Accordingly, in such a situation it is very difficult to distinguish systole from diastole using auscultation. This happens because severe volume overload of the left ventricle prolongs the ejection period, and the diastolic period can become even shorter due to tachycardia. In order not to confuse systole with diastole, it is recommended to palpate the pulse simultaneously with auscultation. carotid artery or apical impulse.
2. Why, with sudden onset of severe aortic regurgitation, the murmur may not be pandiastolic even in cases where the diastole becomes shorter than normal? In sudden severe aortic regurgitation, the left ventricle does not dilate to the same extent as in chronic aortic regurgitation. In other words, in the first case, the left ventricle is less distensible due to the inability of the pericardium to rapidly stretch. In fact, left ventricular pressure during diastole can increase so significantly and so quickly that it can even become equal to the mesodiastolic pressure in the aorta. Equality of intra-aortic and intraventricular pressure limits the amount and duration of aortic regurgitation that can occur (see Fig.
9 on page 396). The murmur of aortic regurgitation may not only be short (not pan-diastolic), but also surprisingly quiet.
Differential diagnosis 1. What murmurs most often mimic the murmur of aortic regurgitation? A. Pulmonary regurgitation noise caused by high blood pressure pulmonary artery(Graham Still noise).
b. High-frequency components of murmurs of mitral stenosis, conducted to the left edge of the sternum.
2. What murmurs in rare cases can imitate the murmur of aortic regurgitation? A. Diastolic component of a quiet continuous murmur due to a fistula coronary artery with the pulmonary artery or right coronary artery with the left ventricle, in cases where the systolic component of this murmur is not heard.
b. Inflation of the intra-aortic balloon pump during diastole produces a short, slightly delayed diastolic noise of a wind-like or roaring timbre.
V. Dangling (flail) rear flap mitral valve at the moment of rapid transition from a prolapsed position (in the left atrium) to an open position (in the left ventricle), blood is pushed from the left atrium into the left ventricle.
d. Similar to the murmur of aortic regurgitation, a quiet diastolic murmur is heard in the second or third intercostal space to the left of the sternum in some patients with moderate (occlusion of no more than 50%) obstruction of the anterior descending coronary artery.
murmurs with stenosis of the anterior descending coronary artery 1. What are they? characteristics diastolic murmur in coronary artery stenosis? This noise:
A. High-frequency and increasingly decreasing in accordance with the pattern of diastolic coronary blood flow, which is maximum in the first quarter of diastole.
b. It is easiest to hear with the patient in a sitting position.
Note:
It has been observed that this murmur may disappear after myocardial infarction and coronary artery bypass grafting.
The diastolic murmur of coronary artery stenosis indicates that the obstruction is minor, i.e. such that the remaining blood flow is sufficient to produce turbulence that can become a source of diastolic murmur.
It is not surprising that all patients studied with this murmur had an obstruction rate of less than 50%.
SOUND OF PULMONARY REGURGITATION Murmurs during high blood pressure in the pulmonary artery (Graham Still murmur) 1. Does the pressure in the pulmonary artery have to be very high for a pulmonary regurgitation murmur to occur? Usually pulmonary pressure is very high (i.e. close to systemic blood pressure). Pulmonary regurgitation murmurs rarely occur when pulmonary artery pressures are below 80 mmHg. Art., except in cases where the pulmonary trunk is significantly dilated.
Notes:
A. A Graham Still murmur is a murmur of pulmonary regurgitation that occurs in the setting of pulmonary hypertension, regardless of whether the pulmonary hypertension is primary or secondary.
b. The murmur of pulmonary regurgitation with a ventricular septal defect can occur even with normal pulmonary vascular resistance, if the pressure in the pulmonary artery exceeds 80 mm Hg. Art.
2. How does a Graham Still murmur differ from an aortic regurgitation murmur? These noises may not be different. In other words, both noises are predominantly high-frequency, can vary in intensity from 1 to degree, at first be increasingly decreasing and - if the intensity is low - become louder on exhalation. At the same time, if the volume of Graham Still's noise is high, it usually intensifies during inspiration (Fig. 13).
Rice. 13. Phonocardiograms of a patient with persistent ductus arteriosus, in whom the pulmonary artery pressure was 145 mm Hg, are presented. Art., and aortic pressure was approximately the same. A loud diastolic murmur (Graham Still's murmur) recorded on phonocardiograms increased significantly during inspiration. The quiet Graham Still noise may not increase during inspiration. HF - high frequencies, MF - mid frequencies Notes:
A. If the volume of the Graham Still murmur is insignificant, then during inspiration it may decrease even more, despite the increase in blood flow in the pulmonary artery. The fact is that the quiet noise of pulmonary regurgitation is usually best heard in the second intercostal space to the left of the sternum, and the increase in the distance between the stethoscope and the heart that occurs during inspiration in this area is most pronounced. In addition, in severe pulmonary hypertension, inspiratory blood flow to the lungs may not increase if there is concomitant tricuspid regurgitation b. Isometric hand clenching and squatting will selectively increase the volume of the aortic regurgitation murmur.
3. How does the Valsalva maneuver help distinguish the murmur of pulmonary regurgitation from the murmur of aortic regurgitation? Immediately after cessation of straining, the volume of the pulmonary regurgitation noise becomes the same as before the Valsalva maneuver. The initial loudness of the murmur of aortic regurgitation is restored only after four or five cardiac cycles.
Notes:
A. In patients with pulmonary artery dilatation, an early diastolic decaying grinding sound may be heard in the absence of aortic or pulmonary regurgitation. This creaking sound is of extracardiac origin and may be caused by adhesions between the pulmonary artery and surrounding lung tissue.
b. Previously, there was a misconception that a Graham Still murmur was often heard in mitral stenosis because the murmur of aortic regurgitation was incorrectly regarded as being due to pulmonary regurgitation.
Pulmonary regurgitation sounds during normal pressure in the pulmonary artery (primary pulmonary regurgitation) 1. Besides the congenital absence of the pulmonary artery, what are the two most common reasons murmurs of primary pulmonary regurgitation? A. Idiopathic dilatation of the pulmonary artery. (Some reports suggest that approximately one third of patients with idiopathic pulmonary artery dilation have pulmonary regurgitation.) b. Surgery pulmonary stenosis. After pulmonary commissurotomy, pulmonary regurgitation of varying degrees always occurs.
Notes:
A. In patients with tetralogy of Fallot and pulmonary regurgitation, the pulmonary valve is almost always absent, and the obstruction of the latter is caused by a narrowed valve ring.
b. Sometimes observed with an atrial septal defect, pulmonary regurgitation may actually be one of the manifestations caused by combined idiopathic dilatation of the pulmonary artery. In one case series, a small number of patients with an uncomplicated atrial septal defect had an early diastolic murmur recorded externally at the base of the heart and on intracardiac phonocardiography exclusively in the right ventricular outflow tract. In another study, in 40% of patients over 20 years of age with an uncomplicated atrial septal defect, a mid-frequency diastolic murmur with an intensity of grade 2 out of 6 was heard, aggravated by inspiration, loudest in the second intercostal space to the left of the sternum and conducted to the right edge of the lower part of the sternum.
V. It has been established that a diastolic murmur that begins simultaneously with the pulmonary component of the second sound near the left edge of the lower part of the sternum in some patients with an atrial septal defect and normal pulmonary artery pressure sometimes represents a diastolic component of a continuous murmur arising at the defect and caused by a combination of high pressure in the left atrium due to mitral regurgitation with small or medium-sized atrial septal defect.
d. Stenosis and/or regurgitation of one or more valves may be caused by long-term use of ergot alkaloids for migraine. In this case, the valve leaflets thicken and tighten, but do not calcify.
2. What are the differences between a primary pulmonary regurgitation murmur and a Graham Still murmur in terms of shape, duration, and frequency? A. With high pulmonary artery pressure, the shape, duration and frequency of the pulmonary regurgitation murmur are the same as with aortic regurgitation. With normal pulmonary artery pressure, there is sometimes a slight delay between the pulmonary component of the second sound and the appearance of any murmur. However, if the noise begins simultaneously with the pulmonary component of the second tone, then such noise is most often short and rough due to the predominance of mid- and low-frequency sound vibrations in its composition.
b. If pulmonary regurgitation is insignificant, then the noise in its characteristics may occupy an intermediate position between the Graham Still noise and the noise of primary pulmonary regurgitation. That is, it may start earlier, last longer, and be of higher frequency than the murmur of more severe primary pulmonary regurgitation.
V. In one study, intracardiac phonocardiography demonstrated that there was no pause between the pulmonary component of the second sound and the appearance of the murmur. At the same time, according to another similar study, the murmur of pulmonary regurgitation occurs with a significant delay.
d. Immediately after the regurgitant pulmonary valve closes, right ventricular pressure drops rapidly, the pressure gradient between the pulmonary artery and right ventricle increases, and the volume of the murmur increases (rising phase). This happens until the right ventricular pressure reaches its minimum. After this, the gradient across the pulmonary valve decreases rapidly and the murmur becomes less loud (waning phase). Thus, the murmur of pulmonary regurgitation with normal pulmonary artery pressure is a short, increasing mid-frequency murmur, because in this case the pressure gradient is not as great as with the high-frequency murmurs of pulmonary hypertension that occur against the background of pulmonary hypertension (Fig. 14).
Rice. 14. This murmur of primary pulmonary regurgitation recorded in a boy adolescence, occurred in early diastole and included many mid- and low-frequency sound vibrations. It did not intensify with inspiration in the second intercostal space to the left of the sternum, because in this area between the stethoscope and the heart there was too much pneumatized lung tissue. The murmur was less loud near the left lower sternal border, although at this location it should have become louder during inspiration 3. Why is the murmur of primary pulmonary regurgitation short? Diastolic pressure in the pulmonary artery falls quickly because its decrease begins with normal values(which corresponds to an incisura on the pulmonary sphygmogram), and the diastolic outflow of blood occurs in two directions. As a result, the pressure in the pulmonary artery and right ventricle quickly becomes equal.
Note:
It has been established that pulmonary regurgitation is caused to a greater extent by deformation rather than dilatation of the annulus fibrosus of the pulmonary valve.
PERICARDIAL FRICTION NOISE Pericarditis 1. What mechanism causes the occurrence of pericardial friction noise? It is generally believed that friction sounds are caused by two hard layers of the pericardium (visceral and parietal) rubbing against each other. If in pathological process The surrounding pleura is also involved, then the cause of the noise may be the friction of the pleura with outer surface pericardium. The murmur that occurs in such cases is a pleuropericardial friction murmur.
Large medical dictionary
Graham Still noise
(Graham Steell, 1851-1942, English doctor; synonym: Graham Still murmur nrk, Still murmur) - diastolic murmur heard in the area of the projection of the pulmonary valve with its relative insufficiency, caused by significant pulmonary hypertension and dilatation of the pulmonary trunk with pronounced narrowing left atrioventricular orifice.
- - the rate of DIFFUSION of a gas is inversely proportional to the square root of its density...
Scientific and technical encyclopedic Dictionary
- - see Graham Still...
Large medical dictionary
- - see Little-Lassuer syndrome...
Large medical dictionary
- - a method for diagnosing helminthiases, which consists in identifying helminth eggs by microscopy of a cellulose tape previously applied to the perianal area of the patient...
Large medical dictionary
- - method for determining the activity of granulocyte peroxidase in blood and bone marrow, based on the oxidation of benzidine by granulocytes in the presence of hydrogen peroxide with the formation of brown granules in them...
Large medical dictionary
- - form rheumatoid arthritis in children, manifested by Still's triad...
Large medical dictionary
- - limited pulsation of the anterior wall chest outside the cardiac impulse zone; sign adjacent to chest wall aortic tumors or aneurysms...
Large medical dictionary
- - combination of magnification lymph nodes, splenomegaly and swelling of symmetrically located joints; observed in Still's disease...
Large medical dictionary
- - see Graham...
Large medical dictionary
- - see Still's disease...
Large medical dictionary
- - see Graham Still...
Large medical dictionary
- - see Graham Still...
Large medical dictionary
"Graham Still's Noise" in books
When Grace met David... and Graham... and Robert...
From the book What Would Grace Do? Secrets of a stylish life from the Princess of Monaco by Gina McKinnonWhen Grace met David... and Graham... and Robert... Although most of Grace's friends were women, she also enjoyed many years of friendships with the most different men, including actor David Niven. The question is whether he and Niven were “just
Editor of Graham's Magazine. 1841–1842
From the author's bookEditor of Graham's Magazine. 1841–1842 In November 1840, the sale of Burton's "gentleman's magazine" was completed, and George Rex Graham (1813–1894) became the new owner of the publication. Despite the fact that he was only twenty-seven years old, he was an energetic, tenacious,
APPENDIX III FRANK GRAHAM'S THEORY OF UNEVEN DEVELOPMENT
From the book How Rich Countries Became Rich [and Why Poor Countries Stay Poor] by Reinert Eric S.APPENDIX III FRANK GRAHAM'S THEORY OF UNEVEN DEVELOPMENT Increasing and diminishing returns in international trade (example in numbers) STAGE 1. WORLD INCOME AND ITS DISTRIBUTION BEFORE TRADE World production: 1600 units. wheat + 1400 units. hours. In wheat: 3200 units. Country income
Two winters in Graham Land
From the book 500 Great Journeys author Nizovsky Andrey YurievichTwo winters on Graham Land From a young age, Australian John Rymill prepared to become a polar explorer. He did difficult things mountain climbing in the Swiss and French Alps, studied flying skills with pilots of the British aircraft corporation De
Concrete landscape of the era. James Graham Ballard's 70th birthday
From the book Did Sholom Aleichem Love Science Fiction? (collection) author Gopman Vladimir LvovichConcrete landscape of the era. For James Graham Ballard's 70th birthday on November 20, 2030. From a special correspondent for the Book Review in Liverpool. Today at the University of Liverpool ended Scientific Conference"Sixth Ballard Readings", organized by
GRAHAM'S HISTORY
From the book Why men lie and women cry by Piz AlanGRAHAM'S STORY Graham thought retirement on the coast would be one long vacation. He will spend his last days in idyllic grace - he will sunbathe, swim, go to restaurants, get up late and constantly relax. And the first few months went just like that.
1. Does the pulmonary artery pressure have to be very high for a pulmonary regurgitation murmur to occur?
Typically, pulmonary pressure is very high (ie, close to systemic arterial pressure). Pulmonary regurgitation murmurs rarely occur when pulmonary artery pressures are below 80 mmHg. Art., except in cases where the pulmonary trunk is significantly dilated.
Notes:
A. A Graham Still murmur is a murmur of pulmonary regurgitation that occurs in the setting of pulmonary hypertension, regardless of whether the pulmonary hypertension is primary or secondary.
b. The murmur of pulmonary regurgitation due to a ventricular septal defect can occur even with normal pulmonary vascular resistance if the pulmonary artery pressure exceeds 80 mmHg. Art.
2. How does a Graham Still murmur differ from an aortic regurgitation murmur?
These noises may not be different. In other words, both noises are predominantly high-frequency, can vary in intensity from 1 to 6 degrees, at first be increasing and decreasing and - if the intensity is low - become louder as you exhale. At the same time, if the volume of Graham Still's noise is high, it usually intensifies during inspiration (Fig. 13).
Rice. 13. Phonocardiograms of a patient with persistent ductus arteriosus, in whom the pulmonary artery pressure was 145 mm Hg, are presented. Art., and aortic pressure was approximately the same. A loud diastolic murmur (Graham Still's murmur) recorded on phonocardiograms increased significantly during inspiration. The quiet Graham Still noise may not increase during inspiration. HF - high frequencies, MF - mid frequencies
Notes:
A. If the volume of the Graham Still murmur is insignificant, then during inspiration it may decrease even more, despite the increase in blood flow in the pulmonary artery. The fact is that the quiet noise of pulmonary regurgitation is usually best heard in the second intercostal space to the left of the sternum, and the increase in the distance between the stethoscope and the heart that occurs during inspiration in this area is most pronounced. In addition, in severe pulmonary hypertension, inspiratory blood flow to the lungs may not increase if there is concomitant tricuspid regurgitation.
b. Isometric hand clenching and squatting will selectively increase the volume of the aortic regurgitation murmur.
3. How does the Valsalva maneuver help distinguish the murmur of pulmonary regurgitation from the murmur of aortic regurgitation?
Immediately after cessation of straining, the volume of the pulmonary regurgitation noise becomes the same as before the Valsalva maneuver. The initial loudness of the murmur of aortic regurgitation is restored only after four or five cardiac cycles.
Notes:
A. In patients with pulmonary artery dilatation, an early diastolic decaying grinding sound may be heard in the absence of aortic or pulmonary regurgitation. This creaking sound is of extracardiac origin and may be caused by adhesions between the pulmonary artery and surrounding lung tissue.
Heart murmurs are peculiar sounds that usually occur when pathological conditions, but sometimes healthy people.
Unlike heart sounds, which are regular, rapidly decaying sound vibrations perceived as a short sound, heart murmurs are irregular sound vibrations that do not decay for a long time and are perceived as a long sound.
Classification of heart murmurs
Intracardiac and extracardiac murmurs are distinguished according to the place of origin.
Intracardiac murmurs occur when conditions are created for their appearance inside the heart itself:
defects in the valvular apparatus of the heart, leading to narrowing of the openings between the cavities of the heart or to narrowing of the pathways for the outflow of blood from the ventricles of the heart into the great vessels;
defects in the valvular apparatus of the heart, leading to regurgitation of blood flow from great vessels into the ventricles of the heart or from the ventricles of the heart into the atria;
acquired lesions of large vessels - aortic atherosclerosis, syphilitic mesaortitis, aortic aneurysm;
congenital defects in the structure of the heart that disrupt intracardiac hemodynamics - ventricular septal defect (Tolochinov-Roger disease), stenosis of the left atrioventricular orifice and patent oval window (atrial septal defect) - Lutembashe disease;
congenital defects of large great vessels, aorta and pulmonary artery: patent ductus arteriosus, or open ductus arteriosus; isolated
with pulmonary artery stenosis (valvular stenosis; subvalvular - infundibular stenosis - narrowing of the pulmonary artery trunk);
isolated stenosis of the aortic mouth (valvular, subvalvular - infundibular stenosis and supravalvular - rarely); Coarctation of the aorta is a congenital narrowing in a limited area, located slightly distal to the origin of the left subclavian artery from the aorta;
congenital combined defects in the structure of the heart and large vessels, for example triad, tetralogy or pentade of Fallot (narrowing of the outflow tract from the right ventricle, defect of the interventricular
daughter septum, change in the position of the initial part of the aorta with its origin above the defect in the septum, hypertrophy of the right ventricle);
damage to the heart muscle (myocarditis, myocardial infarction, cardiosclerosis, dilated cardiomyopathy), leading to a decrease in its tone. In this case, noise is caused by
2 mechanisms: 1) weakening of the papillary muscles that hold the valve leaflets; 2) expansion of the heart chambers (myogenic dilatation), as a result of which the opening between the cavities of the heart widens and the leaflets of unchanged valves are not able to close it;
violation of the rheological properties of blood - a decrease in its viscosity during anemia, when the speed of blood flow increases and turbulence appears as blood passes through the holes
hearts;
an increase in the speed of blood passing through the heart in certain pathological conditions (thyrotoxicosis, infectious diseases, cardiopsychoneurosis).
Extracardiac murmurs: 1) pericardial friction murmur; 2) pleuropericardial murmur; 3) cardiopulmonary murmur. These noises will be discussed in more detail below.
Based on the reason for their occurrence, they distinguish between: a) organic and b) inorganic, or functional, or innocent noises.
Organic murmurs are formed due to the presence in the heart of organic defects of acquired or congenital origin.
To date, it has been proven that both valve insufficiency and stenosis of the orifices are caused by the development of sclerotic changes. Their causes may be rheumatism,
atherosclerosis, infective endocarditis, syphilis, systemic lupus erythematosus.
Functional intracardiac murmurs are caused by a weakening of the tone of the heart muscle, a violation of the rheological properties of the blood, and an acceleration of blood flow. Thus, these murmurs reflect quite serious changes in the heart muscle or in the nature of blood flow and can only rarely occur in healthy people (see below for more details).
In addition, murmurs are divided depending on the phases of cardiac activity: systolic - occurs in systole, determined between the 1st and 2nd sounds; diastolic - occurs in
diastole, determined between the II and I sounds; systole-diastolic - occupies the periods of both systole and diastole.
An example of a systolic-diastolic murmur is the murmur of a patent ductus arteriosus. In this case, the systolic component of the noise is always longer and louder than the diastolic one; the noise has a peculiar timbre - “machine” noise.
Variants of systolic murmur
Pansystolic murmur - occupies the entire systole and merges with the sounds.
Early systolic murmur.
Median systolic murmur, or mesosystolic.
Late systolic murmur.
Holosystolic murmur - occupies the entire systole, but does not merge with the 1st and 2nd sounds.
Functional murmurs, unlike organic ones, are never pansystolic, but occupy only part of the systole.
Variants of diastolic murmur
Protodiastolic. Occurs at the beginning of diastole immediately after the second sound. Associated with insufficiency of the aortic valves and pulmonary valves, since protodiastole occurs
their closure.
Mesodiastolic. Occurs in mid-diastole with pronounced insufficiency of the mitral or tricuspid valves (functional Coombs murmur).
Presystolic. Occurs at the end of diastole before the first sound, more often with mitral stenosis.
Pandiastolic - occupies the entire diastole.
The systolic murmur coincides in time with the apical impulse and the pulse in the carotid artery, and the diastolic murmur coincides with the long pause of the heart preceding the first sound.
Mechanisms of noise generation
There are 7 options for the occurrence of noise.
1. Narrowing of the vessel in a limited area. Fluid turbulence occurs and noise is generated (narrowing of the atrioventricular orifices, aortic orifices, pulmonary artery, coarctation
aorta, etc.). However, with a sharp narrowing of the lumen, the noise is not heard, an example of which is “aphonic” mitral stenosis.
2. Dilation of the vessel in a limited area. Vortex movements of the blood are formed (aneurysm of the aorta and other large vessels).
3. Fluid flow in the opposite direction - regurgitation, reflux (insufficiency of the mitral, tricuspid and semilunar valves of the aorta and pulmonary artery).
4. Model of communicating vessels (patent ducts, arteriovenous aneurysms, etc.).
The remaining 3 mechanisms are associated with functional noise; their occurrence is due to:
5. Decreased myocardial tone.
6. Reduced blood viscosity.
7. Increasing the speed of blood flow.
Taking into account these mechanisms, murmurs in organic heart defects are divided into the following:
1. Return noise (regurgitation) - with valve insufficiency (mitral, aortic, tricuspid, pulmonary).
2. Ejection sounds - with stenosis of the orifices and orifices (left and right atrioventricular orifices and the orifices of the aorta and pulmonary artery).
3. Filling noises - with stenosis of the left and/or right atrioventricular orifices at the time of filling of the ventricles at the beginning of diastole due to acceleration of blood flow from the atria
due to the high pressure gradient.
The characteristics of intracardiac heart murmurs should be reflected by the following data:
a) in what phase of cardiac activity does the murmur occur,
b) the place of his best listening,
c) noise transmission area,
d) noise intensity,
e) duration of noise,
e) timbre of noise,
g) changes in noise intensity,
h) the presence or absence of chest wall tremors accompanying the noise.
NOISE PHASE
Systolic murmur is most often recorded in the following pathologies.
Acquired heart defects:
1. Stenosis of the aortic mouth.
2. Mitral valve insufficiency.
3. Tricuspid valve insufficiency.
Congenital heart defects:
1. Narrowing of the mouth of the pulmonary artery.
2. Ventricular septal defect (VSD).
3. Atrial septal defect (ASD).
4. Coarctation of the aorta and other rare pathologies.
Aortic pathologies:
1. Atherosclerosis of the ascending aorta.
2. Aortic aneurysm.
3. Syphilitic mesaortitis.
Diastolic murmur is recorded with the following acquired heart defects.
1. Narrowing of the mitral orifice.
2. Narrowing of the right atrioventricular opening.
3. Insufficiency aortic valve.
4. Pulmonary valve insufficiency. Most often, relative pulmonary valve insufficiency occurs due to post- and precapillary pulmonary hypertension.
Murmurs at the apex of the heart (at the 1st point) are most often associated with damage to the mitral valve or stenosis of the left atrioventricular orifice.
1. Systolic murmur - with insufficiency or prolapse of the mitral valve.
2. Diastolic murmur - with stenosis of the left atrioventricular orifice.
3. Systolic and diastolic murmurs - with complex (combined) mitral disease. The predominance of any noise may indirectly indicate the predominance of a particular defect.
Noises at the 2nd point (on the right at the sternum in the I intercostal space).
1. Systolic - for stenosis of the aortic mouth, atherosclerosis, aortic aneurysm, syphilitic mesaortitis.
2. Diastolic - with aortic valve insufficiency, but the murmur with this defect is better heard at the 5th point.
3. Combination of systolic and diastolic - for complex (combined) aortic disease.
Noises at the 3rd point (on the left at the sternum in the 2nd intercostal space).
1. Systolic murmur - when the mouth of the pulmonary artery is narrowed.
2. Diastolic (Graham-Still murmur) - with relative insufficiency of the pulmonary valves.
3. Systole-diastolic - when the arterial (botallian) duct is not closed.
Noises at the 4th point (on the lower third of the sternum at the base of the xiphoid process) - damage to the tricuspid valve.
1. Systolic - with tricuspid valve insufficiency.
2. Diastolic - with narrowing of the right atrioventricular opening. However, this noise is best detected in the third intercostal space at the right edge of the sternum.
Murmurs at the 5th point (at the left edge of the sternum in the third intercostal space) are characteristic of damage to the aortic valves.
Functional noise
These noises are caused by 3 groups of reasons: 1) damage to the heart muscle with expansion of the cavities of the heart, a decrease in the tone of the papillary muscles and expansion of the fibrous rings between the cavities
hearts; 2) acceleration of blood flow; 3) decreased blood viscosity.
Characteristics of functional noise:
in the vast majority of cases they are systolic;
the timbre is soft, blowing;
fickle;
are localized and are not carried out beyond the zone of occurrence;
are not accompanied by chest trembling.
Functional noises associated with accelerated blood flow occur during febrile conditions, vegetative-vascular dystonia, thyrotoxicosis, tachycardia of other etiologies.
Functional noises associated with a decrease in blood viscosity are observed in anemia and are called hydremic functional noises.
The following functional murmurs are distinguished, caused by the expansion of the cavities of the heart (myogenic functional murmurs).
1. Systolic murmur at the apex (1st point) with relative mitral valve insufficiency (with stenosis of the aortic mouth, aortic valve insufficiency, myocarditis, infarction
myocardium, arterial hypertension and etc.).
2. Systolic murmur on the lower third of the sternum at the base of the xiphoid process (4th point), associated with relative insufficiency of the tricuspid valve (myogenic
dilatation of the right ventricle with myocarditis, dilated cardiomyopathy, postcapillary and/or precapillary pulmonary hypertension, mitral stenosis, chronic pulmonary
heart, etc.).
3. Protodiastolic Graham-Still murmur in the left 2nd intercostal space (3rd point) with mitral stenosis due to the development of relative pulmonary valve insufficiency
due to high pulmonary hypertension.
4. Presystolic Flint murmur at the 1st point with aortic valve insufficiency. The origin of the murmur is associated with functional mitral stenosis, which occurs due to the fact that the jet of blood from the aorta during regurgitation lifts the mitral valve leaflet towards the flow of blood from the atrium.
Extracardiac murmurs
1. Pericardial friction noise.
2. Pleuropericardial murmur.
3. Cardiopulmonary murmur (“systolic breathing” Po-
tena).
4276 0
All functional noises are conventionally divided into three groups:
Dynamic, which occur with a significant increase in the speed of blood flow through the normal openings of valves or great vessels (for example, dynamic noises during thyrotoxicosis, febrile conditions);
Anemic, associated with a decrease in blood viscosity and some acceleration of blood flow in patients with anemia of various origins;
Noises of relative valve insufficiency or relative narrowing of valve openings.
Often dynamic and anemic noises are combined with the concept of “innocent noises”, since they occur in the absence of any organic diseases hearts.
Functional murmurs of relative valve insufficiency or relative stenosis of the valve openings in most cases are caused by expansion of the fibrous ring of the AV valves with pronounced dilatation of the ventricles, dysfunction of the valve apparatus (chordae and papillary muscles), hemodynamic displacement of the valve leaflets, dilatation of the aorta or pulmonary artery (for example, functional Graham-Still diastolic murmur).
- Expansion of the fibrous ring of the AV valves with severe dilatation of the ventricles leads to incomplete closure of anatomically unchanged AV valve leaflets and the development of relative insufficiency of these valves with turbulent blood flow from the ventricles to the atria. The characteristics of the noise of relative insufficiency of the mitral and tricuspid valves in these cases are similar to those with corresponding organic defects (see above).
- Relative mitral valve insufficiency can develop with LV dilatation in patients with hypertension, aortic heart disease, mainly in the stage of decompensation (the so-called “mitralization” of aortic disease), in patients with congestive heart failure of any origin. Relative tricuspid valve insufficiency, caused by pancreatic dilatation, often develops in late stages mitral stenosis and decompensated cor pulmonale. The functional murmur of regurgitation is detected in patients with dysfunction of the valve apparatus (chordae and papillary muscles), for example, with infarction of the papillary muscle, congenital elongation or acquired rupture of one of the chordae of the AV valves. In these cases, prolapse (protrusion, sagging) of one of the leaflets into the atrium cavity develops during ventricular systole. This leads to incomplete closure of the leaflets and the development of relative insufficiency of the AV valve. In this case, a short systolic murmur (usually meso- or late systolic) is heard, usually with the first sound preserved.
- Graham-Still noise - functional diastolic murmur of relative pulmonary valve insufficiency, which occurs with a prolonged increase in pressure in the pulmonary artery (for example, in patients with mitral stenosis, primary pulmonary hypertension, pulmonary heart). In the second intercostal space to the left of the sternum and along the left edge of the sternum, a quiet, decreasing diastolic murmur is heard, starting immediately with the second sound.
- Flint noise - presystolic murmur of relative (functional) stenosis of the left AV orifice, which sometimes occurs in patients with organic insufficiency of the aortic valve due to elevation of the mitral valve leaflet by a strong stream of blood flowing from the aorta to the LV during diastole. This leads to obstruction of blood flow from the LA to the LV during active atrial systole. At the same time, at the apex of the heart, in addition to the wired organic diastolic murmur of aortic insufficiency, presystolic amplification of the murmur, the functional Flint murmur, is also heard.
- Coombs noise - functional mesodiastolic murmur caused by relative stenosis of the left AV orifice, which occurs in patients with severe organic mitral valve insufficiency under conditions of significant dilatation of the LV and LA and the absence of expansion of the fibrous annulus of the valve. Under these conditions, the heart (LV and LA) resembles in shape hourglass with a relatively narrow “bridge” in the area of the left AV foramen. At the moment of LA emptying in the rapid filling phase, this hole is on a short time becomes relatively narrow for the increased blood volume, and relative stenosis of the left AV orifice occurs with turbulent blood flow from the left atrium. At the apex of the heart, in addition to organic systolic murmur mitral insufficiency, you can listen to a short and quiet mesodiastolic murmur caused by functional mitral stenosis, as well as functional murmurs with abnormally located chords (trabeculae) of the LV, the tension of which leads to the appearance of systolic murmur.
A.V. Strutynsky
Complaints, anamnesis, physical examination
