What is total peripheral resistance? Vascular resistance Decrease in opss

This term is understood total resistance of the entire vascular system flow of blood ejected by the heart. This ratio is described equation:

As follows from this equation, to calculate TPVR, it is necessary to determine the value of systemic arterial pressure and cardiac output.

Direct bloodless methods for measuring total peripheral resistance have not been developed, and its value is determined from Poiseuille equations for hydrodynamics:

where R is the hydraulic resistance, l is the length of the vessel, v is the viscosity of the blood, r is the radius of the vessels.

Since, when studying the vascular system of an animal or a person, the radius of the vessels, their length and blood viscosity usually remain unknown, Franc, using a formal analogy between hydraulic and electrical circuits, led Poiseuille's equation to the following view:

where Р1-Р2 is the pressure difference at the beginning and at the end of a section of the vascular system, Q is the amount of blood flow through this section, 1332 is the conversion coefficient of resistance units to the CGS system.

Frank's equation is widely used in practice to determine vascular resistance, although it does not always reflect the true physiological relationship between volumetric blood flow, blood pressure, and vascular resistance to blood flow in warm-blooded animals. These three parameters of the system are indeed related by the above ratio, but in different objects, in different hemodynamic situations and at different times, their changes can be interdependent to a different extent. So, in specific cases, the level of SBP can be determined mainly by the value of OPSS or mainly by CO.

Rice. 9.3. A more pronounced increase in the resistance of the vessels of the thoracic aortic basin compared with its changes in the basin of the brachiocephalic artery during the pressor reflex.

Under normal physiological conditions OPSS ranges from 1200 to 1700 dyn s ¦ cm, in case of hypertension this value can increase two times against the norm and be equal to 2200-3000 dyn s cm-5.

OPSS value consists of the sums (not arithmetic) of the resistances of the regional vascular departments. In this case, depending on the greater or lesser severity of changes in the regional resistance of the vessels, they will respectively receive a smaller or larger volume of blood ejected by the heart. On fig. 9.3 shows an example of a more pronounced degree of increase in the resistance of the vessels of the basin of the descending thoracic aorta compared to its changes in the brachiocephalic artery. Therefore, the increase in blood flow in the brachiocephalic artery will be greater than in the thoracic aorta. This mechanism is based on the effect of "centralization" of blood circulation in warm-blooded animals, which ensures the redistribution of blood, primarily to the brain and myocardium, under severe or threatening conditions (shock, blood loss, etc.).

Consider for concreteness an example of an erroneous (error when divided by S) calculation of total vascular resistance. During the generalization of clinical results, data from patients of different height, age and weight are used. For a large patient (for example, a hundred kilograms), an IOC of 5 liters per minute at rest may not be sufficient. For the average - within the normal range, and for a patient of low weight, say, 50 kilograms - excessive. How to take into account these circumstances?

Over the past two decades, most doctors have come to an unspoken agreement: to attribute those blood circulation indicators that depend on the size of a person to the surface of his body. The surface (S) is calculated depending on weight and height according to the formula (well-formed nomograms give more accurate relationships):

S=0.007124 W 0.425 H 0.723, W-weight; H-growth.

If one patient is being studied, then the use of indices is not relevant, but when it is necessary to compare the indicators of various patients (groups), to carry out their statistical processing, comparison with the norms, then it is almost always necessary to use indices.

Total vascular resistance of the systemic circulation (RVR) is widely used and, unfortunately, has become a source of unfounded conclusions and interpretations. Therefore, we will dwell on it in detail here.

Recall the formula by which the absolute value of the total vascular resistance is calculated (OSS, or OPS, OPSS, different designations are used):

OSS \u003d 79.96 (BP-VD) IOC -1 din*s*cm - 5 ;

79.96 - coefficient of dimension, BP - mean arterial pressure in mm Hg. Art., VD - venous pressure in mm Hg. Art., IOC - minute volume of blood circulation in l / min)

Let a large person (full adult European) have an IOC \u003d 4 liters per minute, BP-VD \u003d 70, then the OSS approximately (so as not to lose the essence of tenths) will have a value

OSC=79.96 (BP-VD) IOC -1 @ 80 70/[email protected] din*s*cm -5 ;

remember - 1400 din * s * cm - 5 .

Let a small person (thin, short, but quite viable) have an IOC \u003d 2 liters per minute, BP-VD \u003d 70, from here OSS will be approximately

79.96 (BP-VD) IOC -1 @80 70/ [email protected] dyne*s*cm -5 .

OPS in a small person is more than in a large person by 2 times. Both have normal hemodynamics, and comparing OSS indicators with each other and with the norm does not make any sense. However, such comparisons are made and clinical conclusions are drawn from them.

In order to be able to compare, indexes are introduced that take into account the surface (S) of the human body. Multiplying the total vascular resistance (VRS) by S, we get an index (VRS*S=IOVR) that can be compared:

IOSS \u003d 79.96 (BP-VD) IOC -1 S (dyn * s * m 2 * cm -5).

From the experience of measurements and calculations, it is known that for a large person S is about 2 m 2, for a very small one - let's take 1 m 2. Their total vascular resistance will not be equal, but the indices are equal:

ISS=79.96 70 4 -1 2=79.96 70 2 -1 1=2800.

If the same patient is being studied without comparison with others and with standards, it is quite acceptable to use direct absolute estimates of the function and properties of the CCC.

If different, especially differing in size, patients are being studied, and if statistical processing is necessary, then indexes should be used.

Index of elasticity of the arterial vascular reservoir(IEA)

IEA \u003d 1000 SI / [(ADS - ADD) * HR]

is calculated in accordance with Hooke's law and the Frank model. IEA is the greater, the greater the SI, and the less, the greater the product of the heart rate (HR) and the difference between arterial systolic (ADS) and diastolic (ADD) pressures. It is possible to calculate the elasticity of the arterial reservoir (or modulus of elasticity) using the velocity of the pulse wave. In this case, the elastic modulus of only that part of the arterial vascular reservoir, which is used to measure the pulse wave velocity, will be estimated.

Elasticity index of the pulmonary arterial vascular reservoir (IELA)

IELA \u003d 1000 SI / [(LADS - LADD) * HR]

calculated similarly to the previous description: IELA is the greater, the greater the SI and the less, the greater the product of the contraction rate and the difference between the pulmonary arterial systolic (LADS) and diastolic (LADD) pressures. These estimates are very approximate, we hope that with the improvement of methods and equipment they will be improved.

Elasticity index of the venous vascular reservoir(IEV)

IEV \u003d (V / S-BP IEA-LAD IELA-LVD IELV) / VD

calculated using a mathematical model. Actually, the mathematical model is the main tool for achieving systemic indicators. With the available clinical and physiological knowledge, the model cannot be adequate in the usual sense. Continuous individualization and the possibilities of computer technology make it possible to sharply increase the constructiveness of the model. This makes the model useful, despite the weak adequacy in relation to the group of patients and to one for various conditions of treatment and life.

Elasticity index of the pulmonary venous vascular reservoir (IELV)

IELV \u003d (V / S-BP IEA-LAD IELA) / (LVD + V VD)

is calculated, like IEV, using a mathematical model. It averages both the actual elasticity of the pulmonary vascular bed and the influence of the alveolar bed and breathing regimen on it. B is the tuning factor.

Total peripheral vascular resistance index (ISOS) has been discussed earlier. We repeat here briefly for the convenience of the reader:

IOSS=79.92 (BP-VD)/SI

This ratio does not explicitly reflect either the radius of the vessels, or their branching and length, or the viscosity of the blood, and much more. But it displays the interdependence of SI, OPS, AD and VD. We emphasize that given the scale and types of averaging (over time, over the length and cross section of the vessel, etc.), which is characteristic of modern clinical control, such an analogy is useful. Moreover, this is almost the only possible formalization, if, of course, the task is not theoretical research, but clinical practice.

CCC indicators (system sets) for stages of CABG operation. Indexes are in bold

CCC indicators	Designation	Dimensions	Admission to the operating block	End of operation	Average time in intensive care until estubation
Cardiac index	SI	l / (min m 2)	3.07±0.14	2.50±0.07	2.64±0.06
Heart rate	heart rate	bpm	80.7±3.1	90.1±2.2	87.7±1.5
Blood pressure systolic	ADS	mmHg.	148.9±4.7	128.1±3.1	124.2±2.6
Blood pressure diastolic	ADD	mmHg.	78.4±2.5	68.5±2.0	64.0±1.7
Arterial pressure average	HELL	mmHg.	103.4±3.1	88.8±2.1	83.4±1.9
Pulmonary arterial pressure systolic	LADS	mmHg.	28.5±1.5	23.2±1.0	22.5±0.9
Pulmonary arterial pressure diastolic	LADD	mmHg.	12.9±1.0	10.2±0.6	9.1±0.5
Pulmonary arterial pressure mean	LAD	mmHg.	19.0±1.1	15.5±0.6	14.6±0.6
Central venous pressure	CVP	mmHg.	6.9±0.6	7.9±0.5	6.7±0.4
Pulmonary venous pressure	LVD	mmHg.	10.0±1.7	7.3±0.8	6.5±0.5
Left ventricular index	BLI	cm 3 / (s m 2 mm Hg)	5.05±0.51	5.3±0.4	6.5±0.4
Right ventricular index	IPJ	cm 3 / (s m 2 mm Hg)	8.35±0.76	6.5±0.6	8.8±0.7
Vascular resistance index	ISSE	din with m 2 cm -5	2670±117	2787±38	2464±87
Pulmonary vascular resistance index	ILSS	din with m 2 cm -5	172±13	187.5±14.0	206.8±16.6
Vein elasticity index	IEV	cm 3 m -2 mm Hg -1	119±19	92.2±9.7	108.7±6.6
Arterial elasticity index	IEA	cm 3 m -2 mm Hg -one	0.6±0.1	0.5±0.0	0.5±0.0
Pulmonary vein elasticity index	IELV	cm 3 m -2 mm Hg -one	16.3±2.2	15.8±2.5	16.3±1.0
Pulmonary artery elasticity index	IELA	cm 3 m -2 mm Hg -one	3.3±0.4	3.3±0.7	3.0±0.3

The physiological role of arterioles in the regulation of blood flow

On the scale of the body, the total peripheral resistance depends on the tone of the arterioles, which, along with the stroke volume of the heart, determines the magnitude of blood pressure.

In addition, the tone of arterioles can change locally, within a given organ or tissue. A local change in the tone of arterioles, without having a noticeable effect on the total peripheral resistance, will determine the amount of blood flow in this organ. Thus, the tone of arterioles is noticeably reduced in the working muscles, which leads to an increase in their blood supply.

regulation of arteriole tone

Since a change in the tone of arterioles on the scale of the whole organism and on the scale of individual tissues has completely different physiological significance, there are both local and central mechanisms of its regulation.

Local regulation of vascular tone

In the absence of any regulatory influences, an isolated arteriole, devoid of endothelium, retains a certain tone, which depends on the smooth muscles themselves. It is called the basal tone of the vessel. It can be influenced by such environmental factors as pH and CO 2 concentration (a decrease in the first and an increase in the second lead to a decrease in tone). This reaction turns out to be physiologically expedient, since the increase in local blood flow following a local decrease in the tone of arterioles, in fact, will lead to the restoration of tissue homeostasis.

Systemic hormones that regulate vascular tone

Vasoconstrictor and vasodilating nerves

All, or almost all, arterioles of the body receive sympathetic innervation. Sympathetic nerves have catecholamines (in most cases, norepinephrine) as a neurotransmitter and have a vasoconstrictive effect. Since the affinity of β-adrenergic receptors for norepinephrine is low, the pressor effect predominates even in skeletal muscles under the action of sympathetic nerves.

Parasympathetic vasodilatory nerves, whose neurotransmitters are acetylcholine and nitric oxide, occur in the human body in two places: the salivary glands and the cavernous bodies. In the salivary glands, their action leads to an increase in blood flow and increased filtration of fluid from the vessels into the interstitium and further to abundant secretion of saliva, in the cavernous bodies, a decrease in the tone of arterioles under the action of vasodilating nerves provides an erection.

Participation of arterioles in pathophysiological processes

Inflammation and allergic reactions

The most important function of the inflammatory response is the localization and lysis of the foreign agent that caused the inflammation. The functions of lysis are performed by cells that are delivered to the focus of inflammation by the blood stream (mainly neutrophils and lymphocytes. Accordingly, it turns out to be appropriate to increase local blood flow in the focus of inflammation. Therefore, substances that have a powerful vasodilating effect - histamine and prostaglandin E 2. of the five classic symptoms of inflammation (redness, swelling, heat) are caused precisely by vasodilation.An increase in blood flow - hence redness; an increase in pressure in the capillaries and an increase in the filtration of fluid from them - hence edema (however, an increase in the permeability of the walls is also involved in its formation capillaries), an increase in the flow of heated blood from the core of the body - hence, fever (although here, perhaps, an increase in the metabolic rate in the focus of inflammation plays an equally important role).

However, histamine, in addition to a protective inflammatory reaction, is the main mediator of allergies.

This substance is secreted by mast cells when antibodies adsorbed on their membranes bind to antigens from the group of immunoglobulins E.

An allergy to a substance occurs when a sufficiently large number of such antibodies are produced against it and they are massively sorbed on mast cells throughout the body. Then, upon contact of a substance (allergen) with these cells, they secrete histamine, which causes an expansion of arterioles at the site of secretion, followed by pain, redness and swelling. Thus, all allergy options, from the common cold and urticaria, to Quincke's edema and anaphylactic shock, are largely associated with a histamine-dependent drop in arteriole tone. The difference is where and how massively this expansion occurs.

A particularly interesting (and dangerous) variant of allergy is anaphylactic shock. It occurs when an allergen, usually after intravenous or intramuscular injection, spreads throughout the body and causes histamine secretion and vasodilation throughout the body. In this case, all capillaries are filled with blood to the maximum, but their total capacity exceeds the volume of circulating blood. As a result, the blood does not return from the capillaries to the veins and atria, the effective work of the heart is impossible and the pressure drops to zero. This reaction develops within a few minutes and leads to the death of the patient. The most effective measure for anaphylactic shock is the intravenous administration of a substance with a powerful vasoconstrictor effect - best of all, norepinephrine.

Total peripheral resistance (TPR) is the resistance to blood flow present in the vascular system of the body. It can be understood as the amount of force opposing the heart as it pumps blood into the vascular system.

Although total peripheral resistance plays a critical role in determining blood pressure, it is purely an indicator of cardiovascular health and should not be confused with the pressure exerted on the walls of the arteries, which is an indicator of blood pressure.

Components of the vascular system

The vascular system, which is responsible for the flow of blood from and to the heart, can be divided into two components: the systemic circulation (systemic circulation) and the pulmonary vascular system (pulmonary circulation). The pulmonary vasculature delivers blood to and from the lungs, where it is oxygenated, and the systemic circulation is responsible for transporting this blood to the cells of the body through the arteries, and returning the blood back to the heart after being supplied with blood. The total peripheral resistance affects the operation of this system and, as a result, can significantly affect the blood supply to organs.

The total peripheral resistance is described by a particular equation:

CPR = change in pressure / cardiac output

The change in pressure is the difference between mean arterial pressure and venous pressure. Mean arterial pressure equals diastolic pressure plus one third of the difference between systolic and diastolic pressure. Venous blood pressure can be measured using an invasive procedure using special instruments that allows you to physically determine the pressure inside a vein. Cardiac output is the amount of blood pumped by the heart in one minute.

Factors affecting the components of the OPS equation

There are a number of factors that can significantly affect the components of the OPS equation, thus changing the values of the total peripheral resistance itself. These factors include the diameter of the vessels and the dynamics of blood properties. The diameter of the blood vessels is inversely proportional to the blood pressure, so smaller blood vessels increase the resistance, thus increasing the RVR. Conversely, larger blood vessels correspond to a less concentrated volume of blood particles exerting pressure on vessel walls, which means lower pressure.

Blood hydrodynamics

Blood hydrodynamics can also significantly contribute to an increase or decrease in total peripheral resistance. Behind this is a change in the levels of clotting factors and blood components that can change its viscosity. As can be expected, more viscous blood causes more resistance to blood flow.

Less viscous blood moves more easily through the vascular system, resulting in lower resistance.

An analogy is the difference in force required to move water and molasses.

This information is for reference only, consult a doctor for treatment.

Big Encyclopedia of Oil and Gas

Peripheral resistance

Peripheral resistance was set in the range from 0.4 to 2.0 mm Hg. sec / cm in steps of 0.4 mmHg. sec / cm. Contractility is associated with the state of the actomyosin complex, the work of regulatory mechanisms. Contractility is changed by setting MS values from 1.25 to 1.45 in increments of 0.05, as well as by varying active deformities in some periods of the cardiac cycle. The model allows changing active deformities in different periods of systole and diastole, which reproduces the regulation of LV contractile function by separate influence on fast and slow calcium channels. Active deformities were taken constant throughout the entire diastole and equal from 0 to 0.004 with a step of 0.001, first with constant active deformities in systole, then with a simultaneous increase in their value at the end of the isovolumic period of contraction by the amount of deformities in diastole.

The peripheral resistance of the vascular system is the sum of many individual resistances of each vessel.

The main mechanism of redistribution of blood is the peripheral resistance provided to the flowing blood stream by small arterial vessels and arterioles. At that time, only about 15% of the blood enters all other organs, including the kidneys. At rest, only about 20% of the blood ejected by the heart per minute falls on the whole mass of muscles, which make up about half of the body weight. So, a change in the life situation is necessarily accompanied by a kind of vascular reaction in the form of a redistribution of blood.

Changes in systolic and diastolic pressure in these patients occur in parallel, which gives the impression of an increase in peripheral resistance as hyperdynamia of the heart increases.

Over the next 15 s (s), systolic, diastolic and mean pressure, heart rate, peripheral resistance, stroke volume, stroke work, stroke power and cardiac output are determined. In addition, the indicators of already studied cardiac cycles are averaged, as well as the issuance of documents indicating the time of day.

The obtained data suggest that during emotional stress, characterized by a catecholamine burst, a systemic spasm of arterioles develops, which contributes to the growth of peripheral resistance.

Characteristic of changes in blood pressure in these patients is also torpidity in restoring the initial value of diastolic pressure, which, in combination with the data of piezography of the arteries of the extremities, indicates a persistent increase in their peripheral resistance.

The value of the volume of blood that left the chest cavity during the time t from the start of the expulsion of Sam (t) was calculated as a function of arterial pressure, the bulk modulus of the extrathoracic part of the aortic-arterial system, and the peripheral resistance of the arterial system.

The resistance to blood flow varies depending on the contraction or relaxation of the smooth muscles of the vascular walls, especially in the arterioles. With vasoconstriction (vasoconstriction), peripheral resistance increases, and with their expansion (vasodilation) it decreases. An increase in resistance leads to an increase in blood pressure, and a decrease in resistance - to its fall. All these changes are regulated by the vasomotor (vasomotor) center of the medulla oblongata.

Knowing these two values, peripheral resistance is calculated - the most important indicator of the state of the vascular system.

As the diastolic component decreases and the peripheral resistance index increases, according to the authors, the trophism of the eye tissues is disturbed and visual functions decrease even with normal ophthalmotonus. In our opinion, in such situations, the state of intracranial pressure also deserves special attention.

Taking into account that the dynamics of diastolic pressure indirectly reflects the state of peripheral resistance, we believed that it would decrease during physical exertion in the examined patients, since real muscular work would lead to the expansion of muscle vessels to an even greater extent than during emotional stress, which is only provokes the readiness of the muscles for action.

Similarly, multiply connected regulation of arterial pressure and volumetric blood flow velocity is carried out in the body. So, with a decrease in blood pressure, vascular tone and peripheral resistance to blood flow increase compensatory. This, in turn, leads to an increase in blood pressure in the vascular bed to the site of vasoconstriction and to a decrease in blood pressure below the site of narrowing in the direction of blood flow. At the same time, the volumetric velocity of blood flow in the vascular bed decreases. Due to the peculiarities of regional blood flow, blood pressure and blood volume velocity increase in the brain, heart and other organs, and decrease in other organs. As a result, patterns of multiply connected regulation appear: when arterial pressure normalizes, another controlled variable changes - volumetric blood flow.

These figures show that in the background the significance of environmental and hereditary determinants is approximately the same. This indicates that the various components that provide the value of systolic pressure (stroke volume, pulse rate, peripheral resistance value) are clearly inherited and are activated precisely during any extreme effects on the body, while maintaining the homeostasis of the system. High preservation of the value of the Holzinger coefficient in the period of 10 min.

Peripheral vascular resistance (OPVR)

This term is understood as the total resistance of the entire vascular system to the flow of blood ejected by the heart. This ratio is described by the equation:

Used to calculate the value of this parameter or its changes. To calculate TPVR, it is necessary to determine the value of systemic arterial pressure and cardiac output.

The value of OPSS consists of the sums (not arithmetic) of the resistances of the regional vascular departments. In this case, depending on the greater or lesser severity of changes in the regional resistance of the vessels, they will respectively receive a smaller or larger volume of blood ejected by the heart.

This mechanism is based on the effect of "centralization" of blood circulation in warm-blooded animals, which ensures the redistribution of blood, primarily to the brain and myocardium, under severe or threatening conditions (shock, blood loss, etc.).

Resistance, pressure difference and flow are related by the basic equation of hydrodynamics: Q=AP/R. Since the flow (Q) must be identical in each of the consecutive sections of the vascular system, the pressure drop that occurs throughout each of these sections is a direct reflection of the resistance that exists in this section. Thus, a significant drop in blood pressure as blood passes through the arterioles indicates that the arterioles have significant resistance to blood flow. The average pressure decreases slightly in the arteries, as they have little resistance.

Likewise, the modest pressure drop that occurs in capillaries is a reflection of the fact that capillaries have moderate resistance compared to arterioles.

The flow of blood flowing through individual organs can change ten or more times. Since mean arterial pressure is a relatively stable indicator of the activity of the cardiovascular system, significant changes in the blood flow of an organ are a consequence of changes in its total vascular resistance to blood flow. Consistently located vascular departments are combined into certain groups within an organ, and the total vascular resistance of an organ must be equal to the sum of the resistances of its series-connected vascular departments.

Since arterioles have a significantly greater vascular resistance compared to other parts of the vascular bed, the total vascular resistance of any organ is determined to a large extent by the resistance of arterioles. The resistance of arterioles is, of course, largely determined by the radius of the arterioles. Consequently, blood flow through the organ is primarily regulated by changes in the internal diameter of the arterioles by contraction or relaxation of the muscular wall of the arterioles.

When the arterioles of an organ change their diameter, not only does the blood flow through the organ change, but the blood pressure that occurs in this organ also undergoes changes.

Constriction of the arterioles causes a greater pressure drop in the arterioles, which leads to an increase in blood pressure and a simultaneous decrease in changes in arteriole resistance to vascular pressure.

(The function of arterioles is somewhat similar to that of a dam: closing the dam gate reduces flow and raises the level in the reservoir behind the dam and lowers the level after it.)

On the contrary, an increase in organ blood flow caused by the expansion of arterioles is accompanied by a decrease in blood pressure and an increase in capillary pressure. Due to changes in capillary hydrostatic pressure, arteriole constriction leads to transcapillary fluid reabsorption, while arteriole expansion promotes transcapillary fluid filtration.

One of the main diseases of the heart and blood vessels is arterial hypertension (AH). This is one of the most significant non-communicable pandemics, determining the structure of cardiovascular morbidity and mortality.

Remodeling processes in AH involve not only the heart and large elastic and muscular arteries, but also arteries of smaller diameter (resistive arteries). In this regard, the aim of the study was to study the state of peripheral vascular resistance of brachiocephalic arteries in patients with various degrees of hypertension using modern non-invasive research methods.

The study was conducted in 62 AH patients aged 29 to 60 years (mean age 44.3±2.4 years). Among them are 40 women and 22 men. The duration of the disease was 8.75±1.6 years. The study included patients with mild - AH-1 (systolic BP and diastolic BP, respectively, from 140/90 to 160/100 mm Hg) and moderate - AH-2 (systolic BP and diastolic BP, respectively, from 160/90 to 180 /110 mmHg). A subgroup of patients with high normal blood pressure (SBP and DBP, respectively, up to 140/90 mm Hg) was isolated from the group of those examined who consider themselves healthy.

In addition to general clinical parameters, ECHOCG and ABPM parameters were evaluated in all the examined patients; peripheral resistance indices (Pourcelot-Ri and Gosling-Pi), intima-media complex (IMC) were studied in the common carotid (CCA), internal carotid (ICA) arteries using Doppler ultrasound . The total peripheral vascular resistance (TPVR) was calculated by the generally accepted method using the Franck-Poiseuille formula. Statistical processing of the results was carried out using the Microsoft Excel software package.

The analysis of blood pressure and echocardiographic characteristics revealed a significant increase (p<0,01) пульсового давления и толщины межжелудочковой перегородки, особенно в группе больных с АГ-2. В этом контингенте установлены признаки диастолической дисфункции левого желудочка и увеличение общего периферического сосудистого сопротивления (ОПСС) (р<0,05). В группе больных АГ-2 обнаружено утолщение КИМ (р<0,01) в сравнении с показателями здоровых лиц. При сравнительной оценке изучаемого показателя в группе больных АГ-1 и АГ-2 выявлено значительное превалирование комплекса интима- медиа у лиц с АГ-2 (р<0,05). В этой же группе лиц выявлено увеличение внутрипросветного диаметра ОСА и ВСА (р<0,01).

When analyzing the indices of peripheral resistance (Pourcelot-Ri and Gosling-Pi) according to CCA, an increase in Ri was observed in all patients with AH (p<0,05) и тенденция к повышению Pi в группе лиц в высоким нормальным АД. По ВСА- достоверное повышение Pi и Ri в группе больных АГ-2 (р<0,05) и тенденция к повышению Pi в группе лиц с АГ1.

Correlation analysis established a direct relationship between the level of mean blood pressure and the diameter of extracranial vessels (r = 0.51, p<0,01), ОПСС (r =0,56 , р<0,01) и индексами периферического сосудистого сопротивления (Pi и Ri) (r =0,61 и r=0,53 соответственно, р<0,01), что предполагает развитие сосудистого ремоделирования и умеренное уменьшение растяжимости сосудов по мере увеличения уровня среднего АД.

Thus, a persistent chronic increase in blood pressure leads to hypertrophy of the smooth muscle elements of the media with the development of vascular remodeling of the brachiocephalic arteries.

Bibliographic link

URL: http://fundamental-research.ru/ru/article/view?id=3514 (date of access: 03/16/2018).

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Basic Research

The journal has been published since 2003. The journal publishes scientific reviews, articles of a problematic and scientific-practical nature. The journal is presented in the Scientific Electronic Library. The journal is registered with the Center International de l'ISSN. Journal numbers and publications are assigned a DOI (Digital object identifier).

Indices of peripheral resistance

ICA - internal carotid artery

CCA - common carotid artery

ECA - external carotid artery

NBA - supratrochlear artery

VA - vertebral artery

OA - main artery

MCA - middle cerebral artery

ACA - anterior cerebral artery

PCA - posterior cerebral artery

GA - ophthalmic artery

RCA - subclavian artery

PSA - anterior communicating artery

PCA - posterior communicating artery

LBF - linear velocity of blood flow

TKD - transcranial dopplerography

AVM - arteriovenous malformation

BA - femoral artery

RCA - popliteal artery

PTA - posterior tibial artery

ATA - anterior tibial artery

PI - pulsation index

RI - Peripheral Resistance Index

SBI - Spectral Broadening Index

Doppler ultrasound of the main arteries of the head

Currently, cerebral dopplerography has become an integral part of the diagnostic algorithm for cerebrovascular diseases. The physiological basis of ultrasound diagnostics is the Doppler effect, discovered by the Austrian physicist Christian Andreas Doppler in 1842 and described in the work “On the Colored Light of Binary Stars and Some Other Stars in the Heavens”.

In clinical practice, the Doppler effect was first used in 1956 by Satomuru during an ultrasound examination of the heart. In 1959, Franklin used the Doppler effect to study blood flow in the main arteries of the head. Currently, there are several ultrasound techniques based on the use of the Doppler effect, designed to study the vascular system.

Doppler ultrasound is usually used to diagnose the pathology of the main arteries, which have a relatively large diameter and are located superficially. These include the main arteries of the head and limbs. The exception is intracranial vessels, which are also available for examination using a pulsed ultrasonic signal of low frequency (1-2 MHz). The resolution of Doppler ultrasound data is limited by the detection of: indirect signs of stenosis, occlusion of the main and intracranial vessels, signs of arteriovenous shunting. The detection of Dopplerographic signs of certain pathological signs serves as an indication for a more detailed examination of the patient - a duplex study of blood vessels or angiography. Thus, Doppler ultrasound refers to the screening method. Despite this, Doppler ultrasound is widespread, economical and makes a significant contribution to the diagnosis of diseases of the vessels of the head, arteries of the upper and lower extremities.

There is enough special literature on Doppler ultrasound, but most of it is devoted to duplex scanning of arteries and veins. This manual describes cerebral dopplerography, ultrasound Doppler examination of the extremities, their methodology and use for diagnostic purposes.

Ultrasound is a wave-like propagating oscillatory motion of particles of an elastic medium with a frequency above Hz. The Doppler effect consists in changing the frequency of an ultrasonic signal when reflected from moving bodies compared to the original frequency of the sent signal. An ultrasonic Doppler device is a location device, the principle of which is to emit probing signals into the patient's body, receive and process echo signals reflected from moving blood flow elements in the vessels.

Doppler frequency shift (∆f) - depends on the speed of movement of blood elements (v), the cosine of the angle between the axis of the vessel and the direction of the ultrasonic beam (cos a), the speed of propagation of ultrasound in the medium (c) and the primary frequency of radiation (f °). This dependence is described by the Doppler equation:

2 v f° cos a

It follows from this equation that the increase in the linear velocity of blood flow through the vessels is proportional to the velocity of particles and vice versa. It should be noted that the device registers only the Doppler frequency shift (in kHz), while the velocity values are calculated according to the Doppler equation, while the propagation velocity of ultrasound in the medium is assumed to be constant and equal to 1540 m/s, and the primary radiation frequency corresponds to the frequency of the sensor. With a narrowing of the lumen of the artery (for example, by a plaque), the blood flow velocity increases, while in places of vasodilation it will decrease. The frequency difference, which reflects the linear velocity of particles, can be displayed graphically in the form of a curve of velocity change depending on the cardiac cycle. When analyzing the obtained curve and the flow spectrum, it is possible to evaluate the velocity and spectral parameters of blood flow and calculate a number of indices. Thus, by changing the “sound” of the vessel and the characteristic changes in Doppler parameters, one can indirectly judge the presence of various pathological changes in the area under study, such as:

- occlusion of the vessel by the disappearance of sound in the projection of the obliterated segment and a drop in velocity to 0, there may be a variability in the discharge or tortuosity of the artery, for example, the ICA;
- narrowing of the lumen of the vessel due to an increase in the speed of blood flow in this segment and an increase in the “sound” in this area, and after stenosis, on the contrary, the speed will be lower than normal and the sound will be lower;
- arterio - venous shunt, tortuosity of the vessel, kink and, in connection with this, a change in circulation conditions leads to the most diverse modifications of the sound and the velocity curve in this area.

2.1. Characteristics of sensors for dopplerography.

A wide range of ultrasound examinations of blood vessels with a modern Doppler device is provided through the use of sensors for various purposes, which differ in the characteristics of the emitted ultrasound, as well as in design parameters (sensors for screening examinations, sensors with special holders for monitoring, flat sensors for surgical applications).

To study extracranial vessels, sensors with a frequency of 2, 4, 8 MHz are used, intracranial vessels - 2, 1 MHz. The ultrasonic transducer contains a piezoelectric crystal that vibrates when exposed to alternating current. This vibration generates an ultrasonic beam that travels away from the crystal. Doppler transducers have two modes of operation: continuous wave CW and pulsed wave PW. The constant-wave sensor has 2 piezocrystals, one constantly emits, the second - receives radiation. In PW sensors, the same crystal is receiving and emitting. The pulse sensor mode allows location at various, arbitrarily chosen depths, and therefore, it is used for insonation of intracranial arteries. For a 2 MHz probe, there is a 3 cm “dead zone”, with a penetration depth of 15 cm of sounding; for a 4 MHz sensor – 1.5 cm “dead zone”, probing zone 7.5 cm; 8 MHz - 0.25 cm “dead zone”, 3.5 cm probing depth.

III. Doppler ultrasound MAG.

3.1. Analysis of Dopplerogram parameters.

The blood flow in the main arteries has a number of hydrodynamic features, and therefore, there are two main flow options:

- laminar (parabolic) – there is a flow velocity gradient of the central (maximum velocities) and near-wall (minimum velocities) layers. The difference between the speeds is maximum in systole and minimum in diastole. Layers do not mix with each other;
- turbulent - due to unevenness of the vascular wall, high blood flow velocity, the layers are mixed, erythrocytes begin to make a chaotic movement in different directions.

Dopplerogram - a graphical reflection of the Doppler frequency shift over time - has two main components:

- envelope curve - linear velocity in the central layers of the flow;
- Doppler spectrum - a graphical characteristic of the proportional ratio of erythrocyte pools moving at different speeds.

When conducting spectral Doppler analysis, qualitative and quantitative parameters are evaluated. Quality options include:

1. shape of the Doppler curve (envelope of the Doppler spectrum)
2. the presence of a “spectral” window.

Quantitative parameters include:

1. Velocity characteristics of the flow.
2. The level of peripheral resistance.
3. Indicators of kinematics.
4. The state of the Doppler spectrum.
5. Vascular reactivity.

1. The velocity characteristics of the flow are determined by the envelope curve. Allocate:

– systolic blood flow velocity Vs (maximum velocity)
– final diastolic blood flow velocity Vd ;
- average blood flow velocity (Vm) - the average value of blood flow velocity for the cardiac cycle is displayed. The average blood flow velocity is calculated by the formula:

- weighted average blood flow velocity, determined by the characteristics of the Doppler spectrum (reflects the average speed of erythrocytes across the entire diameter of the vessel - the true average blood flow velocity)
- a certain diagnostic value has an indicator of interhemispheric asymmetry of the linear velocity of blood flow (CA) in the same vessels:

where V 1, V 2 - the average linear velocity of blood flow in paired arteries.

2. The level of peripheral resistance - the resulting blood viscosity, intracranial pressure, the tone of the resistive vessels of the pial-capillary vascular network - is determined by the value of the indices:

– systolic-diastolic ratio (SCO) Stuart:

- index of peripheral resistance, or index of resistivity (IR) Pourselot (RI):

The Gosling index is the most sensitive in relation to changes in the level of peripheral resistance.

Interhemispheric asymmetry of peripheral resistance levels is characterized by the transmission pulsation index (TPI) Lindegaard:

where PI ps, PI zs - pulsation index in the middle cerebral artery on the affected and healthy side, respectively.

3. Indices of flow kinematics indirectly characterize the loss of kinetic energy by blood flow and thus indicate the level of “proximal” flow resistance:

The pulse wave rise index (PWI) is determined by the formula:

Where T o is the time of the beginning of systole,

T s is the time to reach peak LSC,

T c - the time occupied by the cardiac cycle;

4. The Doppler spectrum is characterized by two main parameters: frequency (the magnitude of the shift in the linear velocity of blood flow) and power (expressed in decibels and reflects the relative number of red blood cells moving at a given speed). Normally, the vast majority of the spectrum power is close to the envelope velocity. Under pathological conditions leading to a turbulent flow, the spectrum “expands” – the number of erythrocytes increases, making a chaotic movement or moving into the parietal layers of the flow.

Spectral expansion index. It is calculated as the ratio of the difference between the peak systolic blood flow velocity and the time-averaged average blood flow velocity to the peak systolic velocity. SBI = (Vps - NFV) / Vhs = 1 - TAV / Vps.

The state of the Doppler spectrum can be determined using the spread spectrum index (ESI) (stenosis) Arbelli:

where Fo is the spectral expansion in an unchanged vessel;

Fm - spectral expansion in a pathologically altered vessel.

Systolic-diastolic ratio. This ratio of the magnitude of the peak systolic blood flow velocity to the end-diastolic blood flow velocity is an indirect characteristic of the state of the vascular wall, in particular its elastic properties. One of the most frequent pathologies leading to a change in this value is arterial hypertension.

5. Vascular reactivity. To assess the reactivity of the vascular system of the brain, the reactivity coefficient is used - the ratio of indicators characterizing the activity of the circulatory system at rest to their value against the background of exposure to a load stimulus. Depending on the nature of the method of influencing the system under consideration, regulatory mechanisms will tend to return the intensity of cerebral blood flow to the initial level, or change it in order to adapt to new conditions of functioning. The first is typical when using stimuli of a physical nature, the second - chemical. Given the integrity and anatomical and functional interconnectedness of the components of the circulatory system, when assessing changes in blood flow parameters in the intracranial arteries (in the middle cerebral artery) for a certain stress test, it is necessary to consider the reaction of not each isolated artery, but two of the same name at the same time, and it is on this basis to evaluate the type of reaction .

Currently, there is the following classification of types of reactions to functional load tests:

1) unidirectional positive - characterized in the absence of significant (significant for each specific test) third-party asymmetry in response to a functional stress test with a sufficient standardized change in blood flow parameters;
2) unidirectional negative - with a bilateral reduced or absent response to a functional stress test;
3) multidirectional - with a positive reaction on one side and a negative (paradoxical) - on the contralateral, which can be of two types: a) with a predominance of the response on the side of the lesion; b) with a predominance of the answer on the opposite side.

Unidirectional positive reaction corresponds to a satisfactory value of the cerebral reserve, multidirectional and unidirectional negative - reduced (or absent).

Among the functional loads of a chemical nature, the inhalation test with inhalation for 1-2 minutes of a gas mixture containing 5-7% CO2 in the air most fully meets the requirements of the functional test. The ability of cerebral vessels to expand in response to inhalation of carbon dioxide can be sharply limited or completely lost, up to the appearance of inverted reactions, with a persistent decrease in the level of perfusion pressure, which occurs, in particular, in atherosclerotic lesions of the MAH and, especially, insolvency of the collateral blood supply pathways.

In contrast to hypercapnia, hypocapnia causes narrowing of both large and small arteries, but does not lead to abrupt changes in pressure in the microcirculatory bed, which contributes to maintaining adequate brain perfusion.

Similar in mechanism of action to the hypercapnic stress test is the Breath Holding test. The vascular reaction, expressed in the expansion of the arteriolar bed and manifested by an increase in the blood flow velocity in the large cerebral vessels, occurs as a result of an increase in the level of endogenous CO2 due to a temporary cessation of oxygen supply. Holding the breath for approximately one second leads to an increase in systolic blood flow velocity by 20-25% compared with the initial value.

As tests of myogenic orientation, the following are used: a test of short-term compression of the common carotid artery, sublingual intake of 0.25–0.5 mg of nitroglycerin, ortho- and anti-orthostatic tests.

The technique for studying cerebrovascular reactivity includes:

a) assessment of the initial values of LBF in the middle cerebral artery (anterior, posterior) from both sides;

b) carrying out one of the above functional stress tests;

c) reassessment after a standard time interval of LBF in the studied arteries;

d) calculation of the reactivity index, which reflects a positive increase in the parameter of the time-averaged maximum (average) blood flow velocity in response to the applied functional load.

To assess the nature of the reaction to functional load tests, the following classification of types of reactions is used:

1) positive - characterized by a positive change in the evaluation parameters with a reactivity index value of more than 1.1;
2) negative - characterized by a negative change in the evaluation parameters with a reactivity index value in the range from 0.9 to 1.1;
3) paradoxical - characterized by a paradoxical change in the parameters for assessing the reactivity index less than 0.9.

3.2. Anatomy of the carotid arteries and methods of their study.

Anatomy of the common carotid artery (CCA). The brachiocephalic trunk departs from the aortic arch on the right side, which divides at the level of the sternoclavicular articulation into the common carotid artery (CCA) and the right subclavian artery. To the left of the aortic arch, both the common carotid artery and the subclavian artery depart; The CCA goes up and laterally to the level of the sternoclavicular joint, then both CCAs go upwards parallel to each other. In most cases, the CCA is divided at the level of the upper edge of the thyroid cartilage or hyoid bone into the internal carotid artery (ICA) and external carotid artery (ECA). Outside of the CCA lies the internal jugular vein. In people with a short neck, the separation of the CCA occurs more highly. The length of the CCA on the right is on average 9.5 (7-12) cm, on the left 12.5 (10-15) cm. CCA options: short CCA 1-2 cm long; its absence - ICA and ECA begin independently from the aortic arch.

The study of the main arteries of the head is carried out with the patient lying on his back, before the start of the study, the carotid vessels are palpated, their pulsation is determined. A 4 MHz transducer is used to diagnose carotid and vertebral arteries.

For insonation of the CCA, the sensor is placed along the inner edge of the sternocleidomastoid muscle at an angle of degrees in the cranial direction, successively locating the artery along its entire length up to the bifurcation of the CCA. The CCA blood flow is directed away from the sensor.

Fig.1. Dopplerogram of the OSA is normal.

The Dopplerogram of the OSA is characterized by a high systolic-diastolic ratio (normally up to 25-35%), the maximum spectral power at the envelope curve, there is a clear spectral “window”. A staccato rich mid-range sound followed by a sustained low-frequency sound. The Dopplerogram of the OSA has similarities with the Dopplerograms of the NSA and NBA.

The CCA at the level of the upper edge of the thyroid cartilage divides into the internal and external carotid arteries. The ICA is the largest branch of the CCA and most often lies posterior and lateral to the ECA. The tortuosity of the ICA is often noted, it can be unilateral or bilateral. The ICA, rising vertically, reaches the external opening of the carotid canal and passes through it into the skull. Variants of the ICA: unilateral or bilateral aplasia or hypoplasia; independent discharge from the aortic arch or from the brachiocephalic trunk; unusually low start from OCA.

The study is carried out with the patient lying on his back at the angle of the lower jaw with a 4 or 2 MHz sensor at an angle of 45–60 degrees in the cranial direction. The direction of blood flow along the ICA from the sensor.

Normal dopplerogram of the ICA: fast steep ascent, pointed apex, slow sawtooth smooth descent. The systolic-diastolic ratio is about 2.5. The maximum spectral power - the envelope, there is a spectral "window"; characteristic blowing musical sound.

Fig.2. Dopplerogram of the ICA is normal.

Anatomy of the vertebral artery (VA) and research methodology.

PA is a branch of the subclavian artery. On the right, it begins at a distance of 2.5 cm, on the left - 3.5 cm from the beginning of the subclavian artery. The vertebral arteries are divided into 4 segments. The initial segment of the VA (V1), located behind the anterior scalene muscle, goes up, enters the opening of the transverse process of the 6th (rarely 4-5 or 7th) cervical vertebra. Segment V2 - the cervical part of the artery passes in the canal formed by the transverse processes of the cervical vertebrae and rises up. Having exited through the opening in the transverse process of the 2nd cervical vertebra (segment V3), the VA proceeds posteriorly and laterally (1st bend), heading for the opening of the transverse process of the atlas (2nd bend), then turns to the dorsal side of the lateral part of the atlas (3 -th bend) turning medially and reaching the greater foramen magnum (4th bend), it passes through the atlanto-occipital membrane and dura mater into the cranial cavity. Further, the intracranial part of the PA (segment V4) goes to the base of the brain laterally from the medulla oblongata, and then anteriorly from it. Both PAs at the border of the medulla oblongata and the pons merge into one main artery. Approximately in half of the cases, one or both PAs have an S-shaped bend until the moment of confluence.

The study of PA is performed with the patient lying on his back with a 4 MHz or 2 MHz sensor in the V3 segment. The sensor is placed along the posterior edge of the sternocleidomastoid muscle 2-3 cm below the mastoid process, directing the ultrasonic beam to the opposite orbit. The direction of blood flow in the V3 segment, due to the presence of bends and individual characteristics of the course of the artery, can be direct, reverse and bidirectional. To identify the PA signal, a test with cross-clamping of the homolateral CCA is performed, if the blood flow does not decrease, then the PA signal.

The blood flow in the vertebral artery is characterized by continuous pulsation and a sufficient level of the diastolic velocity component, which is also a consequence of low peripheral resistance in the vertebral artery.

Fig.3. Dopplerogram of PA.

Anatomy of the supratrochlear artery and research methodology.

The supratrochlear artery (SAA) is one of the terminal branches of the ophthalmic artery. The ophthalmic artery arises from the medial side of the anterior bulge of the ICA siphon. It enters the orbit through the optic nerve canal and divides on the medial side into its terminal branches. The NMA emerges from the orbital cavity through the frontal notch and anastomoses with the supraorbital artery and with the superficial temporal artery, branches of the ECA.

The study of the NBA is carried out with the eyes closed with an 8 MHz sensor, which is located at the inner corner of the eye towards the upper wall of the orbit and medially. Normally, the direction of blood flow along the NMA to the sensor (antegrade blood flow). The blood flow in the supratrochlear artery has a continuous pulsation, a high level of the diastolic velocity component and a continuous sound signal, which is a consequence of the low peripheral resistance in the basin of the internal carotid artery. Dopplerogram of the NBA is typical for the extracranial vessel (similar to the Dopplerograms of the ECA and CCA). High steep systolic peak with a rapid rise, a sharp peak and a rapid stepped descent followed by a smooth descent into diastole, high systolic-diastolic ratio. The maximum spectral power is concentrated in the upper part of the Dopplerogram, near the envelope; the spectral “window” is expressed.

Fig.4. Dopplerogram of the NBA is normal.

The shape of the blood flow velocity curve in the peripheral arteries (subclavian, brachial, ulnar, radial) differs significantly from the shape of the curve of the arteries supplying the brain. Due to the high peripheral resistance of these segments of the vascular bed, there is practically no diastolic velocity component and the blood flow velocity curve is located on the isoline. Normally, the peripheral arterial flow velocity curve has three components: a systolic pulsation due to direct blood flow, a reverse flow in early diastole due to arterial reflux, and a small positive peak in late diastole after blood is reflected from the aortic valve cusps. This type of blood flow is called main.

Rice. 5. Dopplerogram of peripheral arteries, main type of blood flow.

3.3. Doppler flow analysis.

Based on the results of Doppler analysis, the main flows can be distinguished:

1) main stream,

2) flow stenosis,

4) residual flow,

5) difficult perfusion,

6) embolism pattern,

7) cerebral angiospasm.

1. Main stream characterized by normal (for a specific age group) indicators of linear blood flow velocity, resistivity, kinematics, spectrum, reactivity. This is a three-phase curve, consisting of a systolic peak, a retrograde peak that occurs in diastole due to retrograde blood flow towards the heart until the aortic valve closes, and a third antegrade small peak occurs at the end of diastole, and is explained by the occurrence of weak antegrade blood flow after blood is reflected from the aortic cusps. valve. The main type of blood flow is characteristic of peripheral arteries.

2. With stenosis of the lumen of the vessel(hemodynamic variant: discrepancy between the diameter of the vessel and the normal volumetric blood flow, (narrowing of the lumen of the vessel by more than 50%), which occurs with atherosclerotic lesions, compression of the vessel by a tumor, bone formations, kink of the vessel) due to the D. Bernoulli effect, the following changes occur:

increases the linear predominantly systolic blood flow velocity;
the level of peripheral resistance is slightly reduced (due to the inclusion of autoregulatory mechanisms aimed at reducing peripheral resistance)
flow kinematic indices do not change significantly;
progressive, proportional to the degree of stenosis, expansion of the spectrum (the Arbelli index corresponds to% stenosis of the vessel in diameter)
a decrease in cerebral reactivity, mainly due to a narrowing of the vasodilatory reserve, with preserved opportunities for vasoconstriction.

3. With shunting lesions of the vascular system of the brain - relative stenosis, when there is a discrepancy between the volumetric blood flow and the normal diameter of the vessel (arteriovenous malformations, arteriosinus anastomoses, excessive perfusion,) the Dopplerographic pattern is characterized by:

a significant increase (mainly due to diastolic) linear blood flow velocity in proportion to the level of arteriovenous discharge;
a significant decrease in the level of peripheral resistance (due to organic damage to the vascular system at the level of resistive vessels, which determines the low level of hydrodynamic resistance in the system)
relative preservation of flow kinematic indices;
the absence of pronounced changes in the Doppler spectrum;
a sharp decrease in cerebrovascular reactivity, mainly due to a narrowing of the vasoconstrictor reserve.

4. Residual flow- is registered in vessels located distal to the zone of hemodynamically significant occlusion (thrombosis, occlusion of the vessel, stenosis% in diameter). Characterized by:

a decrease in LBF, mainly in the systolic component;
the level of peripheral resistance decreases due to the inclusion of autoregulatory mechanisms that cause dilation of the pial-capillary vascular network;
sharply reduced kinematics (“smoothed flow”)
doppler spectrum of relatively low power;
a sharp decrease in reactivity, mainly due to the vasodilatory reserve.

5. Difficult perfusion- typical for vessels, segments located proximal to the zone of abnormally high hydrodynamic effect. It is noted with intracranial hypertension, diastolic vasoconstriction, deep hypocapnia, arterial hypertension. Characterized by:

decrease in LBF due to the diastolic component;
a significant increase in the level of peripheral resistance;
indicators of kinematics and spectrum change little;
significantly reduced reactivity: with intracranial hypertension - to hypercapnic load, with functional vasoconstriction - to hypocapnic.

7. Cerebral angiospasm- occurs as a result of contraction of the smooth muscles of the cerebral arteries in subarachnoid hemorrhage, stroke, migraine, arterial hypo and hypertension, dyshormonal disorders and other diseases. It is characterized by a high linear velocity of blood flow, mainly due to the systolic component.

Depending on the increase in LBF, there are 3 degrees of severity of cerebral angiospasm:

mild degree - up to 120 cm / sec,

medium degree - up to 200 cm / sec,

severe degree - over 200 cm / sec.

An increase to 350 cm / sec and above leads to a cessation of blood circulation in the vessels of the brain.

In 1988 K.F. Lindegard proposed to determine the ratio of peak systolic velocity in the middle cerebral artery and the internal carotid artery of the same name. As the degree of cerebral angiospasm increases, the ratio of velocities between MCA and ICA changes (in the norm: V cma/Vvsa = 1.7 ± 0.4). This indicator also allows you to judge the severity of spasm of the MCA:

mild degree 2.1-3.0

average degree 3.1-6.0

severe more than 6.0.

The value of the Lindegard index in the range from 2 to 3 can be assessed as diagnostically significant in individuals with functional vasospasm.

Dopplerographic monitoring of these indicators allows for early diagnosis of angiospasm, when angiographically it may not yet be detected, and the dynamics of its development, which allows for more effective treatment.

The threshold value of the peak systolic blood flow velocity for angiospasm in the ACA according to the literature is 130 cm/s, in the PCA - 110 cm/s. For OA, different authors proposed different threshold values for peak systolic blood flow velocity, which varied from 75 to 110 cm/s. For the diagnosis of angiospasm of the basilar artery, the ratio of the peak systolic velocity of OA and PA at the extracranial level is taken, a significant value = 2 or more. Table 1 shows the differential diagnosis of stenosis, angiospasm and arteriovenous malformation.

Chapter 4
Estimated indicators of vascular tone and tissue blood flow in the systemic circulation

Determining the tone of the arterial vessels of the systemic circulation is a necessary element in the analysis of the mechanisms of changes in systemic hemodynamics. It should be remembered that the tone of various arterial vessels has different effects on the characteristics of the systemic circulation. Thus, the tone of arterioles and precapillaries provides the greatest resistance to blood flow, which is why these vessels are called resistive, or resistance vessels. The tone of large arterial vessels has a lesser effect on peripheral resistance to blood flow.

The level of mean arterial pressure, with certain reservations, can be imagined as the product of cardiac output and the total resistance of resistive vessels. In some cases, for example, with arterial hypertension or hypotension, it is essential to identify the issue on which the shift in the level of systemic blood pressure depends - on changes in the performance of the heart or vascular tone in general. In order to analyze the contribution of vascular tone to the marked shifts in blood pressure, it is customary to calculate the total peripheral vascular resistance.

4.1. Total peripheral vascular resistance

This value shows the total resistance of the precapillary bed and depends on both vascular tone and blood viscosity. The total peripheral vascular resistance (OPVR) is affected by the nature of the branching of the vessels and their length, so usually the greater the body weight, the less the OPSS. Due to the fact that the expression of OPSS in absolute units requires the conversion of pressure into dynes / cm 2 (SI system), the formula for calculating OPSS is as follows:

Units of measurement OPSS - dyne cm -5

Among the methods for assessing the tone of large arterial trunks is the determination of the velocity of propagation of the pulse wave. In this case, it is possible to characterize the elastic-viscous properties of the walls of vessels of both predominantly muscular and elastic types.

4.2. Pulse Wave Velocity and Elasticity Modulus of the Vascular Wall

The speed of propagation of the pulse wave through the vessels of the elastic (S e) and muscular (S m) types is calculated on the basis of either synchronous registration of sphygmograms (SFG) of the carotid and femoral, carotid and radial arteries, or synchronous recording of the ECG and SFG of the corresponding vessels. It is possible to determine C e and C m with synchronous registration of rheograms of the extremities and ECG. The speed calculation is very simple:

C e \u003d L e / T e; C m \u003d L m / T m

where T e is the delay time of the pulse wave in the arteries of the elastic type (determined, for example, by the delay in the rise of the SFG of the femoral artery relative to the rise of the SFG of the carotid artery or from the R or S wave of the ECG to the rise of the femoral SFG); T m - the delay time of the pulse wave in the vessels of the muscular type (determined, for example, by the delay of the SFG of the radial artery relative to the SFG of the carotid artery or the K wave of the ECG); L e - the distance from the jugular fossa to the navel + the distance from the navel to the pulse receiver on the femoral artery (when using the two SFG technique, the distance from the jugular fossa to the sensor on the carotid artery should be subtracted from this distance); L m is the distance from the sensor on the radial artery to the jugular fossa (as in measuring L e, the length to the carotid pulse sensor must be subtracted from this value if the technique of two SFGs is used).

The modulus of elasticity of vessels of the elastic type (E e) is calculated by the formula:

where E 0 - total elastic resistance, w - OPSS. E 0 is found by the Wetzler formula:

where Q is the cross-sectional area of the aorta; T is the time of the main fluctuation of the pulse of the femoral artery (see Fig. 2); With e - the speed of propagation of the pulse wave through the vessels of the elastic type. E 0 can be calculated and but Brezmer and the Bank:

where PI is the duration of the exile period. N.N. Savitsky, taking E 0 as the total elastic resistance of the vascular system or its volumetric elasticity modulus, proposes the following equality:

where PD - pulse pressure; D - duration of diastole; MAP - mean arterial pressure. The expression E 0 /w can, with a known error, also be called the total elastic resistance of the aortic wall, and in this case the formula is more suitable:

where T is the duration of the cardiac cycle, MD is mechanical diastole.

4.3. Regional blood flow index

In clinical and experimental practice, it often becomes necessary to study the peripheral blood flow for the diagnosis or differential diagnosis of vascular diseases. Currently, a sufficiently large number of methods for studying peripheral blood flow have been developed. At the same time, a number of methods characterize only the qualitative features of the state of peripheral vascular tone and blood flow in them (sphygmo- and phlebography), others require sophisticated special equipment (electromagnetic and ultrasonic transducers, radioactive isotopes, etc.) or are feasible only in experimental studies (resistography). ).

In this regard, of considerable interest are indirect, fairly informative and easily implemented methods that allow quantitative study of peripheral arterial and venous blood flow. The latter include plethysmographic methods (VV Orlov, 1961).

When analyzing the occlusal plethysmogram, you can calculate the volumetric blood flow rate (VFR) in cm 3 /100 tissue/min:

where ΔV is the increase in blood flow volume (cm 3) over time T.

With a slow dosed increase in pressure in the occlusal cuff (from 10 to 40 mm Hg), it is possible to determine venous tone (VT) in mm Hg/cm 3 per 100 cm 3 of tissue according to the formula:

where MAP is mean arterial pressure.

To judge the functionality of the vascular wall (mainly arterioles), a calculation of the spasm index (PS) is proposed, which is eliminated by a certain (for example, 5-minute ischemia) vasodilatory effect (N.M. Mukharlyamov et al., 1981):

Further development of the method led to the use of venous occlusive tetrapolar electroplethysmography, which made it possible to detail the calculated indicators, taking into account the values of arterial inflow and venous outflow (D.G. Maksimov et al.; L.N. Sazonova et al.). According to the developed complex methodology, a number of formulas for calculating the indicators of regional blood circulation are proposed:

When calculating the indicators of arterial inflow and venous outflow, the values of K 1 and K 2 are found by preliminary comparison of the data of the impedance method with the data of direct or indirect quantitative research methods that have already been verified and metrologically justified.

The study of peripheral blood flow in the systemic circulation is also possible by the method of rheography. The principles for calculating rheogram indicators are described in detail below.

Source: Brin V.B., Zonis B.Ya. Physiology of systemic circulation. Formulas and calculations. Rostov University Press, 1984. 88 p.

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Table of contents of the subject "Functions of the Circulatory and Lymphatic Circulation Systems. Circulatory System. Systemic Hemodynamics. Cardiac Output.":
1. Functions of the circulatory and lymphatic circulation systems. circulatory system. Central venous pressure.
2. Classification of the circulatory system. Functional classifications of the circulatory system (Folkova, Tkachenko).
3. Characteristics of the movement of blood through the vessels. Hydrodynamic characteristics of the vascular bed. Linear blood flow velocity. What is cardiac output?
4. Blood flow pressure. Blood flow speed. Scheme of the cardiovascular system (CVS).
5. Systemic hemodynamics. Hemodynamic parameters. Systemic arterial pressure. Systolic, diastolic pressure. Medium pressure. pulse pressure.

7. Cardiac output. Minute volume of blood circulation. heart index. Systolic blood volume. Reserve volume of blood.
8. Heart rate (pulse). The work of the heart.
9. Contractility. Contractility of the heart. Myocardial contractility. myocardial automatism. myocardial conduction.
10. Membrane nature of automatism of the heart. Pacemaker. Pacemaker. myocardial conduction. A true pacemaker. latent pacemaker.