SHOCK Stages Classification
Publication Date: January 13, 2022
Last Updated: March 14, 2022
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 | |||
| 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 |
Recommendation Grading
Overview
Title
SHOCK Stages Classification
Authoring Organization
Society for Cardiovascular Angiography and Interventions
Endorsing Organizations
American College of Cardiology
American College of Emergency Physicians
American Heart Association
European Society of Cardiology
International Society for Heart and Lung Transplantation
Society of Critical Care Medicine
Society of Thoracic Surgeons
Publication Month/Year
January 13, 2022
Last Updated Month/Year
April 1, 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