What are the differences in invasive hemodynamic monitoring between pulmonary embolism (PE) and pulmonary edema (PEd)?

Differences in Invasive Hemodynamic Monitoring Between Pulmonary Embolism and Pulmonary Edema

Pulmonary embolism (PE) and pulmonary edema (PEd) show distinctly different hemodynamic patterns on invasive monitoring, with PE characterized by elevated pulmonary vascular resistance, right ventricular dysfunction, and normal pulmonary capillary wedge pressure, while pulmonary edema typically shows elevated left-sided filling pressures with normal pulmonary vascular resistance. 1

Key Hemodynamic Parameters

Pulmonary Embolism

• Right-sided measurements:
  • Elevated pulmonary artery pressure (PAP)
  • Markedly increased pulmonary vascular resistance (PVR)
  • Elevated right ventricular (RV) end-diastolic pressure
  • Normal or low pulmonary capillary wedge pressure (PCWP)
  • Reduced cardiac index, especially in massive PE (often ≤1.8 L/min/m²) 2

Pulmonary Edema

• Left-sided measurements:
  • Elevated pulmonary capillary wedge pressure (PCWP) >18 mmHg
  • Normal or only mildly elevated pulmonary vascular resistance
  • Elevated left ventricular end-diastolic pressure
  • Variable cardiac index (may be reduced in cardiogenic pulmonary edema)

Right Ventricular Function Assessment

Pulmonary Embolism

• RV dilatation (found in at least 25% of PE patients) 1
• RV/LV ratio >1.0 (McConnell sign - hypokinesia of RV free wall with preserved apical contractility) 1
• Flattened interventricular septum with leftward shift (D-shaped left ventricle)
• Tricuspid regurgitation with elevated pressure gradient
• 60/60 sign: acceleration time of pulmonary ejection <60 ms with midsystolic "notch" and peak systolic gradient <60 mmHg 1

Pulmonary Edema

• Typically preserved RV function
• No significant RV dilatation
• Normal interventricular septal position
• May show left ventricular dysfunction

Specific Hemodynamic Patterns

Massive Pulmonary Embolism

• Significant reduction in cardiac index (<1.8 L/min/m²) 2
• Systemic hypotension or shock
• Markedly elevated total pulmonary resistance
• RV failure with increased RV work and oxygen consumption 1
• Decreased LV preload due to reduced pulmonary blood flow

Acute Pulmonary Edema

• Elevated left atrial pressure
• Increased PCWP (>18-20 mmHg)
• Preserved pulmonary blood flow
• Variable cardiac output depending on etiology

Diagnostic Pitfalls

1. Coexisting conditions: Patients with chronic heart failure may develop PE, making interpretation challenging.

2. Right heart thrombi: Present in up to 4% of unselected PE patients (up to 18% in ICU settings), and strongly associated with RV dysfunction and higher mortality 1.

3. Chronic vs. acute findings: Chronic thromboembolic pulmonary hypertension shows RV hypertrophy and very high pulmonary pressures (>60 mmHg), unlike acute PE 1.

4. Misinterpretation of pressure tracings: Damped waveforms can lead to inaccurate measurements.

Clinical Implications

• In suspected massive PE with shock, echocardiography showing RV overload may justify emergency reperfusion treatment if immediate CT angiography isn't feasible 1.

• Absence of echocardiographic signs of RV overload in a patient with shock practically excludes PE as the cause of hemodynamic compromise 1.

• Invasive hemodynamic assessment may help identify higher-risk patients with submassive PE who might benefit from more aggressive interventions despite normal blood pressure 2.

• Hemodynamic monitoring during thrombolytic therapy shows significant decrease in total pulmonary resistance after just 0.5 hours with reteplase and after 2 hours with alteplase 3.

By understanding these distinct hemodynamic patterns, clinicians can more accurately differentiate between PE and pulmonary edema, leading to appropriate therapeutic decisions that can significantly impact morbidity and mortality outcomes.