2025 PACUPrep BCCCP Preparatory Course Cardiogenic Shock Diagnostic Assessment and SCAI Classification in Cardiogenic Shock
Diagnostic and SCAI Classification of Cardiogenic Shock

Diagnostic and SCAI Classification of Cardiogenic Shock

Objective Icon A target symbol, representing a learning objective.

Objective

Apply diagnostic and classification criteria to assess a patient with cardiogenic shock and guide initial management.

1. Introduction

Early recognition of cardiogenic shock (CS) is crucial for reducing mortality and limiting end-organ injury. A structured evaluation confirms CS, helps exclude conditions that mimic CS, and stratifies severity to guide timely escalation of care.

Key Considerations:

  • Impact: Delayed diagnosis significantly increases mortality and the risk of irreversible organ damage.
  • Variability: Institutions may differ in their specific biomarker thresholds, the extent of imaging utilization, and protocols for hemodynamic monitoring.
  • Goals of Evaluation:
    1. Confirm CS by integrating clinical, laboratory, and imaging criteria.
    2. Exclude other shock etiologies (e.g., hypovolemia, cardiac tamponade, massive pulmonary embolism, sepsis).
    3. Assign a SCAI stage (A through E) to inform the urgency of intervention and appropriate resource allocation.
Key Pearl: Multidisciplinary Shock Team

Early activation of a multidisciplinary shock team, typically including specialists from critical care, cardiology, and clinical pharmacy, streamlines the diagnostic process and accelerates the initiation of appropriate therapy. This collaborative approach has been linked to improved patient outcomes.

2. Clinical Presentation

Cardiogenic shock classically presents with hypotension and evidence of tissue hypoperfusion. Rapid recognition of both hemodynamic instability and peripheral signs of poor perfusion is essential for timely intervention.

Common Signs and Symptoms:

  • Hypotension: Systolic blood pressure (SBP) <90 mmHg or Mean Arterial Pressure (MAP) <65 mmHg, sustained for more than 30 minutes, or the requirement for vasoactive medications to maintain these pressures.
  • Signs of Hypoperfusion: Cool, clammy, or mottled extremities; capillary refill time >3 seconds; oliguria (urine output <30 mL/h or <0.5 mL/kg/h).
  • Neurologic Changes: Confusion, agitation, or a decreased level of responsiveness.
  • Pulmonary Findings: Crackles on lung auscultation, or evidence of pulmonary edema on chest X-ray, indicating congestion.
  • Signs of Congestion: Elevated jugular venous pressure (JVP >8 cm H₂O), peripheral edema.
  • Tachycardia: Often a compensatory response, though it may be blunted in patients taking beta-blockers.

SUSPECT CS Mnemonic:

  • S: Symptoms (e.g., chest pain, dyspnea)
  • U: Urine output significantly reduced (<30 mL/h)
  • S: Sustained hypotension (SBP <90 mmHg or MAP <65 mmHg)
  • P: Perfusion markers (cool extremities, delayed capillary refill, mottling)
  • E: ECG changes or Echocardiographic evidence of dysfunction
  • C: Congestion (elevated JVP, pulmonary edema, peripheral edema)
  • T: Triage (consider early shock team activation)

3. Laboratory Assessment

Biomarkers are vital for confirming tissue hypoperfusion, identifying the underlying etiology of shock (especially acute myocardial infarction), and tracking the patient’s response to therapeutic interventions.

Key Laboratory Markers:

  • Lactate: Levels >2 mmol/L are associated with worse outcomes. A therapeutic goal is often ≥10% lactate clearance every 2–4 hours with effective resuscitation.
  • Troponin: Elevated troponin levels detect acute myocardial injury, a common precipitant of CS. Interpret in the context of baseline elevations if known (e.g., in chronic heart failure or renal disease).
  • BNP/NT-proBNP: These markers are typically elevated in both acute and chronic heart failure, reflecting ventricular wall stress. Levels can be influenced by age, renal function, and obesity.
  • End-Organ Function Tests: Rising serum creatinine (kidney), transaminases (liver), and bilirubin (liver) indicate evolving organ dysfunction due to hypoperfusion.
Key Pitfall: Interpreting Lactate Levels

A normal or near-normal lactate level early in the presentation does not definitively exclude cardiogenic shock, especially if other signs of hypoperfusion are present. Always integrate the clinical perfusion exam and monitor lactate trends over time, as a rising lactate is a critical warning sign.

4. Imaging Modalities

Echocardiography and chest radiography are key initial imaging tools. They provide rapid assessment of cardiac function, help identify pulmonary congestion, and can guide the exclusion of mechanical or extracardiac causes of shock.

Primary Imaging Techniques:

  • Echocardiography:
    • Transthoracic Echocardiogram (TTE): Essential for assessing left ventricular ejection fraction (LVEF), regional wall motion abnormalities (suggesting ischemia), right ventricular (RV) function, and estimating pulmonary capillary wedge pressure (PCWP).
    • Transesophageal Echocardiogram (TEE): Used when TTE windows are suboptimal or for more detailed evaluation of valvular structures or the aorta.
    • Detection of Mechanical Complications: Crucial for identifying acute issues like ventricular septal defect (VSD), papillary muscle rupture leading to severe mitral regurgitation, or cardiac tamponade.
  • Chest X-ray: May show signs of pulmonary congestion such as interstitial infiltrates, Kerley B lines, cardiomegaly, or pleural effusions.
  • Advanced Imaging (CT/MRI): Generally reserved for cases with suspected pulmonary embolism, aortic dissection, or other complex intracardiac or extracardiac pathology. These should not delay initial resuscitation and management.
VExUS Score Diagram A diagram showing the three core components of the VExUS (Venous Excess Ultrasound) score used to assess venous congestion in critically ill patients. It shows the Inferior Vena Cava (IVC), Hepatic Vein, and Portal Vein waveforms. VExUS Score Components for Assessing Venous Congestion 1. IVC Diameter Plethoric (>2 cm) 2. Hepatic Vein Pulsatile (S > D wave) 3. Portal Vein Pulsatility Index >30%
Figure 1: The VExUS Score. This POCUS-based score combines assessment of the Inferior Vena Cava (IVC) diameter with Doppler flow patterns in the hepatic, portal, and intrarenal veins to grade the severity of venous congestion, which is a strong predictor of acute kidney injury.
Controversy: Non-invasive PCWP Estimation

Non-invasive estimates of PCWP using Doppler echocardiography are useful for rapid initial assessment and can guide early fluid management. However, their accuracy can be limited in patients with mixed shock states, significant valvular disease, or arrhythmias. Invasive measurements may be necessary for precise hemodynamic guidance in complex cases.

5. Hemodynamic Monitoring

Invasive hemodynamic monitoring, primarily with a pulmonary artery catheter (PAC), provides definitive hemodynamic data. This information is crucial for tailoring therapy when non-invasive assessments are inconclusive or when the patient’s shock state is refractory to initial interventions.

Pulmonary Artery Catheter (PAC):

  • Indications: Diagnostic uncertainty (e.g., differentiating CS from other shock types), refractory hypotension despite initial therapy, or when planning and titrating advanced mechanical circulatory support (MCS).
  • Technical Tips: Ensure accurate zeroing of transducers at the phlebostatic axis (mid-axillary line), confirm characteristic waveform morphology for each pressure, and record serial readings to track trends.
  • Non-invasive Alternatives: Echocardiographic Doppler for cardiac output, and bioreactance/bioimpedance monitors exist. However, these are often more operator-dependent and may be less accurate in hemodynamically unstable patients or those with arrhythmias.
  • Potential Complications: Include catheter-related bloodstream infections, thrombosis, arrhythmias during insertion, and, rarely, pulmonary artery injury or rupture.
Key Hemodynamic Parameters in Cardiogenic Shock (via PAC)
Parameter Typical Value/Threshold in CS Significance
Cardiac Index (CI) <2.2 L/min/m² Indicates reduced cardiac pump function and systemic hypoperfusion.
Pulmonary Capillary Wedge Pressure (PCWP) >15 mmHg (often >18 mmHg) Reflects elevated left ventricular filling pressures and risk of pulmonary edema.
Systemic Vascular Resistance (SVR) >1200 dyn·s/cm⁵ Typically elevated due to compensatory vasoconstriction in classic CS. May be inappropriately low in vasoplegic CS.
Central Venous Pressure (CVP) / Right Atrial Pressure (RAP) >10–12 mmHg Indicates elevated right ventricular preload and systemic venous congestion.
Pulmonary Artery Pulsatility Index (PAPi) <1.5 (often <1.0 in severe RV failure) Suggests right ventricular dysfunction or failure.
Key Pearl: Impact of Hemodynamic Profiling

Studies suggest that early and complete hemodynamic profiling using a PAC in patients with cardiogenic shock is associated with lower in-hospital mortality. This detailed assessment can optimize the selection and timing of vasoactive medications and mechanical circulatory support.

6. Exclusion of Shock Mimics

It is critical to differentiate cardiogenic shock from other types of shock—such as hypovolemic, obstructive, or distributive (septic) shock—to ensure appropriate and timely therapy. Misdiagnosis can lead to harmful interventions.

Differentiating Features of Shock Mimics:

  • Hypovolemic Shock: Characterized by low CVP/PCWP and signs of dehydration or blood loss. Often shows a brisk positive response to a careful fluid challenge.
  • Cardiac Tamponade (Obstructive): Presents with pericardial effusion on echocardiography, often with diastolic chamber collapse. Pulsus paradoxus (>10 mmHg drop in SBP during inspiration) may be present.
  • Massive Pulmonary Embolism (Obstructive): Leads to acute right ventricular dilation and dysfunction, visible on echocardiography. Diagnosis is confirmed with CT angiography.
  • Septic Shock (Distributive): Often features a hyperdynamic cardiac output (initially), low SVR, and an identifiable infectious source. The lactate pattern and response to fluids may differ from CS.
Key Pitfall: Mixed Shock Phenotypes

Mixed shock phenotypes (e.g., cardiogenic shock complicated by sepsis or vasoplegia) are common in critically ill patients. Continual reassessment of hemodynamics, perfusion, and response to therapy is essential as the patient’s condition and treatments evolve.

7. SCAI Shock Classification

The Society for Cardiovascular Angiography & Interventions (SCAI) developed a 5-stage classification system (A through E) to standardize the assessment of cardiogenic shock severity. This system aids in risk stratification, communication among healthcare providers, and guiding resource allocation.

A
At Risk
No signs or symptoms of CS. Large MI without shock.
B
Beginning
Hypotension OR tachycardia alone, without signs of hypoperfusion.
C
Classic
Hypoperfusion present. Needs intervention (drugs or mechanical support).
D
Deteriorating
Worsening despite initial support. Escalating therapies needed.
E
Extremis
Refractory shock, circulatory collapse, or cardiac arrest with CPR.
Figure 2: The SCAI Staging System for Cardiogenic Shock. This classification (Stages A-E) provides a framework for risk stratification and communication. Mortality increases significantly with each advancing stage, from approximately 5% in Stage A to over 50% in Stage E.

SCAI Stages:

  • Stage A (At risk): Patients at risk for CS (e.g., large myocardial infarction) but without current signs of hypotension or hypoperfusion.
  • Stage B (Beginning): Presence of hypotension (SBP <90 mmHg or MAP <70 mmHg) or tachycardia (>100 bpm) without clinical signs of hypoperfusion.
  • Stage C (Classic): Clinical evidence of hypoperfusion (e.g., cool extremities, oliguria, altered mental status, lactate >2 mmol/L) requiring intervention (e.g., inotropes, vasopressors, or mechanical circulatory support). Typically CI <2.2 L/min/m² and PCWP >15 mmHg if measured.
  • Stage D (Deteriorating): Patients in Stage C who are worsening despite initial supportive therapies and require escalation of interventions. May show rising lactate, worsening acidosis, or need for multiple pressors/escalating MCS.
  • Stage E (Extremis): Patients in refractory circulatory collapse, often with ongoing cardiac arrest, or profound shock requiring multiple escalating interventions including CPR or ECLS (ECMO).

Prognostic Correlation: Mortality increases progressively with each stage, from approximately 5% in Stage A to over 50% in Stage E.

Controversies and Considerations with SCAI Staging
  • Interobserver Variability: Some degree of interobserver variability can occur in stage assignment, particularly in patients with chronic hypotension or mixed shock states where distinguishing features might be less clear-cut.
  • Dynamic Nature: SCAI stages are not static; a patient’s condition can change rapidly. Frequent reassessment and restaging are necessary to accurately reflect the patient’s current trajectory and guide ongoing management.

8. Integration and Decision Algorithm

A systematic, stepwise workflow is essential to synthesize multimodal data (clinical, laboratory, imaging, hemodynamic) to confirm CS, exclude mimics, accurately stage severity, and guide initial management decisions effectively.

Stepwise Diagnostic and Management Workflow:

1. Bedside Evaluation
Vitals, perfusion exam, mental status
2. Point-of-Care Labs
Lactate, troponin, BNP, ABG/VBG
3. Urgent TTE
LV/RV function, PCWP est., mechanical complications
4. Initial Measures
Volume optimization (fluid/diuretics), start norepinephrine if MAP <65 mmHg
5. If Refractory/Ambiguous
Insert PAC (CI, PCWP, SVR, PAPi). Exclude mimics via targeted imaging (e.g., CT for PE/dissection).
6. Assign SCAI Stage & Escalate
Escalate to advanced therapies (vasoactives, MCS) for Stage C–E.
Figure 3: Stepwise Diagnostic and Management Workflow for Cardiogenic Shock. This algorithm outlines key steps from initial bedside assessment to advanced interventions and staging. Step 7 (not shown in flow diagram for brevity) is continuous reassessment every 2-4 hours and adjustment of interventions.

Step 7 (Continuous): Reassess clinical status, perfusion, labs, and hemodynamics every 2–4 hours (or more frequently if unstable) and adjust interventions accordingly. Consider repeat imaging or hemodynamic measurements as needed.

Key Pearl: Integrated Approach

Avoid basing critical management decisions on a single isolated parameter (e.g., one blood pressure reading or lactate value). A dynamic, integrated approach that considers all available clinical, laboratory, imaging, and hemodynamic data over time ensures more accurate diagnosis and tailored, effective interventions.

9. Pearls and Pitfalls Summary

Effective management of cardiogenic shock requires attention to detail, continuous reassessment, and a multidisciplinary approach. Here are some summary points:

  • Serial Assessments: Emphasize trends over isolated values for labs (lactate, creatinine), hemodynamics, and clinical signs. A patient’s trajectory is more informative than a single snapshot.
  • SUSPECT CS Mnemonic: Utilize this tool to ensure comprehensive bedside assessment and avoid missing early or subtle signs of cardiogenic shock.
  • Non-invasive Limitations: Be aware of the limitations of non-invasive estimates of filling pressures (e.g., echo-derived PCWP), especially in complex or mixed shock states. Invasive monitoring may be needed for clarity.
  • PAC Use: While early, appropriate use of a Pulmonary Artery Catheter (PAC) for complete hemodynamic profiling can guide therapy and may improve outcomes, always balance the potential benefits against procedural risks.
  • Dynamic SCAI Staging: Re-evaluate the patient’s SCAI shock stage frequently, as their clinical status can change rapidly, necessitating adjustments in management intensity.
  • Multidisciplinary Collaboration: Engage a multidisciplinary shock team early. This collaboration enhances diagnostic accuracy, optimizes resource utilization, and facilitates timely decision-making for advanced therapies.

References

  1. Sinha SS, Morrow DA, Kapur NK, et al. 2025 Concise clinical guidance: an ACC expert consensus statement on evaluation and management of cardiogenic shock. J Am Coll Cardiol. 85(16):1618–1641.
  2. Laghlam D, Benghanem S, Ortuno S, et al. Management of cardiogenic shock: a narrative review. Ann Intensive Care. 14:45.
  3. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update. J Am Coll Cardiol. 79:933–946.
  4. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on classification of cardiogenic shock. Catheter Cardiovasc Interv. 94(1):29–37.
  5. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: AHA scientific statement. Circulation. 136(16):e232–268.
  6. Garan AR, Kanwar M, Thayer KL, et al. Complete hemodynamic profiling with PAC in cardiogenic shock is associated with lower mortality. JACC Heart Fail. 8:903–913.
  7. Tehrani BN, Truesdell AG, Sherwood MW, et al. Standardized team-based care for cardiogenic shock. J Am Coll Cardiol. 73(13):1659–1669.
  8. Waksman R, Pahuja M, van Diepen S, et al. Standardized definitions for cardiogenic shock research and MCS devices: SHARC. Circulation. 148:1113–1126.
  9. Thiele H, Zeymer U, Neumann F, et al. IABP-SHOCK II: long-term outcome of IABP in AMI-CS. Circulation. 139:395–403.
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