Pulmonary vascular resistance

[Northerncardinal]

Can anyone plz explain why the pulmonary vascular resistance increases in Hemorrhagic shock?? I understand that systemic vascular resistance would increase due to Sympathetic activation.

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[Ven0m]

I think it's because of the property of pulmonary vasculature called "hypoxic pulmonary vasoconstriction". If there is less oxygen in those vessels (such as in hemorrhagic shock, where there is too little blood), the vessels will constrict. Its good when there is only a part of the lung that's dysfunctional, so that those vessels can constrict and redirect blood to healthier parts of the lung, but since hemorrhagic shock involves a massive blood loss, all of the pulmonary vessels will constrict due to those unique properties.

Also, if less capillaries are filled in the pulmonary vasculature, it increase the total resistance of the parallel circuit of the pulmonary vasculature. i.e., if you take away an alternative path, then the blood can only go to the open paths, which increases resistance to flow. Check kaplan physiology notes about series and parallel circuits, it explains it well. Conversely, in exercise, the increase in blood flow to the lung recruits additional pulmonary capillaries, decreasing pulmonary resistance. however, other factors during exercise which increase total peripheral resistance overweigh that decrease in pulmonary resistance, so pulmonary pressures increase slightly.

 

[Phloston]

I would imagine that even in a state of hypovolemia that alveolar oxygen shouldn't change.

In hypovolemia you're going to have sympathetic overdrive which will cause a surge in alpha-1 agonism to maintain BP. And you've got alpha-1 receptors in the pulmonary vessels (unrelated to beta-2 on bronchial smooth muscle). I found this article:

https://www.ncbi.nlm.nih.gov/pubmed/10378571

 

[Ven0m]

I would imagine that even in a state of hypovolemia that alveolar oxygen shouldn't change.

In hypovolemia you're going to have sympathetic overdrive which will cause a surge in alpha-1 agonism to maintain BP. And you've got alpha-1 receptors in the pulmonary vessels (unrelated to beta-2 on bronchial smooth muscle). I found this article:

https://www.ncbi.nlm.nih.gov/pubmed/10378571

Actually this does make sense, alveolar oxygen shouldn't change and thus pulmonary vasculature O2 pressure shouldnt change either