U healthy person Under resting conditions, the normal heart rate is 60-90 beats per minute. A heart rate greater than 90 is called tachycardia, less than 60 - bradycardia.

The cardiac cycle consists of three phases: atrial systole, ventricular systole and a general pause (simultaneous atrial and ventricular diastole). Atrial systole is weaker and shorter than ventricular systole and lasts 0.1-0.15 s. Ventricular systole is more powerful and prolonged, equal to 0.3 s. Atrial diastole takes 0.7-0.75 s, ventricular diastole - 0.5-0.55 s. The total cardiac pause lasts 0.4 s. During this period the heart rests. All cardiac cycle lasts 0.8-0.85 s. It is estimated that the ventricles work approximately 8 hours a day (I.M. Sechenov). When the heart rate increases, for example, during muscular work, the cardiac cycle shortens due to a reduction in rest, i.e. general pause. The duration of systole of the atria and ventricles remains almost unchanged. Therefore, if at a heart rate of 70 per minute the total pause is 0.4 s, then when the rhythm frequency doubles, i.e. 140 beats per minute, the total pause of the heart will be correspondingly half as much, i.e. 0.2 s. Conversely, at a heart rate of 35 per minute, the total pause will be twice as long, i.e. 0.8 s.

During a general pause, the muscles of the atria and ventricles relax, the leaflet valves are open, and the semilunar valves are closed. The pressure in the chambers of the heart drops to 0 (zero), resulting in blood from the vena cava and pulmonary veins, where the pressure is 7 mm Hg. Art., flows into the atria and ventricles by gravity, freely (i.e. passively), filling approximately 70% of their volume. Atrial systole, during which the pressure in them increases by 5-8 mm Hg. Art., causes about 30% more blood to be pumped into the ventricles. Thus, the value of the pumping function of the atrial myocardium is relatively small. The atria mainly play the role of a reservoir for inflowing blood, easily changing its capacity due to the small thickness of the walls. The volume of this reservoir can be further increased due to additional containers - atrial appendages, which resemble pouches and can, when expanded, accommodate significant volumes of blood.

Immediately after the end of atrial systole, ventricular systole begins, which consists of two phases: the tension phase (0.05 s) and the blood expulsion phase (0.25 s). The tension phase, including periods of asynchronous and isometric contraction, occurs with the leaflet and semilunar valves closed. At this time, the heart muscle tenses around the incompressible - blood. The length of the myocardial muscle fibers does not change, but as their tension increases, the pressure in the ventricles increases. At the moment when the blood pressure in the ventricles exceeds the pressure in the arteries, the semilunar valves open and blood is ejected from the ventricles into the aorta and pulmonary trunk. The second phase of ventricular systole begins - the phase of blood expulsion, including periods of fast and slow expulsion. Systolic pressure in the left ventricle reaches 120 mmHg. Art., in the right - 25-30 mm Hg. Art. A major role in the expulsion of blood from the ventricles belongs to the atrioventricular septum, which during ventricular systole moves forward to the apex of the heart, and during diastole - back to the base of the heart. This displacement of the atrioventricular septum is called the effect of displacement of the atrioventricular septum (the heart works with its own septum).

After the ejection phase, ventricular diastole begins, and the pressure in them decreases. At the moment when the pressure in the aorta and pulmonary trunk becomes higher than in the ventricles, the semilunar valves slam shut. At this time, the atrioventricular valves open under pressure from the blood accumulated in the atria. A period of general pause begins - a phase of rest and filling of the heart with blood. Then the cycle of cardiac activity is repeated.

12. External manifestations of heart activity and indicators of cardiac activity

TO external manifestations cardiac activities include: apical impulse, heart sounds and electrical phenomena in the heart. Indicators of cardiac activity are systolic and cardiac output.

The apex beat is caused by the fact that the heart turns from left to right during ventricular systole and changes its shape: from ellipsoidal it becomes round. The apex of the heart rises and presses on the chest in the area of ​​the fifth intercostal space on the left. This pressure can be seen, especially in thin people, or palpated with the palm(s) of the hand.

Heart sounds are sound phenomena that occur in the beating heart. They can be heard by placing your ear or stethoscope to your chest. There are two heart sounds: the first sound, or systolic, and the second sound, or diastolic. The first tone is lower, dull and long, the second tone is short and higher. In the origin of the first tone, mainly the atrioventricular valves take part (oscillations of the valves when the valves close). In addition, the myocardium of the contracting ventricles and vibrations of the stretching tendon threads (chords) take part in the origin of the first tone. The semilunar valves of the aorta and pulmonary trunk take the main part in the occurrence of the second tone at the moment of their closure (slamming).

Using the phonocardiography (PCG) method, two more tones were detected: III and IV, which are not audible, but can be recorded in the form of curves. The third tone is caused by vibrations of the walls of the heart due to the rapid flow of blood into the ventricles at the beginning of diastole. It is weaker than tones I and II. IV tone is caused by vibrations of the walls of the heart caused by contraction of the atria and the pumping of blood into the ventricles.

At rest, with each systole, the ventricles of the heart emit 70-80 ml into the aorta and pulmonary trunk, i.e. about half of the blood they contain. This is the systolic, or stroke, volume of the heart. The blood remaining in the ventricles is called reserve volume. There is still a residual volume of blood that is not ejected even with the strongest heart contraction. At 70-75 contractions per minute, the ventricles emit 5-6 liters of blood, respectively. This is the minute volume of the heart. So, for example, if the systolic volume is 80 ml of blood, and the heart contracts 70 times per minute, then the minute volume will be.

Cardiac cycle- this is the systole and diastole of the heart, periodically repeating in a strict sequence, i.e. a period of time involving one contraction and one relaxation of the atria and ventricles.

In the cyclical functioning of the heart, two phases are distinguished: systole (contraction) and diastole (relaxation). During systole, the cavities of the heart are emptied of blood, and during diastole they are filled. The period that includes one systole and one diastole of the atria and ventricles and the following general pause is called cardiac cycle.

Atrial systole in animals lasts 0.1-0.16 s, and ventricular systole lasts 0.5-0.56 s. The total pause of the heart (simultaneous diastole of the atria and ventricles) lasts 0.4 s. During this period the heart rests. The entire cardiac cycle lasts for 0.8-0.86 s.

The work of the atria is less complex than the work of the ventricles. Atrial systole ensures the flow of blood into the ventricles and lasts 0.1 s. Then the atria enter the diastole phase, which lasts for 0.7 s. During diastole, the atria fill with blood.

The duration of the various phases of the cardiac cycle depends on the heart rate. With more frequent heart contractions, the duration of each phase, especially diastole, decreases.

Phases of the cardiac cycle

Under cardiac cycle understand the period covering one contraction - systole and one relaxation - diastole atria and ventricles - general pause. The total duration of the cardiac cycle at a heart rate of 75 beats/min is 0.8 s.

Heart contraction begins with atrial systole, lasting 0.1 s. The pressure in the atria rises to 5-8 mm Hg. Art. Atrial systole is replaced by ventricular systole lasting 0.33 s. Ventricular systole is divided into several periods and phases (Fig. 1).

Rice. 1. Phases of the cardiac cycle

Voltage period lasts 0.08 s and consists of two phases:

• phase of asynchronous contraction of the ventricular myocardium - lasts 0.05 s. During this phase, the excitation process and the subsequent contraction process spread throughout the ventricular myocardium. The pressure in the ventricles is still close to zero. By the end of the phase, the contraction covers all myocardial fibers, and the pressure in the ventricles begins to increase rapidly.
• isometric contraction phase (0.03 s) - begins with the slamming of the atrioventricular valves. In this case, I, or systolic, heart sound occurs. The displacement of the valves and blood towards the atria causes an increase in pressure in the atria. The pressure in the ventricles increases quickly: up to 70-80 mm Hg. Art. in the left and up to 15-20 mm Hg. Art. in the right.

The leaflet and semilunar valves are still closed, the volume of blood in the ventricles remains constant. Due to the fact that the fluid is practically incompressible, the length of the myocardial fibers does not change, only their tension increases. Blood pressure in the ventricles increases rapidly. The left ventricle quickly acquires a round shape and hits the inner surface with force chest wall. In the fifth intercostal space, 1 cm to the left of the midclavicular line, the apical impulse is detected at this moment.

Towards the end of the period of tension, the rapidly increasing pressure in the left and right ventricles becomes higher than the pressure in the aorta and pulmonary artery. Blood from the ventricles rushes into these vessels.

Exile period blood from the ventricles lasts 0.25 s and consists of a fast phase (0.12 s) and a slow ejection phase (0.13 s). At the same time, the pressure in the ventricles increases: in the left one up to 120-130 mm Hg. Art., and in the right up to 25 mm Hg. Art. At the end of the slow ejection phase, the ventricular myocardium begins to relax and diastole begins (0.47 s). The pressure in the ventricles drops, blood from the aorta and pulmonary artery rushes back into the ventricular cavities and “slams” the semilunar valves, and a second, or diastolic, heart sound occurs.

The time from the beginning of ventricular relaxation to the “slamming” of the semilunar valves is called protodiastolic period(0.04 s). After the semilunar valves close, the pressure in the ventricles drops. The leaflet valves are still closed at this time, the volume of blood remaining in the ventricles, and therefore the length of the myocardial fibers, does not change, which is why this period is called the period isometric relaxation(0.08 s). Towards the end, the pressure in the ventricles becomes lower than in the atria, the atrioventricular valves open and blood from the atria enters the ventricles. Begins period of filling the ventricles with blood, which lasts 0.25 s and is divided into phases of fast (0.08 s) and slow (0.17 s) filling.

Vibration of the walls of the ventricles due to the rapid flow of blood to them causes the appearance of the third heart sound. Towards the end of the slow filling phase, atrial systole occurs. The atria pump additional blood into the ventricles ( presystolic period, equal to 0.1 s), after which a new cycle of ventricular activity begins.

Vibration of the walls of the heart, caused by contraction of the atria and additional flow of blood into the ventricles, leads to the appearance of the IV heart sound.

During normal listening of the heart, loud I and II tones are clearly audible, and quiet III and IV tones are detected only with graphical recording of heart sounds.

In humans, the number of heartbeats per minute can fluctuate significantly and depends on various external influences. When performing physical work or sports activity, the heart can contract up to 200 times per minute. In this case, the duration of one cardiac cycle will be 0.3 s. An increase in the number of heartbeats is called tachycardia, at the same time, the cardiac cycle decreases. During sleep, the number of heart contractions decreases to 60-40 beats per minute. In this case, the duration of one cycle is 1.5 s. A decrease in the number of heartbeats is called bradycardia, while the cardiac cycle increases.

Structure of the cardiac cycle

Cardiac cycles follow at a frequency set by the pacemaker. The duration of a single cardiac cycle depends on the frequency of heart contractions and, for example, at a frequency of 75 beats/min it is 0.8 s. The general structure of the cardiac cycle can be represented in the form of a diagram (Fig. 2).

As can be seen from Fig. 1, with a cardiac cycle duration of 0.8 s (beat frequency 75 beats/min), the atria are in a systole state of 0.1 s and in a diastole state of 0.7 s.

Systole- phase of the cardiac cycle, including contraction of the myocardium and expulsion of blood from the heart into the vascular system.

Diastole- phase of the cardiac cycle, including relaxation of the myocardium and filling of the cavities of the heart with blood.

Rice. 2. Scheme of the general structure of the cardiac cycle. Dark squares show the systole of the atria and ventricles, light squares show their diastole.

The ventricles are in systole for about 0.3 s and in diastole for about 0.5 s. At the same time, the atria and ventricles are in diastole for about 0.4 s (total diastole of the heart). Ventricular systole and diastole are divided into periods and phases of the cardiac cycle (Table 1).

Table 1. Periods and phases of the cardiac cycle

Asynchronous contraction phase - the initial stage of systole, during which a wave of excitation spreads across the ventricular myocardium, but there is no simultaneous contraction of cardiomyocytes and the pressure in the ventricles is from 6-8 to 9-10 mm Hg. Art.

Isometric contraction phase - the stage of systole, during which the atrioventricular valves close and the pressure in the ventricles quickly increases to 10-15 mmHg. Art. in the right and up to 70-80 mm Hg. Art. in the left.

Rapid expulsion phase - the stage of systole, during which there is an increase in pressure in the ventricles to a maximum value of 20-25 mm Hg. Art. in the right and 120-130 mm Hg. Art. in the left and blood (about 70% of systolic output) enters the vascular system.

Slow expulsion phase- the stage of systole, in which blood (the remaining 30% of systolic output) continues to flow into the vascular system at a slower rate. The pressure gradually decreases in the left ventricle from 120-130 to 80-90 mmHg. Art., in the right - from 20-25 to 15-20 mm Hg. Art.

Protodiastolic period- the transition period from systole to diastole, during which the ventricles begin to relax. The pressure decreases in the left ventricle to 60-70 mm Hg. Art., in temperament - up to 5-10 mm Hg. Art. Due to greater pressure in the aorta and pulmonary artery, the semilunar valves close.

Isometric relaxation period - stage of diastole, during which the ventricular cavities are isolated by closed atrioventricular and semilunar valves, they relax isometrically, the pressure approaches 0 mmHg. Art.

Rapid filling phase - the stage of diastole, during which the atrioventricular valves open and blood rushes into the ventricles at high speed.

Slow filling phase - the stage of diastole, during which blood slowly flows through the vena cava into the atria and through the open atrioventricular valves into the ventricles. At the end of this phase, the ventricles are 75% filled with blood.

Presystolic period - the stage of diastole coinciding with atrial systole.

Atrial systole - contraction of the atrial muscles, in which the pressure in the right atrium rises to 3-8 mm Hg. Art., in the left - up to 8-15 mm Hg. Art. and each ventricle receives about 25% of the diastolic blood volume (15-20 ml).

Table 2. Characteristics of the phases of the cardiac cycle

Contraction of the myocardium of the atria and ventricles begins following their excitation, and since the pacemaker is located in the right atrium, its action potential initially spreads to the myocardium of the right and then the left atrium. Consequently, the myocardium of the right atrium responds with excitation and contraction somewhat earlier than the myocardium of the left atrium. IN normal conditions The cardiac cycle begins with atrial systole, which lasts 0.1 s. The non-simultaneous coverage of the myocardial excitation of the right and left atria is reflected by the formation of the P wave on the ECG (Fig. 3).

Even before atrial systole, the AV valves are open and the cavities of the atria and ventricles are already largely filled with blood. Stretch Rate the thin walls of the atrial myocardium with blood is important for irritation of mechanoreceptors and the production of atrial natriuretic peptide.

Rice. 3. Changes in heart performance indicators in different periods and phases of the cardiac cycle

During atrial systole, pressure in the left atrium can reach 10-12 mm Hg. Art., and in the right - up to 4-8 mm Hg. Art., the atria additionally fill the ventricles with a volume of blood that at rest is about 5-15% of the volume located in the ventricles by this time. The volume of blood entering the ventricles during atrial systole can increase during physical activity and amount to 25-40%. The volume of additional filling can increase to 40% or more in people over 50 years of age.

The flow of blood under pressure from the atria promotes stretching of the ventricular myocardium and creates conditions for their more efficient subsequent contraction. Therefore, the atria play the role of a kind of amplifier of the contractile capabilities of the ventricles. With this atrial function (for example, with atrial fibrillation) the efficiency of the ventricles decreases, a decrease in their functional reserves develops, and the transition to insufficiency of myocardial contractile function accelerates.

At the moment of atrial systole, an a-wave is recorded on the venous pulse curve; in some people, when recording a phonocardiogram, a 4th heart sound may be recorded.

The volume of blood located after atrial systole in the ventricular cavity (at the end of their diastole) is called end-diastolic. It consists of the volume of blood remaining in the ventricle after the previous systole ( end-systolic volume), the volume of blood that filled the cavity of the ventricle during its diastole before atrial systole, and the additional volume of blood that entered the ventricle during atrial systole. The amount of end-diastolic blood volume depends on the size of the heart, the volume of blood flowing from the veins and a number of other factors. In a healthy young man at rest, it can be about 130-150 ml (depending on age, gender and body weight, it can range from 90 to 150 ml). This volume of blood slightly increases the pressure in the ventricular cavity, which during atrial systole becomes equal to the pressure in them and can fluctuate in the left ventricle within 10-12 mm Hg. Art., and in the right - 4-8 mm Hg. Art.

For a period of time 0.12-0.2 s, corresponding to the interval PQ on the ECG, the action potential from the SA node spreads to the apical region of the ventricles, in the myocardium of which the excitation process begins, quickly spreading in the directions from the apex to the base of the heart and from the endocardial surface to the epicardial. Following the excitation, myocardial contraction or ventricular systole begins, the duration of which also depends on the heart rate. Under resting conditions it is about 0.3 s. Ventricular systole consists of periods voltage(0.08 s) and exile(0.25 s) blood.

Systole and diastole of both ventricles occur almost simultaneously, but occur under different hemodynamic conditions. A further, more detailed description of the events occurring during systole will be considered using the example of the left ventricle. For comparison, some data for the right ventricle are provided.

The period of ventricular tension is divided into phases asynchronous(0.05 s) and isometric(0.03 s) contractions. The short-term phase of asynchronous contraction at the beginning of ventricular myocardial systole is a consequence of the non-simultaneous coverage of excitation and contraction various departments myocardium. Excitation (corresponds to the wave Q on the ECG) and myocardial contraction occurs initially in the area of ​​the papillary muscles, the apical part of the interventricular septum and the apex of the ventricles and spreads to the remaining myocardium in about 0.03 s. This coincides with registration on ECG wave Q and the ascending part of the tooth R to its top (see Fig. 3).

The apex of the heart contracts before its base, so the apical part of the ventricles is pulled towards the base and pushes the blood in the same direction. At this time, areas of the ventricular myocardium that are not affected by excitation can stretch slightly, so the volume of the heart practically does not change, the blood pressure in the ventricles does not yet change significantly and remains lower than the blood pressure in large vessels above the tricuspid valves. Blood pressure in the aorta and others arterial vessels continues to fall, approaching the value of the minimum, diastolic, pressure. However, the tricuspid vascular valves remain closed.

At this time, the atria relax and the blood pressure in them decreases: for the left atrium, on average, from 10 mm Hg. Art. (presystolic) up to 4 mm Hg. Art. By the end of the phase of asynchronous contraction of the left ventricle, the blood pressure in it rises to 9-10 mm Hg. Art. Blood, under pressure from the contracting apical part of the myocardium, picks up the leaflets of the AV valves, they close, taking a position close to horizontal. In this position, the valves are held by tendon threads of the papillary muscles. The shortening of the size of the heart from its apex to the base, which, due to the unchanged size of the tendon filaments, could lead to eversion of the valve leaflets into the atria, is compensated by contraction of the papillary muscles of the heart.

At the moment of closure of the atrioventricular valves, the 1st systolic sound heart, the asynchronous phase ends and the isometric contraction phase begins, which is also called the isovolumetric (isovolumic) contraction phase. The duration of this phase is about 0.03 s, its implementation coincides with the time interval in which the descending part of the wave is recorded R and the beginning of the tooth S on the ECG (see Fig. 3).

From the moment the AV valves close, under normal conditions the cavity of both ventricles becomes sealed. Blood, like any other fluid, is incompressible, so contraction of myocardial fibers occurs at their constant length or in an isometric mode. The volume of the ventricular cavities remains constant and myocardial contraction occurs in an isovolumic mode. The increase in tension and force of myocardial contraction under such conditions is converted into rapidly increasing blood pressure in the cavities of the ventricles. Under the influence of blood pressure on the area of ​​the AV septum, a short-term shift occurs towards the atria, is transmitted to the inflowing venous blood and is reflected by the appearance of a c-wave on the venous pulse curve. Within a short period of time - about 0.04 s, the blood pressure in the cavity of the left ventricle reaches a value comparable to its value at this moment in the aorta, which decreased to a minimum level - 70-80 mm Hg. Art. Blood pressure in the right ventricle reaches 15-20 mm Hg. Art.

The excess of blood pressure in the left ventricle over the diastolic blood pressure in the aorta is accompanied by the opening aortic valves and the replacement of the period of myocardial tension by the period of blood expulsion. The reason for the opening of semilunar valves of blood vessels is the blood pressure gradient and the pocket-like feature of their structure. The valve leaflets are pressed against the walls of the vessels by the flow of blood expelled into them by the ventricles.

Exile period blood lasts about 0.25 s and is divided into phases quick expulsion(0.12 s) and slow exile blood (0.13 s). During this period, the AV valves remain closed, the semilunar valves remain open. The rapid expulsion of blood at the beginning of the period is due to a number of reasons. About 0.1 s has passed since the onset of cardiomyocyte excitation and the action potential is in the plateau phase. Calcium continues to flow into the cell through open slow calcium channels. Thus, the tension of the myocardial fibers, which was already high at the beginning of expulsion, continues to increase. The myocardium continues to compress the decreasing blood volume with greater force, which is accompanied by a further increase in its pressure in the ventricular cavity. The blood pressure gradient between the ventricular cavity and the aorta increases and blood begins to be expelled into the aorta at high speed. During the rapid ejection phase, more than half of the stroke volume of blood expelled from the ventricle during the entire ejection period (about 70 ml) is ejected into the aorta. By the end of the phase of rapid expulsion of blood, the pressure in the left ventricle and aorta reaches its maximum - about 120 mm Hg. Art. in young people at rest, and in the pulmonary trunk and right ventricle - about 30 mm Hg. Art. This pressure is called systolic. The phase of rapid expulsion of blood occurs during the period of time when the end of the wave is recorded on the ECG S and isoelectric part of the interval ST before the beginning of the tooth T(see Fig. 3).

Under the condition of rapid expulsion of even 50% of the stroke volume, the rate of blood flow into the aorta per a short time will be about 300 ml/s (35 ml/0.12 s). Average speed of blood outflow from the arterial part vascular system is about 90 ml/s (70 ml/0.8 s). Thus, more than 35 ml of blood enters the aorta in 0.12 s, and during the same time about 11 ml of blood flows out of it into the arteries. Obviously, in order to accommodate for a short time a larger volume of inflowing blood compared to outflow, it is necessary to increase the capacity of the vessels receiving this “excess” volume of blood. Part of the kinetic energy of the contracting myocardium will be spent not only on the expulsion of blood, but also on stretching the elastic fibers of the wall of the aorta and large arteries to increase their capacity.

At the beginning of the phase of rapid expulsion of blood, stretching of the vessel walls is relatively easy, but as more blood is expelled and the vessels are stretched more and more, the resistance to stretching increases. The stretching limit of the elastic fibers is exhausted and the hard collagen fibers of the vessel walls begin to undergo stretching. The flow of blood is prevented by resistance peripheral vessels and the blood itself. The myocardium needs to spend a large amount of energy to overcome these resistances. Potential energy accumulated during the isometric tension phase muscle tissue and the elastic structures of the myocardium itself are exhausted and the force of its contraction decreases.

The rate of blood expulsion begins to decrease and the rapid expulsion phase is replaced by the slow blood expulsion phase, which is also called phase of reduced expulsion. Its duration is about 0.13 s. The rate of decrease in ventricular volume decreases. At the beginning of this phase, blood pressure in the ventricle and aorta decreases at almost the same rate. By this time, the slow calcium channels close, and the plateau phase of the action potential ends. Calcium entry into cardiomyocytes decreases and the myocyte membrane enters phase 3—terminal repolarization. Systole, the period of blood expulsion, ends and ventricular diastole begins (corresponding in time to phase 4 of the action potential). The implementation of reduced expulsion occurs during the period of time when a wave is recorded on the ECG T, and the end of systole and the beginning of diastole occur at the end of the tooth T.

During the systole of the ventricles of the heart, more than half of the end-diastolic volume of blood (about 70 ml) is expelled from them. This volume is called stroke volume of blood. Stroke blood volume can increase with increasing myocardial contractility and, conversely, decrease with insufficient contractility (see below for indicators of the pumping function of the heart and myocardial contractility).

The blood pressure in the ventricles at the beginning of diastole becomes lower than the blood pressure in the arterial vessels leaving the heart. The blood in these vessels experiences the forces of stretched elastic fibers of the vessel walls. The lumen of the vessels is restored and a certain amount of blood is displaced from them. Part of the blood flows to the periphery. The other part of the blood is displaced in the direction of the ventricles of the heart, and during its reverse movement fills the pockets of the tricuspid vascular valves, the edges of which are closed and held in this state by the resulting difference in blood pressure.

The time interval (about 0.04 s) from the beginning of diastole to the closure of the vascular valves is called protodiastolic interval. At the end of this interval, the 2nd diastolic beat of the heart is recorded and audible. When recording an ECG and a phonocardiogram simultaneously, the onset of the 2nd sound is recorded at the end of the T wave on the ECG.

Diastole of the ventricular myocardium (about 0.47 s) is also divided into periods of relaxation and filling, which, in turn, are divided into phases. From the moment the semilunar vascular valves close, the ventricular cavities become 0.08 closed, since the AV valves still remain closed at this time. Relaxation of the myocardium, caused mainly by the properties of the elastic structures of its intra- and extracellular matrix, is carried out under isometric conditions. In the cavities of the ventricles of the heart, less than 50% of the end-diastolic volume of blood remains after systole. The volume of the ventricular cavities does not change during this time, the blood pressure in the ventricles begins to decrease rapidly and tends to 0 mmHg. Art. Let us remember that by this time blood continued to return to the atria for about 0.3 s and the pressure in the atria gradually increased. At the moment when the blood pressure in the atria exceeds the pressure in the ventricles, the AV valves open, the phase of isometric relaxation ends and the period of filling the ventricles with blood begins.

The filling period lasts about 0.25 s and is divided into fast and slow filling phases. Immediately after the opening of the AV valves, blood quickly flows along a pressure gradient from the atria into the ventricular cavity. This is facilitated by a certain suction effect of the relaxing ventricles, associated with their straightening under the action of elastic forces that arise during compression of the myocardium and its connective tissue framework. At the beginning of the rapid filling phase, sound vibrations in the form of the 3rd diastolic heart sound can be recorded on the phonocardiogram, which are caused by the opening of the AV valves and the rapid passage of blood into the ventricles.

As the ventricles fill, the difference in blood pressure between the atria and ventricles decreases, and after about 0.08 s, the rapid filling phase is replaced by a slow filling phase of the ventricles with blood, which lasts about 0.17 s. The filling of the ventricles with blood in this phase is carried out mainly due to the preservation in the blood moving through the vessels of the residual kinetic energy imparted to it by the previous contraction of the heart.

0.1 s before the end of the phase of slow filling of the ventricles with blood, the cardiac cycle ends, and new potential action in the pacemaker, the next atrial systole occurs and the ventricles are filled with end-diastolic volumes of blood. This period of time of 0.1 s, which completes the cardiac cycle, is sometimes also called period additional filling ventricles during atrial systole.

An integral indicator characterizing mechanical is the volume of blood pumped by the heart per minute, or minute blood volume (MBV):

IOC = heart rate. UO,

where heart rate is the heart rate per minute; SV - stroke volume of the heart. Normally, at rest, the IOC for a young man is about 5 liters. Regulation of the IOC is carried out by various mechanisms through changes in heart rate and (or) stroke volume.

The influence on heart rate can be exerted through changes in the properties of cardiac pacemaker cells. The influence on stroke volume is achieved through the effect on the contractility of myocardial cardiomyocytes and the synchronization of its contraction.

breathing - respiratory arrhythmia. At the end of exhalation, the heart rate decreases, while inhaling it increases.

In pathology, rapid and asynchronous contractions of the fibers of the atria or ventricles are sometimes observed; contractions up to 400 per minute are called myocardial flutter, up to 600 per minute - flicker (fibrillation).

Electrocardiography allows you to analyze the nature of heart rhythm disturbances, the localization of the source of excitation (in the atria, AV node, ventricles), the degree and localization of disturbances in the conduction of excitation in the heart (blockade). ECG is used to diagnose ischemia, infarction, and dystrophic changes in the myocardium.

Vectorcardiography

This is a method of recording changes in tension and direction of vector movement electric field, which occurs when the myocardium is excited. A cathode ray tube is used, onto the plates of which (horizontal and vertical) 2 ECG leads are simultaneously supplied. In this way, the resulting voltage of the heart biocurrents from two ECG leads. On the screen of the vectorcardioscope, VCH is observed in the form of 3 closed loops P, QRS, T.

TOPIC 7 CARDIAC CYCLE. PHASE ANALYSIS OF SYSTOLE

VENTRICULAR AND VENTRICULAR DIASTOLS. REGULATION OF HEART ACTIVITY

Lecture outline

1. Periods and phases of the cardiac cycle.

2. Mechanical and acoustic manifestations of cardiac activity. Tones of hearts.

3. Systolic and minute blood volumes.

4. Nervous-reflex And humoral regulation hearts.

Conclusion.

1. Periods and phases of the cardiac cycle

Systole and diastole are coordinated and constitute the cardiac cycle. Each cardiac cycle consists of atrial systole, ventricular systole and a general pause. At a heart rate of 75 beats/min, the cardiac cycle lasts 0.8 s: the atria contract for 0.1 s, the ventricles contract for 0.3 s, and the total pause lasts 0.4 s. Atrial diastole lasts 0.7 s, ventricular diastole - 0.5 s. The atria act as a reservoir in which blood collects while the ventricles contract and eject blood into the great vessels.

The cycle of ventricular contraction consists of several periods and phases that make up the structure of systole and diastole. As criteria for dividing the cardiac cycle, changes in pressure in the atria, ventricles and great vessels are taken, compared with the recording of heart biocurrents - ECG, as well as the moments of opening and closing of the heart valves.

Ventricular systole divided into 2 periods: tension and exile.

Voltage period lasts 0.08 s and consists of two phases with different characteristics:

- phases of asynchronous contraction (0.05 s);

- phases of isometric contraction(0.03–0.05s).

Asynchronous contraction phase- the initial part of systole, during

which results in sequential coverage of the ventricular myocardium by the contractile process. The beginning of this phase coincides with the beginning of depolarization of the fibers of the ventricular muscles (Q wave on the ECG). The end of this phase coincides with the beginning sharp increase intraventricular pressure. During the phase of asynchronous contraction, intraventricular pressure either does not increase or increases little.

Isometric contraction phase - part of ventricular systole,

occurring when the heart valves are closed. During this phase, the pressure in the cavities of the ventricles rises to the level of pressure in the aorta (or pulmonary artery), i.e., until the semilunar valves open. The beginning of this phase coincides with the beginning of a sharp increase in pressure in the ventricle, and the end coincides with the beginning of an increase in pressure in the aorta and pulmonary artery.

The ejection period (0.25 s) extends to the second major part of ventricular systole. It lasts from the moment the semilunar valves open

And until the end of systole and is divided into:

- phase of rapid expulsion of blood (0.12 s);

- phase of slow blood expulsion (0.13 s).

When analyzing the cardiac cycle, general and mechanical systole are distinguished. General systole is that part of the cycle during which the contractile process occurs in the myocardium. It includes periods of tension and exile. Mechanical systole includes only the isometric contraction phase and the expulsion period, that is, it represents that part of the cycle during which the pressure in the ventricles increases and is maintained above the pressure in the great vessels.

Ventricular diastole is divided into following periods and phases.

Protodiastolic period (0.04 s) - time from the beginning to relax-

ventricles until the semilunar valves close.

Isometric relaxation period (0.08 s) - period of relaxation

heart failure with all valves closed. After the semilunar valves close, the pressure in the ventricles drops. The leaflet valves are still closed, the volume of remaining blood and the length of myocardial fibers do not change. By the end of the period, the pressure in the ventricles becomes lower than in

the atria, the leaflet valves open, blood enters the ventricles. The next period is coming.

The period of filling the ventricles with blood (0.25 s) includes:

- rapid filling phase (0.08 s);

- slow filling phase (0.17 s).

Then comes the presystolic period (0.1 s) - The atria pump additional blood into the ventricles. After which a new cycle of ventricular activity begins.

2. Mechanical and sound manifestations cardiac activity. Heart sounds

Apex impulse. As the pressure in the ventricles increases, the left ventricle becomes rounded and hits the inner surface chest. At this moment, in the 5th intercostal space, 1 cm to the left of the midclavicular line, the apical (cardiac) impulse is detected.

Heart sounds are sound phenomena accompanying cardiac activity. They are listened to by the ear using a stethophonendoscope and recorded by devices - phonocardiographs. There are several heart sounds. The first heart sound appears at the beginning of ventricular systole (therefore called systolic). Its occurrence is based on vibrations of the atrioventricular valve leaflets, their tendon threads, and vibrations of the ventricular muscle. The second sound (diastolic) occurs as a result of the slamming of the semilunar valves.

The third and fourth sounds are not heard by the ear. They can only be determined by a phonocardiogram. The third sound is formed by vibrations of the walls of the ventricles during rapid filling of them with blood, the fourth sound is formed by additional filling of the ventricles during atrial systole.

Heart sounds and the rhythm of their occurrence are used in clinical medicine to assess cardiac activity.

3. Systolic and minute blood volumes

JR is the amount of blood that each ventricle ejects into main vessel for one systole. At rest it is from 1/3 to half total number of blood contained in this chamber of the heart at the end of diastole. CO2 in a state of physiological rest in a horizontal position of a person is often 75–100 ml (at a heart rate of 70–75 beats/min). When moving from a horizontal to a vertical position, the CVR decreases by 30–40%, as blood is deposited in the vessels of the lower half of the body. During physical work, the CO increases due to the reserve volume of emission.

IOC is the volume of blood that the left or right ventricle of the heart ejects in 1 minute. IOC in a state of physiological (physical and mental) rest and horizontal position of the body fluctuates pre-

business 4.5–6 l/min. During a passive transition from horizontal position in the vertical IOC decreases by 15–20%. To level out the influence of individual anthropometric differences on the value of the IOC, the latter is expressed in SI form. SI is the IOC value divided by the body surface area in m2. SI ranges from 3–3.5 l/min/m2.

4. Neuro-reflex and humoral regulation of the heart

The mechanisms regulating the activity of the heart are divided into intracardiac and extracardiac. Intracardiac include intracellular, intercellular and intracardiac nervous mechanisms carried out by the cardiac metasympathetic nervous system. Intracellular, in turn, are divided into heterometric and homeometric. Extracardiac include nervous ones, carried out by the sympathetic and parasympathetic nervous system, and humoral regulatory mechanisms. Regulatory influences can be:

1. Chronotropic - affecting heart rate.

2. Inotropic - on the strength of contractions.

3. Batmotropic - on myocardial excitability.

4. Dromotropic - on conductivity (the speed of excitation propagation throughout the myocardium).

Myogenic (hemodynamic) autoregulation is carried out by one of two mechanisms:

Heterometric regulation

Studied by Starling. Starling's law states that the more the ventricles are filled (stretched) with blood during diastole, the stronger their contraction during the next systole, i.e., other things being equal, the force of contraction of myocardial fibers is a function of their end-diastolic length. It follows from the law that an increase in the filling of the heart with blood, caused either by an increase in venous inflow or a decrease in the release of blood into the arteries, leads to an increase in the stretching of the ventricles and an increase in their contractions. Thus, the reaction caused by the stretching of the heart leads to the elimination of this stretching. The “law of the heart” is based on the molecular relationship “sarcomere length - force”. With a diastolic pressure of 10–15 mm Hg. Art. the length of the sarcomere is 2.1 μm, at which the ratio between actin and myosin filaments is optimal, leading to maximum interaction between them during contraction and maximum contractile force.

Homeometric regulation of cardiac activity

The mechanism of increased heart contractions, not caused by changes in the diastolic length of muscle fibers, is called homeometric self-regulation. These include enhancing heart contraction:

1) under the influence of an increase in aortic pressure (Anrep effect - Russian physiologist, employee of I.P. Pavlov, who worked during an internship in Starling’s laboratory);

2) with an increase in heart rate (the Bowditch effect or “ladder”). This phenomenon can be reproduced both on an isolated strip and on hearts as a whole. Serial irritation of the heart with stimuli of the same strength leads to a gradual increase in the amplitude of contractions. These phenomena are calledcontraction potentiation and are associated with changes in the intervals between contractions and are therefore referred to as chronoinotropic dependence or “interval-force”). It is based on the accumulation of calcium ions in myocardiocytes.

Mechanism of long-term adaptation of the heart based on enhancing protein synthesis and increasing the numberfunctional-structuralelements that provide increased cardiac output.

Intercellular and intraorgan mechanisms of intracardial regulation

Intercellular regulation is associated with the presence between muscle cells myocardium intercalary disc nexuses providing transport nutrients and metabolites, connection of myofibrils, transfer of excitation from cell to cell. Intercellular regulation also includes the interaction of cardiomyocytes with connective tissue cells that make up the stroma of the heart muscle, which perform a trophic function in relation to myocardiocytes.

Nervous-reflex regulation covers all 4 types of influences on the heart: chrono-, ino-, batmo- and dromotropic. It is carried out in the form of extero- and interoreceptive reflexes that arise in the reflexogenic zones of the body. The heart acts as an effector organ in these reflexes.

Preganglionic fibers vagus nerve are axons nerve cells, located in the medulla oblongata, mainly in its parvocellular part - in the mutual nucleus, the nucleus of the solitary tract and the dorsal motor nucleus. Efferent vagal neurons in the medulla oblongata have mono- and polysynaptic connections with afferent fibers of the aortic and sinus nerves, with the nuclei of the hypothalamus, cerebral cortex and spinal cord.

Extracardiac nerve plexuses (superficial and deep) are formed mainly due to branches cervical spine border trunk and branches extending from the cervical and thoracic parts of the vagus nerve. The right vagus innervates mainly the sinoatrial node, the left one innervates the muscle fibers of the atria and the upper parts of the atrioventricular conduction system, a small number of fibers also reach the muscles of the ventricles.

Preganglionic sympathetic fibers are axons of neurons located in the lateral horns of the 5 upper thoracic segments of the spinal cord and end in the lower cervical and upper thoracic (stellate) sympathetic ganglia. Sympathetic fibers pass through various parts of the epicardium and innervate all parts of the heart; several sympathetic axons pass along one muscle fiber. The atria contain more adrenergic fibers than the ventricles.

In humans, ventricular activity is controlled primarily by sympathetic nerves. The atria and sinoatrial node are under constant antagonistic influence from the vagus and sympathetic nerves. Turning off parasympathetic influences in a dog increases the heart rate from 100 to 150 beats/min, and when sympathetic activity is suppressed, the frequency drops to 60 beats/min. At rest, the tone of the vagus nerves prevails over the tone of the sympathetic nerves.

Most of the afferent fibers of the heart come as part of the vagus and sympathetic nerves. There are 2 types of mechanoreceptors in the atria: B-receptors (response to passive stretch) and A-receptors (response to active tension).

The vagus, along with the negative chronotropic effect, also has a negative foreign-, as well as batmo- and dromotropic effect on the heart, i.e. irritation of the vagus reduces the strength of heart contractions, inhibits the automatism of the sinoatrial node, the excitability and conductivity of the atrioventricular node. The vagus does not affect conduction in the His bundle and Purkinje fibers. Due to the suppression of the automaticity of the sinoatrial node and the conduction block in the atrioventricular node, irritation causes complete cardiac arrest. The mediator of the vagus nerve in its influence on the heart is the ACh mediator. The main consequence of the interaction of acetylcholine with the m-cholinergic receptor is an increase in membrane permeability for potassium ions. As a result, irritation of the vagus leads to hyperpolarization of the membrane of pacemaker cells. A certain role is also played by a decrease in the entry into the cell of calcium ions necessary for the development of contraction, since the flow of calcium is hampered by accelerated repolarization due to increased potassium permeability. In addition, ACH reduces the production of cAMP in the heart, which stimulates heart contractions.

With prolonged irritation of the vagus, the phenomenon of the heart escaping from its influence develops: despite the ongoing irritation of the vagus, heart contractions resume, but their rhythm remains slow. False escape develops due to the occurrence of automatic activity of the His bundle and Purkinje fibers. True escape is the result, according to some, of a decrease in the number of impulses entering the vagus. According to other scientists, it is more likely that escape develops due to a compensatory increase in sympathetic nervous influences on the heart.

Stimulation of the sympathetic nerves of the heart leads to increased heart contractions, increased heart rate (positive ino- and chronotropic effects), stimulation of metabolism in the heart muscle (trophic effect). Sympathetic nerves also have a positive batmo- and dromotropic effect on the heart. The mediator of the sympathetic nerves in the heart of warm-blooded animals is NA. In addition, AN, a sympathomimetic formed in the adrenal medulla and adsorbed by the heart from the blood, acts in the myocardium. Catecholamines interact withbeta-adrenergic receptormembranes of the myocardial cell, representing adenylate cyclase. In the cells of working muscles, interaction withbeta-adrenergic receptorsNA and AN increase permeability to calcium ions, resulting in increased contractile force. Apparently the inotropic effect of catecholamines is carried out in the same way as the chronotropic one - through the activation of adenylate cyclase and cAMP, which activates protein kinase, which is integral part myofibril troponin.

Tone of the centrifugal nerves of the heart has a central origin

denition. Vagal neurons in the nuclei medulla oblongata are in constant excitement. These neurons constitute the cardiac inhibitory center. In the medulla oblongata, next to this center, there are structures, the excitation of which is transmitted to the sympathetic neurons of the spinal cord, stimulating the activity of the heart. These structures constitute the cardiac accelerator center of the medulla oblongata.

Intracardiac level of regulation is autonomous, although it is also included in the complex hierarchy of the central nervous regulation. It is carried out by the MNS, the neurons of which are located in the intramural ganglia of the heart. The MNS has a full set of functional elements necessary for independent reflex activity: sensory cells, integrating interneuron apparatus, motor neurons. Axons sensory neurons pass as part of the vagus and sympathetic nerves, so sensitive impulses from the heart can reach the higher parts nervous system. Preganglionic fibers of the vagus nerve and cardiac sympathetic branches terminate on the intercalary and motor neurons of the MNS, i.e., metasympathetic neurons are the common final pathway for impulses of intracardiac and central origin. Intracardial MHC regulates the rhythm of heart contractions, speedatrioventricularconduction, repolarization of cardiomyocytes, rate of diastolic relaxation. This system ensures the adaptation of the circulatory system to changing physical activity on the body even in persons after heart transplantation. Professor G.I. Kositsky found that stretching of the myocardium of the right ventricle of an isolated heart is accompanied by increased contraction of the myocardium of the left ventricle. This reaction disappears with the action of ganglion blockers, which turn off

functioning of the MNS. Local cardiac reflexes, carried out by the MNS, regulate the level of cardiac activity in accordance with the needs of the general hemodynamics of the body. Irritation of stretch receptors due to increased blood flow and congestion coronary vessels accompanied by a weakening of the force of heart contractions; with insufficient stretching of the mechanoreceptors of the heart due to reduced filling of its chambers with blood, it leads to a reflex increase in the force of contractions.

Reflex changes in heart activity when irritating the receptors of reflexogenic zones

Increased pressure in the aorta and sinocarotid vascular area irritates pressoreceptors, increases the tone of the cardioinhibitory center and the vagus nerve, which is accompanied by a decrease in heart rate and force, reduction and normalization blood pressure(depressor reflex). On the contrary, a decrease in pressure in the vessels reduces the excitability of vasoreceptors and vagal tone, which leads to increased heart rate and an increase in CO2. Irritation of receptors eyeball when pressing on the eyes, it causes a sharp slowdown in heart rate - the Danini-Aschner reflex. Cardiac reflexes are known. Bezold-Jarisch reflex - a decrease in heart rate when the alkaloid veratrine or other is introduced into the coronary bed chemical substances, bradycardia due to distension of the heart cavities. When chemicals (nicotine) are introduced into the pericardium, bradycardia occurs - epicardial Chernigovsky reflexes.

The role of the higher parts of the central nervous system in the regulation of cardiac activity

The cardiovascular system, through the suprasegmental sections of the autonomic nervous system - the thalamus, hypothalamus, and cerebral cortex, is integrated into the behavioral, somatic, and autonomic reactions of the body. The influence of the cerebral cortex (motor and premotor zones) on the circulatory center of the medulla oblongata underlies conditioned reflex cardiovascular reactions. Irritation of the structures of the central nervous system, as a rule, is accompanied by an increase in heart rate and an increase in blood pressure.

Humoral regulation of the heart

In response to the release of catecholamines, a 2-phase reaction is observed: an increase in heart rate and a rise in blood pressure and, in connection with the depressor reflex, a secondary decrease in blood pressure. The activity of the heart is stimulated by thyroid hormones, adrenal hormones, and sex hormones. An excess of potassium ions is accompanied by cardiac arrest in the diastole stage. Increased ion concentration calcium enhances heart contractions, complicates diastole and causes cardiac arrest in systole.

The heart beats rhythmically. Contraction of the heart causes blood to be pumped from the atria to the ventricles and from the ventricles to blood vessels, and also creates a difference in blood pressure in the arterial and venous system, thanks to which the blood moves. The contraction phase of the heart is designated as systole, and the relaxation phase as diastole.

The cardiac cycle consists of atrial systole and diastole and ventricular systole and diastole. The cycle begins with contraction of the right atrium, and immediately the left atrium begins to contract. Atrial systole begins 0.1 s before ventricular systole. During systole, the atria cannot flow from the right atrium into the vena cava, since the contracting atrium closes the openings of the veins. The ventricles are relaxed at this time, so venous blood enters the right ventricle through the open tricuspid valve, and arterial blood from the left atrium, which enters it from the lungs, is pushed through the open bicuspid valve into the left ventricle. During this time, blood from the aorta and pulmonary artery cannot enter the heart because the semilunar valves are closed by the blood pressure in these blood vessels.

Then the diastole of the atria begins and as their walls relax, blood from the veins fills their cavity.

Immediately after the end of atrial systole, the ventricles begin to contract. At first, only part of the muscle fibers of the ventricles contracts, while the other part stretches. In this case, the shape of the ventricles changes, but the pressure in them remains the same. This is the phase of asynchronous contraction or change in the shape of the ventricles, which lasts approximately 0.05 s. After complete contraction of all muscle fibers of the ventricles, the pressure in their cavities increases very quickly. This causes the tricuspid and bicuspid valves to close and the openings to the atria to close. The semilunar valves remain closed because the pressure in the ventricles is even lower than in the aorta and pulmonary artery. This phase in which muscle wall The ventricles tense, but their volume does not change until the pressure in them exceeds the pressure in the aorta and pulmonary artery, called the isometric contraction phase. It lasts about 0.03 s.

During isometric contraction of the ventricles, the pressure in the atria during their diastole reaches zero and even becomes negative, i.e. less than atmospheric, so the atrioventricular valves remain closed, and the semilunar valves are closed by the reverse flow of blood from the arterial vessels.

Both phases of asynchronous and isometric contractions together constitute the period of ventricular tension. In humans, the semilunar valves of the aorta open when the pressure in the left ventricle reaches 65-75 mmHg. Art., and the semilunar valves of the pulmonary artery open when the pressure in the right ventricle reaches - 12 mm Hg. Art. In this case, the ejection phase begins, or systolic ejection of blood, in which the blood pressure in the ventricles increases sharply within 0.10-0.12 s (fast ejection), and then, as the blood in the ventricles decreases, the increase in pressure stops and by the end of systole it begins to fall within 0.10-0.15 s (slow ejection).

After the semilunar valves open, the ventricles contract, changing their volume and using some of the tension to work to push blood into the blood vessels (auxotonic contraction). During isometric contraction, the blood pressure in the ventricles becomes greater than in the aorta and pulmonary artery, which causes the opening of the semilunar valves and a phase of rapid and then slow expulsion of blood from the ventricles into the blood vessels. After these phases, a sudden relaxation of the ventricles occurs, their diastole. The pressure in the aorta becomes higher than in the left ventricle, and therefore the semilunar valves close. The time interval between the beginning of ventricular diastole and the closure of the semilunar valves is called the protodiastolic period, which lasts 0.04 s.

During diastole, the ventricles relax for approximately 0.08 s with the atrioventricular and semilunar valves closed, until the pressure in them drops below that in the atria, already filled with blood. This is the isometric relaxation phase. Ventricular diastole is accompanied by a drop in pressure in them to zero.

A sharp drop in pressure in the ventricles and an increase in pressure in the atria as their contraction begins opens the tricuspid and bicuspid valves. The phase of rapid filling of the ventricles with blood begins, which lasts 0.08 s, and then, due to a gradual increase in pressure in the ventricles as they are filled with blood, the filling of the ventricles slows down, and a slow filling phase begins for 0.16 s, which coincides with the late diastolic phase.

In humans, ventricular systole lasts about 0.3 s, ventricular diastole - 0.53 s, atrial systole - 0.11 s, atrial diastole - 0.69 s. The entire cardiac cycle lasts an average of 0.8 seconds in humans. Time total diastole the atria and ventricles are sometimes called a pause. In the work of the heart of humans and higher animals under physiological conditions there is no pause, other than diastole, which distinguishes the activity of the heart of humans and higher animals from the activity of the heart of cold-blooded animals.

In a horse, when cardiac activity increases, the duration of one cardiac cycle is 0.7 s, of which atrial systole lasts 0.1 s, ventricular systole lasts 0.25 s, and total cardiac systole lasts 0.35 s. Since the atria are also relaxed during ventricular systole, atrial relaxation lasts 0.6 s, or 90% of the duration of the cardiac cycle, and ventricular relaxation lasts 0.45 s, or 60-65%.

This duration of relaxation restores the performance of the heart muscle.

The work of the heart is accompanied by changes in pressure in the cavities of the heart and in the vascular system, the appearance of heart sounds, the appearance of pulse fluctuations, etc. The cardiac cycle is a period spanning one systole and one diastole. At a heart rate of 75 per minute, the total duration of the cardiac cycle will be 0.8 s; at a heart rate of 60 per minute, the cardiac cycle will take 1 s. If the cycle takes 0.8 s, then of this ventricular systole accounts for 0.33 s, and ventricular diastole accounts for 0.47 s. Ventricular systole includes the following periods and phases:

1) tension period. This period consists of a phase of asynchronous contraction of the ventricles. During this phase, the pressure in the ventricles is still close to zero, and only at the end of the phase does a rapid increase in pressure in the ventricles begin. The next phase of the tension period is the phase of isometric contraction, i.e. this means that the length of the muscles remains unchanged (iso – equal). This phase begins with the slamming of the atrioventricular valves. At this time, the 1st (systolic) heart sound occurs. The pressure in the ventricles increases quickly: up to 70-80 in the left and up to 15-20 mm Hg. in the right. During this phase, the leaflet and semilunar valves are still closed and the volume of blood in the ventricles remains constant. It is no coincidence that some authors, instead of the phases of asynchronous contraction and isometric tension, distinguish the so-called phase of isovolumetric (iso - equal to volume - volume) contraction. There is every reason to agree with this classification. Firstly, the statement about the presence of asynchronous contraction of the working ventricular myocardium, which works as a functional syncytium and has a high speed of propagation of excitation, is very doubtful. Secondly, asynchronous contraction of cardiomyocytes occurs during ventricular flutter and fibrillation. Thirdly, during the phase of isometric contraction, the length of the muscles decreases (and this no longer corresponds to the name of the phase), but the volume of blood in the ventricles at this moment does not change, because Both the atrioventricular and semilunar valves are closed. This is essentially a phase of isovolumetric contraction or tension.

2) period of exile. The expulsion period consists of a fast expulsion phase and a slow expulsion phase. During this period, the pressure in the left ventricle increases to 120-130 mm Hg, in the right - up to 25 mm Hg. During this period, the semilunar valves open and blood is released into the aorta and pulmonary artery. Stroke volume of blood, i.e. the volume ejected per systole is about 70 ml, and the end-diastolic volume of blood is approximately 120-130 ml. About 60-70 ml of blood remains in the ventricles after systole. This is the so-called end-systolic, or reserve, blood volume. The ratio of stroke volume to end-diastolic volume (for example, 70:120 = 0.57) is called the ejection fraction. It is usually expressed as a percentage, so 0.57 must be multiplied by 100 and in this case we get 57%, i.e. ejection fraction = 57%. Normally, it is 55-65%. A decrease in the ejection fraction is an important indicator of weakened contractility of the left ventricle.

Ventricular diastole has the following periods and phases: 1) protodiastolic period, 2) period of isometric relaxation and 3) filling period, which in turn is divided into a) fast filling phase and b) slow filling phase. The protodiastolic period takes place from the beginning of ventricular relaxation to the closure of the semilunar valves. After these valves close, the pressure in the ventricles drops, but the leaflet valves are still closed at this time, i.e. the ventricular cavities have no communication with either the atria or the aorta and pulmonary artery. At this time, the volume of blood in the ventricles does not change and therefore this period is called the period of isometric relaxation (or more correctly it should be called the period of isovolumetric relaxation, since the volume of blood in the ventricles does not change). During the period of rapid filling, the atrioventricular valves are open and blood from the atria quickly enters the ventricles (it is generally accepted that blood at this moment enters the ventricles by gravity.). The main volume of blood from the atria into the ventricles enters precisely during the rapid filling phase, and only about 8% of the blood enters the ventricles during the slow filling phase. Atrial systole occurs at the end of the slow filling phase and due to atrial systole, the remaining blood is squeezed out of the atria. This period is called presystolic (meaning ventricular presystole), and then a new cycle of the heart begins.

Thus, the heart cycle consists of systole and diastole. Ventricular systole consists of: 1) a period of tension, which is divided into a phase of asynchronous contraction and a phase of isometric (isovolumetric) contraction, 2) a period of ejection, which is divided into a phase of fast ejection and a phase of slow ejection. Before the onset of diastole, there is a proto-diastolic period.

Ventricular diastole consists of: 1) a period of isometric (isovolumetric) relaxation, 2) a period of filling with blood, which is divided into a fast filling phase and a slow filling phase, 3) a presystolic period.

Phase analysis of the heart is carried out using polycardiography. This method is based on synchronous recording of ECG, FCG (phonocardiogram) and sphygmogram (SG) carotid artery. The duration of the cycle is determined by the R–R teeth. The duration of systole is determined by the interval from the beginning of the Q wave on the ECG to the beginning of the 2nd tone on the FCG, the duration of the ejection period is determined by the interval from the beginning of anacrotism to incisura on the SG, the duration of the ejection period is determined by the difference between the duration of systole and the ejection period - the period of tension, by the interval between the beginning of the Q wave ECG and the beginning of the 1st tone of the FCG - the period of asynchronous contraction, according to the difference between the duration of the period of tension and the phase of asynchronous contraction - the phase of isometric contraction.