Diastolic heart murmur. Heart murmurs in a child

Heart murmurs This is a relatively long series of audible vibrations that differ from each other in volume, character, shape, frequency and location.

Heart murmurs are heard in the vast majority of children. They are divided into “functional” - in the absence of significant anatomical defects (transient noises developing heart and “small” hemodynamically insignificant anomalies and dysfunctions) and “organic” - associated with congenital anomalies, rheumatic and non-rheumatic heart lesions.

Functional heart murmurs(accidental, atypical, innocent, inorganic, benign) are heard very often in children. They are characterized by: 1) low intensity; 2) variability when the child’s position changes, with physical activity; 3) impermanence; 4) localization within the boundaries of area C; 5) occurrence during systole.

Organic heart murmurs meet less often. They are characterized by:

high intensity
constancy
conduction outside the heart
occurring during both systole and diastole.

Let's note the areas where the child's heart is listened to:

Left ventricular zone
Right ventricular zone
Left atrium zone
Right atrium zone
Aortic zone
Zone pulmonary artery
Area of the descending thoracic aorta

Features of examination of children with heart murmurs

If a child has a functional heart murmur, it is necessary to:

carefully analyze the medical history for the possibility of cardiac disease;
conduct initial examination, which necessarily includes electrocardiography (ECG);
if you suspect cardiac disease perform echocardiography (ultrasound of the child’s heart with Doppler ultrasound)
refer the child for consultation to a pediatric cardiologist.

It is advisable to divide children with functional heart murmurs into three categories:

healthy children with functional noise hearts;
children with noises of muscle origin requiring immediate or planned in-depth examination;
children with noises requiring dynamic monitoring.

Children with organic noise(or if a child is diagnosed pathological changes in the heart and large vessels) must be referred for consultation to pediatric cardiologist for the purpose of immediate or planned specialized examination and treatment.

The main characteristics of heart murmurs heard by auscultation:

Location of the noise: there are systolic, diastolic and systole-diastolic (long-lasting).

Loudness (intensity): assessed at the location where it is greatest. A heart murmur loudness gradation scale has been developed.

I degree: a very weak noise that can be heard even in silence, not immediately, but after persistent and careful auscultation.
Grade II: weak but easily recognizable murmur that can be heard under normal conditions.
III degree: moderately expressed without trembling chest.
IV degree: pronounced noise with moderate tremors of the chest.
V degree: loud, heard immediately after applying the stethoscope to the skin of the chest, with pronounced trembling of the chest.
Grade VI: exceptionally loud, which can be heard even when the stethoscope is removed from the skin of the chest, with pronounced trembling of the chest.

The special tonality of the heart murmur and its individual timbre can be perceived subjectively (by the human ear). Its character is described by the following terms: “blowing”, “scraping”, “snow crunching noise”, “rumbling”, “machine”, “rough”, “ soft”, “gentle”, “musical”, etc.

Duration and form (configuration).

A long murmur occupies almost the entire systole or diastole or both phases, while a short murmur occupies only a part cardiac cycle. The shape is determined by changes in the volume of a long noise along its length. It is customary to highlight various options.

in the form of a “plateau” - with a constant volume throughout.
in the form of “crescendo-decrescendo” - when the volume first grows to a maximum (towards the middle of the cycle) and then decreases.
in the form of “decrescendo” - decreasing, the volume of which decreases and gradually fades away.
in the form of a “crescendo” - increasing with a progressive increase in its volume.

Systolic heart murmurs

Occurs during systole, following the 1st sound C.

By nature they are usually “rough”, “scraping”; in children they can be relatively “soft”, with a “musical” tint.

Diastolic murmurs

They occur during diastole, following the second heart sound.

Early (protodiastolic) - with insufficiency aortic valve, infective endocarditis. By nature, it is usually “soft”, “blowing”, and therefore is often missed by doctors with inattentive auscultation.
Middle (mesodiastolic) - with stenosis mitral valve(timbre - “roar”, “roll”); may also be heard as there is increased blood flow into the ventricles through a normal or dilated atrioventricular orifice.
Late (presystolic) - with stenosis of the tricuspid valve (timbre - “squeak”); may also be integral part heart murmur with mitral stenosis.

Systole-diastolic

They arise at the beginning of systole and, without a pause, covering the second sound, continue during diastole. The unidirectionality of blood flow gives them a unique “machine” character.

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Auscultation of the heart with tricuspid stenosis

- Itone at the base of the xiphoid it is strengthened and even “popping”, especially at the height of inspiration.

Reducing intensity IItones above the pulmonary artery due to a decrease in blood flow into the pulmonary circulation with isolated tricuspid stenosis. When combined with stenosis of the left atrioventricular orifice, the second tone above the pulmonary artery can be normal or accentuated.

With sinus rhythm in the projection of the tricuspid valve (at the lower part of the sternum, at the insertion of the 5th rib) in diastole, sound (click) of tricuspid valve opening, better determined during inspiration.

- At the base of the xiphoid process, in the IV-V intercostal space at the left edge of the sternum, an increasing-decreasing protodiastolic murmur or presystolic murmur of a grinding timbre is heard, intensifying at the height of inspiration (Rivero-Corvallo sign), especially when the patient is positioned on the right side or standing. The area of best listening to diastolic murmur in tricuspid stenosis is located medially from the left midclavicular line, and in mitral stenosis - lateral from it. The noise decreases during the Valsalva maneuver (due to decreased blood flow through the valve), and increases in the clinostatic position.

Auscultation of the heart in pulmonary valve insufficiency

- Weakening Itones at the xiphoid process.

- AccentIItones in the second intercostal space to the left of the sternum as a manifestation of hypertension with relative insufficiency of the pulmonary valve. Split II tone in the II intercostal space to the left of the sternum due to the delay of its pulmonary component.

- With absence pulmonary hypertension and organic insufficiency of the pulmonary artery valve, diastolic murmur is heard in the III-IV intercostal space at the left edge of the sternum, being low-frequency, increasing-decreasing, short. In cases of relative valve insufficiency against the background of pulmonary hypertension and clefting of the pulmonary artery trunk, a diastolic murmur is detected in the II-III intercostal space to the left of the sternum (Graham Still's murmur) and is conducted towards the clavicle or is heard in the III-IV intercostal space on the right. This is a high-frequency, blowing, quiet, decreasing noise that increases with inspiration and decreases in the tension phase when performing the Valsalva maneuver.

Auscultation of the heart with ventricular septal defect

-I tone strengthened for small defects or weakened.

-II tone not changed or split over the pulmonary artery as a result of prolonged systole and volume overload of the right ventricle.

Sharp rough, scraping pansystolic murmur along the left edge of the sternum with the epicenter in the III-IV intercostal spaces and at the xiphoid process. This is one of the loudest noises (grade 4-5 according to Lewin). It covers the first sound, maintaining its full intensity, irradiates from the epicenter to both sides of the sternum, to the back, into the interscapular space (girdling noise). May be carried out bone tissue and listen with a stethoscope placed on the ribs, collarbone, and head of the humerus. The noise is more audible when the patient is lying down and increases in intensity when performing movements or isometric load.

In the III-IV intercostal spaces to the left of the sternum and at the apex of the heart, a short, soft mesodiastolic timbre is sometimes heard Coombs noise, caused by the flow of a large volume of blood from the lungs through the mitral orifice into the left atrium, which characterizes the hemodynamic picture of relative mitral stenosis. The noise decreases in an upright position and with a decrease in arteriovenous discharge (against the background of increasing pulmonary hypertension) it can completely disappear.

Short, soft, protodiastolic murmur in the second intercostal space on the left, occurring immediately after the second sound (Graham-Still noise), indicates relative insufficiency of the pulmonary valve. Appears in the late stages of the defect, when the pulmonary artery trunk expands and the pulmonary valve leaflets do not close completely.

With significant dilatation of the right ventricle, systolic noise of relative tricuspid valve insufficiency, heard over the xiphoid process and intensifying with inspiration.

Auscultation of the heart with atrial septal defect

- I tone the heart at the apex is not changed or increased due to reduced blood filling of the left ventricle due to the discharge of part of the blood into the right atrium.

Accent and cleavage II tones in the second intercostal space on the left as a result of increased pressure in the pulmonary circulation and a lag in the pulmonary component of the tone.

Pathological right ventricular III tone, caused by volume overload of the right atrium and right ventricle.

As a result of the ejection of a large volume of blood by the right ventricle, systolic murmur medium intensity and duration over the pulmonary artery, radiating to the left clavicle. The noise is better detected in the supine position, intensifying with physical activity. The murmur is caused by relative stenosis of the normal pulmonary fibrous opening with significantly increased blood flow through the dilated trunk of the pulmonary artery.

A low-frequency short mesodiastolic sound may be heard above the tricuspid valve. noise, increasing with inspiration, indicating an increase in blood flow through the tricuspid valve and the development relative tricuspid stenosis with right ventricular hypertrophy.

In conditions of significant dilation of the pulmonary artery trunk, in a third of patients in the late stages of the disease, a quiet, gentle protodiastolic murmur of relative insufficiency of the pulmonary valve appears with a blowing timbre. (Graham-Still noise).

Auscultation of the heart with a patent ductus arteriosus

- Itone not changed or, with severe hypertrophy and overload of the ventricular myocardium, weakened.

When equalizing pressure in the aorta and pulmonary artery accentIItones above the pulmonary artery.

With pronounced dilatation of the left cavities of the heart at the apex IIItone.

Intense (4-6th degree according to Lewin), scraping (“machine”, “trains in a tunnel”) continuous Gibson's systole-diastolic murmur at the base of the heart, especially in the second intercostal space to the left of the sternum. The murmur is associated with the flow of blood from the aorta to the pulmonary artery and begins after the first sound, increases in the second half of systole, absorbing the second sound, and weakens in proto- or mesodiastole. The noise radiates along the left edge of the sternum, is determined on the back between the upper angle of the scapula and the spine. It intensifies in the supine position, with pressure on the area of the abdominal aorta, weakens at the height of a deep forced inspiration with breath holding and during the Valsalva maneuver.

Auscultation of the heart with tetralogy of Fallot

- Itone at the top is not changed.

- IItone over the pulmonary artery is weakened.

Rough, scraping, medium intensity (grade 3-5) systolic murmur of right ventricular outflow tract stenosis in the II-III intercostal spaces to the left of the sternum with valvular stenosis of the pulmonary artery and in the III-IV intercostal spaces on the left - with infundibular stenosis. Occupies the entire systole, is not associated with sounds, has greater intensity in horizontal position. It is carried out on the vessels of the neck, to the collarbones and in the interscapular space.

- Systolic murmur of ventricular septal defect in the III-IV intercostal spaces to the left of the sternum.

While maintaining a functioning patent ductus arteriosus systole-diastolic murmur in the left subclavian region with maximum sound in the second intercostal space on the left.

Auscultation of the heart in fibrinous pericarditis

- IAndIItones hearts are muffled.

- Pericardial friction rub between the left edge of the sternum and the apex, often in the area absolute stupidity hearts. It resembles the crunch of snow underfoot, the rustle of paper, the creaking of skin, and consists of three components: atrial systole - ventricular systole - ventricular protodiastole, two components: ventricular systole - ventricular diastole, or only one component (ventricular systole). Often, a pericardial friction murmur begins in systole and passes into diastole without any interruption (continuous systole-diastolic murmur). The pericardial friction noise intensifies when the patient bends forward, tilts the head back, or with strong pressure with a phonendoscope; the noise is better heard in vertical position the patient and while holding his breath while exhaling.

Auscultation of the heart for cardiac myxoma

- Itone at the apex of the heart (at the xiphoid process) with myxoma of the left (right) atrium, it can be loud, increasing, and decreasing in the supine position.

At the very beginning of diastole with myxoma, an additional tone is “tumor cotton” is recorded when a pedunculated tumor sags into the lumen of the mitral valve (or tricuspid valve) and can impact the endocardium of the left ventricle. Determined at the apex of the heart (or at the xiphoid process), decreases or disappears in the supine position.

- IItone above the pulmonary artery may be accentuated with myxoma of the left atrium.

- Systolic murmur at the apex (with myxoma of the left atrium), in the region of the xiphoid process or at the left edge in the IV intercostal space (with myxoma of the right atrium) due to the development of relative valve insufficiency and systolic regurgitation in the atrium. Decreases when lying down.

- Diastolic murmur at the apex (with myxoma of the left atrium), in the region of the xiphoid process or at the left edge in the IV intercostal space (with myxoma of the right atrium) is due to relative stenosis of the atrioventricular orifice due to myxoma. The noise decreases or disappears in the supine position, whereas with organic stenosis it weakens in the vertical position. The degree of covering of the atrioventricular orifice by the tumor can vary in different cardiac cycles, leading to the fact that the diastolic noise migrates during diastole: in some cardiac cycles it is protodiastolic, in others it is mesodiastolic or even presystolic, which is not observed with organic stenosis.

Treatment of patients with congenital and acquired heart defects includes compensation for congestive heart failure through drug treatment and, if indicated, surgical correction of the defects. The nature of the surgical intervention is determined by the morphology of the existing changes and the patient’s condition.

Great importance is given to preventive measures to prevent the formation of heart defects in children, aimed at promoting a healthy lifestyle for mothers during pregnancy, sanitizing foci of infection, limiting the use of medications, and timely medical examination of pregnant women (especially those with a family history).

Prevention of acquired heart defects includes, first of all, the prevention of rheumatic defects. Primary prevention is antimicrobial therapy for acute and chronic recurrent upper respiratory tract infections. Secondary prevention is prescribed to patients who have suffered acute rheumatic fever. Its goal is to prevent recurrent attacks and progression of the disease. As a rule, it should be for patients who have had acute rheumatic fever without carditis (arthritis, chorea), at least 5 years after the attack or up to 18 years of age. For patients with cured carditis without heart defects - at least 10 years after the attack or 25 years of age. For patients with established defects (including those undergoing surgery) – for life.

Appendix 2. Test tasks:

1. Early signs of rheumatism include: a) minor chorea; b) diastolic murmur over the aorta; c) arthritis; d) ring-shaped erythema; e) erythema nodosum. Choose the correct combination of answers:

2. Late signs of rheumatism include:

1) polyarthritis

2) valvulitis

4) carditis

5) erythema nodosum

3. How does the presystolic murmur change in patients with mitral stenosis when atrial fibrillation occurs?

1) is significantly enhanced

2) increases slightly

3) does not change

4) disappears

5) decreases

4. For secondary seasonal prevention of rheumatism, the following drug is used:

1) ampicillin

2) digoxin

3) delagil

4)bicillin

5) gentamicin

5. With mitral stenosis the following is observed:

1) deviation of the esophagus along a large radius arc

2) deviation of the esophagus along a small radius arc

3) enlargement of the left ventricle

4) expansion of the ascending aorta

6. Auscultatory signs of combined mitral heart disease with a predominance of stenosis of the left atrioventricular orifice are:

1) strengthening of the first tone at the apex of the heart

3) apical systolic murmur associated with the first sound

4) mesodiastolic murmur

5) all of the above

7.Which of the following symptoms allows us to suspect concomitant mitral regurgitation in the presence of mitral stenosis?

1) high-frequency systolic murmur immediately adjacent to the first sound

2) the tone of the mitral valve opening

3) loud I tone

8. What diseases can lead to aortic valve insufficiency?

1) rheumatism

3)syphilis

4) atherosclerosis of the aorta

5) all of the above

9. Clinical signs of aortic valve insufficiency are: a) carotid dance; b) diastolic murmur at the V point; c) undulation of the neck veins; d) systolic murmur in the second intercostal space on the left; e) diastolic murmur in the second intercostal space on the left. Choose the correct combination of answers:

10. In case of aortic valve insufficiency, the following symptoms may be detected: a) strengthening of the first tone; b) quail rhythm; c) weakening of the second tone over the aorta; d) double Traube tone on large vessels; e) Flint noise. Choose the correct combination of answers:

11. The cause of organic damage to the tricuspid valve is:

1) rheumatism

2) infective endocarditis

3) Ebstein's anomaly

4) injury

5) all of the above

12. Tetralogy of Fallot consists of the following components except:

1) narrowing of the outflow tract of the right ventricle

2) ventricular septal defect

4) atrial septal defect

5) hypertrophy of the right ventricular myocardium

13. The characteristics of noise with a patent ductus arteriosus include all except:

4) has a scraping character

The murmur caused by atrial septal defect is caused by:

1) relative stenosis of the pulmonary opening

2) turbulent blood flow through the defect

3) reverse blood flow from the aorta to the left ventricle

4) reverse blood flow from the left ventricle to the left atrium

5) the presence of communication between the aorta and the pulmonary trunk

15. Rheumatic endocarditis corresponds to: a) valvulitis; b) formation of defects; c) disturbance of atrioventricular conduction; d) deformation in the joints; e) negative T wave on the ECG. Choose the correct combination of answers:

16. Rheumatic myocarditis corresponds to: a) disturbance of atrioventricular conduction; b) expansion of the cavities of the heart; c) additional third tone; d) formation of defects; e) valvulitis. Choose the correct combination of answers:

17. The characteristics of noise with a patent ductus arteriosus include all except:

1) noise intensity of 4-6 degrees according to Levin

2) heard at the base of the heart, especially in the 2nd intercostal space to the left of the sternum

3) is continuous systole-diastolic

4) has a scraping character

5) with the development of pulmonary hypertension it becomes more intense

18. Erythrocytosis most often appears with:

1) aortic insufficiency

2) mitral stenosis

3) tetralogy of Fallot

4) open ductus arteriosus

5) coarctation of the aorta

19. Features of functional noise include all except:

1) is a rough scraper

2) is of short duration

3) varies from one cardiac cycle to another

4) not accompanied by trembling

5) not accompanied by changes in I and II tones

20. Which of the following symptoms are characteristic of tricuspid stenosis?

1) weakening of the first tone at the base of the xiphoid process

2) strengthening of the second tone above the pulmonary artery

3) systolic murmur at the base of the xiphoid process

4) diastolic murmur at the base of the xiphoid process

5) continuous systole-diastolic murmur

Answers to test tasks: 1 – 3; 2 – 3; 3 – 4; 4 – 4; 5 – 2; 6 – 5; 7 – 1; 8 – 5; 9 – 1; 10 – 5; 11 – 5; 12 – 4; 13 – 5; 14 – 1; 15 – 1; 16 – 4; 17 – 5; 18 – 3; 19 – 1; 20 – 4.

Appendix 3. Situational tasks:

Task 1.

A 24-year-old patient complains of shortness of breath when walking. In childhood I had frequent tonsillitis, at the age of 15 I had minor chorea, and from the age of 20 I had a heart murmur. Shortness of breath for a year, received outpatient digoxin and periodic diuretics. Worsening within a month. Objectively: body weight - 73 kg, height - 170 cm. No edema. Increased pulsation of the carotid arteries. The apical impulse is strengthened, diffuse, in the 5th intercostal space. On auscultation, there is a blowing protodiastolic murmur in the second intercostal space to the right of the sternum and a systolic murmur at the apex of the heart. Pulse - 80 per minute, rhythmic, full. Blood pressure - 150/mm Hg. Art. The liver is at the edge of the costal arch, pulsating. With fluoroscopy the heart has an aortic configuration, the apex is rounded, pulsation is reduced.

ECG: left ventricular hypertrophy, R<=0,24 sec. Blood analysis:НБ - 120 g/l, leuk. - 9.0x10 9 /l, ESR - 39 mm/hour.

1) Diagnosis, rationale.

2) Etiology, phase of the process, state of blood circulation.

3) Additional tests for process activity.

4) Treatment tactics.

Task 2.

A 52-year-old patient was admitted with complaints of shortness of breath at rest, swelling and abdominal enlargement. She suffered from polyarthritis as a child. At the age of 26, a heart defect was discovered. 10 years - interruptions, shortness of breath on exertion, for 2 years - swelling and enlargement of the abdomen. Objectively: height - 165 cm, body weight - 89 kg. Swelling on the legs. There is hard breathing in the lungs, no wheezing. NPV - 20 per minute. The neck veins are swollen.

Heart rate - 115 per minute. Pulse - 90 per minute. Blood pressure -110/80 mm Hg. Art. The abdomen is enlarged in volume, ascites is detected. The liver is 5 cm below the edge of the costal arch, dense, with a sharp edge, pulsating. On the ECG: atrial fibrillation, right gram, signs of right ventricular hypertrophy.

1) The patient has been diagnosed with mitral stenosis. Give arguments “for” the diagnosis.

2) How to explain the noise at the xiphoid process and changes in the liver?

3) Full diagnosis?

4) How will you begin treating the patient?

5) After 5 days, heart rate is 88 per minute. Pulse - 44 per minute, nausea, anorexia. What happened?

6) Tactics regarding atrial fibrillation?

Task 3.

A 28-year-old patient was admitted with complaints of pain in the joints of the arms and legs, dizziness, and fever up to 37.5°C.

Objectively: the skin and visible mucous membranes are pale. Sharply expressed pulsation of the carotid and subclavian arteries. The apical impulse in the VI intercostal space 1 cm to the left of the midclavicular line, diffuse, strengthened. Auscultation: protodiastolic murmur at the Botkin-Erb point, weakening of the second sound in the aorta. Pulse - 90 per minute, rhythmic, fast, high. Blood pressure - 180/40 mm Hg. Art. The liver is not enlarged, there is no edema. ECG: levogram, left ventricular hypertrophy.

1) Diagnosis and its rationale?

2) Direct and indirect signs of heart disease?

3) Additional research methods?

4) Treatment tactics?

5) Is surgical intervention possible for heart defects at the moment?

Task 4.

A 40-year-old patient has been under the supervision of a rheumatologist for a long time. Recently, shortness of breath has increased, and swelling has appeared in the legs.

During the examination - cyanotic blush on the cheeks, pulsation in the epigastric region under the xiphoid process. The heart is expanded to the left and up; trembling over the apical region. On auscultation above the apex there is a loud 1st sound, a bifurcation of the 2nd tone, and the rhythm of cardiac activity is abnormal. The liver is 3 cm below the costal arch, swelling of the legs.

1) What is missing in the description of auscultatory data?

2) What causes the second tone to split?

3) What does epigastric pulsation indicate?

4) Stage of heart failure?

5) The drug of choice for the correction of heart failure, given the presence of a permanent form of atrial fibrillation.

Task 5.

Make a table in the form of a table of the main auscultatory differential diagnostic differences in diastolic murmur in the diseases under study, indicating such characteristics as localization, duration of murmur, intensity, irradiation, connection with the second sound, dependence on physical activity, changes in body position, breathing, use of vasopressors and vasodilators .

Detection and interpretation of heart murmurs are often difficult and require experience and knowledge of physiology and cardiology. Currently, if a murmur is present, the patient is immediately referred for echocardiography. Murmurs are audible vibrations caused by turbulent blood flow. They are described using a large number of characteristics given in table. 1. Noises vary in intensity (loudness), as described in table. 2.

Table 1.

Description of noise

Intensity (loudness)	Degrees 1-6 (or 1-4) (see table 1)
Duration	Short to long noise
Character (shape)	Crescendo, decrescendo, variable, plateau, crescendo-decrescendo
Time	In relation to the phases of the cardiac cycle, for example mid-systolic, pan-systolic, late systolic, early diastolic
Frequency	High or low frequency
Character	For example, blowing, rough, scratching, gurgling, scraping, etc.
Localization	Maximum intensity
Carrying out	Conducting noise to auscultation points (including the vessels of the neck)
Variability	Variability depending on the phases of breathing

Table 2.

Noise intensity gradations

Degrees 1-6	Degrees 1-4	Description
1	1	Very little noise. Usually only an experienced doctor can listen to him
2	2	Faint but distinct noise
3	3	Loud noise without accompanying vibration
4	4	Loud noise accompanied by subtle shaking
5	4	Loud noise accompanied by distinct shaking
6	4	Loud noise accompanied by shaking, audible when the stethoscope is removed from the surface of the chest

Functional noise

Not all noises are pathological; quite often there are functional noises that occur during hyperkinetic blood circulation, for example in healthy children, as well as during pregnancy, thyrotoxicosis, against the background of fever and anemia. Their presence may require an echocardiogram to ensure that the murmur is truly functional. Such murmurs are always systolic, usually quiet or of moderate intensity, have a “musical” tone, and are not rough or blowing.

Systolic murmurs

Blood flow through pathologically altered structures leads to the formation of noise due to the presence of a pressure gradient (on a pathologically altered valve, in the area of a septal defect, with coarctation, etc.). The louder the noise, the greater the pressure gradient and the higher the blood flow velocity. The murmur does not occur until the expulsion of blood from the left ventricle begins, and reaches a maximum at the moment of greatest blood flow through the narrowed opening. Consequently, in severe stenosis, the peak of the murmur is recorded in late systole. The murmur stops before the start of the second sound, as cardiac output stops. Therefore, the noise has a crescendo-decrescendo shape. This noise is called ejection noise. Since the murmur is dependent on blood flow, it may weaken or disappear when the degree of valve damage is very severe and leads to HF. The systolic murmur of regurgitation on the MV can occur as soon as the isovolemic contraction begins, that is, before the onset of ejection, since the reverse flow of blood occurs simultaneously with the beginning of an increase in pressure in the ventricle and continues until the appearance of the second sound or ends a little earlier. This occurs due to the pressure difference between the LV and LA during systole. Often the second tone is covered by noise. Murmurs of this type, occupying the entire systole, are called pansystolic or holosystolic. Pansystolic murmur also occurs with a ventricular septal defect (VSD). However, in many patients with mitral regurgitation, the valve failure is incomplete, and then the murmur begins in the middle or even at the end of systole and continues until the second sound. Late systolic murmurs may have a crescendo shape, which resembles an ejection murmur, but they arise much later in systole, cover the second sound, and then suddenly stop. It is not difficult for an experienced doctor to determine this, especially in the absence of pronounced tachycardia, but sometimes a systolic click in the middle or end of diastole is mistaken for the second sound, and the murmur is interpreted as diastolic.

Diastolic murmurs

Diastolic murmurs on the AV valves are very difficult to hear. These noises are usually low-frequency and may be mistaken for external noise by an inexperienced physician. Typically, diastolic murmur is a sign of mitral stenosis (sometimes TC stenosis), and these defects are becoming less common in developed countries. The diastolic murmur of mitral stenosis intensifies when the patient is positioned on the left side when listening to the apex area with a phonendoscope cone and/or after physical activity. Mid-diastolic murmurs intensify immediately before the onset of the next systole, since in presystole the blood flow through the MV increases due to atrial contraction (Table 3). This presystolic enhancement usually disappears as AF progresses, but may sometimes persist.

Table 3.

Differential diagnosis of systolic murmurs

	Cause	Localization	A comment
Systolic ejection murmur	Aortic stenosis	To the left of the sternum in the area of the upper third, also often at the apex. Performed on the carotid arteries	Slow pulse in the carotid arteries, but not always detected in the elderly. The apical impulse is usually elevating, but not displaced. In young people, the noise may be preceded by an ejection tone. The II tone varies, with severe valve calcification there is no splitting
	Pulmonary artery (PA) stenosis	To the left of the upper edge of the sternum	Intensifies on inspiration. Ejection tone, possibly delayed pulmonary component II tone
			Fixed splitting of the second tone. With a large discharge, you can palpate the contracting pancreas along the left edge of the sternum
	Functional	All points. "Musical"	May appear with high cardiac output
Pansystolic	Mitral regurgitation	At the apex, carried into the axillary region	It varies greatly, but with valvular regurgitation it often blows and covers the second sound. Pulsating top. In case of severe defect, mid-diastolic murmur and III tone may appear
	Tricuspid regurgitation	Along the left edge of the sternum	It intensifies on inspiration, the v-wave of the pulse is pronounced in the jugular veins, and pulsation of the liver is possible. Pulsation to the left of the sternum is also possible - a sign of pulmonary hypertension
		Along the left edge of the sternum	Usually rough, often accompanied by trembling. Single II tone with a large defect
Late systolic	Mitral regurgitation associated with damage to subvalvular structures (MVP, chord avulsion)	At the apex, carried into the axillary region, but can also carried out in the back and neck area	Often rough, the murmur may be preceded by a systolic click. Elevating apical impulse, mid-diastolic murmur and III sound with severe mitral regurgitation. Can be confused with an early diastolic murmur if it is preceded by a late click, which is mistaken for the second tone
Presystolic	Mitral stenosis (and also TC stenosis - very rare)	At the apex and left edge of the sternum	Sometimes it is difficult to recognize. The murmur is often mistaken for systolic and associated with mitral regurgitation. It is necessary to carefully compare the noise with the pulsation of the carotid arteries

Early diastolic murmur

Early diastolic murmurs occur due to regurgitation of blood at the AC or PC. They have a decrescendo shape and follow directly the second tone. This results from the fact that the maximum pressure difference between the vessel and the ventricular cavity occurs at the beginning of diastole. Minor aortic regurgitation results in a short, soft early diastolic murmur that is difficult to hear, but the intensity of the murmur may increase as the patient bends forward and exhales. These actions make regurgitation better audible due to the closer location of the heart to the anterior surface of the chest. An increase in noise intensity may be associated with an increase in the degree of the defect, but sometimes paradoxical situations arise. When chronic aortic regurgitation is very severe, backflow of blood from the aorta into the ventricle occurs very quickly and the murmur becomes loud but very short. This phenomenon is even more pronounced with the development of acute aortic regurgitation due to valve damage due to endocarditis, dissecting aneurysm or trauma. Before the defect occurs, the LV is of normal size, and a sudden large volume of regurgitation instantly fills it to its maximum limit, leading to slamming of the MV. This leads to extremely low cardiac output and a very short murmur. Clinical signs include collapse, sinus tachycardia and the appearance of an auscultatory pattern resembling a gallop rhythm. An experienced cardiologist will immediately recognize severe acute aortic regurgitation and prescribe appropriate testing, including emergency echocardiography. Often, emergency surgery for AK can save the patient's life, but if the diagnosis is not made in a timely manner, the consequences can be fatal. Pulmonary hypertension produces an early diastolic murmur that is lower in pitch than that of aortic regurgitation. An early diastolic murmur is heard in the upper part of the sternum along its left edge and follows the loud pulmonary component of the second sound (a sign of pulmonary hypertension).

Systole-diastolic murmurs

Systole-diastolic murmurs are rare in adults. These are murmurs heard throughout the entire cardiac cycle. The systolic component is usually louder than the diastolic component, but there seems to be no interval between them, and they are well named "engine noises" because they are similar to the sound of a running engine. A systole-diastolic murmur may be a sign of a patent ductus arteriosus that was undiagnosed in childhood. However, most often in adults, systolic-diastolic murmur is a sign of an acutely developed fistula between the right and left chambers of the heart. In this case, blood flow occurs in both systole and diastole. The most common example is a rupture of the sinus of Valsalva, although infective endocarditis can lead to the formation of an arteriovenous and right-sided shunt.

Carotid murmurs

Systolic murmur on the carotid arteries has the following properties.

1.Can be performed from the heart valves - usually the aortic, although loud mitral murmurs may also be heard in the neck. The same noise will be heard above the surface of the chest.

2. It may occur due to damage to the carotid arteries, in this case it is heard only in the neck. It is sometimes difficult to understand whether there is a combined lesion of the valve and carotid arteries or an isolated lesion of the AV.

Noise irradiation

The irradiation of noises is complex, and in general any noise can be carried out to any point in the chest. However, typical sites include the apical/mitral, pulmonary, aortic, and tricuspid regions, with radiation to the carotid arteries, the back, and/or the axilla. It must be remembered that loud noises during MVP and chord rupture can be carried out anywhere, including to the vessels of the neck, and resemble the noise during aortic stenosis. Moreover, the noise of aortic stenosis in elderly patients is characterized by a louder sound at the apex than at classical auscultation points. This occurs due to emphysema in the elderly and interferes with auscultation, especially at the base of the heart. Aortic murmurs, heard only at the apex, are often carried out on the carotid arteries.

Other auscultatory phenomena

The pericardial friction noise that occurs with pericarditis is caused by the friction of the inflamed pericardial layers against each other with each contraction of the heart. It is an intermittent scraping sound with systolic and diastolic components. It is better heard when the patient is lying on his back, and may disappear when the patient sits down and bends forward - in this position, as a rule, the pain associated with pericarditis decreases. You should always think about the presence of pericarditis when you see a patient sitting on the bed, leaning forward.

Roger Hall, Iain Simpson

History taking and physical examination of patients with cardiovascular diseases

Early diastolic murmurs appear simultaneously with the second heart sound or follow immediately after it, as soon as the pressure in the ventricle decreases so much that it is lower than the pressure in the aorta or pulmonary artery. High-frequency murmurs due to aortic valve insufficiency or pulmonary valve insufficiency caused by pulmonary hypertension usually have a descending shape, as during diastole there is a gradual decrease in the volume and speed of regurgitation. The gentle, high-frequency sounds of aortic valve insufficiency are difficult to auscultate. They cannot be heard by chance. Careful auscultation along the left sternal border is necessary. The phonendoscope should be pressed tightly to the chest. In this case, the patient must change position: sit, lean forward, hold a deep exhalation. The diastolic murmur of aortic valve insufficiency increases with a sudden increase in blood pressure, as with the wrist squeeze test, and becomes weaker as the blood pressure decreases, as with amyl nitrite inhalation. Diastolic murmur with congenital pulmonary valve insufficiency, not accompanied by pulmonary hypertension, is characterized by low or medium height. This noise appears somewhat later, since at the moment the pulmonary valve closes, the reverse flow of blood is minimal, since the pressure gradient leading to regurgitation is insignificant at this moment.

Middiastolic murmurs usually appear at the level of the atrioventricular valves during early ventricular filling. Like most midsystolic murmurs, middiastolic murmurs result from a mismatch between the valve lumen and blood flow. They can be quite loud, despite the slight stenosis of the atrioventricular orifice, even if the blood flow is unchanged or slightly increased. In contrast, the murmur may be weak or absent in patients with severe valve disease, but with a marked decrease in cardiac output. Severe stenosis is accompanied by a prolonged diastolic murmur. Moreover, the duration of the noise is a more reliable sign of the degree of narrowing of the hole than its intensity.

A characteristic feature of the low-frequency middiastolic murmur of left atrioventricular orifice stenosis (mitral stenosis) is its occurrence after the opening click. The stethoscope should be placed over the area of the left ventricular impulse, which is best detected with the patient lying on the left side. The murmur of mitral stenosis is often heard only in the area of the apex of the left ventricle. It may be aggravated by mild physical exertion with the patient lying down or by inhalation of amyl nitrite. In patients with right atrioventricular orifice stenosis, the middiastolic murmur is localized to a relatively limited area along the left sternal border and may become aggravated with inspiration.

The left atrioventricular (mitral) valve may be the source of a middiastolic murmur in patients with a ventricular septal defect, patent ductus arteriosus, or mitral regurgitation. In case of an atrial septal defect or insufficiency of the right atrioventricular (tricuspid) valve, the origin of the middiastolic murmur is the tricuspid valve. These noises are caused by blood rushing through the valve. As a rule, this occurs after the third heart sound. A predisposing factor for the appearance of murmurs is a large shunt of blood from left to right or severe atrioventricular valve insufficiency. A soft middiastolic murmur can sometimes be heard in patients with acute rheumatic fever (Carey-Coombs murmur). Its appearance is associated with inflammation of the edges of the left atrioventricular (mitral) valve or excessive accumulation of blood in the left atrium due to mitral regurgitation.

In the case of acute aortic valve insufficiency, the diastolic pressure in the left ventricle may exceed the pressure in the left atrium, which will lead to the development of so-called diastolic mitral regurgitation, accompanied by a middiastolic murmur. In severe chronic aortic insufficiency, a middiastolic or presystolic murmur (Flint murmur) can often be detected. It is believed that this noise occurs when blood entering the cavity of the left ventricle simultaneously from the aortic root and left atrium collides with the anterior leaflet of the mitral valve.

The onset of presystolic murmurs coincides with the period of ventricular filling, i.e., follows atrial contraction. In this regard, the condition for the occurrence of these noises is the preservation of sinus rhythm. They are usually caused by stenosis of the atrioventricular orifice. They have the same characteristics as middiastolic filling murmurs, however, they have an ascending shape. The peak of their intensity coincides in time with the loud first heart sound. The intensity of the presystolic murmur is determined by the magnitude of the pressure gradient across the atrioventricular valve, which may remain minimal until the right or left atrium contracts. The presence of presystolic murmur to a much greater extent than middiastolic murmur is characteristic of stenosis of the right atrioventricular orifice (tricuspid stenosis), combined with preserved sinus rhythm. Sometimes a myxoma of the right or left atrium may be accompanied by the appearance of middiastolic or presystolic murmurs, reminiscent of the murmurs of mitral or tricuspid stenosis.

Constant murmurs begin in systole, reach a maximum approaching the second heart sound, and continue throughout diastole or part of it. The presence of these noises indicates the preservation of constant blood flow between the high and low pressure sections in the period from the end of systole to the beginning of diastole. In the case of a patent ductus arteriosus, the murmur persists until the pressure in the pulmonary artery becomes significantly lower than the pressure in the aorta. This noise increases with increasing systemic blood pressure and becomes weaker with inhaled amyl nitrite. With pulmonary hypertension, the diastolic component of the murmur may disappear. In this case, the murmur becomes exclusively systolic. A continuous murmur is rare in aortopulmonary septal defects because this malformation is usually accompanied by severe pulmonary hypertension. Surgically created aortopulmonary connections and anastomoses between the subclavian and pulmonary arteries lead to the appearance of murmurs similar to those of a patent ductus arteriosus.

Persistent murmurs may result from congenital or acquired systemic arteriovenous fistulas, coronary arteriovenous fistulas, anomalous origin of the left coronary artery from the pulmonary artery, or connections between the sinus of Valsalva and the right heart. The cause of persistent murmurs may also be high pressure in the left atrium, causing a constant discharge of blood through a small defect in the interatrial septum. Murmurs associated with pulmonary arteriovenous fistulas may be continuous, but are usually only systolic. Persistent murmurs may also result from impaired blood flow in stenotic systemic (eg, renal) or pulmonary arteries, when there is a noticeable pressure difference at the ends of the narrowed segment. In patients with coarctation of the aorta, a continuous murmur may be heard from the back. Pulmonary embolism, leading to partial closure of the lumen, can also cause constant noise.

Constant noise may be a consequence of the rapid passage of blood through unchanged but tortuous vessels. An example illustrating this situation would be the occurrence of a constant murmur in patients with severe cyanosis caused by severe obstruction of blood outflow from the lungs. In such a case, the place of origin of noise is the collaterals of the bronchial arteries. In late pregnancy and early postpartum, women may hear a milky murmur, a harmless systolic or continuous murmur. An innocuous cervical venous hum is a constant noise usually heard in the medial aspect of the right supraclavicular fossa when the patient is in an upright position. This buzzing usually increases during diastole and can be instantly relieved by finger pressure on the internal jugular vein on the same side. Radiation of a loud venous hum below the collarbones may lead to an erroneous diagnosis of patent ductus arteriosus.

The pericardial friction rub consists of presystolic, systolic and early diastolic components, which have a scratchy sound. If only the systolic component is heard, the murmur may be confused with some other cardiac or extracardiac murmur. For better auscultation of the pericardial friction rub, the patient should be in an upright position, bending forward. The noise intensifies on inspiration.

A murmur is the sound produced by turbulent blood flow. Under normal conditions, the movement of blood in the vascular bed is laminar and silent. However, as a result of hemodynamic and/or structural changes in the vascular system, the silent flow of blood is disrupted and audible noises may occur

Mechanism

Noise is based on the following mechanisms:
1. Blood flow through a narrowed area (for example, with aortic stenosis)
2. Acceleration of blood flow through a normal structure (for example, aortic systolic murmur may occur due to an increase in cardiac output, in particular with anemia)
3. Blood flow into the dilated area (for example, aortic systolic murmur caused by aneurysmal dilatation of the aorta)
4. Regurgitation due to valve insufficiency (eg, mitral regurgitation)
5. Pathological discharge of blood from a chamber with high pressure to a chamber with lower pressure (for example, with a ventricular septal defect)

Listening areas

Listening area- this is the zone of maximum noise intensity; special auscultation points are usually used to describe the listening area (see figure)
- Point of the aortic valve (2 - 3 intercostal spaces at the right edge of the sternum).
- Pulmonary valve point (2 - 3 intercostal spaces at the left edge of the sternum)
- Tricuspid valve point (at the left edge of the sternum at the level of the xiphoid process)
- Mitral valve point (apex of the heart)
- Botkin point 3 - 4 intercostal space to the left of the sternum - aorta

Noises are divided into systolic, heard after S1 - I tone and diastolic, heard after S2 - II tone.

Systolic murmurs

- aortic stenosis
- pulmonary artery stenosis
- mitral valve insufficiency
- insufficiency of TC
- ventricular septal defect
- mitral valve prolapse

Diastolic murmurs

They are heard with the following heart defects:
- aortic valve insufficiency
- pulmonary valve insufficiency
- MV stenosis
- TC stenosis