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Valvular Disease and Murmurs

Introduction

 

The heart contains four valves, which open and close in response to pressure changes during the cardiac cycle. These valves are one-way and thus prevent the backflow of blood ensuring blood is pumped in the right direction through the heart and into the arteries. These valves are composed of dense connective tissue and are covered by endocardium. All valves have three cusps, apart from the mitral valve which only has two leaflets.

 

On the left side of the heart, the left ventricle is separated from the left atrium by the mitral valve, also known as the left atrioventricular valve. Following this, the left ventricle is seperated from the aorta by the aortic valve. Conversely, on the right side of the heart, the right ventricle is seperated from the right atrium by the tricuspid valve, also known as the right atrioventricular valve. In turn, the right ventricle is separated from the pulmonary trunk by the pulmonary valve

 

NB See below for Cardiac Cycle figure illustrating valve opening and closing in response to left atrial, aortic and ventricular pressure changes. Diagram also illustrates the relationship between heart sounds 1 and 2 to the closing of the mitral/tricuspid and aortic/pulmonary valves respectively. Also included are ventricular volume and ECG changes too.

 

A disease of the valves within the heart is commonly reffered to as valvular disease and consequently, the valves ability to perform its normal function is impaired. A single valve may be affected initially but over time other valves may become involved too, complicating the clinical picture. 

 

Valvular disease can be divided into two types: stenosis or regurgitation . Stenosis, refers to a narrowing of the valve, in other words the valve cannot fully open and as a result there is a decreased blood flow across the valve. Regurgitation, is the failure of the valve to close completely, allowing the backflow of blood. More importantly, valvular disease has serious implications leading to induce strokeatrial fibrillation (AF)heart failure (HF) and even sudden cardiac death (SCD).  

 

Auscultation Sites

Auscultation sites for valves of the heart

Cardiac Cycle

Cardiac Cycle Figure illustrating valve opening and closing in response left atrial, aortic and vent

Aortic Valve Disease

Aortic Stenosis (AS)

 

Incidence

Aortic Stenosis (AS) is the most common type of valvular disease, continuing to increase in incidence. This may be due to the development of better diagnostic tools thus increasing its detection as well as an ageing population. As much as up to 2% of the population, over the age of 65, have features of AS on echocardiography.

 

Causes

Congenital: Bicuspid aortic valve (1-2% of population) or William's syndrome

Acquired: Senile calcification is the most common cause but other causes include rheumatic heart disease (RHD), end-stage renal failure or Pagets disease of the bone

 

Pathophysiology

The pathophysiology of AS varies according to the aetiology, although most aetiologies share a final common pathway. The effect, is an increased end-diastolic pressure (EDP) and compensatory left ventricular hypertrophy (LVH). Senile calcification progresses over several years with inflammation and calcium deposition resulting in reduced opening of the aortic valve. In the case of a congenital bicuspid aortic valve, chronic turbulent blood flow leads to early calcification and fibrosis. Nevertheless, regardless of the cause, the effect of a narrowed aortic valve is obstruction of blood flow from the heart, which contributes to symptoms discussed below.  

 

Symptoms  

  • Angina
  • Syncope
  • Dysponea (typically "on effort")
  • Exertional syncope
  • Palpitations
  • Dizziness

 

Signs  

  • Soft S2
  • Low volume
  • Slow rising pulse (best felt at carotids)    
  • Narrow pulse pressure (systolic pressure - diastolic pressure)
  • Ejection systolic murmur (ESM)
  • Heaving apex beat (non-displaced)
  • LV heave
  • Systolic ejection click
  • S4 may be audible in severe AS
  • Systolic thrill (best felt in aortic area during complete expiration)

 

NB The ESM is heard loudest in the aortic area, during full expiration but is also heard at other sites and radiating to the carotids. The loudness of the murmur itself does not correlate with the severity of AS. Instead, it is the loudness of S2 that indicates severity, with a quieter S2 implying a more severe AS.

 

Investigations

  • ECG - LVH with strain pattern, left/right bundle branch block (LBBB/RBBB) or complete atrioventricular (AV) block
  • CXR - LVH, calcification or post stenotic dilatation of ascending aorta
  • Echocardiogram - Assesses severity of calcified valve and gradient across it 
  • Cardiac catheterisation - Assesses the extent of pre-existing coronary heart disease (CHD) as well as LV function
  • Cardiac MRI - Provides important anatomical, functional and haemodynamical information

 

Management

Medical: The severity of AS will dictate the management, although without surgery the prognosis is poor, as AS is a progressive disease. Medical therapy, is primarily aimed at reducing the demand on the heart through reducing myocardial oxygen consumption and increasing coronary blood flow. Thus, beta-blockers and loop diuretics are useful since they decrease preload on the heart. Patients with aortic stenosis are at risk of syncope and often have preexisting cardiovascular disease. Thus in these patients medications including nitrates, ACE inhibitors, nitroglycerin and hydralazine should be best avoided as all lead to peripheral vasodilation, which may reduce the gradient across the valve, exacerbating symptoms such as syncope. 

Surgical: Surgery offers a cure to those with AS and is the treatment of choice in patients who are symptomatic. This involves aortic valve replacement. However, the risks of having surgery must be weighed against the benefits, as there are associated complications including long term valve failure, arrhythmias, formation of blood clots and death.

Balloon aortic valvuloplasty: This is an alternative to open invasive surgery but is currently restricted to those with non-calcified AS, due to the high procedural complication rate which can cause myocardial infarction (MI), perforation or aortic regurgitation (AR).

Novel Treatments: Trans-aortic valve implantation (TAVI) is a novel, minimally invasive technique, that follows the principles of cardiac catheterisation. This includes the use of catheters to guide the aortic valve from the site of entry (often via the femoral route) to the heart itself, where it is then deployed. This is a suitable alternative procedure for those patients who are not fit for surgical replacement. In one study involving patients with symptomatic severe AS, who were not fit for surgical replacement, the use of TAVI was associated with an improvement in survival, symptoms and quality of life, when compared to standard treatment.

 

Murmur of AS

An ejection systolic murmur associated with aortic stenosis. Alternatively, described as a cresendo-

Aortic Regurgitation (AR)

 

Incidence

Aortic regurgitation (AR) is becoming less and less common due to a decline in the incidence of rheumatic fever (RF). The remaining cases are instead related to aortic root disease.

 

Aetiology

Acute: Infective endocarditis (IE), ascending aortic root disease or trauma especially to the chest.

Chronic: Congenital, Marfan's syndrome, systemic lupus erythematosus (SLE) or RHD.

 

Alternatively, causes can be divided into:

 

Aortic valve: Congenital bisuspic aortic valve, IE, RF and collegen vascular diseases.

Aortic root (in the absence of valve pathology): Uncontrolled hypertension, Marfans syndrome, aortic dilation, ankylosing spondylitis. 

 

NB A good menomic for the causes of AR: SCREAM AR 

  • Syphilis
  • Congenital
  • Rheumatic fever
  • Endocarditis
  • Aortic root disease
  • Marfan's syndrome
  • Ankylosing spondylitis
  • Rheumatoid arthritis

 

Pathophysiology

The destruction or fusion/fibrosis, of the cusps of the aortic valve, results in its failure to close completely. This allows the backflow of blood into the left ventricle. Consequently, there is an increase in end diastolic volume (EDV) with compensatory LV dilatation and associated myocyte dysfunction.

 

Symptoms 

  • Dysponea
  • Orthopnea
  • Paroxysmal nocturnal dysponea (PND)
  • Angina
  • Palpitations
  • Syncope

 

Signs  

  • Wide pulse pressure
  • Collapsing pulse
  • Decresendo early diastolic murmur (EDM)
  • Displaced and heaving apex beat
  • Apical systolic thrill
  • S3 may be heard due to dilated LV
  • Corrigan's sign (Visible carotid pulsation)
  • de Musset's sign (Head nodding with each heart beat)
  • Traube sign (Pistol shot femorals, which are loud noises heard over the femoral artery)
  • Muller's sign (Visible pulsation of the uvula)
  • Quincke's sign (Capillary pulsations in the nailbed)
  • Duroziez's sign (When femorals are compressed a systolic murmur is audible 2cm proximal to the stethoscope and diastolic murmur 2cm distal)

 

Associated conditions (found on examination): 

  •  Argyl-roberston pupil (Syphilis)
  •  Apical lung fibrosis (Ankolysing spondylitis)
  •  High arched palate (Marfan's syndrome)

 

NB Decresendo early diastolic murmur, heard best at the lower left sternal edge, during expiration, with patient sitting forward. Importantly, in cases of severe AR an Austin Flint murmur may be heard. This is a mid diastolic murmur best heard at the apex that results from functional stenosis of the mitral valve, due to regurgitant blood flow hitting the mitral valve leaflets.

  

Investigations 

  • ECG - LVH with strain or left axis deviation
  • CXR - Cardiomegaly, dilated ascending aorta or pulmonary oedema
  • Echocardiogram - Assesses severity and gradient across the valve
  • Cardiac catheterisation - Identifies pre-existing CHD, aortic root disease and LV function
  • Cardiac MRI - Provides important anatomical, functional and haemodynamical information

 

Management 

Medical: The main aim of medical therapy is to ensure symptomatic control, which may require the use of loop diuretics, digoxin and vasodilators including ACE-I and Ca channel blockers. For those patients who are asymptomatic and have mild-moderate AS, routine follow-up should be performed every 1-2 years. If patients are asymptomatic but have severe AS then routine follow-up should be performed more frequently, at every 6 months.

Surgery: Those patients who cannot be managed medically and have continuing symptoms of AR or evidence of LV dysfunction should be treated surgically, with aortic valve or aortic root replacement.

 

Murmur of AR

An early diastolic murmur associated with AR

Mitral Valve Disease

Mitral Stenosis (MS)

 

Aetiology

Mitral stenosis (MS), is commonly caused by RF but other rarer causes include congenital, malignant carcinoid or endocardial fibroelastosis.

 

Pathophysiology 

A narrowing of the mitral orifice results in an increased left atrial pressure, which is needed to push blood through into the left ventricle. This leads to increased pulmonary venous presure, along with pulmonary hypertension and compensated right ventricular hypertrophy (RVH), that may lead to RV failure.  

 

Symptoms 

  • Dysponea
  • Orthopnea
  • PND
  • Fatigue
  • Angina
  • Palpitations
  • Haemoptysis

 

Signs 

  • Loud S1
  • Opening snap
  • Rumbling mid-diastolic murmur
  • Low volume pulse 
  • Diastolic thrill at apex
  • Tapping non-displaced apex beat
  • Left parasternal heave
  • Malar flush
  • Prominent "a" wave in JVP
  • Atrial fibrillation (AF)

 

NB A rumbling mid-diastolic murmur is heard best during expiration, in the left lateral decibutus position, at the apex. As the stenosis becomes more severe, the murmur becomes longer in duration, with the opening snap becoming closer to S2.

NB An early diastolic murmur resulting from pulmonary regurgitation may also be heard and is commonly referred to as a Graham Steell murmur.

 

Investigations 

  • ECG - Bifid P wave indicating left atrial enlargement, AF or RVH
  • CXR - Prominent upper lobe veins, pulmonary artery or left atrial enlargement, straightening of the left heart border or pulmonary oedema
  • Echo - Enlarged atrium, calcification and assessment of flow across the valve
  • Cardiac catherisation - Assessment of CAD, presence of other valvular lesions and may identify increased pulmonary capillary wedge pressure (PCWP)
  • Cardiac MRI - Provides important anatomical, functional and haemodynamical information

 

Management 

Medical: Those patients who are asymptomatic require no treatment, apart from IE prophylaxis. For those patients who are symptomatic, diuretics may be useful, which reduce preload on the heart as well as pulmonary venous congestion. Furthermore, as MS may trigger the onset of AF, rate control may be necessary, requiring beta blockers, calcium channel blockers or digoxin. In addition, anticoagulants such as warfarin may be considered. 

Mitral Balloon Valvuloplasty: Those patients with moderate to severe symptoms of pulmonary hypertension (PHT) may undergo percutaneous mitral balloon valvuloplasty. This is where a balloon is directed across the mitral valve and inflated at the orifice. However, this is not without complications, including pulmonary hypertension, emboli and pressure from a large left atrium on local adjacent structures that may cause hoarseness or dysphagia. 

Surgery: Those patients with more severe MS may undergo surgery, with several options available:

1. Closed valvotomy, where cusps are seperated by a dilator introduced through the LV apex

2. Open valvotomy, where cusps are seperated through direct supervision.

3. Mitral valve replacement, in cases of severe disease or significant accompanying mitral regurgitation

 

Murmur of MS

A mid diastolic murmur associated with MS

Mitral Regurgitation (MR)

 

Aetiology  

Acute: IE, acute myocardial infarction (AMI) or trauma

Chronic: RHD, mitral valve prolapse (MVP), degenertion of valve cusps, hypertrophic/dilated cardiomyopathy and heart failure (HF)

 

Pathophysiology  

In MR, during systole, the LV is decompressed into the left atrium (LA). Consequently, there is a raised LA pressure that results in pulmonary oedema. In longstanding severe MR, there is enlargement of the LA, attempting to accomodate the volume overload but with a minimal rise in LA pressure.

 

Symtoms 

  • Pulmonary oedema (acute)
  • Fatigue
  • Dysponea
  • Palpitations

 

Signs 

  • Pansystolic murmur (PSM)
  • Forceful displaced apex
  • Rapid upstroke in arterial pulse
  • Systolic thrill at apex
  • RV heave
  • Soft S1
  • Splitting of S2
  • Loud P2
  • Prominent "a" waves in JVP
  • Left atrial enlargement leading to AF

 

NB PSM is heard loudest at the apex and radiates to the axilla

 

Investigations 

  • ECG - LA or RA enlargement, LVH and AF
  • CXR - Cardiomegaly, LA or LV enlargment and pulmonary oedema   
  • Echocardiogram - Assess LV function as well as identify potential aetiology
  • Cardiac catheterisation - Asssess severity of the lession, extent of CAD and presence of other valvular lesions
  • Cardiac MRI - Provides important anatomical, functional and haemodynamical information

 

Management  

Medical: Those patients asymptomatic MR only require IE prophylaxis and a regular review involving echocardiography. In those with symptomatic MR, vasodilators may be utilised to increase cardiac output and reduce regurgitant blood volume. If in AF, rate control is recommended, along with anticoagulation in those with a history of embolisms, prosthetic valve implantation or additional mitral stenosis.

Surgical: Those patients who cannot be managed medically and have worsening symptoms will require surgery. Mitral valve repair or mitral valve replacement may be necessary, if valve leaflets are severely damaged with calcification. In addition, long term anticoagulation will also be required.

 

Murmur of MR

A pansystolic murmur associated with MR

Mitral Valve Prolapse (MVP)

 

Aetiology 

The most common cause of mitral valve prolapse (MVP) is idiopathic but it can also occur in combination with other conditions, such as atrial septal defects, patent ductus arteriosus (PDA), cardiomyopathy, Turner's syndrome, Marfan's syndome and osteogensis imperfecta.

 

Pathophysiology

MVP is caused by the mitral valve leaflet prolapsing into the left atrium during contraction of the LV. This can result from dysfunction of the papillary muscles, chordae tendinae or the presence of a large mitral annulus.

 

Symptoms

  • Angina
  • Palpitations

 

Signs

  • Mid/late systolic click
  • Late systolic murmur

 

Complications 

  • MR
  • Cerebral emboli
  • Arrhythmia
  • Sudden cardiac death (SCD)

 

Investigations 

  • ECG - Often normal, although inferior T-wave inversion may be seen
  • CXR - Normal
  • Echocardiogram - Assess gradient across valve, calcification and identify possible aetiology

 

Management 

Beta-blockers may be useful in the treatment of symptoms such as angina or palpitations. However, in cases of severe MR, surgery will often be necessary (see MR for management)

 

Right Heart Valve Disease

Tricuspid Stenosis

 

Aetiology 

Tricuspid stenosis, is most commonly due to RF but can be congenital, carcinoid or IE related.

 

Symtoms 

  • Fatigue
  • Ascites
  • Peripheral oedema
  • Anorexia

 

Signs

  • Early/mid diastolic murmur
  • Elevated JVP with prominent "a" waves 
  • Opening snap
  • Wasting
  • Oedema
  • Hepatomegaly
  • AF may be present

 

NB Early-mid diastolic murmur, heard best at the lower left sternal edge during inspiration

 

Investigation

  • ECG - Normal sinus rhythm but with evidence of right atrial (RA) enlargement
  • CXR - Illustrates signs of RA enlargement
  • Echocardiogram - Assesses the severity of calcification and gradient across the valve
  • Cardiac MRI - Provides valuable anatomical, functional and haemodynamical information

 

Management

Management for tricuspid stenosis involves providing symptomic relief through the use of diuretics and salt restriction. Occasionally however, trisuspid valve (TV) replacement or TV balloon valvuloplasty may be considered.

 

Tricuspid Regurgitation

 

Aetiology

Tricuspid regurgitation (TR) has numerous causes including: IE, RF, Marfan's syndrome, congenital heart disease or carcinoid.

 

Symptoms

    • Abdonimal pain
    • Dysponea
    • Orthopnea
    • Fatigue
    • Oedema
    • Ascites
    • Nausea
    • Anorexia

     

    Signs 

    • Pansystolic murmur (PSM)
    • S3, often heard on inspiration 
    • Jaundice
    • Ascites
    • Hepatomegaly
    • Oedema
    • Cachexia
    • Elevated JVP with cannon "v" waves 
    • RV heave
    • AF may be present

     

    NB PSM heard best at lower left sternal edge, during inspiration

     

    Investigation

    • ECG - Often non-specific
    • CXR - May show cardiomegaly or pleural effusion
    • Echocardiogram - Assesses calcification and gradient across the valve
    • Cardiac MRI - Provides important anatomical, funcional and haemodynamical information

     

    Management

    Often TR is well tolerated and consequently does not require any intervention. However, symptomatic treatment may include diuretics and salt/fluid restriction. If there is coexisting valvular disease trisuspid valve (TV) replacement or TV valvuloplasty may be considered.

     

    Pulmonary Stenosis

     

    Aetiology

    Congenital: Turners syndrome, Williams syndrome, Tetrology of Fallot or rubella

    Acquired: Carcinoid, RHD or a result of extrinsic compression

     

    Symptoms

    • Dysponea
    • Dizziness
    • Fatigue
    • Oedema
    • Ascites

     

    Signs

    • Ejection systolic murmur (ESM)
    • Ejection click
    • Prominent "a" wave in JVP
    • RV heave
    • Widely split S2 and P2
    • Thrill felt in 2nd intercostal space

     

    NB ESM heard best at the left upper sternal edge, during inspiration and radiating towards the left shoulder

     

    Investigation

    • ECG - Signs of RVH, RA enlargement and RBBB
    • CXR - Dilated pulmonary arteries with calcified valve may be present
    • Echocardiogram - Assesses severity of calcification and level of stenosis
    • Cardiac catheterisation - Assesses severity of calcification and identifies pre-existing CHD

     

    Management

    Medical: Aims to treat symptoms resulting from RV failure, including the use of diuretics and fluid restriction.

    Pulmonary balloon valvuloplasty: Treatment of choice for stenosis at the level of the valve.

    Surgical: In those patients where the gradient across the pulmonary valve (PV) is greater than 50mmHg or have continuing symptoms despite medical therapy, valvotomy can be effective. PV replacement is indicated if patients develop severe pulmonary regurgitation or do not respond to treatments mentioned above.

     

    Pulmonary Regurgitation

     

    Aetiology

    Pulmonary regurgitation can be caused by IE, carcinoid, Marfan's syndrome or from any cause of pulmonary hypertension (PHT).

     

    Symptoms

    • Dysponea
    • Lethargy
    • Peripheral oedema
    • Abdominal pain

     

    Signs

    • Descrendo murmur
    • RV heave
    • Thrill in pulmonary area
    • P2 may be delayed 

     

    NB: Descrendo murmur heard best in the 3rd/4th intercostal space, at left sternal edge during inspiration

     

    Investigations

    • ECG - RVH, RBBB, RSR pattern in V1
    • CXR - Enlarged pulmonary artery and RV
    • Echocardiogram - RV dilatation or hypertrophy
    • Cardiac catheterisation - Assessment of pre-existing CHD

     

    Management

    Medical: Treatment of RV failure may involve the use of diuretics.

    Surgical: If there is severe RV failure then PV replacement should be considered.

     

    Rheumatic Fever (RF)

     

    Epidemiology

    The incidence of rheumatic fever (RF) is now less than 1/1000 in developed countries. The peak incidence is between the ages of 5-15yrs. The decline in the incidence of RF has most likely been brought about by improved living conditions and improved access to medical care.

     

    Pathology

    This is a systemic infection, occuring a few weeks after a pharyngeal infection. This is usually caused by Group A beta-haemolytic streptococci. Consequently, antibodies are produced in response to this infection towards the carbohydrate cell wall of the streptococcus, cross-reacting with the proteins in the cardiac valves. RF develops approximately 3-4 weeks after the initial acute infection and can lead to pancarditis.

     

    Clinical Features

    • A sore throat during the first 1-5 weeks
    • Fever, abdominal pain and epistaxis
    • Polyarthritis causing severe pain and tenderness
    • Pancarditis develops in 50% of cases
    • Chorea develops in 10-30% of cases, occuring 1-6 months after pharygitis. Patients often exhibit difficulties in writing, speaking and emotional disturbances. Joints are hyperextended with hypotonia, diminished tendon reflexes and tongue fasiculation.
    • Erythema marginatum seen in 5-13% of cases, appearing as erythematous non-pruiritic papules and macules that spread out onto the trunk and proximal limbs.
    • Subcutanous nodules seen in up to 8% of cases, occuring after the onset of pancarditis. 

     

    Diagnostic criteria for RF (revised Jones criteria)

     

    The diagnosis of RF is made on the evidence of group A beta-haemolytic streptococcal infection AND 2 major criteria OR 1 major and 2 minor criteria

     

    Evidence of group A beta-haemolytic streptococcal infection:

    • Positive throat culture
    • Rapid steptococcal antigen test
    • Elevated streptococcal antibody titre
    • Recent scarlet fever

     

    Major

    • Polyarthritis - Inflammation at common joint sites including the knees, ankles, wrists and elbows
    • Carditis - Inflammation throughout all layers of the heart including the pericardium, epicardium, myocardium and endocardium. There may also be an associated new or changing murmur.
    • Chorea - These are sudden involuntary rapid movements of the face and arms but may also manifest as emotional disturbances as well
    • Erthema marginatum - This presents as a well-defined non-pruritic rash affecting the trunk and proximal extremities that migrates to the peripheries 
    • Subcutaneous nodules - Are painless nodules often located over bones and tendons

     

    Minor

    • Fever - 38.2-38.9 °C
    • Arthralgia - Joint pain without swelling
    • Prolonged PR interval on ECG
    • Elevated ESR and CRP
    • Leukocytosis
    • Previous RF or RHD

     

    Management

    The management for RF has a well defined treatment algorithm centering around antibiotic usage and bed rest:

    • Oral benzylpenacillin or penacillin V for 10 days
    • OR intramsucular penicillin G to treat acute infection
    • OR alternatively, oral erythromycin, if penacillin alergic for 10 days
    • Oral aspirin 4-8g daily until ESR and CRP normal
    • Prednisolone 2mg/kg/day for 2-4 weeks, if moderate-severe carditis
    • Oral haloperidol or diazepman for chorea
    • Diuretics, ACE-I and digoxin for treatment of heart failure symptoms.

     

    Prognosis

    Prognosis varies according to the severity of RF. Those individuals with carditis can go on to develop chronic RHD. RF recurrence is precipitated by further streptococcal infections, pregnancy or the use of the pill.

     

    References

     

    1) P Ramrakha and J. Hill. Oxford Handbook of Cardiology. 2nd Edition. Oxford University Press. 2012.

    2) Longmore M, Wilkinson I, Turmezei T et al. Oxford Handbook of Clinical Medicine. Seventh Edition. Oxford University Press. 2008.

    3) Kumar P and Clark M. Kumar & Clark’s Clinical Medicine. Seventh Edition. Saunders Elsevier. 2009.

    4) ESC Guidelines - Guidelines on the management of valvular heart disease. http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-VHD-FT.pdf 

    5) Patient UK - Valvular heart disease. http://www.patient.co.uk/health/Heart-Valves-and-Valve-Disease.htm

    6) TAVI for aortic stenosis in patients who cannot undergo surgery - http://www.nejm.org/doi/full/10.1056/NEJMoa1008232

     

    Images

    1) Cardiac Cycle - Image reproduced with the kind permission of Dave Klemm at Faculty & Curriculum Support (FACS),Illustration and Graphics, Preclinical Science Bldg, Room GM-6, Box 571419, Washington, DC 20057-1417. American Academy of Family Physicians (AAFP): http://www.aafp.org/afp/2004/0601/p2609.html  

    2) Auscultation Sites - Image reproduced from Stethographics, Inc. 2007. http://www.stethographics.com/heart/main/sites.htm 

     

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