2025 PACUPrep BCCCP Preparatory Course Atrial Fibrillation and Flutter Diagnosis and Classification of Atrial Arrhythmias
Cardiogenic Shock: Assessment, Monitoring, and Classification

Cardiogenic Shock: Assessment, Monitoring, and Classification

Objectives Icon A checkmark inside a circle, symbolizing achieved goals.

Learning Objectives

  • Recognize bedside signs and laboratory markers of cardiogenic shock.
  • Apply point-of-care echocardiography for rapid differential diagnosis.
  • Understand indications and measurements from pulmonary artery catheterization.
  • Use the SCAI 5-stage system to stratify shock severity and guide interventions.
  • Identify current gaps and research directions in shock monitoring.

1. Bedside Assessment and Laboratory Evaluation

Rationale: Early recognition and differentiation of cardiogenic shock (CS) from other shock states are paramount for initiating life-saving therapies. The initial assessment combines physical examination with key laboratory markers to confirm the presence of both cardiac dysfunction and end-organ hypoperfusion.

A. Vital Signs and Physical Exam

The classic presentation of CS involves hypotension and tachycardia. However, the physical exam provides a more nuanced picture of the underlying hemodynamics.

  • Hypotension: Defined as a sustained systolic blood pressure (SBP) < 90 mm Hg for over 30 minutes, or the need for vasopressor support to maintain an SBP ≥90 mm Hg.
  • Signs of Hypoperfusion (The “Cold” Profile): Cool, clammy, or mottled extremities signal intense peripheral vasoconstriction. A capillary refill time greater than 3 seconds and a quantitative mottling score are strongly associated with increased mortality. Oliguria (<30 mL/h) and altered mental status (confusion, lethargy) are also critical indicators of end-organ malperfusion.
  • Signs of Congestion (The “Wet” Profile): Jugular venous distension (JVD) is a direct sign of elevated right atrial pressure and systemic congestion. Pulmonary rales on auscultation indicate pulmonary edema from elevated left-sided filling pressures. A narrow pulse pressure (<25% of SBP) suggests a critically low stroke volume.
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: Detecting “Preshock”

A significant portion of patients present with “normotensive shock” or “preshock” (SCAI Stage B). They may have a normal or near-normal SBP but exhibit clear signs of malperfusion, such as rising lactate or cool extremities. Identifying these patients early, before the onset of profound hypotension, is crucial for preventing progression to more advanced shock stages.

B. Key Laboratory Biomarkers

Laboratory tests are essential to confirm the diagnosis, assess severity, and monitor response to therapy. They provide objective evidence of organ injury and metabolic derangement.

Key Biomarkers in the Evaluation of Cardiogenic Shock
Biomarker Typical Threshold Clinical Interpretation Therapeutic Goal / Note
Lactate >2 mmol/L Gold standard for tissue hypoperfusion and anaerobic metabolism. Target ≥10% clearance every 2-6 hours as a marker of successful resuscitation.
BNP/NT-proBNP Significantly elevated Indicates high ventricular filling pressures and wall stress. A 30–50% reduction from peak levels suggests effective decongestion.
High-Sensitivity Troponin Elevated (often markedly) Confirms acute myocardial injury, the most common cause of CS. Trend is more important than absolute value; interpret in clinical context.
Arterial Blood Gas (ABG) pH < 7.35 Metabolic acidosis (lactic acidosis) confirms systemic hypoperfusion. Monitor for worsening acidemia, which indicates failing compensation.
Liver Function Tests (ALT/AST) >2x Upper Limit of Normal “Shock liver” indicates severe hepatic hypoperfusion. Rapid rises are common and can be an early indicator of SCAI Stage C/D.

2. Advanced Imaging and Point-of-Care Ultrasound (POCUS)

Rationale: Rapid, non-invasive imaging is essential to confirm the etiology of shock, rule out mechanical complications, and guide initial therapy.

A. Formal Echocardiography

A comprehensive transthoracic or transesophageal echocardiogram is the cornerstone of diagnostic imaging in CS. It provides critical information on:

  • Left and Right Ventricular Function: Assesses global and regional wall motion abnormalities to confirm ischemic etiology and quantifies ejection fraction.
  • Valvular Integrity: Can rapidly diagnose acute, severe mitral regurgitation (e.g., from papillary muscle rupture) or aortic regurgitation.
  • Mechanical Complications: The only reliable non-invasive tool to identify ventricular septal defects, free wall rupture, or cardiac tamponade.
  • Hemodynamic Estimation: Doppler imaging can estimate filling pressures, stroke volume, and cardiac output, providing a non-invasive hemodynamic profile.

B. Point-of-Care Ultrasound (POCUS)

POCUS has emerged as a vital bedside tool for the initial assessment and ongoing monitoring of shock. Protocols like the RUSH (Rapid Ultrasound for Shock and Hypotension) exam allow clinicians to quickly assess the “pump, tank, and pipes.” More recently, the VExUS (Venous Excess Ultrasound) score has gained prominence for quantifying systemic venous congestion, which is a key driver of end-organ injury in CS.

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.

3. Invasive Hemodynamic Monitoring

Rationale: While POCUS provides excellent qualitative data, the pulmonary artery catheter (PAC) remains the gold standard for quantitative hemodynamic assessment, enabling precise titration of therapies in complex or refractory shock.

A. The Pulmonary Artery Catheter (PAC)

The PAC provides direct measurement of intracardiac pressures and cardiac output, allowing for the calculation of key hemodynamic parameters:

  • Central Venous Pressure (CVP): Reflects right atrial pressure and systemic venous congestion.
  • Pulmonary Capillary Wedge Pressure (PCWP): An estimate of left atrial pressure; a key marker of left-sided filling pressures and pulmonary congestion. A PCWP >18 mm Hg is highly suggestive of cardiogenic pulmonary edema.
  • Cardiac Output/Index (CO/CI): The definitive measure of pump function. A CI < 2.2 L/min/m² is a diagnostic criterion for CS.
  • Systemic Vascular Resistance (SVR): Calculated to assess afterload. In classic CS, SVR is high as a compensatory response to low CO.
  • Pulmonary Artery Pulsatility Index (PAPi): A specific marker of right ventricular function. A PAPi < 1.0 is highly suggestive of severe RV failure.
Controversy Icon A chat bubble with a question mark, indicating a point of controversy or debate. Controversy: Routine vs. Selective PAC Use

The routine use of PACs in all CS patients has been debated for decades. The ESCAPE trial (2005) showed no benefit for routine PAC use in advanced heart failure. However, modern consensus suggests a paradigm of “selective early use.” In undifferentiated shock, when response to initial therapy is poor, or when considering advanced mechanical support, the PAC provides invaluable data that can guide therapy and improve outcomes. The PAC is a tool for diagnosis and management, not a therapy itself.

4. Shock Classification and Staging

Rationale: Standardized classification systems are essential for communication, risk stratification, and guiding the escalation of care.

A. Hemodynamic Profiles (Forrester Classification)

The original Forrester classification stratified patients based on clinical signs of perfusion (“cold” vs. “warm”) and congestion (“wet” vs. “dry”), which correlated with PAC-derived CI and PCWP. This simple 2×2 table remains a useful conceptual framework at the bedside. Most CS patients present as “Cold and Wet” (low CI, high PCWP).

B. The SCAI 5-Stage Classification

In 2019, the Society for Cardiovascular Angiography & Interventions (SCAI) introduced a 5-stage classification (A through E) to provide a more granular and dynamic description of shock severity. This system has been widely adopted and validated, showing a stepwise increase in mortality with each stage.

Figure 2: The SCAI Staging System for Cardiogenic Shock. This classification provides a framework for risk stratification, with mortality increasing significantly from Stage A (<5%) to Stage E (>60%). It emphasizes the continuum of shock and the importance of early intervention.

5. Pearls, Pitfalls, and Research Gaps

Rationale: Mastery of CS management requires understanding clinical nuances and recognizing the limits of current evidence.

Key Clinical Pearls

  • Right Ventricular (RV) Failure is Different: CS from RV failure presents with high CVP and JVD but often clear lungs (“cold and dry”). These patients are preload-dependent and may worsen with diuretics but improve with cautious fluid administration.
  • The “Shock Team” Approach: A multidisciplinary team (Cardiology, Critical Care, Cardiac Surgery) approach to CS, often guided by a standardized protocol, has been shown to improve outcomes by facilitating rapid diagnosis and timely escalation to mechanical circulatory support.

Common Pitfalls

  • Misattributing AKI: Attributing oliguria and rising creatinine solely to “cardiorenal syndrome” without recognizing severe hypoperfusion as the primary driver, thereby delaying inotropes or MCS.
  • Over-diuresis: Aggressive diuresis in a patient who is “wet” but also profoundly “cold” can reduce preload to a critical point, worsening cardiac output and hypoperfusion.

Knowledge Gaps and Future Directions

Despite advances, many questions remain. Optimal timing and selection of mechanical circulatory support devices are subjects of ongoing trials. The role of novel biomarkers for predicting recovery versus deterioration is an active area of research. Finally, developing personalized resuscitation strategies based on unique patient phenotypes, rather than a one-size-for-all approach, represents the future of cardiogenic shock care.

References

  1. Sinha SS, Morrow DA, Kapur NK, et al. 2025 Concise clinical guidance: An ACC expert consensus statement on the evaluation and management of cardiogenic shock. J Am Coll Cardiol. 2025;85(16):1618–1641.
  2. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: A scientific statement from the American Heart Association. Circulation. 2017;136(16):e232-e268.
  3. Laghlam D, Benghanem S, Ortuno S, et al. Management of cardiogenic shock: a narrative review. Ann Intensive Care. 2024;14(1):45.
  4. Jones AE, Shapiro NI, Trzeciak S, et al; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010;303(8):739-746.
  5. Samsky MD, Morrow DA, Proudfoot AG, et al. Cardiogenic Shock After Acute Myocardial Infarction: A Review. JAMA. 2021;326(18):1840–1850.
  6. Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J. 2020;12(1):16.
  7. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv. 2019;94(1):29-37.
  8. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies. J Am Coll Cardiol. 2022;79(10):933-946.
  9. Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018;137(20):e578-e622.
  10. Binanay C, Califf RM, Hasselblad V, et al; ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005;294(13):1625-1633.
  11. Ranka S, Mastoris K, Kapur NK. The Role of Invasive Hemodynamics in the Management of Cardiogenic Shock. Curr Heart Fail Rep. 2021;18(5):266-277.
  12. Mullens W, Damman K, Harjola VP, et al. The use of diuretics in heart failure with congestion — a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2019;21(2):137-155.
  13. Forrester JS, Diamond G, Chatterjee K, Swan HJ. Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts). N Engl J Med. 1976;295(24):1356-1362.
  14. Tehrani BN, Truesdell AG, Sherwood MW, et al. Standardized team-based care for cardiogenic shock. J Am Coll Cardiol. 2019;73(13):1659-1669.
  15. Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is a determinant of survival in patients with severe sepsis and septic shock. Crit Care Med. 2004;32(8):1637-1642.
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