SHOCK Stages Classification

Publication Date: January 14, 2022
Last Updated: March 14, 2022

Key Summary Points

  1. The SCAI SHOCK stage is an indication of shock severity and comprises one component of mortality risk prediction in patients with CS, along with etiology/phenotype and other risk modifiers; a 3-axis model of risk stratification in CS has been proposed to position the SCAI SHOCK stage in context.
  2. Validation studies have underscored the correlation of the SCAI SHOCK stage with mortality across all clinical subgroups, including CS with and without acute coronary syndrome (ACS), cardiac intensive care unit (CICU) patients, and those presenting with out-of-hospital cardiac arrest (OHCA).
  3. Progression across the SCAI SHOCK stage continuum is a dynamic process, incorporating new information as available, and patient trajectories are important both for communication among clinicians and for decision-making regarding the next level of care and therapeutics.
  4. A hub and spoke model for transfer of higher-risk patients including those with a deteriorating SCAI SHOCK stage has been proposed.
  5. Cardiac arrest (CA) as described herein relates to that accompanied by coma, defined as the inability to respond to verbal stimuli, most commonly associated with Glasgow Coma Scale <9, where there is concern for significant anoxic brain injury.
  6. The SCAI SHOCK pyramid and associated figure now reflect gradations of severity within each stage and pathways by which patients progress or recover.
  7. A streamlined table incorporating variables that are most typically seen, and the revised CA modifier definition, is also provided and incorporates lessons learned from validation studies and clinician experience.
  8. The lactate level and thresholds have been highlighted to detect hypoperfusion but may be dissociated from hemodynamics in cases such as chronic heart failure (HF). In addition, patients may demonstrate other manifestations of end-organ hypoperfusion with a normal lactate level, and there are also important causes of an elevated lactate level other than shock.

Descriptors of shock stages: Physical examination, biochemical markers, and hemodynamics

Stage Description Physical examination/bedside findings Biomechanical markers Hemodynamics
Typically includes May include Typically includes May include Typically includes May include
A - At Risk A patient who is not currently experiencing signs or symptoms of CS, but is at risk for its development.
These patients may include those with large acute myocardial infarction or prior infarction and/or acute or acute-on-chronic heart failure symptoms.		 Normal JVP
Warm and well-perfused•Strong distal pulses•Normal mentation		 Clear lung sounds Normal lactate Normal labs•Normal (or at baseline) renal function Normotensive (SBP ≥100 ​mmHg or at baseline) If invasive hemodynamics are assessed:•Cardiac Index ≥2.5 ​L/min/m2 (if acute)•CVP ≤10 ​mmHg•PCWP ≤15 ​mmHg•PA saturation ≥65%
B - Beginning CS A patient who has clinical evidence of hemodynamic instability (including relative hypotension or tachycardia) without hypoperfusion. Elevated JVP
Warm and well-perfused•Strong distal pulses•Normal mentation		 Rales in lung fields Normal lactate Minimal acute renal function impairment
Elevated BNP		 Hypotension•SBP <90 ​mmHg•MAP <60 ​mmHg•> 30 ​mmHg drop from baselineTachycardia•Heart rate ≥100 bpm
C - Classic CS A patient who manifests with hypoperfusion and who requires one intervention (pharmacological or mechanical) beyond volume resuscitation.
These patients typically present with relative hypotension (but hypotension is not required).		 Volume overload Looks unwell
Acute alteration in mental status
Feeling of impending doom
Cold and clammy
Extensive rales
Ashen, mottled, dusky, or cool extremities
Delayed capillary refill
Urine Output
<30 ​mL/h		 Lactate ≥2 mmol/L Creatinine increase to 1.5 x baseline (or 0.3 ​mg/dL) or ​> ​50% drop in GFR
Increased LFTs
Elevated BNP		 If invasive hemodynamics assessed (strongly recommended)•Cardiac index <2.2 ​L/min/m2•PCWP >15 ​mmHg
D - Deteriorating A patient who is similar to category C but is getting worse. Failure of initial support strategy to restore perfusion as evidenced by worsening hemodynamics or rising lactate. Any of stage C and worsening (or not improving) signs/symptoms of hypoperfusion despite the initial therapy. Any of stage C and lactate rising and persistently >2 mmol/L Deteriorating renal function
Worsening LFTs
Rising BNP		 Any of stage C and requiring escalating doses or increasing numbers of pressors or addition of a mechanical circulatory support device to maintain perfusion
E - Extremis Actual or impending circulatory collapse Typically unconscious Near pulselessness
Cardiac collapse
Multiple defibrillations		 Lactate ≥8 mmol/La CPR (A-modifier)
Severe acidosis•pH ​< ​7.2•Base deficit >10 mEq/L		 Profound hypotension despite maximal hemodynamic support Need for bolus doses of vasopressors
Link to External Table Unavailable

Recommendation Grading

Overview

Title

SHOCK Stages Classification

Authoring Organization

Endorsing Organizations

Publication Month/Year

January 14, 2022

Last Updated Month/Year

February 12, 2024

Supplemental Implementation Tools

Document Type

Consensus

Country of Publication

US

Inclusion Criteria

Male, Female, Adolescent, Adult, Child, Older adult

Health Care Settings

Emergency care, Hospital, Medical transportation

Intended Users

Paramedic emt, nurse, nurse practitioner, physician, physician assistant

Scope

Assessment and screening, Management, Prevention

Diseases/Conditions (MeSH)

D012770 - Shock, Cardiogenic, D012769 - Shock

Keywords

shock, Shock stages

Source Citation

SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies
Naidu, Srihari S. et al. Journal of the Society for Cardiovascular Angiography & Interventions, Volume 1, Issue 1, 100008

Supplemental Methodology Resources

Evidence Tables