Practical monitoring of hemodynamics during shock. Watching the Breath

Methodological development of the lecture

“PHYSIOLOGY OF THE VASCULAR SYSTEM.

BLOOD PRESSURE AND PULSE"

Blood pressure as the main indicator of hemodynamics. Factors determining the magnitude of arterial and venous pressure. Research methods.

Arterial and venous pulse, their origin. Analysis of sphygmogram and venogram.

Blood pressure - this is the pressure produced by blood on the walls of blood vessels and the cavities of the heart - is the main indicator of hemodynamics.

1st factor in the movement of blood through arterial vessels. The central organ of the entire circulatory system is the heart. Thanks to its pumping activity, blood pressure is created, which promotes its movement through the vessels: during the systole of the ventricles of the heart, portions of blood are released into the aorta and pulmonary arteries under a certain pressure. This leads to an increase in pressure and stretching of the elastic walls of the vascular pool. During diastole, the arterial vessels stretched with blood contract and push blood towards the capillaries, thereby maintaining the necessary blood pressure. The amount of blood pumped into the vascular system per unit time – Q.

2nd factor of blood movement through arterial vessels. The level of capillary pressure (CP) from the aorta to the periphery gradually decreases: The pressure difference present at the beginning and end of the vascular system ensures the movement of blood through the arterial vessels and promotes continuous blood flow.

Changes in blood pressure levels along the vascular system are facilitated by friction of blood against the walls of blood vessels - peripheral resistance, which prevents blood movement.

Thus, blood pressure depends on the amount of blood that is pumped by the heart into the arterial system per unit time and the resistance that blood flow encounters in the vessels. These factors are interrelated and can be expressed by the equation:

This formula follows from the basic equation of hydrodynamics:

Factors that determine blood pressure.

I factor - heart function . Cardiac activity provides the amount of blood entering the vascular system within 1 minute, i.e. minute volume of blood circulation. It is 4-5 liters in humans (Q=MOC). This amount of blood is quite enough to provide all the needs of the body at rest: transport of oxygen to the tissues and removal of carbon dioxide, metabolism in the tissues, a certain level of activity of the excretory organs, thanks to which the constancy of the mineral composition of the internal environment is maintained, thermoregulation. The value of the minute volume of blood circulation at rest is characterized by great constancy and is one of the biological constants of the body. A change in minute volume of blood circulation can be observed during blood transfusion, as a result of which blood pressure increases. With blood loss or bloodletting, the volume of circulating blood decreases, causing blood pressure to drop.

On the other hand, when performing heavy physical activity, the minute volume of blood circulation reaches 30-40 l, since muscular work leads to the emptying of blood depots and vessels of the lymphatic system (V.V. Petrovsky, 1960), which significantly increases the mass of circulating blood and stroke volume heart and heart rate. As a result, the minute volume of blood circulation increases 8-10 times. However, in a healthy body, blood pressure increases slightly, by only 20-40 mmHg.

The absence of a pronounced increase in blood pressure with a significant increase in minute volume is explained by a decrease in the peripheral resistance of blood vessels and the activity of the blood depot.

II factor - blood viscosity. According to the basic laws of hemodynamics, the greater the resistance to fluid flow, the greater its viscosity (the viscosity of blood is 5 times higher than water, the viscosity of which is considered to be 1), the longer the tube through which the fluid flows, and the smaller its lumen. It is known that blood moves in blood vessels due to the energy that the heart imparts to it during its contraction. During ventricular systole, the blood inflow into the aorta and pulmonary artery becomes greater than its outflow from them and the blood pressure in these vessels increases. Part of this pressure is spent on overcoming friction. There is a distinction between external friction - this is the friction of blood cells, for example, red blood cells, against the walls of blood vessels (it is especially high in precapillaries and capillaries), and internal friction of particles against each other. If blood viscosity increases, the friction of the blood against the walls of blood vessels and the mutual friction of the formed elements against each other increases. Thickening of the blood increases external and internal friction, increases resistance to blood flow and leads to a rise in blood pressure.

III factor – peripheral vascular resistance. Since blood viscosity is not subject to rapid changes, the main importance in the regulation of blood circulation belongs to the indicator of peripheral resistance, caused by friction of blood against the walls of blood vessels. The greater the total area of ​​contact of blood with the walls of blood vessels, the greater the friction of blood. The largest area of ​​​​contact between blood and vessels falls on thin blood vessels - arterioles and capillaries. Arterioles have the greatest peripheral resistance, which is associated with the presence of smooth muscle sphincter, so blood pressure when blood passes from arteries to arterioles drops from 120 to 70 mm Hg. Art. In the capillaries the pressure drops to 30-40 mmHg. Art., which is explained by a significant increase in their total lumen, and therefore resistance

Changes in blood pressure along the vascular bed (according to Folkov B., 1967)

From the above data it is clear that the first significant drop in blood pressure is observed in the area of ​​the arterioles, i.e. precapillary section of the vascular system. According to the functional classification of B. Folkov, vessels that resist blood flow are designated as resistive, or resistance vessels. Arterioles are the most active in the vasomotor (lat. vas - vessels, motor - engine) relation. The most significant changes in the peripheral resistance of the vascular bed are caused by:

changes in the lumen of arterioles – with a significant increase in their tone, resistance to blood flow increases, blood pressure rises above normal throughout the entire vascular system. Arises hypertension. Increased pressure in certain areas of the vascular system, for example, in the vessels of the pulmonary circulation or blood vessels abdominal cavity, called hypertension. Hypertension typically results from local increases in resistance to blood flow. Significant and persistent hypertension can occur only as a result of a violation of the neurohumoral regulation of vascular tone.

The speed of blood flow through the vessels – the higher the speed, the greater the resistance. With increasing resistance, maintaining the minute volume of blood is possible only if the linear speed of blood flow in them increases. This additionally increases the resistance of blood vessels. With a decrease in vascular tone, the linear speed of blood flow decreases, and the friction of the blood stream against the walls of the vessels becomes less. The peripheral resistance of the vascular system decreases, and the maintenance of minute volume is ensured at lower blood pressure.

In the body, due to the regulation of vascular tone, a relative constancy of blood pressure is ensured.. For example, when the minute volume of blood circulation decreases (with weakening of cardiac activity or as a result of blood loss), a drop in blood pressure does not occur, since vascular tone increases, R increases, and P, as the product of Q by R, remains constant. On the contrary, during physical or mental work, which is accompanied by an increase in minute blood volume (due to an increase in heart rate), a regulatory decrease in vascular tone occurs, mainly in the precapillary section, due to which the total lumen of the arterioles increases and the peripheral resistance of the vascular pool decreases. Thus, fluctuations in vascular tone actively change the resistance of the vascular bed and, thereby, ensure relative constancy of blood pressure.

4 factor – elasticity of the vascular wall : the more elastic the vascular wall, the lower the blood pressure, and vice versa.

5th factor - circulating blood volume (CBV) - so, blood loss reduces blood pressure, on the contrary, transfusion of large amounts of blood increases blood pressure.

Thus, blood pressure depends on many factors, which can be grouped as follows:

Factors related to the work of the heart itself (strength and frequency of heart contractions), which provides blood flow to the arterial system.

Factors associated with the state of the vascular system - tone of the vessel wall, elasticity of the vessel wall, surface condition vascular wall.

Factors associated with the state of blood circulating through the vascular system - its viscosity, quantity (BCV).

BLOOD PRESSURE FLUCTUATIONS. ASSESSMENT OF SYSTOLIC, DIASTOLIC AND PULSE PRESSURE.

Blood pressure in the arteries makes constant continuous fluctuations from some average level. When directly recording blood pressure on a kymogram, 3 types of waves are distinguished: 1) systolic waves of the first order, 2) respiratory waves of the second order, 3) vascular waves of the third order.

Waves I order – caused by the systole of the ventricles of the heart. During the expulsion of blood from the ventricles, the pressure in the aorta and pulmonary artery increases and reaches a maximum of 140 and 40 mm Hg, respectively. Art. This is the maximum systolic pressure ( SD). During diastole, when blood does not enter the arterial system from the heart, but only the outflow of blood from large arteries to the capillaries occurs, the pressure in them drops to a minimum, and this pressure is called minimal, or diastolic(DD). Its value largely depends on the lumen (tone) of the blood vessels and is equal to 60-80 mm Hg. Art. The difference between systolic and diastolic pressure is called pulse(PD), and ensures the appearance of a sitole wave on the kymogram, equal to 30-40 mm Hg. Art. Pulse pressure is directly proportional to the stroke volume of the heart and indicates the strength of heart contractions: The more blood the heart ejects during systole, the greater the pulse pressure will be. There is a certain quantitative relationship between systolic and diastolic pressures: the maximum pressure corresponds to the minimum pressure. It is determined by dividing the maximum pressure in half and adding 10 (for example, SD = 120 mm Hg, then DD = 120: 2 + 10 = 70 mm Hg).

The highest value of pulse pressure is observed in the vessels located closer to the heart - in the aorta, and large arteries. In small arteries the difference between systolic and diastolic pressures is smoothed out, but in arterioles and capillaries the pressure is constant and does not change during systole and diastole. This is important for stabilizing the metabolic processes occurring between the blood flowing through the capillaries and the tissues surrounding them. The number of first order waves corresponds to the heart rate.

Waves II order – respiratory, reflect changes in blood pressure associated with respiratory movements. Their number corresponds to the number of breathing movements. Each second order wave includes several first order waves. The mechanism of their occurrence is complex: when inhaling, conditions are created for the flow of blood from the systemic circulation into the small circle, due to an increase in the capacity of the pulmonary vessels and a slight decrease in their resistance to blood flow, an increase in the flow of blood from the right ventricle to the lungs. This is also facilitated by the difference in pressure between the vessels of the abdominal cavity and chest, which arises as a result of an increase in negative pressure in the pleural cavity, on the one hand, and the lowering of the diaphragm and “pressing” blood from the venous vessels of the intestines and liver, on the other. All this creates conditions for the deposition of blood in the vessels of the lungs and reduces its exit from the lungs to the left half of the heart. Therefore, at the height of inspiration, blood flow to the heart decreases and blood pressure decreases. Toward the end of inhalation, blood pressure rises.

The factors described are mechanical. However, in the formation of waves of the second order, nervous factors are important: when the activity of the respiratory center changes, which occurs during inhalation, the activity of the vasomotor center increases, increasing the tone of the vessels of the systemic circulation. Fluctuations in blood flow volume may also secondary cause changes in blood pressure by activating vascular reflexogenic zones. For example, the Bainbridge reflex when there is a change in blood flow in the right atrium.

Waves III order (Hering-Traube waves) are even slower increases and decreases in pressure, each of which covers several respiratory waves of the second order. They are caused by periodic changes in the tone of the vasomotor centers. They are most often observed when there is insufficient oxygen supply to the brain (high-altitude hypoxia), after blood loss or poisoning with certain poisons.

METHODS AND TECHNIQUES FOR STUDYING BLOOD PRESSURE

Blood pressure was first measured by Stefan Hels (1733). He determined blood pressure by the height of the column to which the blood rose in a glass tube inserted into the horse's artery.

Currently, there are 2 ways to measure blood pressure: the first is direct, or bloody, used mainly on animals; the second - indirect, bloodless - on a person.

Bloody or direct research method . A cannula or flattened needle is inserted into the artery, connected to a manometer filled with mercury - a curved glass tube shaped like the Latin letter U. Fluctuations in blood pressure are transmitted to a column of mercury with a float, to which a recorder is attached, sliding along a paper tape. The result is a record of changes in blood pressure.

They use it in the clinic indirect, bloodless method (without opening the blood vessels) using a sphygmomanometer by D. Riva-Rocci. In 1905, I.S. Korotkov proposed a method of sound auscultatory determination of pressure, based on listening with a phonendoscope to the sound phenomenon, or vascular tones, on the brachial artery. The data obtained by the Korotkov method exceed the actual data (obtained by the direct method) for SD - by 7-10%, for DD - by 28%.

To more accurately determine blood pressure, it is advisable to use an oscillographic method based on recording vibrations of the arterial wall distal to the site of compression of the limb. A sphygmogram (blood pressure recording curve obtained using this technique) can be recorded from the forearm, shoulder, lower leg, and thigh.

CLINICAL SIGNIFICANCE OF BLOOD PRESSURE INDICATORS

A significant number of methods for studying the activity of the heart and circulatory system as a whole are based on determining systolic and diastolic blood pressure while simultaneously taking into account heart rate.

SYSTOLIC PRESSURE– or maximum (MP) blood pressure normally ranges from 105 to 120 mmHg. Art. By doing physical work it increases by 20-80 mm Hg. Art. and depends on its severity. After stopping operation, the SD is restored within 2-3 minutes.

Slower recovery of initial DM values ​​is considered as evidence of cardiovascular failure.

DM changes with age. In older people it increases, there is a gender difference - in men it is slightly lower than in women of the same age. DM depends on constitutional features human: height and weight have a direct correlative positive relationship with diabetes. In newborns, the maximum blood pressure is 50 mm Hg. Art., and by the end of the 1st month of life it already increases to 80 mm Hg. Art.

Age-related relationships between blood pressure and pulse.

Systolic pressure and pulse vary somewhat throughout the day, reaching the highest values ​​at 18-20 hours and the lowest at 2-4 hours in the morning (circadian rhythm).

DIASTOLIC PRESSURE (PP)– 60-80 mm Hg. Art. After physical activity and various kinds of influences (for example, emotions), it usually does not change or several goes down(by 10 mmHg). A sharp decrease in the level of diastolic pressure during work or its increase and a slow (within 2-3 minutes) return to initial values ​​is regarded as an unfavorable symptom indicating insufficiency of the cardiovascular system.

During the contraction of the heart, another portion of blood is pushed into the vascular system. Its impact on the wall of the artery creates vibrations, which, spreading through the vessels, gradually fade to the periphery. They are called the pulse.

What is the pulse like?

There are three types of veins and capillaries in the human body. The release of blood from the heart affects each of them in one way or another, causing their walls to vibrate. Of course, arteries, as the vessels closest to the heart, are more susceptible to the influence of cardiac output. Vibrations of their walls are well determined by palpation, and in large vessels they are even noticeable to the naked eye. That is why arterial pulse most significant for diagnosis.

Capillaries are the smallest vessels in the human body, but even they affect the work of the heart. Their walls vibrate in time with heart contractions, but normally this can only be determined using special devices. A capillary pulse visible to the naked eye is a sign of pathology.

The veins are so far away from the heart that their walls do not vibrate. The so-called venous pulse is transmitted vibrations from nearby large arteries.

Why measure your pulse?

What is the significance of vascular wall vibrations for diagnosis? Why is this so important?

The pulse makes it possible to judge hemodynamics, how effectively it contracts, the fullness of the vascular bed, and the rhythm of heartbeats.

In many pathological processes, the pulse changes, and the pulse characteristic no longer corresponds to the norm. This allows us to suspect that not everything is in order in the cardiovascular system.

What parameters determine the pulse? Pulse characteristics

1. Rhythm. Normally, the heart contracts at regular intervals, which means the pulse should be rhythmic.
2. Frequency. Normally, there are as many pulse waves as there are heart beats per minute.
3. Voltage. This indicator depends on the value of systolic blood pressure. The higher it is, the more difficult it is to compress the artery with your fingers, i.e. Pulse tension is high.
4. Filling. Depends on the volume of blood ejected by the heart during systole.
5. Magnitude. This concept combines filling and tension.
6. Shape is another parameter that determines the pulse. The characteristics of the pulse in this case depend on the change in blood pressure in the vessels during systole (contraction) and diastole (relaxation) of the heart.

Rhythm disorders

If there are disturbances in the generation or conduction of impulses through the heart muscle, the rhythm of heart contractions changes, and with it the pulse changes. Individual vibrations of the vascular walls begin to fall out, or appear prematurely, or follow each other at irregular intervals.

What are the types of rhythm disturbances?

Arrhythmias due to changes in the functioning of the sinus node (the area of ​​the myocardium that generates impulses leading to contraction of the heart muscle):

1. Sinus tachycardia - increased contraction frequency.
2. Sinus bradycardia - decreased contraction frequency.
3. Sinus arrhythmia - contractions of the heart at irregular intervals.

Ectopic arrhythmias. Their occurrence becomes possible when a focus appears in the myocardium with activity higher than that of the sinus node. In such a situation, the new pacemaker will suppress the activity of the latter and impose its own rhythm of contractions on the heart.

1. Extrasystole - the appearance of an extraordinary heart rate. Depending on the location of the ectopic focus of excitation, extrasystoles are atrial, atrioventricular and ventricular.
2. Paroxysmal tachycardia is a sudden increase in heart rate (up to 180-240 heart beats per minute). Like extrasystoles, it can be atrial, atrioventricular and ventricular.

Impaired conduction of impulses through the myocardium (blockade). Depending on the location of the problem that prevents normal progression from the sinus node, blockades are divided into groups:

1. (the impulse does not go further than the sinus node).
2. (the impulse does not pass from the atria to the ventricles). With complete atrioventricular block (III degree), a situation becomes possible when there are two pacemakers (the sinus node and the focus of excitation in the ventricles of the heart).
3. Intraventricular block.

Separately, we should dwell on the flickering and fluttering of the atria and ventricles. These conditions are also called absolute arrhythmia. In this case, the sinus node ceases to be a pacemaker, and multiple ectopic foci of excitation are formed in the myocardium of the atria or ventricles, setting the heart rhythm with a huge contraction frequency. Naturally, under such conditions the heart muscle is not able to contract adequately. That's why this pathology(especially from the ventricles) poses a threat to life.

Heart rate

The resting heart rate of an adult is 60-80 beats per minute. Of course, this indicator changes throughout life. Pulse varies significantly by age.

There may be a discrepancy between the number of heart contractions and the number of pulse waves. This occurs if a small volume of blood is released into the vascular bed (heart failure, decreased amount of circulating blood). In this case, vibrations of the vessel walls may not occur.

Thus, a person’s pulse (the norm for age is indicated above) is not always determined in the peripheral arteries. This, however, does not mean that the heart does not contract either. Perhaps the reason is a decrease in ejection fraction.

Voltage

Depending on changes in this indicator, the pulse also changes. The characteristics of the pulse according to its voltage include division into the following types:

1. Firm pulse. Caused by high blood pressure (BP), primarily systolic. In this case, it is very difficult to squeeze the artery with your fingers. The appearance of this type of pulse indicates the need for urgent correction of blood pressure with antihypertensive drugs.
2. Soft pulse. The artery contracts easily, and this is not very good, because this type of pulse indicates that the blood pressure is too low. It can be due to various reasons: a decrease in the volume of circulating blood, a decrease in vascular tone, and ineffective heart contractions.

Filling

Depending on changes in this indicator, there are the following types pulse:

1. Full. This means that the blood supply to the arteries is sufficient.
2. Empty. Such a pulse occurs when the volume of blood ejected by the heart during systole is small. The causes of this condition may be heart pathology (heart failure, arrhythmias with too high heart rate) or a decrease in blood volume in the body (blood loss, dehydration).

Pulse value

This indicator combines the filling and tension of the pulse. It depends primarily on the expansion of the artery during contraction of the heart and its collapse during relaxation of the myocardium. The following types of pulse are distinguished by size:

1. Big (tall). It occurs in a situation where the ejection fraction increases and the tone of the arterial wall is reduced. At the same time, the pressure in systole and diastole is different (during one cycle of the heart it increases sharply, and then decreases significantly). The reasons leading to the occurrence of a high pulse may be aortic insufficiency, thyrotoxicosis, fever.
2. Small pulse. Little blood is released into the vascular bed, the tone of the arterial walls is high, and pressure fluctuations in systole and diastole are minimal. Causes of this condition: aortic stenosis, heart failure, blood loss, shock. In especially severe cases, the pulse value may become insignificant (this pulse is called threadlike).
3. Uniform pulse. This is how the normal heart rate is characterized.

Pulse form

According to this parameter, the pulse is divided into two main categories:

1. Fast. In this case, during systole, the pressure in the aorta increases significantly, and during diastole it quickly drops. A rapid pulse is a characteristic sign of aortic insufficiency.
2. Slow. The opposite situation, in which there is no room for significant pressure drops in systole and diastole. Such a pulse usually indicates the presence of aortic stenosis.

How to properly examine the pulse?

Probably everyone knows what needs to be done to determine what a person’s pulse is. However, even such a simple manipulation has features that you need to know.

The pulse is examined in the peripheral (radial) and main (carotid) arteries. It is important to know that with weak cardiac output in the periphery, pulse waves may not be detected.

Let's look at how to palpate the pulse in the hand. The radial artery is accessible for examination at the wrist just below the base thumb. When determining the pulse, both arteries (left and right) are palpated, because Situations are possible when pulse fluctuations will be different on both hands. This may be due to compression of the vessel from the outside (for example, a tumor) or blockage of its lumen (thrombus, atherosclerotic plaque). After comparison, the pulse is assessed on the arm where it is better palpated. It is important that when examining pulse fluctuations, there is not one finger on the artery, but several (it is most effective to clasp your wrist so that 4 fingers, except the thumb, are on the radial artery).

How is the pulse in the carotid artery determined? If the pulse waves at the periphery are too weak, the pulse in the great vessels can be examined. The easiest way is to try to find it on the carotid artery. To do this, two fingers (index and middle) must be placed on the area where the indicated artery is projected (at the anterior edge of the sternocleidomastoid muscle above the Adam's apple). It is important to remember that it is impossible to examine the pulse on both sides at once. Pressure of two carotid arteries can cause circulatory problems in the brain.

The pulse at rest and with normal hemodynamic parameters is easily determined both in peripheral and central vessels.

A few words in conclusion

(the age norm must be taken into account during the study) allows us to draw conclusions about the state of hemodynamics. Certain changes in the parameters of pulse fluctuations are often characteristic signs of certain pathological conditions. That is why pulse examination is important diagnostic value.

The main factors characterizing the state of blood circulation and its effectiveness are MOS, total peripheral vascular resistance and bcc (Table 10.1). These factors are interdependent and interconnected and are decisive. Measuring blood pressure and heart rate alone cannot give a complete picture of the state of blood circulation. Determining MOC, BCC and calculating some indirect indicators allow us to obtain the necessary information.

Minute volume of the heart, or cardiac output, is the amount of blood passing through the heart in 1 minute; cardiac index - the ratio of CO to body surface area: CO averages 5-7 l/min.

Stroke volume is the amount of blood ejected by the heart in one systole; left ventricular work - mechanical work performed by the heart in 1 minute; pulmonary artery wedge pressure or pulmonary capillary wedge pressure - pressure in the distal branch of the pulmonary artery when the balloon is inflated; central venous pressure - pressure at the mouth of the vena cava or in the right atrium; total peripheral vascular resistance - an indicator of the total resistance of the vascular system to the volume of blood ejected by the heart:

Table 10.1.

By means of a coefficient of 80, pressure and volume values ​​​​are converted into dyn-s/cm5. In fact, this value is an index of OPSS.

The main function of blood circulation is to deliver the required amount of oxygen and nutrients to tissues. Blood carries energy substances, vitamins, ions, hormones and biologically active substances from the place of their formation to various organs. The balance of fluid in the body, maintaining a constant body temperature, releasing cells from waste and delivering them to the excretory organs occur due to the constant circulation of blood through the vessels.

The heart consists of two “pumps”: the left and right ventricles, which must push the same amount of blood to prevent stagnation in the arterial and venous systems (Fig. 10.1). The left ventricle, which has powerful muscles, can create high pressure. With sufficient oxygenation, it easily adapts to sudden demands for increased CO. The right ventricle, while providing sufficient MVR, cannot function adequately with a sudden increase in resistance.

Every cardiac cycle lasts 0.8 s. Ventricular systole occurs within 0.3 s, diastole - 0.5 s. Heart rhythm in a healthy heart is regulated in the sinus node, which is located at the point where the vena cava enters the right atrium. The excitation impulse spreads through the atria and then to the atrioventricular node, located between the atria and ventricles. From the atrioventricular node, the electrical impulse travels through the right and left branches of the His bundle and Purkinje fibers (cardiac conduction myocytes), covering the endocardial surface of both ventricles.

Rice. 10.1. Heart.

1 - aorta, 2 - pulmonary artery; 3 - aortic arch; 4 - superior vena cava; 5 - bottom hollow foam; b - pulmonary veins. RA - right atrium; RV - right ventricle, LA - left atrium; LV - left ventricle.

Minute volume of the heart (cardiac output). IN healthy body The main regulatory factor of MOS is peripheral vessels. Spasm and dilatation of arterioles affect the dynamics of arterial circulation, regional and organ blood supply. Venous tone, changing the capacity of the venous system, ensures the return of blood to the heart.

In case of diseases or functional overload of the heart, MOS almost entirely depends on the efficiency of its “pump”, i.e. functional ability myocardium. The ability to increase CO in response to increased tissue demand for blood supply is called cardiac reserve. In healthy adults it is 300-400% and is significantly reduced in heart disease.

In the regulation of cardiac reserve, the main role is played by Starling's law, the nervous regulation of the strength and frequency of heart contractions. This law reflects the ability of the heart to increase the force of contraction with greater filling of its chambers. According to this law, the heart “pumps” an amount of blood equal to the venous inflow, without a significant change in central venous pressure. However, in the whole organism, neuro-reflex mechanisms make the regulation of blood circulation more subtle and reliable, ensuring continuous adaptation of the blood supply to the changing internal and external environment.

Myocardial contractions occur when there is sufficient oxygen supply. Coronary blood flow provides blood supply to the myocardium in accordance with the needs of cardiac activity. Normally, it is 5% of DM, on average 250-300 ml/min. The filling of the coronary arteries is proportional to the average pressure in the aorta. Coronary blood flow increases with a decrease in blood oxygen saturation and an increase in the concentration of carbon dioxide and adrenaline in the blood. Under stress conditions, CO and coronary blood flow increase proportionally. With significant physical activity, CO can reach 37-40 l/min, coronary blood flow - 2 l/min. When coronary circulation is impaired, cardiac reserve is significantly reduced.

Venous flow to the heart. In a clinical setting, it is difficult to determine the amount of venous blood flow to the heart. It depends on the magnitude of capillary blood flow and the pressure gradient in the capillaries and right atrium. Pressure in the capillaries and capillary blood flow are determined by the value of CO and the propulsive action of the arteries. Pressure gradients in each part of the vascular system and the right atrium are different. They are approximately 100 mmHg. in the arterial bed, 25 mm Hg. in capillaries and 15 mm Hg. Art. at the beginning of the venules. The zero point for measuring venous pressure is considered to be the pressure level in the right atrium. This point was called the “physiological zero of hydrostatic pressure.”

The venous system plays a large role in regulating blood flow to the heart. Venous vessels have the ability to expand when blood volume increases and to narrow when it decreases. The state of venous tone is regulated by the autonomic nervous system. With a moderately reduced blood volume, its flow to the heart is ensured by an increase in venous tone. With severe hypovolemia, venous inflow becomes insufficient, which leads to a decrease in MOS. Transfusion of blood and solutions increases venous return and increases MOS. At heart failure and increased pressure in the right atrium, conditions are created for a decrease in venous return and MOS. Compensatory mechanisms are aimed at overcoming the decrease in venous flow to the heart. With weakness of the right ventricle and stagnation of blood in the vena cava, the central venous pressure increases significantly.

Pumping function of the heart. The adequacy of blood circulation depends primarily on the function of the ventricles, which determine the functioning of the heart as a pump. Measurement of PCWP has become a huge step forward in assessing cardiovascular function. Previously established criteria for venous inflow based on the CVP level were revised, since in some cases, focusing on the CVP level during infusion therapy led to catastrophic results. This indicator could be normal and even reduced, while the PCWP increased more than 2 times, which was the cause of pulmonary edema. When considering preload options, one cannot fail to take into account the value of PCWP, which is normally 5-12 mmHg. The development of the Swan-Ganz catheterization method has opened up new opportunities in hemodynamic monitoring. It became possible definition intraatrial pressure, CO, saturation and oxygen tension in mixed venous blood.

Normal pressure values ​​in the cavities of the heart and pulmonary artery are presented in table. 10.2. Despite the importance of measuring PCWP and CO, these indicators cannot be considered absolute criteria for the adequacy of tissue perfusion. However, the use of this method allows you to control the amount of preload and create the most economical modes of heart operation.

Table 10.2. Pressure in the cavities of the heart and pulmonary artery

Suction force of the heart. During ventricular systole, the atrioventricular septum moves toward the ventricles and the volume of the atria increases. The resulting vacuum in the atria facilitates the absorption of blood from the central veins into the heart. When the ventricles relax, the tension of their walls ensures the absorption of blood from the atria into the ventricles.

The value of negative pressure in the chest cavity. Respiratory excursions are among the extracardiac factors regulating MOS. During inspiration, intrapleural pressure becomes negative. The latter is transmitted to the atria and vena cava and blood flow into these veins and the right atrium increases. When you exhale, the pressure in the abdominal cavity increases, as a result of which the blood is squeezed out of the abdominal veins into the chest veins. Negative pressure in the pleural cavity increases afterload, while positive pressure (during mechanical ventilation) has the opposite effect. This may explain the decrease in systolic pressure during the inspiratory phase.

Total peripheral resistance. The term “total peripheral vascular resistance” refers to the total resistance of the arterioles. However, changes in tone in different parts of the cardiovascular system are different. In some vascular areas there may be pronounced vasoconstriction, in others - vasodilation. Nevertheless, the peripheral vascular resistance is important for the differential diagnosis of the type of hemodynamic disorders.

In order to imagine the importance of TPR in the regulation of MOS, it is necessary to consider two extreme options - an infinitely large TPR and the absence of it in the blood flow. With a large peripheral vascular resistance, blood cannot flow through the vascular system. Under these conditions, even with good heart function, blood flow stops. In some pathological conditions, blood flow in tissues decreases as a result of an increase in peripheral vascular resistance. A progressive increase in the latter leads to a decrease in MOC. With zero resistance, blood could flow freely from the aorta into the vena cava and then into the right heart. As a result, the pressure in the right atrium would become equal to the pressure in the aorta, which would greatly facilitate the release of blood into the arterial system, and the MVR would increase 5-6 times or more. However, in a living organism, OPSS can never become equal to 0, just as it can never become infinitely large. In some cases, peripheral vascular resistance decreases (liver cirrhosis, septic shock). When it increases by 3 times, MVR can decrease by half at the same pressure values ​​in the right atrium.

Division of vessels according to their functional significance. All vessels of the body can be divided into two groups: resistance vessels and capacitive vessels. The former regulate the value of peripheral vascular resistance, blood pressure and the degree of blood supply to individual organs and systems of the body; the latter, due to their large capacity, are involved in maintaining venous return to the heart, and consequently, MOS.

The vessels of the “compression chamber” - the aorta and its large branches - maintain a pressure gradient due to distensibility during systole. This softens the pulsatile release and makes the flow of blood to the periphery more uniform. Precapillary resistance vessels - small arterioles and arteries - maintain hydrostatic pressure in the capillaries and tissue blood flow. It falls to their lot most of resistance to blood flow. Precapillary sphincters, changing the number of functioning capillaries, change the exchange surface area. They contain a-receptors, which, when exposed to catecholamines, cause spasm of the sphincters, impaired blood flow and cell hypoxia. α-blockers are pharmacological agents, reducing irritation of a-receptors and relieving spasm in the sphincters.

Capillaries are the most important vessels of exchange. They carry out the process of diffusion and filtration - absorption. Solutes pass through their wall in both directions. They belong to the system of capacitive vessels and in pathological conditions can accommodate up to 90% of the blood volume. Under normal conditions, they contain up to 5-7% blood.

Post-capillary resistance vessels - small veins and venules - regulate hydrostatic pressure in the capillaries, resulting in the transport of the liquid part of the blood and interstitial fluid. Humoral factor is the main regulator of microcirculation, but neurogenic stimuli also have an effect on pre- and postcapillary sphincters.

Venous vessels, containing up to 85% of the blood volume, do not play a significant role in resistance, but act as a container and are most susceptible to sympathetic influences. General cooling, hyperadrenalineemia and hyperventilation lead to venous spasm, which has great importance in the distribution of blood volume. Changing the capacity of the venous bed regulates the venous return of blood to the heart.

Shunt vessels - arteriovenous anastomoses - in internal organs function only in pathological conditions; in the skin they perform a thermoregulatory function.

Circulating blood volume. It is quite difficult to define the concept of “circulating blood volume”, since it is a dynamic quantity and constantly changes over a wide range. At rest, not all blood takes part in circulation, but only a certain volume, which completes the circulation in a relatively short period of time necessary to maintain blood circulation. On this basis, the concept of “circulating blood volume” entered clinical practice.

In young men, the blood volume is 70 ml/kg. It decreases with age to 65 ml/kg body weight. In young women, the BCC is 65 ml/kg and also tends to decrease. U two year old child blood volume is 75 ml/kg body weight. In an adult man, plasma volume averages 4-5% of body weight. Thus, a man weighing 80 kg has an average blood volume of 5600 ml and a plasma volume of 3500 ml. More accurate values ​​of blood volumes are obtained taking into account the body surface area, since the ratio of blood volume to body surface does not change with age. In obese patients, the volume of blood volume per 1 kg of body weight is less than in patients with normal weight. For example, in obese women the BCC is 55-59 ml/kg body weight. Normally, 65-75% of blood is contained in the veins, 20% in the arteries and 5-7% in the capillaries (Table 10.3).

A loss of 200-300 ml of arterial blood in adults, equal to approximately 1/3 of its volume, can cause pronounced hemodynamic changes; the same loss of venous blood is only l/10-1/13 of it and does not lead to any circulatory disorders.

Table 10.3.

Distribution of blood volumes in the body

A decrease in blood volume during blood loss is due to the loss of red blood cells and plasma, during dehydration - due to loss of water, during anemia - due to loss of red blood cells, and during myxedema - a decrease in the number of red blood cells and plasma volume. Hypervolemia is characteristic of pregnancy, heart failure and polyglobulia.

Metabolism and blood circulation. There is a close correlation between the state of blood circulation and metabolism. The amount of blood flow to any part of the body increases in proportion to the metabolic rate. In various organs and tissues, blood flow is regulated by different substances: for muscles, heart, liver, the regulators are oxygen and energy substrates, for brain cells - the concentration of carbon dioxide and oxygen, for the kidneys - the level of ions and nitrogenous wastes. Body temperature regulates blood flow in the skin. What is certain, however, is the fact that there is a high degree of correlation between the level of blood flow in any part of the body and the concentration of oxygen in the blood. An increase in tissue oxygen demand leads to an increase in blood flow. The exception is brain tissue. Both a lack of oxygen and an excess of carbon dioxide are equally powerful stimulants of cerebral circulation. Cells react differently to the lack of certain substances involved in metabolism. This is due to different needs for them, different utilization and their reserve in the blood.

The amount of reserve of a particular substance is called the “safety factor” or “recycling coefficient”. This reserve of the substance is utilized by tissues under emergency conditions and completely depends on the state of the MOS. At a constant level of blood flow, oxygen transport and utilization can increase 3 times due to a more complete release of oxygen by hemoglobin. In other words, the oxygen reserve can only increase 3 times without increasing the MOC. Therefore, the “safety factor” for oxygen is 3. For glucose it is also equal to 3, and for other substances it is much higher - for carbon dioxide - 25, amino acids - 36, fatty acids - 28, protein metabolism products - 480. The difference between the "safety factor" The safety of oxygen with glucose and that of other substances is enormous.

Preload and afterload. Myocardial preload is defined as the force that stretches the heart muscle before it contracts. For an intact ventricle, preload is the end-diastolic volume of the left ventricle. Since this volume is difficult to determine at the patient’s bedside, an indicator such as left ventricular end-diastolic pressure (LVEDP) is used. If the distensibility of the left ventricle is normal, then the PCWP will be equal to the LVEP. For patients in departments intensive care, the compliance of the left ventricle is usually changed. The distensibility of the left ventricle can be significantly reduced by ischemic heart disease, the action of calcium channel blockers, and the influence of positive pressure during mechanical ventilation. Thus, PCWP determines pressure in the left atrium, but is not always an indicator of preload on the left ventricle.

Afterload is defined as the force that opposes or resists ventricular contraction. It is equivalent to the stress that occurs in the wall of the ventricle during systole. This transmural stress of the ventricular wall in turn depends on the systolic pressure, the radius of the chamber (ventricle), the impedance of the aorta and its components - the distensibility and resistance of the arteries. Afterload includes preload and pressure in the pleural cavity (cleft). The load characteristics of the heart are expressed in units of pressure and blood volume [Marino P., 1998].

Oxygen transport. Oxygen bound to hemoglobin (Hb) in arterial blood is determined taking into account its real level, the saturation of arterial blood with oxygen (SaO2) and the Hüfner constant of 1.34, indicating that 1 g of hemoglobin is fully saturated (SaO2 = 100%) binds 1.34 ml of oxygen:

Oxygen contained in blood plasma in a free (dissolved) state:

0.003 x PaO2.

CaO2 = 1.34 x Hb (g/l) x SaO2 + 0.003 x PaO2.

It is easy to see that the contribution of the PaO2 value to the oxygen content in arterial blood is insignificant. Much more informative in assessing oxygen transport is the SaO2 indicator.

Oxygen delivery to tissues (DO2) is determined by two indicators - the CO value (l/min) and the oxygen content in arterial blood CaO2:

DO2 = CB x CaO2.

If you use the SI value and not the MOC value, then the calculation of oxygen transport should be carried out using the following formula:

DO2 = SI x (1.34 x Hb x SaO2) x 10,

Where coefficient 10 is the conversion factor for volumetric processes (ml/s).

Normally, DO2 is 520-720 ml/(min-m2). This value is actually the DO2 index, since it is calculated per 1 m2 of body surface.

Oxygen consumption by tissues. Oxygen consumption by tissues (VO2) is the final stage of its transport. VO2 is determined by multiplying CO values ​​by the arteriovenous oxygen difference. In this case, one should use absolute values ​​not MOS, but SI, as a more accurate indicator. The arteriovenous difference is determined by subtracting the oxygen content of mixed venous blood (i.e., pulmonary artery) from the oxygen content of arterial blood:

VO2 = SI x (CaO2 – CVO2).

At normal SI values, the VO2 value ranges from 110 to 160 ml/(min-m2).

Oxygen utilization. Oxygen utilization coefficient (ORU2) is an indicator of absorbed oxygen from the capillary bed. CO2 is defined as the ratio of oxygen consumption to its delivery rate:

KUO2 can fluctuate within wide limits; at rest it is equal to 22-32%.

For a summary assessment of oxygen transport, you should use not only these, but also other indicators.

Great diagnostic importance is attached to the values ​​of PvO2 and SvO2. Normally, PVO2 in mixed venous blood is 33-53 mmHg. PvO2 level is below 30 mmHg. indicates a critical state of oxygen transport [Ryabov G.A., 1994]. The oxygen saturation of hemoglobin in mixed venous blood in a healthy person is 68-77%. It should be emphasized that the indicators SaO2 and SvO2 are more significant in assessing oxygen transport than PaO2 and PvO2. In itself, a decrease in PaO2, even below 60 mm Hg, does not indicate the development of anaerobic glycolysis. It all depends on the value of CO, hemoglobin concentration and capillary blood flow. An important indicator in assessing oxygen transport is the level of serum lactate (norm 0-2 mmol/l), especially in combination with pH, ​​PCO2 and BE.

Hypoxia does not always have a clear clinical picture. However Clinical signs hypoxia and oxygen transport data are decisive today. There is no single criterion for hypoxia. The clinical picture of hypoxia is characterized by the variability of many signs. In the initial stage, hypoxia is accompanied by inappropriate behavior of the patient, slowness of thinking and speech, and absence of cyanosis. Breathing rhythm disturbances, tachypnea, tachycardia, transient arterial hypertension. As hypoxia progresses, loss of consciousness, irregular breathing, and cyanosis may suddenly occur. Subsequently, in the absence of treatment, deep coma, apnea, vascular collapse and cardiac arrest.

Determining the type of hemodynamics is possible by measuring three important parameters: CI, OPSS and LVDP, which is normally 12-18 mm Hg. (Table 10.4).

Table 10.4.

In table 10.4 does not show all hemodynamic options. The advantage of these parameters is the possibility of their bloodless determination. The values ​​of SI, OPSS and LVDN can vary widely depending on the method of their determination. Most accurate results in critically ill patients are achieved using invasive research methods.

How to manage hemodynamics? First of all, it is necessary to become familiar with the laws and formulas that determine the interdependence of the most important hemodynamic parameters. You need to know that blood pressure depends on CO and TPSS. The formula defining this dependence can be presented as follows:

SBP = SV x OPSS,

Where SBP is mean arterial pressure, CO is cardiac output, TPVR is total peripheral vascular resistance. SV is calculated using the formula:

CO = HR x SV.

Normally, CO, or MOC, is 5-7 l/min. UO, i.e. the amount of blood ejected by the heart in one systole is 70-80 ml and depends on the volume of blood flowing to the heart and the contractility of the myocardium. This dependence is determined by the Frank-Starling law: the greater the filling of the heart chambers, the greater the stroke volume. This position is correct for a normally functioning healthy heart. It is clear that stroke volume can be regulated by creating adequate venous inflow, i.e. a volume of blood that is determined by the ability of the heart to work as a pump. Contractility of the heart muscle can be increased by administering positive inotropic agents. In this case, you must always keep in mind the state of preload. The amount of preload depends on the filling of the venous bed and venous tone. It is possible to reduce venous tone with vasodilators and thus reduce preload. Incorrect actions by the doctor can sharply increase preload (for example, as a result of excessive infusion therapy) and create unfavorable conditions for the functioning of the heart. If venous flow is reduced, the use of positive inotropic agents will not be justified.

So, the problem of reduced blood volume should be solved first of all by adequate infusion therapy. With relative hypovolemia associated with vasodilation and blood redistribution, treatment also begins with an increase in blood volume, while simultaneously prescribing drugs that increase venous tone. In patients with insufficient myocardial contractility, increased filling of the heart chambers is almost always observed, leading to an increase in ventricular filling pressure and pulmonary edema. In such clinical situations, infusion therapy is contraindicated; treatment consists of prescribing agents that reduce pre- and afterload. With anaphylaxis, a decrease in afterload leads to a decrease in blood pressure and determines the use of drugs that increase arteriolar tone.

CO and blood pressure can be significantly reduced with severe tachycardia or bradycardia. These changes can be associated with both cardiac (impaired conduction and automatism) and extracardiac factors (hypoxia, hypovolemia, the influence of increased vagal tone, etc.). If it is possible to find the cause of rhythm disturbances, then the etiological treatment of these disturbances will be most correct.

The most important condition normal operation the heart is the oxygen balance. The heart muscle, which performs a tremendous amount of work, has an extremely high level of oxygen consumption. The oxygen saturation of blood in the coronary sinus is 25%, i.e. much less than in mixed venous blood. How more work heart, the greater its need for oxygen and nutrients. It is not difficult to imagine that in non-ischemic healthy myocardium, oxygen consumption depends on heart rate, contractility, and resistance to contraction of cardiac fibers. The delivery of oxygen to the heart is ensured by the normal content of oxygen carriers, i.e. hemoglobin, PaO2, 2,3-DPG, general and coronary circulation. Any decrease in oxygen delivery or inability to consume oxygen (blockage of the coronary artery) immediately leads to dysfunction of the cardiovascular system. Coronary blood flow is directly proportional to the pressure and the radius of the vessel and inversely proportional to the viscosity of the blood and the length of the vessel (Hagen-Poiseuille law). This relationship is not linear because the coronary vessel is not a tube with laminar flow. Deterioration of coronary circulation and increased EDP of the left ventricle lead to a decrease in blood circulation in the subendocardial zone. Blood viscosity increases with a high concentration of hemoglobin, a high hematocrit number, and an increase in the concentration of proteins (especially fibrinogen) in the plasma. By reducing blood viscosity by prescribing crystalloid solutions and rheological agents, maintaining the hematocrit number at 30-40% and the concentration of plasma proteins slightly below normal, we create optimal conditions for coronary blood flow.

The metabolic needs of the heart are maximally satisfied under conditions of aerobic glycolysis. Normally, the energy needs of the myocardium are met mainly due to aerobic metabolism of glucose, at rest mainly due to carbohydrates and, only slightly, due to fatty acids. Hypoxia and acidosis, changes in the metabolism of potassium, magnesium and other electrolytes are accompanied by disruption of the normal metabolism of the heart muscle.

To control hemodynamics, monitoring of the cardiovascular system is necessary. In general intensive care units, preference should be given to the use of non-invasive methods (to the extent possible). Among the invasive indicators, PDLC is especially important. Hemodynamics is closely related to the function of the central nervous system, lungs, kidneys and other organs and systems.

TOPIC 6.

DETERMINATION OF THE MAIN INDICATORS OF HEMODYNAMICS AND RESPIRATION OF A PATIENT

Determination of basic hemodynamic parameters

The main indicators of hemodynamic status are pulse and blood pressure.

Pulse- These are jerky vibrations of the walls of the arteries as a result of the movement of blood and changes in pressure during the contraction of the heart. The characteristics of the pulse depend on the activity of the heart and the condition of the arteries, and also change with mental excitement, physical work, fluctuations in ambient temperature, under the influence of certain medications, and alcohol.

The simplest pulse method is its palpation, which is carried out where the arteries are located superficially. For diagnostic purposes, the pulse is determined in different arteries: carotid, temporal, femoral, subclavian, brachial, radial, popliteal, arteries of the dorsum of the foot. Most often, the pulse is determined by palpation on the radial artery between the styloid process of the radius and the tendon of the internal radial muscle (Fig. 6.1). First evaluate pulse symmetry, defining it simultaneously on both hands. The patient's hands should be at the level of the heart in a position midway between supination and pronation. The hand of the subject is taken in the area of ​​the wrist joint with the thumb from the outside and below, and with the pads of the fourth, middle and index finger- from above and, feeling the pulsating artery in the marked place, press it with moderate force inner surface radius bone. If the pulse is the same on both hands, the studies continue on one hand, paying attention to the rhythm of the pulse, its frequency, filling and tension. If there is a difference in the filling of the pulse (anomalies of development, narrowing or compression of one of the arteries), then its other properties are determined on the radial artery where the pulse waves are clearer.

Rice. 6.1. Pulse detection:

a) on both hands; b) on the temporal artery; c) on the carotid artery.

Pulse rhythm assessed by the regularity of pulse waves that occur one after another. If pulse waves appear at regular intervals, this indicates correct rhythm (rhythmic pulse); at different intervals between pulse waves, pulse rhythm irregular (irregular pulse). In a healthy person, the heart contracts rhythmically, with equal intervals between pulse waves, and so-called respiratory arrhythmia can also be observed - an increase in the pulse rate during inhalation and a slowdown during exhalation, which disappears when holding the breath.

Pulse rate – this is the number of pulse fluctuations per minute, which depends on the activity of the heart. In a healthy person, the number of pulse waves corresponds to the number of heart contractions and is 60-80 beats per minute. To determine the pulse rate per minute, it is assessed for 15 seconds and the resulting number is multiplied by 4. If the pulse is arrhythmic, then it is counted for 1 minute. A pulse rate over 90 beats per minute is called tachycardia, and the frequency is less than 60 beats per minute - bradycardia. Under physiological conditions, the pulse rate depends on many factors: age - the highest pulse rate in the first years of life; gender – women’s pulse is 5-10 beats higher than men’s; from physical work and mental state(fear, anger, pain) - the pulse accelerates, and during sleep the pulse slows down. Reason prolonged tachycardia There may be an increase in body temperature: An increase in body temperature of 1° C speeds up the pulse by 8-10 beats per minute. A particularly alarming symptom is a decrease in temperature with increasing tachycardia. Bradycardia observed in patients recovering from severe infectious diseases, brain diseases, and damage to the conduction system of the heart.

Pulse voltage - this is the degree of resistance of the artery to finger pressure. It is determined by the force with which it is necessary to press the artery wall to stop the pulsation. The voltage depends on the blood pressure in the artery, which is predetermined by the activity of the heart and the tone of the vascular wall. For diseases that are accompanied by increased arterial tone ( hypertonic disease, atherosclerosis), it is difficult to compress the vessel - such a pulse is called tense or hard. On the contrary, with a sharp drop in arterial tone (collapse) - pulse soft(light pressure on the artery is enough for the pulse to disappear).

Pulse filling - this is the degree of filling of the artery with blood during the systole of the heart, depending on the magnitude of cardiac output, that is, on the amount of blood that the heart throws into the vessels during its contraction.

Determination of pulse filling: initial position of the palpating hand (see above): with a proximally placed finger, press on the wall of the radial artery, and at this time, with a distally located finger, palpate and determine the nature of the artery (when it is not filled with blood); then the proximally located finger is raised, reducing the pressure on the vessel, and the distally located finger receives a palpation sensation at the moment of maximum filling of the artery with blood and determines the degree of filling of the artery full or empty pulse. With good filling we feel a high pulse wave under our fingers, and with poor filling we feel small pulse waves.

Pulse value . The magnitude of the pulse impulse combines the filling and tension of the pulse. It depends on the degree of expansion of the artery during systole and on its collapse at the time of diastole. This in turn depends on the filling of the pulse, the magnitude of the fluctuation in blood pressure and the elasticity of the vessel. With an increase in stroke volume of blood, a significant fluctuation in pressure in the artery and a decrease in the tone of the artery wall, the magnitude of the pulse wave increases, and the pulse becomes big or high. A decrease in stroke volume, the amplitude of blood pressure fluctuations, and an increase in the tone of the arterial wall reduce the magnitude of pulse waves - small pulse. In acute heart failure, shock, significant blood loss, the pulse value becomes so insignificant that it can barely be determined - this is filiform pulse.

Pulse shape (speed) is the rate of change in the volume of the palpated artery. With rapid stretching of the artery wall and its equally rapid collapse, it is determined fast pulse, and with a slow rise and slow fall of the pulse wave - slow pulse.

Pulse registration. The frequency, rhythm, filling and tension of the pulse are recorded daily in the medical history, and on the temperature sheet the pulse frequency is marked in red, followed by a curved line, similar to body temperature. It must be remembered that on the “P” (pulse) scale there are divisions of the pulse rate from 50 to 160 beats per minute. At heart rate values ​​from 50 to 100 beats, the “price” of one division is equal to 2, and at pulse rates above 100 beats per minute, the “price” of one division is equal to 4.

The most important for assessing the state of human health are arrhythmias, which occur mainly in diseases of the heart muscle or conduction system of the heart, less often as a result of a disorder of the vagus or sympathetic nerves. These types of arrhythmias include extrasystole and flickering arrhythmia. E extrasystolic arrhythmia, in which an additional systole (extrasystole) occurs between two successive contractions of the heart; the pause that occurs after the extrasystole (compensatory pause) is much longer than usual. Extrasystoles can be single or group. Attacks of tachycardia that last from a few seconds to several days are called paroxysmal tachycardia. Flickering arrhythmia characterized by a lack of regularity in the rhythm and filling of the pulse; small and large pulse waves arise chaotically, which indicates severe damage to the myocardium. Often with flickering arrhythmia it can develop heart rate deficiency in which not all heart contractions push a sufficient amount of blood into the arteries, and some contractions are so weak that the pulse wave does not reach the peripheral arteries and is not detected by palpation. Therefore, with flickering arrhythmia, it is imperative to first calculate the heart rate, and then the pulse rate in the radial arteries - the difference between these two indicators determines the pulse deficit.

Blood pressure (BP) is the force with which the blood exerts pressure on the walls of the arteries and on the underlying fluid. Blood pressure measurement is an important diagnostic method that reflects the strength of heart contraction, blood flow into the arterial system, resistance and elasticity of peripheral vessels. The level of blood pressure is influenced by the magnitude and speed of cardiac emissions, the frequency and rhythm of heart contractions, and the peripheral resistance of the walls of arterioles. The blood pressure that occurs in the arteries during ventricular systole and the maximum increase in pulse waves is called systolic, and the pressure that is maintained in the arteries during diastole as a result of a decrease in their tone is diastolic. The difference between systolic and diastolic pressure is called pulse pressure.

Currently, there are direct and indirect methods for measuring blood pressure. Direct methods are used in cardiac surgery. Among the methods in clinical practice, the generally accepted auscultatory method using a mercury, membrane or electronic sphygmomanometer, which is the most accurate. The sphygmomanometer consists of a 14 cm wide cuff that compresses the artery when air is pumped, a mercury column membrane manometer, and a rubber bulb that pumps air into the cuff. A phonendoscope is used to determine arterial sounds.

When studying blood pressure, you must adhere to the following requirements:

· 30 minutes before measuring blood pressure, do not smoke, do not drink alcohol, strong tea, coffee, do not take medications with caffeine, or adrenergic stimulants;

· do not exercise for 1 hour before measuring blood pressure;

· in the case of taking antihypertensive drugs, blood pressure measurements should be carried out after the end of the action of the drugs, before taking the next dose;

· during the initial study, measurements should be taken on both arms; subsequently, blood pressure should be measured where the pressure is higher; if the blood pressure level is the same in both arms, blood pressure measurements should be carried out on right hand.

Method of measuring blood pressure:

- research is carried out in a quiet room;

- the patient lies or sits, being in a comfortable, relaxed state (muscle tension in the limbs, abdominals leads to increased blood pressure);

- measurements are carried out first on the right hand, freeing the hand from tight clothing;

- If possible, the hand of the person being examined should be located at the level of his heart;

- if the shoulder diameter is less than 42 cm, a standard cuff is used, if the diameter is more than 42 cm, a special one is used;

- the cuff should be positioned 2-3 cm above the elbow bend;

- the cuff should fit tightly around the shoulder, but not lead to compression;

- the rubber tube that connects the cuff to the device and the balloon should be located lateral to the patient;

- when pumping air into the cuff, palpate the pulse on the radial artery and monitor the mercury column; after the pulse disappears, the pressure is increased by 20-30 mmHg. Art.;

- the rate of pressure reduction in the cuff is 2 mm Hg. per second (for arrhythmias, slow decompression is necessary, because the auscultatory interval is possible - 5-10 mm Hg);

- systolic blood pressure is determined when pulsation appears, diastolic blood pressure is determined when it disappears;

- the measurement result is determined by the nearest paired digit with an accuracy of 2 mm Hg, which is equal to one scale division;

- Blood pressure is measured twice with an interval of 2-3 minutes;

- The average of two measurements is taken as the blood pressure level in the subject.

The results of blood pressure measurements are recorded daily in the medical history in the form of a fraction: in the numerator - systolic blood pressure, in the denominator - diastolic blood pressure, and are also recorded in the temperature sheet (scale "BP") in the form of columns: systolic blood pressure is marked with a red column, and diastolic blood pressure - blue (“the price” of one division on the “BP” scale is 5 mm Hg).

Normal blood pressure numbers range from 100/60 to 139/89 mm Hg. Depending on various physiological processes (fatigue, excitement, food intake, etc.), blood pressure levels may change. Its daily fluctuations are within 10-20 mmHg. In the morning the pressure is lower than in the evening. With age, blood pressure increases slightly. Increases in blood pressure above normal levels (>140/90 mm Hg) are called arterial hypertension, and the decrease – arterial hypotension. The classification of arterial hypertension by blood pressure level is presented in Table 6.1.

Table 6.1

Classification of arterial hypertension according to blood pressure level

First aid for patients with increased or decreased blood pressure. A sharp increase in blood pressure may result from mental trauma or nervous strain, when using certain antihypertensive drugs in patients with arterial hypertension. The most constant symptom is a sharp headache, combined with dizziness, tinnitus, often with nausea and vomiting, and nosebleeds. The intensity of the pain is such that it is difficult for the patient to withstand minor noise, talk, or turn his head.

First aid for high blood pressure :

1) measure blood pressure and determine the main parameters of the pulse;

2) call a doctor;

3) put the patient in bed with the head of the bed raised and provide him with complete physical and mental rest;

4) provide access fresh air(can be inhaled oxygen);

5) place mustard plasters on the back of the head and calf muscles;

6) make hot or mustard foot baths, warm hand baths, cold compress to the head;

7) prepare the necessary medications.

After a crisis, change the patient's underwear; explain to him that after antihypertensive therapy he should lie down for 2-3 hours to prevent collapse. Measure blood pressure for 2-3 hours.

A decrease in blood pressure is an important diagnostic sign acute vascular insufficiency, which has the following forms: fainting, collapse, shock .

Fainting– sudden short-term loss of consciousness caused by cerebral ischemia. Sometimes fainting is preceded by a semi-conscious state - sudden weakness, dizziness, darkening of the eyes, ringing in the ears, nausea, then the patient loses consciousness and falls.

At collapse and shock there is a pronounced and prolonged decrease in blood pressure, tachycardia, and peripheral signs of circulatory disorders. The cause of collapse may be bleeding, diseases of the cardiovascular system, infectious diseases (foodborne illness, lobar pneumonia). Collapse poses an immediate threat to the patient's life and requires immediate treatment.

Collapse Clinic: sudden onset, complaints of severe weakness and chilliness, Hippocrates face (thin face, sunken eyes, dry skin, pale earthy color, cyanosis), low position of the patient in bed, indifference to the environment; extremities are cold to the touch with a cyanotic tint to the skin (peripheral sign of collapse), breathing is accelerated, superficial; the pulse is very frequent, weak filling and tension (“thread-like”), veins collapse, blood pressure is sharply reduced.

First aid for a patient with low blood pressure . Since a decrease in vascular tone and a decrease in venous return to the heart play an important role in the mechanism of collapse development, immediate measures should be aimed primarily at increasing venous and arterial tone and increasing the volume of fluid in the bloodstream. First of all, the patient is placed horizontally, without a high pillow (sometimes with his legs raised); vascular drugs are administered subcutaneously, which excite the vasomotor and respiratory centers (cordiamin, mesatone, strychnine).

A decrease in blood pressure is an important diagnostic sign of acute vascular insufficiency (fainting, collapse). Fainting – short-term loss of consciousness as a result of anemia of the brain. The causes of fainting can be anemia, heart defects, heart block, sudden changes in body position, staying in a position, standing for a long time, negative emotions, severe pain, fasting.

The main clinical symptoms of fainting: pale and moist skin, rare shallow breathing, decreased blood pressure, weak pulse and tension, pupils are moderately dilated, actively reacts to light.

First aid to a patient : 1) the patient is laid horizontally with his legs raised at 45°; 2) provide access to fresh air; 3) free the neck and chest from compressive clothing; 4) spray your face cold water; 5) give a swab moistened with ammonia solution to sniff; 6) pat on the cheeks; 7) rub the body with a piece of cloth.

Collapse – acute vascular insufficiency associated with a pronounced and prolonged decrease in vascular tone and a decrease in circulating blood volume. The causes of collapse may be blood loss, myocardial infarction, pulmonary embolism, infectious and acute inflammatory diseases, trauma, and drug allergies.

Main clinical symptoms: sudden onset, impaired consciousness, Hippocratic face (pale earthy color with pointed features), indifference to the environment, decreased body temperature; pallor of the skin, limbs cold to the touch with a cyanotic tint to the skin (peripheral sign of collapse), shallow rapid breathing; the pulse is very frequent, weak filling and tension (“thread-like”), low blood pressure.

First aid for a patient with low blood pressure : 1) eliminate the causes of collapse (stop bleeding, remove poison from the body); 2) warm the patient; 3) give oxygen to breathe; 4) quickly transport the patient in a horizontal position to the appropriate department of the hospital; 5) medications are administered that increase blood pressure (adrenaline, mezaton, glucocorticoids).

Bleeding and basic rules for stopping it

Bleeding - this is the flow of blood from its bed into the tissues and cavities of the body or out. Normally, the amount of blood in a person is 7% or 1/13 of body weight, of which 80% of the blood circulates in the cardiovascular system, and 20% is in the parenchymal organs (liver, spleen, Bone marrow). A decrease in circulating blood volume (CBV) by 30-50% leads to the development of severe disorders in the body, which are called critical condition. Losing half or more of total number blood is lethal. Blood loss is especially difficult for children and the elderly.

The cause of bleeding is: a violation of the integrity of the walls of blood vessels as a result of diseases, injuries or damage, leading to the development of hypovolemia and a complex set of hemodynamic disorders. Depending on the principle underlying the classification, arterial, venous, capillary and parenchymal bleeding are distinguished, differing in the characteristics of the clinical picture and methods of stopping.

With external arterial bleeding blood flows out in a stream, the height of which changes with each pulse wave, the blood is bright red. Venous bleeding characterized by a continuous flow of dark blood; when large veins are injured with high intravenous pressure, blood may also flow out in a trickle, but it does not pulsate. At capillary and parenchymal bleeding, the entire wound surface, small vessels and capillaries bleed. If damaged parenchymal organs More often mixed bleeding occurs, which does not stop for a long time and often leads to acute anemia.

If bleeding occurs, to save the life of the victim, it is necessary to stop the bleeding and replace the blood loss. There are temporary and final stops of bleeding. A temporary stop is carried out by medical workers, the victim himself or eyewitnesses of the accident.

Main types of bleeding control : temporary - tight bandage, finger pressure, tight wound tamponade, maximum flexion of the limbs, circular tugging with a rubber band; final - ligation of the vessel in the wound or outside it in the operating room (Fig. 6.2).

d Fig. 6.2. Types of bleeding control:

a, b) finger pressure of the artery; c) circular constriction of the artery; d) applying a tourniquet; d)

maximum flexion of the limbs.

Tight bandage - a method of temporarily stopping bleeding, which is used for minor bleeding from soft tissues with a bone base. The skin around the wound is treated with a 5% iodine solution, the pad of an individual dressing bag is placed on the wound and firmly fixed with a bandage, adhering to the general rules of bandaging. The limbs are fixed in the position in which they will remain after applying the bandage: the arm is usually bent at a right angle at the elbow joint, and the leg at the knee; the foot is fixed in a position at right angles to the shin. A tight bandage is usually circular - all circles of the bandage are applied in layers to the same place. If there is no bandage or dressing bag, you can use clean ironed fabric, scraps of sheets, towels, etc.

Finger pressure on the artery- a method of emergency short-term stopping of bleeding, which is used only at certain anatomical points where the vessels are located superficially and close to the bones to which they can be pressed (Fig. 6.2 a). If the lumen of the vessel is completely blocked, the pulsation of the artery in the underlying area stops and the bleeding stops. Pressing of the vessels can be done with several fingers of one hand, the thumbs of both hands, the palm or a fist. Long-term pressure of the vessels is carried out with the thumbs of both hands: place one finger on the second and take turns using the pressure of the fingers on the vessels.

In case of wounds of the extremities, the vessels are pressed above the wound, in case of damage to the vessels of the neck - below. Bleeding from head and neck wounds is stopped by applying pressure common carotid artery in the middle of the posterior edge of the sternocleidomastoid muscle to the transverse processes of the cervical vertebrae, in particular to the tubercle of the sixth cervical vertebra - C VI (Fig. 6.2b).

External jaw the artery is pressed to the lower edge of the lower jaw at the border of its posterior and middle third. The temporal artery is pressed against the temple. Bleeding in upper section the shoulders are stopped by pressing subclavian artery up to 1 rib. To do this, the victim’s arm is lowered down and pulled back, after which the artery is pressed behind the collarbone.

Rice. 6.3. Places for digital pressure on the arteries to stop arterial bleeding:

a) diagram of the main human vessels; b) internal carotid artery; external carotid artery; c) supraclavicular artery; e) submandibular artery; e) temporal artery; g, h) brachial artery; i) axillary artery.

Axillary artery pressed in the axillary fossa to the head of the humerus (Fig. 6.3 i) When bleeding from the shoulder and forearm, the brachial artery is pressed with fingers to the humerus near the inner edge of the biceps muscle. Radial artery pressed against the radius where the pulse is detected, ulna- to the ulna. For bleeding on the thigh and lower leg femoral artery pressed in the middle of the inguinal ligament and below it to the horizontal branch of the pubic bone. This vessel can also be fixed between the superior anterior spine ilium and pubic symphysis. popliteal artery pressed to the middle of the popliteal fossa, dorsal artery– to its back surface in the middle between the outer and inner bones (below the knee joint). When wounded abdominal aorta Temporary stopping of bleeding can be achieved by firmly pressing the abdominal aorta to the spinal column with a fist (to the left of the navel).

Tight wound tamponade- a method of temporarily stopping bleeding, used for deep bleeding wounds when digital pressure is impossible. Use tweezers to tightly fill the wound with a sterile gauze swab or apply a special hemostatic sponge to the wound, which is pressed with a gauze swab. Then a tight compressive bandage is applied, to which an ice bag is placed in the wound area.

Rice. 6.4. Stopping bleeding by maximally flexing the limbs:

a) scheme to stop bleeding, b) compression subclavian artery, c, d) brachial artery, e) femoral artery, f) arterial columns of the thigh and foot.

Maximum limb flexion- a method of temporarily stopping bleeding used when bleeding from wounds near the base of the limb, which is fixed in a state of maximum flexion in order to compress great vessels(Fig. 6.4).

To increase pressure on the vessel under the knee or in the armpit, it is necessary to place a thick cloth roller. If the subclavian artery is injured or there is bleeding from a wound of the upper limb, the subclavian or brachial artery is clamped. For compression subclavian artery The arms bent at the elbows are pulled back and secured in this position with several turns of the bandage (Fig. 6.4 b). Brachial artery and its branch is blocked by maximally bending the arm at the elbow joint and fixing it in this position. This technique can be used for arterial bleeding from the vessels of the forearm and hand (Fig. 6.4 c, d).

When bleeding from the femur arteries the leg is bent as far as possible hip joint and bandaged to the body (Fig. 6.4 f). When bleeding from arterial trunks of the lower leg and foot squeeze popliteal artery(Fig. 6.4 d). To do this, insert a tightly twisted roller into the popliteal fossa, then bend the leg at the knee joint as much as possible and fix it in this position with several turns of a bandage or a belt.

Circular drag- the most common and most reliable method of temporarily stopping bleeding on the extremities, which is performed using a standard rubber tourniquet, a rubber tube or an improvised twist tourniquet (Fig. 6.5).

The hemostatic tourniquet is a rubber band 125 cm long and 3-4 mm wide. There is a hook at one end of the ribbon and a metal chain at the other.

Rice. 6.5. The procedure for stopping bleeding by circular tugging:

a, b) application of an improvised tourniquet-twist, c) fixation of the tourniquet-twist.

The tourniquet is applied to the shoulder and thigh, with the exception of: the upper third of the shoulder (the radial nerve can be injured), the lower third of the thigh (compression of the femoral artery is accompanied by damage to soft tissues), the lower thirds of the forearm and shins (the arteries pass between the bones and cannot be compressed, except In addition, there are no muscles in these places and skin necrosis may develop under the tourniquet) (Fig. 6.6).

Rice. 6.6. Application of a hemostatic tourniquet.

Rules for applying a hemostatic tourniquet :

· The tourniquet is applied over clothing or on a flat pad, without folds, so as not to pinch the skin between its turns, as close to the wound as possible.

· With one hand, grab the end of the tourniquet, with the other - its middle and, stretching it strongly, circle it 2-3 times around the limb; the free ends of the tourniquet are tied with a knot or secured with a hook and chain.

· A note is attached to the tourniquet or to the victim’s clothing indicating the time it was applied.

· If the tourniquet is applied correctly, bleeding from the wound stops, the limb becomes pale and cold, and the peripheral pulse is not detected.

· In the cold season, after applying a tourniquet, the limb should be wrapped in a warm blanket to prevent frostbite.

· After applying a tourniquet, the limb is immobilized transport bus, administer painkillers and hospitalize the patient.

· The tourniquet can be left on the limb for no longer than 1.5 hours, and in the cold season - 30 minutes.

· If the bleeding has not stopped during this time, the tourniquet should be loosened for a few minutes and then tightened again. In general, a tourniquet can be applied to a limb for no more than 2 hours.

· If the tourniquet needs to be held longer, it must be removed and applied 1.5-2 cm higher. During relaxation of the tourniquet, finger pressure is applied to the main vessel.

Complications that are predetermined by an incorrectly applied tourniquet: impaired motor function of the limb as a result of injury to the nerve trunks (paralysis), venous congestion in the limb, increased venous bleeding, tissue necrosis, development of gangrene. It is a mistake to apply a tourniquet for venous or capillary bleeding, when a tight bandage can be used.

Determination of basic breathing indicators

When caring for patients with respiratory diseases, it is necessary to monitor the frequency, depth and rhythm of breathing. Normally, a person’s breathing is silent and invisible to others. A person usually breathes through the nose with the mouth closed. In an adult at rest, the respiratory rate is 16-20 per minute, with inhalation being 2 times shorter than exhalation. Breathing is characterized by frequency, rhythm, depth and periodicity.

Breathing rate . The number of respiratory movements (RR) is determined by counting the movements of the chest or abdominal wall for 1 minute. The counting is carried out unnoticed by the patient, holding his hands, as for counting the pulse. The results obtained are recorded daily on a temperature sheet using a blue pencil in the form of a graph of respiration rate. Respiration rate depends on age, gender, position. In an adult at rest, it is 16-20 respiratory movements per minute. Women have a slightly higher NPV than men. In infants, the number of respiratory movements reaches 40-45 per minute, with age it decreases and by the age of 20 it reaches the frequency of an adult. In a standing position, the respiratory rate is higher (18-20) than in a lying position (12-14). Athletes breathe at 8-10 breaths per minute. Changes in breathing frequency: rapid - tachypnea and rare - bradypnea.

Tachypnea– frequent breathing due to dysfunction of the respiratory center. Under physiological conditions (excitement, physical activity, eating), tachypnea is short-term and quickly passes after the cessation of the provoking factor.

Pathological tachypnea can be caused by the following reasons:

§ damage to the lungs, accompanied by: a decrease in their respiratory surface; limitation of lung excursion as a result of decreased elasticity of lung tissue; disturbance of gas exchange in the alveoli (accumulation of carbon dioxide in the blood);

§ damage to the bronchi, accompanied by difficulty in accessing air to the alveoli and partial or complete blockage of their lumen;

§ defeat respiratory muscles and pleura, accompanied by difficult contraction of the intercostal muscles and diaphragm as a result of sharp pain, paralysis of the diaphragm, increased intra-abdominal pressure, which is one of the reasons for the decrease in respiratory excursion of the lungs;

§ damage to the central nervous system due to its intoxication and disruption of the respiratory center.

§ pathology of the cardiovascular system and hematopoietic organs, accompanied by the development of hypoxemia.

Most often, increased breathing is caused by a combination of several reasons. For example, with lobar pneumonia, the causes of increased breathing are a decrease in the respiratory surface of the lungs (accumulation of exudate in the alveoli, swelling of the alveolar walls), pain in the chest when breathing (as a result of the development of concomitant pleurisy), intoxication of the central nervous system (toxins circulating in the blood).

Thus, increased breathing may be caused not only by pathology of the respiratory system, but also by disorders of the cardiovascular and nervous systems. For the differential diagnosis of tachypnea, the ratio of respiratory rate (RR) and heart rate (HR) is used. In healthy individuals, the respiratory rate/heart rate ratio is 1:4, that is, the respiratory rate is ahead of the respiratory rate; for respiratory diseases, the respiratory rate/heart rate ratio is 4:2, that is, the respiratory rate is ahead of the heart rate; with high fever, on the contrary, the heart rate is much ahead of the respiratory rate.

Bradypnea– decreased breathing due to decreased excitability of the respiratory center. Physiological bradypnea can be observed during sleep and hypnosis.

Pathologically, a decrease in breathing occurs when the respiratory center is depressed and its excitability decreases, caused by a number of reasons, primarily by damage to the central nervous system: increased intracranial pressure (brain tumor, adhesions, hernia); hemodynamic disturbances and the development of hypoxia (stroke, cerebral edema, agony); exo- and endointoxication (meningitis, uremia, hepatic and diabetic coma); use of anesthetics and other dosage forms (morphine poisoning).

Severe bradypnea is observed in chronic obstructive pulmonary diseases (chronic obstructive bronchitis, pulmonary emphysema, bronchial asthma). These patients experience forced (increased) exhalation with the participation of auxiliary muscles of the neck and shoulder girdle. A type of slow breathing is stridor breathing– rare loud breathing caused by sharp compression of the larynx (tumor, enlarged goiter, laryngeal edema, less often – aortic aneurysm).

Depth of breathing. The depth of breathing is determined by the volume of air inhaled and exhaled at rest. In a healthy person, under physiological conditions, the volume of respiratory air is 500 ml. Depending on the change in the depth of respiratory movements, shallow and deep breathing are distinguished.

Shallow breathing (hypopnea) is observed with a pathological increase in breathing due to shortening of both phases of breathing (inhalation and exhalation). Deep breathing (hyperpnea) is often combined with pathological slow breathing. For example, " Kussmaul's big breath" or “air hunger” - rare, deep, loud breathing due to the development metabolic acidosis followed by irritation of the respiratory center by acidic products; observed in patients with diabetic, uremic and hepatic coma.

Breathing rhythm . The breathing of a healthy person is rhythmic, of the same depth, duration and alternation of inhalation and exhalation phases. When the central nervous system is damaged, breathing becomes arrhythmic: individual respiratory movements of different depths occur more often, sometimes less often. Sometimes, with arrhythmic breathing, after a certain number of respiratory movements, an extended pause or short-term breath holding (apnea) appears. This kind of breathing is called periodic. It includes the following pathological types of breathing: Cheyne-Stokes breathing, wave-like Grokk breathing and Biot breathing.

Cheyne-Stokes breathing– periodic pathological breathing, characterized by a long (from several seconds to 1 minute) respiratory pause (apnea), after which silent shallow breathing quickly increases in depth, becomes loud and reaches a maximum at 5-7 breaths, then decreases in the same breathing sequence and ends with the next short pause (apnea). During a pause, the patient is poorly oriented in the environment or may completely lose consciousness, which returns when breathing movements resume. Cheyne-Stokes breathing is caused by a decrease in the excitability of the respiratory center, acute or chronic cerebral circulatory failure, brain hypoxia, severe intoxication and is a prognostically unfavorable sign. Often manifests itself in sleep in elderly people with severe cerebral atherosclerosis, in patients with chronic failure cerebral circulation, chronic renal failure(uremia), taking drugs (morphine).

"Wave-shaped breathing" by Grokka or dissociated breathing, is characterized by a wave-like change in the depth of breathing and differs from Cheyne-Stokes breathing in the absence of periods of apnea. Grokk's breathing is caused by damage to the respiratory coordination center and is caused by chronic cerebrovascular accident. More often observed with brain abscess, meningitis, brain tumor.

Breath Biota– periodic pathological breathing, characterized by rhythmic but deep respiratory movements, which alternate at regular intervals with a long (from several seconds to half a minute) respiratory pause. Biot's breathing is caused by a deep disorder of cerebral circulation and is observed in patients with meningitis and in agony.

Thus, disturbances in frequency, rhythm, depth, or the appearance of pathological forms of breathing (Cheyne-Stokes, Biot, Grock, Kussmaul) identified during a static examination are characteristic symptoms of damage to the respiratory system.

Dyspnea – a feeling of lack of air, accompanied by impaired breathing in frequency, rhythm and depth, which is based on the development of tissue hypoxia.

There are physiological and pathological shortness of breath. Physiological shortness of breath is a compensatory reaction of the body by the respiratory system in response to significant physical or emotional stress. Physiological shortness of breath manifests itself in the form of short, frequent and deep breathing, resolves spontaneously with rest within 3-5 minutes and is not accompanied by unpleasant sensations.

Pathological shortness of breath– a more persistent violation of the frequency, rhythm and depth of breathing, accompanied by unpleasant sensations (compression in the chest, a feeling of lack of air) and caused by damage to various organs and systems, primarily the respiratory and cardiovascular.

The main causes of pathological shortness of breath:

I. Disturbance in the process of blood oxygenation in the lungs is caused by: a) disruption of the airway patency; entry of a foreign object into the respiratory tract; chest injuries; congenital pathologies respiratory and chest organs; b) damage to the lung parenchyma; c) changes in the pleural cavity, with limited respiratory excursion and compression of the lung tissue; d) changes in the tissues of the chest, limiting its mobility and ventilation of the lungs.

II. Disorders of gas transport caused by damage to the cardiovascular system (heart defects, cardiosclerosis, myocarditis, arterial hypertension) and hematopoietic organs (anemia, leukemia).

III. Metabolic disorder accompanied by an increased need for oxygen in the body: endocrine diseases(thyrotoxicosis, diabetes mellitus, Itsenko-Cushing's disease); malignant neoplasms.

IV. Violation of the regulatory mechanisms of breathing (disease of the central nervous and endocrine systems).

V. Changes in the composition of inhaled air (humidity, pressure, temperature, pollution, occupational hazards and poisoning with toxic substances and poisons).

Pathological shortness of breath distinguished: in relation to the patient (subjective, objective, mixed); by time of appearance (constant, prolonged, paroxysmal or paroxysmal); according to the structure of the respiratory cycle (inspiratory, expiratory, mixed).

Clinically, shortness of breath can be manifested by subjective and objective signs; from here shortness of breath is distinguished: subjective, objective and mixed. Subjective shortness of breath– breathing disorder, manifested by a subjective feeling of compression in the chest, lack of air, difficulty inhaling or exhaling; characteristic of hysteria, neurasthenia. Objective shortness of breath– breathing disorder, manifested by intermittent speech (the patient gasps for air when speaking), tachypnea (respiratory rate more than 30 per minute), disturbance of the breathing rhythm, participation of auxiliary muscles in breathing (tension of the cervical and trapezius muscles), the appearance of cyanosis; observed in diseases of the lungs, heart, central nervous system, and muscular system.

Depending on the structure of the respiratory cycle and the characteristics of its phases, three types of shortness of breath are distinguished: inspiratory, expiratory and mixed. Inspiratory dyspnea– breathing disorder with difficult (prolonged) inspiration. A type of inspiratory dyspnea can be classified as stridor breathing– loud breathing with difficulty inhaling, accompanied by whistling (with severe narrowing of the upper respiratory tract and trachea); observed when a foreign object enters the respiratory tract or is compressed from the outside by a tumor, scars, or enlarged lymph nodes. Expiratory dyspnea– breathing disorder with difficult (prolonged) exhalation, caused by impaired passage of small bronchi and bronchioles (bronchial asthma, chronic obstructive bronchitis, bronchiolitis). The mechanism of expiratory dyspnea is based on the early expiratory closure (collapse) of small bronchi (bronchial collapse) in response to an increase in the linear velocity of air entering and a decrease in its lateral pressure, which leads to bronchospasm (Bernoulli phenomenon), as well as mucosal edema and congestion in the enlightenment of the bronchi of heavy secretions, which are difficult to separate, a decrease in the elastic properties of the bronchial wall. Mixed shortness of breath– breathing disorder in the form of simultaneous difficulty in inhaling and exhaling; more often observed with a decrease in the respiratory surface of the lungs (pneumonia, hydro- and pneumothorax, pulmonary atelectasis, pulmonary infarction), less often with a high position of the diaphragm, which limits the excursion of the lungs (pregnancy, ascites, flatulence, massive tumors of the abdominal cavity, including the liver and spleen ), as well as with a combination of heart and lung damage.

According to the frequency and time of occurrence, they distinguish constant, periodic and paroxysmal (paroxysmal) shortness of breath. Constant shortness of breath persists at rest and intensifies with the least physical exertion; observed when severe forms respiratory and heart failure, emphysema, pneumosclerosis, heart defects . Periodic(long-term) shortness of breath can develop in the midst of severe illnesses (lobar pneumonia, exudative pleurisy, obstructive bronchitis, pneumo- and hydrothorax, myocarditis, pericarditis) and disappear upon recovery. Paroxysmal shortness of breath, which suddenly appeared in the form of an attack (asthma), is observed in bronchial and cardiac asthma.

Choking (asthma)– a sudden attack of shortness of breath, caused by a sharp disruption of the respiratory center, is an objective sign of acute respiratory failure as a result of a sudden spasm, swelling of the bronchial mucosa or entry of a foreign object. Basic and characteristic clinical manifestation suffocation is its sudden occurrence, intensity; a feeling of lack of air, a rapid increase in objective signs of respiratory failure - diffuse cyanosis, swelling of the neck veins, tachypnea more than 30 per minute; forced position - orthopnea with arm support (bronchial asthma) and without arm support (cardiac asthma).

Clinical characteristics of the attack bronchial asthma: begins suddenly during the day, but more often at night, the attack is often preceded by precursors (nasal congestion, sneezing, watery discharge from the nose, dry cough, drowsiness, yawning, feeling of tightness in the chest and acute shortage air). The patient is unable to push out the air that fills the chest and, in order to enhance exhalation, he sits on the bed and rests his hands on it, thus including in the act of breathing not only the respiratory muscles, but also the auxiliary muscles of the shoulder girdle and chest. Some patients are excited, run up to the window and open it wide, stand near it, leaning their hands on the table or window sill. Characteristic is rare breathing with prolonged noisy exhalation, a lot of dry wheezing. The chest seems to freeze in the position of maximum inspiration with raised ribs and “exploding” intercostal spaces. Often an attack of suffocation is accompanied by a cough with the release of a small amount of viscous, difficult to separate glassy sputum, after which the patient’s condition improves.

First aid for suffocation : 1) sit the patient down or help him take a half-sitting position; 2) free the chest from tight clothing; 3) ensure the flow of fresh air and oxygen; 4) apply a heating pad to lower limbs. 5) inform the doctor and follow all his instructions after emergency care.

Cough– a reflexive protective act in the form of a jerky forced sonorous exhalation in response to irritation of the receptors of the respiratory tract and pleura, is important symptom damage to the respiratory system. In heart failure, the occurrence of cough is caused by congestion in the lungs (congestive bronchitis, hypostatic pneumonia). The coughing mechanism is a deep inhalation and a rapid, forceful exhalation with the glottis closed at the beginning of exhalation, the sound effect being compared to an “air shot through a narrowed glottis.”

According to the rhythm, cough is divided into: constant, periodic, paroxysmal cough. Constant cough in the form of separate cough impulses (coughing), observed in chronic laryngitis, tracheitis, bronchitis, the initial form of tuberculosis, circulatory failure, sometimes with neuroses, often in smokers in the morning. Periodic (bronchopulmonary) cough in the form of coughing impulses following one another, repeated at certain intervals; observed in chronic diseases (during exacerbation): bronchitis, pulmonary tuberculosis. Paroxysmal cough with coughing impulses quickly following each other, which are interrupted by a loud exhalation; observed when a foreign object enters the respiratory tract, whooping cough, cavities, or damage to the bronchial lymph nodes.

Coughs can be classified according to their timbre: cautious, barking, hoarse, silent. A mild, short cough that accompanied by a painful grimace, observed with dry pleurisy, the onset of lobar pneumonia. Barking cough– loud, abrupt, dry, caused by swelling of predominantly false or simultaneously false and true vocal cords; observed with laryngitis, as well as compression of the trachea (tumor, goiter), hysteria. Hoarse cough caused by damage to the true vocal cords; observed with laryngitis. Silent cough caused by ulcer and destruction of the vocal cords (cancer, tuberculosis, syphilis of the larynx) or paralysis of their muscles, leading to insufficient closure of the glottis. Cough also becomes silent with severe general weakness in patients with severe debilitating diseases.

Coughs are classified according to their nature: non-productive (dry, without sputum) and productive (wet, with sputum). Dry (non-productive) cough without sputum production; occurs in so-called dry bronchitis, early stages of pneumonia (especially viral), pulmonary infarction, which begins with an attack of bronchial asthma, pleurisy, embolism of small branches of the pulmonary artery. Wet (productive)cough accompanied by sputum production; characteristic of acute stage bacterial or viral infection (bronchitis, pneumonia, tracheitis); cavity formations in the lungs (bronchiectasis, abscess, cancer in the decay stage, cavernous form of tuberculosis). The quantity, character, color and smell of sputum are of important diagnostic value for diseases of the bronchopulmonary system.

Coughs are classified according to the time of appearance: morning, evening, night. Morning cough– “cough when washing” (5-7 a.m.) is caused by the accumulation of sputum overnight and difficulty in clearing it; observed in chronic inflammatory processes of the upper respiratory tract (nasopharynx, paranasal sinuses, pharynx, larynx, trachea); in patients with cavity formations in the lungs, in alcoholics and smokers. Evening cough caused by vagotonia in the evening hours; observed in bronchitis and pneumonia. Night cough associated with nocturnal vagotonia; observed with enlarged bronchopulmonary lymph nodes and pulmonary tuberculosis.

First aid for cough: 1) create a comfortable position for the patient (sitting or half-sitting), which reduces coughing; 2) give warm drink, preferably milk with sodium bicarbonate or mineral water such as Borzhom; 3) cover warmly to prevent hypothermia; 4) ensure a flow of fresh air; 5) if the cough is accompanied by the release of a significant amount of sputum, provide the patient with a drainage position for several hours a day to facilitate better discharge of sputum; 6) teach the patient to properly handle sputum, collect sputum only in a spittoon or a jar with a tight lid.

Control questions

1. How to determine the pulse on the radial artery?
2. Describe the basic properties of the pulse.
3. Rules and methods for determining blood pressure.
4. Standard indicators blood pressure.
5. First aid for high blood pressure.
6. First aid for a patient with low blood pressure.
7. Name the main types of bleeding control
8. Rules for applying a hemostatic tourniquet
9. How to determine the frequency of respiratory movements?
10. What types of shortness of breath do you know? Their diagnostic value.
11. Name the pathological types of breathing, their characteristics and diagnostic significance.
12. First aid for suffocation.

Study of primary indicators.

– Pulse counting;
– Blood pressure measurement: diastolic, systolic, pulse, average dynamic, minute blood volume, peripheral resistance;

Study of initial and final indicators during test actions:


– Ruffier's test - dynamic load tolerance; endurance coefficient);
Vegetative status assessment:



–
–
Calculated index of the adaptive potential of the cardiovascular system.
– Index R.M. Baevsky et al., 1987.

DESCRIPTION OF METHODS

STUDY OF PRIMARY INDICATORS.
Assessment of the degree of tension of regulatory mechanisms:
– Pulse counting;
– Blood pressure measurement: diastolic, systolic, pulse, average dynamic, minute blood volume, peripheral resistance;
Pulse counting. Normal indicator: 60 – 80 beats. per minute
Diastolic or minimum pressure (MP).
Its height is mainly determined by the degree of patency of the precapillaries, heart rate and the degree of elasticity of the blood vessels. The greater the resistance of the precapillaries, the lower the elastic resistance of large vessels, and the greater the heart rate, the higher the DD. Normally, in a healthy person, DD is 60-80 mm Hg. Art. After loads and various types of influences, DD does not change or decreases slightly (up to 10 mm Hg). A sharp decrease in the level of diastolic pressure during work or, conversely, its increase and a slow (more than 2 minutes) return to initial values ​​is regarded as an unfavorable symptom. Normal indicator: 60 – 89 mm. rt. Art.
Systolic or maximum pressure (MP).
This is the entire energy reserve that a blood stream actually possesses in a given area of ​​the vascular bed. The lability of systolic pressure depends on the contractile function of the myocardium, the systolic volume of the heart, the state of elasticity of the vascular wall, hemodynamic shock and heart rate. Normally, in a healthy person, DM ranges from 100 to 120 mm Hg. Art. With load, DM increases by 20-80 mmHg. Art., and after its cessation returns to the original level within 2-3 minutes. Slow recovery of initial DM values ​​is considered as evidence of insufficiency of the cardiovascular system. Normal indicator: 110-139 mm. rt. Art.
When assessing changes in systolic pressure under the influence of load, the resulting shifts in maximum pressure and heart rate are compared with the same indicators at rest:
(1)

where SDr, heart rate is systolic pressure and heart rate during work;
MDP, HRSP - the same indicators at rest.
This comparison allows us to characterize the state of cardiovascular regulation. Normally, it is carried out due to changes in pressure (1 greater than 2); in heart failure, regulation occurs due to an increase in heart rate (2 greater than 1).
Pulse pressure (PP).
Normally, in a healthy person it is about 25-30% of the minimum pressure. Mechanocardiography allows you to determine the true value of PP, equal to the difference between the lateral and minimum pressure. When determining PP using the Riva-Rocci apparatus, it turns out to be somewhat overestimated, since in this case its value is calculated by subtracting the minimum value from the maximum pressure (PD = SD - PP).
Mean dynamic pressure (SDP).
It is an indicator of the consistency of the regulation of cardiac output and peripheral resistance. In combination with other parameters, it makes it possible to determine the state of the precapillary bed. In cases where the determination of blood pressure is carried out according to N. S. Korotkov, the ADD can be calculated using the formulas:
(1)

SDD = DD + 0.42 x PD.
The value of the SDD calculated using formula (2) is slightly higher. Normal indicator: 75-85 mm. rt. st.
Minute blood volume (MO).
This is the amount of blood pumped by the heart per minute. MO is used to judge the mechanical function of the myocardium, which reflects the state of the circulatory system. The value of MO depends on age, gender, body weight, ambient temperature, and intensity of physical activity. Normal value: 3.5 – 5.0 l.
The MO norm for the resting state has a fairly wide range and significantly depends on the determination method:
The simplest way to determine the MO, which allows you to roughly determine its value, is to determine the MO using the Starr formula:
CO = 90.97 + 0.54 x PD – 0.57 x DD – 0.61V;
MO = CO-HR
where CO is the systolic blood volume, Ml; PP - pulse pressure, mm Hg. st; DD - minimum pressure, mm Hg. Art.; B - age, in years.
Liljetrand and Zander proposed a formula for calculating MO, based on the calculation of the so-called reduced pressure. To do this, first determine the SDD using the formula:

hence MO = RAD x HR.
In order to possibly more objectively assess the observed changes in MO, you can also calculate the proper minute volume: DMO = 2.2 x S,
where 2.2 is cardiac index, l;
S is the surface of the subject’s body, determined by the Dubois formula:
S = 71.84 M ° 425 R 0725
where M is body weight, kg; P - height, cm;
or

where DOO is the proper basal metabolic rate, calculated in accordance with the data of age, height and body weight according to the Harris-Benedict tables.
A comparison of MO and DME allows us to more accurately characterize the specifics of functional changes in the cardiovascular system caused by the influence of various factors.
Peripheral resistance (PR).
Determines the constancy of the average dynamic pressure (or its deviation from the norm). Calculated using the formulas:

where SI is the cardiac index, equal on average to 2.2 ±0.3 l/min-m2.
Peripheral resistance is expressed either in conventional units or in dynes. Normal indicator: 30 - 50 conventional units. units The change in PS during work reflects the reaction of the precapillary bed, depending on the volume of circulating blood.

STUDY OF INITIAL AND FINAL INDICATORS WHEN CARRYING OUT TEST IMPACTS.
Assessment of functional reserves:
– Martinet test - assessment of the ability to recover after physical exercise. loads;
– Squat test - a characteristic of the functional usefulness of the cardiovascular system;
– Flack test - allows you to evaluate the function of the heart muscle;
– Ruffier's test - dynamic load tolerance; endurance coefficient;
1. Martinet's test(simplified technique) is used in mass studies and allows assessing the ability of the cardiovascular system to recover after physical activity. Depending on the population of subjects, 20 squats at 30C and squats at the same pace for 2 minutes can be used as a load. In the first case, the period lasts 3 minutes, in the second - 5. Before the load and 3 (or 5) minutes after its completion, the subject’s heart rate, systolic and diastolic pressure are measured. The sample is assessed based on the difference between the studied indicators before and after the load:
if the difference is no more than 5 - “good”;
with a difference from 5 to 10 - “satisfactory”;
if the difference is more than 10 - “unsatisfactory”.
2. Squat test. Serves to characterize the functional usefulness of the cardiovascular system. Methodology: a person’s heart rate and blood pressure are calculated twice before exercise. Then the subject performs 15 squats in 30 seconds or 60 in 2 minutes. Immediately after the end of the load, the pulse is counted and the pressure is measured. The procedure is repeated after 2 minutes. If the subject is in good physical condition, the test at the same pace can be extended to 2 minutes. To evaluate the sample, the reaction quality indicator is used:

where PD2 and PD1) are pulse pressure before and after exercise; P 2 and P1 - heart rate before and after exercise.
3. Flack test. Allows you to evaluate the function of the heart muscle. Methodology: the subject maintains a pressure of 40 mm Hg in the U-shaped tube of a mercury manometer with a diameter of 4 mm for the maximum possible time. Art. The test is performed after a forced inhalation with the nose pinched. During its implementation, the heart rate is determined every 5C. The evaluation criterion is the degree of increase in heart rate in relation to the initial one and the duration of maintaining pressure, which in trained people does not exceed 40-50C. According to the degree of heart rate increase over 5C, the following reactions differ: no more than 7 beats. - good; up to 9 beats - satisfactory; up to 10 beats - unsatisfactory.
Before and after the test, the subject's blood pressure is measured. Impaired functions of the cardiovascular system lead to a decrease in blood pressure, sometimes by 20 M;M Hg. Art. and more. The sample is assessed according to the reaction quality indicator:

where DM 1 and DM2 are systolic pressure initially and after the test.
When the cardiovascular system is overloaded, the RCC value exceeds 0.10-0.25 rel. units
systems.
4. Ruffier's test (dynamic load tolerance)
The subject is in a standing position for 5 minutes. The pulse /Pa/ is calculated in 15 seconds, after which physical activity is performed / 30 squats per minute /. The pulse is re-calculated for the first /Рб/ and last /Рв/ 15 seconds of the first minute of recovery. When counting the pulse, the subject must stand. The calculated indicator of cardiac activity /CDA/ is a criterion for the optimal autonomic support of the cardiovascular system when performing low-power physical activity

Sample interpretation: if the PSD is less than 5, the test is performed “excellent”;
if the PSD is less than 10, the test is performed “good”;
if PSD is less than 15 – “satisfactory”;
if the PSD is more than 15, it is “bad.”
Our studies suggest that in healthy subjects the PSD does not exceed 12, and patients with neurocircular dystonia syndrome, as a rule, have a PSD of more than 15.
Thus, periodic monitoring of PSD provides the doctor with a fairly informative criterion for assessing the adaptive potential of the cardiovascular system.
5. Endurance factor. It is used to assess the degree of fitness of the cardiovascular system to perform physical activity and is determined by the formula:

where HR is heart rate, beats/min;
PP - pulse pressure, mm Hg. Art.
Normal indicator: 12-15 conventional units. units (according to some authors 16)
An increase in KB associated with a decrease in PP is an indicator of detraining of the cardiovascular system, a decrease in fatigue.

ASSESSMENT OF VEGETATIVE STATUS:
– Kerdo index - the degree of influence of the autonomic nervous system on the cardiovascular system;
– Active orthotest - level of vegetative-vascular stability;
– Orthostatic test - serves to characterize the functional usefulness of reflex mechanisms for regulating hemodynamics and assessing the excitability of the centers of sympathetic innervation;
– Ocular heart test - used to determine the excitability of the parasympathetic centers for regulating heart rate;
– Clinostatic test - characterizes the excitability of the centers of parasympathetic innervation.
1. Kerdo index (degree of influence on the cardiovascular system of the autonomic nervous system)

DD - diastolic pressure, mmHg;
Heart rate - heart rate, beats/min.

Normal indicator: from – 10 to + 10%
Sample interpretation: a positive value - the predominance of sympathetic influences, a negative value - the predominance of parasympathetic influences.
2. Active orthotest (level of vegetative-vascular resistance)
The test is one of the functional stress tests; it allows you to assess the functionality of the cardiovascular system, as well as the state of the central nervous system. A decrease in the tolerance of orthostatic tests (active and passive) is often observed in hypotonic conditions in diseases accompanied by vegetative-vascular instability, in asthenic conditions and fatigue.
The test should be carried out immediately after a night's sleep. Before starting the test, the subject must lie quietly on his back for 10 minutes, without a high pillow. After 10 minutes, the subject’s pulse rate is counted three times in a lying position (counting for 15 s) and the blood pressure is determined: maximum and minimum.
After obtaining background values, the subject quickly gets up, takes a vertical position and stands for 5 minutes. In this case, every minute (in the second half of each minute) the frequency is calculated and blood pressure is measured.
Orthostatic test (OI - orthostatic index) is assessed according to the formula proposed by Burchard-Kirhoff.

Sample interpretation: Normally, the orthostatic index is 1.0 - 1.6 relative units. For chronic fatigue, RI = 1.7-1.9, for overfatigue, RI = 2 or more.
3. Orthostatic test. Serves to characterize the functional usefulness of reflex mechanisms for regulating hemodynamics and assessing the excitability of the centers of sympathetic innervation.
After 5 minutes of lying down, the subject's heart rate is recorded. Then, on command, the subject calmly (without jerking) takes a standing position. The pulse is counted at the 1st and 3rd minutes of being in vertical position, blood pressure is determined at the 3rd and 5th minutes. The sample can be assessed by pulse alone or by pulse and blood pressure.

The excitability of the centers of sympathetic innervation is determined by the degree of heart rate increase (PS), and the usefulness of autonomic regulation is determined by the time of pulse stabilization. Normally (in young people), the pulse returns to its original values ​​at 3 minutes. The criteria for assessing the excitability of sympathetic units according to the SUP index are presented in the table.

4. Ocular heart test. Used to determine the excitability of the parasympathetic centers for regulating heart rate. It is carried out against the background of continuous ECG recording, during which pressure is applied to the eyeballs of the subject for 15 C (in the direction of the horizontal axis of the orbits). Normally, pressure on the eyeballs causes the heart rate to slow down. Increased rhythm is interpreted as a perversion of the reflex, which occurs according to the sympathicotonic type. You can monitor your heart rate by palpation. In this case, the pulse is counted 15C before the test and during pressure.
Sample rating:
decrease in heart rate by 4 - 12 beats. in min – normal;
decrease in heart rate by 12 beats. per minute – sharply enhanced;
no reduction – areactive;
no increase in frequency – perverted.

5. Clinostatic test.
Characterizes the excitability of the centers of parasympathetic innervation.
Method of behavior: the subject smoothly moves from a standing position to a lying position. The pulse rate in vertical and horizontal positions is counted and compared. The clinostatic test is normally manifested by a slowing of the pulse by 2-8 beats.
Assessment of excitability of parasympathetic innervation centers

CALCULATION INDEX OF ADAPTATION POTENTIAL OF THE CARDIOVASCULAR SYSTEM.
1. Calculated index of the adaptive potential of the cardiovascular system R.M. Baevsky et al., 1987.
Recognition of functional states based on the analysis of data on autonomic and myocardial-hemodynamic homeostasis requires certain experience and knowledge in the field of physiology and clinical practice. In order to make this experience available to a wide range of doctors, a number of formulas have been developed that make it possible to calculate the adaptive potential of the circulatory system according to a given set of indicators using multiple regression equations. One of the simplest formulas, providing recognition accuracy of 71.8% (compared to expert assessments), is based on the use of the simplest and most commonly available research methods - measuring heart rate and blood pressure levels, height and body weight:

AP = 0.011(PP) + 0.014(SBP) + 0.008(DBP) + 0.009(MT) - 0.009(R) + 0.014(V)-0.27;

Where AP- adaptive potential of the circulatory system in points, Emergency- pulse rate (bpm); GARDEN And DBP- systolic and diastolic blood pressure (mm Hg); R- height (cm); MT- body weight (kg); IN- age (years).
Based on the values ​​of adaptation potential, the patient’s functional state is determined:
Sample interpretation: below 2.6 - satisfactory adaptation;
2.6 - 3.09 - tension of adaptation mechanisms;
3.10 - 3.49 - unsatisfactory adaptation;
3.5 and higher - adaptation failure.
A decrease in adaptation potential is accompanied by a slight shift in the indicators of myocardial-hemodynamic homeostasis within the limits of their so-called normal values, the tension of regulatory systems increases, and the “payment for adaptation” increases. Failure of adaptation as a result of overstrain and depletion of regulatory mechanisms in older people is different sharp drop reserve capacity of the heart, while in at a young age At the same time, there is even an increase in the level of functioning of the circulatory system.

OTHER METHODS

Determination of the type of self-regulation of blood circulation makes it possible to assess the level of tension in the regulation of the cardiovascular system. An express method for diagnosing the type of self-regulation of blood circulation (TSC) has been developed:

TSC from 90 to 110 reflects the cardiovascular type. If the index exceeds 110, then the type of self-regulation of blood circulation is vascular, if less than 90 – cardiac. The type of self-regulation of blood circulation reflects the phenotypic characteristics of the organism. A change in the regulation of blood circulation towards the predominance of the vascular component indicates its economization and an increase in functional reserves.