Pulmonary embolism pathophysiology
|
Pulmonary Embolism Microchapters |
|
Diagnosis |
|---|
|
Pulmonary Embolism Assessment of Probability of Subsequent VTE and Risk Scores |
|
Treatment |
|
Follow-Up |
|
Special Scenario |
|
Trials |
|
Case Studies |
|
Pulmonary embolism pathophysiology On the Web |
|
Directions to Hospitals Treating Pulmonary embolism pathophysiology |
|
Risk calculators and risk factors for Pulmonary embolism pathophysiology |
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 this formation is termed thromboembolism.
Pathophysiology
- Most pulmonary embolisms 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 nature to which it occludes the vascular tree and its subsequent branches.
Thrombus travels to the lung, and depending on its size, produce variable outcomes.
- Large thrombus: lodge at the bifurcation of the main pulmonary artery or lobar branches, and causes hemodynamic compromise.
- Small thrombus: travel distally and initiate an inflammatory response adjacent to the parietal pleura causing pleuritis and pleuritic chest pain.
Chronic pulmonary hypertension may occur when the initial embolus fail to lyses and also in patients with recurrent thromboembolism.
Gas exchange abnormalities, if present, happen due to a mix of the following factors:
- Mechanical obstruction of the vascular bed.
- Alterations in the ventilation to perfusion ratio.
- Release of inflammatory mediators causing atelectasis and surfactant dysfunction.
Mechanism
The following figure explains the pathophysiology and the cause of death in Pulmonary embolism.[2]
In conditions where more than 2/3rd of the pulmonary artery is occluded, in order to preserve pulmonary perfusion, the right ventricle is forced to: a). Generate a systolic pressure (SBP) in excess of 50 mmHg and b). Maintain a mean pulmonary artery pressure approximating 40 mmHg. Failure to do so would eventually lead to right heart failure.[3]
Patients with underlying cardiopulmonary disease experience more substantial deterioration in cardiac output as compared with otherwise healthy individuals. Also, right ventricular failure following PE is more common in patients with coexisting coronary artery disease.
The following video explains the pathophysiology of DVT and its most common complication, PE. {{#ev:youtube|gGrDAGN5pC0}}
References
- ↑ Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
- ↑ 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.