Systolic noises

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-as an expression of mitral valve prolapse-was first described by Cuffer and Barbillon in 1887.

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 1961, Ried described phonocardiograms of 8 patients who had a mesosystolic click with or without a murmur and considered these murmurs to be a murmur phenomenon 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 systolic murmur is a high-frequency ejection murmur that can be heard auscultatorily (Kasper 2015), usually originating in the aortic or pulmonary valves (Attenhofer Jost 2004).

Systolic heart murmurs are characterized by

• Loudness:
  • 1 / 6: Very quiet murmur, which can only be auscultated 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 even without stethoscope
• Frequency
• Punctum maximum
• Conduction
• Position in relation to heart sounds
• Palpation of the carotid pulse
• Type of sound:
  • Decrescendo-
  • Spindle-
  • Band-
  • crescendo form (Herold 2022)
• Duration:
  • holosystolic (sustained throughout systole)
  • early or protosystolic
  • late or telesystolic
  • mid- or mesosystolic (Haas 2017)

• Systolic murmurs:

This is an abnormal heart murmur occurring during systole.

Systolic murmurs are differentiated between:

- Ejection murmurs: Ejection murmurs result from obstruction between ventricles and great vessels.

- Regurgitant murmurs: These are caused by AV valve insufficiency, in which blood returns from the ventricles to the atria during systole.

- Ejection- click: This is a short early systolic high-frequency murmur that results from the opening of a pathologically altered semilunar valve (Haas 2017).

• Functional systolic heart murmurs:

Functional systolic heart murmurs are quiet, low-frequency 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).

A functional systolic occurs after S1, is short-lived, and ceases before S2. The p. m. are apex, base or left parasternal (Attenhofer Jost 2004).

• Accidental systolic murmurs (also called Still'smurmur in infants):

These result from structural or hemodynamic changes in healthy hearts and are considered harmless. They are quiet, systolic murmurs that are parasternal auscultable in the 2nd / 3rd ICR and are not propagated (Füeßl 2010), never louder than 3 / 6 degrees (Haas 2017). The noise is probably due to vibrations of the pulmonary valve (Attenhofer Jost 2004).

• Continuous systolic-diastolic heart murmurs:

These are also called systolic-diastolic machine murmurs. They are caused by a vortex formation. If the vortex formation goes posteriorly, stenosis occurs; if it goes anteriorly, insufficiency occurs (Herold 2022).

These noise phenomena result from a shunt connection between the high and low pressure systems (Herold 2022).

• Systolic click:

A systolic click involves high-frequency oscillations, some of whose amplitude may exceed that of the 1st and 2nd heart sounds. It occurs in the middle or at the end of systole (Schmidt- Voigt 1982) and is found, for example, in mitral valve prolapse (Herold 2022).

• Nuns' Fe ver:

So-called barnacle murmur is systolic-diastolic murmur 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).

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

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 those over 50 years of age. However, the incidence increases with age (Attenhofer Jost 2004).

A systolic murmur may occur in the following conditions:

• Insufficiency of the AV- valves:
  • Mitral regurgitation: Mostly organic, sounding immediately after the 1st heart sound, decrescendo or band-like (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
    • by 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 annulus, the valve leaflets no longer completely cover the orifice
  • myxomatous degeneration:
    • by a genetic 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 regurgitation: Rarely occurring, this results in relative tricuspid regurgitation due to overstretching of the valve annulus (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 occur.
    • Trauma
    • Collagenosis: changes in collagen and connective tissue result in a flaccid valve (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 of serotonin, plaques occur on or around the pulmonary valve
    • 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).

• Continuous systolic-diastolic murmurs (so-called machine murmurs).

The cause of machine murmurs are congenital or acquired coronary AV- fistulas or an open ductus botalli(Attenhofer Jost 2004).

This noise phenomenon occurs in the following diseases:

- aorto-pulmonary window

- ruptured sinus- Valsalva- aneurysm

- coronary fistulas

- arteriovenous fistulas due to e.g. pulmonary angioma or posttraumatic (Herold 2022)

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).

The systolic murmur depends on blood flow through the pocket valves. It is offset from S1 and begins when the ventricular pressure exceeds the diastolic pulmonary artery or aortic pressure (Attenhofer Jost 2004).

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

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).

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