EM · Shock
Shock states — the recognition and the approach
Also known as Circulatory shock · Acute circulatory failure · Tissue hypoperfusion
Shock — the definition (the inadequate tissue perfusion and the cellular hypoxia); the four patterns by the haemodynamics (the hypovolaemic, the distributive, the cardiogenic, the obstructive); the compensated vs the decompensated phases; the clinical signs (the compensatory tachycardia, the vasoconstriction, the tachypnoea that precede the hypotension); the lactate as the occult-shock marker; the bedside ultrasound (the IVC, the cardiac); and the management framework (the treat-the-cause, the fluid, the vasopressor, the transfusion, the targets). ACEM-primary, globally tagged.
Checked against its sources on 3 Sept 2026
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Target exams
Red flags
- The hypotension is a LATE sign — the compensatory mechanisms maintain the blood pressure until a large fraction of the circulating volume is lost
- The lactate greater than 2 mmol/L (or the failure of the lactate to clear) is the marker of the occult shock, even with a normal blood pressure
- The mottled skin, the delayed capillary refill (over 3 seconds) and the cold extremities are the bedside signs of the poor perfusion
- The anaphylactic and the neurogenic shock are WARM and DRY (the distributive pattern) — do not be reassured by the warm skin
Shock is the emergency physician's bread and butter — the recognition of the tissue hypoperfusion before the blood pressure drops, the classification by the haemodynamic pattern, and the rapid correction with the fluid, the vasopressor and the treat-the-cause approach. The Fellowship candidate must know the four patterns, the compensated vs the decompensated phases, the role of the lactate, and the targets for the resuscitation, because the shock is the final common pathway of every acute presentation from the trauma to the sepsis to the MI.[1][2]
Definition
Shock is the state of inadequate cellular oxygen delivery — the oxygen supply to the tissues falls below the oxygen demand, producing the anaerobic metabolism, the lactate generation and, if untreated, the multi-organ failure and the death. The definition is haemodynamic: the cardiac output (the stroke volume times the heart rate) is insufficient to meet the tissue demand, whether because of the low preload (the hypovolaemic), the low contractility (the cardiogenic), the low systemic vascular resistance (the distributive), or the external obstruction to the flow (the obstructive).[1][10]
References16ShowHide
- [1]Standl T, Annecke T, Cascorbi I, et al. The Nomenclature, Definition and Distinction of Types of Shock Dtsch Arztebl Int, 2018.PMID 30573009
- [2]Chioncel O, Parissis J, Mebazaa A, et al. Epidemiology, pathophysiology and contemporary management of cardiogenic shock - a position statement from the Heart Failure Association of the European Society of Cardiology Eur J Heart Fail, 2020.PMID 32469155
- [3]Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med, 2001.PMID 11794169
- [4]Yealy DM, Kellum JA, Huang DT, et al. A randomized trial of protocol-based care for early septic shock N Engl J Med, 2014.PMID 24635773
- [5]Peake SL, Delaney A, Bailey M, et al. Goal-directed resuscitation for patients with early septic shock N Engl J Med, 2014.PMID 25272316
- [6]Mouncey PR, Osborn TM, Power GS, et al. Trial of early, goal-directed resuscitation for septic shock N Engl J Med, 2015.PMID 25776532
- [7]Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically lll Emerg Med Clin North Am, 2010.PMID 19945597
- [8]Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903338
- [9]Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021 Intensive Care Med, 2021.PMID 34599691
- [10]Vincent JL, De Backer D Circulatory shock N Engl J Med, 2013.PMID 24171518
- [11]Shakur H, Roberts I, Bautista R, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2) Lancet, 2010.PMID 20554319
- [12]Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma (PROPPR) JAMA, 2015.PMID 25647203
- [13]Monnet X, Messina A, Greco M, et al. ESICM guidelines on circulatory shock and hemodynamic monitoring 2025 Intensive Care Med, 2025.PMID 41236566
- [14]Marik PE, Baram M, Vahid B Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares Chest, 2008.PMID 18628220
- [15]Moturi SV, Thiyagarajan PR, Dominic M, et al. Comparative Evaluation of Shock Index and Modified Shock Index in Predicting Outcomes of Sepsis Patients with and without Comorbidities Ann Afr Med, 2026.PMID 42390434
- [16]Roberts I, Shakur H, Afolabi A, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients Lancet, 2011.PMID 21439633