This book is a translation of the latest, third, world-renowned edition of the fundamental manual written by University of Pennsylvania professor Paul Marino, "The ICU Book". It presents the most modern and relevant information on hemodynamic and metabolic monitoring, on the pathophysiology of critical conditions, modern methods of their diagnosis and treatment. Particular attention is paid to the selection of adequate treatment, which is very valuable given the tendency of many doctors to polypharmacy, as a result of which the risk of iatrogenic complications increases and the economic costs increase unreasonably. The material is accompanied by numerous clinical examples and summary tables that facilitate the perception of information. The appendices tell about the features of pharmacotherapy, about the doses and routes of administration of a number of drugs, provide schemes and algorithms for resuscitation and diagnostic measures, reference tables for calculating various needs of the body, international systems for assessing the severity of the patient's condition, and outline measures to prevent infections and the hemodynamic profile. The book will be useful not only for specialists in the field of intensive care and resuscitation, but also for doctors of other specialties, as well as senior students of medical institutions.

Preface by the scientific editor to the publication in Russian

List of abbreviations

Basic scientific concepts

Circulation

Transport of oxygen and carbon dioxide

SECTION II

Preventive measures for critical conditions

Infection control in the intensive care unit

Preventive treatment of the gastrointestinal tract

Venous thromboembolism

SECTION III

Vascular access

Creation of venous access

Staying the catheter in the vessel

SECTION IV

Hemodynamic monitoring

Blood pressure

Pulmonary artery catheterization

Central venous pressure and wedge pressure

Oxygenation of tissues

Circulatory disorders

Bleeding and hypovolemia

Replacement with colloidal and crystalloid solutions

Acute heart failure syndromes

Heart failure

Infusion of drugs with hemodynamic action

SECTION VI

Critical conditions in cardiology

Early treatment of acute coronary syndrome

Tachyarrhythmias

SECTION VII

Acute respiratory failure

Hypoxemia and hypercapnia

Oximetry and Capnography

Inhalation oxygen therapy

Acute Respiratory Distress Syndrome

Severe airway obstruction

SECTION VIII

Artificial lung ventilation

Principles of artificial ventilation

Assisted ventilation modes

Patient on artificial lung ventilation

Termination of artificial ventilation

SECTION IX

Acid-base disorders

Interpretation of the acid-base state

Organic acidosis

Metabolic alkalosis

SECTION X

Renal and electrolyte disorders

Oliguria and Acute Renal Failure

Hypertensive and hypotonic states

Calcium and Phosphorus

SECTION XI

The practice of transfusion therapy in critical medicine

Anemia and red blood cell transfusion in the intensive care unit

Platelets in critical conditions

SECTION XII

Body temperature disorders

Hyper- and hypothermic syndromes

Fever

SECTION XIII

Inflammation and infection in the intensive care unit

Infection, inflammation and multiple organ failure

Pneumonia

Sepsis in pathology of the abdominal cavity and small pelvis

Immunocompromised patients

Antibacterial therapy

SECTION XIV

Nutrition and metabolism

Metabolic needs

Enteral tube feeding

Parenteral nutrition

Adrenal and thyroid dysfunctions

SECTION XV

Intensive care in neurology

Pain relief and sedation

Thinking disorders

Disorders of motor function

Stroke and related disorders

SECTION XVI

Poisoning

Toxic reactions to drugs and antidotes to them

SECTION XVII

Applications

Annex 1

Units and Conversions

Appendix 2

Selected Reference Tables

Appendix 3

Clinical grading systems

Subject index

Once a child is diagnosed with diabetes, parents often go to the library for information on the subject and face the possibility of complications. After a period of related anxiety, parents take the next blow when they find out the statistics of morbidity and mortality associated with diabetes.

Viral hepatitis in early childhood

Relatively recently, the hepatitis alphabet, in which hepatitis A, B, C, D, E, G viruses were already listed, was replenished with two new DNA-containing viruses, TT and SEN. We know that hepatitis A and hepatitis E do not cause chronic hepatitis and that hepatitis G and TT viruses are most likely “innocent bystanders” that are transmitted vertically and do not affect the liver.

Measures for the treatment of chronic functional constipation in children

When treating chronic functional constipation in children, important factors in the child's medical history must be considered; establish a good relationship between the healthcare provider and the child-family to implement the proposed treatment properly; a lot of patience on both sides with repeated guarantees that the situation will gradually improve, and courage in cases of possible relapses are the best way to treat constipated children.

Scientists' study results challenge the concept of diabetes management

The results of a ten-year study indisputably proved that frequent self-monitoring and maintenance of blood glucose levels close to normal leads to a significant decrease in the risk of late complications caused by diabetes mellitus and a decrease in their severity.

Manifestations of rickets in children with impaired formation of the hip joints

In the practice of pediatric orthopedic traumatologists, the question of the need to confirm or exclude violations of the formation of the hip joints (dysplasia of the hip joints, congenital dislocation of the hip) in infants is often raised. The article shows the analysis of the examination of 448 children with clinical signs of disorders in the formation of the hip joints.

Medical gloves as a means of ensuring infectious safety

Gloves are disliked by most nurses and doctors, and for good reason. In gloves, the sensitivity of the fingertips is lost, the skin on the hands becomes dry and flaky, and the instrument strives to slip out of the hands. But gloves have been and remain the most reliable means of protection against infection.

Lumbar osteochondrosis

It is believed that every fifth adult on earth suffers from lumbar osteochondrosis, this disease occurs both in young and old age.

Epidemiological control of health workers who have been in contact with the blood of HIV-infected

(to help medical workers of medical and preventive institutions)

The guidelines cover the issues of monitoring medical workers who had contact with the blood of a patient infected with HIV. Actions are proposed to prevent occupational HIV infection. A logbook and an official investigation report in case of contact with the blood of an HIV-infected patient have been developed. The procedure for informing higher authorities about the results of medical supervision of medical workers who came into contact with the blood of an HIV-infected patient has been determined. Designed for medical workers of medical institutions.

Chlamydial infection in obstetrics and gynecology

Chlamydia of the genitals is the most common sexually transmitted disease. Worldwide, there is an increase in chlamydia infections among young women who have just entered the period of sexual activity.

Cycloferon in the treatment of infectious diseases

Currently, there is an increase in certain nosological forms of infectious diseases, primarily viral infections. One of the directions for improving treatment methods is the use of interferons as important nonspecific factors of antiviral resistance. These include cycloferon - a low molecular weight synthetic inducer of endogenous interferon.

Dysbacteriosis in children

The number of microbial cells present on the skin and mucous membranes of the macroorganism in contact with the external environment exceeds the number of cells of all its organs and tissues combined. The weight of the microflora of the human body is on average 2.5-3 kg. The importance of microbial flora for a healthy person was first noticed in 1914 by I.I. Mechnikov, who suggested that the cause of many diseases are various metabolites and toxins produced by various microorganisms that inhabit the organs and systems of the human body. The problem of dysbiosis in recent years has caused a lot of discussions with an extreme range of judgments.

Diagnosis and treatment of female genital infections

In recent years, throughout the world and in our country, there has been an increase in the incidence of sexually transmitted infections among the adult population and, which is of particular concern, among children and adolescents. The incidence of chlamydia and trichomoniasis is increasing. According to WHO, trichomoniasis ranks first in frequency among sexually transmitted infections. Every year 170 million people fall ill with trichomoniasis in the world.

Intestinal dysbiosis in children

Intestinal dysbiosis and secondary immunodeficiency are increasingly common in the clinical practice of doctors of all specialties. This is due to changing living conditions, the harmful effects of the preformed environment on the human body.

Viral hepatitis in children

The lecture "Viral hepatitis in children" presents data on viral hepatitis A, B, C, D, E, F, G in children. All clinical forms of viral hepatitis, differential diagnosis, treatment and prevention that exist at present are presented. The material is presented from a modern perspective and is designed for senior students of all faculties of medical universities, interns, pediatricians, infectious disease specialists and doctors of other specialties who are interested in this infection.

Resuscitation is a theoretical discipline, the scientific findings of which are used in resuscitation in a clinic, or, more precisely, a science that studies the patterns of dying and revitalization of the body in order to develop the most effective methods of prevention and ... ... Wikipedia

THERAPY, and, wives. 1. The branch of medicine dealing with the treatment of internal diseases by conservative (in 2 meanings), non-surgical methods and their prevention. 2. The very treatment. Intensive t. (Aimed at saving the patient's life). | adj. ... ... Ozhegov's Explanatory Dictionary

Complex T., carried out in severe and life-threatening conditions of the patient ... Comprehensive Medical Dictionary

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A system of therapeutic measures aimed at correcting disturbed vital functions (breathing, blood circulation, metabolism) or preventing these disorders. The need for I. t. Arises in acute serious illnesses and critical conditions ... ... Medical encyclopedia

- (late lat. infectio infection) a group of diseases that are caused by specific pathogens, characterized by infectiousness, cyclic course and the formation of post-infectious immunity. The term "infectious diseases" was introduced ... ... Medical encyclopedia

I Preoperative period is the period of time from the moment of establishing the diagnosis and indications for the operation to the beginning of its implementation. The main task of P. p. Is to maximize the risk of developing various complications associated with anesthesia and ... ... Medical encyclopedia

I Sepsis Sepsis (Greek sēpsis decay) is a common non-cyclic infectious disease caused by constant or periodic penetration of various microorganisms and their toxins into the bloodstream under conditions of inadequate resistance ... ... Medical encyclopedia

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The relevance of the subject matter of the article is questioned. Please show in the article the significance of its subject by adding evidence of significance to it according to particular criteria of significance or, if the particular criteria of significance for ... ... Wikipedia

Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 1-2.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 1-3.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 1-4.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 1-5.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 1-7.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 1.html Contents The activity of the heart In this chapter we will consider the forces that affect the effective activity of the heart, the formation of its stroke volume, and their interaction under normal conditions and at various stages of development heart failure. Most of the terms and concepts that you will come across in this chapter are well known to you, but now you can apply this knowledge at the patient's bedside. MUSCLE CONTRACTION The heart is a hollow muscular organ. Despite the fact that skeletal muscles differ in structure and physiological properties from the heart muscle (myocardium), apparently, in a simplified way, they can be used to demonstrate the basic mechanical regularities of muscle contraction. For this, a model is usually used in which the muscle is rigidly suspended on a support. 1. If a load is applied to the free end of the muscle, then the muscle will stretch and its length at rest will change. The force that stretches a muscle before contracting it is referred to as preload. 2. The length to which the muscle is stretched after applying the preload is determined by the “elasticity” of the muscle. Elasticity (resilience) - the ability of an object to take its original shape after deformation. The more elastic a muscle is, the less it lends itself to stretching by preload. To characterize the elasticity of a muscle, the term “extensibility” is traditionally used; in its meaning, this term is the reverse of the concept of “elasticity”. 3. If a limiter is attached to the muscle, it is possible to increase the load with an additional weight without additional stretching of the muscle. With electrical stimulation and removal of the restraint, the muscle contracts and lifts both weights. The load that the contracting muscle must lift is referred to as afterload. Note that afterload includes preload. 4. The ability of a muscle to move the load is considered an index of the strength of muscle contraction and is defined by the term contractility. Table 1-1. Parameters that determine the contraction of skeletal muscle Preload Strength that stretches the muscle at rest (before contraction) Afterload Weight that the muscle must lift during contraction Contraction Strength of muscle contraction with constant pre- and afterload Stretch Length by which preload stretches the muscle DEFINITIONS C positions of mechanics, muscle contraction is determined by several forces (tab. 1-1). These forces act on the muscle either at rest or during active contractions. At rest, the state of the muscle is determined by the applied preload and the elastic properties (extensibility of the constituent parts) of the tissue. During contraction, the state of the muscle depends on the properties of the contractile elements and the load that must be lifted (afterload). Under normal conditions, the heart functions in a similar way (see below). However, when transferring the mechanical laws of muscle contraction to the activity of the heart muscle as a whole (i.e., its pumping function), the load characteristics are described in units of pressure, not forces, in addition, blood volume is used instead of length. Pressure-Volume Curves The pressure-volume curves are shown in Figure 1-2 to explain the contraction of the left ventricle and the forces that affect this process. The loop inside the graph describes one heart cycle. CARDIAC CYCLE Point A (see Fig. 1-2) is the beginning of filling of the ventricle when the mitral valve opens and blood flows from the left atrium. The volume of the ventricle gradually increases until the pressure in the ventricle exceeds the pressure in the atrium and the mitral valve closes (point B). At this point, the ventricular volume is the end diastolic volume (EDV). This volume is similar to the preload in the model considered above, since it will lead to stretching of the fibers of the ventricular myocardium to a new residual (diastolic) length. In other words, the end-diastolic volume is equivalent to preload. Rice. 1-2 Pressure-volume curves for the left ventricle of an intact heart. 2. Point B - the beginning of the left ventricle contraction with closed aortic and mitral valves (isometric contraction phase). The pressure in the ventricle rises rapidly until it exceeds the pressure in the aorta and the aortic valve opens (point B). The pressure at this point is similar to afterload in the model discussed above, since it is applied to the ventricle after the onset of contraction (systole) and is the force that must be overcome by the ventricle in order to “eject” the systolic (stroke) blood volume. Therefore, the pressure in the aorta is similar to afterload (in fact, afterload consists of several components, but see below for more on this). 3. After the aortic valve opens, blood flows into the aorta. When the ventricular pressure drops below the aortic pressure, the aortic valve closes. The force of ventricular contraction determines the volume of expelled blood at a given pre- and afterload values. In other words, the pressure at point G is a function of contractility if the values ​​of B (preload) and C (afterload) do not change. Thus, systolic pressure is similar to contractility when pre- and afterload are constant. When the aortic valve closes at point H, the pressure in the left ventricle drops sharply (period of isometric relaxation) until the next moment of opening of the mitral valve at point A, i.e. the beginning of the next cardiac cycle. 4. The area bounded by the pressure-volume curve corresponds to the work of the left ventricle during one cardiac cycle (work of force is a value equal to the product of the moduli of force and displacement). Any processes that increase this area (for example, an increase in pre- and afterload or contractility), increase the heart beat. Impact work is an important indicator, as it determines the energy expended by the heart (oxygen consumption). This issue is discussed in Chapter 14. STARLING CURVE A healthy heart primarily depends on the volume of blood in the ventricles at the end of diastole. This was first discovered in 1885 on a frog heart preparation by Otto Frank. Ernst Starling continued these studies on the mammalian heart, and in 1914 he obtained very interesting data. In fig. 1-2 shows the Starling (Frank-Starling) curve showing the relationship between EDV and systolic pressure. Note the steep ascending part of the curve. The steep slope of the Starling curve indicates the importance of preload (volume) for enhancing the release of blood from a healthy heart; in other words, with an increase in the blood supply of the heart in diastole and, therefore, with an increase in the stretching of the heart muscle, the force of the heart contractions increases. This dependence is a fundamental law (“law of the heart”) of the physiology of the cardiovascular system, in which a heterometric (ie, carried out in response to a change in the length of myocardial fibers) mechanism of regulation of the heart's activity is manifested. DOWN PART OF STARLING CURVE With an excessive increase in EDV, a drop in systolic pressure is sometimes observed with the formation of a descending part of the Starling curve. This phenomenon was originally attributed to overstretching of the heart muscle, when the contractile filaments are significantly separated from each other, which reduces the contact between them, which is necessary to maintain the force of contraction. However, the descending part of the Starling curve can be obtained with an increase in afterload, and not only due to an increase in the length of the muscle fiber at the end of diastole. If afterload is kept constant, then in order to decrease the stroke volume of the heart, the end diastolic pressure (EDP) must exceed 60 mmHg. Since this pressure is rarely seen in the clinic, the meaning of the descending part of the Starling curve remains a matter of debate. Rice. 1-3. Functional curves of the ventricles. In clinical practice, there is not enough data to support the descending part of the Starling curve. This means that with hypervolemia, cardiac output should not decrease, and with hypovolemia (for example, due to increased diuresis), it cannot increase. Special attention should be paid to this, as diuretics are often used in the treatment of heart failure. This issue is discussed in more detail in Chapter 14. FUNCTIONAL HEART CURVE In the clinic, the analogue of the Starling curve is the functional heart curve (Fig. 1-3). Note that the stroke volume replaces the systolic pressure, and the CDP replaces the EDV. Both indicators can be determined at the patient's bedside using pulmonary artery catheterization (see Chapter 9). The slope of the functional curve of the heart is caused not only by myocardial contractility, but also by afterload. As seen in Fig. 1-3, decreasing contractility or increasing afterload decreases the slope of the curve. It is important to take into account the effect of afterload, since it means that the functional curve of the heart is not a reliable indicator of myocardial contractility, as previously assumed [b]. EXTENSION CURVES The ability of the ventricle to fill during diastole can be characterized by the relationship between pressure and volume at the end of diastole (EDV and EDV), which is shown in Fig. 1-4. The slope of the pressure-volume curves during diastole reflects the distensibility of the ventricle. Ventricular compliance = AKDO / AKDD. Rice. 1-4 Pressure-Volume Curves During Diastole As shown in fig. 1-4, a decrease in elongation will lead to a shift of the curve down and to the right, the KDV will be higher for any BWD. Increasing the elongation has the opposite effect. Preload - the strength that stretches the muscle at rest is equivalent to the BWD, not the BDC. However, EDV cannot be determined routinely at the bedside, and EDV measurement is the standard clinical procedure for determining preload (see Chapter 9). When using KDD to assess the preload, one should take into account the dependence of KDD on the change in elongation. In fig. 1-4, it can be seen that the EDV can be increased, although the EDV (preload) is actually reduced. In other words, the CDP indicator will overestimate the preload value with a reduced ventricular compliance. CDV allows to reliably characterize preload only with normal (unchanged) ventricular compliance. Some therapeutic measures in critically ill patients can lead to a decrease in ventricular compliance (for example, artificial ventilation of the lungs with positive inspiratory pressure), and this limits the value of CDP as an indicator of preload. These issues are discussed in more detail in Chapter 14. AFTERLOAD Above, afterload has been defined as a force that prevents or resists ventricular contraction. This force is equivalent to the stress in the ventricular wall during systole. The components of the transmural stress of the ventricular wall are shown in Fig. 1-5. Rice. 1-5. Afterload components. According to Laplace's law, wall tension is a function of systolic pressure and chamber (ventricular) radius. Systolic pressure depends on the impedance of blood flow in the aorta, while chamber size is a function of the EDV (i.e., preload). Above, it was shown in the model that preload is part of the afterload. VASCULAR RESISTANCE Impedance is a physical quantity characterized by the resistance of the medium to the propagation of a pulsating fluid flow. Impedance has two components: extensibility, which prevents changes in velocity in the flow, and resistance, which limits the average flow velocity [b]. Arterial compliance cannot be measured routinely, so arterial resistance (BP) is used to assess afterload, which is defined as the difference between mean arterial pressure (inflow) and venous pressure (outflow) divided by blood flow velocity (cardiac output). Pulmonary vascular resistance (PVR) and total peripheral vascular resistance (OPSR) are determined as follows: PVR = (Dla-Dlp) / SV; OPSS = (SBP - ATP) CB, where SV is cardiac output, Dla is the mean pressure in the pulmonary artery, Dlp is the mean pressure in the left atrium, SBP is the mean systemic arterial pressure, Dp is the mean pressure in the right atrium. The presented equations are similar to the formulas used to describe the resistance to direct electric current (Ohm's law), i.e. there is an analogy between hydraulic and electrical circuits. However, the behavior of the resistor in the electrical circuit will differ significantly from that of the impedance of the fluid flow in the hydraulic circuit due to the presence of pulsation and capacitive elements (veins). TRANSMURAL PRESSURE True afterload is transmural force and therefore includes a component that is not part of the vascular system: pressure in the pleural cavity (fissure). Negative pleural pressure increases afterload because it increases transmural pressure at a specific intraventricular pressure, while positive intrapleural pressure has the opposite effect. This may explain the decrease in systolic pressure (stroke volume) during spontaneous inspiration, when the negative pressure in the pleural cavity decreases. The effect of pleural pressure on cardiac activity is discussed in Chapter 27. Finally, a number of issues related to vascular resistance to blood flow as an indicator of afterload should be noted, since experimental evidence suggests that vascular resistance is an unreliable indicator of ventricular afterload. Measurement of vascular resistance can be informative when vascular resistance is used as a factor in determining blood pressure. Due to the fact that mean blood pressure is a derivative of cardiac output and vascular resistance, the measurement of the latter helps to investigate the features of hemodynamics in arterial hypotension. The use of OPSS for the diagnosis and treatment of shock conditions is discussed in Chapter 12. BLOOD CIRCULATION IN HEART FAILURE The regulation of blood circulation in heart failure can be described if cardiac output is taken as an independent value, and CDP and OPSS - as dependent variables (Fig. 1-6). With a decrease in cardiac output, an increase in CDP and OPSS occurs. This explains the clinical signs of heart failure: Increased CDP = venous congestion and edema; Increased OPSS = vasoconstriction and hypoperfusion. At least in part, these hemodynamic changes arise from the activation of the renin-angiotensin-aldosterone system. The release of renin in heart failure is due to a decrease in renal blood flow. Then, under the action of renin, angiotensin I is formed in the blood, and from it, with the help of an angiotensin-converting enzyme, angiotensin II, a powerful vasoconstrictor that has a direct effect on the vessels. The release of aldosterone from the adrenal cortex caused by angiotensin II leads to a delay in the body of sodium ions, which contributes to an increase in venous pressure and the formation of edema. PROGRESSIVE HEART FAILURE Hemodynamic parameters in progressive heart failure are shown in Fig. 1-7. The solid line represents the plot of cardiac output versus preload (i.e. functional curve of the heart), dashed - cardiac output from OPSS (afterload). The intersection points of the curves reflect the relationship between preload, afterload, and cardiac output at each stage of ventricular dysfunction. Rice. 1-6. Influence of cardiac output on the final Fig. 1-7. Changes in hemodynamics in cardiac diastolic pressure and general peripheral failure. H - norm, U - moderate cardiac vascular resistance. insufficiency, T - severe heart failure 1. Moderate heart failure As ventricular function deteriorates, the slope of the functional curve of the heart decreases, and the intersection point shifts to the right along the OPSS-SV curve (afterload curve) (Fig. 1-7). In the early stages of mild heart failure, there is still a steep slope of the KDD-SW (preload curve), and the point of intersection (point Y) is defined on the flat part of the afterload curve (Fig. 1-7). In other words, in moderate heart failure, ventricular activity depends on preload and does not depend on afterload. The ability of the ventricle to respond to preload in moderate heart failure means that the level of blood flow can be maintained, but when filling pressures are higher than normal. This explains why dyspnea is the most prominent symptom in moderate heart failure. 2. Severe heart failure With a further decrease in heart function, ventricular activity becomes less dependent on preload (ie, the slope of the functional curve of the heart decreases) and cardiac output begins to decrease. The functional heart curve shifts to the steep part of the afterload curve (point T) (Fig. 1-7): in severe heart failure, ventricular activity is independent of preload and depends on afterload. Both factors are responsible for the decrease in blood flow seen in the later stages of heart failure. The role of afterload is especially important, since arterial vasoconstriction not only decreases cardiac output, but also decreases peripheral blood flow. The increasing importance of afterload in the development of severe heart failure is the basis for its treatment with peripheral vasodilators. This issue is discussed in more detail below (Chapter 14). REFERENCES Berne RM, Levy MN. Cardiovascular physiology, 3rd ed. St. Louis: C.V. Mosby, 1981. Little RC. Physiology of the heart and circulation, 3rd ed. Chicago: Year Book Medical Publishers, 1985. Reviews Parmley WW, Talbot L. Heart as a pump. In: Berne RM ed. Handbook of physiology: The cardiovascular system. Bethesda: American Physiological Society, 1979; 429-460. Braunwald E, Sonnenblick EH, Ross J Jr. Mechanisms of cardiac contraction and relaxation. In: Braunwald E. ed. Heart disease. A textbook of cardiovascular medicine, 3rd ed. Philadelphia: W.B. Saunders, 1988; 383-425. Weber K, Janicki JS, Hunter WC, et al. The contractile behavior of the heart and its functional coupling to the circulation. Prog Cardiovasc Dis 1982; 24: 375-400. Rothe CF. Physiology of venous return. Arch Intern Med 1986; 246: 977-982. Katz AM. The descending limb of the Starling curve and the failing heart. Circulation 1965; 32: 871-875. Nichols WW, Pepine CJ. Left ventricular afterload and aortic input impedance: Implications of pulsatile blood flow. Prog Cardiovasc Dis 1982; 24: 293-306. Harizi RC, Bianco JA, Alpert JS. Diastolic function of the heart in clinical cardiology. Arch Intern Med 1988; 148: 99-109. Robotham JL, Scharf SM. Effects of positive and negative pressure ventilation on cardiac performance. Clin Chest Med 1983; 4: 161-178. Lang RM, Borow KM, Neumann A, et al. Systemic vascular resistance: An unreliable index of left ventricular afterload. Circulation 1986; 74: 1114-1123. Zeiis R, Flaim SF. Alterations in vasomotor tone in congestive heart failure. Prog Cardiovasc Dis 1982; 24: 437-459. Cohn JN, Franciosa JA. Vasodilator therapy of cardiac failure (first of two parts). N Engin Med 1977; 297: 27-31. Dzau VJ, Colucci WS, Hollenberg NK, Williams GH. Relation of the renin-angiotensin-aldosterone system to clinical state in congestive heart failure. Circulation 1981; 63: 645-651. Contents Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 10-1.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 10-2.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 10-3.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 10-4.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 10.html 10 Jamming pressure In the exact sciences, the idea of ​​relativity dominates B. Paccell Jamming pressure in pulmonary capillaries (PLCP) is traditionally used in the practice of critical care medicine, and the term “jamming pressure ”Has already become quite familiar to doctors. Despite the fact that this indicator is used quite often; it is not always critically examined. This chapter identifies some of the limited ”applications of DZLK and discusses the misconceptions that arise when this indicator is used in clinical practice. KEY FEATURES There is an opinion that DCLK is a universal indicator, but this is not so. Below is the characteristic of this parameter. DZLK: Determines the pressure in the left atrium. Not always indicative of left ventricular preload. May reflect pressure in nearby alveoli. Does not allow accurate assessment of the hydrostatic pressure in the pulmonary capillaries. Not indicative of transmural pressure. Each of these statements is disclosed below. Additional information about DZLK can be obtained from the reviews. WEDDING PRESSURE AND PRE-LOADING PLC is used to determine the pressure in the left atrium. The information obtained allows the assessment of intravascular blood volume and left ventricular function. PRINCIPLE OF MEASURING DZLK The principle of measuring DZLK is shown in Fig. 10-1. The balloon at the distal end of a catheter inserted into the pulmonary artery is inflated until blood flow is obstructed. This will cause a column of blood to form between the end of the catheter and the left atrium, and the pressure from both ends of the column will be balanced. The pressure at the end of the catheter then becomes equal to the pressure in the left atrium. The indicated principle expresses the hydrostatic equation: Дк - Длп = Q x Rv Fig. 10-1. DZLK measurement principle. The lungs are divided into 3 functional zones on the basis of the ratio of alveolar pressure (Ralv), mean pressure in the pulmonary artery (compare for Dla) and pressure in the pulmonary capillaries (Dc). DZLK allows you to accurately determine the pressure in the left atrium (Lp) only when Dk exceeds Ralv (zone 3). Further explanations in the text. where Dk is the pressure in the pulmonary capillaries, Dlp is the pressure in the left atrium, Q is the pulmonary blood flow, Rv is the resistance of the pulmonary veins. If Q = 0, then Дк - Длп = 0 and, therefore, Дк - Длп = ДЗЛК. The pressure at the end of the catheter at the time of occlusion of the pulmonary artery with a balloon is called DZLK, which, in the absence of an obstruction between the left atrium and the left ventricle, is considered equal to the end-diastolic pressure in the left ventricle (LVEDP). TERMINAL DIASTOLIC PRESSURE IN THE LEFT VENTRICLE AS A PRE-LOAD CRITERION In Chapter 1, resting preload on the myocardium is defined as the force that stretches the heart muscle. For an intact ventricle, preload is the end-diastolic volume (EDV). Unfortunately, EDV is difficult to determine directly at the patient's bedside (see. 14); therefore, end-diastolic pressure (EDP) is used to assess preload. Normal (unchanged) compliance of the left ventricle makes it possible to use CDP as a measure of preload. This is represented by tensile curves (see Figure 1-4 and Figure 14-4). Briefly, this can be characterized as follows: LVEDV (DLVD) is a reliable indicator of preload only when the distensibility of the left ventricle is normal (or unchanged). It is unlikely that ventricular compliance is normal or abnormal in adult intensive care units. At the same time, the prevalence of diastolic dysfunction in such patients has not been studied, although in some conditions their ventricular distensibility is undoubtedly changed. Most often, this pathology occurs due to mechanical ventilation of the lungs with positive pressure, especially when the inspiratory pressure is high (see chapter 27). Ventricular distensibility can also change myocardial ischemia, ventricular hypertrophy, myocardial edema, cardiac tamponade and a number of drugs (calcium channel blockers, etc.). When ventricular distensibility is reduced, an increase in PCD will be observed in both systolic and diastolic heart failure. This issue is discussed in detail in Chapter 14. WEDGING PRESSURE AND HYDROSTATIC PRESSURE OF PLCP are used as an indicator of hydrostatic pressure in pulmonary capillaries, which makes it possible to assess the possibility of developing hydrostatic pulmonary edema. However, the problem is that DZLK is measured in the absence of blood flow, including in capillaries. The features of the dependence of the DZLK on the hydrostatic pressure are shown in Fig. 10-2. When the balloon at the end of the catheter is deflated, blood flow is restored, and the pressure in the capillaries will be higher than the DZLK. The magnitude of this difference (Dk - DZLK) is determined by the values ​​of blood flow (Q) and resistance to blood flow in the pulmonary veins (Rv). Below is the equation of this dependence (note that, unlike the previous formula, in this one, instead of Dlp, there is DZLK): Dk - DZLK - Q x Rv. If Rv = 0, then Dk - DZLK = 0 and, therefore, Dk = DZLK. Rice. 10-2. The difference between the hydrostatic pressure in the pulmonary capillaries (DC) and PLC. The following important conclusion follows from this equation: DZLK is equal to the hydrostatic pressure in the pulmonary capillaries only when the resistance of the pulmonary veins approaches zero. However, the pulmonary veins create most of the total vascular resistance in the pulmonary circulation because the resistance of the pulmonary arteries is relatively low. Pulmonary circulation occurs under low pressure conditions (due to the thin-walled right ventricle), and the pulmonary arteries are not as stiff as the arteries of the systemic circulation. This means that the bulk of the total pulmonary vascular resistance (PVR) is created by the pulmonary veins. Animal studies have shown that the pulmonary veins create at least 40% of PVR [b]. These ratios in humans are not exactly known, but are likely similar. If we assume that the resistance of the venous part of the pulmonary circulation is 40% of the PVR, then the decrease in pressure in the pulmonary veins (Dk - Dlp) will be 40% of the total pressure drop between the pulmonary artery and the left atrium (Dla - Dlp). The above can be expressed by the formula, assuming that DZLK is equal to Dlp. Dk - DZLK = 0.4 (Dla - Dlp); Dk = DZLK + 0.4 (Dla - DZLK). In healthy people, the difference between DK and PZLK approaches zero, as shown below, because the pressure in the pulmonary artery is low. However, with pulmonary hypertension or increased resistance of the pulmonary veins, the difference may increase. This is illustrated below using adult respiratory distress syndrome (ARDS), in which pressure increases in both the pulmonary artery and the pulmonary veins (see Chapter 23). DZLK is taken equal to 10 mm Hg. both normal and with ARDS: DZLK = 10 mm Hg. Normally, Dc = 10 + 0.4 (15 - 10) = 12 mm Hg. With ARDS, Dk = 10 + 0.6 (30 - 10) = 22 mm Hg. If the average pressure in the pulmonary artery increases by 2 times, and venous resistance by 50%, then the hydrostatic pressure exceeds the DZLK by more than 2 times (22 versus 10 mm Hg). In this situation, the choice of treatment is influenced by the method of assessing the hydrostatic pressure in the pulmonary capillaries. If the calculated capillary pressure (22 mm Hg) is taken into account, then therapy should be aimed at preventing the development of pulmonary edema. If DZLK is taken into account as a criterion for DC (10 mm Hg), then no therapeutic measures are indicated. This example illustrates how DZLK (more precisely, its incorrect interpretation) can be misleading. Unfortunately, the resistance of the pulmonary veins cannot be directly determined, and the above equation is practically not applicable to a specific patient. However, this formula gives a more accurate estimate of the hydrostatic pressure than the DZLK, and therefore it is advisable to use it until a better estimate of Dk exists. CHARACTERISTIC OF OCCLUSIVE PRESSURE The decrease in pressure in the pulmonary artery from the moment of occlusion of the blood flow by the balloon is accompanied by an initial rapid drop in pressure followed by a slow decrease in pressure. The point dividing these two components is proposed to be considered equal to the hydrostatic pressure in the pulmonary capillaries. However, this view is controversial, since it is not mathematically supported. Moreover, it is not always possible to clearly separate the fast and slow components of the pressure at the patient's bedside (personal observations of the author), so the issue requires further study. ARTIFACTS DUE TO PRESSURE IN THE CHEST The effect of pressure in the chest on the PPC is based on the difference between intraluminal (inside the vessel) and transmural (transmitted through the vascular wall and represents the difference between intra- and extravascular pressure) pressure. Intraluminal pressure is traditionally considered a measure of vascular pressure, but it is transmural pressure that influences preload and the development of edema. Alveolar pressure can be transmitted to the pulmonary vessels and change the intravascular pressure without changing the transmural pressure, depending on several factors, including the thickness of the vascular wall and its extensibility, which, naturally, will be different in healthy and sick people. When measuring CPLC to reduce the effect of pressure in the chest on CPLC, the following should be remembered. In the chest, the vascular pressure recorded in the lumen of the vessel corresponds to the transmural pressure only at the end of expiration, when the pressure in the surrounding alveoli is equal to atmospheric (zero level). It should also be remembered that the vascular pressure that is recorded in the ICU (i.e., intraluminal pressure) is measured relative to atmospheric pressure (zero) and does not accurately reflect transmural pressure until tissue pressure approaches atmospheric pressure. This is especially important when, when determining the CPLK, shifts associated with breathing are recorded (see below). CHANGES ASSOCIATED WITH BREATHING 10-3. This action is associated with a change in pressure in the chest, which is transmitted to the capillaries. The true (transmural) pressure on this recording can be constant throughout the entire breathing cycle. DZLK, which is determined at the end of expiration, with artificial lung ventilation (ALV) is represented by the lowest point, and with spontaneous breathing - the highest. Electronic pressure monitors in many ICUs record the pressure at 4 s intervals (corresponds to 1 wave pass through the oscilloscope screen). At the same time, 3 different pressures can be observed on the monitor screen: systolic, diastolic and average. Systolic pressure is the highest point in every 4-second interval. Diastolic is the lowest pressure, and the average corresponds to the average pressure. In this regard, DZLK at the end of expiration during spontaneous breathing of the patient is determined selectively according to the systolic wave, and during mechanical ventilation - according to the diastolic wave. Note that the mean pressure is not recorded on the monitor screen when breathing changes. Rice. 10-3. Dependence of DZLK on changes in breathing (spontaneous breathing and mechanical ventilation). The transmural phenomenon is determined at the end of expiration, it coincides with the systolic pressure during spontaneous breathing and with diastolic pressure during mechanical ventilation. POSITIVE END-EXPIRED PRESSURE When breathing with positive end-expiratory pressure (PEEP), the alveolar pressure at the end of the expiration does not return to atmospheric pressure. As a result, the DZLK value at the end of expiration exceeds its true value. PEEP is created artificially or it can be characteristic of the patient himself (auto-PEEP). Auto-PEEP is the result of incomplete expiration, which is often found during mechanical ventilation in patients with obstructive pulmonary disease. It should be remembered that auto-PEEP during mechanical ventilation is often asymptomatic (see chapter 29). If an agitated patient with tachypnea has an unexpected or unexplained increase in PEP, then auto-PEEP is considered the cause of these changes. The phenomenon of auto-PEEP is described in more detail at the end of Chapter 29. The effect of PEEP on PPCV is ambiguous and depends on lung compliance. When registering DZLK against the background of PEEP, it is necessary to reduce the latter to zero, and without disconnecting the patient from the respirator. By itself, disconnecting a patient from the ventilator (PEEP mode) can have various consequences. Some researchers believe that this manipulation is dangerous and leads to a deterioration in gas exchange. Others report only the development of transient hypoxemia. The risk of disconnecting the patient from the respirator can be significantly reduced by creating positive pressure during ventilation when PEEP is temporarily interrupted. There are 3 possible reasons for an increase in CPLP in PEEP: PEEP does not change transmural capillary pressure. PEEP leads to compression of the capillaries, and against this background, PCP is the pressure in the alveoli, and not in the left atrium. PEEP acts on the heart and reduces the distensibility of the left ventricle, which leads to an increase in PEP at the same EDV. Unfortunately, it is often impossible to single out one or another reason for changing the DCLK. The last two circumstances may indicate hypovolemia (relative or absolute), for the correction of which infusion therapy is necessary. LUNG ZONES The accuracy of determining the PPC depends on the direct communication between the end of the catheter and the left atrium. If the pressure in the surrounding alveoli is higher than the pressure in the pulmonary capillaries, then the latter are compressed and the pressure in the pulmonary catheter, instead of the pressure in the left atrium, will reflect the pressure in the alveoli. Based on the ratio of alveolar pressure and pressure in the pulmonary circulation system, the lungs were conditionally divided into 3 functional zones, as shown in Fig. 10-1, sequentially from the tops of the lungs to their base. It should be emphasized that only in zone 3 the capillary pressure exceeds the alveolar pressure. In this zone, the vascular pressure is the highest (as a result of pronounced gravitational influence), and the pressure in the alveoli is the lowest. When registering DZLK, the end of the catheter should be located in zone 3 (below the level of the left atrium). In this position, the effect of alveolar pressure on the pressure in the pulmonary capillaries decreases (or eliminates). However, if a patient has hypovolemia or is undergoing mechanical ventilation with a high PEEP, then this condition is not necessary [I]. Without X-ray control directly at the patient's bedside, it is almost impossible to place a catheter into zone 3, although in most cases, due to the high blood flow velocity, it is in these areas of the lungs that the end of the catheter gets to its destination. On average, out of 3 catheterizations, only in 1 case the catheter enters the upper zones of the lungs, which are located above the level of the left atrium [I]. ACCURACY OF WIDING PRESSURE MEASUREMENT UNDER CLINICAL CONDITIONS When measuring DZLK, there is a high probability of obtaining an erroneous result. In 30% of cases, there are various technical problems, and in 20% of cases, errors arise due to incorrect interpretation of the received data. The nature of the pathological process can also affect the measurement accuracy. Some practical issues related to the accuracy and reliability of the results obtained are discussed below. VERIFICATION OF THE OBTAINED RESULTS Position of the end of the catheter. Usually, catheterization is performed with the patient lying on his back. In this case, the end of the catheter with blood flow enters the posterior parts of the lungs and is located below the level of the left atrium, which corresponds to zone 3. Unfortunately, portable X-ray machines do not allow taking pictures in frontal projection and thereby determining the position of the catheter, therefore, for this purpose, it is recommended to use lateral projection [I]. However, the significance of lateral X-ray images is questionable, since there are reports in the literature that the pressure in the ventral areas (located both above and below the left atrium) does not practically change compared to the dorsal ones. In addition, such x-ray examination (in lateral projection) is difficult, expensive, and possibly not in every clinic. In the absence of X-ray control, the catheter not falling into zone 3 is indicated by the following change in the pressure curve, which is associated with breathing. With mechanical ventilation in the PEEP mode, the DZLK value increases by 50% or more. Oxygenation of blood in the field of measurement of DZLK. To determine the location of the catheter, it is recommended to draw blood from its end while the balloon is inflated. If the saturation of hemoglobin of a blood sample with oxygen reaches 95% or more, then the blood is considered arterial. In one work, it is indicated that in 50% of cases, the area of ​​measurement of the DZLK does not satisfy this criterion. Consequently, its role in reducing the error in measuring the DCL is minimal. At the same time, in patients with lung pathology, such oxygenation may not be observed due to local hypoxemia, and not to an incorrect position of the end of the catheter. It seems that a positive result of this test can help, and a negative one has almost no prognostic value, especially in patients with respiratory failure. We use continuous monitoring of the oxygen saturation of mixed venous blood, which has already become common in our intensive care unit when measuring PWD, without increasing the incidence of complications and costs. Atrial pressure waveform. The PPCR waveform can be used to confirm that PPCR reflects left atrial pressure. The atrial pressure curve is shown in Fig. 10-4, which also shows a parallel ECG recording for clarity. The following components of the intra-atrial pressure curve are distinguished: A-wave, which is caused by atrial contraction and coincides with the RNA wave of the ECG. These waves disappear during atrial fibrillation and flutter, as well as in acute pulmonary embolism. X-wave, which corresponds to atrial relaxation. A pronounced decrease in the amplitude of this wave is noted with cardiac tamponade. C-wave means the beginning of the contraction of the ventricle and corresponds to the moment when the mitral valve begins to close. The V-wave appears at the time of ventricular systole and is caused by the depression of the valve leaflets into the left atrial cavity. Y-descending - the result of rapid atrial emptying, when the mitral valve breaks off at the beginning of diastole. With cardiac tamponade, this wave is weak or absent. A giant V-wave when registering atrial pressure corresponds to mitral valve insufficiency. These waves occur as a result of the reverse flow of blood through the pulmonary veins, which can even reach the valves of the pulmonary valve. Rice. 10-4. Schematic representation of the atrial pressure curve versus ECG. Explanation in the text. A high V-wave leads to an increase in the average PPCR to a level exceeding the diastolic pressure in the pulmonary artery. At the same time, the value of the mean PCV will also exceed the value of the filling pressure of the left ventricle, therefore, for greater accuracy, it is recommended to measure the pressure in diastole. (defect of the interventricular septum) VARIABILITY The values ​​of PCV in most people fluctuate within 4 mm Hg, but in some cases their deviation can reach 7 mm Hg. A statistically significant change in PCV should exceed 4 mm Hg. And LVEDV In most cases, the value of PCVD corresponds to the value of CDVD [I]. However, this may not be the case in the following situations: 1. In case of insufficiency of the aortic valve. into the ventricle 2. Atrial contraction with a rigid ventricular wall leads to rapid thrombus increase in CDP with premature closure of the mitral valve. As a result, DZLK is lower than KDDLZh [I]. 3. In case of respiratory failure, the value of DZLK in patients with pulmonary pathology may exceed the value of EDLVH. A possible mechanism of this phenomenon is the contraction of small veins in the hypoxic zones of the lungs, therefore, in this situation, the accuracy of the results obtained cannot be guaranteed. The risk of such an error can be reduced by placing a catheter in areas of the lungs that are not involved in the pathological process. REFERENCES REVIEWS Marini JJ, Pulmonary artery occlusion pressure: Clinical physiology, measurement and interpretation. Am Rev Respir Dis 1983; 125: 319-325. Sharkey SW. Beyond the wedge: Clinical physiology and the Swan-Ganz catheter. Am J Med 1987; 53: 111-122. Raper R, Sibbald WJ. Misled by the wedge? The Swan-Ganz catheter and leftventric-ular preload. Chest 1986; 59: 427-434. Weidemann HP, Matthay MA, Matthay RA. Cardiovascular-pulmonary monitoring in the intensive care unit (part 1). Chest 1984; 55: 537-549. CHARACTERISTICS Harizi RC, Bianco JA, Alpert JS. Diastolic function of the heart in clinical cardiology. Arch Intern Med 1988; 145: 99-109. Michel RP, Hakim TS, Chang HK. Pulmonary arterial and venous pressures measured with small catheters. J Appi Physiol 1984; 57: 309-314. Alien SJ, Drake RE, Williams JP, et al. Recent advances in pulmonary edema. Crit Care Med 1987; 15: 963-970. Cope DK, Allison RC, Parmentier JL, ef al. Measurement of effective pulmonary capillary pressure using the pressure profile after pulmonary artery occlusion. Crit Care Med 1986; 14: 16-22. Seigel LC, Pearl RG. Measurement of the longitudinal distribution of pulmonary vascular resistance from pulmonary artery occlusion pressure profiles. Anesthesiology 1988; 65: 305-307. ARTIFACTS RELATED TO CHEST PRESSURE LEVEL Schmitt EA, Brantigan CO. Common artifacts of pulmonary artery and pulmonary artery wedge pressures: Recognition and management. J Clin Monit 1986; 2: 44-52. Weismann IM, Rinaldo JE, Rogers RM. Positive end-expiratory pressure in adult respiratory distress syndrome. N Engi J Med 1982; 307: 1381-1384. deCampo T, Civetta JM. The effect of short term discontinuation of high-level PEEP in patients with acute respiratory failure. Crit Care Med 1979; 7: 47-49. WEDDING PRESSURE MEASUREMENT ACCURACY Morris AN, Chapman RH, Gardner RM. Frequency of technical problems encountered in the measurement of the pulmonary artery wedge pressure. Crit Care Med 1984; 12: 164-170. Wilson RF, Beckman B, Tyburski JG, et al. Pulmonary artery diastolic and wedge pressure relationships in critically ill patients. Arch Surg 1988; 323: 933-936. Henriquez AN, Schrijen FV, Redondo J, et al. Local variations of pulmonary arterial wedge pressure and wedge angiograms in patients with chronic lung disease. Chest 1988; 94: 491-495. Morris AH, Chapman RH. Wedge pressure confirmation by aspiration of pulmonary capillary blood. Crit Care Med 1985; 23: 756-759. Nemens EJ, Woods SL. Normal fluctuations in pulmonary artery and pulmonary capillary wedge pressures in acutely ill patients. Heart Lung 1982; P: 393-398. Johnston WE, Prough DS, Royster RL. Pulmonary artery wedge pressure may fail to reflect left ventricular end-diastolic pressure in dogs with oleic acid-induced pulmonary edema. Crit Care Med 1985: 33: 487-491. Contents Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 11-1.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 11-2.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 12-1.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 12-2.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 12-3.JPG Intensive Care ~ Paul L. Marino. "" The ICU Book "" (2nd Ed) - Rus / 12.html 12 Structural Approach to the Problem of Clinical Shock This chapter will introduce you to a simple approach to the diagnosis and treatment of shock, which is based on the analysis of only 6 indicators (most are measured using catheterization pulmonary artery) and is carried out in two stages. This approach does not define shock as arterial hypotension or hypoperfusion, but rather as a state of inadequate tissue oxygenation. The ultimate goal of this approach is to match the delivery of oxygen to tissues and their metabolic rate. Normalization of blood pressure and blood flow is also considered, but not as an end goal. The fundamental provisions that are used in our approach are set out in Chapters 1, 2, 9, and are also considered in works (see the end of this chapter). There is one central theme in the approach to shock in this book: to strive to always clearly define the state of tissue oxygenation. The shock "lurks" in the latter, and you will not detect it by listening to the organs of the chest cavity or by measuring the pressure in the brachial artery. It is necessary to search for new approaches to the problem of shock. “Black box” - an approach widely used to determine damage in technology, is applicable, in our opinion, to the study of complex pathological processes in the human body. GENERAL CONCEPTS Our approach is based on the analysis of a number of indicators that can be presented in the form of two groups: “pressure / blood flow” and “oxygen transport”. Indicators of the “pressure / blood flow” group: 1. The pressure of wedging in the pulmonary capillaries (DZLK); 2. Cardiac output (CO); 3. Total peripheral vascular resistance (OPSS). Indicators of the "oxygen transport" group: 4. Oxygen delivery (UOg); 5. Oxygen consumption (VC ^); 6 Serum lactate content. 1. At the first stage, a set of “pressure / blood flow” parameters is used to determine and correct the leading hemodynamic disorders. The indicators combined into such a group have certain values, on the basis of which it is possible to characterize the entire complex (in other words, to describe or create a small hemodynamic profile, a “formula”), which is used to diagnose and evaluate the effectiveness of treatment. The final goal of this stage is to restore blood pressure and blood flow (if possible) and to establish the root cause of the pathological process. II. At stage II, the effect of the initial therapy on tissue oxygenation is assessed. The purpose of this stage is to achieve a correspondence between the oxygen consumption of tissues and the level of metabolism in them, for which such an indicator as the concentration of lactate in the blood serum is used. Oxygen delivery is changed (if necessary) to correct the VO2 value. STAGE I: LOW HEMODYNAMIC PROFILES (“FORMULAS”) For simplicity, we consider that each factor from the group of “pressure / blood flow” indicators plays a leading role in one of the main types of shock, as, for example, shown below. Indicator Type of shock Cause of PCVD Hypovolemic Blood loss (more precisely, a decrease in BCC, as in bleeding or dehydration SVCardiogenic Acute myocardial infarction OPSS Vasogenic Sepsis The relationship of DPLK, SV and OPSS with these types of shock can be represented by the so-called small hemodynamic profiles in each individual The relationship of DZLK, SV and OPSS is normally considered in Chapter 1. Small hemodynamic profiles, characterizing the 3 main types of shock, are shown in Fig. 12-1. Fig. 12.1 Small hemodynamic profiles ("formulas"), characterizing the 3 main types shock HYPOVOLEMIC SHOCK In this case, a decrease in ventricular filling (low PCV) is of paramount importance, leading to a decrease in CO, which in turn causes vasoconstriction and an increase in OPSS. high OPSS. CARDIOGENIC SHOCK In this case the leading factor is a sharp decrease in CO, followed by stagnation of blood in the pulmonary circulation (high DZLK) and peripheral vasoconstriction (high OPSS). The “formula” of cardiogenic shock is as follows: high CPLK / low SV / high TPR. VASOGENIC SHOCK- A feature of this type of shock is a drop in the tone of the arteries (low OPSS) and, to varying degrees, veins (low PWD). Cardiac output is usually high, but its magnitude can vary considerably. The “formula” of vasogenic shock is as follows: low CPLK / high SV / low TPVR. The magnitude of the DZLK can be normal if the venous tone is not changed or the stiffness of the ventricle is increased. These cases are discussed in Chapter 15. The main causes of vasogenic shock: 1. Sepsis / multiple organ failure. 2. Postoperative condition. 3. Pancreatitis. 4. Trauma. 5. Acute adrenal insufficiency. 6. Anaphylaxis. DIFFICULT COMBINATIONS OF HEMODYNAMIC INDICATORS These three main hemodynamic indices, when combined in different ways, can create more complex profiles. For example, the “formula” might look like this: normal PCR / low SV / high TPR. However, it can be presented as a combination of two main “formulas”: 1) cardiogenic shock (high PCVD / low SV / high TPVR) + 2) hypovolemic shock (low PCVD / low SV / high TPVR). There are only 27 minor hemodynamic profiles (since each of the 3 variables has 3 more characteristics), but each can be interpreted based on 3 main “formulas”. INTERPRETATION OF LOW HEMODYNAMIC PROFILES (“FORMULAS”) The informational capabilities of small hemodynamic profiles are shown in table. 12-1. First, the leading circulatory disorder should be identified. So, in this case, the characteristics of the indicators resemble the “formula” of hypovolemic shock, with the exception of the normal value of OPSS. Consequently, the main hemodynamic disorders can be formulated as a decrease in the volume of circulating blood plus a low vascular tone. This determined the choice of therapy: infusion and drugs that increase the systemic vascular resistance (for example, dopamine). So, each of the main pathological processes accompanied by circulatory disorders will have a small hemodynamic profile. Table 12-1 such disorders were decreased circulating blood volume and vasodilation. * In the domestic literature, the concept of "vasogenic shock" is not found. A sharp drop in the tone of arterial and venous vessels is observed in acute adrenal insufficiency, anaphylactic shock, in the late stage of septic shock, multiple organ failure syndrome, etc. turn by a drop in vascular tone, and also by a decrease in the volume of circulating blood. Collapse develops most often as a complication of serious diseases and pathological conditions. Distinguish (depending on etiological factors) infectious, hypoxemic. pancreatic, orthostatic collapse, etc. - Approx. ed. Table 12-1 Application of small hemodynamic profiles Information Example A profile has been formed Determination of the pathological process Targeted therapy Possible causes Low PPC / low CO / normal OPSS Decreased BCC and vasodilation Increase in BCC before setting PPC = 12 mm Hg. Dopamine, if necessary Adrenal insufficiency Sepsis Anaphylaxis REGULATION OF BLOOD CIRCULATION The following diagram shows which therapeutic measures can be used to correct hemodynamic disturbances. The pharmacological properties of the drugs mentioned in this section are discussed in detail in Chapter 20. For simplicity, the drugs and their action are described rather briefly and simply, for example, alpha: vasoconstriction (ie stimulation of a-adrenergic receptors produces a vasoconstrictor effect), (beta: vasodilation and increased cardiac activity (ie stimulation of the beta-adrenergic receptors of the vessels causes their expansion, and the heart - an increase in the frequency and strength of heart contractions.) Condition Therapy 1. Low or normal CPLC Infusion therapy Fluids are always preferable to vasoconstrictor agents. in an increase in CPL or up to 18-20 mm Hg, or to a level equal to the colloidal osmotic pressure (COP) of plasma. Methods for measuring COP are discussed in the 1st part of Chapter 23. 2. Low SV a. High OPSS Dobutamine b Normal OPSS Dopamine Selective (beta-agonists like dobutamine (beta1-adrenomimetic) are indicated for low cardiac output without arterial hypotension and. Dobutamine is less valuable in cardiogenic shock, since it does not always increase blood pressure; but, by decreasing the OPSS, it significantly increases cardiac output. In cases of pronounced arterial hypotension (beta-agonists, together with some alpha-adrenergic agonists, are most suitable for increasing blood pressure, since stimulation of vascular a-adrenergic receptors, causing their narrowing, will prevent a decrease in OPSS in response to an increase in CO. 3. Low OPSS a. Decreased or normal CO alpha-, beta-Agonists b.High CO alpha-agonists * * The use of vasoconstrictors should be avoided if possible, as they increase systemic blood pressure at the cost of deteriorating blood supply to tissues due to spasm of arterioles. β-agonists are preferable to selective alpha-agonists, which can cause severe vasoconstriction.Dopamine is often used in combination with other drugs; in addition, it stimulates special dopamine receptors of vascular smooth muscles, causing their expansion, which allows you to maintain blood flow in the kidneys. It should be noted that the arsenal of medicines is essential. about affecting blood circulation in shock, is small. We have to mainly limit ourselves to the drugs listed below. Expected effect Medicines Beta: increased cardiac activity Dobutamine alpha, beta and dopamine receptors: cardiotonic action and dilatation of renal and mesenteric vessels Dopamine in medium doses alpha vasoconstriction, increased blood pressure Large doses of dopamine The presence of dopamine in medium doses of cardiotonic activity, with an effect on the resistance of regional vessels, and in high - pronounced alpha-adrenomimetic properties makes it a very valuable anti-shock drug. A decrease in the effectiveness of dopamine after several days of administration is possible due to the depletion of stores of norepinephrine, which it releases from granules of presynaptic nerve endings. In some cases, norepinephrine can replace dopamine, for example, if there is a need to quickly obtain a vasoconstrictor effect (in particular, in septic shock) or increase blood pressure. It should be remembered that in hemorrhagic and cardiogenic shock with a sharp drop in blood pressure, norepinephrine cannot be used (due to deterioration of the blood supply to the tissues), but infusion therapy is recommended to normalize blood pressure. In addition, the aforementioned drugs stimulate metabolism and increase tissue energy requirements, while their energy supply is in jeopardy. POST-REANIMATION INJURIES The period following the recovery of systemic blood pressure may be accompanied by ongoing ischemia and progressive organ damage. The three postresuscitation injury syndromes are summarized in this section to show the importance of monitoring tissue oxygenation and to justify the feasibility of stage II in the treatment of shock. UNRESOLVED ORGAN BLOOD FLOW The phenomenon of non-restoration of blood flow (no-reflow) is characterized by persistent hypoperfusion after resuscitation in ischemic stroke. It is believed that this phenomenon is due to the accumulation of calcium ions in vascular smooth muscle during ischemia caused by vasoconstriction, which then persists for several hours after resuscitation. The vessels of the brain and internal organs are especially susceptible to this process, which significantly affects the outcome of the disease. Ischemia of internal organs, in particular of the gastrointestinal tract, can disrupt the barrier of the mucous membrane of the intestinal wall, which will make it possible for the intestinal microflora to enter the systemic circulation through the intestinal wall (translocation phenomenon). Persistent cerebral ischemia causes permanent neurological deficits, which may explain the predominance of cerebral disorders after revival of patients with cardiac arrest [b]. In the long term, the phenomenon of non-restoration of blood flow clinically manifests itself as a syndrome of multiple organ failure, often leading to death. REPERFUSION INJURY Reperfusion injury differs from the phenomenon of non-restoration of blood flow, since in this case the blood supply is restored after ischemic stroke. The fact is that during ischemia, toxic substances accumulate, and during the period of restoration of blood circulation, they are washed out and carried by the blood stream throughout the body, falling into distant organs. As you know, free radicals and other reactive oxygen species (superoxide anion radical, hydroxyl radical, hydrogen peroxide and singlet oxygen), as well as lipid peroxidation (LPO) products, can change membrane permeability and thereby cause metabolic shifts at the cellular and tissue levels. ... (Free radicals are particles that have unpaired electrons in the outer orbital and, as a result, have a high chemical reactivity.) It should be recalled that most LPO products (lipid hydroperoxides, aldehydes, aldehyde acids, ketones) are highly toxic and can disrupt the structure of biological membranes up to the formation of intramembrane stitching and tearing. Such changes significantly disrupt the physicochemical properties of membranes and, first of all, their permeability. LPO products inhibit the activity of membrane enzymes, blocking their sulfhydryl groups, inhibit the sodium-potassium pump, thereby aggravating membrane permeability disorders. It was found that the increase

Name: Intensive therapy. 3rd edition
Paul L. Marino
The year of publishing: 2012
The size: 243.35 MB
Format: pdf
Language: Russian

Intensive Care, edited by Paul L. Marino, discusses basic therapy that requires intensive care. The third edition of the famous book contains modern data on the pathogenesis and clinical picture, as well as methods of diagnosis and intensive treatment of various nosologies. The main issues of clinical anesthesiology from the position of an anesthesiologist-resuscitator, the principles of infection prevention when providing assistance to critical patients are presented. The issues of monitoring and interpretation of clinical and laboratory data are highlighted. The topical issues of infusion therapy are stated. Critical conditions in cardiology, neurology are described in more detail. surgery, pulmonology and so on. The issues of tactics of carrying out artificial lung ventilation, transfusion therapy, acute poisoning are considered in detail. For anesthesiologists-resuscitators.

Name: Ultrasound in the intensive care unit
Killou K., Dalchevski S., Koba B
The year of publishing: 2016
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Language: Russian
Description: The Practical Guide "Ultrasound in the Intensive Care Unit", ed., Keith Keelu et al., Discusses the current issues of the use of ultrasound in critically ill patients ... Download the book for free

Name: General and private anesthesiology. Volume 1
A. V. Schegolev
The year of publishing: 2018
The size: 32.71 MB
Format: pdf
Language: Russian
Description: The textbook "General and private anesthesiology", ed., A. Shchegolev, examines the issues of general anesthesiological practice from the perspective of modern international data. In the first volume of the manual ... Download the book for free

Name: Neonatal intensive care
Alexandrovich Yu.S., Pshenisnov K.V.
The year of publishing: 2013
The size: 41.39 MB
Format: pdf
Language: Russian
Description: The practical guide "Intensive care of newborns", ed., Aleksandrovich Yu.S., et al., Considers modern, relevant information about the principles of intensive care for children of the new age ... Download the book for free

Name: General anesthesia in the pediatric oncology clinic
Saltanov A.I., Matinyan N.V.
The year of publishing: 2016
The size: 0.81 MB
Format: pdf
Language: Russian
Description: The book "General Anesthesia in the Clinic of Pediatric Oncology" edited by A.I. Saltanova et al., Considers the features of pediatric oncology, the principles of general balanced anesthesia, its components, as well as ... Download the book for free

Name: Algorithms of actions in critical situations in anesthesiology. 3rd edition
McCormick B.
The year of publishing: 2018
The size: 27.36 MB
Format: pdf
Language: Russian
Description: A practical guide "Algorithms of actions in critical situations in anesthesiology" ed., McCormick B., in an adapted guide for the Russian-speaking population, ed., Nedashkovsky E. V., ... Download the book for free

Name: Critical situations in anesthesiology
Borshoff D.S.
The year of publishing: 2017
The size: 36.27 MB
Format: pdf
Language: Russian
Description: The practical guide "Critical situations in anesthesiology", ed., Borshoff DS, considers clinical situations that are critical in the practice of an anesthesiologist-resuscitator .... Download the book for free

Name: Anesthesiology, resuscitation and intensive care in children
Stepanenko S.M.
The year of publishing: 2016
The size: 46.62 MB
Format: pdf
Language: Russian
Description: The textbook "Anesthesiology, resuscitation and intensive care in children" under the editorship of Stepanenko S.M., considers the main issues of intensive care, anesthesiology and resuscitation in children ...

Name: Ambulance and emergency care. General questions of resuscitation
Gekkieva A.D.
The year of publishing: 2018
The size: 2.3 MB
Format: pdf
Language: Russian
Description: The textbook "Ambulance and emergency care. General issues of resuscitation", ed., Gekkieva A.D., considers in the aspect of modern standards the algorithm of doctor's actions in the development of terminal s ...