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.

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.

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.

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.

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.

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-fits-all approach, represents the future of cardiogenic shock care.