Modern concept of etiopathogenesis and diagnosis of shock
Modern concept of shock
Keywords:
shock, hemodynamic disorder, sepsis, etiopathogenesis
Abstract
Introduction: Shock is a life-threatening condition that occurs due to a mismatch in the supply and consumption of oxygen, which leads to cell and tissue hypoxia, resulting in cell death and dysfunction of vital organs. The effects of shock are reversible in the early stages, but delay in diagnosis and initiation of treatment can lead to irreversible changes, including multiorgan failure (MODS) and death. There are four main categories of shock: hypovolemic, distributive, cardiogenic, and obstructive. Etiology: Hypovolemic shock can occur due to hemorrhagic and non-hemorrhagic causes. Distributive shock is divided into septic, systemic inflammatory response syndrome (SIRS), anaphylactic, neurogenic and endocrine due to differences in etiopathogenesis. Cardiogenic shock occurs due to intracardiac causes, while obstructive shock occurs due to extracardiac causes. Pathogenesis: The pathogenesis of each type of shock is different depending on the etiology. Generally speaking, shock has three phases: compensated, cellular distress phase, and decompensated. When the shock progress into an irreversible phase, usually it ends with MODS and death. Clinical presentation: Symptoms may vary depending on the type and stage of shock. The most important changes that occur during this syndrome are at the level of hemodynamics, so the most common clinical signs indicating shock are hypotension, tachycardia, tachypnea, disturbed mental status, cold extremities, blue skin and oliguria. Diagnosis: The diagnosis of shock is based on history, clinical presentation, physical examination, vital parameters and biochemical analyses, SOFA criteria (sequential organ failure assessment score), SIRS criteria, acid-base status, blood count, hemodynamic monitoring, diuresis measurement, etc.
References
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2. Vincent JL, Rello J, Marshall J, et al. International study of the prevalence and outcomes of infection in intensive care units. JAMA. 2009;302(21):2323-2329. [PubMed]
3. Cohen J, Cristofaro P, Carlet J, Opal S. New method of classifying infections in critically ill patients. Crit Care Med. 2004;32(7):1510-1526. [PubMed]
4. Angus DC, van der Poll T. Severe sepsis and septic shock [published correction appears in N Engl J Med. 2013 Nov 21;369(21):2069]. N Engl J Med. 2013;369(9):840-851. [PubMed]
5. Ring J, Beyer K, Biedermann T, et al. Guideline for acute therapy and management of anaphylaxis: S2 Guideline of the German Society for Allergology and Clinical Immunology (DGAKI), the Association of German Allergologists (AeDA), the Society of Pediatric Allergy and Environmental Medicine (GPA), the German Academy of Allergology and Environmental Medicine (DAAU), the German Professional Association of Pediatricians (BVKJ), the Austrian Society for Allergology and Immunology (ÖGAI), the Swiss Society for Allergy and Immunology (SGAI), the German Society of Anaesthesiology and Intensive Care Medicine (DGAI), the German Society of Pharmacology (DGP), the German Society for Psychosomatic Medicine (DGPM), the German Working Group of Anaphylaxis Training and Education (AGATE) and the patient organization German Allergy and Asthma Association (DAAB). Allergo J Int. 2014;23(3):96-112. [PubMed]
6. Taylor MP, Wrenn P, O'Donnell AD. Presentation of neurogenic shock within the emergency department. Emerg Med J. 2017;34(3):157-162. [PubMed]
7. Tewelde SZ, Liu SS, Winters ME. Cardiogenic Shock. Cardiol Clin. 2018;36(1):53-61. [PubMed]
8. Palacios Ordonez C, Garan AR. The landscape of cardiogenic shock: epidemiology and current definitions. Curr Opin Cardiol. 2022;37(3):236-240. [PubMed]
9. Pich H, Heller AR. Obstruktiver Schock [Obstructive shock]. Anaesthesist. 2015;64(5):403-419. [PubMed]
10. Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000;48(1):23-33. [PubMed]
11. Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996;4(2):161-167. [PubMed]
12. Furer A, Wessler J, Burkhoff D. Hemodynamics of Cardiogenic Shock. Interv Cardiol Clin. 2017;6(3):359-371. [PubMed]
13. Blumlein D, Griffiths I. Shock: aetiology, pathophysiology and management. Br J Nurs. 2022;31(8):422-428. [PubMed]
14. Gasparetto A. Risonanze endocrine nello shock [Endocrine repercussions of shock]. Minerva Anestesiol. 1980;46(9):1047-1056. [PubMed]
15. Patel S, Holden K, Calvin B, DiSilvio B, Dumont T. Shock. Crit Care Nurs Q. 2022;45(3):225-232. [PubMed]
16. Deitch EA, Condon M, Feketeova E, et al. Trauma-hemorrhagic shock induces a CD36-dependent RBC endothelial-adhesive phenotype. Crit Care Med. 2014;42(3):e200-e210. [PubMed]
17. Slaughter AL, Nunns GR, D'Alessandro A, et al. The Metabolopathy of Tissue Injury, Hemorrhagic Shock, and Resuscitation in a Rat Model. Shock. 2018;49(5):580-590. [PubMed]
18. Lodha R, Kapoor V. Peripheral circulatory failure. Indian J Pediatr. 2003;70(2):163-168. [PubMed]
19. Salmon AH, Satchell SC. Endothelial glycocalyx dysfunction in disease: albuminuria and increased microvascular permeability. J Pathol. 2012;226(4):562-574. [PubMed]
20. Martin L, Koczera P, Zechendorf E, Schuerholz T. The Endothelial Glycocalyx: New Diagnostic and Therapeutic Approaches in Sepsis. Biomed Res Int. 2016;2016:3758278. [PubMed]
21. Jeschke MG, van Baar ME, Choudhry MA, Chung KK, Gibran NS, Logsetty S. Burn injury. Nat Rev Dis Primers. 2020;6(1):11. Published 2020 Feb 13. [PubMed]
22. Spapen H. Liver perfusion in sepsis, septic shock, and multiorgan failure. Anat Rec (Hoboken). 2008;291(6):714-720. [PubMed]
23. Chang JC. Thrombogenesis and thrombotic disorders based on 'two-path unifying theory of hemostasis': philosophical, physiological, and phenotypical interpretation. Blood Coagul Fibrinolysis. 2018;29(7):585-595. [PubMed]
24. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2015;372(11):1078-1079. [PubMed]
25. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. [PubMed]
26. Lier H, Bernhard M, Hossfeld B. Hypovolämisch-hämorrhagischer Schock [Hypovolemic and hemorrhagic shock]. Anaesthesist. 2018;67(3):225-244. [PubMed]
27. Gotts JE, Matthay MA. Sepsis: pathophysiology and clinical management. BMJ. 2016;353:i1585. Published 2016 May 23. [PubMed]
28. Triggiani M, Montagni M, Parente R, Ridolo E. Anaphylaxis and cardiovascular diseases: a dangerous liaison. Curr Opin Allergy Clin Immunol. 2014;14(4):309-315. [PubMed]
29. Vincent JL, de Mendonça A, Cantraine F, et al. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Working group on "sepsis-related problems" of the European Society of Intensive Care Medicine. Crit Care Med. 1998;26(11):1793-1800. [PubMed]
30. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003;31(4):1250-1256. [PubMed]
31. Shokoohi H, Boniface KS, Pourmand A, et al. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit Care Med. 2015;43(12):2562-2569. [PubMed]
32. Estrada-Y-Martin RM, Oldham SA. CTPA as the gold standard for the diagnosis of pulmonary embolism. Int J Comput Assist Radiol Surg. 2011;6(4):557-563. [PubMed]
Published
2025/11/19
Section
Pregledni rad / Review article
