SCAI SHOCK Stages Classification Guideline Summary

Key Summary Points

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.
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).
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.
A hub and spoke model for transfer of higher-risk patients including those with a deteriorating SCAI SHOCK stage has been proposed.
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.
The SCAI SHOCK pyramid and associated figure now reflect gradations of severity within each stage and pathways by which patients progress or recover.
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.
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
Stage	Description	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

SHOCK Stages Classification

Key Summary Points

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

Overview

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