Pulmonary hypertension pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assistant Editor(s)-in-Chief: Ralph Matar,
Overview
- Whatever the cause is, an initiating factor leads to increased resistance in the pulmonary vasculature causing narrowing of the vessels and impaired blood flow, much as it is harder to make water flow through a narrow pipe as opposed to a wide one.
- As a consequence, the right ventricle adapts by increasing right ventricular systolic pressures to preserve the cardiac output from the right heart.
- Over time, increasing right ventricular systolic pressures will subsequently result in chronic changes in the pulmonary circulation and progressively the affected blood vessels become both stiffer and thicker, further increasing the blood pressure within the lungs and impairing blood flow.
- In addition, the increased workload of the heart causes thickening and enlargement of the right ventricle, making the heart less able to pump blood through the lungs, causing right heart failure.
- As the blood flowing through the lungs decreases, the left side of the heart receives less blood. This blood may also carry less oxygen than normal. Therefore it becomes harder and harder for the left side of the heart to pump to supply sufficient oxygen to the rest of the body, especially during physical activity.
A role for endothelial injury
All classes of pulmonary hypertension are associated with narrowing and obliteration of the pulmonary arterioles due to thickening of the intima by fibromuscular dysplasia.This constant finding has created increased our interest in the role of endothelial injury and the release of vasoactive mediators in the pathogenesis of pulmonary hypertension.These mediators include both vasoconstrictors and vasodilators.The main vasoconstrictor is Endothelin, whereas Nitric Oxide (NO), PGI2 and endothelium derived hyperpolarizing factor (EDHF) are vasodilators of which NO is the most potent in reversing the effects of Endothelin.[1]
Factors determining the ability of the RV to adapt to increased PVR
- Age of the patient at onset.
- Rapidity of onset of pulmonary hypertension.
- Coexisting hypoxemia.
- ↑ Higenbottam Tim(1994) "Pathophysiology of Pulmonary Hypertension, A role for endothelial dysfunction" Chest journal"