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 in-traventricular 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
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
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, decompen-sated 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.