Answer:
HPV is an autoregulatory mechanism to prevent ventilation/perfusion mismatch and improve arterial oxygenation. Proposed mechanisms include an increase in reactive oxygen species in the pulmonary arterial smooth muscle, activation of redox-based oxygen sensors, and an increase in intracellular calcium. HPV is triggered by a decrease in PaO2 within the lung from low FIO2, hypoventilation, or atelectasis. The selective increase of vascular resistance in the hypoxic parenchyma diverts blood away to the better ventilated normoxic lung, decreasing the amount of shunt flow. This is a biphasic response that starts within 15 to 30 minutes from lung collapse, culminates at 120 minutes, and takes hours to reverse after normoxia is restored.
Increasing evidence indicates that significant systemic oxidative stress can be elicited by hyperoxic reperfusion of a lung in which HPV has been sustained for an extended period of time. Although the exact ramifications of this insult remain to be clarified, clinical data suggest an association between the magnitude of the oxidative stress and postoperative cardiopulmonary complications. Recommendations to decrease reexpansion injury include reinflating the collapsed lung with less than 100% FIO2 as well as using protective lung strategies. The lowest FIO2 possible is also recommended.
Reference(s):
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