Show Summary Details
Page of

Structure and function of the pulmonary circulation 

Structure and function of the pulmonary circulation

Chapter:
Structure and function of the pulmonary circulation
Author(s):

Nicholas W. Morrell

DOI:
10.1093/med/9780199204854.003.161501_update_001

Update:

Chapter reviewed; minor alterations made, now includes content from retired Chapter 16.15.3.

Updated on 27 Nov 2014. The previous version of this content can be found here.
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy).

date: 23 April 2017

The normal pulmonary circulation distributes deoxygenated blood at low pressure and high flow to the pulmonary capillaries for the purposes of gas exchange. The structure of pulmonary blood vessels varies with their function—from large elastic conductance arteries, to small muscular arteries, to thin-walled vessels involved in gas exchange.

Pulmonary vascular resistance (PVR) is about one-tenth of systemic vascular resistance, with the small muscular and partially muscular arteries of 50 to 150 µm diameter being the site of the greatest contribution to resistance. The gas-exchanging capillary surface area (c.125 m2) contains a blood volume of about 150 ml at any one time, with the blood–gas barrier being only 0.2 to 0.3 µm thick at its thinnest part. In the normal pulmonary circulation, a large increase in cardiac output causes only a small rise in mean pulmonary arterial pressure because PVR falls on exercise: this is accomplished by a combination of vascular distensibility and recruitment. Pulmonary blood flow is heterogeneous: gravity causes increased blood flow in the more dependent parts of the lung; within a horizontal region—or within an acinus—blood-flow heterogeneity is imposed by the branching pattern of the vessels.

Many neural and humoral mediators can influence pulmonary vascular tone, including nitric oxide and prostacyclin. Alveolar hypoxia causes constriction of the small pulmonary arteries, whereas systemic arteries dilate when hypoxic: this hypoxic pulmonary vascoconstriction can reduce venous admixture and improve arterial oxygenation in the presence of bronchial obstruction. Despite large regional differences in the matching of ventilation and perfusion within the normal lung, the overall lung ventilation–perfusion ratio is maintained remarkably steady at around 0.85.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.