Intensive care by Paul Marino, edited by Zilber. Marino, Paul L

Current issues in surgical hepatology, gastroenterology and transfusiology Sheshunov I.V. (ed.).rar -

Current problems of anesthesiology and resuscitation. Refreshing course of lectures 2006 Nedashkovsky E.V. (Ed.).rar -

Current problems of anesthesiology and resuscitation. Refreshing course of lectures Nedashkovsky E.V. (Ed.).rar -

Algorithms for action in critical situations in anesthesiology McCormick B..rar -

Algorithms for difficult tracheal intubation Chuev P.N., Budnyuk A.A., Basenko I.L.rar -

Alcoholic delirium shock Galankin L.N., Livanov G.A., Burov V.V.rar -

Anaphylactic reactions during anesthesia and intensive care Levy D.X..rar -

Anaphylactic shock, Emelyanov A.V.rar -

Anesthesiology, resuscitation and intensive care of emergency conditions Kovalchuk.zip -

Anesthesiology, resuscitation and intensive care of emergency conditions Kovalchuk L.Ya..rar -

Anesthesiology and intensive care. Etaloni practical skills Shlapak.zip -

Anesthesiology and intensive care Paliy L.V..rar -

Anesthesiology and intensive care Chepky L.P..rar -

Anesthetic management for cardiogenic shock Kheraskov V.Yu., Plotnikov G.P., Shukevich D.L.rar -

Anesthesiology, resuscitation and intensive care in dentistry and maxillofacial surgery Agapov V.S., Emelyanova N.V., Shipkova T.P.rar -

Anesthesiology, resuscitation and intensive care Spas V.V., Bushma K.M..rar -

Anesthesiology and intensive care in tables Lebedinsky K.M.rar -

Anesthesiology and intensive care in tables Lebedinsky K.M..rar -

Anesthesiology and intensive care Gelfand.zip -

Anesthesiology and intensive care Gelfand B.R., Kirienko P.A., Grinenko T.F..rar -

Anesthesiology and intensive care of children Kurek V.V., Kulagin A.E.rar -

Anesthesiology and resuscitation - lecture notes by Kolesnikov M.A..rar -

Anesthesiology and resuscitation - Sepsis at the beginning of the 21st century.rar -

Anesthesiology and resuscitation. Guide for doctors) ed. Polushina Yu.S.rar -

Anesthesiology and resuscitation. Cheat sheets by Kolesnikov A..rar -

Anesthesiology and resuscitation Dolina O.A. (ed.)..rar -

Anesthesiology and resuscitation Kizimenko A.N..rar -

Anesthesiology and resuscitation Sumin S.A., Rudenko M.V., Borodinov I.M..rar -

Anesthesiology and resuscitation Cribs.rar -

Anesthetic and resuscitation support for operations on the pancreas Zubkov V.I., Dubitsky A.E. etc..rar -

Anesthesia and intensive care in obstetrics Kalinin A.L..rar -

Anesthesia and intensive care in pediatrics.rar -

Anesthesia and intensive care in pediatrics V.A. Mikhelson V.A. Sidorov S.M. Stepanenko.rar -

Anesthesia and intensive care in endoscopic surgery Butrov A.V.rar -

Anesthesia and intensive care Koryachkin V.A., Strashnov V.I..rar -

Anesthesia and intensive care Koryachkin Strashnov.zip -

Anesthesia and intensive care in children Kurek V.V., Kulagin A.E., Furmanchuk D.A.rar -

Anesthesia and resuscitation in obstetrics and gynecology Kulakov V.I., Serov V.N., Abubakirova A.M., Chernukha E.A..rar -

Anesthesia and resuscitation at the stages of medical evacuation Darbinyan T.M., Zvyagin A.A., Tsitovsky Yu.I..zip -

Asthmatic status in the practice of anesthesiologist-resuscitator Zaprudin G.G.rar -

Atlas Intensive care of emergency conditions. Pathophysiology, clinic, treatment Butylin.rar -

Atlas of thoracic resuscitation in Ukrainian.rar -

Basic and advanced resuscitation in children Aleksandrovich Yu.S., Gordeev V.I.rar -

Sudden cardiac arrest. Resuscitation measures Kudryashov V.G.rar -

Intrauterine hypoxia. Asphyxia and resuscitation of newborns Neiman E.G..rar -

Water-electrolyte and acid-base balance M.M. Horn.rar -

Water-electrolyte metabolism, disorders and correction Sukhorukov V.P.rar -

Military and extreme medicine. Part 1 Drokin A.V..rar -

Military and extreme medicine. Part 2 Prokhorov I.I..rar -

Issues of military field surgery and post-mortem blood transfusion Yudin S.S..rar -

Restoring biostability in sepsis, Shifrin G.A., Gorenshtein M.L.rar -

Medical manipulations, Kondratenko P.G..rar -

Gastrointestinal insufficiency, ways of diagnosis and correction Maltseva Usenko.zip -

Hemorrhagic shock in obstetrics Klimov V. A., Chibisova I. V., School L.I..rar -

Blood transfusions - an anesthesiological and resuscitation view on the problem Polushin Yu.S..rar -

Hydroxyethyl starches in the treatment of critical conditions Cherny Kobanko.zip -

Hypoxia of critical conditions Ryabov G.A..rar -

Graphic monitoring of respiratory support Gritsan A.I., Kolesnichenko A.P..rar -

Pediatric anesthesiology and resuscitation Mikhelson, V.A. Grebennikov.zip -

Pediatric anesthesiology and resuscitation Mikhelson V.A., Grebennikov V.A.rar -

Pediatric anesthesiology and resuscitation Mikhelson V.A., Grebennikov V.A..rar -

Diagnosis and treatment of cardiac arrhythmias in anesthesiology and intensive care. Methodological recommendations - Kyiv, 2003.rar -

Diagnosis and treatment of cardiac arrhythmias in anesthesiology and intensive care Cherniy V.I., Novikova R.I., Shramenko E.K..rar -

Diagnosis and treatment of shock Weil M.G., Shubin G..rar -

Dosimetric planning of radiation therapy. Part 3. Radiation therapy with intensity-modulated beams Klimanov V.A..rar -

Shine's Common Sense in Emergency Abdominal Surgery Moshe Shine, Paul Rogers, Ahmad Assaly.rar -

Mechanical ventilation, basics and concepts. The best book for anesthesiologists.rar -

Acupuncture in anesthesiology and resuscitation Staroverov A.T., Barashkov G.N..rar -

Selected lectures on anesthesiology and resuscitation Churlyaev Yu.A. (general ed.).rar -

Invasive hemodynamic monitoring in intensive care and anesthesiology Kuzkov V.V., Kirov M.Yu.rar -

Invasive monitoring of hemodynamics in intensive care and anesthesiology Kuzkov V.V., Kirov M.Yu..rar -

Intensive rehabilitation of victims with combined trauma Kachesov V.A.rar -

Intensive therapy. National leadership in 2 volumes (Volume II) Gelfand B.R., Saltanov A.I. (ed.).rar -

Intensive therapy. National leadership in 2 volumes (Volume I) Gelfand B.R., Saltanov A.I. (ed.).rar -

Intensive therapy. National leadership. B.R. Gelfand, I.B. Zabolotskikh 2017.pdf -

Intensive therapy. Resuscitation. First aid Ed. Malysheva V.D..zip -

Intensive care Marino Paul L..rar -

Intensive care in obstetrics and gynecology Kulakov V.I., Serov V.N., Abubakirova A.M., Fedorova T.A..rar -

Intensive care in neonatology Romanenko V.A..rar -

Intensive care in pediatrics Grebennikov V.I., Lazarev V.V., Lekmanov A.U.rar -

Intensive care in pediatrics, ed. prof. Mikhelson V.A.rar -

Intensive care of critical conditions at the prehospital stage Balatanova E.A., Volny I.F., Pomerantseva T.I.rar -

Intensive therapy for blood loss Kligunenko E.N., Kravets O.V.rar -

Intensive care Malyshev V.D., Vedenina I.V..rar -

Intensive care Marino P.L., editor-in-chief of the Russian translation Martynov A.I..rar -

Intensive care of emergency conditions. In the drawings. Yu.P. Butylin.rar -

Intensive therapy of burn disease Kligunenko Leshchev.zip -

Intensive therapy of acute water and electrolyte disturbances Malyshev V.D..rar -

Intensive therapy of acute poisoning Kurashov O.V.rar -

Intensive therapy for blood loss Usenko L.V., Shifrin G.A..rar -

Intensive care for burns. Methodical recommendations.rar -

Intensive therapy for pulmonary embolism Clinical guidelines (draft).rar -

Intensive therapy of threatening conditions. Ed. Koryachkina V. A., Strashnova, V. I.rar -

Intensive therapy of acute liver failure Usenko.zip -

Intensive therapy for comatose states of various movements Usenko Maltseva.zip -

Intensive therapy for emergency conditions Navc. Companion Chuev P. M., Vladika A. S.rar -

Interpretation of blood and urine tests and their clinical significance Kozinets.rar -

Tracheal intubation. Bogdanov A.B., Koryachkin V.A.rar -

Infusion therapy, Gumenyuk N.I., Kirkilevsky S.I.rar -

Infusion therapy of the perioperative period E. M. Shifman, A. D. Tikanadze.rar -

Artificial ventilation (principles, methods, equipment) Burlakov R.I., Galperin Yu.Sh., Yurevich V.M.rar -

Artificial ventilation in intensive care. Kassil V.L. - Moscow, Medicine, 1987.rar -

Artificial ventilation Hess D.R., Kaczmarek R.M..rar -

Artificial and assisted ventilation Kassil V.L., Vyzhigina M.A., Leskin G.S..rar -

Artificial nutrition Bakhman A.L.rar -

Results and prospects for the use of low-intensity EHF therapy for chronic dermatoses Kurnikov G.Yu., Klemenova I.A..rar -

IT for blood loss. Usenko L.V., Shifrin G.A. - Dnepropetrovsk, New Ideology, 2007.rar -

Ischemic stroke through the eyes of an anesthesiologist. Modern approaches to intensive care Usenko L.V., Maltseva L.A., Tsarev A.V., Chernenko V.G.rar -

Cardiogenic shock Golub I.E., Sorokina L.V..rar -

Acid-base state and water-electrolyte balance in intensive care Malyshev V.D..rar -

Acid-base balance in intensive care Kostyuchenko S.S 2008.rar -

Classification of errors and complications of catheterization of the subclavian veins Starberg A.I.rar -

Wedge. Guidelines for the management of patients with sepsis, septic shock during treatment. and in the postpartum period.rar -

Clinical neuroreanimation. Guide for doctors. Starchenko A.A. Under general ed. acad. RAMS, prof. V.A. Khilko.rar -

Clinical neuroreanimatology. Guide for doctors Starchenko.zip -

Clinical transfusiology, Rumyantsev A.G., Agranenko V.A.rar -

Clinical physiology in anesthesiology and resuscitation. Zilber A.P.rar -

Clinical physiology in anesthesiology and resuscitation Zilber A.P.rar -

Clinical physiology in anesthesiology and resuscitation Zilber A.P.rar -

Key facts in anesthesiology and intensive care Gomez A.S.rar -

Key facts in anesthesiology and intensive care Park Gilbert R., Serrano Gomez A.rar -

KOS and VEB in IT. Malyshev V.D.rar -

Critical situations in anesthesiology Gaba David M., Fish Kevin J., Howard Stephen K..rar -

Critical conditions in obstetrics Serov.rar -

Critical conditions in obstetrics Serov V.N., Markin S.A..rar -

Blood loss and blood transfusion. Principles and methods of bloodless surgery. Zilber A.P.rar -

Xenon and inert gases in medicine. Proceedings of the conference of anesthesiologists and resuscitators of medical institutions of the Ministry of Defense of the Russian Federation.rar -

Lectures on neuroreanimation Krylov V.V., Petrikov S.S., Belkin A.A.rar -

Therapeutic nutrition for children in critical conditions Gurova.rar -

Master class on neuroanesthesiology and neuroreanimatology. Lectures Kondratyev A.N. (prev)..rar -

Critical Care Medicine John Marini.rar -

Critical care medicine Zilber A.P..zip -

Little things in intensive care Polyakov G.A..rar -

Methods and modes of modern artificial lung ventilation Brygin P.A..rar -

Mechanical ventilation Satishur.zip -

Mechanical ventilation Satishur O.E..rar -

Breath monitoring - pulse oximetry, capnography, oximetry, Shurygin I.A.rar -

Adrenal insufficiency, V.V. Fadeev, G.A. Melnichenko.rar -

Circulatory failure. Methodological manual in tables and diagrams Dzyak G.V., Drynovets J..rar -

Non-invasive ventilation Skryagin A.E. etc..rar -

Non-invasive mask ventilation of the lungs in acute respiratory failure Moroz V.V., Marchenkov Yu.V., Kuzovlev A.N..rar -

Neurogenic hyperventilation Vein A.M., Moldovanu I.V.rar -

Neuroreanimatology. Intensive therapy of traumatic brain injury Tsarenko S.V..rar -

Neuroreanimatology_ neuromonitoring, principles of intensive care, neurorehabilitation Usenko Mal.zip -

Neuroreanimatology neuromonitoring, principles of intensive care, neurorehabilitation Usenko Mal.zip -

Neuroreanimatology neuromonitoring, principles of intensive care, neurorehabilitation Usenko Maltseva.zip -

Emergency care for acute poisoning Golikov S.N.rar -

Emergency therapy, anesthesia and resuscitation. Short course François J., Cara M., Deleuze R., Poiver M..rar -

Nosocomial pneumonia in adults Chuchalin A.G., Sinopalnikov A.I.rar -

Burns Guide for doctors Paramonov B.A., Porembsky Ya.O., Yablonsky V.G.rar -

Operational management of the anesthesiology and resuscitation service of a multidisciplinary hospital_ monograph Nedashkovsky E.V.rar -

Determination of the rate of protein catabolism in patients with acute renal failure Yampolsky A.F.rar -

Optimization of intensive care in surgical gastroenterology Zabolotskikh I.B., Malyshev Yu.P., Klevko V.A., Filippova E.G.rar -

Optimization of intensive care in surgical gastroenterology Zabolotskikh I.B., Malyshev Yu.P., Klevko V.A., Filippova E.G.pdf.rar -

Organization of anesthesiology and resuscitation service Popov A.S., Ekstrem A.V..rar -

Organization and principles of work of the department of anesthesiology, intensive care and resuscitation Prasmytsky O.T., Rzheutskaya R.E., Ivankovich N.K..rar -

Organization and standardization of intensive care and pain management Shifrin G.A..rar -

Complications of resuscitation and intensive care Permyakov N.K.rar -

Basics of intensive care. Head of publication Usenko Krishtafor Sizonenko.zip -

Basics of blood transfusion Ligonenko O.V., Girin L.V..rar -

Basics of blood transfusion Ligonenko O.V., Girin L.V..pdf.rar -

Fundamentals of anesthesiology and resuscitation Volodchenko N.P..rar -

Fundamentals of basic and advanced resuscitation in children M.D.Ivaneev, O.Yu.Kuznetsova, E.V.Parshin.rar -

Fundamentals of mechanical ventilation 2009 Goryachev A.S., Savin I.A..rar -

Fundamentals of mechanical ventilation 2013 Goryachev A.S., Savin I.A..rar -

Fundamentals of mechanical ventilation Goryachev A.S., Savin I.A.rar -

Basics of intensive rehabilitation. Injury of the spine and spinal cord, Kachesov V. A.rar -

Fundamentals of intensive rehabilitation of cerebral palsy, Kachesov V. A.rar -

Fundamentals of intensive rehabilitation of cerebral palsy Kachesov V.A.rar -

Fundamentals of intensive self-rehabilitation, Kachesov V. A.rar -

Fundamentals of intensive care Gordeev V.I., Lebedinsky K.M.rar -

Fundamentals of Intensive Care McCormick B.rar -

Fundamentals of resuscitation Negovsky N.A..rar -

Fundamentals of respiratory support in anesthesiology, resuscitation and intensive care Kolesnichenko A.P., Gritsan A.I..rar -

Fundamentals of respiratory support Lebedinsky K.M., Mazurok V.A., Nefedov A.V..rar -

Features of pathological diagnosis of ion-osmotic complications of intensive care and resuscitation Permyakov N.K., Tumansky V.A.rar -

Features of transfusion support for planned orthopedic operations in patients with hemophilia V.D. Kargin, L.P. Papayan.rar -

Features of transfusion support for planned orthopedic operations in patients with hemophilia Kargin V.D., Papayan L.P..pdf.rar -

Acute obstruction of the upper respiratory tract in children. Educational and methodological manual. Zhuchenko V.K., Poltarin V.P., Romanenko V.A.rar -

Acute heart failure. Guidelines for the diagnosis and treatment of AHF ACG Clinic.rar -

Acute poisoning. Ludevig R., Los K.rar -

Acute poisoning diagnostics, emergency care Luzhnikov E.A., Aleksandrovsky V.N.rar -

Acute pancreatitis. Surgical treatment, intensive care Maltseva Usenko.zip -

Acute coronary syndrome Stelmashok V.I., Petrov Yu.P..doc.rar -

Oto- and rhinosinusogenic sepsis in children Sergeev M.M., Zinkin A.N., Gornostaev A.A..rar -

Poisoning in childhood Zabolotskikh T.V., Grigorenko G.V., Klimova N.V..rar -

Rating and prognostic scales in critical care medicine Aleksandrovich Yu.S..rar -

Transfusion of blood, blood products and blood substitutes, Ostrovsky A.G., Karashurov E.S..rar -

Transfusion of blood and its components A.V. Fedoseev, S.A. Pigin, L.A. Novikov, B.I. Gureev.rar -

Blood transfusion and blood substitutes in surgery and pediatrics.rar -

Perftoran in intensive care of critical conditions Usenko Kligulenko.zip -

Perftoran in intensive care for blood loss Kligulenko Kravets Novikovi.zip -

Liver failure. Pathophysiological and clinical aspects Chesnokova N.P., Nevvazhay T.A. (comp.).rar -

A guide to respiratory support Shlapak Pilipenko.zip -

A guide to practical work in anesthesiology and resuscitation Usenko Zueva Sizonenko.zip -

The sequence of performing basic manipulations in neonatal practice Tsaregorodtsev A.D., Baibarina E.N., Ryumina I.I..rar -

Intensive care attendant's manual.rar -

Manual on intensive care in military medical institutions of the SA and Navy Nechaev E.A..rar -

Post-resuscitation illness, V. A. Negovsky, A. M. Gurevich, E. S. Zolotokrylina.rar -

Practical transfusiology Kozinets G.I..zip -

Practical course of artificial lung ventilation Tsarenko.zip -

Presentation - Anaphylactic shock. Asthmatic condition and its therapy.rar -

Presentation - Anaphylactic shock. Etiology. Pathogenesis. Treatment.rar -

Presentation - Autodonation. Autohemotransfusion.rar -

Presentation - Autodonation. Autohemotransfusion.ppt.rar -

Presentation - For or Against blood transfusion.rar -

Presentation - For or Against blood transfusion.ppt.rar -

Principles and methods for assessing the severity of the condition of patients in intensive care Shano Cherniy.zip -

Decision making in intensive care Don H.rar -

Protocols for diagnostics, anesthesia, resuscitation and intensive care of critical conditions in inpatient conditions Kolbanov V.V., Tsybin A.K. etc. (comp.).rar -

Punctures and catheterization in practical medicine. Practical guide by V.M. Binewich.rar -

Puncture and catheterization in practical medicine Binewich V.M..rar -

Resuscitation and intensive care for a practicing physician Radushkevich V.L., Bartashevich B.I.zip -

Regional anesthesia. The most necessary things in anesthesiology Rafmell D.P.rar -

Regional anesthesia Pashchuk A.Yu.rar -

Register of Medicines of Russia RLS Doctor Surgery and Intensive Care. 18th issue Vyshkovsky G.L.rar -

Register of Medicines of Russia Radar Doctor Surgery and Intensive Care Vyshkovsky G.L.rar -

Respiratory support Kassil V.L., Leskin G.S., Vyzhigina M.A..rar -

Respiratory support during anesthesia, resuscitation and intensive care Levshankov A.I..rar -

Respiratory support in children Gordeev V.I., Aleksandrovich Yu.S., Parshin E.V.rar -

Respiratory therapy in newborns Fomichev M.V..zip - -

Cardiopulmonary resuscitation Safar P.rar -

Nursing in anesthesiology and resuscitation Levshankov A.I., Klimov A.G.rar -

Syndromes of critical conditions Ryabov G.A.rar -

System of intensive neurophysiological rehabilitation. Kinesitherapy block, Kozyavkin V.I.rar -

System of Intensive Neurophysiological Rehabilitation Kozyavkin V.I.rar -

Ambulance. Guide for paramedics and nurses, Vertkin A.L..rar - -

Spirographic diagnosis of disorders of the ventilation function of the lungs Perelman Yu.M., Prikhodko A.G.rar -

Directory for emergency care Eliseev O.M.rar -

Standards of medical care for emergency medical care, Miroshnichenko A.G., Shaytor V.M.rar -

Theoretical background and practical basis of nutritional support in a critical illness clinic. Ed. Usenko L.V., Maltseva L.A.rar -

Test tasks in anesthesiology and resuscitation Lyzikova T.V., Alekseeva L.A..rar -

Techniques of intensive care in pediatrics. Ed. Romanenko V.A., Sparlinga D.rar -

Technical techniques of intensive care in pediatrics Gromov Yu.A. Zhuchenko V.K.rar -

Transfusiology in resuscitation. Ragimov A.A., Eremenko A.A., Nikiforov Yu.V.rar -

Transfusiology for anesthesiologist-resuscitator Shlakhter S.M.rar -

Tracheostomy. Modern technologies, Sukhorukov V.P.rar -

Tracheostomy in neurosurgical patients Fokin Goryachev.zip -

Tracheostomy Shlyaga I.D., Ermolin S.V.rar -

Difficulties in tracheal intubation Latto I.P., Rosen M..rar -

Difficult airway from the position of an anesthesiologist-resuscitator - a manual for doctors. Molchanov I.V.rar -

Difficult airway from the position of an anesthesiologist-resuscitator Molchanov I.V., Zabolotskikh I.B., Magomedov M.A..rar -

Ultrasound studies in the provision of infusion therapy in intensive care units Bykov M.V.rar -

Ultrasound studies in the provision of infusion therapy in intensive care units Bykov M.V..rar -

Urgent sonography of the lungs in acute respiratory failure Kyiv, Sonomir, 2012.rar -

Pharmacotherapy of acute pain Lebedeva R.N., Nikoda V.V..zip -

Physiology and pathophysiology of artificial lung ventilation Belebezev G.I., Kozyar V.V..rar -

Functional and laboratory tests in intensive care Koryachkin V.A., Strashnov V.I., Chufarov V.N., Shelukhin D.A..zip -

Traumatic brain injury. Current principles of uncomplicated assistance Pedachenko.rar -

Percutaneous catheterization of central veins Rosen M., Latto Y. P., Ng W. Sheng.rar -

Shock. Theory, clinic, organization of anti-shock care Mazurkevich Bagnenko.zip -Get a book on medicine

Emergency medical care at the prehospital stage Volny I.F., Posternak G.I., Peshkov Yu.V., Tkacheva M.Yu.rar -Get a book on medicine

Emergency medical care for poisoning R. Hoffman, L. Nelson, M.-E. Howland, N. Lewin, N. Flomenbau.m, L. Goldfrank.rar -

Emergency care for injuries, pain shocks and inflammations. Experience in emergency situations Yakovlev V..rar -

Enteral clinical nutrition in intensive care medicine Luft V.M..rar -

Etudes of critical medicine Volume 1. Medicine of critical conditions_ general problems Zilber A.P..rar -

Efferent methods of treatment of acute poisoning. Dedenko I.K., Starikov A.V., Litvinyuk V.A., Torbin V.F.rar -

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Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/1-2.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/1-3.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/1-4.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/1-5.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/1-7.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/1.html Contents Heart activity In this chapter we will consider the forces influencing 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 you will encounter in this chapter are familiar to you, but now you will be able to apply this knowledge at the bedside. MUSCLE CONTRACTION The heart is a hollow muscular organ. Despite the fact that skeletal muscles differ in structure and physiological properties from cardiac muscle (myocardium), apparently in a simplified manner they can be used to demonstrate the basic mechanical laws of muscle contraction. For this purpose, 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, the muscle will stretch and its length at rest will change. The force that stretches a muscle before it contracts is referred to as preload. 2. The length to which a muscle is stretched after applying a preload is determined by the “elasticity” of the muscle. Elasticity (strength) is the ability of an object to return to its original shape after deformation. The more elastic a muscle is, the less susceptible it is to stretching by preload. To characterize the elasticity of muscles, the concept of “extensibility” is traditionally used; in its meaning, this term is the opposite of the concept of “elasticity”. 3. If you attach a limiter to the muscle, you can increase the overload with an additional load without additional stretching of the muscle. When electrical stimulation is applied and the restraint is removed, the muscle contracts and lifts both weights. The load that the contracting muscle must lift is referred to as afterload. Please note that afterload also includes preload. 4. The ability of a muscle to move a 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 a skeletal muscle Preload The force that stretches a muscle at rest (before contraction) Afterload The load that a muscle must lift during contraction Contractility The force of muscle contraction under constant pre- and afterload Extensibility The length to which the preload stretches the muscle DEFINITIONS C mechanical positions, muscle contraction is determined by several forces (Table. 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 condition of the muscle depends on the properties of the contractile elements and the load that needs to 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 force, and in addition, instead of length, blood volume is used. Pressure-volume curves Pressure-volume curves are presented in Fig. 1-2, explaining the contraction of the left ventricle and the forces influencing this process. The loop located inside the graph describes one cardiac cycle. CARDIAC CYCLE Point A (see Fig. 1-2) - the beginning of ventricular filling, 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 volume in the ventricle is the end-diastolic volume (EDV). This volume is similar to the preload on the model discussed above, since it will lead to stretching of the ventricular myocardial fibers to a new residual (diastolic) length. In other words, 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 contraction of the left ventricle with the aortic and mitral valves closed (isometric contraction phase). The pressure in the ventricle increases rapidly until it exceeds the pressure in the aorta and the aortic valve opens (point B). The pressure at this point is similar to the afterload in the model discussed above, since it is applied to the ventricle after the onset of contraction (systole) and is the force that the ventricle must overcome in order to “throw out” the systolic (stroke) volume of blood. Therefore, aortic pressure is similar to afterload (in reality, afterload is made up of several components, but see below for more on this). 3. Once the aortic valve opens, blood flows into the aorta. When the pressure in the ventricle becomes lower than the pressure in the aorta, the aortic valve closes. The force of ventricular contraction determines the volume of expelled blood at given pre- and afterload values. In other words, the pressure at point G is a function of contractility if the values ​​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 D, the pressure in the left ventricle decreases sharply (period of isometric relaxation) until the next moment the mitral valve opens at point A, i.e. the beginning of the next cardiac cycle. 4. The area limited 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 force and displacement modules). Any processes that increase this area (for example, an increase in pre- and afterload or contractility) increase the stroke work of the heart. Impact work is an important indicator, since it determines the energy consumed by the heart (oxygen consumption). This issue is discussed in Chapter 14. STARLING CURVE The work of 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 specimen by Otto Frank. Ernest Starling continued these studies on the heart of mammals and in 1914 obtained very interesting data. In Fig. Figure 1-2 shows the Starling (Frank-Starling) curve, demonstrating the relationship between EDV and systolic pressure. Note the steep upward portion of the curve. The steep slope of the Starling curve indicates the importance of preload (volume) in increasing blood output in a healthy heart; in other words, with an increase in the blood supply to the heart in diastole and, therefore, with an increase in the stretching of the heart muscle, the force of heart contraction increases. This dependence is a fundamental law (“law of the heart”) of the physiology of the cardiovascular system, in which a heterometric (i.e., carried out in response to changes in the length of myocardial fibers) mechanism of regulation of cardiac activity is manifested. DESCENDING PART OF THE 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 explained by hyperextension of the cardiac muscle, where the contractile filaments move significantly away from each other, reducing the contact between them necessary to maintain the force of contraction. However, the downward part of the Starling curve can also 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 the afterload remains constant, then in order for the stroke volume of the heart to decrease, the end-diastolic pressure (EDP) must exceed 60 mmHg. Because such pressures are rarely observed clinically, the significance of the downward portion of the Starling curve remains a matter of debate. Rice. 1-3. Functional curves of the ventricles. In clinical practice, there is not enough evidence to support the downward portion 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. Particular attention should be paid to this, since diuretics are often used in the treatment of heart failure. This issue is discussed in more detail in Chapter 14. FUNCTIONAL CURVE OF THE HEART In the clinic, an analogue of the Starling curve is the functional curve of the heart (Fig. 1-3). Please note that stroke volume replaces systolic pressure, and EDP replaces 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 determined not only by myocardial contractility, but also by afterload. As can be seen in Fig. 1-3, a decrease in contractility or an increase in afterload reduces the steepness of the slope of the curve. It is important to consider the effect of afterload because it means that the cardiac function curve is not a reliable indicator of myocardial contractility, as previously assumed [b]. EXTENSIBILITY 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 (EPV and EDV), which is presented in Fig. 1-4. The slope of pressure-volume curves during diastole reflects ventricular compliance. Ventricular compliance = ACDO/ACDD. Rice. 1-4 Pressure-volume curves during diastole As shown in Fig. 1-4, a decrease in extensibility will lead to a shift of the curve down and to the right, the EDC will be higher for any EDV. Increasing extensibility has the opposite effect. Preload - the force that stretches the muscle at rest, is equivalent to EDV, not EDD. However, EDV cannot be determined by conventional bedside methods, and measurement of EDV is a standard clinical procedure for determining preload (see Chapter 9). When using FDC to estimate preload, the dependence of FDC on changes in extensibility should be taken into account. In Fig. 1-4 it can be seen that the EDD may be increased, although the EDL (preload) is actually reduced. In other words, the EDP indicator will overestimate the preload value with reduced ventricular compliance. EDC makes it possible to reliably characterize preload only with normal (unchanged) ventricular compliance. Some therapeutic interventions in critically ill patients can lead to a decrease in ventricular compliance (for example, mechanical ventilation with positive inspiratory pressure), and this limits the value of EDP as an indicator of preload. These issues are discussed in more detail in Chapter 14. AFTERLOAD Above, afterload has been defined as the force that opposes or resists contraction of the ventricles. This force is equivalent to the stress generated 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 stress is a function of systolic pressure and the radius of the chamber (ventricle). Systolic pressure depends on the impedance of blood flow in the aorta, while chamber size is a function of EDV (i.e. preload). It was shown in the model above that preload is part of 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: compliance, which prevents changes in speed in the flow, and resistance, which limits the average speed of the flow [b]. Arterial compliance cannot be measured routinely, so afterload is assessed using arterial resistance (BP), 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 (TPVR) are determined as follows: PVR = (Pla-Dlp)/SV; OPSS = (SBP - DPP)CB, where CO is cardiac output, Dla is the average pressure in the pulmonary artery, Dlp is the average pressure in the left atrium, SBP is the average systemic arterial pressure, Dpp is the average pressure in the right atrium. The presented equations are similar to the formulas used to describe resistance to direct electric current (Ohm's law), i.e. There is an analogy between hydraulic and electrical circuits. However, the behavior of a resistor in an electrical circuit will be significantly different from that of the fluid flow impedance in a hydraulic circuit due to the presence of pulsation and capacitive elements (veins). TRANSMURAL PRESSURE True afterload is a transmural force and therefore includes a component that is not part of the vascular system: pressure in the pleural cavity (cleft). Negative pleural pressure increases afterload because it increases transmural pressure at a given 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 cavity pressure on cardiac performance is discussed in Chapter 27. In conclusion, there are a number of problems associated with vascular resistance to blood flow as an indicator of afterload, 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 determining blood pressure. Due to the fact that mean blood pressure is a derivative of cardiac output and vascular resistance, measuring the latter helps to study the characteristics of hemodynamics during arterial hypotension. The use of OPSS for the diagnosis and treatment of shock conditions is discussed in Chapter 12. CIRCULATION IN HEART FAILURE The regulation of blood circulation in heart failure can be described if we take cardiac output as an independent value, and EDP and OPSS as dependent variables (Fig. 1-6). As cardiac output decreases, cardiopulmonary resistance and peripheral vascular resistance increase. This explains the clinical signs of heart failure: Increased EVP = venous congestion and edema; Increased peripheral vascular resistance = vasoconstriction and hypoperfusion. At least in part, these hemodynamic changes arise from activation of the renin-angiotensin-aldosterone system. Renin release in heart failure is due to decreased renal blood flow. Then, under the influence of renin, angiotensin I is formed in the blood, and from it, with the help of angiotensin-converting enzyme, angiotensin II, a powerful vasoconstrictor that has a direct effect on blood vessels. The release of aldosterone from the adrenal cortex caused by angiotensin II leads to the retention of sodium ions in the body, 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 indicates the graphical dependence of cardiac output on preload (i.e. functional curve of the heart), dotted line - cardiac output from peripheral vascular resistance (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. Effect of cardiac output on final Fig. 1-7. Changes in hemodynamics with cardiac diastolic pressure and general peripheral failure. N - normal, U - moderate cardiac vascular resistance. failure, 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 TPR-CO curve (afterload curve) (Fig. 1-7). In the early stage of moderate heart failure, the slope of the EDC-CO curve (preload curve) is still steep, and the intercept point (point Y) is determined on the flat part of the afterload curve (Fig. 1-7). In other words, in moderate heart failure, ventricular activity is dependent on preload and independent of afterload. The ability of the ventricle to respond to preload in moderate heart failure means that blood flow levels can be maintained but at higher than normal filling pressures. This explains why the most prominent symptom in moderate heart failure is dyspnea. 2. Severe heart failure With a further decrease in cardiac function, ventricular activity becomes less dependent on preload (i.e., the slope of the functional curve of the heart decreases) and cardiac output begins to decrease. The functional curve of the heart shifts to the steep part of the afterload curve (point T) (Fig. 1-7): in severe heart failure, ventricular activity does not depend on preload and depends on afterload. Both factors are responsible for the decrease in blood flow observed in late stages of heart failure. The role of afterload is especially important, since arterial vasoconstriction not only reduces cardiac output, but also reduces peripheral blood flow. The increasing importance of afterload during 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 R.C. 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/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/10-1.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/10-2.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/10-3.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/10-4.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/10.html 10 Wedge pressure The exact sciences are dominated by the idea of ​​relativity B. Paccell Pulmonary capillary wedge pressure (PCWP) is traditionally used in the practice of critical care medicine, and the term “wedge pressure ” has become quite familiar to doctors. Despite the fact that this indicator is used quite often; it is not always thought through critically. This chapter identifies some of the limitations of the use of the PCI and discusses misconceptions that arise when using this indicator in clinical practice. MAIN FEATURES There is an opinion that DZLK is a universal indicator, but this is not so. Below is a description of this parameter. DZLK: Determines pressure in the left atrium. It is not always an indicator of preload on the left ventricle. May reflect pressure in nearby alveoli. Does not allow accurate assessment of hydrostatic pressure in the pulmonary capillaries. Not an indicator of transmural pressure. Each of these statements is explained below. Additional information about DZLK can be obtained from reviews. WEGGING PRESSURE AND PRELOAD DPLC is used to determine left atrial pressure. The information obtained allows us to assess intravascular blood volume and left ventricular function. PRINCIPLE OF MEASUREMENT OF DZLK The principle of measurement of DZLK is shown in Fig. 10-1. The balloon at the distal end of the catheter inserted into the pulmonary artery is inflated until blood flow is obstructed. This will cause a column of blood to form between the tip of the catheter and the left atrium, and the pressure at the two ends of the column will equalize. The pressure at the end of the catheter becomes equal to the pressure in the left atrium. This principle expresses the hydrostatic equation: Dk - Dlp = Q x Rv Fig. 10-1. The principle of measuring DZLK. The lungs are divided into 3 functional zones based on the ratio of alveolar pressure (Palv), mean pressure in the pulmonary artery (avg. Dla) and pressure in the pulmonary capillaries (Pk). DZLK allows you to accurately determine the pressure in the left atrium (LAP) only when Dc 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 Dk - Dlp = 0 and, therefore, Dk - Dlp = DZLK. The pressure at the tip of the catheter at the time of balloon occlusion of the pulmonary artery is called LVP, which, in the absence of an obstruction between the left atrium and the left ventricle, is considered equal to the left ventricular end-diastolic pressure (LVEDP). END-DIASTOLIC PRESSURE IN THE LEFT VENTRICLE AS A CRITERION FOR PRELOAD In Chapter 1, preload on the myocardium at rest is defined as the force that stretches the heart muscle. For an intact ventricle, the preload is the end-diastolic volume (EDV). Unfortunately, EDV is difficult to determine directly at the patient's bedside (see. Chapter 14), therefore, to assess preload, an indicator such as end-diastolic pressure (EDP) is used. Normal (unchanged) compliance of the left ventricle makes it possible to use EDC 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: LVEDP (LVED) is a reliable indicator of preload only when left ventricular compliance is normal (or unchanged). The assumption that ventricular compliance is normal or unchanged in adult patients in intensive care units is unlikely. At the same time, the prevalence of impaired diastolic function in such patients has not been studied, although in some conditions their ventricular compliance is undoubtedly altered. This pathology is most often observed due to mechanical positive pressure ventilation, especially when inspiratory pressure is high (see Chapter 27). Ventricular compliance can also be altered by myocardial ischemia, ventricular hypertrophy, myocardial edema, cardiac tamponade, and a number of drugs (calcium channel blockers, etc.). When ventricular compliance is reduced, an increase in PCWP will be observed in both systolic and diastolic heart failure. This issue is discussed in detail in Chapter 14. WEDGE PRESSURE AND HYDROSTATIC PRESSURE DPLP is used as an indicator of hydrostatic pressure in the pulmonary capillaries, which makes it possible to assess the possibility of developing hydrostatic pulmonary edema. However, the problem is that PCWP is measured in the absence of blood flow, including in capillaries. Features of the dependence of the DPLC on hydrostatic pressure are presented 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 maximum permissible pressure. 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 for this relationship (note that, unlike the previous formula, this one has DZLK instead of Dlp): Dk - DZLK - Q x Rv. If Rv = 0, then Dk - DZLK = 0 and, therefore, Dk = DZLK. Rice. 10-2. The difference between hydrostatic pressure in the pulmonary capillaries (Pc) and the pulmonary capillaries. The following important conclusion follows from this equation: the pulmonary capillary pressure 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 small. The pulmonary circulation occurs under conditions of low pressure (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 main part of the total pulmonary vascular resistance (PVR) is created by the pulmonary veins. Animal studies have shown that the pulmonary veins account for at least 40% of PVR [b]. These ratios in humans are not precisely known, but are probably 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 account for 40% of the total pressure drop between the pulmonary artery and the left atrium (Dl - 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 DP and PCWP approaches zero, as shown below, because the pressure in the pulmonary artery is low. However, with pulmonary hypertension or increased pulmonary venous resistance, the difference may increase. This is illustrated below by the example of adult respiratory distress syndrome (ADRS), in which pressure increases in both the pulmonary artery and pulmonary veins (see Chapter 23). PCWP is assumed to be 10 mm Hg. both normally and with ARDS: PCWP = 10 mm Hg. Normally Dk = 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 PCWP by more than 2 times (22 versus 10 mm Hg). In this situation, the choice of treatment is influenced by the method of assessing hydrostatic pressure in the pulmonary capillaries. If the calculated pressure in the capillaries (22 mm Hg) is taken into account, then therapy should be aimed at preventing the development of pulmonary edema. If PCWP is taken into account as a criterion for DK (10 mm Hg), then no therapeutic measures are indicated. This example illustrates how the DZLK (more precisely, its incorrect interpretation) can be misleading. Unfortunately, it is impossible to directly determine the resistance of the pulmonary veins, 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. CHARACTERISTICS OF OCCLUSAL PRESSURE A decrease in pressure in the pulmonary artery from the moment of occlusion of blood flow by a balloon is accompanied by an initial rapid drop in pressure followed by a slow decrease. The point separating these two components is proposed to be considered equal to the hydrostatic pressure in the pulmonary capillaries. However, this idea is controversial, since it is not confirmed mathematically. Moreover, it is not always possible to clearly separate the fast and slow components of pressure at the bedside (personal observations of the author), so the issue requires further study. ARTIFACTS CAUSED BY PRESSURE IN THE CHEST The influence of pressure in the chest on PCWP 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 intravascular pressure without changing transmural pressure, depending on several factors, including the thickness of the vascular wall and its distensibility, which, naturally, will be different in healthy and sick people. When measuring PCWP, the following should be kept in mind to reduce the effect of chest pressure on PCWP. 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 pressure (zero level). It must also be remembered that vascular pressures recorded in intensive care units (ie, intraluminal pressure) are measured relative to atmospheric pressure (zero) and do not accurately reflect transmural pressure until tissue pressure approaches atmospheric pressure. This is especially important when changes associated with breathing are recorded when determining PCWP (see below). CHANGES RELATED TO BREATHING The effect of chest pressure on PCWP is shown in Fig. 10-3. This action is associated with a change in pressure in the chest, which is transmitted to the capillaries. The true (transmural) pressure in this recording may be constant throughout the respiratory cycle. PCWP, which is determined at the end of exhalation, during artificial pulmonary ventilation (ALV) is represented by the lowest point, and during independent breathing - the highest. Electronic pressure monitors in many intensive care units record pressure at 4 s intervals (corresponding to 1 wave pass through the oscilloscope screen). In this case, 3 different pressures can be observed on the monitor screen: systolic, diastolic and average. Systolic pressure is the highest point in each 4-second interval. Diastolic is the lowest pressure, and average corresponds to the average pressure. In this regard, PCWP at the end of expiration during spontaneous breathing of the patient is determined selectively by the systolic wave, and during mechanical ventilation - by the diastolic wave. Please note that the average pressure is not recorded on the monitor screen as breathing changes. Rice. 10-3. Dependence of PCWP 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 the diastolic pressure during mechanical ventilation. POSITIVE END-EXPIRATORY PRESSURE When breathing with positive end-expiratory pressure (PEEP), the alveolar pressure does not return to atmospheric pressure at the end of expiration. As a result, the value of the EPC at the end of expiration exceeds its true value. PEEP is created artificially or it may be characteristic of the patient himself (auto-PEEP). Auto-PEEP is the result of incomplete exhalation, which often occurs during mechanical ventilation in patients with obstructive pulmonary diseases. It must be remembered that auto-PEEP during mechanical ventilation often remains asymptomatic (see Chapter 29). If an excited patient with tachypnea experiences an unexpected or unexplained increase in PCWP, 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 PCWP is ambiguous and depends on the compliance of the lungs. When registering PCWP against the background of PEEP, it is necessary to reduce the latter to zero, without disconnecting the patient from the respirator. In itself, disconnecting the 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 that arises when a patient is disconnected from a respirator can be significantly reduced by creating positive pressure ventilation when PEEP is temporarily stopped. There are 3 possible reasons for the increase in PCWP with PEEP: PEEP does not change transmural capillary pressure. PEEP leads to compression of the capillaries, and against this background, PEEP represents the pressure in the alveoli, and not in the left atrium. PEEP affects the heart and reduces the compliance of the left ventricle, which leads to an increase in PCWP at the same EDV. Unfortunately, it is often impossible to identify one or another reason for the change in PCWP. The last two circumstances may indicate hypovolemia (relative or absolute), the correction of which requires infusion therapy. LUNG ZONES The accuracy of determining pulmonary pulmonary artery disease depends on the direct communication between the tip 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 relationship between alveolar pressure and pressure in the pulmonary circulation system, the lungs were conventionally 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, vascular pressure is highest (as a result of the pronounced gravitational influence), and pressure in the alveoli is lowest. When recording PCWP, the end of the catheter should be located in zone 3 (below the level of the left atrium). In this position, the influence of alveolar pressure on the pressure in the pulmonary capillaries is reduced (or eliminated). However, if the patient has hypovolemia or is undergoing mechanical ventilation with high PEEP, then this condition is not necessary [I]. Without X-ray control directly at the patient's bedside, it is almost impossible to insert a catheter into zone 3, although in most cases, due to the high speed of blood flow, it is in these areas of the lungs that the end of the catheter reaches its intended destination. On average, out of 3 catheterizations, only in 1 case does the catheter enter the upper zones of the lungs, which are located above the level of the left atrium [I]. ACCURACY OF MEASUREMENT OF JAW PRESSURE IN CLINICAL CONDITIONS When measuring the PCWP, there is a high probability of obtaining an erroneous result. In 30% of cases there are various technical problems, and in 20% errors arise due to incorrect interpretation of the received data. The accuracy of the measurement can also be affected by the nature of the pathological process. Some practical issues related to the accuracy and reliability of the results obtained are discussed below. VERIFICATION OF THE RESULTS OBTAINED Position of the catheter end. Typically, catheterization is performed with the patient lying on his back. In this case, the end of the catheter with the blood flow enters the posterior sections 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 photographs in a direct projection and thereby determining the position of the catheter, therefore it is recommended to use lateral projection [I]. However, the significance of x-rays taken in the lateral projection is questionable, since there are reports in the literature that the pressure in the ventral areas (located both above and below the left atrium) remains virtually unchanged compared to the dorsal ones. In addition, such an X-ray examination (in a lateral projection) is difficult to perform, expensive, and not possible in every clinic. In the absence of x-ray control, the catheter does not enter zone 3, which is indicated by the following change in the pressure curve, which is associated with breathing. During mechanical ventilation in the PEEP mode, the PCWP value increases by 50% or more. Blood oxygenation in the area of ​​measurement of pulmonary arterial pressure. To determine the location of the catheter, it is recommended to take blood from its end with the balloon inflated. If the hemoglobin saturation of a blood sample with oxygen reaches 95% or more, then the blood is considered arterial. One work indicates 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 PCWP is minimal. At the same time, in patients with lung pathology, such oxygenation may not be observed due to local hypoxemia, and not due to incorrect position of the catheter end. 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 oxygen saturation of mixed venous blood, which has become routine in our intensive care unit when measuring PCWP, without increasing the incidence of complications and costs. Shape of the atrial pressure curve. The shape of the PCWP waveform can be used to confirm that the PCWP 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 intraatrial pressure curve are distinguished: A-wave, which is caused by atrial contraction and coincides with the Pna wave of the ECG. These waves disappear during atrial fibrillation and flutter, as well as during acute pulmonary embolism. X-wave, which corresponds to atrial relaxation. A pronounced decrease in the amplitude of this wave is observed with cardiac tamponade. The C wave marks the onset of ventricular contraction and corresponds to the moment when the mitral valve begins to slam shut. The V wave appears at the moment of ventricular systole and is caused by the pressing of the valve leaflets into the cavity of the left atrium. Y-descending is the result of rapid emptying of the atrium when the mitral valve ruptures early in diastole. With cardiac tamponade, this wave is weakly expressed or absent. A giant V wave when recording atrial pressure corresponds to mitral valve insufficiency. These waves arise as a result of the reverse flow of blood through the pulmonary veins, which can even reach the valve flaps of the pulmonary trunk. Rice. 10-4. Schematic representation of the atrial pressure waveform compared to the ECG. Explanation in the text. A high V-wave leads to an increase in the average PCWP to a level exceeding the diastolic pressure in the pulmonary artery. In this case, the value of the average PCWP will also exceed the filling pressure of the left ventricle, therefore, for greater accuracy, it is recommended to measure pressure in diastole. A high V-wave is not pathognomonic for mitral regurgitation. This wave is also observed with left atrial hypertrophy (cardiomyopathy) and high pulmonary blood flow (ventricular septal defect). VARIABILITY The values ​​of PCWP in most people fluctuate within 4 mm Hg, but in some cases their deviation can reach 7 mm Hg. A statistically significant change in PCWP should exceed 4 mm Hg. PCWP AND LVEDP In most cases, the LVEP value corresponds to the value of LVEDP [I].However, this may not be the case in the following situations: 1. In case of aortic valve insufficiency. In this case, the level of LVEDP exceeds that of the LVEDP, since the mitral valve slams prematurely due to retrograde blood flow into the ventricle 2. Contraction of the atrium with a rigid ventricular wall leads to a rapid increase in EDP with premature closure of the mitral valve. As a result, PCWP is lower than LVEF [I]. 3. In case of respiratory failure, the value of LVAD in patients with pulmonary pathology may exceed the value of LVED. A possible mechanism for this phenomenon is the contraction of small veins in hypoxic areas of the lungs, so in this situation the accuracy of the results cannot be guaranteed. The risk of such an error can be reduced by placing the catheter in areas of the lungs that are not involved in the pathological process. LITERATURE 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 left ventricular 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. CHARACTERISTIC FEATURES 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. ACCURACY OF STALL PRESSURE MEASUREMENT 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 AN, 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/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/11-1.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/11-2.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/12-1.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/12-2.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/12-3.JPG Intensive Care~Paul L. Marino/Paul L.Marino. ""The ICU Book"" (2nd Ed) - Rus/12.html 12 A 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 hypotension or hypoperfusion, but rather as a state of inadequate tissue oxygenation. The ultimate goal of this approach is to achieve a match between the delivery of oxygen to tissues and the level of metabolism in them. Normalization of blood pressure and blood flow is also taken into account, but not as the final goal. The fundamental principles that are used in our proposed approach are set out in Chapters 1, 2, 9, and are also discussed in the works (see the end of this chapter). In this book, there is one central theme in approaching the problem of shock: to always strive to clearly determine the state of tissue oxygenation. The shock is “hidden” in the latter, and you will not detect it by listening to the organs of the chest cavity or measuring the pressure in the brachial artery. It is necessary to search for new approaches to the problem of shock. The “black box” 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 VIEWS The approach we propose 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. Wedge pressure in the pulmonary capillaries (PCP); 2. Cardiac output (CO); 3. Total peripheral vascular resistance (TPVR). Indicators of the “oxygen transport” group: 4. Oxygen delivery (UOg); 5. Oxygen consumption (VC^); 6 Lactate content in blood serum. 1. At stage I, a set of “pressure/blood flow” parameters is used to determine and correct leading hemodynamic disorders. Indicators combined into such a group have certain values, on the basis of which the entire complex can be characterized (in other words, described or created a small hemodynamic profile, “formula”), which is used for diagnosis and evaluation of treatment effectiveness. The final goal of this stage is to restore blood pressure and blood flow (if possible) and determine the underlying cause of the pathological process. II. At stage II, the effect of initial therapy on tissue oxygenation is assessed. The goal of this stage is to achieve a correspondence between oxygen consumption by tissues and the level of metabolism in them, for which an indicator such as the concentration of lactate in the blood serum is used. Oxygen delivery is modified (if necessary) to correct VO2. STAGE I: MAIN HEMODYNAMIC PROFILES (“FORMULAS”) To simplify, we believe that each factor from the “pressure/blood flow” group of indicators plays a leading role in one of the main types of shock, as, for example, shown below. Indicator Type of shock Cause PCOS Hypovolemic Blood loss (more precisely, a decrease in volume of blood volume, as with bleeding or dehydration SV Cardiogenic Acute myocardial infarction OPSS Vasogenic Sepsis The relationship between PALS, SV and OPSS in these types of shock can be represented by so-called small hemodynamic profiles, which help determine an individual approach in each specific case. The relationship between PC, CO and TPSS is normally discussed 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 With it, the primary importance is a decrease in ventricular filling (low PCWP), leading to a decrease in CO, which in turn causes vasoconstriction and an increase in OPSS. Taking into account the above, the “formula" of hypovolemic shock will be as follows: low PCWP/low CO/ high TOP. CARDIOGENIC SHOCK In this case, the leading factor is a sharp decrease in CO with subsequent stagnation of blood in the pulmonary circulation (high PAWP) and peripheral vasoconstriction (high TOP). The “formula” of cardiogenic shock is as follows: high PCOS/low CO/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 in the veins (low PCWP). Cardiac output is usually high, but its value can vary significantly. The “formula” of vasogenic shock is as follows: low PCOS/high CO/low TPR. The value of PVLC 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 are: 1. Sepsis/multiple organ failure. 2. Postoperative condition. 3. Pancreatitis. 4. Trauma. 5. Acute adrenal insufficiency. 6. Anaphylaxis. COMPLEX COMBINATIONS OF HEMODYNAMIC INDICATORS The three indicated basic hemodynamic indicators, when combined in different ways, can create more complex profiles. For example, the “formula” may look like this: normal PA/low CO/high OPSS. However, it can be presented as a combination of two main “formulas”: 1) cardiogenic shock (high PA/low CO/high TPR) + 2) hypovolemic shock (low PC/low CO/high TPR). 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 SMALL HEMODYNAMIC PROFILES (“FORMULAS”) The information capabilities of small hemodynamic profiles are demonstrated in Table. 12-1. First, the leading circulatory disorder must be determined. Thus, in the case under consideration, the characteristics of the indicators resemble the “formula” of hypovolemic shock, with the exception of the normal value of TPVR. Consequently, the main hemodynamic disorders can be formulated as a decrease in circulating blood volume plus low vascular tone. This determined the choice of therapy: infusion and drugs that increase peripheral vascular resistance (for example, dopamine). So, each of the main pathological processes accompanied by circulatory disorders will correspond to a small hemodynamic profile. In table 12-1 such disorders were a decrease in circulating blood volume and vasodilation. * The concept of “vasogenic shock” does not appear in Russian literature. 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. In the domestic literature, the concept of “collapse” is close in meaning to vasogenic shock - an acutely developing vascular insufficiency, characterized primarily turn a decrease in vascular tone, and also a decrease in the volume of circulating blood. Collapse most often develops as a complication of serious diseases and pathological conditions. There are (depending on the 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 Definition of the pathological process Targeted therapy Possible causes Low PCWP/low CO/normal TPR Decrease in volumetric blood volume and vasodilation Increase in volumetric volume until PCWP is established = 12 mm Hg. Dopamine, if necessary Adrenal insufficiency Sepsis Anaphylaxis NORMALIZATION OF BLOOD CIRCULATION The following diagram shows what therapeutic measures can be used to correct hemodynamic disorders. The pharmacological properties of the drugs mentioned in this section are discussed in detail in Chapter 20. To simplify, the drugs and their actions are described quite briefly and simply, for example, alpha: vasoconstriction (i.e. stimulation of α-adrenergic receptors gives a vasoconstrictor effect), (beta: vasodilation and increased cardiac activity (i.e., stimulation of beta-adrenergic receptors of blood vessels causes their dilation, and the heart - an increase in the frequency and strength of heart contractions) Condition Therapy 1. Low or normal PCWP Infusion therapy Fluids are always preferable to vasoconstrictors.The goal of infusion therapy is in increasing PCWP either to 18-20 mm Hg, or to a level equal to the colloid osmotic pressure (COP) of plasma.Methods for measuring COP are discussed in the 1st part of Chapter 23. 2. Low CO a. High TOP Dobutamine b Normal peripheral vascular resistance Dopamine Selective (beta-agonists like dobutamine (beta1-adrenergic agonist) are indicated for low cardiac output without hypotension. Dobutamine is less valuable in cardiogenic shock, since it does not always increase blood pressure; but, by reducing peripheral vascular resistance, it significantly increases cardiac output. In cases of severe arterial hypotension (beta-agonists, together with some alpha-adrenergic agonists, are most suitable for increasing blood pressure, since stimulation of the α-adrenergic receptors of blood vessels, causing their constriction, will prevent a decrease in OPSS in response to an increase in CO. 3. Low OPSS a. Reduced or normal CO alpha-, beta-Agonists b. High CO alpha-Agonists* * Prescription of vasoconstrictors should be avoided if possible, as they increase systemic blood pressure at the cost of deterioration of blood supply to tissues due to spasm of arterioles. If the administration of vasoconstrictors is necessary, then alpha-, beta -agonists are preferred over selective alpha-agonists, which can cause severe vasoconstriction.Dopamine is often used in combination with other drugs and, by stimulating special dopamine receptors on vascular smooth muscle, causes them to dilate, which helps maintain blood flow in the kidneys. It should be noted that the arsenal of drugs that significantly affect blood circulation during shock is small. You have to basically limit yourself to the drugs listed below. Expected effect Drugs Beta: increased cardiac activity Dobutamine alpha, beta and dopamine receptors: cardiotonic effect 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 has cardiotonic activity, combined with an effect on the resistance of regional vessels, and in high - pronounced alpha-adrenomimetic properties makes it a very valuable anti-shock drug. The effectiveness of dopamine may decrease after several days of administration due to the depletion of norepinephrine, which it releases from the 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, with septic shock) or to increase blood pressure. It should be remembered that in case of hemorrhagic and cardiogenic shock with a sharp drop in blood pressure, norepinephrine cannot be used (due to deterioration of blood supply to tissues), and infusion therapy is recommended to normalize blood pressure. In addition, the drugs mentioned above stimulate metabolism and increase the energy demand of tissues, while their energy supply is in jeopardy. POST-RESuscitation INJURY The period following the restoration of systemic blood pressure may be accompanied by ongoing ischemia and progressive organ damage. The three post-resuscitation injury syndromes are briefly presented in this section to demonstrate the importance of monitoring tissue oxygenation and to justify the appropriateness of stage II treatment of shock. NON-RESTORED ORGAN BLOOD FLOW The phenomenon of non-restoration of blood flow (no-reflow) is characterized by persistent hypoperfusion after resuscitation measures for ischemic stroke. This phenomenon is believed to be 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 the gastrointestinal tract, can disrupt the mucosal barrier of the intestinal wall, which makes it possible for 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 dysfunction after resuscitation of patients with cardiac arrest [b]. In the long term, the phenomenon of non-restoration of blood flow clinically manifests itself as multiple organ failure syndrome, often leading to death. REPERFUSION INJURY Reperfusion injury differs from the phenomenon of non-restoration of blood flow because in this case the blood supply is restored after an 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 distributed throughout the body by the blood flow, reaching distant organs. As is known, free radicals and other reactive oxygen species (superoxide anion radical, hydroxyl radical, hydrogen peroxide and singlet oxygen), as well as products of lipid peroxidation (LPO) are capable of changing membrane permeability and thereby causing metabolic changes at the cellular and tissue levels . (Free radicals are particles that have unpaired electrons in the outer orbital and, as a result, have 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 stitches and breaks. Such changes significantly disrupt the physicochemical properties of membranes and, first of all, their permeability. LPO products inhibit the activity of membrane enzymes by blocking their sulfhydryl groups and suppress the functioning of the sodium-potassium pump, thereby aggravating membrane permeability disorders. It has been established that the increase

Name: Intensive therapy. 3rd edition
Paul L. Marino
The year of publishing: 2012
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Language: Russian

The book Intensive Care, edited by Paul L. Marino, examines a basic course of therapy that requires intensive treatment. 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 care to critically ill patients are presented. The issues of monitoring and interpretation of clinical and laboratory data are covered. Current issues of infusion therapy are outlined. Critical conditions in cardiology and neurology are described in more detail. surgery, pulmonology and so on. The issues of tactics for artificial ventilation, transfusion therapy, and acute poisoning are discussed in detail. For anesthesiologists and resuscitators.

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