Pulmonary embolism pathophysiology: Difference between revisions
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*Release of inflammatory mediators causing [[atelectasis]] and [[surfactant]] dysfunction. | *Release of inflammatory mediators causing [[atelectasis]] and [[surfactant]] dysfunction. | ||
==Mechanism== | ==Mechanism== | ||
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Revision as of 18:42, 21 December 2011
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Pulmonary Embolism Microchapters |
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Diagnosis |
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Pulmonary Embolism Assessment of Probability of Subsequent VTE and Risk Scores |
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Treatment |
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Follow-Up |
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Special Scenario |
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Trials |
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Pulmonary embolism pathophysiology On the Web |
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Directions to Hospitals Treating Pulmonary embolism pathophysiology |
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Risk calculators and risk factors for Pulmonary embolism pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editors-in-Chief: Ujjwal Rastogi, MBBS [2]
Overview
Pulmonary embolism (PE) occurs when there is an acute obstruction of the pulmonary artery (or one of its branches). Most often this is due to a venous thrombus (blood clot from a vein), which dislodges from its site of formation and embolizes to the arterial blood supply of one of the lungs. This process is termed thromboembolism.
Pathophysiology
Iliofemoral veins are the source of most clinically recognized PE. It can cause death and significant disability.
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
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:
- Generate a systolic pressure (SBP) in excess of 50 mmHg
- Maintain a mean pulmonary artery pressure approximating 40 mmHg
Failure to do so would eventually lead to right heart failure.[1]
Patients with underlying cardiopulmonary disease experience more substantial deterioration in cardiac output than 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}}