PULMONARY EMBOLISM-PATHOLOGY

SUMMARY

1. Summary: Pulmonary artery (PA) occlusion → increased alveolar dead space → V/Q mismatch → vascular constriction → loss of alveolar surfactant with atelectasis.

2. Increased pulmonary vascular resistance leads to increased PA pressure & RV afterload leading to RV dilatation and dysfunction.

3. The pulmonary circulatory system is highly compliant and therefore inherently has high capacitance.

4. Consequently, up to 50% of the lung vasculature can be blocked before increased workload on the right ventricle becomes significant in a normal individual.

5. Massive PE occurs when > 2/3 of functioning lung vasculature is compromised.

6. Lung infarction is rare as the parenchyma is perfused by multiple sources (bronchial & PA circulation, back diffusion through venous system).

7. RV dysfunction → decreased LV preload → hypotension → RV ischemia.

Reference(s)

Wilkinson, I., Furmedge, D. and Sinharay, R. (2017). Oxford handbook of clinical medicine. Oxford: Oxford University Press. Get it on Amazon.
Feather, A., Randall, D. and Waterhouse, M. (2020). Kumar And Clark’s Clinical Medicine. 10th ed. S.L.: Elsevier Health Sciences. Get it on Amazon.
Hannaman, R. A., Bullock, L., Hatchell, C. A., & Yoffe, M. (2016). Internal medicine review core curriculum, 2017-2018. CO Springs, CO: MedStudy.
Therapeutic Guidelines. Melbourne: Therapeutic Guidelines Limited. https://www.tg.org.au [Accessed 2021].