Hypoxic Pulmonary Vasoconstriction (HPV)

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’ve seen patients with severe COPD (who have established an HPV pattern chronically) have profound hemoglobin oxygen desaturations when drugs like nicardipine drips are started. Why? Because pulmonary vessels which were previously constricted by HPV and now dilated but still supplying alveoli that are poorly ventilated. This worsens V/Q matching and results in hypoxemia.

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. 🙂

Drop me a comment below with questions!

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  1. Question, does short-duration systemic hypoxemia cause HPV?

    By short duration I mean seconds to say 30 minutes.
    By hypoxemia, I mean SpO2 percentages <90% as measured by a pulse oximeter. Or more extreme, SpO2 <85%.

    Background: I've been repeatedly told to avoid SpO2 percentages <90% when exercising. Ideally, I should keep SpO2 at 93% or higher. The reason I was told was that low SpO2 levels would (further) constrict the blood vessels in my lungs. I just can't see the connection between systemic hypoxemia and blood vessel constriction due to lack of air in the alveoli. I mean, regardless of systemic SpO2, my lungs are being ventilated.

    I was diagnosed with CTEPH in early 2022. We started a therapy of sildenafil and oral anticoagulation (warfarin). I used to be a very active endurance athlete. With my doctors' permission, I added exercise to this cocktail. After 3 months, I can say that the therapy seems to be working. My 6MWD improved from 395m to 510m.

    I am not a doctor or medical professional of any kind. I am a certified personal trainer and running coach. I am not looking for medical advice. But I'd be happy to get an answer to my question.

    Thank you!

    • Hey Greg! Wonderful question! HPV is the pulmonary blood vessels’ response to alveolar hypoxemia. The partial pressure of oxygen in the alveolus (PAO2) is a very important determinant in this response; however, HPV is also attenuated by the partial pressure of oxygen in the arterial and venous blood. I think the recommendation is erring on the side of safety to avoid anything that could compound any increase in pulmonary vascular resistance caused by CTEPH. Sildenafil will also attenuate the HPV response (hard to constrict if you’re on a pulmonary vasodilator).

      The physiology is interesting, but at the end of the day, everyone’s body responds differently. I’m happy to hear the medical regimen is working well for you! Best wishes!

      • Thank you very much! You replied promptly, something rarely seen these days. Thanks for that as well.

  2. I’ve come across this article before but I had trouble understanding it. Now it made more sense to me since we’re done with cardio-pulmonary physiology. Thank you so much!

  3. Love the picture and the explanation! I tried to make similar pictures but with the effect of inhaled prostacyclin or nitric oxide – but yours is better.


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