EM · ABCDE approach
ABCDE approach to the deteriorating patient
A structured, prioritised approach to the recognition and resuscitation of the deteriorating emergency department patient — airway, breathing, circulation, disability, exposure — built on oxygen-delivery physiology, early-warning scoring, the pathophysiology of compensated shock, and time-critical sepsis care. ACEM-primary, globally tagged.
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Target exams
Red flags
- Airway obstruction, stridor, or a silent chest
- Respiratory rate below 8 or above 30, or oxygen saturation below 90 percent on supplemental oxygen
- Systolic blood pressure below 90 mmHg, a rising or persistently elevated lactate, or cold poorly perfused peripheries
- New confusion, agitation, or a Glasgow Coma Score below 12
- A time-critical cause such as anaphylaxis, sepsis, or major haemorrhage
The ABCDE approach is a prioritised, repeatable framework for assessing and resuscitating the acutely ill or deteriorating patient. It treats problems in the order in which they threaten life — airway first, then breathing, then circulation, then disability, then exposure — so that the clinician corrects the most immediately fatal derangement before moving to the next step.[11] Its purpose is not to reach a diagnosis but to keep the patient alive, to buy time, and to reveal the diagnosis as resuscitation proceeds. In the emergency department it is applied to every undifferentiated, potentially unstable patient: the collapsed patient in the resus bay, the breathless patient pulled forward from the waiting room because of abnormal observations, and the patient who is stable by numbers but quietly deteriorating. The assessment is rapid, performed in parallel with treatment and investigation, and repeated as a loop after every intervention.
Three principles govern the whole approach. First, treat first what kills first: a blocked airway kills the patient long before the cause of the blockage is known, so it is managed immediately. Second, resuscitate and investigate simultaneously: intravenous access, bloods, a gas and an electrocardiogram are obtained while the airway and breathing are secured, not deferred until afterwards. Third, call for help early: a deteriorating patient is managed by a team, and senior, anaesthetic and critical-care assistance should be summoned at the first sign of instability rather than when resuscitation has failed. [11]
The physiology that underpins resuscitation
Every step of ABCDE exists to preserve oxygen delivery to the tissues, and a Fellowship candidate must be able to defend the approach from first principles. Global oxygen delivery is the product of cardiac output and arterial oxygen content: DO2 = CO × CaO2. The arterial oxygen content is CaO2 = (1.34 × Hb × SaO2) + (0.003 × PaO2), so it depends overwhelmingly on haemoglobin and saturation, with dissolved oxygen contributing negligibly. Cardiac output is CO = stroke volume × heart rate, and stroke volume is determined by preload, afterload and contractility. Mean arterial pressure approximates to MAP = CO × systemic vascular resistance (SVR), which is why a falling output can be masked for a time by rising SVR (vasoconstriction). [6]
This physiology dictates both the order and the content of the assessment. The airway and breathing exist to maintain the SaO2 term; the circulation exists to maintain the CO term; together they protect DO2 and therefore cerebral and myocardial oxygenation. A blocked airway removes SaO2 within minutes; a failing circulation removes CO. The same framework explains why a patient can look well while dying: healthy adults compensate for a falling output through sympathetic tachycardia, vasoconstriction and tachypnoea, holding MAP and cerebral perfusion until reserve is exhausted. Decompensation is then abrupt — the blood pressure falls, the conscious level drops, and the patient arrests. [11]
Three clinical consequences follow, and they are the heart of safe emergency practice. A normal blood pressure does not exclude shock, particularly in the young, pregnant, athlete and the chronically hypertensive, who may hold a normal pressure until a substantial fraction of circulating volume is lost. A rising heart rate, a rising respiratory rate and cold, clammy peripheries are the footprints of compensation and may precede hypotension by minutes or hours. A raised lactate signals that DO2 has fallen behind demand and anaerobic metabolism has begun, and it may be the first objective marker of occult shock. The resuscitation team must therefore act on the trend and the compensatory signs, not wait for the blood pressure to collapse. [6]
References13ShowHide
- [1]Gao H, McDonnell A, Harrison DA, et al. Systematic review and evaluation of physiological track and trigger warning systems for identifying at-risk patients on the ward Intensive Care Med, 2007.PMID 17318499
- [2]Subbe CP, Davies RG, Williams E, et al. Effect of introducing the Modified Early Warning score on clinical outcomes, cardio-pulmonary arrests and intensive care utilisation in acute medical admissions Anaesthesia, 2003.PMID 12859475
- [3]Subbe CP, Gao H, Harrison DA. Reproducibility of physiological track-and-trigger warning systems for identifying at-risk patients on the ward Intensive Care Med, 2007.PMID 17235508
- [4]Kostakis I, Smith GB, Prytherch D, et al. The performance of the National Early Warning Score and National Early Warning Score 2 in hospitalised patients infected by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Resuscitation, 2021.PMID 33176170
- [5]Smith GB, Redfern O, Maruotti A, et al. The association between nurse staffing levels and a failure to respond to patients with deranged physiology: A retrospective observational study in the UK Resuscitation, 2020.PMID 31945427
- [6]Monnet X, Messina A, Greco M, et al. ESICM guidelines on circulatory shock and hemodynamic monitoring 2025 Intensive Care Med, 2025.PMID 41236566
- [7]Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903338
- [8]Shankar-Hari M, Phillips GS, Levy ML, et al. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903336
- [9]Seymour CW, Gesten F, Prescott HC, et al. Time to Treatment and Mortality during Mandated Emergency Care for Sepsis N Engl J Med, 2017.PMID 28528569
- [10]Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903335
- [11]Thim T, Krarup NH, et al. [ABCDE--a systematic approach to critically ill patients]. Ugeskr Laeger, 2010.PMID 21092723
- [12]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): a randomised, placebo-controlled trial. Lancet, 2010.PMID 20554319
- [13]Roberts I, Shakur H, Afolabi A, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet, 2011.PMID 21439633