Last updated: 05/28/2019
Hypoxic pulmonary vasoconstriction (HPV)refers to the phenomenon of reflexive contraction of smooth muscle in the vasculature of the pulmonary circulation in response to regional low alveolar oxygen tension. This is in contrast to the systemic circulation, where regional hypoxemia typically results in vasodilation..
HPV can be inhibited by several agents commonly used in anesthetic practice. The physiologic consequences of HPV inhibition are of much greater relative importance during one-lung ventilation compared to dual-lung.
Volatile anesthetics: The three mostcommonly used volatile anesthetics (sevoflurane, isoflurane, desflurane) all inhibit HPV in a dose-dependent fashion. Halothane inhibits HPV to a greater extent.As these agents act locally, if there is no ventilation to a given area of the lung, there will not be inhibition of HPV.
Inhaled nitric oxide: inhibits HPV by the well described vasodilatoryeffect of NO. In comparison, nitrous oxide, much more common in clinical use,has no significant effect on HPV.
Systemic agents: non-inhaled drugs are not dependent on ventilation to inhibit HPV.
- Nitroprusside and nitroglycerin – these agents produce nitric oxide, which then causes inhibition of HPV as described above.
- Phosphodiesterase inhibitors: impede the breakdown of cGMP, resulting in more NO, leading to increased pulmonary arterial dilation.
Other agents relevant to anesthetic practice that cause inhibition of HPV:
- Calcium channel blockers
- ACE inhibitors
It is worthwhile to note that while having well-known systemic vasodilatory effects, propofol has not been shown to inhibit HPV.
- Lumb AM, Slinger P. Hypoxic Pulmonary Vasoconstriction: Physiology and Anesthetic Implications. Anesthesiology 4 2015, Vol.122, 932-946. Link
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