Pulmonary Embolism ABG Question

Sorry in advanced if this is a stupid question. I've been trying to figure out why a PE is considered respiratory alkalosis. I thought it would be a metabolic acidosis with respiratory compensation. Isn't the mechanism for a pulmonary embolism: PE -> decrease PO2 -> lactic acid generation(metabolic acidosis) -> tachypnea (respiratory compensation) I would appreciate any help on what I am missing. This has really been nagging at me today.
Source: Student Doctor Network - Category: Universities & Medical Training Authors: Source Type: forums