Pulmonary embolism pathophysiology
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Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Pulmonary embolism 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.
Pathophysiology
Clot Formation
- Most pulmonary emboli commonly originate in the iliofemoral vein, deep within the vasculature of the lower extremity.
- Less commonly, a pulmonary embolism may also arise in the upper extremity veins, renal veins, or pelvic veins.
- The nature of the clinical manifestation of a pulmonary embolism depends on a number of factors:[1]
- The presence of any preexisting cardiopulmonary conditions.
- The role of chemical vasoconstriction as it is insinuated by platelets releasing serotonin and thromboxane which adhere to the embolus.
- The presence of pulmonary artery dilatation and subsequent reflex vasoconstriction.
- The size of the embolus and the degree to which it occludes the vascular tree and its subsequent branches.
Embolization
- After formation, a thrombus will travel from the site of origin and circulate through the inferior vena cava into the right ventricle and on into the pulmonary vasculature where it will lodge.[2]
- Depending upon the patient, there can be one or many pulmonary emboli present. The size of the clot(s) and their physiologic impact will depend largely on the individual patient and subsequent anatomy of the vasculature. [2]
Physiologic Complications
- Hemodynamic complications arise as a result of the obstruction of flow within the pulmonary arteries.
- When there is a 50-60% reduction in perfusion, the following complications may arise:[2]
- Increased resistence in the pulmonary vessels.
- Pulmonary hypertension
- Right ventricular strain
- Congestive heart failure
- Vasoconstriction
- In 10% of all pulmonary embolism cases, the pulmonary embolism develops into a pulmonary infarction. This is an exceedingly rare complication.[2]
- Long term complications:[2]
- [[Chronic obstructive pulmonary hypertension]]
- Ventilation/perfusion ratio (V/Q ratio)
Mechanism
- Current research suggests that a pulmonary embolism arises through the following progression of events.[3]
Comorbidites
- In circumstances where more than two-thirds of the pulmonary artery is occluded, the right ventricle needs to find ways to preserve pulmonary perfusion. Some of the adaptation techniques displayed by the right ventricle are as follows:
- Generate a systolic blood pressure in excess of 50 mmHg.
- Maintain an average pulmonary artery pressure of approximately 40 mmHg.
- Without these adapations, a pulmonary embolism will lead to right heart failure.[4]
- In patients with underlying cardiopulmonary disease, the cardiac output suffers substantial deterioration in overall output as compared to otherwise healthy individuals.
- In patients with coexisting coronary artery disease, right ventricular failure is more common following a pulmonary embolism as compared to those without coexisting CAD.
References
- ↑ Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
- ↑ 2.0 2.1 2.2 2.3 2.4 McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.
- ↑ Fengler BT, Brady WJ (2009). "Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm". Am J Emerg Med. 27 (1): 84–95. doi:10.1016/j.ajem.2007.10.021. PMID 19041539. Retrieved 2011-12-21. Unknown parameter
|month=ignored (help) - ↑ Benotti JR, Dalen JE (1984). "The natural history of pulmonary embolism". Clin Chest Med. 5 (3): 403–10. PMID 6488744.