Deterioration in blood flow is typical for patients in the intensive care unit. Increased blood viscosity creates additional resistance to blood flow and is therefore associated with excessive cardiac afterload, microcirculatory disorders, tissue hypoxia. During a hemodynamic crisis, blood viscosity also increases due to a decrease in blood flow velocity. A vicious circle arises that maintains stasis and shunting of blood in the microvasculature.
Disorders in the hemorheological system represent a universal mechanism for the pathogenesis of critical conditions, therefore optimization of the rheological properties of blood is the most important tool intensive care. Reducing blood viscosity helps accelerate blood flow, increase DO2 to tissues, and facilitate heart function. Using rheological active funds it is possible to prevent the development of thrombotic, ischemic and infectious complications underlying disease.
Applied hemorheology is based on a number of physical principles blood fluidity. Understanding them helps you choose optimal method diagnosis and treatment.
Physical Basics hemorheology. IN normal conditions In almost all parts of the circulatory system, a laminar type of blood flow is observed. It can be represented as an infinite number of layers of liquid that move in parallel without mixing with each other. Some of these layers come into contact with a stationary surface - the vascular wall and their movement, accordingly, slows down. The adjacent layers still tend to move in the longitudinal direction, but the slower wall layers retard them. Inside the flow, friction occurs between the layers. A parabolic velocity distribution profile appears with a maximum in the center of the vessel. The near-wall layer of liquid can be considered stationary (Fig. 23.1). The viscosity of a simple fluid remains constant (8 cPoise), while the viscosity of blood varies depending on blood flow conditions (from 3 to 30 cPoise).
The property of blood to provide “internal” resistance to those external forces that set it in motion is called viscosity
Viscosity is due to the forces of inertia and adhesion.
Rice. 23.1. Viscosity as a coefficient of proportionality between stress and shear rate.
Rice. 23.2. Dependence of relative blood viscosity (without taking into account shear rate) on hematocrit.
When the hematocrit is 0, the viscosity of the blood approaches the viscosity of plasma.
To correctly measure and mathematically describe viscosity, concepts such as shear stress c and shear rate y are introduced. The first indicator is the ratio of the friction force between adjacent layers to their area - F/S. It is expressed in dynes/cm2 or pascals*. The second indicator is the velocity gradient of the layers - deltaV/L. It is measured in s-1.
In accordance with Newton's equation, shear stress is directly proportional to shear rate: . This means that what more difference speed between layers of liquid, the stronger their friction. And, conversely, equalizing the speed of fluid layers reduces mechanical stress along the watershed line. Viscosity in this case acts as a proportionality coefficient.
The viscosity of simple, or Newtonian, liquids (for example, water) is constant under any conditions of movement, i.e. There is a linear relationship between shear stress and shear rate for these fluids.
Unlike simple liquids, blood can change its viscosity when the speed of blood flow changes. So, in the aorta and main arteries blood viscosity approaches 4-5 relative units (if we take the viscosity of water at 20 °C as a reference measure). In the venous section of the microcirculation, despite the low shear stress, the viscosity increases 6-8 times relative to its level in the artery (i.e., up to 30-40 relative units). At extremely low, non-physiological shear rates, blood viscosity can increase 1000 times (!).
Thus, the relationship between shear stress and shear rate for whole blood is nonlinear, exponential. This “rheological behavior of blood”* is called “non-Newtonian” (Fig. 23.2).
The reason for the “non-Newtonian behavior” of blood. The “non-Newtonian behavior” of blood is due to its roughly dispersed nature. From a physicochemical point of view, blood can be represented as a liquid medium (water) in which a solid, insoluble phase is suspended ( shaped elements blood and high molecular weight substances). The dispersed phase particles are large enough to resist Brownian motion. That's why common property of such systems is their nonequilibrium. The components of the dispersed phase constantly strive to separate and precipitate cellular aggregates from the dispersed medium.
The main and rheologically most significant type of cellular blood aggregates is erythrocyte. It is a multidimensional cellular complex with a typical “coin column” shape. Its characteristic features are the reversibility of the connection and the absence of functional activation of cells. The structure of the erythrocyte aggregate is maintained mainly by globulins. It is known that the patient's erythrocytes with an initially increased sedimentation rate after their addition to the plasma of the same group healthy person begin to settle at normal speed. And vice versa, if the red blood cells of a healthy person with a normal sedimentation rate are placed in the plasma of a patient, then their precipitation will significantly accelerate.
Natural inducers of aggregation include primarily fibrinogen. The length of its molecule is 17 times greater than its width. Thanks to this asymmetry, fibrinogen is able to spread in the form of a “bridge” from one cell membrane to another. The bond formed in this case is fragile and breaks under the influence of minimal mechanical force. A2- and beta-macroglobulins, fibrinogen degradation products, and immunoglobulins act in a similar way. A closer approach of red blood cells and their irreversible binding to each other is prevented by a negative membrane potential.
It should be emphasized that erythrocyte aggregation is a normal rather than pathological process. Its positive side is that it facilitates the passage of blood through the microcirculation system. When aggregates form, the surface to volume ratio decreases. As a result, the frictional resistance of the unit turns out to be significantly less than the resistance of its individual components.
Main determinants of blood viscosity. Blood viscosity is influenced by many factors (Table 23.1). All of them realize their effect by changing the viscosity of plasma or the rheological properties of blood cells.
Red blood cell content. The erythrocyte is the main cellular population of the blood, actively participating in the processes of physiological aggregation. For this reason, changes in hematocrit (Ht) significantly affect blood viscosity (Fig. 23.3). Thus, when Ht increases from 30 to 60%, the relative viscosity of blood doubles, and when Ht increases from 30 to 70%, it triples. Hemodilution, on the contrary, reduces blood viscosity.
The term “rheological behavior of blood” is generally accepted and emphasizes the “non-Newtonian” nature of blood fluidity.
Rice. 23.3. Relationship between DO2 and hematocrit.
Table 23.1.
Deformability of erythrocytes. The diameter of the red blood cell is approximately 2 times the lumen of the capillary. Because of this, the passage of an erythrocyte through the microvasculature is possible only if its volumetric configuration changes. Calculations show that if the erythrocyte were not capable of deformation, then blood with Ht 65% would turn into a dense homogeneous formation and into peripheral parts the circulatory system would experience a complete stop of blood flow. However, due to the ability of red blood cells to change their shape and adapt to environmental conditions, blood circulation does not stop even at Ht 95-100%.
There is no coherent theory of the deformation mechanism of erythrocytes. Apparently this mechanism is based on general principles transition of sol to gel. It is assumed that the deformation of erythrocytes is an energy-dependent process. Perhaps hemoglobin A takes an active part in it. It is known that the content of hemoglobin A in the erythrocyte decreases with certain hereditary diseases blood (sickle cell anemia), after operations in conditions cardiopulmonary bypass. At the same time, the shape of red blood cells and their plasticity change. Increased blood viscosity is observed, which does not correspond to low Ht.
Plasma viscosity. Plasma as a whole can be classified as a “Newtonian” fluid. Its viscosity is relatively stable in various departments circulatory system and is mainly determined by the concentration of globulins. Among the latter, fibrinogen is of primary importance. It is known that the removal of fibrinogen reduces the viscosity of plasma by 20%, so the viscosity of the resulting serum approaches the viscosity of water.
Normally, plasma viscosity is about 2 rel. units This is approximately 1/15 of the internal resistance that develops with whole blood in the venous microcirculation. However, plasma has a very significant effect on peripheral blood flow. In capillaries, blood viscosity is reduced by half compared to proximal and distal vessels of larger diameter (phenomenon §). This “prolapse” of viscosity is associated with the axial orientation of red blood cells in a narrow capillary. In this case, the plasma is pushed to the periphery, to the wall of the vessel. It serves as a “lubricant”, which ensures the sliding of the chain of blood cells with minimal friction.
This mechanism functions only under normal conditions protein composition plasma. An increase in the level of fibrinogen or any other globulin leads to difficulty in capillary blood flow, sometimes of a critical nature. Thus, multiple myeloma, Waldenström's macroglobulinemia and some collagenoses are accompanied by excessive production of immunoglobulins. In this case, the plasma viscosity increases relative to normal level 2-3 times. The clinical picture begins to be dominated by symptoms of severe microcirculation disorders: decreased vision and hearing, drowsiness, adynamia, headache, paresthesia, bleeding of the mucous membranes.
Pathogenesis of hemorheological disorders. In intensive care practice, hemorheological disorders arise under the influence of a complex of factors. The action of the latter in a critical situation is universal.
Biochemical factor. On the first day after surgery or injury, fibrinogen levels usually double. The peak of this increase occurs on days 3-5, and normalization of fibrinogen levels occurs only at the end of the 2nd postoperative week. In addition, fibrinogen degradation products, activated platelet procoagulants, catecholamines, prostaglandins, and lipid peroxidation products appear in the bloodstream in excess quantities. All of them act as inducers of red blood cell aggregation. A peculiar biochemical situation is formed - “rheotoxemia”.
Hematological factor. Surgery or trauma is also accompanied by certain changes in the cellular composition of the blood, which are called hematological stress syndrome. Young granulocytes, monocytes and platelets of increased activity enter the bloodstream.
Hemodynamic factor. The increased aggregation tendency of blood cells under stress is superimposed on local hemodynamic disturbances. It has been shown that during uncomplicated abdominal interventions, the volumetric velocity of blood flow through the popliteal and iliac veins drops by 50%. This is due to the fact that immobilization of the patient and muscle relaxants are blocked during surgery. physiological mechanism"muscle pump" In addition, under the influence of mechanical ventilation, anesthetics or blood loss, systemic pressure decreases. IN similar situation the kinetic energy of systole may not be enough to overcome the adhesion of blood cells to each other and to the vascular endothelium. The natural mechanism of hydrodynamic disaggregation of blood cells is disrupted, and microcirculatory stasis occurs.
Hemorheological disorders and venous thrombosis. Slowing down the speed of movement in the venous circulation provokes aggregation of red blood cells. However, the inertia of movement may be quite large and the blood cells will experience increased deformation load. Under its influence, ATP is released from red blood cells - a powerful inducer of platelet aggregation. Low shear rate also stimulates the adhesion of young granulocytes to the venule wall (Farheus-Vejiens phenomenon). Irreversible aggregates are formed that can form the cellular core of a venous thrombus.
Further development of the situation will depend on the activity of fibrinolysis. As a rule, an unstable balance arises between the processes of formation and resorption of a blood clot. For this reason, most cases of deep vein thrombosis of the lower extremities in hospital practice are hidden and resolve spontaneously, without consequences. The use of disaggregants and anticoagulants is a highly effective way to prevent venous thrombosis.
Methods for studying the rheological properties of blood. The “non-Newtonian” nature of blood and the associated shear rate factor must be taken into account when measuring viscosity in clinical laboratory practice. Capillary viscometry is based on the flow of blood through a graduated vessel under the influence of gravity, and therefore is physiologically incorrect. Real blood flow conditions are simulated on a rotational viscometer.
The fundamental elements of such a device include a stator and a rotor congruent with it. The gap between them serves as a working chamber and is filled with a blood sample. The movement of the liquid is initiated by the rotation of the rotor. This, in turn, is arbitrarily specified in the form of a certain shear rate. The measured quantity is the shear stress, which occurs as a mechanical or electrical torque necessary to maintain the selected speed. Blood viscosity is then calculated using Newton's formula. The unit of measurement for blood viscosity in the GHS system is Poise (1 Poise = 10 dynes x s/cm2 = 0.1 Pa x s = 100 relative units).
It is mandatory to measure blood viscosity in the range of low (100 s-1) shear rates. The low range of shear rates reproduces the conditions of blood flow in the venous section of the microcirculation. The determined viscosity is called structural. It mainly reflects the tendency of red blood cells to aggregate. High shear rates (200-400 s-1) are achieved in vivo in the aorta, great vessels and capillaries. In this case, as rheoscopic observations show, red blood cells occupy a predominantly axial position. They stretch in the direction of movement, their membrane begins to rotate relative to the cellular contents. Due to hydrodynamic forces, almost complete disaggregation of blood cells is achieved. Viscosity, determined at high shear rates, depends primarily on the plasticity of the red blood cells and the shape of the cells. It is called dynamic.
As a standard for research on a rotational viscometer and the corresponding norm, you can use the indicators according to the method of N.P. Alexandrova et al. (1986) (Table 23.2).
Table 23.2.
To provide a more detailed picture of the rheological properties of blood, several more specific tests are performed. The deformability of erythrocytes is assessed by the speed of passage of diluted blood through a microporous polymer membrane (d=2-8 μm). The aggregation activity of red blood cells is studied using nephelometry by measuring the change in the optical density of the medium after adding aggregation inducers (ADP, serotonin, thrombin or adrenaline) to it.
Diagnosis of hemorheological disorders. Disorders in the hemorheological system, as a rule, occur latently. Their clinical manifestations non-specific and inconspicuous. Therefore, the diagnosis is determined mainly by laboratory data. Its leading criterion is the value of blood viscosity.
The main direction of shifts in the hemorheology system in patients in critical condition is the transition from high viscosity blood to low. This dynamics, however, is accompanied by a paradoxical deterioration in blood fluidity.
Syndrome of increased blood viscosity. It is nonspecific in nature and is widespread in the clinic of internal diseases: with atherosclerosis, angina pectoris, chronic obstructive bronchitis, gastric ulcer, obesity, diabetes mellitus, obliterating endarteritis, etc. In this case, a moderate increase in blood viscosity is noted to 35 cPoise at y = 0.6 s-1 and 4.5 cPoise at y = 150 s-1. Microcirculatory disorders are usually mild. They progress only as the underlying disease develops. Hyperviscosity syndrome in patients admitted to the intensive care unit should be considered as an underlying condition.
Low blood viscosity syndrome. As the critical condition unfolds, blood viscosity decreases due to hemodilution. Viscometry indicators are 20-25 cPoise at y=0.6 s-1 and 3-3.5 cPoise at y=150 s-1. Similar values can be predicted from Ht, which usually does not exceed 30-35%. IN terminal state the decrease in blood viscosity reaches the stage of “very low” values. Severe hemodilution develops. Ht decreases to 22-25%, dynamic blood viscosity - to 2.5-2.8 cPoise and structural blood viscosity - to 15-18 cPoise.
The low value of blood viscosity in a patient in critical condition creates a misleading impression of hemorheological well-being. Despite hemodilution, with low blood viscosity syndrome, microcirculation significantly deteriorates. The aggregation activity of red blood cells increases 2-3 times, and the passage of the erythrocyte suspension through nucleopore filters slows down 2-3 times. After restoration of Ht by hemoconcentration in vitro, blood hyperviscosity is found in such cases.
Against the background of low or very low blood viscosity, massive aggregation of red blood cells can develop, which completely blocks the microvasculature. This phenomenon described by M.N. Knisely in 1947 as a “sludge” phenomenon, indicates the development of a terminal and apparently irreversible phase of a critical condition.
The clinical picture of low blood viscosity syndrome consists of severe microcirculatory disorders. Note that their manifestations are nonspecific. They may be caused by other, non-rheological mechanisms.
Clinical manifestations of low blood viscosity syndrome:
Tissue hypoxia (in the absence of hypoxemia);
Increased peripheral vascular resistance;
Deep vein thrombosis of the extremities, recurrent pulmonary thromboembolism;
Adynamia, stupor;
Deposition of blood in the liver, spleen, subcutaneous vessels.
Prevention and treatment. Patients admitted to the operating room or intensive care unit need to optimize the rheological properties of blood. This prevents the formation of venous blood clots, reduces the likelihood of ischemic and infectious complications, and alleviates the course of the underlying disease. The most effective methods of rheological therapy are blood dilution and suppression of the aggregation activity of its formed elements.
Hemodilution. The red blood cell is the main carrier of structural and dynamic resistance to blood flow. Therefore, hemodilution turns out to be the most effective rheological agent. Its beneficial effect has been known for a long time. For many centuries, bloodletting was perhaps the most common method of treating diseases. The appearance of low molecular weight dextrans was the next stage in the development of the method.
Hemodilution increases peripheral blood flow, but at the same time reduces the oxygen capacity of the blood. Under the influence of two differently directed factors, DO2 ultimately develops in the tissues. It can increase due to blood dilution or, on the contrary, significantly decrease under the influence of anemia.
The lowest Ht that corresponds to safe level DO2 is called optimal. Its exact size is still a matter of debate. The quantitative relationships between Ht and DO2 are well known. However, it is not possible to assess the contribution of individual factors: tolerance of anemia, tension of tissue metabolism, hemodynamic reserve, etc. According to the general opinion, the goal of therapeutic hemodilution is Ht 30-35%. However, experience in treating massive blood loss without blood transfusion shows that greater reduction Ht up to 25 and even 20% is quite safe from the point of view of oxygen supply to tissues.
Currently, three techniques are used to achieve hemodilution.
Hemodilution in the hypervolemic mode implies a fluid transfusion that leads to a significant increase in blood volume. In some cases, a short-term infusion of 1-1.5 liters of plasma substitutes precedes induction of anesthesia and surgery; in other cases, requiring longer hemodilution, a decrease in Ht is achieved by a constant fluid load at the rate of 50-60 ml/kg of the patient’s body weight per day. A decrease in the viscosity of whole blood is the main consequence of hypervolemia. The viscosity of plasma, the plasticity of erythrocytes and their tendency to aggregation do not change. The disadvantages of the method include the risk of volume overload of the heart.
Norvolemic hemodilution was initially proposed as an alternative to heterologous transfusions in surgery. The essence of the method is the preoperative collection of 400-800 ml of blood into standard containers with a stabilizing solution. Controlled blood loss, as a rule, is replenished simultaneously with the help of plasma substitutes at a rate of 1:2. With some modification of the method, it is possible to collect 2-3 liters of autologous blood without any adverse hemodynamic and hematological consequences. The collected blood is then returned during or after surgery.
Normovolemic hemodilution is not only a safe, but also a low-cost method of autodonation, which has a pronounced rheological effect. Along with a decrease in Ht and the viscosity of whole blood after exfusion, there is a persistent decrease in plasma viscosity and the aggregation ability of erythrocytes. The flow of fluid between the interstitial and intravascular spaces is activated, along with it the exchange of lymphocytes and the flow of immunoglobulins from tissues increase. All this ultimately leads to a reduction in postoperative complications. This method can be widely used for planned surgical interventions.
Endogenous hemodilution develops with pharmacological vasoplegia. The decrease in Ht in these cases is due to the fact that protein-depleted and less viscous fluid enters the vascular bed from the surrounding tissues. Epidural blockade, halogen-containing anesthetics, ganglion blockers and nitrates have a similar effect. The rheological effect accompanies the main therapeutic effect these funds. The degree of reduction in blood viscosity is not predicted. It is determined by the current state of volume and hydration.
Anticoagulants. Heparin is obtained by extraction from biological tissues (lungs of large cattle). The final product is a mixture of polysaccharide fragments with different molecular weights, but with similar biological activity.
The largest heparin fragments in complex with antithrombin III inactivate thrombin, while heparin fragments with a molecular weight of 7000 act predominantly on activated factor X.
The administration of high molecular weight heparin in a dose of 2500-5000 units subcutaneously 4-6 times a day in the early postoperative period has become a widespread practice. Such a prescription reduces the risk of thrombosis and thromboembolism by 1.5-2 times. Low doses of heparin do not prolong the activated partial thromboplastin time (aPTT) and, as a rule, do not cause hemorrhagic complications. Heparin therapy, along with hemodilution (intentional or collateral), are the main and most effective methods for the prevention of hemorheological disorders in surgical patients.
Low molecular weight fractions of heparin have less affinity for platelet von Willebrand factor. Because of this, compared to high molecular weight heparin, they are even less likely to cause thrombocytopenia and bleeding. First use experience low molecular weight heparin(clexane, fraxiparine) in clinical practice gave encouraging results. Heparin preparations turned out to be equipotential to traditional heparin therapy, and according to some data even exceeded its preventive and therapeutic effect. In addition to safety, low-molecular-weight heparin fractions are also distinguished by their economical administration (once daily) and the absence of the need for aPTT monitoring. The dose selection is usually made without taking into account body weight.
Plasmapheresis. The traditional rheological indication for plasmapheresis is primary hyperviscosity syndrome, which is caused by excessive production of abnormal proteins (paraproteins). Their removal leads to rapid reversal of the disease. The effect, however, is short-lived. The procedure is symptomatic.
Currently, plasmapheresis is actively used for preoperative preparation patients with obliterating diseases of the lower extremities, thyrotoxicosis, gastric ulcer, and purulent-septic complications in urology. This leads to an improvement in the rheological properties of blood, activation of microcirculation, and a significant reduction in the number of postoperative complications. Replace up to 1/2 of the volume of the central processing unit.
The decrease in globulin levels and plasma viscosity after one plasmapheresis procedure can be significant, but short-lived. The main beneficial effect of the procedure, which applies to the entire postoperative period, is the so-called resuspension phenomenon. Washing of erythrocytes in a protein-free environment is accompanied by a stable improvement in the plasticity of erythrocytes and a decrease in their aggregation tendency.
Photomodification of blood and blood substitutes. With 2-3 procedures intravenous irradiation blood helium-neon laser (wavelength 623 nm) low power(2.5 mW) a clear and long-lasting rheological effect is observed. According to precision nephelometry, under the influence of laser therapy, the number of hyperergic reactions of platelets decreases, and the kinetics of their aggregation in vitro is normalized. Blood viscosity remains unchanged. Similar effect They also have UV rays (with a wavelength of 254-280 nm) in the extracorporeal circuit.
The mechanism of the disaggregation action of laser and ultraviolet radiation not entirely clear. It is assumed that photomodification of blood first causes the formation of free radicals. In response, mechanisms are activated antioxidant protection, which block the synthesis of natural inducers of platelet aggregation (primarily prostaglandins).
Ultraviolet irradiation of colloidal preparations (for example, rheopolyglucin) has also been proposed. After their administration, the dynamic and structural viscosity of blood decreases by 1.5 times. Platelet aggregation is also significantly inhibited. It is characteristic that unmodified rheopolyglucin is not able to reproduce all these effects.
Blood is a suspension (suspension) of cells that are found in plasma, consisting of protein and fat molecules. Rheological properties include viscosity and stability of the suspension. They determine the ease of its movement - fluidity. To improve microcirculation, infusion therapy and drugs that reduce coagulation and combination of cells into clots are used.
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Violation of blood rheology
The properties of blood that determine its passage through the circulatory system depend on the following factors:
- the ratio of the liquid (plasma) part and cells (mainly erythrocytes);
- plasma protein composition;
- cell shapes;
- movement speed;
- temperature.
Violations of rheology manifest themselves in the form of changes in the viscosity and stability of the suspension. They can be local (with inflammation or venous stagnation), as well as general – with shock or weakness of the heart. The supply of oxygen and nutrients to the cells depends on the rheological properties.
Blood viscosity
When blood flow slows down, red blood cells are not located along the vessel (as is normal), but in different planes, which reduces blood fluidity. In this case, the blood vessels and heart require increased efforts to move it. To measure viscosity, an indicator such as . It is calculated by dividing the volume of blood cells by the entire volume. At in good condition
Viscosity in the blood is 45% of cells and 55% of plasma. The hematocrit of a healthy person is 0.45.
The higher this indicator, the worse the rheological characteristics of the blood, since its viscosity is higher. The hematocrit level can be affected by bleeding, dehydration, or, conversely, excessive blood dilution (for example, during intense infusion therapy
). Cooling increases the hematocrit by more than 1.5 times.
Sludge phenomenon
If suspension stability, that is, the suspended state of red blood cells, is disrupted, then the blood can be divided into a liquid part (plasma) and a clot of red blood cells, platelets and leukocytes.
- This becomes possible due to the association, adhesion, and gluing of cells. This phenomenon is called sludge, which means silt or thick mud. Sludge of blood cells leads to severe disruption of microcirculation.
- Reasons for the phenomenon of blood separation:
- circulatory failure due to heart weakness;
- stagnation of blood in the veins;
- spasm of arteries or blockage of their lumen;
- blood diseases with excessive cell formation;
- dehydration due to vomiting, diarrhea, taking diuretics;
- inflammation of the vessel wall;
- allergic reactions;
- tumor processes;
disruption of cellular charge due to electrolyte imbalance; increased protein content in plasma. The sludge phenomenon leads to a decrease in the speed of blood flow, up to its complete stop. The straight-line direction changes to turbulent, that is, flow turbulence occurs. Because of large quantities accumulations of blood cells are discharged from arterial to
venous vessels
(shunts open), blood clots form.
At the tissue level, the processes of transport of oxygen and nutrients are disrupted, metabolism and cell restoration slow down when damaged.
To study blood viscosity, instruments called viscometers or rheometers are used. There are currently two common types:
- rotational - blood rotates in a centrifuge, its shear flow is calculated using hemodynamic formulas;
- capillary - blood flows through a tube of a given diameter under the influence of a known pressure difference at the ends, that is, the physiological regime of blood flow is reproduced.
Rotational viscometers consist of two cylinders of different diameters, one of which is nested inside the other. The inner one is connected to the dynamometer, and the outer one rotates. Between them there is blood, it begins to move due to its viscosity. A modification of the rotational rheometer is a device with a cylinder that floats freely in a liquid (Zakharchenko apparatus).
Rotational rheometer Why you need to know about hemodynamics
Since the state of blood flow is greatly influenced by mechanical factors such as pressure in the vessels and the speed of flow, the basic laws of hemodynamics are applicable to their study.
With their help, it is possible to establish a connection between the main parameters of blood circulation and the properties of blood. Movement of blood through vascular system
carried out due to the pressure difference, it moves from the high to low zone. This process is influenced by viscosity, suspension stability and arterial wall resistance. The latter indicator is the highest in arterioles, since they have the greatest length with a small diameter. The main force of heart contractions is spent precisely on moving blood into these vessels. The resistance of arterioles, in turn, strongly depends on their lumen, which is affected by various environmental factors and autonomic stimuli. nervous system
. These vessels are called the taps of the human body. The length may change during growth, as well as during work. skeletal muscles
(regional arteries).
In all other cases, length is considered a constant factor, and the lumen of the vessel and blood viscosity are variable values, they determine the state of blood flow.
Evaluation of indicators
- The main characteristics of hemodynamics in the body are:
- Stroke volume is the amount of blood that enters the vessels when the heart contracts; its norm is 70 ml. Ejection Fraction – Ratio in ml to the residual blood volume at the end of diastole. It is about 60%, if it decreases to 45, then this is a sign of systolic dysfunction (heart failure). If it falls below 40%, the condition is considered critical.
- Blood pressure – systolic from 100 to 140, diastolic from 60 to 90 mm Hg. Art. Any reading below this range is a sign of hypotension, while anything higher is indicative of hypertension.
- Total peripheral resistance is calculated as the ratio of the average blood pressure(diastolic indicator and a third of the pulse rate) to the ejection of blood per minute. Measured in din x s x cm-5, the normal range is from 700 to 1500 units.
To assess rheological parameters, determine:
- Red blood cell content. Normally 3.9 - 5.3 million/µl, it is reduced in case of anemia and tumors. High rates occur with leukemia, chronic oxygen deficiency, and blood thickening.
- Hematocrit In healthy people it ranges from 0.4 to 0.5. Increased with breathing problems, kidney tumors or cysts, and dehydration. Decreases with anemia and excessive fluid infusion.
- Viscosity. About 23 mPa×s is considered normal. Increases with atherosclerosis, diabetes mellitus, respiratory diseases, digestive systems, pathology of the kidneys, liver, taking diuretics, alcohol. Decreases with anemia and intense fluid intake.
Drugs that improve blood rheology
To facilitate the movement of blood with increased viscosity, use:
- Hemodilution - dilution of blood using transfusion of plasma substitutes (Reopoliglyukin, Gelofusin, Voluven, Refortan, Stabizol, Poliglyukin);
- anticoagulant therapy - Fraxiparine, Fragmin, Phenilin, Sinkumar, Wessel Due F, Tsibor, Pentasan;
- antiplatelet agents - Plavix, Ipaton, Cardiomagnil, Aspirin, Curantil, Ilomedin, Brilinta.
In addition to drugs, plasmapheresis is used to remove excess protein from plasma and improve the suspension stability of red blood cells, as well as ultraviolet light.
The rheological and hemodynamic properties of blood determine the delivery of oxygen and nutrients to tissues.
Hemodynamic parameters of blood flow are determined by measuring pressure, cardiac output and peripheral resistance. Impaired blood flow speed leads to a slowdown in tissue metabolism. To improve fluidity, medications are used - plasma expanders, anticoagulants, antiplatelet agents.
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Rheology is the science of flow and deformation.
The rheological properties of blood depend on:
1. Hemodynamic parameters - changes in the properties of blood during its movement. Hemodynamic parameters are determined by the propulsive ability of the heart, functional state bloodstream and the properties of the blood itself.
2. Cellular factors(quantity, concentration - hematocrit, deformability, shape, functional state).
3. Plasma factors – content of albumins, globulins, fibrinogen, FFA, TT, cholesterol, pH, electrolytes.
4. Interaction factors - intravascular aggregation of formed elements.
A dynamic process of “aggregation - disaggregation” constantly occurs in the blood. Normally, disaggregation dominates over aggregation. The resulting direction of the “aggregation - disaggregation” process is determined by the interaction of the following factors: hemodynamic, plasma, electrostatic, mechanical and conformational.
The hemodynamic factor determines the shear stress and the distance between individual cells in the flow.
Plasma and electrostatic factors determine the bridging and electrostatic mechanisms.
The bridging mechanism consists in the fact that the connecting element in the aggregate between red blood cells are macromolecular compounds, the ends of the molecules of which, adsorbed on neighboring cells, form a kind of bridges. The distance between red blood cells in an aggregate is proportional to the length of the connecting molecules. The main plastic materials for intererythrocyte bridges are fibrinogen and globulins. A necessary condition for the implementation of the bridging mechanism is the bringing together of red blood cells at a distance not exceeding the length of one macromolecule. It depends on the hematocrit. The electrostatic mechanism is determined by the charge on the surface of red blood cells. With acidosis, the accumulation of lactate, the (-) potential decreases and the cells do not repel each other.
The gradual elongation and branching of the aggregate triggers the conformational mechanism and the aggregates form a three-dimensional spatial structure.
5. External conditions - temperature. As temperature increases, blood viscosity decreases.
Among intravascular microcirculation disorders, aggregation of erythrocytes and other blood cells should be placed in one of the first places.
The founders of the doctrine of “sludge”, i.e. blood condition, which is based on the aggregation of erythrocytes, are Knisese (1941) and his student Blosh. The term “sluge” itself literally translated from English means “thick mud”, “mud”, “silt”. It is necessary, first of all, to distinguish between aggregation of blood cells (mainly erythrocytes) and agglutination of erythrocytes. The first process is reversible, while the second always seems to be irreversible, associated mainly with immune phenomena. The development of sludge represents an extreme degree of expression of aggregation of blood cells. Sludged blood has a number of differences from normal blood. The main features of sludged blood should be the adhesion of red blood cells, leukocytes or platelets to each other and an increase in blood viscosity. This leads to a blood condition that makes its perfusion through microvessels very difficult.
There are several types of sludge depending on the structural features of the unit.
I. Classic type. It is characterized by relatively large aggregates and dense packing of red blood cells with uneven contours. This type of sludge develops when an obstruction (such as a ligature) interferes with the free movement of blood through a vessel.
II. Dextran type. The units have different sizes, dense packing, rounded outlines, free spaces in aggregates in the form of cavities. This type of sludge develops when dextran with a molecular weight of 250-500 or higher CDN is introduced into the blood.
III. Amorphous type. This type is characterized by the presence of a huge number of small aggregates similar to granules. In this case, the blood takes on the appearance of a coarse liquid. The amorphous type of sludge develops when ethyl, ADP and ATP, thrombin, serotonin, and norepinephrine are introduced into the blood. Only a few red blood cells are involved in the formation of an aggregate in the amorphous type of sludge. The small size of the aggregates can pose no less, but even a greater danger to microcirculation, since their size allows them to penetrate into the smallest vessels up to and including the capillaries.
Sludge can also develop due to poisoning with arsenic, cadmium, ether, chloroform, benzene, toluene, and aniline. Depending on the dose of the substance administered, sludge may be reversible or irreversible. Numerous clinical observations have established that changes in the protein composition of the blood can lead to the development of sludge. Conditions such as increased fibrinogen content or decreased albumin, microglobulinemia increase blood viscosity and reduce its suspension stability.
Rheology is a field of mechanics that studies the characteristics of the flow and deformation of real continuous media, one of the representatives of which are non-Newtonian fluids with structural viscosity. A typical non-Newtonian fluid is blood. Blood rheology, or hemorheology, studies mechanical patterns and especially changes in the physical colloidal properties of blood during circulation at different speeds and in different parts of the vascular bed. The movement of blood in the body is determined by the contractility of the heart, the functional state of the bloodstream, and the properties of the blood itself. At relatively low linear flow velocities, blood particles move parallel to each other and the axis of the vessel. In this case, the blood flow has a layered character, and such a flow is called laminar.
If the linear speed increases and exceeds a certain value, different for each vessel, then the laminar flow turns into a disorderly, vortex flow, which is called “turbulent”. The speed of blood movement, at which laminar flow becomes turbulent, is determined using the Reynolds number, which for blood vessels is approximately 1160. Data on Reynolds numbers indicate that turbulence is possible only at the beginning of the aorta and in the areas of branching of large vessels. The movement of blood through most vessels is laminar. In addition to the linear and volumetric velocity of blood flow, the movement of blood through a vessel is characterized by two more important parameters, the so-called “shear stress” and “shear rate”. Shear stress means the force acting on a unit surface of a vessel in a direction tangential to the surface and is measured in dynes/cm2, or Pascals. Shear rate is measured in reciprocal seconds (s-1) and means the magnitude of the velocity gradient between parallel moving layers of fluid per unit distance between them.
Blood viscosity is defined as the ratio of shear stress to shear rate, and is measured in mPas. The viscosity of whole blood depends on the shear rate in the range of 0.1 - 120 s-1. At a shear rate of >100 s-1, changes in viscosity are not so pronounced, and after reaching a shear rate of 200 s-1, blood viscosity remains virtually unchanged. The viscosity value measured at high shear rates (more than 120 - 200 s-1) is called asymptotic viscosity. The principal factors influencing blood viscosity are hematocrit, plasma properties, aggregation and deformability of cellular elements. Given the vast majority of red blood cells compared to white blood cells and platelets, the viscosity properties of blood are determined mainly by red cells.
The main factor determining blood viscosity is the volumetric concentration of red blood cells (their content and average volume), called hematocrit. The hematocrit, determined from a blood sample by centrifugation, is approximately 0.4 - 0.5 l/l. Plasma is a Newtonian fluid, its viscosity depends on temperature and is determined by the composition of blood proteins. Plasma viscosity is most affected by fibrinogen (plasma viscosity is 20% higher than serum viscosity) and globulins (especially Y-globulins). According to some researchers, more important factor What leads to a change in plasma viscosity is not the absolute amount of proteins, but their ratios: albumin/globulins, albumin/fibrinogen. The viscosity of blood increases during its aggregation, which determines the non-Newtonian behavior of whole blood; this property is due to the aggregation ability of erythrocytes. Physiological aggregation of erythrocytes is a reversible process. IN healthy body The dynamic process of “aggregation - disaggregation” continuously occurs, and disaggregation dominates over aggregation.
The ability of erythrocytes to form aggregates depends on hemodynamic, plasma, electrostatic, mechanical and other factors. Currently, there are several theories explaining the mechanism of erythrocyte aggregation. The most well-known theory today is the theory of the bridging mechanism, according to which bridges from fibrinogen or other large-molecular proteins, in particular Y-globulins, are adsorbed on the surface of the erythrocyte, which, with a decrease in shear forces, contribute to the aggregation of erythrocytes. Pure Power aggregation is the difference between the force in the bridges, the force of electrostatic repulsion of negatively charged red blood cells and the shear force causing disaggregation. The mechanism of fixation of negatively charged macromolecules on erythrocytes: fibrinogen, Y-globulins is not yet completely clear. There is a point of view that the adhesion of molecules occurs due to weak hydrogen bonds and van der Waals dispersion forces.
There is an explanation for the aggregation of erythrocytes through depletion - the absence of high molecular weight proteins near erythrocytes, resulting in the appearance of “interaction pressure”, similar in nature to osmotic pressure macromolecular solution, which leads to the convergence of suspended particles. In addition, there is a theory according to which erythrocyte aggregation is caused by erythrocyte factors themselves, which lead to a decrease in the zeta potential of erythrocytes and a change in their shape and metabolism. Thus, due to the relationship between the aggregation ability of erythrocytes and blood viscosity, a comprehensive analysis of these indicators is necessary to assess the rheological properties of blood. One of the most accessible and widely used methods for measuring erythrocyte aggregation is the assessment of erythrocyte sedimentation rate. However, in his traditional version this test is not very informative because it does not take into account the rheological characteristics of the blood.
Ministry of Education of the Russian Federation
Penza State University
Medical Institute
Department of Therapy
Head Department of Doctor of Medical Sciences
“RHEOLOGICAL PROPERTIES OF BLOOD AND THEIR DISTURBANCES DURING INTENSIVE CARE”
Completed by: 5th year student
Checked by: Ph.D., Associate Professor
Penza
Plan
Introduction
1. Physical foundations of hemorheology
2. The reason for the “non-Newtonian behavior” of blood
3. Main determinants of blood viscosity
4. Hemorheological disorders and venous thrombosis
5. Methods for studying the rheological properties of blood
Literature
Introduction
Hemorheology studies the physicochemical properties of blood, which determine its fluidity, i.e. the ability to undergo reversible deformation under the influence of external forces. A generally accepted quantitative measure of blood fluidity is its viscosity.
Deterioration in blood flow is typical for patients in the intensive care unit. Increased blood viscosity creates additional resistance to blood flow and is therefore associated with excessive cardiac afterload, microcirculatory disorders, and tissue hypoxia. During a hemodynamic crisis, blood viscosity also increases due to a decrease in blood flow velocity. A vicious circle arises that maintains stasis and shunting of blood in the microvasculature.
Disorders in the hemorheological system represent a universal mechanism for the pathogenesis of critical conditions, therefore optimization of the rheological properties of blood is the most important tool in intensive care. Reducing blood viscosity helps accelerate blood flow, increase DO 2 to tissues, and facilitate heart function. With the help of rheologically active agents, the development of thrombotic, ischemic and infectious complications of the underlying disease can be prevented.
Applied hemorheology is based on a number of physical principles of blood fluidity. Understanding them helps to choose the optimal method of diagnosis and treatment.
1. Physical foundations of hemorheology
Under normal conditions, a laminar type of blood flow is observed in almost all parts of the circulatory system. It can be represented as an infinite number of layers of liquid that move in parallel without mixing with each other. Some of these layers come into contact with a stationary surface - the vascular wall and their movement, accordingly, slows down. The adjacent layers still tend to move in the longitudinal direction, but the slower wall layers retard them. Inside the flow, friction occurs between the layers. A parabolic velocity distribution profile appears with a maximum in the center of the vessel. The near-wall layer of liquid can be considered stationary. The viscosity of the simple fluid remains constant (8 s. Poise), while the viscosity of blood varies depending on the blood flow conditions (from 3 to 30 s. Poise).
The property of blood to provide “internal” resistance to those external forces that set it in motion is called viscosity η . Viscosity is due to the forces of inertia and adhesion.
When the hematocrit is 0, the viscosity of the blood approaches the viscosity of plasma.
To correctly measure and mathematically describe viscosity, concepts such as shear stress are introduced With and shear rate at . The first indicator is the ratio of the friction force between adjacent layers to their area - F / S . It is expressed in dynes/cm2 or pascals*. The second indicator is the velocity gradient of the layers - delta V / L . It is measured in s -1.
According to Newton's equation, shear stress is directly proportional to shear rate: τ= η·γ. This means that the greater the speed difference between the layers of fluid, the greater their friction. And, conversely, equalizing the speed of fluid layers reduces mechanical stress along the watershed line. Viscosity in this case acts as a proportionality coefficient.
The viscosity of simple, or Newtonian, liquids (for example, water) is constant under any conditions of movement, i.e. There is a linear relationship between shear stress and shear rate for these fluids.
Unlike simple liquids, blood can change its viscosity when the speed of blood flow changes. Thus, in the aorta and main arteries, blood viscosity approaches 4-5 relative units (if we take the viscosity of water at 20 °C as a reference measure). In the venous section of the microcirculation, despite the low shear stress, the viscosity increases 6-8 times relative to its level in the artery (i.e., up to 30-40 relative units). At extremely low, non-physiological shear rates, blood viscosity can increase 1000 times (!).
Thus, the relationship between shear stress and shear rate for whole blood is nonlinear, exponential. This “rheological behavior of blood”* is called “non-Newtonian.”
2. The reason for the “non-Newtonian behavior” of blood
The “non-Newtonian behavior” of blood is due to its roughly dispersed nature. From a physicochemical point of view, blood can be represented as a liquid medium (water) in which a solid, insoluble phase (blood elements and high-molecular substances) is suspended. The dispersed phase particles are large enough to resist Brownian motion. Therefore, a common property of such systems is their nonequilibrium. The components of the dispersed phase constantly strive to separate and precipitate cellular aggregates from the dispersed medium.
The main and rheologically most significant type of cellular blood aggregates is erythrocyte. It is a multidimensional cellular complex with a typical “coin column” shape. Its characteristic features are the reversibility of the connection and the absence of functional activation of cells. The structure of the erythrocyte aggregate is maintained mainly by globulins. It is known that the erythrocytes of a patient with an initially increased sedimentation rate, after they are added to the same-group plasma of a healthy person, begin to sediment at a normal rate. And vice versa, if the red blood cells of a healthy person with a normal sedimentation rate are placed in the plasma of a patient, then their precipitation will significantly accelerate.
Natural inducers of aggregation include primarily fibrinogen. The length of its molecule is 17 times greater than its width. Thanks to this asymmetry, fibrinogen is able to spread in the form of a “bridge” from one cell membrane to another. The bond formed in this case is fragile and breaks under the influence of minimal mechanical force. They act in a similar way A 2- and beta-macroglobulins, fibrinogen degradation products, immunoglobulins. A closer approach of red blood cells and their irreversible binding to each other is prevented by a negative membrane potential.
It should be emphasized that erythrocyte aggregation is a normal rather than pathological process. Its positive side is that it facilitates the passage of blood through the microcirculation system. When aggregates form, the surface to volume ratio decreases. As a result, the frictional resistance of the unit turns out to be significantly less than the resistance of its individual components.
3. Main determinants of blood viscosity
Blood viscosity is influenced by many factors. All of them realize their effect by changing the viscosity of plasma or the rheological properties of blood cells.
Red blood cell content. The erythrocyte is the main cellular population of the blood, actively participating in the processes of physiological aggregation. For this reason, changes in hematocrit (Ht) significantly affect blood viscosity. Thus, when Ht increases from 30 to 60%, the relative viscosity of blood doubles, and when Ht increases from 30 to 70%, it triples. Hemodilution, on the contrary, reduces blood viscosity.
The term “rheological behavior of blood” is generally accepted and emphasizes the “non-Newtonian” nature of blood fluidity.
Deformability of erythrocytes. The diameter of the red blood cell is approximately 2 times the lumen of the capillary. Because of this, the passage of an erythrocyte through the microvasculature is possible only if its volumetric configuration changes. Calculations show that if the erythrocyte were not capable of deformation, then blood with Ht 65% would turn into a dense homogeneous formation and a complete stop of blood flow would occur in the peripheral parts of the circulatory system. However, due to the ability of red blood cells to change their shape and adapt to environmental conditions, blood circulation does not stop even at Ht 95-100%.
There is no coherent theory of the deformation mechanism of erythrocytes. Apparently, this mechanism is based on the general principles of the transition of a sol to a gel. It is assumed that the deformation of erythrocytes is an energy-dependent process. Perhaps hemoglobin A takes an active part in it. It is known that the content of hemoglobin A in the erythrocyte decreases in some hereditary blood diseases (sickle cell anemia), after operations under artificial circulation. At the same time, the shape of red blood cells and their plasticity change. Increased blood viscosity is observed, which does not correspond to low Ht.
Plasma viscosity. Plasma as a whole can be classified as a “Newtonian” fluid. Its viscosity is relatively stable in various parts of the circulatory system and is mainly determined by the concentration of globulins. Among the latter, fibrinogen is of primary importance. It is known that the removal of fibrinogen reduces the viscosity of plasma by 20%, so the viscosity of the resulting serum approaches the viscosity of water.
Normally, plasma viscosity is about 2 rel. units This is approximately 1/15 of the internal resistance that develops with whole blood in the venous microcirculation. However, plasma has a very significant effect on peripheral blood flow. In capillaries, blood viscosity is reduced by half compared to proximal and distal vessels of larger diameter (phenomenon §). This “prolapse” of viscosity is associated with the axial orientation of red blood cells in a narrow capillary. In this case, the plasma is pushed to the periphery, to the wall of the vessel. It serves as a “lubricant”, which ensures the sliding of the chain of blood cells with minimal friction.
This mechanism functions only when the plasma protein composition is normal. An increase in the level of fibrinogen or any other globulin leads to difficulty in capillary blood flow, sometimes of a critical nature. Thus, multiple myeloma, Waldenström's macroglobulinemia and some collagenoses are accompanied by excessive production of immunoglobulins. In this case, the viscosity of the plasma increases relative to the normal level by 2-3 times. The clinical picture begins to be dominated by symptoms of severe microcirculation disorders: decreased vision and hearing, drowsiness, adynamia, headache, paresthesia, bleeding of the mucous membranes.
Pathogenesis of hemorheological disorders. In intensive care practice, hemorheological disorders arise under the influence of a complex of factors. The action of the latter in a critical situation is universal.
Biochemical factor. On the first day after surgery or injury, fibrinogen levels usually double. The peak of this increase occurs on days 3-5, and normalization of fibrinogen levels occurs only at the end of the 2nd postoperative week. In addition, fibrinogen degradation products, activated platelet procoagulants, catecholamines, prostaglandins, and lipid peroxidation products appear in the bloodstream in excess quantities. All of them act as inducers of red blood cell aggregation. A peculiar biochemical situation is formed - “rheotoxemia”.
Hematological factor. Surgery or trauma is also accompanied by certain changes in the cellular composition of the blood, which are called hematological stress syndrome. Young granulocytes, monocytes and platelets of increased activity enter the bloodstream.
Hemodynamic factor. The increased aggregation tendency of blood cells under stress is superimposed on local hemodynamic disturbances. It has been shown that during uncomplicated abdominal interventions, the volumetric velocity of blood flow through the popliteal and iliac veins drops by 50%. This is due to the fact that immobilization of the patient and muscle relaxants block the physiological mechanism of the “muscle pump” during surgery. In addition, under the influence of mechanical ventilation, anesthetics or blood loss, systemic pressure decreases. In such a situation, the kinetic energy of systole may not be enough to overcome the adhesion of blood cells to each other and to the vascular endothelium. The natural mechanism of hydrodynamic disaggregation of blood cells is disrupted, and microcirculatory stasis occurs.
4. Hemorheological disorders and venous thrombosis
Slowing down the speed of movement in the venous circulation provokes aggregation of red blood cells. However, the inertia of movement may be quite large and the blood cells will experience increased deformation load. Under its influence, ATP is released from red blood cells - a powerful inducer of platelet aggregation. Low shear rate also stimulates the adhesion of young granulocytes to the venule wall (Farheus-Vejiens phenomenon). Irreversible aggregates are formed that can form the cellular core of a venous thrombus.
Further development of the situation will depend on the activity of fibrinolysis. As a rule, an unstable balance arises between the processes of formation and resorption of a blood clot. For this reason, most cases of deep vein thrombosis of the lower extremities in hospital practice are hidden and resolve spontaneously, without consequences. The use of disaggregants and anticoagulants is a highly effective way to prevent venous thrombosis.
5. Methods for studying the rheological properties of blood
The “non-Newtonian” nature of blood and the associated shear rate factor must be taken into account when measuring viscosity in clinical laboratory practice. Capillary viscometry is based on the flow of blood through a graduated vessel under the influence of gravity, and therefore is physiologically incorrect. Real blood flow conditions are simulated on a rotational viscometer.
The fundamental elements of such a device include a stator and a rotor congruent with it. The gap between them serves as a working chamber and is filled with a blood sample. The movement of the liquid is initiated by the rotation of the rotor. This, in turn, is arbitrarily specified in the form of a certain shear rate. The measured quantity is the shear stress, which occurs as a mechanical or electrical torque necessary to maintain the selected speed. Blood viscosity is then calculated using Newton's formula. The unit of measurement for blood viscosity in the GHS system is Poise (1 Poise = 10 dynes x s/cm 2 = 0.1 Pa x s = 100 relative units).
It is mandatory to measure blood viscosity in the low range (<10 с -1) и высоких (>100 s -1) shear rates. The low range of shear rates reproduces the conditions of blood flow in the venous section of the microcirculation. The determined viscosity is called structural. It mainly reflects the tendency of red blood cells to aggregate. High shear rates (200-400 s -1) are achieved in vivo in the aorta, great vessels and capillaries. In this case, as rheoscopic observations show, red blood cells occupy a predominantly axial position. They stretch in the direction of movement, their membrane begins to rotate relative to the cellular contents. Due to hydrodynamic forces, almost complete disaggregation of blood cells is achieved. Viscosity, determined at high shear rates, depends primarily on the plasticity of the red blood cells and the shape of the cells. It is called dynamic.
As a standard for research on a rotational viscometer and the corresponding norm, you can use the indicators according to the method of N.P. Alexandrova and others.
To provide a more detailed picture of the rheological properties of blood, several more specific tests are performed. The deformability of erythrocytes is assessed by the speed of passage of diluted blood through a microporous polymer membrane (d=2-8 μm). The aggregation activity of red blood cells is studied using nephelometry by measuring the change in the optical density of the medium after adding aggregation inducers (ADP, serotonin, thrombin or adrenaline) to it.
Diagnosis of hemorheological disorders . Disorders in the hemorheological system, as a rule, occur latently. Their clinical manifestations are nonspecific and subtle. Therefore, the diagnosis is determined mainly by laboratory data. Its leading criterion is the value of blood viscosity.
The main direction of shifts in the hemorheology system in patients in critical condition is the transition from increased to decreased blood viscosity. This dynamics, however, is accompanied by a paradoxical deterioration in blood fluidity.
Syndrome of increased blood viscosity. It is nonspecific in nature and is widespread in the clinic of internal diseases: with atherosclerosis, angina pectoris, chronic obstructive bronchitis, gastric ulcer, obesity, diabetes mellitus, obliterating endarteritis, etc. In this case, a moderate increase in blood viscosity to 35 cPoise is noted at y = 0, 6 s -1 and 4.5 cPoise at y = = 150 s -1 . Microcirculatory disorders are usually mild. They progress only as the underlying disease develops. Hyperviscosity syndrome in patients admitted to the intensive care unit should be considered as an underlying condition.
Low blood viscosity syndrome. As the critical condition unfolds, blood viscosity decreases due to hemodilution. Viscometry indicators are 20-25 cPoise at y=0.6 s -1 and 3-3.5 cPoise at y=150 s -1 . Similar values can be predicted from Ht, which usually does not exceed 30-35%. In the terminal state, the decrease in blood viscosity reaches the stage of “very low” values. Severe hemodilution develops. Ht decreases to 22-25%, dynamic blood viscosity - to 2.5-2.8 cPoise and structural blood viscosity - to 15-18 cPoise.
The low value of blood viscosity in a patient in critical condition creates a misleading impression of hemorheological well-being. Despite hemodilution, with low blood viscosity syndrome, microcirculation significantly deteriorates. The aggregation activity of red blood cells increases 2-3 times, and the passage of the erythrocyte suspension through nucleopore filters slows down 2-3 times. After restoration of Ht by in vitro hemoconcentration, blood hyperviscosity is detected in such cases.
Against the background of low or very low blood viscosity, massive aggregation of red blood cells can develop, which completely blocks the microvasculature. This phenomenon described by M.N. Knisely in 1947 as a “sludge” phenomenon, indicates the development of a terminal and apparently irreversible phase of a critical condition.
The clinical picture of low blood viscosity syndrome consists of severe microcirculatory disorders. Note that their manifestations are nonspecific. They may be caused by other, non-rheological mechanisms.
Clinical manifestations of low blood viscosity syndrome:
Tissue hypoxia (in the absence of hypoxemia);
Increased peripheral vascular resistance;
Deep vein thrombosis of the extremities, recurrent pulmonary thromboembolism;
Adynamia, stupor;
Deposition of blood in the liver, spleen, subcutaneous vessels.
Prevention and treatment. Patients admitted to the operating room or intensive care unit need to optimize the rheological properties of blood. This prevents the formation of venous blood clots, reduces the likelihood of ischemic and infectious complications, and alleviates the course of the underlying disease. The most effective methods of rheological therapy are blood dilution and suppression of the aggregation activity of its formed elements.
Hemodilution. The red blood cell is the main carrier of structural and dynamic resistance to blood flow. Therefore, hemodilution turns out to be the most effective rheological agent. Its beneficial effect has been known for a long time. For many centuries, bloodletting was perhaps the most common method of treating diseases. The emergence of low molecular weight dextrans was the next stage in the development of the method.
Hemodilution increases peripheral blood flow, but at the same time reduces the oxygen capacity of the blood. Under the influence of two differently directed factors, DO 2 ultimately develops in the tissues. It can increase due to blood dilution or, on the contrary, significantly decrease under the influence of anemia.
The lowest possible Ht, which corresponds to a safe level of DO 2, is called optimal. Its exact size is still a matter of debate. The quantitative relationships between Ht and DO 2 are well known. However, it is not possible to assess the contribution of individual factors: tolerance of anemia, tension of tissue metabolism, hemodynamic reserve, etc. According to the general opinion, the goal of therapeutic hemodilution is Ht 30-35%. However, experience in treating massive blood loss without blood transfusion shows that an even greater reduction in Ht to 25 and even 20% is quite safe from the point of view of oxygen supply to tissues.
Currently, three techniques are used to achieve hemodilution.
Hemodilution in hypervolemic mode implies a fluid transfusion that leads to a significant increase in blood volume. In some cases, a short-term infusion of 1-1.5 liters of plasma substitutes precedes induction of anesthesia and surgery; in other cases, requiring longer hemodilution, a decrease in Ht is achieved by a constant fluid load at the rate of 50-60 ml/kg of the patient’s body weight per day. A decrease in the viscosity of whole blood is the main consequence of hypervolemia. The viscosity of plasma, the plasticity of erythrocytes and their tendency to aggregation do not change. The disadvantages of the method include the risk of volume overload of the heart.
Hemodilution in normovolemia was originally proposed as an alternative to heterologous transfusions in surgery. The essence of the method is the preoperative collection of 400-800 ml of blood into standard containers with a stabilizing solution. Controlled blood loss, as a rule, is replenished simultaneously with the help of plasma substitutes at a rate of 1:2. With some modification of the method, it is possible to collect 2-3 liters of autologous blood without any adverse hemodynamic and hematological consequences. The collected blood is then returned during or after surgery.
Normovolemic hemodilution is not only a safe, but also a low-cost method of autodonation, which has a pronounced rheological effect. Along with a decrease in Ht and the viscosity of whole blood after exfusion, there is a persistent decrease in plasma viscosity and the aggregation ability of erythrocytes. The flow of fluid between the interstitial and intravascular spaces is activated, along with it the exchange of lymphocytes and the flow of immunoglobulins from tissues increase. All this ultimately leads to a reduction in postoperative complications. This method can be widely used for planned surgical interventions.
Endogenous hemodilution develops with pharmacological vasoplegia. The decrease in Ht in these cases is due to the fact that protein-depleted and less viscous fluid enters the vascular bed from the surrounding tissues. Epidural blockade, halogen-containing anesthetics, ganglion blockers and nitrates have a similar effect. The rheological effect accompanies the main therapeutic effect of these drugs. The degree of reduction in blood viscosity is not predicted. It is determined by the current state of volume and hydration.
Anticoagulants. Heparin is obtained by extraction from biological tissues (cattle lungs). The final product is a mixture of polysaccharide fragments with different molecular weights, but with similar biological activity.
The largest heparin fragments in complex with antithrombin III inactivate thrombin, while heparin fragments with a molecular weight of 7000 act predominantly on the activated factor X.
The administration of high molecular weight heparin in a dose of 2500-5000 units subcutaneously 4-6 times a day in the early postoperative period has become a widespread practice. Such a prescription reduces the risk of thrombosis and thromboembolism by 1.5-2 times. Low doses of heparin do not prolong the activated partial thromboplastin time (aPTT) and, as a rule, do not cause hemorrhagic complications. Heparin therapy, along with hemodilution (intentional or collateral), are the main and most effective methods for the prevention of hemorheological disorders in surgical patients.
Low molecular weight fractions of heparin have less affinity for platelet von Willebrand factor. Because of this, compared to high molecular weight heparin, they are even less likely to cause thrombocytopenia and bleeding. The first experience of using low molecular weight heparin (Clexane, Fraxiparin) in clinical practice gave encouraging results. Heparin preparations turned out to be equipotential to traditional heparin therapy, and according to some data even exceeded its preventive and therapeutic effect. In addition to safety, low-molecular-weight heparin fractions are also distinguished by their economical administration (once daily) and the absence of the need for aPTT monitoring. The dose selection is usually made without taking into account body weight.
Plasmapheresis. The traditional rheological indication for plasmapheresis is primary hyperviscosity syndrome, which is caused by excessive production of abnormal proteins (paraproteins). Their removal leads to rapid reversal of the disease. The effect, however, is short-lived. The procedure is symptomatic.
Currently, plasmapheresis is actively used for the preoperative preparation of patients with obliterating diseases of the lower extremities, thyrotoxicosis, gastric ulcer, and purulent-septic complications in urology. This leads to an improvement in the rheological properties of blood, activation of microcirculation, and a significant reduction in the number of postoperative complications. Replace up to 1/2 of the volume of the central processing unit.
The decrease in globulin levels and plasma viscosity after one plasmapheresis procedure can be significant, but short-lived. The main beneficial effect of the procedure, which extends throughout the entire postoperative period, is the so-called resuspension phenomenon. Washing of erythrocytes in a protein-free environment is accompanied by a stable improvement in the plasticity of erythrocytes and a decrease in their aggregation tendency.
Photomodification of blood and blood substitutes. With 2-3 procedures of intravenous irradiation of blood with a helium-neon laser (wavelength 623 nm) of low power (2.5 mW), a clear and long-lasting rheological effect is observed. According to precision nephelometry, under the influence of laser therapy, the number of hyperergic reactions of platelets decreases, and the kinetics of their aggregation in vitro is normalized. Blood viscosity remains unchanged. UV rays (with a wavelength of 254-280 nm) in the extracorporeal circuit also have a similar effect.
The mechanism of the disaggregation effect of laser and ultraviolet radiation is not entirely clear. It is assumed that photomodification of blood first causes the formation of free radicals. In response, antioxidant defense mechanisms are activated, which block the synthesis of natural inducers of platelet aggregation (primarily prostaglandins).
Ultraviolet irradiation of colloidal preparations (for example, rheopolyglucin) has also been proposed. After their administration, the dynamic and structural viscosity of blood decreases by 1.5 times. Platelet aggregation is also significantly inhibited. It is characteristic that unmodified rheopolyglucin is not able to reproduce all these effects.
Literature
1. “Emergency Medical Care,” ed. J.E. Tintinally, Rl. Kroma, E. Ruiz, Translation from English by Dr. med. Sciences V.I. Kandrora, Doctor of Medical Sciences M.V. Neverova, Dr. med. Sciences A.V. Suchkova, Ph.D. A.V. Nizovoy, Yu.L. Amchenkova; edited by Doctor of Medical Sciences V.T. Ivashkina, D.M.N. P.G. Bryusova; Moscow "Medicine" 2001
2. Intensive therapy. Resuscitation. First aid: Tutorial/ Ed. V.D. Malysheva. - M.: Medicine. - 2000. - 464 p.: ill. - Textbook. lit. For students of the postgraduate education system. - ISBN 5-225-04560-Х
