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I'm not sure what the mechanism is, but the nurse is only partially right. An increase in pCO2 causes vasoconstriction in the pulmonary vasculature and vasodilation EVERYWHERE else. CO2 causes constriction in the pulmonary vasculature because an increase in pC02 sends the message there is damage/shunting here, sending blood here will not effectively oxygenate it so blood is preferentially sent to a different part of the lung where it will receive better oxygenation.
Decreased PCO2 causes cerebral vasoconstriction thereby decreasing cerebral blood flow and decreasing intracranial pressure. Ideal PCO2 levels to treat increased intracranial pressure are 30 to 35. Levels < 30 cause excessive vasoconstriction and secondary ischemia and should not be used. Continuous ETCO2 monitoring is helpful. Abrupt cessation of hyperventilation may cause rebound cerebral vasodilitation and increased intracranial pressure.