Explain the pathophysiology of pulmonary embolism


Assignment task:

Explain the Pathophysiology of Pulmonary Embolism caused by a Venous Thrombosis:

A pulmonary embolism (PE) is an emergent respiratory complication. This is because an embolus from another area of the body, typically the lower extremities, migrates into the pulmonary circulation. The most frequent cause is a blood clot. This is why, when patients have a pulmonary embolism, a d-dimer may be drawn as well as an ultrasound of the lower extremities to determine where the clot came from. Although the most common cause, a blood clot is not the only cause of a PE. Simply put, it can be material that is brought to the lungs from another part of the body, such as fat from a femoral fracture. (PE). To continue, when discussing blood clots, Virchow's Triad becomes relevant. It highlights a group of risk factors for developing a blood clot. The 3 factors are endothelial injury, blood stasis, and hypercoagulable states (Kushner, et al. 2024). Each factor has a multitude of examples.

To begin, endothelial injury can be caused by uncontrolled hypertension, diabetes, metabolic syndrome, smoking, as well as a PICC line. Although very uncommon, a PICC line can cause endothelial damage upon insertion of the line (Gao, et al. 2024). Not only do PICCs present a minimal risk for a VTE, but they can also cause an air embolism if improperly flushed as well as if they are not removed correctly (Gonzalez and Cassaro, 2023). Proper removal of a PICC requires a patient to hold their breath during removal as the nurse incrementally withdraws the catheter as well as remaining in a supine position for up to 30 minutes to prevent an air embolism. If they are unable to hold their breath to cause a Valsalva response, then they can also exhale during removal.

For blood stasis, there are a multitude of conditions and behaviors that cause this. For example, blood stasis can be caused by a sedentary lifestyle. Also, a malignancy can compress a vein leading to stagnancy of blood (Kushner, et al. 2024). The same can occur in pregnancy. During pregnancy, the release of a hormone called progesterone leads to venous dilation as well as renal vasodilation. To sustain blood pressure due to progesterone's vasodilatory effects, increased sodium retention and ultimately water retention occurs in the kidneys (Kushner, et al. 2024). Due to possible compression from the amniotic sac, as well as increased volume, blood stasis and lower extremity edema can occur (Kushner, et al. 2024). Another cause of blood stasis is atrial fibrillation (Kushner, et al. 2024). In the left atrium, specifically, there is a structure called a left atrial appendage that is like a sac and can lead to blood pooling, causing a clot (Kushner, et al. 2024). However, blood may pool in all chambers of the heart during atrial fibrillation and drastically increase one's risk for an embolic event. Also, after an MI affecting the left ventricle, blood pooling and clot formation can occur due to left ventricular myocardial dysfunction (Kushner, et al. 2024). These are examples of conditions that can cause blood stasis.

The hypercoagulability of blood has a multitude of causes as well. For example, some genetic factors are involved with deficiencies of anti-clotting factors, such as a deficiency in antithrombin III. Also, mutations of factor V Leiden and prothrombin G2021A (Senst, et al. 2023). Malignancy can also lead to hypercoagulable blood due to its production of tissue factor and "cancer procoagulant" (Senst, et al. 2023). Also, for women, "oral contraception and hormone replacement therapy are a risk factor for thrombosis" (Senst, et al. 2023). So, it has been shown that there are a multitude of factors that can lead to a pulmonary embolism.

During a PE, most commonly a thrombus disrupts blood flow in the pulmonary circulation (Vyas, et al. 2024). There are two types of PE: hemodynamically unstable, in which the patient develops hypotension due to obstructive shock, and hemodynamically stable PE (Vyas, et al. 2024). As a result of the occlusion of pulmonary blood flow, impaired gas exchange occurs as well as a ventilation/ perfusion (V/Q) mismatch. Ventilation remains the same, but alveolar perfusion decreases (Vyas, et al. 2024). This leads to dead space ventilation and hypoxemia (low oxygen levels in the blood). To continue, serotonin and inflammatory mediators are released, and the SNS is activated due to decreased oxygen states. The result is an increased oxygen demand and vasoconstriction, which worsens blood flow to the lungs and may cause respiratory alkalosis and hypocapnia. Lung surfactant secretion diminishes, also contributing to an increased respiratory drive. If a large embolus is present, this can lead to pulmonary infarction, dysrhythmias, heart failure, shock, and death (Winton and Brashers, 2023, p. 1180). If the emboli is small enough that pulmonary infarction does not occur, the body naturally dissolves the clot utilizing the fibrinolytic system. Pulmonary function will eventually return to near baseline functioning (Winton and Brashers, 2023, p. 1180). Treatment, once diagnosed, is mainly composed of symptom management until the clot resolves. Also, the patient will be started on anticoagulant therapy and will be discharged on a long-term anticoagulant medication regimen, such as Eliquis. Need Assignment Help?

References:

Gao, X., Mi, X., Hou, S., & Kang, C. (2024). Analysis of Factors Related to Thrombosis in Patients with PICC Placements. Medicine, 103(5), e37168.

Gonzalez, R. and Cassaro, S. (2023). Percutaneous Central Catheter. StatPearls.

Kushner, A., West, W., Khan Suheb, M., and Pillarisetty, L. (2024). Virchow Triad. StatPearls.

Senst, B., Tadi, P., Basit, H., and Jan, A. (2023). Hypercoagulability. StatPearls.

Vyas, V., Sankari, A., and Goyal, A. (2024). Acute Pulmonary Embolism. StatPearls.

Winton, M. and Brashers, V. (2023). Chapter 35 Alterations of Pulmonary Function. In: Rogers, J. McCance and Huether's Pathophysiology: The Biologic Basis for Disease in Adults and Children, 9th ed. Elsevier, p. 1180.

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