SCAI Classification for Cardiogenic Shock
The SCAI (Society for Cardiovascular Angiography and Interventions) classification is a five-stage system (A through E) that risk-stratifies patients with cardiogenic shock based on physical examination findings, biochemical markers, and hemodynamics, with validated stepwise increases in mortality from Stage A to Stage E. 1, 2
The Five SCAI Stages
Stage A: At Risk
- Clinical Profile: Patients are normotensive with normal tissue perfusion, clear lung fields, and no signs of hypoperfusion 1, 3
- Hemodynamics: Normal cardiac index and blood pressure 3
- Typical Patients: Those with large acute myocardial infarction, prior infarction, or acute-on-chronic heart failure symptoms who have not yet developed shock 1
- Key Feature: No current signs or symptoms of shock, but at elevated risk for deterioration 1, 2
Stage B: Beginning Cardiogenic Shock
- Clinical Profile: Relative hypotension or tachycardia without evidence of end-organ hypoperfusion 1, 3, 2
- Distinguishing Feature: Normal lactate levels, adequate urine output, and preserved mental status despite hemodynamic abnormalities 3, 2
- Critical Point: This is the pre-hypoperfusion stage—patients show early warning signs but have not yet crossed into true shock 2
Stage C: Classic Cardiogenic Shock
- Clinical Profile: Hypoperfusion requiring intervention (inotropes, pressors, or mechanical support including ECMO) beyond volume resuscitation 1, 2
- Hemodynamic Criteria:
- Physical Findings: Cold extremities, oliguria, altered mental status, and relative hypotension 1, 3
- Key Threshold: Presence of tissue hypoperfusion distinguishes Stage C from Stage B 2
Stage D: Deteriorating/Doom
- Clinical Profile: Similar presentation to Stage C but worsening despite initial interventions 1, 2
- Temporal Criterion: Failure to respond after ≥30 minutes of observation and treatment 3, 2
- Management Implication: Initial therapy has failed; escalation to advanced mechanical circulatory support is typically required 3
- Prognosis: Significantly higher mortality than Stage C due to refractory nature 1, 4
Stage E: Extremis
- Clinical Profile: Cardiac arrest with ongoing CPR and/or ECMO support, accompanied by refractory hypotension and hypoperfusion 1, 3
- Hemodynamics: Cardiovascular collapse requiring multiple simultaneous interventions 1
- Mortality: In-hospital mortality approaches 50% or higher 3, 4
- Key Feature: Represents the most severe end of the shock spectrum with circulatory collapse 2
Hemodynamic Parameters for Classification
Cardiac Index Thresholds:
Blood Pressure Criteria:
- Stage C and higher: Systolic BP <90 mmHg for ≥30 minutes or requiring vasopressors to maintain >90 mmHg 1, 3
Lactate as Perfusion Marker:
Cardiac Power Output:
- Refractory shock threshold: <0.6 W (most critical marker for identifying need for mechanical support) 3
Filling Pressures:
- Pulmonary capillary wedge pressure >15 mmHg indicates left ventricular failure 3
- Central venous pressure >15 mmHg suggests right ventricular or biventricular involvement 3
Shock Phenotypes Within SCAI Stages
Left Ventricular-Dominant:
Right Ventricular-Dominant:
Biventricular:
- Both PCWP >15 mmHg and CVP >15 mmHg 3
- Combined pulmonary and systemic congestion; typically requires biventricular support 3
Cardiac Arrest Modifier
Critical Consideration: At every SCAI stage, the presence of cardiac arrest significantly increases mortality 1, 5
- Cardiac arrest is common across all stages and confers independent mortality risk 5
- Stage E specifically includes ongoing cardiac arrest requiring CPR 1
- Post-arrest patients who are comatose (Glasgow Coma Scale <8) should receive targeted temperature management 5
Validated Prognostic Value
Mortality Increases Stepwise:
- Multiple validation studies demonstrate progressive mortality increases from Stage A through E 1, 4
- The Mayo Clinic series of 10,004 patients showed stepwise mortality increases after multivariable adjustment 1
- The National Cardiogenic Shock Initiative demonstrated survival rates of 76% (Stage C), 76% (Stage D), and 58% (Stage E) 6
Reproducibility:
- Near-perfect inter-rater agreement (kappa = 0.975-0.985) between independent clinicians 6
- Classification remains relatively stable after the first 6-12 hours of admission 7
Practical Application Algorithm
Step 1: Initial Assessment
- Measure systolic blood pressure, heart rate, and calculate shock index (HR ÷ SBP) 8
- Assess for hypoperfusion: lactate level, urine output (<0.5 mL/kg/h), mental status, extremity temperature 1, 3
- Obtain cardiac index via echocardiography or pulmonary artery catheter if available 1, 3
Step 2: Assign SCAI Stage
- No hypotension or hypoperfusion but high-risk features → Stage A 1
- Hypotension or tachycardia WITHOUT hypoperfusion → Stage B 1, 2
- Hypoperfusion requiring pharmacologic/mechanical support → Stage C 1, 2
- Stage C features but worsening after 30 minutes of treatment → Stage D 1, 2
- Cardiac arrest with ongoing CPR/ECMO → Stage E 1, 2
Step 3: Identify Phenotype (Stages C-E)
- Obtain invasive hemodynamics via pulmonary artery catheter 1, 3
- Measure PCWP and CVP to determine LV-dominant, RV-dominant, or biventricular pattern 3
- Calculate cardiac power output if considering mechanical support 3
Step 4: Reassess Every 6-12 Hours
- Most patients reach their maximum stage within 6 hours of admission 7
- Stage progression or regression guides treatment escalation or de-escalation 7
- Patients in Stage E at 24 hours have <20% survival regardless of baseline stage 6
Common Pitfalls and Caveats
Pitfall 1: Assuming Normal Blood Pressure Excludes Shock
- Stage B patients may have near-normal systolic pressure despite early shock physiology 1
- "Preshock" patients with compensatory vasoconstriction can maintain BP >90 mmHg despite tissue hypoperfusion 1
- Always assess lactate and end-organ perfusion markers, not just blood pressure 3
Pitfall 2: Delayed Recognition of Stage Progression
- 78% of patients change SCAI stage within 6 hours of admission 7
- Failure to reassess frequently can miss deterioration from Stage C to D 7
- Implement continuous monitoring protocols rather than single time-point assessments 4
Pitfall 3: Confusing Distributive and Cardiogenic Shock
- Late-stage septic shock can develop myocardial depression but maintains decreased SVR (distributive pattern) 3
- Cardiogenic shock has elevated SVR as a compensatory mechanism 3
- Use hemodynamic profiling (cardiac index, SVR, PCWP) to differentiate when clinical picture is unclear 3
Pitfall 4: Underestimating Cardiac Arrest Impact
- Cardiac arrest at any stage dramatically worsens prognosis 1
- Do not assume electrolyte abnormalities caused the arrest; treat underlying shock 5
- Hypokalemia often results from cardiac arrest itself rather than being the primary cause 5
Pitfall 5: Inadequate Phenotyping
- Failing to distinguish LV-dominant, RV-dominant, and biventricular patterns leads to inappropriate mechanical support selection 3
- Biventricular shock requires different support strategies than isolated LV failure 3
- Obtain invasive hemodynamics early in Stage C or higher 1
Integration with Treatment Decisions
Stage A: Close monitoring, optimize medical therapy, address precipitating factors 1
Stage B: Initiate inotropes/pressors if hemodynamics worsen, prepare for potential escalation 1, 2
Stage C: Immediate coronary angiography if AMI-related (within 2 hours), consider mechanical support if cardiac power output <0.6 W 1, 3
Stage D: Escalate to advanced mechanical circulatory support (Impella, VA-ECMO) based on phenotype 3
Stage E: Ongoing CPR/ECMO, multidisciplinary shock team activation, consider palliative care consultation if futile 1