Hypoxic pulmonary vasoconstriction (HPV) is an intrinsic property of the lung where vascular smooth muscle will constrict pulmonary circulation in response to areas of hypoxia. In other words, if an alveolus is not being well ventilated (shunt), why waste perfusion on it? Edema, infection, atelectasis, and mucous plugging are just a few examples of etiologies of a hypoxic alveolus. By constricting the pulmonary vessels associated with these alveoli and redistributing that blood to better ventilated pulmonary segments, ventilation-perfusion (V/Q) mismatch is improved.
HPV is divided into two phases: phase 1 begins in several seconds and peaks at 15 minutes and phase 2 begins around 45 minutes and peaks at 2 hours. It is enhanced in the neonatal/fetal circulations, in periods of acidosis (either respiratory or metabolic), hypercapnia, hypoxia (hence the name), and even in iron deficiency.
HPV can be affected by many drugs including ACE inhibitors/ARBs, acetazolamide, inhaled nitric oxide, corticosteroids, PDE inhibitors, calcium channel blockers, and higher concentrations of halogenated volatile agents (isoflurane, desflurane, sevoflurane). Intravenous anesthetics tend to spare HPV. I have seen patients with severe COPD (who have established an HPV pattern chronically) have profound desaturations when drugs like nicardipine drips are started. And it all deals in part with altering their baseline HPV. 🙂
Now how about a classic example we face in cardiothoracic surgery – one lung ventilation (OLV). During OLV, an entire lung is not ventilated. This creates a massive shunt which can lead to hypoxemia… especially in very sick patients with baseline pulmonary pathology. We rely on HPV to improve V/Q mismatch. Arterial blood gases typically show the PaO2 reach its nadir 30 minutes into OLV with a slow improvement over the following 1-2 hours. 🙂
Overall, HPV is a very cool, protective mechanism that is inherent to our pulmonary vasculature. Even denervated transplanted lungs retain this amazing property. 🙂
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