Decoding Pulmonary Embolism: Pathophysiology, Diagnosis, and Treatment

Figures

• 

  Figure 1. Diagnostic Algorithm for pulmonary embolism (PE) depending on the patient’s risk category score using the Geneva Clinical Prediction or Wells Criteria. Abbreviations: Pulmonary Embolism Rule Out Criteria (PERC), Pulmonary embolism (PE), Computed tomography pulmonary angiography (CTPA), ventilation/perfusion (V/Q), and extremity compression ultrasonography (CUS).

• 

  Figure 2. Schematic Representation of Coagulation and Clotting Factor Signaling in Thrombus Formation. The cascade involves key coagulation factors such as XII, XIIa, IXa, VIIIa, VIIa, Xa, and XIIIa, which play pivotal roles in the propagation of clotting events. The principles of the coagulation cascade pathways are detailed, highlighting the coordinated activation of these cellular components. The anticoagulant treatments for PE are detailed, encompassing conventional anticoagulants, novel oral anticoagulants, and thrombolytic agents.

• 

  Figure 3. Effects of pulmonary embolism (PE) in the vascular endothelium. PE disrupts normal endothelial function, which can be attributed to multiple factors: vascular remodeling alterations, vasoconstrictor–vasodilator imbalance, anticoagulant levels and procoagulant factors, synthesis of pro-inflammatory molecules, and an increase in oxidative stress, among others. Abbreviations: Nitric oxide (NO), Tissue factor pathway inhibitor (TFPI), heparin sulfate (HS), Tissue factor (TF), von Willebrand Factor (vWF), interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), cell adhesion molecules (CAMs), Nuclear Factor-kappa B (NF-kB), Reactive oxygen species (ROS), and endothelial nitric oxide synthase (eNOS).