orifice because systolic tension of the myocardium grows slowly when the blood flow from the left ventricle is obstructed and it is overfilled with blood; the amplitude of the sound vibrations decreases. In diffuse affections of the myocardium (due to dystrophy, cardiosclerosis or myocarditis), the first heart sound only may be diminished because its muscular component also diminishes in these cases.
The first sound increases at the heart apex if the left ventricle is not adequately filled with blood during diastole. The first sound often becomes louder in stenosis of the left atrioventricular orifice, when less than normal amount of blood is discharged from atrium to the ventricle during diastole. The muscle of the left ventricle is therefore less distended by the blood by the start of systole; it is more relaxed and therefore contracts more rapidly and energetically to intensify the first sound. The first sound increases in stenosed right atrioventricular orifice at the base of the xiphoid process. This sound is also intensified during extrasystole (premature contraction of the heart) due to inadequate diastolic filling of the ventricles.
The variation of the first sound at the heart base is not important because this sound is transmitted here from its best auscultative area, i.e. from the cardiac apex area.
The second heart sound is heard over the base. In normal cases the intensity of this sound over the aorta is the same as over the pulmonary trunk. Although the blood pressure in the aorta is higher and the cusps of its valve are closed with a greater force than those of the pulmonary valve, the sound produced by the closing aortic valve is perceived by the examiner as being of the same intensity as the sound of the pulmonary valve, because of the deeper location of the aortic valve.
The second sound over the aorta is diminished in aortic valve affections because either the cusps of the valve are destroyed or their vibrating power decreases due to developing cicatrices. Moreover, the thrust of the blood discharged at early diastole from the aorta to the cusps of the aortic valve is weaker than in normal persons because part of the blood is regurgitated to the ventricle through an incompletely closed aortic orifice. The second sound can be inaudible over the aorta if the aortic valve is much destroyed. The second sound diminishes over the aorta in cases of marked hypotension; the second sound diminishes over the pulmonary trunk in cases of aortic valve incompetence (in very rare cases) and in decreased pressure in the lesser circulation.
The second sound may increase (accent) either over the aorta or over the pulmonary trunk. If the sound is more intense over the aorta, it is said to be accentuated over the aorta, and if it is stronger over the pulmonary trunk, accentuation of the second sound over pulmonary artery is meant.
The aortic second sound is accentuated when the blood pressure in aorta increases (in essential hypertension, during heavy exercise, in psychic
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excitation), because during early diastole, the aortic valve cusps are closed with a greater force due to increased blood pressure in the aorta. The tone of the second heart sound over the aorta often varies. For example, in patients with sclerotic aortic valve, the second sound over the aorta acquires a metallic character which, however, can be heard in normal arterial pressure as well.
The accentuated second sound over the pulmonary artery occurs when pressure in the lesser circulation is elevated or when the vessels of the lesser circulation are overfilled with blood (e.g. in mitral heart diseases), deranged circulation in the lungs and stenosed pulmonary artery (in lung emphysema or pneumosclerosis).
Reduplication of the heart sounds may be revealed by auscultation. Two short sounds which quickly follow one another are heard instead of one. Reduplication of the sounds occurs in asynchronous work of the left and right chambers of the heart. Asynchronous closure of the atrioventricular valves splits the first sound while asynchronous closure of the semilunar valves causes reduplication of the second heart sound. If the two short sounds follow one another at a short interval, they are not perceived as two separate sounds, the sound is said to be split. Both physiological and pathological splitting of the heart sounds is possible. Physiological reduplication or splitting of the first sound is due to asynchronous closure of the atrioventricular valves, e.g. during very deep expiration, when the blood is ejected into the left atrium with a greater force to prevent the closure of the mitral valves; the valvular component of the left ventricle is therefore split and is perceived as a separate sound.
Pathological reduplication of the first sound can occur in impaired intraventricular conduction (through the His bundle) as a result of delayed systole of one of the ventricles.
The second sound is reduplicated more frequently than the first heart sound. Reduplication occurs due to asynchronous closure of the valve of the aorta and pulmonary trunk because of the different length of contractions of the left and the right ventricles. The length of the ventricular systole depends on the volume of the ejected blood and the pressure in that vessel (aorta or the pulmonary artery) into which the blood is expelled. When the amount of blood in the left ventricle decreases and the pressure in the aorta is low, systole of the left ventricle ends sooner and the aortic valve cusps will close earlier than the cusps of the valve of the pulmonary trunk. The second heart sound can therefore be duplicated in cases with diminished or increased filling of one of the ventricles or when pressure in the aorta or the pulmonary artery changes. Physiological reduplication of the second sound is mostly connected with various respiratory phases: the filling of the right and left ventricles differs during inspiration and expiration and the length of their systole changes accordingly, as well as the time of closure of the valve of the
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aorta and pulmonary trunk. The amount of blood flowing to the left ventricle decreases during inspiration because part of blood is retained in the distended vessels of the lungs. The left-ventricular systolic blood volume decreases during inspiration, its systole ends earlier, and the aortic valve therefore closes earlier as well. At the same time, the stroke volume of the right ventricle increases, its systole prolongs, the pulmonary valve closure is delayed and the second sound is thus doubled.
Pathological reduplication of the second sound can be due to delayed closure of the aortic valve in persons suffering from essential hypertension, or if the closure of the pulmonary valve is delayed at increased pressure in the lesser circulation (e.g. in mitral stenosis or emphysema of the lungs), delayed contraction of one of the ventricles in patients with bundle-branch block.
True reduplication of the heart sounds should be differentiated from apparent doubling which is connected with the appearance of adventitious sounds. The mitral valve opening sound is an example. This sound is heard at the heart apex of patients with mitral stenosis. The sound is heard 0.07-0.13 s following the second sound, during diastole. In normal conditions, the cusps of the atrioventricular valves open noiselessly; they are freely forced back by the blood flow ejected from the atria to the ventricles. In mitral stenosis, the cusps of the sclerosed valve adhere to each other by their edges and cannot freely move to the walls of the ventricle. Therefore, blood thrusts against the valve as it passes from the atrium to generate sound vibrations that are responsible for the appearance of adventitious sounds.
The mitral valve opening sound follows soon after the second heart sound to give it the character of reduplication. This sound is best heard at the heart apex rather than at the heart base; it is characterized by stability and is combined with other auscultative signs of mitral stenosis. The mitral valve opening sound is heard together with a loud (snapping) first sound characteristic of mitral stenosis, and the second sound, to form a specific triple rhythm - “rhythm of quail”.
An extrapericardial sound can occur in pericardial adhesion. It originates during diastole, 0.08-0.14s after the second sound, and is generated by the vibrating pericardium during the rapid dilatation of the ventricles at the beginning of diastole. The extra sound in adhesions in the pericardium can also arise during systole, between the first and the second heart sounds. This short and loud sound is also known as the systolic click.
Changes in heart sounds in heart diseases can be due to intensified physiological third or fourth sound. In normal subjects these sounds are better revealed in graphic recording (phonocardiography). But if the ventricular myocardium is much weakened, these sounds can be revealed by auscultation. Intensification of one of these sounds gives a three-sound rhythm, known as the gallop rhythm (because it resembles the galloping of a
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horse). The sounds of the gallop rhythm are usually soft and low, always attended by a thrust, for which reason they are best heard on direct auscultation; the gallop rhythm can also be heard in auscultation with a phonendoscope, but the patient should lie on the left side after a mild exercise. Protodiastolic (at the beginning of diastole), mesodiastolic (in the middle of diastole), and presystolic (at the end of diastole) gallop rhythms are distinguished by the time of appearance of the extra sound in diastole. Gallop rhythm is also classified as ventricular or atrial, according to its origin.
Protodiastolic gallop rhythm arises in considerably diminished tone of the ventricular myocardium. The ventricles distend quickly during their filling with blood at the beginning of diastole and the vibrations thus generated are audible as an extra sound. The sound appears 0.12 - 0.2 s after the second heart sound and is an increased physiological third sound.
Presystolic gallop rhythm arises in intensification of the physiological fourth sound, which is due to the diminished tone of the ventricular myocardium and a stronger atrial contraction. Intensified contraction of the overfilled atrium increases blood ejection into the ventricle, while a diminished tone of the ventricular myocardium causes quicker distention of its walls. The presystolic gallop rhythm is better detected in delayed atrioventricular conduction, when atrial systole is separated from the ventricular systole by a longer than normal period.
Both the third and the fourth heart sounds can intensify significantly in grave myocardial affection, but in tachycardia they sum up to give a mesodiastolic or summation gallop rhythm. Gallop rhythm is an important sign of myocardial weakness, and it has a great diagnostic and prognostic value. It develops in severe heart affections in patients with myocardial infarction, essential hypertension, myocarditis, chronic nephritis, decompensated heart diseases.
A. pronounced acceleration of the cardiac rhythm makes the diastolic pause shorter so that it becomes almost as short as the systolic one. If the heart sounds heard at the cardiac apex are similar in intensity, a peculiar auscultative picture resembles the tic-tac or fetal rhythm, known also as embryocardial or pendulum rhythm. It occurs in severe cardiac failure, attacks of paroxysmal tachycardia, high fever, etc.
Auscultation of heart: cardiac murmurs
Cardiac murmurs
Physical and hemodynamic bases of originating of cardiac murmurs
In addition to the normal heart sounds, abnormal sounds known as murmurs may be heard. Cardiac murmurs may be both endoand exocardiac.
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Endocardiac murmurs occur most frequently. These may occur in anatomical changes of the structure of the heart (organic murmurs) or in dysfunction of the intact valves (functional murmurs). Functional murmurs may be heard with increased rate of blood flow or decreased blood viscosity. The mechanism of endocardiac murmurs can be easier understood if one remembers the laws of physics concerning the flow of liquids in tubes. If a tube has a point where its otherwise even lumen is narrowed, the passing liquid produces noise. This noise is associated with turbulent flow of liquid above the narrowed portion of the tube, which causes vibration of the tube. The intensity of noise depends on two factors, viz., the liquid velocity and the extent of narrowing. The higher the velocity of the liquid, the more intense is the noise; when the liquid velocity decreases, the noise lessens or disappears. As to the extent of tube narrowing, its influence on noise intensity is directly proportional only within a certain range. If the lumen is narrowed to a very high degree, noise may weaken or even disappear. Liquid is also set in vortex movement when it passes a narrow portion of the tube and enters its wider part again. The same reasons account for the murmurs that arise in the heart. If the passage is narrowed or on the contrary widened, blood is set in turbulent flow which generates murmurs. If the vascular lumen remains unchanged, murmurs may be produced by the changes in the blood flow rate, as is the case with thyrotoxicosis, fever, or nervous excitation. Decreased blood viscosity (e.g. in anemia) increases the flow rate of blood and can also be the cause of murmurs. The most frequent cause of endocardiac murmur is various heart defects.
According to the time of appearance, murmurs are classified as systolic and diastolic (Table 6). Systolic murmur occurs in cases when, during systole, blood moves from one chamber of the heart to another or from the heart to the main vessels and meets an obstacle. Systolic murmur is heard in the stenotic orifice of the aorta or the pulmonary trunk because blood ejected from the ventricles meets a narrowed vessel (ejection murmur). Systolic murmur is also heard in cases with mitral and tricuspid incompetence (regurgitation murmur). Generation of systolic murmur is explained by regurgitation of blood which is not completely expelled into the aorta and pulmonary trunk during the ventricular systole, but is partly returned to the atrium through an incompletely closed mitral or tricuspid orifice. Since this partly closed orifice is actually a narrow slit, murmur is generated as blood passes through it.
Diastolic murmur occurs if blood meets a narrowed passage during diastole (ejection murmur). This murmur is heard in a stenosed left or right atrioventricular orifice, since blood meets a narrow passage in its flow from the atria into the ventricles. Diastolic murmur also occurs in aortic or pulmonary valve incompetence. Murmur is generated when blood flows back from the vessels into the ventricles through a slit formed by incomplete
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