Pulmonary embolism pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] The APEX Trial Investigators; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Overview

Pulmonary embolism (PE) occurs when there is an acute obstruction of the pulmonary artery or one of its branches. It is commonly caused by a venous thrombus that has dislodged from its site of formation and embolized to the arterial blood supply of one of the lungs. The process of clot formation and embolization is termed thromboembolism. PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the capillary by the embolism, but also due to pulmonary vasoconstriction. When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload might lead to the dilatation of the right ventricular wall and subsequent right heart failure.[1][2]

Pathophysiology

Clot Formation

  • Most PE commonly originate from a thrombus that has formed in the iliofemoral vein, deep within the vasculature of the lower extremity.
  • Less commonly, a PE may also arise from a thrombus in the upper extremity veins, renal veins, or pelvic veins.
  • The development of thrombosis is classically due to a group of conditions referred to as Virchow's triad. Virchow's triad includes alterations in blood flow, factors in the vessel wall, and factors affecting the properties of the blood. It is common for more than one risk factor to be present. Shown below is an image depicting Virchow's triad.

Embolization

  • After its formation, a thrombus might dislodge from the site of origin and circulate through the inferior vena cava, into the right ventricle, and into the pulmonary vasculature.[3]

Hemodynamic Consequences

  • Hemodynamic complications and the nature of the clinical manifestations of a PE depend on a number of factors:[4]
    • The size of the embolus and the degree to which it occludes the vascular tree and its subsequent branches
    • The presence of any preexisting cardiopulmonary conditions
    • The role of chemical vasoconstriction as it is insinuated by platelets releasing serotonin and thromboxane in addition to other vasoconstrictors
    • The presence of pulmonary artery dilatation and subsequent reflex vasoconstriction
  • PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the capillary by the embolism, but also due to pulmonary vasoconstriction. Pulmonary vasoconstriction can be either biochemically mediated, hypoxia induced, or reflex-induced.[5][6]
  • When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload might lead to the dilatation of the right ventricular wall and subsequent right heart failure. In addition, the elevated pulmonary vascular resistance causes a decrease in the left ventricular preload and consequently leads to systemic hypotension.[1][2] In patients with underlying cardiopulmonary disease, the cardiac output suffers substantial deterioration in overall output as compared to otherwise healthy individuals.

Abnormalities in Gas Exchange

  • In PE, hypoxemia occurs mainly due to the ventilation perfusion mismatch.[7] In fact, in the setting of an acute PE, the ventilation to perfusion ratio (V/Q) increases and the dead space enlarges.[8]

References

  1. 1.0 1.1 1.2 Wiedemann HP, Matthay RA (1985). "Acute right heart failure". Crit Care Clin. 1 (3): 631–61. PMID 3916797.
  2. 2.0 2.1 2.2 Lualdi JC, Goldhaber SZ (1995). "Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications". Am Heart J. 130 (6): 1276–82. PMID 7484782.
  3. McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.
  4. Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
  5. Elliott CG (1992). "Pulmonary physiology during pulmonary embolism". Chest. 101 (4 Suppl): 163S–171S. PMID 1555481.
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 Smulders YM (2000). "Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction". Cardiovasc Res. 48 (1): 23–33. PMID 11033105.
  7. 7.0 7.1 7.2 7.3 7.4 Goldhaber SZ, Elliott CG (2003). "Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis". Circulation. 108 (22): 2726–9. doi:10.1161/01.CIR.0000097829.89204.0C. PMID 14656907.
  8. Itti E, Nguyen S, Robin F, Desarnaud S, Rosso J, Harf A; et al. (2002). "Distribution of ventilation/perfusion ratios in pulmonary embolism: an adjunct to the interpretation of ventilation/perfusion lung scans". J Nucl Med. 43 (12): 1596–602. PMID 12468507.

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