USMLE INICET FMGE NEET:
Heart Murmurs
Introduction
A heart murmur is a sound produced due to turbulent blood flow within the heart.Heart Murmurs
Heart murmurs are heard by auscultation with a stethoscope as part of the cardiovascular examination.
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The cardiac cycle
The cardiac cycle refers to a series of physiological events making up a single heartbeat. The cycle involves contraction (systole) and relaxation (diastole) of the atria and ventricles to effectively pump blood.
The cardiac cycle starts with the atria and ventricles in diastole. Blood enters the right atrium (from the vena cava) and the left atrium (from the pulmonary vein). At this point, the mitral and tricuspid valves are open. This allows blood to flow freely into the right ventricle and left ventricle from the atria. The aortic and pulmonary valves are shut, which prevents an abnormal backflow of blood into the ventricles from the aorta and pulmonary artery.
The next stage of the cycle is atrial systole, contraction of the atria to finish “filling” the ventricles with blood.
Ventricular systole occurs as the ventricles contract, increasing the pressure within the ventricles. The increased pressure causes the closure of the mitral and tricuspid valves, this prevents regurgitation of blood from the ventricles into the atria.
At this point, the volume of blood within the ventricles remains constant as the aortic and pulmonary valves have not yet opened. This phase of ventricular systole is called isovolumetric contraction.
Eventually, the pressure within the ventricles exceeds the pressure in the pulmonary artery and aorta causing the pulmonary and aortic valves to open. Blood is ejected from the ventricles during ventricular ejection phase.
The ventricles then begin to relax following contraction (ventricular diastole). The drop in pressure within the ventricle causes the aortic and pulmonary valves to close, to prevent backflow (regurgitation) of blood into the ventricles.
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Normal heart sounds
Normal heart sounds are caused by the closure of heart valves.
First heart sound (S1)
The first heart sound (S1) is caused by the closure of the mitral and tricuspid valves. It marks the start of ventricular systole, and a peripheral pulse is felt at the same time (or shortly after) S1.
Second heart sound (S2)
The second heart sound (S2) is caused by the closure of aortic and pulmonary valves. It marks the end of ventricular systole, and the start of diastole.
The pulmonary valve may close just after the aortic valve. Closure of the pulmonary valve just after the aortic valve is prolonged during inspiration, or in defects which cause more blood to be pumped out of the right ventricle.
Therefore, S2 may not always be heard as one discrete sound but may be muffled or have two discrete sounds (split S2).
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How to approach heart murmurs
It is important to have a structured approach to interpreting heart murmurs. See the Geeky Medics guide to cardiovascular examination for more information on how to perform auscultation.
If a murmur is heard during auscultation, consider the following questions:
When during the cardiac cycle is the murmur heard?
What are the characteristics of the murmur? What is the intensity (Table 1)?
Is the murmur heard loudest using the bell or the diaphragm of the stethoscope?
Where is the murmur heard the loudest?
Do any manoeuvres exaggerate the murmur?
Heard loudest on inspiration or expiration?
Does the murmur radiate?
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Aortic stenosis
Aortic stenosis (AS) refers to a tightening of the aortic valve at the origin of the aorta.
Aortic stenosis is associated with an ejection systolic murmur heard loudest over the aortic valve. The murmur is described as having a ‘crescendo-decrescendo’ quality (it appears as diamond-shaped on a phonogram). The murmur of aortic stenosis commonly radiates to the carotid arteries.
Aetiology
Causes of aortic stenosis include:
Calcification of the aortic valves: this is the most common cause of AS in developed countries, typically occurring in elder
ly adults.
Congenital abnormality of the aortic valve: the aortic valve is normally composed of three cusps (known as a tricuspid valve), but in some cases, individuals have only two cusps (known as a bicuspid valve) which predisposes them to the development of AS as well as aortic regurgitation.
Rheumatic heart disease: a rare cause of AS in developed countries.
Clinical features
Typical features of an aortic stenosis murmur include:
Ejection systolic murmur heard loudest over the aortic area
Radiates to the carotid arteries
Loudest on expiration and when the patient is sitting forwards
Other clinical features of aortic stenosis may include:
Slow rising pulse with narrow pulse pressure
Non-displaced, heaving apex beat (if present indicates left ventricular hypertrophy)
Reduced or absent S2 (a sign of moderate-severe aortic stenosis)
Reverse splitting of S2: aortic valve closes after pulmonary valve (due to the longer time required for blood to exit the left ventricle)
For more information, see the Geeky Medics guide to aortic stenosis examination.
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Mitral regurgitation
Mitral regurgitation (MR) occurs when there is backflow (regurgitation) of blood from the left ventricle into the left atria (through the mitral valve) during ventricular systole.
Mitral regurgitation is associated with a pansystolic murmur heart loudest over the mitral area and radiating to the axilla.
Aetiology
Mitral regurgitation can be either acute or chronic.
Causes of mitral regurgitation include:
Infective endocarditis
Acute myocardial infarction with rupture of papillary muscles
Rheumatic heart disease
Congenital defects of the mitral valve
Cardiomyopathy
Clinical features
Typical features of mitral regurgitation murmur include:
A pansystolic murmur heard loudest over mitral area
Radiation of the murmur to the axilla
Heard loudest using the bell of the stethoscope
Loudest on expiration in the left lateral decubitus position
Other clinical features may include:
Displaced, hyperdynamic apex beat
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Aortic regurgitation
Aortic regurgitation (AR) occurs when there is backflow of blood from the aorta into the left ventricle during ventricular diastole.
Aortic regurgitation is associated with an early diastolic murmur heard loudest at the left sternal edge
Aetiology
Aortic regurgitation can be either acute or chronic. Chronic AR is often asymptomatic.
AR can occur due to a disease process affecting the valve itself, or due to dilatation of the aortic root.
Diseases affecting the valve include:
Congenital bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis
Causes of aortic root dilatation include:
Aortic dissection: can result in acute aortic regurgitation
Connective tissue diseases (e.g. Marfan’s)
Aortitis
Typical clinical features
Typical features of an aortic regurgitation murmur include:
Decrescendo early diastolic murmur
Heard loudest at left sternal edge (the direction that the turbulent blood flows) sometimes heard loudest over the aortic area
Austin Flint murmur: a low pitched rumbling mid-diastolic murmur heard best at the apex. This is caused by the regurgitated blood through the aortic valve mixing with blood from the left atrium, during atrial contraction. An Austin Flint murmur is a sign of severe aortic regurgitation.
Other clinical features of aortic regurgitation may include:
Collapsing pulse (a ‘water hammer pulse’ with wide pulse pressure)
Displaced, hyperdynamic apex beat
Mitral stenosis
Mitral stenosis (MS) is narrowing of the mitral valve, which results in decreased filling of the left ventricle during systole and increased left atrial pressure (due to incomplete left atrial emptying).
Mitral stenosis is associated with a low-pitched, rumbling, mid-diastolic murmur heard loudest over the apex.
Aetiology
Rheumatic heart disease is the most common cause of mitral stenosis.
Other rarer causes include:
Congenital
Left atrial myxoma
Connective tissue disorders
Mucopolysaccharidosis
Clinical features
Typical features of a mitral stenosis murmur include:
Low-pitched, rumbling mid-diastolic murmur with an opening click (click heard in mid-diastole when the mitral valve opens)
Murmur is heard loudest over the apex
Loudest in left lateral decubitus position on expiration
Other clinical features of mitral stenosis may include:
A low-volume pulse which may be irregularly, irregular (atrial fibrillation is common in mitral stenosis)
Loud first heart sound with tapping apex beat (due to a palpable closing of the mitral valve)
A malar flush (plum-red discolouration of the cheeks)
Aortic stenosis
Aortic stenosis (AS) refers to a tightening of the aortic valve at the origin of the aorta.
Aortic stenosis is associated with an ejection systolic murmur heard loudest over the aortic valve. The murmur is described as having a ‘crescendo-decrescendo’ quality (it appears as diamond-shaped on a phonogram). The murmur of aortic stenosis commonly radiates to the carotid arteries.
Aetiology
Causes of aortic stenosis include:
Calcification of the aortic valves: this is the most common cause of AS in developed countries, typically occurring in elderly adults.
Congenital abnormality of the aortic valve: the aortic valve is normally composed of three cusps (known as a tricuspid valve), but in some cases, individuals have only two cusps (known as a bicuspid valve) which predisposes them to the development of AS as well as aortic regurgitation.
Rheumatic heart disease: a rare cause of AS in developed countries.
Clinical features
Typical features of an aortic stenosis murmur include:
Ejection systolic murmur heard loudest over the aortic area
Radiates to the carotid arteries
Loudest on expiration and when the patient is sitting forwards
Other clinical features of aortic stenosis may include:
Slow rising pulse with narrow pulse pressure
Non-displaced, heaving apex beat (if present indicates left ventricular hypertrophy)
Reduced or absent S2 (a sign of moderate-severe aortic stenosis)
Reverse splitting of S2: aortic valve closes after pulmonary valve (due to the longer time required for blood to exit the left ventricle)
Mitral regurgitation
Mitral regurgitation (MR) occurs when there is backflow (regurgitation) of blood from the left ventricle into the left atria (through the mitral valve) during ventricular systole.
Mitral regurgitation is associated with a pansystolic murmur heart loudest over the mitral area and radiating to the axilla.
Aetiology
Mitral regurgitation can be either acute or chronic.
Causes of mitral regurgitation include:
Infective endocarditis
Acute myocardial infarction with rupture of papillary muscles
Rheumatic heart disease
Congenital defects of the mitral valve
Cardiomyopathy
Clinical features
Typical features of mitral regurgitation murmur include:
A pansystolic murmur heard loudest over mitral area
Radiation of the murmur to the axilla
Heard loudest using the bell of the stethoscope
Loudest on expiration in the left lateral decubitus position
Other clinical features may include:
Displaced, hyperdynamic apex beat
Aortic regurgitation
Aortic regurgitation (AR) occurs when there is backflow of blood from the aorta into the left ventricle during ventricular diastole.
Aortic regurgitation is associated with an early diastolic murmur heard loudest at the left sternal edge
Aetiology
Aortic regurgitation can be either acute or chronic. Chronic AR is often asymptomatic.
AR can occur due to a disease process affecting the valve itself, or due to dilatation of the aortic root.
Diseases affecting the valve include:
Congenital bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis
Causes of aortic root dilatation include:
Aortic dissection: can result in acute aortic regurgitation
Connective tissue diseases (e.g. Marfan’s)
Aortitis
Typical clinical features
Typical features of an aortic regurgitation murmur include:
Decrescendo early diastolic murmur
Heard loudest at left sternal edge (the direction that the turbulent blood flows) sometimes heard loudest over the aortic area
Austin Flint murmur: a low pitched rumbling mid-diastolic murmur heard best at the apex. This is caused by the regurgitated blood through the aortic valve mixing with blood from the left atrium, during atrial contraction. An Austin Flint murmur is a sign of severe aortic regurgitation.
Other clinical features of aortic regurgitation may include:
Collapsing pulse (a ‘water hammer pulse’ with wide pulse pressure)
Displaced, hyperdynamic apex beat
Mitral stenosis
Mitral stenosis (MS) is narrowing of the mitral valve, which results in decreased filling of the left ventricle during systole and increased left atrial pressure (due to incomplete left atrial emptying).
Mitral stenosis is associated with a low-pitched, rumbling, mid-diastolic murmur heard loudest over the apex.
Aetiology
Rheumatic heart disease is the most common cause of mitral stenosis.
Other rarer causes include:
Congenital
Left atrial myxoma
Connective tissue disorders
Mucopolysaccharidosis
Clinical features
Typical features of a mitral stenosis murmur include:
Low-pitched, rumbling mid-diastolic murmur with an opening click (click heard in mid-diastole when the mitral valve opens)
Murmur is heard loudest over the apex
Loudest in left lateral decubitus position on expiration
Other clinical features of mitral stenosis may include:
A low-volume pulse which may be irregularly, irregular (atrial fibrillation is common in mitral stenosis)
Loud first heart sound with tapping apex beat (due to a palpable closing of the mitral valve)
A malar flush (plum-red discolouration of the cheeks)
Mitral valve prolapse
A mitral valve prolapse occurs when the mitral valve leaflets prolapse into the left atrium during systole.
Mitral valve prolapse is associated with a combination of a mid-systolic click and mid to late-systolic murmur.
Aetiology
Mitral valve prolapse is the most common valvular abnormality with a prevalence of approximately 5%.
The exact underlying cause of mitral valve prolapse is unknown. Primary mitral valve prolapse is caused by myxomatous degeneration of the mitral valve and is associated with connective tisuse diseases. Secondary mitral valve prolapse occurs when a ‘normal’ valve prolapses.
Typical clinical features
Typical features of a mitral valve prolapse murmur include:
Mid-systolic click (prolapse of the mitral valve into left atrium)
Followed by a mid or late-systolic murmur
Heard loudest at the apex
Loudest in expiration
Tricuspid regurgitation
Tricuspid regurgitation occurs when there is backflow of blood from the right ventricle into the right atrium during ventricular systole. This causes an increase in right atrial pressure and elevated venous pressures.
Tricuspid regurgitation is associated with a pansystolic murmur heard loudest over the tricuspid region.
Aetiology
Causes of tricuspid regurgitation include:
Right ventricular dilatation (e.g. secondary to pulmonary stenosis or pulmonary hypertension)
Rheumatic fever
Infective endocarditis (intravenous drug users are at high risk of endocarditis affecting the tricuspid valve)
Carcinoid syndrome
Congenital (e.g. atrial septal defect, AV canal, Ebstein anomaly)
The Ebstein anomaly (i.e. congenital isolated tricuspid regurgitation) is abnormal attachment of tricuspid valve leaflets causes the tricuspid valve to displace downwards into the right ventricle.
Typical clinical features
Typical features of a tricuspid regurgitation murmur include:
Pansystolic murmur
Heard loudest over the tricuspid region
Loudest during inspiration
Other clinical features of tricuspid regurgitation may include:
Large ‘v-waves’ visible in the jugular veins: caused by the right atrial filling of blood against a closed tricuspid valve
Visible/palpable hepatic pulsations
Signs of right-sided heart failure: right ventricular heave, peripheral oedema, hepatomegaly, ascites
Pulmonary stenosis
Pulmonary stenosis (PS) refers to narrowing of the pulmonary valve. It is commonly associated with other congenital heart defects.
Aetiology
Causes of pulmonary stenosis include:
Congenital: Turner’s, Noonan’s and Williams syndromes. Tetralogy of Fallot (pulmonary stenosis, right ventricular hypertrophy, ventricular septal defect and an overriding aorta).
Rheumatic fever
Carcinoid syndrome
Typical clinical features
Typical features of a pulmonary stenosis murmur include:
Ejection systolic murmur heard loudest over pulmonary area
Loudest during inspiration
Radiates to left shoulder/left infraclavicular region
In severe pulmonary stenosis, the murmur is longer and may obscure the sound of A2
Other clinical features of pulmonary stenosis may include:
Prominent ‘a waves’ in the jugular veins
Widely split S2: blood from the ventricles takes longer to pass through a narrow pulmonary valve, so pulmonary valve closure occurs much later than aortic valve closure
P2 may be soft and inaudible
Right ventricular dilatation can lead to a right ventricular heave, tricuspid regurgitation and peripheral signs of right-sided heart failure (e.g. peripheral oedema, ascites etc)
Pulmonary regurgitation
Pulmonary regurgitation (PR) occurs when there is backflow of blood from the pulmonary artery into the right ventricle during ventricular diastole. Pulmonary regurgitation is rare.
Aetiology
Causes of pulmonary regurgitation include:
Pulmonary hypertension
Infective endocarditis
Congenital valvular heart disease
Typical clinical features
Pulmonary regurgitation is usually asymptomatic.
Typical features of a pulmonary regurgitation murmur include:
Early decrescendo murmur heard loudest over the left sternal edge
Loudest during inspiration
Usually due to pulmonary hypertension: known as a Graham Steell murmur when associated with mitral stenosis
Tricuspid stenosis
Tricuspid stenosis (TS) refers to narrowing of the tricuspid valve.
Tricuspid stenosis is associated with a soft diastolic murmur loudest at 3rd – 4th intercostal space at the left sternal edge
Aetiology
Causes of tricuspid stenosis include:
Rheumatic fever (most common)
Congenital disease
Infective endocarditis
Clinical features
Typical features of a tricuspid stenosis murmur include:
Mid-diastolic murmur (rarely audible)
Loudest at 3rd-4th intercostal space at the left sternal edge
Loudest during inspiration
Other clinical features of tricuspid stenosis may include:
Raised JVP with giant ‘a waves’
Peripheral oedema, ascites
Jugular Venous Pressure (JVP)
ugular venous pressure (JVP) provides an indirect measure of central venous pressure. This is possible because the internal jugular vein (IJV) connects to the right atrium without any intervening valves, resulting in a continuous column of blood. The presence of this continuous column of blood means that changes in right atrial pressure are reflected in the IJV (e.g. raised right atrial pressure results in distension of the IJV).
The IJV runs between the medial end of the clavicle and the ear lobe, under the medial aspect of the sternocleidomastoid, making it difficult to visualise (its double waveform pulsation is, however, sometimes visible due to transmission through the sternocleidomastoid muscle).
Because of the inability to easily visualise the IJV, it’s tempting to use the external jugular vein (EJV) as a proxy for assessment of central venous pressure during clinical assessment. However, because the EJV typically branches at a right angle from the subclavian vein (unlike the IJV which sits in a straight line above the right atrium) it is a less reliable indicator of central venous pressure.
Differentiating venous and arterial pulsation
When trying to identify the venous pulsation associated with the JVP, it’s important to distinguish it from the arterial pulsation of the nearby carotid artery.
Differences between the venous pulsation of the JVP and the arterial pulsation of the carotid artery include:
Number of pulses: the JVP has a double waveform pulse (i.e. 2 pulses) whereas the carotid artery has a single pulsation for each cardiac cycle.
Palpability: the pulse of the JVP is not easily palpable, whereas the carotid pulse is typically easy to feel.
The double waveform pulsation associated with the JVP reflects pressure changes within the right atrium. Think of the pressure changes as a Mexican wave; starting in the right atrium and travelling to the IJV where we observe the pulsations.
How do we assess the JVP?
Assessment of the JVP
1. Position the patient in a semi-recumbent position (at 45°).
2. Ask the patient to turn their head slightly to the left.
3. Inspect for evidence of the IJV, running between the medial end of the clavicle and the ear lobe, under the medial aspect of the sternocleidomastoid (it may be visible just above the clavicle between the sternal and clavicular heads of the sternocleidomastoid). The IJV has a double waveform pulsation, which helps to differentiate it from the pulsation of the external carotid artery.
4. Measure the JVP by assessing the vertical distance between the sternal angle and the top of the pulsation point of the IJV (in healthy individuals, this should be no greater than 3cm).
Causes of a raised JVP
A raised JVP indicates the presence of venous hypertension. Cardiac causes of a raised JVP include:
Right-sided heart failure: commonly caused by left-sided heart failure. Pulmonary hypertension is another cause of right-sided heart failure, often occurring due to chronic obstructive pulmonary disease or interstitial lung disease.
Tricuspid regurgitation: causes include infective endocarditis and rheumatic heart disease.
Constrictive pericarditis: often idiopathic, but rheumatoid arthritis and tuberculosis are also possible underlying causes.
JVP waveform
The JVP has its own waveform which consists of 5 parts:
A wave
X descent (part 1)
C wave
X descent (part 2)
V wave
Y descent
A wave
The A wave is caused by the contraction of the right atrium, where blood is being pumped through the tricuspid valve into the right ventricle. Increased pressure in the right atrium also forces blood upwards towards and into the IJV. This influx of venous blood into the IJV is known as the A wave.
X descent (part 1)
The first part of the X descent is caused by relaxation of the right atrium, which results in blood filling the right atrium from the superior vena cava, reducing the height of the column of blood sitting in the IJV (i.e. causing a drop in the JVP). The right ventricles relaxation also contributes to the X descent, as blood exits the right atrium into the right ventricle, further reducing the column of blood in the SVC and IJV.
C wave
The C wave is caused by the forceful contraction of the right ventricle which ejects blood out of the heart into the pulmonary artery. As this occurs, the pressure within the right ventricle increases significantly, forcing the tricuspid valve upwards so much so that it projects partially into the right atrium. This sudden projection of the tricuspid valve into the right atrium generates upwards force which is transmitted into the SVC and ultimately the IJV, causing a temporary rise in the JVP referred to as the C wave.
X descent (part 2)
The second part of the X descent occurs during the final phase of right ventricular contraction. When the ventricle reaches its most contracted state, it is physically much smaller than when in its relaxed state, resulting in the creation of extra space within the pericardium. This extra space within the pericardium allows the right atrium to expand and begin filling with blood. This initial phase of atrial filling results in a drop in venous pressure within the SVC and IVC, producing the second part of the X descent.
V wave
The V wave is caused by the relaxation of the right atrium whilst the tricuspid valve is still closed. The relaxation of the right atrium combined with a closed tricuspid valve results in blood being drawn into the column of blood that begins at the right atrium and extends up to the IJV. As blood is drawn into the column, whilst the tricuspid valve is closed, the level of the JVP is temporality increased.
Y descent
The Y descent occurs when the tricuspid valve opens, resulting in blood from the right atrium filling the right ventricle and blood from the SVC and IJV filling the right atrium. This results in a decrease in the height of the column of blood and thus a decrease in the JVP.
Paediatric Cardiovascular Examination
The paediatric cardiovascular exam can be a logistical minefield, requiring a good understanding of cardiac anatomy and possible congenital anomalies. With babies especially, it’s important to be opportunistic with your examination – doing the three ‘quiet things’ first: auscultation of heart sounds, auscultation of breath sounds and palpation of femoral pulses.
With all children, don’t expect to follow a pre-defined order. Be creative and playful, making the examination into a game involving parents, siblings and the toys available to you.
General inspection
Appearance and behaviour
Observe the child in their environment (e.g. waiting room, hospital bed) and take note of their appearance and behaviour:
Activity/alertness: note if the child appears alert and engaged, or quiet and listless.
Cyanosis: bluish discolouration of the skin due to poor circulation (e.g. peripheral vasoconstriction secondary to hypovolaemia) or inadequate oxygenation of the blood (e.g. right-to-left cardiac shunting).
Shortness of breath: may indicate underlying cardiovascular (e.g. congenital heart disease) or respiratory disease (e.g. asthma).
Pallor: a pale colour of the skin that can suggest underlying anaemia (e.g. blood dyscrasia, chronic disease) or poor perfusion (e.g. congestive cardiac failure).
Oedema: typically presents with swelling of the limbs (e.g. pedal oedema) or abdomen (i.e. ascites). There are many causes of oedema including cardiac failure and nephrotic syndrome.
Rashes: note the characteristics and distribution of any skin rashes (e.g. petechiae suggesting clotting disorder).
Weight: note if the child appears a healthy weight for their age and height.
Syndromic features
Pay attention to features that may indicate the presence of an underlying genetic condition:
Stature (e.g. tall/short)
Syndromic facial features
See the end of this guide for a non-exhaustive list of clinical syndromes which can be associated with cardiovascular system pathology.
Equipment
Observe for any equipment in the child’s immediate surroundings and consider why this might be relevant to the cardiovascular system:
Oxygen: saturation probe, mask, nasal prongs, oxygen tank and other breathing support.
Mobility equipment: wheelchair, crutches and walking frame.
Medications
Note any medications by the bedside or in the child’s room and consider what underlying diagnoses they may indicate:
Anticoagulants (e.g. warfarin/heparin): commonly prescribed for children with artificial heart valves.
Antihypertensives (e.g. ACE inhibitors)
Diuretics (e.g. furosemide): often used in the management of heart failure.
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