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.

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.

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.

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.

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.

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.

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.

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:

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.

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.