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HPV Inhibition: Drugs

Hypoxic pulmonary vasoconstriction (HPV) is a physiologic mechanism by which lung perfusion is adjusted to match ventilation through the contraction of vascular smooth muscle in the pulmonary circulation in response to low regional partial pressure of oxygen. It is of particular importance in patients with lung disease and during one-lung ventilation, when there is significant heterogeneity in alveolar ventilation throughout the lungs, and attenuation of the reflex may lead to arterial hypoxemia. HPV is affected by numerous factors, including pH, PCO2, temperature, cardiac output, and several drugs, including anesthetic agents.

Drugs that potentiate HPV:

  • Catecholamines (epinephrine, norepinephrine, phenylephrine, dopamine, dobutamine)
  • Almitrine (respiratory stimulant)
  • NSAIDS (animal studies only, inhibits production of prostacyclin)

Drugs that inhibit HPV:

  • Acetazolamide (high doses only)
  • Nitric Oxide (causes localized pulmonary vasodilation in ventilated lung regions)
  • Nitric Oxide Donors (nitroprusside, nitroglycerine)
  • Corticosteroids
  • Phosphodiesterase Inhibitors (“oral sildenafil almost abolishes the HPV response in healthy volunteers”)
  • Prostacyclin (systemic or inhaled, with inhaled form primarily affecting the ventilated lung region)
  • Calcium Channel Blockers (verapamil, nifedipine)
  • ACE Inhibitors & Angiotensin Receptor Blockers
  • Endothelin Antagonists (sitaxsentan, bosentan)
  • Halogenated Volatile Anesthetics (isoflurane, sevoflurane, desflurane)
    • No difference between these three agents at equal MAC

Drugs that have not been demonstrated to affect HPV:

  • IV Anesthetics
  • Nitrous Oxide


  1. Lumb AB, Slinger P. Hypoxic pulmonary vasoconstriction: physiology and anesthetic implications. Anesthesiology. 2015 Apr;122(4):932-46. Link