Heart murmurs

The first heart murmurs were described more than 200 years ago (Rishaniw 2018).

The Parisian physician Rene Theophile Hyacinthe Laennec (1781 - 1826) regularly used the ear trumpet he had developed during his rounds in a clinic for lung patients and thus developed a vocabulary for normal, abnormal, and pathological sounds (Schoon 2012).

The mesosystolic click (expressing mitral valve prolapse) was first described by Cuffer and Barbillon in 1887.

The Graham- Steell sound is named after its first describer (Graham Steell 1851 - 1942) (Kasper 2015).

In the early 20th century, an apical systolic could be attributed to rheumatic mitral regurgitation for the first time. Many patients were subsequently written invalids. This was the reason for Sir James Mackenzie to give systolic murmurs no more importance. However, this changed decisively after the invention of phonocardiography in 1908 (Attenhofer Jost 2004).

In 1907, Carey Franklin Coombs (1879 - 1932) described for the first time the Carey- Coombs sound named after him (Robbins 2022).

Austin Flint (1812 - 1886), a New York internist, suspected the mechanism of origin to be aortic valve insufficiency as early as the mid-19th century, and therefore the Austin- Flint murmur was named after him (Gahl 2014).

In 1961, Ried described phonocardiograms of 8 patients who had a mesosystolic click with or without a murmur and considered these sounds to be caused by the mitral valve apparatus through tendon filaments. In 1963, Barlow et al angiographically demonstrated that late systolic murmurs were caused by mitral regurgitation (Brandis 1989).

Still's murmur was first described by Still in 1918 (Begic 2017).

A heart murmur - in contrast to heart sounds - is understood to be longer lasting sound phenomena that occur during systole (as systolic) or diastole (as diastolic). These sounds occur in special situations or due to turbulence of blood flow (Füeßl 2010).

Heart murmurs are composed of a sum of audible oscillations with different frequencies between 20 - 1,000 Hz, different temporal occurrence and intensities (Attenhofer Jost 2004).

1st heart sound

According to traditional doctrine, the 1st heart sound (S1) is produced by the closure of the mitral and tricuspid valves and by ventricular tension. According to a second hypothesis, it is generated by the sudden deceleration of the blood during valve closure. This causes vibration of the ventricles, chordae tendinae, and blood (Dennis 2019).

S1 occurs approximately 0.02 - 0.04 sec after the onset of the QRS complex (Herold 2022). The mitral valve can be auscultated in the 5th ICR medioclavicularly, the tricuspid valve in the region of the 4th rib right parasternal (Balletshofer 2006).

The intensity of the sound depends on the:

• Distance required for the anterior valve leaflet to return to the annular plane.
• contractility of the left ventricle
• mobility of the valve leaflet
• the PR interval (Kasper 2015).

The loudness of the 1st heart sound is high in:

• in patients with hyperkinetic circulation
• in the early phase of rheumatic mitral stenosis (MS)
• in case of a short PR interval (Kasper 2015)
• Ventricular septal defect
• high cardiac output
• Atrial myxoma (Dennis 2019)

Volume decreases with:

• therapy with beta-adrenergic receptor blockers
• in later stages of mitral stenosis due to calcification and rigidity of the valve
• in case of left ventricular dysfunction of contraction
• long PR intervals (Kasper 2015)
• severe mitral regurgitation(this prevents complete closure of the valve leaflets by returning blood [Dennis 2019])
• due to large distance between stethoscope and heart due to e.g.:
  • obesity
  • obstructive lung diseases
  • mechanical ventilation
  • Pericardial effusion
  • pneumothorax (Kasper 2015)

2nd heart sound

The 2nd heart sound (S2) occurs due to closure of the aortic and pulmonary valves. It is brighter and shorter than S1. It occurs at the end of the T wave.

It is best auscultated in the 2nd ICR parasternal right (aortic valve) and left (pulmonary valve). When there is an increase in pressure in the great circulation, the sound is louder over the aorta; when there is an increase in pressure in the pulmonary circulation, the sound is louder over the pulmonary artery (Herold 2022).

Physiologically, the A2- P2 interval (aortic valve closure = A2, P2 = pulmonary valve closure) increases during inspiration and narrows during expiration (Kasper 2015).

• Amplified 2nd heart sound by:
  • Pulmonary hypertension (Here, the pulmonary component of S2 is louder than normal [Dennis 2019]).

• Physiological splitting of the 2nd heart sound:

This results from a delayed closure of the aortic or pulmonary valve. It is said to be a physiological split if the gap is up to 0.08 sec during deep inspiration. The splitting is audible due to the negative pressure in the thorax and the transient increased diastolic filling of the right ventricle during inspiration (Herold 2022).

This physiologic split during inspiration is usually absent in patients >50 years of age (Mewis 2006).

• Wide splitting of the 2nd heart sound:

This results from delayed closure of the pulmonic valve or premature closure of the aortic valve (Dennis 2019).

Here, during expiration, the closing sounds of the aortic or pulmonic valves are split. The distance between the closure of the two valves is longer than normal during inspiration. (Dennis 2019).

One finds a wide split of the 2nd heart sound, for example, in:

• Right bundle branch block (Herold 2022).
• Pulmonary valve stenosis
• Mitral valve regurgitation
• Ventricular tachycardia
• Pacing in the left ventricle (Dennis 2019).

• Wide fixed division of the 2nd heart sound:

In this case, there is constant prolongation of the closing sounds of the aortic and pulmonary valves during both inspiration and expiration. This form of splitting can occur in:

• Atrial septal defect (Dennis 2019).
• Pulmonary stenosis (Herold 2022).

With fixed cleavage, sensitivity is 92% and specificity is 65% (Dennis 2019).

• Paradoxical cleavage of the 2nd heart sound:

It represents the opposite of the physiological cleft. In this form, the split disappears during inspiration and is instead auscultated expiratory. It results from a delay in the aortic valve closure tone. Paradoxical splitting is found in:

• Aortic valve stenosis
• Left bundle branch block (Dennis 2019)
• severe aortic isthmus stenosis
• pacemaker in the right ventricle (Herold 2022)
• hypertrophic obstructive cardiomyopathy = HOCM (often with a gradient > 300 mmHg [Dennis 2019])
• acute myocardial ischemia
• right ventricular pacemaker (Kasper 2015).

For paradoxical cleavage, sensitivity is 50% and specificity is 79% (Dennis 2018).

• Narrowly split 2nd heart sound up to singular S2 at:
  • Pulmonary arterial hypertension

• Decreasing intensity of A2 and P2 at:
  • Aortic stenosis
  • pulmonarystenosis (Kasper 2015)

• Widening of A2- P2- interval and lack of inspiratory change at:
  • Secondary atrial septal defect(Kasper 2015).

• Lengthening of the A2- P2- interval possible by:
  • right bundle branch block (causes delayed closure of the pulmonary valve)
  • Severe mitral valve regurgitation (due to premature closure of the aortic valve) (Kasper 2015)

3rd heart sound

The 3rd heart sound is a dull, low-frequency soft sound in the mitral valve area that occurs in early diastole (Dennis 2019). It becomes auscultable approximately 0.15 sec after the 2nd heart sound and is an expression of a so-called "diastolic overloading" (Herold 2022).

It may occur in the context:

• physiologically in adults < 40 years of age
• any ventricular dysfunction can cause a 3rd heart sound
• Hyperthyroidism
• Anemia
• Mitral valve regurgitation
• Aortic valve regurgitation
• tricuspid regurgitation
• hypertrophic obstructive cardiomyopathy (Dennis 2019)

4th heart sound

The 4th heart sound is low frequency and quiet. It coincides with late diastole and can be auscultated before the 1st heart sound (Herold 2022). It occurs in conditions associated with stiffening of the left ventricle (Dennis 2019).

It is commonly found in:

• Aortic valve stenosis
• ischemic changes
• arterial hypertension with left ventricular hypertrophy
• hypertrophic cardiomyopathy
• in advanced age

Rarely, it may occur in the setting of:

• Mitral valve regurgitation
• Diseases associated with rapid blood inflow such as anemia (Dennis 2019)

Different types of heart sounds

• Valve opening sounds: These are caused by a sudden stop in the opening movement of the stuck AV valves and occur with:
  • Mitralstenosis as mitral opening tone
  • Mitral valve prosthesis as prosthetic opening tone
  • Tricuspid stenosis (very rarely occurring) as tricuspid opening tone (Herold 2022)

• Ejection clicks:
  • Aortic ejection click: This is usually heard 40 - 60 msec after M1. It is best auscultated at the apex of the heart. The sound is louder the more mobile the aortic valve is and finally disappears in a highly stenosed, calcified valve. It occurs in a bicuspid aortic valve, valvular aortic stenosis, but not in infravalvular or supravalvular aortic stenosis (Mewis 2006).
  • Pulmonary ejection click: This is best auscultated in the area of the left sternal border. It is produced by opening of the pulmonary valve. It disappears during inspiration. Pulmonary ejection click occurs in valvular pulmonary stenosis (Mewis 2006).

• Systolic click:

This is found, for example, in mitral valve prolapse (Herold 2022). See also Systolic murmur

• Ventricular systole:

It includes the interval between 1st heart sound (S1) and the 2nd heart sound (S2).

(Kasper 2015).

Heart murmurs

Cardiac murmurs are caused by a whorl formation. If the whorling goes posteriorly, stenosis occurs; if it goes anteriorly, insufficiency occurs (Herold 2022).

Heart murmurs are characterized by

• the loudness, measured in degrees according to Samuel A. Levine 1933 (Attenhofer Jost 2004 / Hofbeck 2007):
  • 1 / 6: Very quiet murmur, which can be auscultated only with difficulty.
  • 2 / 6: Quiet, but clearly audible
  • 3 / 6: Loud heart murmur without buzzing
  • 4 / 6: Loud murmur with murmur
  • 5 / 6: Very loud heart murmur, audible immediately after placing the stethoscope on the patient's head
  • 6 / 6: Loud murmur which can be heard without stethoscope
• Frequency
• Punctum maximum
• Conduction
• Position in relation to heart sounds
• Palpation of the carotid pulse
• type of sound:
  • Decrescendo- (decreasing volume)
  • Spindle- (first louder, then softer)
  • Band- (continuous)
  • Crescendo form (increasingly louder)

(Herold 2022 / Hofbeck 2007)

• duration:
  • holosystolic (persistent throughout systole)
  • early- or protosystolic
  • late or telesystolic
  • mid- or mesosystolic
  • early or protodiastolic
  • late- or teldiastolic
  • mid- or mesodiastolic (Haas 2017 / Hofbeck 2007).

Cardiac murmurs include the following murmurs:

• Functional systolic heart murmurs
• Accidental systolic heart murmurs (also known as Still's murmur in infants).
• Barnacle murmur
• Organic murmurs
• Continuous systolic-diastolic murmurs (so-called machine murmurs)
• Diastolic murmurs
• Systolic murmurs

For more details see "Etiology

The systolic murmur is the most common auscultation murmur (Attenhofer Jost 2004).

Acute systolic murmurs are not uncommon, especially in children and adolescents. The prevalence is > 50%. Without hemodynamic or structural changes, these are considered harmless (Herold 2022).

In Switzerland, it is even said that up to 80% of children present with systolic murmurs and ≥ 50% of all adults over 50 years of age. However, the incidence increases with age (Attenhofer Jost 2004).

Functional systolic heart murmurs:

They are caused by flow phenomena due to increased stroke volume (Füeßl 2010) in e.g. anemia, fever, hyperthyroidism (Haas 2017), bradycardia, pregnancy (Herold 2022).

Functional systolic heart murmurs are quiet, low-frequency murmurs. A functional systolic occurs after S1, is of short duration, and ceases before S2. The auscultatory p. m. are apex, base or left parasternal (Attenhofer Jost 2004).

Accidental systolic heart murmurs:

These occur due to structural or hemodynamic changes in healthy hearts and are considered harmless.

The murmur is probably due to vibrations of the pulmonary valve (Attenhofer Jost 2004). These are quiet, systolic murmurs that are parasternal auscultable in the 2nd / 3rd ICR and are not propagated (Füeßl 2010). They are never louder than 3 / 6 degrees (Haas 2017).

Nun's foot:

So-called barnacle murmurs are systolic-diastolic murmurs occurring in children between 3 - 6 years of age due to turbulence in the jugular veins. Punctum maximum is located left or right infraclavicularly. The murmur is exclusively auscultable in the upright position and disappears when the head is turned (Haas 2017).

Organic heart murmurs:

In organic murmurs, there is always a pathological change in the cardiovascular system (Herold 2022). They are found in acquired valvular defects and / or in congenital heart defects (Füeßl 2010).

Continuous systolic-diastolic murmurs (so-called machine murmurs):

These are also called systolic-diastolic machine murmurs. These noise phenomena are caused by a shunt connection between the high and low pressure systems (Herold 2022).

They may occur in the following conditions:

• aorto-pulmonary window
• ruptured sinus- Valsalva- aneurysm
• open ductus botalli
• Coronary fistulas
• Arteriovenous fistulas due to e.g. pulmonary angioma or posttraumatic (Herold 2022)
• Extracardiac murmurs:

The murmur results from inflammatory altered surfaces rubbing against each other. This includes pericardial rubbing(Haas 2017).

Diastolic murmurs:

Diastolic murmur is always pathological (Herold 2022). It occurs during diastole. It is etiologically differentiated between:

• diastolic regurgitation murmurs: These regurgitation murmurs are caused by an insufficiency of the semilunar valves (Haas 2017).
• diastolic filling murmurs: These are caused by an increased blood volume flowing across an AV valve. An increased blood volume can occur, for example, due to a shunt vitium. This is therefore referred to as "relative AV valve stenosis". True AV valve stenosis occurs only very rarely (Haas 2017).

It is found in the following clinical pictures:

• Stenosis of the AV- valves (primarily caused by mitral valve stenosis and referred to as "mitral orifice tone").
• Functional AV- valve murmur due to increased blood flow in e.g:
  • AV-valve insufficiency see also mitral valve insufficiency and tricuspid valve insufficiency
• Insufficiency of the semilunar valves
  • due to organically caused valve defects such as aortic valve insufficiency
  • due to overstretching of the valve annulus together with pulmonary hypertension in e.g. relative pulmonary valve insufficiency (Herold 2022).
  • functional noises of the AV-valves caused by increased blood flow e.g. in AV-valve insufficiency(Herold 2022)
• Tricuspid valve stenosis (however, this occurs only rarely)
• severe mitral regurgitation as Carey-Combs murmur
• severe aortic regurgitation as Austin- Flint- murmur
• atrial myxoma
• Atrial septal defect: In addition to the systolic, there may be a low-frequency diastolic with p. m. above the inferior sternal border or a high-frequency diastolic with p. m. above the base (Gahl 2005).
• Ventricular septal defect: Again, in addition to the systolic [Siegenthaler 2005]), a diastolic may exist with a large shunt due to relative mitral stenosis(Gahl 2005).
• After mitral valve replacement (Sato 2016).

For more details see Diastolic murmurs

Systolic murmurs:

A systolic murmur occurs during systole , i.e., after S1 to before or to S2. It is not - like the diastolic murmur - exclusively pathological (Attenhofer 2004).

One differentiates etiologically in systolic murmurs between:

• Ejection murmurs: Expulsion murmurs result from obstruction between the ventricles and the great vessels.
• Regurgitant murmur: This is a result of AV valve regurgitation, in which blood flows back from the ventricles to the atria during systole.
• Ejection- click: This is a short early systolic high-frequency murmur resulting from the opening of a pathologically altered semilunar valve (Haas 2017).

Systolic murmurs may occur in the following conditions:

• insufficiency of the AV-valves:
  • Mitral regurgitation: Mostly organic, sounding immediately after 1st heart sound, decrescendo or band (Herold 2022). Punctum maximum is located in left lateral position at the apex (Attenhofer Jost 2004), conduction to the left axilla. Cause of mitral valve regurgitation may be:
    • Mitral valve prolapse
    • infective endocarditis:
      • by inflammatory destruction of the valve apparatus
    • rheumatic heart disease:
      • due to thickening of the valve leaflets and stiffening of the commissures
  • Cardiomyopathy due to:
    • dysfunction of the papillary muscles
    • Alteration of ventricular size and function:
      • due to enlargement of the left ventricle and the annulus, the valve leaflets no longer cover the opening completely
  • myxomatous degeneration:
    • by a genetically caused defect of the collagen composition
  • coronary artery disease:
    • a tear of a papillary muscle or elongation leads to a prolapse of the valve leaflet
    • regional remodeling of the ventricle size and dilatation of the annulus
    • dysfunction of the papillary muscles (Dennis 2019)
  • Tricuspid reg urgitation: Only rarely occurring, due to overstretching of the valve annulus, relative tricuspid regurgitation occurs in this case (Herold 2022). Also described as "Rivero-Carvallo sign". It is a high-frequency, pansystolic murmur that becomes louder on inspiration with p. m. in the 4th ICR left parasternal (Dennis 2019). Associated conditions include:
    • right ventricular dilatation (most common)
    • infective endocarditis
    • rheumatic heart disease due to scarring and stiffening of the valve
    • prolapse
    • Ebstein anomaly
    • disorder of papillary muscle function
    • Carcinoid syndrome: In this case the fibroblasts are activated by serotonin excess and plaques of the valve apparatus and the endocardium are formed.
    • Trauma
    • Collagenosis: due to changes in collagen and connective tissue, a flaccid valve occurs (Dennis 2019).
• Stenosis of the semilunar valves:
  • Pulmonary stenosis: Punctum maximum of pulmonary stenosis is located in the 2nd ICR on the left. It is a harsh, spindle-shaped expulsion sound (Attenhofer Jost 2004). Associated diseases are:
    • Congenital heart disease (most common cause).
    • Carcinoid syndrome: Due to excess serotonin, plaques on or around the pulmonary valve occur.
    • rheumatic heart disease (Dennis 2019)
  • Aortic stenosis: In this case, the p. m. is located in the 2nd ICR right parasternal (Attenhofer Jost 2004) and is transmitted to the carotids (Herold 2022). The murmur is short with mild stenosis and has an early systolic maximum. A late systolic maximum of longer duration characterizes severe aortic stenosis (Attenhofer Jost2004).
• Hypertrophic obstructive cardiomyopathy (HOCM): Here, the p. m. is located on the left parasternal side in the 4th ICR or at the apex. In up to 40% there is radiation to the axilla, only rarely to the carotids (Attenhofer Jost 2004).
• Aortic isthmus stenosis: This murmur is best auscultated between the scapulae (Herold 2022).
• isolated aortic or pulmonary root dilatation in normal semilunar valves
• Congenital bicuspid aortic valve disease: In this case, the murmur becomes quieter to inaudible as the valve becomes more calcified and stiff (Kasper 2015).
• Ventricular septal defect:

This is a pansystolic, high frequency murmur with p. m. in the 5th - 6th ICR. This does not increase during inspiration and is not transmitted to the axilla. One can draw conclusions about the defect size: the quieter the murmur, the larger the defect (Dennis 2019). For more details, see systolic.

Heart murmurs are caused by the formation of a vortex. If this goes posteriorly, stenosis occurs; if it goes anteriorly, insufficiency occurs (Herold 2022).

The diastolic murmur is inversely proportional to the magnitude of the diastolic pressure gradient between the left atrium and left ventricle (Kasper 2015). For more details, see diastolic.

The systolic murmur depends on blood flow through the pocket valves. It is separated from S1 and starts when the ventricular pressure exceeds the diastolic pulmonary artery or aortic pressure (Attenhofer Jost 2004).For more details see systolic.

The diagnosis of heart murmurs includes auscultation, echocardiography, pulse oximetry, ECG, MRI, CT (Haas 2017).

A diastolic murmur is always an indication for echocardiography (Haas 2017). For more details, see diastolic.

A quiet mesosystolic murmur in young, lean, asymptomatic patients does not require further workup. In patients with cardiac symptoms, any loud or quiet systolic must be clarified by echocardiography (Attenhofer Jost 2004). For more details see Systolic.

The prognosis depends on the cause of the murmur. The performance of patients with accessory or functional heart murmurs is not impaired (Haas 2017).

1. Attenhofer Jost C H et al (2004) Systolic heart murmur. Switzerland Med Forum (4) 49 - 55
2. Balletshofer B et al (2006) Tübingen curriculum: heart and vessels - an action-oriented guide for medical students. Georg Thieme Verlag Stuttgart / New York 64
3. Begic E et al. (2017) Accidental heart murmurs. Med. arch. 71 (4) 284 - 287
4. Brandis M et al (1989) Results of internal medicine and pediatrics. Springer Verlag Berlin / Heidelberg / New York / London / Paris / Tokyo / Hong Kong 122.
5. Dennis M et al (2019) Understanding symptoms: interpreting clinical signs. Elsevier Urban and Fischer Publishers 182 - 186.
6. Frey S M et al (2020) The heart murmur as an incidental finding. Therapeutische Umschau 77 (8) DOI: https://doi.org./10.1024/0040-5930/a001203.
7. Füeßl H et al. (2010) Dual series: anamnesis and clinical examination Georg Thieme Verlag Stuttgart 181.
8. Gahl K et al (2005) Auscultation and percussion - inspection and palpation. Georg Thieme Verlag Stuttgart / New York 166
9. Haas N A et al. (2017) DGPK (German Society for Pediatric Cardiology) guideline: Abklärung eines Herzgeräusches im Kindes- und Jugendalter AWMF- Register Nr. 023 / 001.
10. Herold G et al (2022) Internal Medicine. Herold Publishers 154 - 156
11. Hofbeck M et al (2007) Heart murmurs. Pediatrics Up2date (2) 105 - 123.
12. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1447 - 1450
13. Mewis C et al (2006) Auscultation of the heart. Cardiology compact 21 - 23 DOI: 10.1055/b-0034-24163.
14. Rishaniw M (2018) Murmur grading in humans and animals: past and present. J Vet Cardiolog. 20 (4) 223 - 233
15. Robbins A et al (2022) Carey Coombs murmur. Bristol Medico- Surgical Journal
16. Sato Y et al (2016) Diastolic murmur in mid-ventricular obstructive hypertrophic cardiomyopathy: A case report. J Cardiol Cases. 15 (2) 46 - 49
17. Siegenthaler W et al. (2005) Siegenthaler's differential diagnosis: internal diseases - from symptom to diagnosis. Georg Thieme Verlag Stuttgart / New York 695, 712
18. Schoon A et al. (2012) The trained ear: a cultural history of sonification. Transcript Verlag Bielefeld 78