This term means total resistance of the entire vascular system the flow of blood emitted by the heart. This relationship is described equation:

As follows from this equation, to calculate the peripheral vascular resistance, it is necessary to determine the value of systemic blood 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 human, the radius of the vessels, their length and blood viscosity usually remain unknown, Franc, using a formal analogy between hydraulic and electrical circuits, cited Poiseuille's equation to the following form:

where P1-P2 is the pressure difference at the beginning and end of the section of the vascular system, Q is the amount of blood flow through this section, 1332 is the coefficient of conversion 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 varying degrees. Thus, in specific cases, the level of SBP can be determined primarily by the value of TPSS or mainly by CO.

Rice. 9.3. A more pronounced increase in vascular resistance in the thoracic aorta basin compared to its changes in the brachiocephalic artery basin during the pressor reflex.

Under normal physiological conditions OPSS ranges from 1200 to 1700 dynes per cm; with hypertension, this value can double the norm and be equal to 2200-3000 dynes per cm-5.

OPSS value consists of sums (not arithmetic) of the resistances of regional vascular sections. At the same time, depending on the greater or lesser severity of changes in regional vascular resistance, they will accordingly receive a smaller or larger volume of blood ejected by the heart. In Fig. Figure 9.3 shows an example of a more pronounced degree of increase in vascular resistance 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 the basis for the effect of “centralization” of blood circulation in warm-blooded animals, which ensures redistribution of blood, primarily to the brain and myocardium, in difficult or life-threatening conditions (shock, blood loss, etc.).

For specificity, let us consider an example of an erroneous (error when dividing by S) calculation of total vascular resistance. When summarizing clinical results, data from patients of different heights, ages and weights are used. For a large patient (for example, a hundred kilogram patient), an IOC of 5 liters per minute at rest may not be sufficient. For an average person - within the normal range, and for a patient of low weight, say, 50 kilograms - excessive. How to take these circumstances into account?

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

S=0.007124 W 0.425 H 0.723 , W–weight; H–height.

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

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

Let us recall the formula by which the absolute value of total vascular resistance is calculated (TVR, or TPR, TPR, different notations are used):

OSS=79.96 (BP-BP) IOC -1 din*s*cm - 5 ;

79.96 – dimension coefficient, BP – mean arterial pressure in mmHg. art., VP - venous pressure in mm Hg. Art., MOC – minute volume of blood circulation in l/min)

Let a large person (full adult European) have IOC = 4 liters per minute, BP-BP = 70, then OVR approximately (so as not to lose the essence behind tenths) will have the value

OCC=79.96 (AD-BP) IOC -1 @ 80 70/4@1400 din*s*cm -5 ;

remember - 1400 din*s*cm - 5 .

Let a small person (thin, short, but quite viable) have IOC = 2 liters per minute, BP-BP = 70, from here OVR will be approximately

79.96 (AD-BP) IOC -1 @80 70/2@2800 din*s*cm -5 .

The OPS of a small person is 2 times greater than that of a large person. 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.

To make comparisons possible, indices are introduced that take into account the surface (S) of the human body. By multiplying total vascular resistance (TVR) by S, we get an index (TVR*S=IOVR), which can be compared:

IOSS = 79.96 (BP-BP) IOC -1 S (din*s*m 2 *cm -5).

From the experience of measurements and calculations it is known that for a large person S is approximately 2 m2, for a very small person we take 1 m2. Their total vascular resistances will not be equal, but the indices will be equal:

IOSS=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 cardiovascular system.

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

Elasticity index of the arterial vascular reservoir(IEA)

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

calculated in accordance with Hooke's law and Frank's model. The greater the IEA, the greater the SI, and the smaller the greater the product of the contraction frequency (HR) and the difference between arterial systolic (APS) and diastolic (APP) pressures. It is possible to calculate the elasticity of the arterial reservoir (or elastic modulus) using the velocity of the pulse wave. In this case, the elastic modulus of only that part of the arterial vascular reservoir that is used to measure the pulse wave velocity will be assessed.

Pulmonary arterial vascular reservoir elasticity index (IELA)

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

is calculated similarly to the previous description: the greater the SI, the greater the IELA and the smaller, the greater the product of the contraction frequency and the difference between pulmonary arterial systolic (PAS) and diastolic (PADP) 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 = (V/S-BP IEA-LAD IELA-LVD IELV)/VD

calculated using a mathematical model. Actually, the mathematical model is the main tool for achieving systematic indicators. Given the existing clinical and physiological knowledge, the model cannot be adequate in the usual sense. Continuous customization and computing capabilities allow the constructability of the model to dramatically increase. This makes the model useful, despite its poor adequacy in relation to a group of patients and to one patient for various treatment and life conditions.

Pulmonary venous vascular reservoir elasticity index (IELV)

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

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

Total peripheral vascular resistance index (IOSS) has been reviewed previously. Let us repeat here briefly for the convenience of the reader:

IOSS=79.92 (AD-BP)/SI

This ratio does not explicitly reflect the radius of the vessels, their branching and length, the viscosity of the blood, and much more. But it displays the interdependence of SI, OPS, AD and VD. We emphasize that taking into account 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, unless, of course, the task is not theoretical research, but clinical practice.

SSS indicators (system sets) for stages of CABG surgery. Indexes are in bold

CV indicators	Designation	Dimensions	Admission to the operating unit	End of operation	Average for the period of 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	beats/min	80.7±3.1	90.1±2.2	87.7±1.5
Systolic blood pressure	ADS	mmHg.	148.9±4.7	128.1±3.1	124.2±2.6
Diastolic blood pressure	ADD	mmHg.	78.4±2.5	68.5±2.0	64.0±1.7
Average blood pressure	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 diastolic pressure	LADD	mmHg.	12.9±1.0	10.2±0.6	9.1±0.5
Pulmonary arterial pressure average	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	FTD	mmHg.	10.0±1.7	7.3±0.8	6.5±0.5
Left ventricular index	ILZH	cm 3 / (s m 2 mm Hg)	5.05±0.51	5.3±0.4	6.5±0.4
Right ventricular index	IPI	cm 3 / (s m 2 mm Hg)	8.35±0.76	6.5±0.6	8.8±0.7
Vascular resistance index	IOSS	din s m 2 cm -5	2670±117	2787±38	2464±87
Pulmonary vascular resistance index	ILSS	din s 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 -1	0.6±0.1	0.5±0.0	0.5±0.0
Pulmonary vein elasticity index	IELV	cm 3 m -2 mm Hg -1	16.3±2.2	15.8±2.5	16.3±1.0
Pulmonary artery elasticity index	IELA	cm 3 m -2 mm Hg -1	3.3±0.4	3.3±0.7	3.0±0.3

Owners of patent RU 2481785:

The group of inventions relates to medicine and can be used in clinical physiology, physical culture and sports, cardiology, and other areas of medicine. In healthy subjects, heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) are measured. Determines the proportionality coefficient K depending on body weight and height. Calculate the value of OPSS in Pa mL -1 s using the original mathematical formula. Then the minute blood volume (MBV) is calculated using a mathematical formula. The group of inventions makes it possible to obtain more accurate values of TPSS and IOC, to assess the state of central hemodynamics through the use of physically and physiologically based calculation formulas. 2 n.p.f-ly, 1 pr.

The invention relates to medicine, in particular to the determination of indicators reflecting the functional state of the cardiovascular system, and can be used in clinical physiology, physical culture and sports, cardiology, and other areas of medicine. For most physiological studies conducted on humans, in which pulse, systolic (SBP) and diastolic (DBP) blood pressure are measured, integral indicators of the state of the cardiovascular system are useful. The most important of these indicators, reflecting not only the functioning of the cardiovascular system, but also the level of metabolic and energy processes in the body, is the minute blood volume (MBV). Total peripheral vascular resistance (TPVR) is also the most important parameter used to assess the state of central hemodynamics.

The most popular method for calculating stroke volume (SV), and based on it the IOC, is Starr’s formula:

VR=90.97+0.54 PD-0.57 DBP-0.61 V,

where PP is pulse pressure, DBP is diastolic pressure, B is age. Next, the IOC is calculated as the product of SV and heart rate (IOC = SV·HR). But the accuracy of Starr's formula has been questioned. The correlation coefficient between the SV values obtained by impedance cardiography methods and the values calculated using the Starr formula was only 0.288. According to our data, the discrepancy between the value of SV (and, consequently, IOC), determined using the tetrapolar rheography method and calculated using the Starr formula, in some cases exceeds 50%, even in a group of healthy subjects.

There is a known method for calculating the IOC using the Lilje-Strander and Zander formula:

IOC=AD ed. · Heart rate,

where is AD ed. - reduced blood pressure, blood pressure ed. = PP·100/Avg.Da, HR is heart rate, PP is pulse pressure, calculated by the formula PP=SBP-DBP, and Avg.Da is the average pressure in the aorta, calculated by the formula: Avg.Da=(SBP+ DBP)/2. But in order for the Lilje-Strander and Zander formula to reflect the IOC, it is necessary that the numerical value of AD ed. , which is PP multiplied by a correction factor (100/Sr.Da), coincided with the value of stroke ejected by the ventricle of the heart during one systole. In fact, with a value of Av.Da = 100 mm Hg. blood pressure value ed. (and, consequently, SV) is equal to the value of PD, with Average Yes<100 мм рт.ст. - АД ред. несколько превышает ПД, а при Ср.Да>100 mmHg - AD ed. becomes less than PD. In fact, the value of PD cannot be equated to the value of SV even with Average Da=100 mmHg. Normal average values of PP are 40 mm Hg, and SV are 60-80 ml. A comparison of the IOC values calculated using the Lilje-Strander and Zander formula in a group of healthy subjects (2.3-4.2 l) with the normal IOC values (5-6 l) shows a discrepancy between them of 40-50%.

The technical result of the proposed method is to increase the accuracy of determining minute blood volume (MVR) and total peripheral vascular resistance (TPVR) - the most important indicators reflecting the functioning of the cardiovascular system, the level of metabolic and energy processes in the body, assessing the state of central hemodynamics through the use of physical and physiologically based calculation formulas.

A method is claimed for determining integral indicators of the state of the cardiovascular system, which consists in measuring the subject's heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), weight and height at rest. After this, total peripheral vascular resistance (TPVR) is determined. The value of TPSS is proportional to diastolic blood pressure (DBP) - the higher the DBP, the greater the TPSS; time intervals between periods of ejection (Tpi) of blood from the ventricles of the heart - the longer the interval between periods of ejection, the greater the TPR; circulating blood volume (CBV) - the more BCC, the lower the OPSS (CBV depends on a person’s weight, height and gender). OPSS is calculated using the formula:

OPSS=K·DAD·(Tsts-Tpi)/Tpi,

where DBP is diastolic blood pressure;

Tstc - period of the cardiac cycle, calculated by the formula Tstc=60/HR;

Tpi is the expulsion period, calculated by the formula:

Tpi=0.268·Tsc 0.36 ≈Tsc·0.109+0.159;

K is a proportionality coefficient depending on body weight (BW), height (P) and gender of a person. K=1 in women with MT=49 kg and P=150 cm; in men with MT=59 kg and P=160 cm. In other cases, K for healthy subjects is calculated according to the rules presented in Table 1.

MOK=Avg.Da·133.32·60/OPSS,

Avg.Yes=(GARDEN+DBP)/2;

Table 2 shows examples of calculations of the IOC (RMOC) using this method in 10 healthy subjects aged 18-23 years, compared with the IOC value determined using the non-invasive monitor system "MARG 10-01" (Microlux, Chelyabinsk), the basis of the work which is the method of tetrapolar bioimpedance rheocardiography (error 15%).

Table 2.
Floor	№	R, cm	MT, kg	Heart rate beats/min	SBP mmHg	DBP mmHg	IOC, ml	RMOC, ml	Deviation %
and	1	154	42	72	117	72	5108	5108	0
	2	157	48	75	102	72	4275	4192	2
	3	172	56	57	82	55	4560	4605	1
	4	159	58	85	107	72	6205	6280	1
	5	164	65	71	113	71	6319	6344	1
6	167	70	73	98	66	7008	6833	3
m	7	181	74	67	110	71	5829	5857	0,2
	8	187	87	69	120	74	6831	7461	9
	9	193	89	55	104	61	6820	6734	1
10	180	70	52	113	61	5460	5007	9
Average deviation between the MOC and RMOC values in these examples	2,79%

The deviation of the calculated value of the IOC from its measured value using the method of tetrapolar bioimpedance rheocardiography in 20 healthy subjects aged 18-35 years averaged 5.45%. The correlation coefficient between these values was 0.94.

The deviation of the calculated values of OPSS and IOC using this method from the measured values can be significant only if there is a significant error in determining the proportionality coefficient K. The latter is possible with deviations in the functioning of the regulation mechanisms of OPSS and/or with excessive deviations from the norm of MT (MT>>P (cm) -101). However, errors in determining TPR and MOC in these patients can be leveled out either by introducing an amendment to the calculation of the proportionality coefficient (K), or by introducing an additional correction factor into the formula for calculating TPR. These amendments can be either individual, i.e. based on preliminary measurements of the assessed indicators in a particular patient, and group, i.e. based on statistically identified changes in K and OPSS in a certain group of patients (with a certain disease).

The method is implemented as follows.

To measure heart rate, SBP, DBP, weight and height, any certified devices for automatic, semi-automatic, manual measurement of pulse, blood pressure, weight and height can be used. The subject's heart rate, SBP, DBP, body mass (weight) and height are measured at rest.

After this, the proportionality coefficient (K) is calculated, which is necessary to calculate the OPSS and depends on the body weight (BW), height (P) and gender of the person. For women, K=1 with MT=49 kg and P=150 cm;

at MT≤49 kg K=(MT·P)/7350; at MT>49 kg K=7350/(MT·P).

For men, K=1 with MT=59 kg and P=160 cm;

at MT≤59 kg K=(MT·P)/9440; at MT>59 kg K=9440/(MT·P).

After this, the OPSS is determined using the formula:

OPSS=K·DAD·(Tsts-Tpi)/Tpi,

Tstc=60/HR;

Tpi is the expulsion period, calculated by the formula:

Tpi=0.268·Tsc 0.36 ≈Tsc·0.109+0.159.

The IOC is calculated using the equation:

MOK=Avg.Da·133.32·60/OPSS,

where Avg.Da is the average pressure in the aorta, calculated by the formula:

Avg.Yes=(GARDEN+DBP)/2;

133.32 - amount of Pa in 1 mm Hg;

TPVR - total peripheral vascular resistance (Pa ml -1 s).

The implementation of the method is illustrated by the example below.

Woman - 34 years old, height 164 cm, MT=65 kg, pulse (HR) - 71 beats/min, SBP=113 mmHg, DBP=71 mmHg.

K=7350/(164·65)=0.689

Tsts=60/71=0.845

Tpi≈Tsc·0.109+0.159=0.845·0.109+0.159=0.251

OPSS=K·DAD·(Tsc-Tpi)/Tpi=0.689·71·(0.845-0.251)/0.251=115.8≈116 Pa·ml -1 ·s

Average Yes=(SBP+DBP)/2=(113+71)/2=92 mmHg.

IOC=Avg.Da·133.32·60/OPSS=92·133.32·60/116=6344 ml≈6.3 l

The deviation of this calculated IOC value for this subject from the IOC value determined using tetrapolar bioimpedance rheocardiography was less than 1% (see Table 2, subject No. 5).

Thus, the proposed method allows one to quite accurately determine the values of OPSS and MOC.

BIBLIOGRAPHY

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3. Karpman V.L. Phase analysis of cardiac activity. M., 1965. 275 p., p. 111.

4. Murashko L.E., Badoeva F.S., Petrova S.B., Gubareva M.S. Method for integral determination of central hemodynamic parameters. // RF Patent No. 2308878. Published 10/27/2007.

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8. Ctarr I // Circulation, 1954. - V.19 - P.664.

1. A method for determining integral indicators of the state of the cardiovascular system, which consists in determining the total peripheral vascular resistance (TPVR) in healthy subjects, including measuring heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), different in that they also measure body weight (MW, kg), height (P, cm) to determine the proportionality coefficient (K), in women with MT≤49 kg according to the formula K=(MW·P)/7350, with MT>49 kg according to the formula K=7350/(MW·P), for men with MT≤59 kg according to the formula K=(MW·P)/9440, for MT>59 kg according to the formula K=9440/(MW·P), the value OPSS is calculated using the formula
OPSS=K·DAD·(Tsts-Tpi)/Tpi,
where Tc is the period of the cardiac cycle, calculated by the formula
Tstc=60/HR;
Tpi - period of expulsion, Tpi=0.268·Tsc 0.36 ≈Tsc·0.109+0.159.

2. A method for determining integral indicators of the state of the cardiovascular system, which consists in determining the minute blood volume (MBV) in healthy subjects, characterized in that the MVC is calculated using the equation: MVC=Avg.Da·133.32·60/OPSS,
where Av.Da is the average pressure in the aorta, calculated by the formula
Avg.Yes=(GARDEN+DBP)/2;
133.32 - amount of Pa in 1 mm Hg;
TPVR - total peripheral vascular resistance (Pa ml -1 s).

Similar patents:

The invention relates to medical equipment and can be used to perform various medical procedures. .

8) classification of blood vessels.

Blood vessels- elastic tubular formations in the body of animals and humans, through which the force of a rhythmically contracting heart or a pulsating vessel carries out the movement of blood throughout the body: to organs and tissues through arteries, arterioles, arterial capillaries, and from them to the heart - through venous capillaries, venules and veins .

Among the vessels of the circulatory system there are arteries, arterioles, capillaries, venules, veins And arteriole-venous anastomoses; The vessels of the microcirculatory system mediate the relationship between arteries and veins. Vessels of different types differ not only in their thickness, but also in tissue composition and functional features.

Arteries are vessels through which blood moves away from the heart. Arteries have thick walls that contain muscle fibers as well as collagen and elastic fibers. They are very elastic and can contract or expand, depending on the amount of blood pumped by the heart.

Arterioles are small arteries that immediately precede capillaries in the blood flow. Smooth muscle fibers predominate in their vascular wall, thanks to which arterioles can change the size of their lumen and, thus, resistance.

Capillaries are tiny blood vessels, so thin that substances can freely penetrate their walls. Through the capillary wall, nutrients and oxygen are released from the blood into cells and carbon dioxide and other waste products are transferred from cells to the blood.

Venules are small blood vessels that provide in a large circle the outflow of oxygen-depleted blood saturated with waste products from the capillaries into the veins.

Veins are vessels through which blood moves to the heart. The walls of veins are less thick than the walls of arteries and contain correspondingly fewer muscle fibers and elastic elements.

9) Volumetric blood flow velocity

The volumetric flow rate of the blood (blood flow) of the heart is a dynamic indicator of the activity of the heart. The variable physical quantity corresponding to this indicator characterizes the volumetric amount of blood passing through the cross section of the flow (in the heart) per unit time. The volumetric blood flow velocity of the heart is estimated using the formula:

CO = HR · SV / 1000,

Where: HR- heart rate (1/ min), SV- systolic blood flow volume ( ml, l). The circulatory system, or cardiovascular system, is a closed system (see diagram 1, diagram 2, diagram 3). It consists of two pumps (right heart and left heart), connected in series by blood vessels of the systemic circulation and blood vessels of the pulmonary circulation (vessels of the lungs). In any aggregate cross section of this system, the same amount of blood flows. In particular, under the same conditions, the flow of blood flowing through the right heart is equal to the flow of blood flowing through the left heart. In a person at rest, the volumetric velocity of blood flow (both right and left) of the heart is ~4.5 ÷ 5.0 l / min. The purpose of the circulatory system is to ensure continuous blood flow to all organs and tissues in accordance with the needs of the body. The heart is a pump that pumps blood through the circulatory system. Together with the blood vessels, the heart actualizes the purpose of the circulatory system. Hence, the volumetric blood flow velocity of the heart is a variable that characterizes the efficiency of the heart. Heart blood flow is controlled by the cardiovascular center and is influenced by a number of variables. The main ones are: the volumetric flow rate of venous blood to the heart ( l / min), end-diastolic blood flow volume ( ml), systolic blood flow volume ( ml), end-systolic blood flow volume ( ml), heart rate (1/ min).

10) Linear speed of blood flow (blood flow) is a physical quantity that is a measure of the movement of blood particles that make up the flow. Theoretically, it is equal to the distance traveled by a particle of the substance that makes up the flow per unit time: v = L / t. Here L- path ( m), t- time ( c). In addition to the linear velocity of blood flow, there is a distinction between the volumetric velocity of blood flow, or volumetric blood flow velocity. Average linear velocity of laminar blood flow ( v) is estimated by integrating the linear velocities of all cylindrical flow layers:

v = (dP r 4 ) / (8η · l ),

Where: dP- difference in blood pressure at the beginning and end of a section of a blood vessel, r- radius of the vessel, η - blood viscosity, l - length of the vessel section, coefficient 8 - this is the result of integrating the velocities of the blood layers moving in the vessel. Volumetric blood flow velocity ( Q) and linear blood flow velocity are related by the relationship:

Q = vπ r 2 .

Substituting into this relation the expression for v we obtain the Hagen-Poiseuille equation (“law”) for the volumetric blood flow rate:

Q = dP · (π r 4 / 8η · l ) (1).

Based on simple logic, it can be argued that the volumetric velocity of any flow is directly proportional to the driving force and inversely proportional to the resistance to flow. Similarly, the volumetric velocity of blood flow ( Q) is directly proportional to the driving force (pressure gradient, dP), providing blood flow, and is inversely proportional to the resistance to blood flow ( R): Q = dP / R. From here R = dP / Q. Substituting expression (1) into this relation for Q, we obtain a formula for estimating blood flow resistance:

R = (8η · l ) / (π r 4 ).

From all these formulas it is clear that the most significant variable that determines the linear and volumetric velocity of blood flow is the lumen (radius) of the vessel. This variable is the main variable in controlling blood flow.

Vascular resistance

Hydrodynamic resistance is directly proportional to the length of the vessel and blood viscosity and inversely proportional to the radius of the vessel to the 4th power, that is, it most depends on the lumen of the vessel. Since arterioles have the greatest resistance, peripheral vascular resistance depends mainly on their tone.

There are central mechanisms for regulating arteriolar tone and local mechanisms for regulating arteriolar tone.

The first includes nervous and hormonal influences, the second - myogenic, metabolic and endothelial regulation.

Sympathetic nerves have a constant tonic vasoconstrictor effect on the arterioles. The magnitude of this sympathetic tone depends on the impulse received from the baroreceptors of the carotid sinus, aortic arch and pulmonary arteries.

The main hormones normally involved in the regulation of arteriolar tone are adrenaline and norepinephrine, produced by the adrenal medulla.

Myogenic regulation is reduced to contraction or relaxation of vascular smooth muscle in response to changes in transmural pressure; at the same time, the tension in their wall remains constant. This ensures autoregulation of local blood flow - constancy of blood flow under changing perfusion pressure.

Metabolic regulation ensures vasodilation with an increase in basal metabolism (due to the release of adenosine and prostaglandins) and hypoxia (also due to the release of prostaglandins).

Finally, endothelial cells release a number of vasoactive substances - nitric oxide, eicosanoids (arachidonic acid derivatives), vasoconstrictor peptides (endothelin-1, angiotensin II) and oxygen free radicals.

12) blood pressure in different parts of the vascular bed

Blood pressure in various parts of the vascular system. The average pressure in the aorta is maintained at a high level (approximately 100 mmHg) as the heart continually pumps blood into the aorta. On the other hand, blood pressure varies from a systolic level of 120 mm Hg. Art. up to a diastolic level of 80 mm Hg. Art., since the heart pumps blood into the aorta periodically, only during systole. As blood moves through the systemic circulation, the average pressure steadily decreases, and at the point where the vena cava enters the right atrium it is 0 mmHg. Art. The pressure in the capillaries of the systemic circulation decreases from 35 mm Hg. Art. at the arterial end of the capillary up to 10 mm Hg. Art. at the venous end of the capillary. The average “functional” pressure in most capillary networks is 17 mmHg. Art. This pressure is sufficient to force a small amount of plasma through small pores in the capillary wall, while nutrients easily diffuse through these pores to the cells of nearby tissues. The right side of the figure shows the change in pressure in different parts of the pulmonary (pulmonary) circulation. In the pulmonary arteries, pulse pressure changes are visible, as in the aorta, but the pressure level is much lower: systolic pressure in the pulmonary artery is on average 25 mm Hg. Art., and diastolic - 8 mm Hg. Art. Thus, the average pulmonary artery pressure is only 16 mmHg. Art., and the average pressure in the pulmonary capillaries is approximately 7 mm Hg. Art. At the same time, the total volume of blood passing through the lungs per minute is the same as in the systemic circulation. Low pressure in the pulmonary capillary system is necessary for the gas exchange function of the lungs.

Peripheral resistance determines the so-called subsequent cardiac load. It is calculated by the difference in blood pressure and CVP and by MOS. The difference between mean arterial pressure and CVP is designated by the letter P and corresponds to a decrease in pressure within the systemic circulation. To convert the total peripheral resistance to the DSS system (length cm -5), it is necessary to multiply the obtained values by 80. The final formula for calculating peripheral resistance (Pk) looks like this:

1 cm water. Art. = 0.74 mm Hg. Art.

In accordance with this ratio, it is necessary to multiply the values in centimeters of water column by 0.74. So, the central venous pressure is 8 cm of water. Art. corresponds to a pressure of 5.9 mmHg. Art. To convert millimeters of mercury to centimeters of water, use the following ratio:

1 mmHg Art. = 1.36 cm water. Art.

CVP 6 cm Hg. Art. corresponds to a pressure of 8.1 cm water. Art. The value of peripheral resistance, calculated using the above formulas, reflects the total resistance of all vascular sections and part of the resistance of the systemic circle. Peripheral vascular resistance is therefore often referred to in the same way as total peripheral resistance. Arterioles play a decisive role in vascular resistance and are called resistance vessels. The dilation of arterioles leads to a drop in peripheral resistance and an increase in capillary blood flow. The narrowing of the arterioles causes an increase in peripheral resistance and at the same time the blocking of the disabled capillary blood flow. The latter reaction can be observed especially well in the centralization phase of circulatory shock. Normal values of total vascular resistance (Rl) in the systemic circulation in the supine position and at normal room temperature are in the range of 900-1300 dyne s cm -5.

In accordance with the total resistance of the systemic circulation, the total vascular resistance in the pulmonary circulation can be calculated. The formula for calculating pulmonary vascular resistance (Pl) is:

This also includes the difference between the mean pressure in the pulmonary artery and the pressure in the left atrium. Since the systolic pressure in the pulmonary artery at the end of diastole corresponds to the pressure in the left atrium, the pressure determination necessary to calculate pulmonary resistance can be performed using a single catheter inserted into the pulmonary artery.

What is total peripheral resistance?

Total peripheral resistance (TPR) is the resistance to blood flow present in the body's vascular system. 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 solely an indicator of cardiovascular health and should not be confused with the pressure exerted on arterial walls, 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 vascular system delivers blood to and from the lungs, where it is oxygenated, and the systemic circulation is responsible for transporting this blood to the body's cells through the arteries, and returning the blood back to the heart after being supplied. Total peripheral resistance affects the functioning of this system and can ultimately significantly affect the blood supply to organs.

The total peripheral resistance is described by the partial equation:

OPS = 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 physically detects the pressure inside the vein. Cardiac output is the amount of blood pumped by the heart in one minute.

Factors influencing the components of the OPS equation

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

Hydrodynamics of blood

Blood hydrodynamics can also significantly contribute to an increase or decrease in total peripheral resistance. Behind this is a change in the levels of coagulation factors and blood components that can change its viscosity. As one might expect, more viscous blood causes greater 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 your information only; please consult your doctor for treatment.

Peripheral vascular resistance

The heart can be thought of as a flow generator and a pressure generator. With low peripheral vascular resistance, the heart acts as a flow generator. This is the most economical mode, with maximum efficiency.

The main mechanism for compensating for increased demands on the circulatory system is a constantly decreasing peripheral vascular resistance. Total peripheral vascular resistance (TPVR) is calculated by dividing mean arterial pressure by cardiac output. During a normal pregnancy, cardiac output increases, but blood pressure remains the same or even tends to decrease. Consequently, peripheral vascular resistance should decrease, and during the weeks of pregnancy it decreases to one cm-sec."5 This occurs due to the additional opening of previously non-functioning capillaries and a decrease in the tone of other peripheral vessels.

The constantly decreasing resistance of peripheral vessels with increasing gestational age requires the precise operation of mechanisms that maintain normal blood circulation. The main control mechanism of acute changes in blood pressure is the sinoaortic baroreflex. In pregnant women, the sensitivity of this reflex to the slightest changes in blood pressure increases significantly. On the contrary, with arterial hypertension that develops during pregnancy, the sensitivity of the sinoaortic baroreflex is sharply reduced, even in comparison with the reflex in non-pregnant women. As a result, the regulation of the ratio of cardiac output to the capacity of the peripheral vascular bed is disrupted. Under such conditions, against the background of generalized arteriolospasm, cardiac performance decreases and myocardial hypokinesia develops. However, thoughtless administration of vasodilators without taking into account the specific hemodynamic situation can significantly reduce uteroplacental blood flow due to a decrease in afterload and perfusion pressure.

A decrease in peripheral vascular resistance and an increase in vascular capacity must also be taken into account when administering anesthesia during various non-obstetric surgical interventions in pregnant women. They have a higher risk of developing hypotension and, therefore, should be particularly careful to adhere to the technology of preventive fluid therapy before performing various methods of regional anesthesia. For the same reasons, the volume of blood loss, which in a non-pregnant woman does not cause significant changes in hemodynamics, can lead to severe and persistent hypotension in a pregnant woman.

The increase in blood volume due to hemodilution is accompanied by a change in cardiac performance (Fig. 1).

Fig.1. Changes in cardiac performance during pregnancy.

An integral indicator of the performance of the heart pump is cardiac minute volume (MCV), i.e. the product of stroke volume (SV) and heart rate (HR), characterizing the amount of blood ejected into the aorta or pulmonary artery in one minute. In the absence of defects connecting the systemic and pulmonary circulation, their minute volume is the same.

The increase in cardiac output during pregnancy occurs in parallel with an increase in blood volume. At 8-10 weeks of pregnancy, cardiac output increases by 30-40%, mainly due to an increase in stroke volume and, to a lesser extent, due to an increase in heart rate.

During labor, cardiac output (CV) increases sharply, reaching 1/min. However, in this situation, MOS increases to a greater extent due to an increase in heart rate than stroke volume (SV).

Our previous ideas that cardiac performance is associated only with systole have recently undergone significant changes. This is important for a correct understanding of not only the work of the heart during pregnancy, but also for intensive care of critical conditions accompanied by hypoperfusion in the “small output” syndrome.

The value of SV is largely determined by the end-diastolic volume of the ventricles (EDV). The maximum diastolic capacity of the ventricles can be divided into three fractions: the SV fraction, the reserve volume fraction and the residual volume fraction. The sum of these three components is the EDC contained in the ventricles. The volume of blood remaining in the ventricles after systole is called end-systolic volume (ESV). EDV and ESV can be represented as the smallest and largest points of the cardiac output curve, which allows you to quickly calculate stroke volume (E0 = EDV - ESV) and ejection fraction (FI = (EDV - ESV) / EDV).

Obviously, you can increase the operating efficiency either by increasing the EDC or decreasing the ESR. Note that ESV is divided into residual blood volume (the part of blood that cannot be expelled from the ventricles even with the most powerful contraction) and basal reserve volume (the amount of blood that can be additionally expelled when myocardial contractility increases). The basal reserve volume is that part of cardiac output that we can count on when using drugs with a positive inotropic effect during intensive care. The value of EDV can actually suggest the advisability of infusion therapy in a pregnant woman based not on some traditions or even instructions, but on specific hemodynamic indicators in this particular patient.

All of the mentioned indicators, measured by echocardiography, serve as reliable guidelines in the selection of various means of circulatory support during intensive care and anesthesia. For our practice, echocardiography is everyday life, and we focused on these indicators because they will be required for subsequent discussions. We must strive to introduce echocardiography into the daily clinical practice of maternity hospitals in order to have these reliable guidelines for hemodynamic correction, and not read the opinion of authorities from books. As Oliver W. Holmes, who is related to both anesthesiology and obstetrics, argued, “you shouldn’t trust authority if you can have facts, don’t guess if you can know.”

During pregnancy, a very slight increase in myocardial mass occurs, which can hardly be called hypertrophy of the left ventricular myocardium.

Dilatation of the left ventricle without myocardial hypertrophy can be considered as a differential diagnostic criterion between chronic arterial hypertension of various etiologies and arterial hypertension caused by pregnancy. Due to a significant increase in the load on the cardiovascular system during pregnancy, the size of the left atrium and other systolic and diastolic sizes of the heart increase.

An increase in plasma volume as pregnancy progresses is accompanied by an increase in preload and an increase in ventricular EDV. Since stroke volume is the difference between EDV and end-systolic volume, a gradual increase in EDV during pregnancy, according to the Frank-Starling law, leads to an increase in cardiac output and a corresponding increase in the useful work of the heart. However, there is a limit to such growth: with KDOml, the increase in SV stops, and the curve takes on the shape of a plateau. If we compare the Frank-Starling curve and the graph of changes in cardiac output depending on the duration of pregnancy, it will seem that these curves are almost identical. It is during the weeks of pregnancy, when the maximum increase in BCC and EDV is noted, that the growth of MOS stops. Therefore, when these deadlines are reached, any hypertransfusion (sometimes not justified by anything other than theoretical considerations) creates a real danger of reducing the useful work of the heart due to an excessive increase in preload.

When choosing the volume of infusion therapy, it is more reliable to focus on the measured EDV than on the various guidelines mentioned above. Comparison of end-diastolic volume with hematocrit numbers will help create a real idea of volemic disorders in each specific case.

The work of the heart ensures normal volumetric blood flow in all organs and tissues, including uteroplacental blood flow. Therefore, any critical condition associated with relative or absolute hypovolemia in a pregnant woman leads to “small output” syndrome with tissue hypoperfusion and a sharp decrease in uteroplacental blood flow.

In addition to echocardiography, which is directly related to everyday clinical practice, pulmonary artery catheterization with Swan-Ganz catheters is used to assess cardiac activity. Pulmonary artery catheterization allows you to measure pulmonary capillary wedge pressure (PCWP), which reflects end-diastolic pressure in the left ventricle and allows you to assess the hydrostatic component in the development of pulmonary edema and other circulatory parameters. In healthy non-pregnant women, this figure is 6-12 mm Hg, and these numbers do not change during pregnancy. The modern development of clinical echocardiography, including transesophageal echocardiography, hardly makes cardiac catheterization necessary in everyday clinical practice.

I saw something

Peripheral vascular resistance is increased in the basin of the vertebral arteries and in the basin of the right internal carotid artery. The tone of large arteries is reduced in all basins. Hello! The result indicates a change in vascular tone, which may be caused by changes in the spine.

In your case, it indicates a change in vascular tone, but does not allow any significant conclusions to be drawn. Hello! Based on this study, we can talk about vascular dystonia and difficult outflow of blood through the vertebral and basilar artery system, which are aggravated when turning the head. Hello! According to the REG conclusion, there is a violation of vascular tone (mainly a decrease) and difficulty in venous outflow.

Hello! Spasm of small vessels in the brain and venous congestion can cause headaches, but the cause of these changes in vascular tone cannot be determined by REG; the method is not sufficiently informative. Hello! Based on the results of the REG, we can talk about the unevenness and asymmetry of the blood filling of the vessels and their tone, but this research method does not show the reason for such changes. Hello! This means that there are changes in the tone of the brain vessels, but it is difficult to associate them with your symptoms, and even more so, REG does not indicate the cause of vascular disorders.

Vessels leading to the “center”

Hello! Please help me decipher the results of the REG: Volumetric blood flow is increased in all pools on the left and right in the carotid zone with difficulty in venous outflow. Vascular tone according to the normotype. Dystonic type of REG. Manifestation of vegetative-vascular dystonia of the hypertensive type with symptoms of venous insufficiency.

Norms of REG graphs, depending on age

According to REG, we can only talk about vegetative-vascular dystonia, but the presence of symptoms, complaints, and the results of other examinations are also important. Hello! There is a change in vascular tone, but probably not related to the condition of the spine.

Hypotonicity of the arteries most often accompanies vegetative-vascular dystonia. Yes, vascular tone is changed with asymmetry of blood flow, venous outflow is complicated, but the REG does not indicate the reason for the changes, this is not an informative enough method.

In this case, REG of cerebral vessels will be the first step in studying the problem. They cannot adapt to temperature fluctuations and changes in atmospheric pressure, and lose the ability to easily move from one climate zone to another.

REG and “non-serious” diseases

A prescribed and performed REG of the head solves the problem in a matter of minutes, and the use of adequate medications relieves the patient of the fear of monthly physiological conditions. Few people know that migraine should not be considered frivolous, because not only women suffer from it, and not only at a young age.

And the disease can manifest itself to such an extent that a person completely loses his ability to work and needs to be assigned a disability group. The REG procedure does not cause harm to the body and can be performed even in early infancy. To solve large problems and record the work of several pools, polyreogreographs are used. However, the patient is very eager to find out what is going on in his vessels and what the graph on the tape means, because, as REG is done, he already has a good idea and can even reassure those waiting in the corridor.

Of course, the standards for tone and elasticity will be different for a young and an elderly person. The essence of REG is to record waves that characterize the filling of certain areas of the brain with blood and the reaction of blood vessels to blood filling. The hypertensive type according to REG is somewhat different in this regard; here there is a persistent increase in the tone of the afferent vessels with obstructed venous outflow.

Often, when signing up for an REG head examination at medical centers, patients confuse it with other studies that contain the words “electro,” “graphy,” and “encephalo” in their names. This is understandable, all the designations are similar and sometimes it is difficult for people who are far from this terminology to understand.

Where, how and how much does it cost?

Attention! We are not a “clinic” and have no interest in providing medical services to readers. Hello! According to REG, there is a decrease in blood supply to the brain vessels and their tone. This result must be compared with your complaints and data from other examinations, which is usually done by a neurologist.

Consult a neurologist about what is most appropriate based on your condition and the presence of other diseases (osteochondrosis, for example). Hello! The result of the REG may indicate functional disorders of cerebral vascular tone, but the study is not informative enough to draw any conclusions.

A 33-year-old woman has been suffering from migraines and simple headaches in different areas since childhood. Thank you in advance! With the result of this study, you should contact a neurologist, who, in accordance with your complaints, will clarify the diagnosis and prescribe treatment, if necessary. We can only say that the tone of cerebral vessels is changed and, possibly, intracranial pressure is increased (REG speaks about this only indirectly). The cause is most likely not related to problems in the spine.

Hello! This result may indicate increased blood flow to the brain and difficulty in its outflow from the cranial cavity. Hello! We do not prescribe medications over the Internet, and based on the results of the REG, even a neurologist at the clinic will not do this. Good afternoon Help me decipher the results of the REG. Decreased tone of the distribution arteries in lead FM (by 13%). On the FP “Fn after the test” the following are observed: NO SIGNIFICANT CHANGES DETECTED.

The causes of vascular dystonia are not clear, but you can additionally undergo ultrasound or MR angiography. When turning the head to the sides, there are no special changes. Hello! REG is not a sufficiently informative study to talk about the nature of the disorders and their cause, so it is better to additionally undergo an ultrasound scan or MR angiography.

Peripheral vascular resistance in all pools is increased. Changes in vascular tone often accompany vegetative-vascular dystonia and functional changes in childhood and adolescence. In the basin of the right vertebral artery, the venous outflow worsened, in all basins on the left and in the carotid system on the right it did not change.

What is opps in cardiology

Peripheral vascular resistance (PVR)

This term refers to the total resistance of the entire vascular system to the blood flow emitted by the heart. This relationship is described by the equation:

Used to calculate the value of this parameter or its changes. To calculate the peripheral vascular resistance, it is necessary to determine the value of systemic blood pressure and cardiac output.

This mechanism is the basis for the effect of “centralization” of blood circulation in warm-blooded animals, which ensures redistribution of blood, primarily to the brain and myocardium, in difficult or life-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 successive sections of the vascular system, the drop in pressure that occurs throughout each of these sections is a direct reflection of the resistance that exists in that 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 moderate pressure drop that occurs in the 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 tenfold or more. 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 general vascular resistance to blood flow. Consistently located vascular sections are combined into certain groups within the organ, and the total vascular resistance of the organ must be equal to the sum of the resistances of its sequentially connected vascular sections.

Since arterioles have 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 the arterioles. Arteriolar resistance is, of course, largely determined by arteriolar radius. Therefore, blood flow through the organ is primarily regulated by changes in the internal diameter of the arterioles through 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 drop in blood pressure that occurs in that organ also undergoes changes.

Arteriolar constriction causes a greater drop in arteriolar pressure, resulting in an increase in blood pressure and a concomitant decrease in changes in arteriolar resistance to vascular pressure.

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

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

Definition of basic concepts in intensive care

Basic Concepts

Blood pressure is characterized by systolic and diastolic pressure, as well as an integral indicator: mean arterial pressure. Mean arterial pressure is calculated as the sum of one third of the pulse pressure (the difference between systolic and diastolic) and the diastolic pressure.

Mean arterial pressure alone does not adequately describe cardiac function. The following indicators are used for this:

Cardiac Output: The volume of blood ejected by the heart per minute.

Stroke Volume: The volume of blood ejected by the heart in one beat.

Cardiac output is equal to stroke volume multiplied by heart rate.

The cardiac index is cardiac output adjusted for patient size (body surface area). It more accurately reflects the function of the heart.

Preload

Stroke volume depends on preload, afterload and contractility.

Preload is a measure of the tension of the left ventricular wall at the end of diastole. It is difficult to directly quantify.

Indirect indicators of preload are central venous pressure (CVP), pulmonary artery wedge pressure (PAWP), and left atrial pressure (LAP). These indicators are called “filling pressures”.

Left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic pressure are considered more accurate measures of preload, but are rarely measured in clinical practice. The approximate dimensions of the left ventricle can be obtained using transthoracic or (more precisely) transesophageal ultrasound of the heart. In addition, the end-diastolic volume of the heart chambers is calculated using some methods of studying central hemodynamics (PiCCO).

Afterload

Afterload is a measure of the stress on the left ventricular wall during systole.

It is determined by preload (which causes stretching of the ventricle) and the resistance that the heart encounters during contraction (this resistance depends on total peripheral vascular resistance (TPVR), vascular compliance, mean arterial pressure and the gradient in the left ventricular outflow tract).

TPR, which typically reflects the degree of peripheral vasoconstriction, is often used as an indirect indicator of afterload. Determined by invasive measurement of hemodynamic parameters.

Contractility and compliance

Contractility is a measure of the force of contraction of myocardial fibers under certain pre- and afterload conditions.

Mean arterial pressure and cardiac output are often used as indirect measures of contractility.

Compliance is a measure of the distensibility of the left ventricular wall during diastole: a strong, hypertrophied left ventricle may be characterized by low compliance.

Compliance is difficult to quantify in a clinical setting.

Left ventricular end-diastolic pressure, which can be measured during preoperative cardiac catheterization or assessed by echoscopy, is an indirect measure of LVDP.

Important formulas for calculating hemodynamics

Cardiac output = SV * HR

Cardiac index = CO/PPT

Impact index = SV/PPT

Mean arterial pressure = DBP + (SBP-DBP)/3

Total peripheral resistance = ((MAP-CVP)/SV)*80)

Total peripheral resistance index = TPSS/PPT

Pulmonary vascular resistance = ((PAP - PCWP)/SV)*80)

Pulmonary vascular resistance index = TPVR/PPT

CO = cardiac output, 4.5-8 l/min

SV = stroke volume, ml

BSA = body surface area, 2- 2.2 m2

CI = cardiac index, 2.0-4.4 l/min*m2

SVI = stroke volume index, ml

MAP = Mean arterial pressure, mm Hg.

DD = Diastolic pressure, mm Hg. Art.

SBP = Systolic pressure, mm Hg. Art.

TPR = total peripheral resistance, dyn/s*cm 2

CVP = central venous pressure, mm Hg. Art.

IOPSS = index of total peripheral resistance, dyn/s*cm 2

SLS = pulmonary vascular resistance, SLS = dyn/s*cm 5

PAP = pulmonary artery pressure, mm Hg. Art.

PAWP = pulmonary artery wedge pressure, mm Hg. Art.

ISLS = index of pulmonary vascular resistance = din/s*cm 2

Oxygenation and ventilation

Oxygenation (oxygen content in arterial blood) is described by such concepts as partial pressure of oxygen in arterial blood (P a 0 2) and saturation (saturation) of hemoglobin in arterial blood with oxygen (S a 0 2).

Ventilation (the movement of air into and out of the lungs) is described by the concept of minute volume of ventilation and is assessed by measuring the partial pressure of carbon dioxide in arterial blood (P a C0 2).

Oxygenation is, in principle, independent of minute ventilation unless it is very low.

In the postoperative period, the main cause of hypoxia is pulmonary atelectasis. An attempt should be made to eliminate them before increasing the oxygen concentration in the inspired air (Fi0 2).

Positive end expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) are used to treat and prevent atelectasis.

Oxygen consumption is assessed indirectly by oxygen saturation of hemoglobin in mixed venous blood (S v 0 2) and by oxygen uptake by peripheral tissues.

External respiratory function is described by four volumes (tidal volume, inspiratory reserve volume, expiratory reserve volume and residual volume) and four capacities (inspiratory capacity, functional residual capacity, vital capacity and total lung capacity): in NICU, only tidal volume measurement is used in daily practice .

A decrease in functional reserve capacity due to atelectasis, supine position, compaction of lung tissue (congestion) and lung collapse, pleural effusion, and obesity lead to hypoxia. CPAP, PEEP and physical therapy are aimed at limiting these factors.

Total peripheral vascular resistance (TPVR). Frank's equation.

This term refers to the total resistance of the entire vascular system to the blood flow emitted by the heart. This relationship is described by the equation.

As follows from this equation, to calculate the peripheral vascular resistance, it is necessary to determine the value of systemic blood pressure and cardiac output.

Direct bloodless methods for measuring total peripheral resistance have not been developed, and its value is determined from the Poiseuille equation 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, Frank. using a formal analogy between hydraulic and electrical circuits, he brought Poiseuille’s equation to the following form:

The Frank 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 varying degrees. Thus, in specific cases, the level of SBP can be determined primarily by the value of TPSS or mainly by CO.

Rice. 9.3. A more pronounced increase in vascular resistance in the thoracic aorta basin compared to its changes in the brachiocephalic artery basin during the pressor reflex.

Under normal physiological conditions, TPSS ranges from 1200 to 1700 dynes per cm. With hypertension, this value can double the norm and be equal to 2200-3000 dynes per cm-5.

The value of the peripheral vascular resistance consists of the sums (not arithmetic) of the resistances of the regional vascular sections. At the same time, depending on the greater or lesser severity of changes in regional vascular resistance, they will accordingly receive a smaller or larger volume of blood ejected by the heart. In Fig. Figure 9.3 shows an example of a more pronounced degree of increase in vascular resistance 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 the basis for the effect of “centralization” of blood circulation in warm-blooded animals, which ensures redistribution of blood, primarily to the brain and myocardium, in difficult or life-threatening conditions (shock, blood loss, etc.).