Vasodilators may be used while the patient is awaiting surgery.[B Evidence]
All symptomatic patients require surgery, regardless of their LV function and dilation.[B Evidence] If the patient is not a surgical candidate due to comorbidities, long-term therapy with vasodilators or angiotensin convertingenzyme inhibitors (e.g. enalapril) is recommended.[1] [22] The surgical options are aortic valve replacement (AVR) or repair. There is no difference in the indications for replacement or repair. AVR is performed in most patients requiring surgery. Aortic valve repair is possible in selected patients but is only performed in specialist centres. Following surgery, most of the patients show reversal of LV dilation and improvement in EF. Preoperative LV function is the best predictor of long-term prognosis in patients undergoing AVR. [23] Patients with normal preoperative EF or a brief duration of LV dysfunction (<14 months) have greater improvement in LV diameters and early and late postoperative improvement in LV function. [24] Among patients with LV dysfunction, patients with impaired preoperative LV function have a greater risk of developing CHF and are at a higher risk of death compared with patients with normal preoperative LV function. [25] Survival among patients with preoperative severe LV dysfunction has improved dramatically since 1985 and has become almost equivalent to that among patients with non-severe LV dysfunction.
Monitoring
Patients who present to their physician with AR on initial evaluation need to be followed up closely due to the protracted course and potential
complications of the disease. These patients need to be serially monitored based on the severity of AR, left ventricular ejection fraction (LVEF), and left ventricular (LV) diameters. Asymptomatic patients with mild chronic AR and normal LVEF can be seen yearly, and routine echocardiography can be done every 2 to 3 years. Asymptomatic patients with chronic severe AR and normal LVEF are serially monitored based on LV diameters. [1] Those with LV end-systolic diameter <45 mm and end-diastolic diameter <60 mm need clinical evaluation every 6 to 12 months, and echocardiography every 12 months. [1] In patients with LV end-systolic diameter 45-50 mm and end-diastolic diameter 60-70 mm, clinical evaluation every 6 months and echocardiography every 12 months is required. [1] Those with LV end-systolic diameter 50-55 mm and end-diastolic diameter 70-75 mm and normal haemodynamic response to exercise need clinical evaluation every 6 months and echocardiography every 6 months. [1] Patients with aortic root dilation and diameter >4 cm should undergo serial evaluations of aortic root and ascending aorta by echocardiography, CT scan, or MRI yearly. [1] Patients who undergo aortic valve replacement/repair need close follow-up during the early and late postoperative course and need to be serially monitored. Asymptomatic patients need to be followed up yearly for a complete history and physical examination. [1] Any change in clinical status demands echocardiography. Prosthetic valve patients are at high risk for thromboembolism and need antithrombotic therapy. The risk of bleeding must be weighed against the benefit of anticoagulation.
Patient Instructions
Patients are encouraged to do moderate exercise, but patients with severe AR and LV end-diastolic diameter >65 mm should be advised to avoid active sport. [38] Those on anticoagulation are advised to avoid contact sport. Patients should be advised of the possible complications of having a prosthetic valve, such as thromboembolism, infective endocarditis, haemolysis, structural valve failure, and arrhythmias. They are advised to seek medical help if they become suddenly breathless, develop a fever, or experience palpitations or sudden onset of weakness of a limb, or complete or partial loss of sight.
Patients should also be advised about the risks of being on anticoagulation, the main one being haemorrhage. The patient should report unusual bruises, bleeding gums, coughing up blood, dark urine, and black bowel movements. Ideally, they are advised to avoid any activity that may increase their chances of bruising or bleeding, such as contact sport. They are also reminded that they should tell the pharmacist, doctor, and dentist that they are taking warfarin, as some medications affect how the drug works: for example, broad-spectrum antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs). Patients are encouraged to attend every appointment to have their INR checked.
Complications
Complicationhide all
operative mortality There is a 4% risk of death with AVR, and the risk increases to 6.8% if performed along with CABG. [33] [37] CHF see our comprehensive coverage of Chronic congestive heart failure The most common complication of severe AR. Mild to moderate AR may remain asymptomatic throughout patient's life or may progress to severe AR and then CHF. Chronic severe AR patients should be referred for aortic valve replacement/repair (AVR) as soon as they develop any symptoms, impaired exercise tolerance, or decreased ejection fraction. [31] [33] Patients with severe left ventricular dysfunction and symptoms of CHF should be started on medical therapy (inotropes and vasodilators) and referred for AVR. arrhythmias see our comprehensive coverage of Overview of dysrhythmias (cardiac) Stretching and dilation of the left atrium results in atrial fibrillation, which leads to weakness, dyspnoea, palpitations, and occasionally syncope. The AV node, due to its proximity to the aortic valve, may be damaged secondary to stretching and scarring, which sometime results in bradyarrhythmias and different degrees of block that are treated with medications and/or a pacemaker. infective endocarditis see our comprehensive coverage of Infective endocarditis Bacteraemia with organisms likely to cause endocarditis results in this complication in patients with underlying structural valvular defects.
Patients with AR are considered to be at low risk of developing endocarditis, and prophylactic antibiotics are not required before bacteraemia-causing procedures. [34] sudden death Sudden death is rare in patients with severe AR and normal ventricular function. Annual mortality is 0.4%. One paper reported unexpected sudden deaths in patients with maintained systolic function but severe ventricular dilation. [32] myocardial ischaemia see our comprehensive coverage of Overview of acute coronary syndrome Patients with AR may complain of angina without CAD due to increased myocardial oxygen requirement and decreased coronary flow reserve. [35] [36]
Prognosis
Mortality is low (<0.4 % per year) in this group and therefore aortic valve replacement is not required, but patients do need to be monitored closely for developing symptoms or LV dysfunction. [31] These patients are at risk of progressing to symptoms and/or LV dysfunction at the rate of 5% per year with a mortality of 0.2% per year. [32] In patients with more severe LV dilation (end-systolic diameter >50 mm or end-diastolic diameter >70 mm), there is an even higher risk of developing LV dysfunction (19%) or symptoms (10%). [1] [32] The outcome and prognosis of patients depends on the magnitude of LV function and symptoms. [25] [24] The 5-year survival in patients with normal LV function has been reported as 96% whereas that in patients with reduced LV function is 62%. [25] Long-term improvement in LV function is related to the immediate and short-term (first 6 months) response to surgery. Patients who have an immediate reduction in LV dilatation following surgery are more likely to have short- and long-term improvements in the ejection fraction (EF). Furthermore, patients who have an improvement in EF within the first 6 months following surgery are likely to have further late improvements in LV function after this time. The EF is unlikely to improve in patients who do not have an improvement in EF within the first 6 months of surgery. [24]
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Parasternal long-axis view demonstrating aortic regurgitation jet From authors' collection
Parasternal long-axis view demonstrating aortic regurgitation jet width and height From authors' collection
Parasternal long-axis view demonstrating left ventricular outflow tract diameter From authors' collection
Parasternal long-axis view showing vena contracta of the aortic regurgitation jet From authors' collection
Pulsed wave Doppler of the regurgitant jet From authors' collection
Continuous wave Doppler of the regurgitant jet demonstrating pressure half-time of the aortic regurgitant velocity From authors' collection

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Aortic regurgitation

History & exam

Other diagnostic factors

Other related conditions

History & examination

diastolic murmur (common)

Sign of cardiogenic shock.

Austin Flint murmur (uncommon)

Muller's sign (uncommon) Pulsations of the uvula. Traube's sign (uncommon)

Quincke's sign (uncommon)

Duroziez's sign (uncommon)

Rare presentation. factorshide all

Strong bicuspid aortic valve

Marfan's syndrome and related connective tissue disease aortitis

pulsed wave Doppler

Tests to considerhide all

Mitral regurgitation (MR)

ECG: can present with atrial fibrillation.

Echocardiography: for MR it is used to assess left ventricula

CXR: pulmonary oedema, enlarged left atrium, and mitral va

Presentation includes dyspnoea, dizziness, fainting, and congestive cardiac failure.

CXR: LVH, calcified aortic valve.

Echocardiography: diagnostic for aortic stenosis.

and P2 is loud in the presence of pulmonary artery hypertension.

Step-by-step diagnostic approach

Acute AR: clinical presentation

Acute AR: investigation and imaging

Chronic AR: clinical symptoms

Chronic AR: clinical signs

Chronic AR: imaging and investigations

Regurgitant orifice area (cm^2): 0.10-0.29.

Stages of chronic aortic regurgitation assessed by echocardiogram and cardiac catheterisation

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Patients with normal left ventricular function (ejection

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

investigation and treatment of alternative underlying cause

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Medical therapy and surgery are not recommended,

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

as an alternative cause is likely. Patient should be

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

investigated for alternative causes for the symptoms

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

of left ventricular dysfunction: for example,

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

hypertension, CAD, or a cardiomyopathy.

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Treatment Patient group acute AR line 1st Treatmenthide all

inotropes + vasodilators + urgent aortic valve replacement

Treatment Patient group acute AR line 1st Treatmenthide all