Create a one‑page infographic classifying cardiogenic shock by (1) SCAI severity stages A (at‑risk) through E (extremis) with their defining hemodynamic features, (2) hemodynamic phenotypes—left‑ventricular dominant (pulmonary capillary wedge pressure >15 mm Hg, central venous pressure <15 mm Hg), right‑ventricular dominant (central venous pressure >15 mm Hg, pulmonary capillary wedge pressure <15 mm Hg), and biventricular (both pressures >15 mm Hg), and (3) typical etiologies such as acute myocardial infarction, mechanical complications of myocardial infarction, acute decompensated heart failure, severe valvular disease, myocarditis, and malignant arrhythmias, with a concise caption summarizing the definition and progression.

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Cardiogenic Shock Classification Infographic

SCAI Severity Stages (A through E)

The Society for Cardiovascular Angiography and Interventions (SCAI) classification provides the standard framework for staging cardiogenic shock severity, progressing from at-risk patients through extremis, with mortality increasing stepwise through each stage. 1, 2

Stage A: At Risk

  • Clinical features: Normotensive, normal perfusion, clear lungs, no hypoperfusion 1
  • Hemodynamics: Normal cardiac index, normal blood pressure 3
  • Population: Large acute myocardial infarction, prior infarction, acute-on-chronic heart failure symptoms 1
  • Mortality: Lowest risk 3

Stage B: Beginning Shock

  • Clinical features: Relative hypotension OR tachycardia WITHOUT hypoperfusion 1, 2
  • Hemodynamics: Systolic blood pressure may be borderline but tissue perfusion remains adequate 2
  • Key distinction: No evidence of end-organ hypoperfusion (normal lactate, adequate urine output, normal mentation) 2

Stage C: Classic Cardiogenic Shock

  • Clinical features: Hypoperfusion REQUIRING intervention (inotropes, pressors, or mechanical support including ECMO) beyond volume resuscitation 1, 2
  • Hemodynamics:
    • Systolic blood pressure <90 mmHg 1
    • Cardiac index <2.2 L/min/m² 1, 3
    • Lactate >2 mmol/L 1, 3
  • End-organ signs: Cold extremities, confusion, oliguria (<0.5 mL/kg/h) 1, 3
  • Key distinction: Presence of hypoperfusion differentiates Stage C from Stage B 2

Stage D: Deteriorating/Doom

  • Clinical features: Similar to Stage C but WORSENING despite initial interventions 1, 2
  • Temporal criterion: Failure to respond after at least 30 minutes of observation and treatment 2
  • Hemodynamics: Progressive decline in cardiac power output despite escalating support 3
  • Management implication: Requires escalation to advanced mechanical circulatory support 3

Stage E: Extremis

  • Clinical features: Cardiac arrest with ongoing CPR and/or ECMO, supported by multiple interventions 1, 2
  • Hemodynamics: Cardiovascular collapse, refractory hypotension and hypoperfusion 1, 3
  • Key distinction: Requires CPR or equivalent life-sustaining intervention 2
  • Mortality: Highest risk, approaching 50% in-hospital mortality 1, 3

Hemodynamic Phenotypes

Cardiogenic shock phenotypes are defined by filling pressures in the left and right ventricles, guiding mechanical circulatory support selection. 3, 4

Left-Ventricular Dominant Shock

  • Hemodynamic criteria:
    • Pulmonary capillary wedge pressure (PCWP) >15 mmHg 3
    • Central venous pressure (CVP) or right atrial pressure <15 mmHg 3
  • Clinical presentation: Prominent pulmonary congestion, rales, dyspnea, clear jugular veins 3
  • Pathophysiology: Left ventricular failure with backward transmission of pressure into pulmonary circulation 1

Right-Ventricular Dominant Shock

  • Hemodynamic criteria:
    • Central venous pressure (CVP) >15 mmHg 3
    • Pulmonary capillary wedge pressure (PCWP) <15 mmHg 3
  • Clinical presentation: Jugular venous distension, hepatomegaly, peripheral edema, clear lung fields 3
  • Pathophysiology: Right ventricular failure with systemic venous congestion but preserved left-sided function 3

Biventricular Shock

  • Hemodynamic criteria:
    • BOTH pulmonary capillary wedge pressure >15 mmHg AND central venous pressure >15 mmHg 3
  • Clinical presentation: Combined pulmonary congestion AND systemic venous congestion 3
  • Pathophysiology: Failure of both ventricles with elevated filling pressures bilaterally 1
  • Prognosis: Typically requires biventricular mechanical support and carries worse outcomes 3

Common Etiologies

Acute myocardial infarction accounts for 81% of cardiogenic shock cases, but non-ischemic etiologies are increasing in contemporary practice. 5, 6

Acute Myocardial Infarction

  • Incidence: Occurs in 7-10% of acute myocardial infarction cases 3
  • Mechanism: Ischemic myocardial damage reduces contractility, decreasing cardiac output 1, 5
  • Management priority: Immediate coronary angiography within 2 hours with intent to revascularize 3

Mechanical Complications of Myocardial Infarction

  • Types: Ventricular septal rupture, acute mitral regurgitation from papillary muscle rupture, free wall rupture with tamponade 3
  • Timing: Typically occur 3-7 days post-infarction 3
  • Management: Requires urgent surgical intervention; IABP may provide temporary stabilization 3

Acute Decompensated Heart Failure

  • Mechanism: Acute-on-chronic heart failure with progressive pump failure 1
  • Hemodynamic pattern: Follows indolent course, more commonly requires biventricular support compared to acute myocardial infarction-related shock 3
  • Precipitants: Medication non-adherence, arrhythmias, infection, uncontrolled hypertension 7

Severe Valvular Disease

  • Acute presentations: Acute aortic regurgitation (endocarditis, dissection), acute mitral regurgitation (chordae rupture, endocarditis) 3
  • Chronic presentations: Critical aortic stenosis, severe mitral stenosis with acute decompensation 3
  • Management: Urgent valve repair or replacement often required 3

Myocarditis

  • Mechanism: Inflammatory myocardial injury causing acute contractile dysfunction 6
  • Presentation: May present with fulminant shock requiring mechanical circulatory support 3
  • Prognosis: Potential for complete recovery if bridged successfully through acute phase 3

Malignant Arrhythmias

  • Types: Sustained ventricular tachycardia, ventricular fibrillation, complete heart block, supraventricular tachycardia with rapid ventricular response 3
  • Mechanism: Loss of coordinated atrial-ventricular contraction or critically reduced diastolic filling time 3
  • Management: Immediate cardioversion or pacing; treat underlying ischemia or electrolyte abnormalities 3

Defining Hemodynamic Features

Cardiogenic shock diagnosis requires the combination of systolic blood pressure <90 mmHg, end-organ hypoperfusion, lactate >2 mmol/L, and cardiac index <2.2 L/min/m². 1, 3

Core Hemodynamic Parameters

  • Cardiac index: <2.2 L/min/m² (severe dysfunction <1.8 L/min/m²) 1, 3
  • Systolic blood pressure: <90 mmHg for ≥30 minutes or requiring vasopressors/inotropes to maintain >90 mmHg 3
  • Cardiac power output: <0.6 W identifies refractory shock requiring mechanical circulatory support 3
  • Systemic vascular resistance: Elevated (compensatory vasoconstriction) 1, 3

Filling Pressures

  • Pulmonary capillary wedge pressure: >15 mmHg (often >20 mmHg in severe cases) 1, 3
  • Central venous pressure: >15 mmHg in right ventricular or biventricular involvement 3

Perfusion Markers

  • Lactate: >2 mmol/L indicates anaerobic metabolism 1, 3
  • Mixed venous oxygen saturation (SvO₂): <70% reflects inadequate oxygen delivery 8
  • Urine output: <0.5 mL/kg/h indicates renal hypoperfusion 3

Pathophysiology Summary

Cardiogenic shock results from primary cardiac dysfunction creating a vicious cycle: reduced cardiac output triggers compensatory vasoconstriction that increases afterload, further impairing the failing heart and leading to multi-organ dysfunction. 1

The pathophysiology involves:

  • Reduced cardiac output from depressed contractility 1
  • Compensatory systemic vasoconstriction to maintain perfusion pressure, paradoxically increasing cardiac afterload 1
  • Neurohormonal activation (renin-angiotensin-aldosterone system, sympathetic nervous system) perpetuating the cycle 1
  • Systemic inflammation with pathological vasodilation from nitric oxide, interleukins, and tumor necrosis factors 1
  • Macro- and micro-hemodynamic alterations culminating in multi-organ dysfunction 1

References

1
Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

3
Guideline

Hemodynamic Differentiation of Shock Types

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

7
Guideline

Cardiorenal Syndrome: Definition, Pathophysiology, and Clinical Presentation

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

8
Guideline

Shock Management Guidelines

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

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