This is my best interpretation with a source and paragraph from the source listed:
In anemia, hemoglobin available is decreased. This causes decreased oxygen binding, and ultimately less oxygen is available for release onto tissues.
"The circulatory adjustments in response to anemia will be similar to those of the preceding case. In order to maintain tissue oxygen consumption at baseline levels associated with a normal oxygen carrying capacity of blood, the reduction in oxygen delivery will lead to an increase in capillary perfusion, and oxygen extraction will increase. Arteriolar dilation and viscosity reduction (for the case of a reduction in Hct) will cause blood flow and oxygen delivery to increase. Both oxygen extraction and oxygen delivery will continue to increase until the oxygen requirements of the tissues are met or until the capacity to increase oxygen extraction and delivery has been reached. The resulting situation is one in which venous oxygen content and PvO2 are less than normal. Since PaO2 is normal for all the anemic situations considered, this defect is not sensed by the respiratory chemoreceptors. Thus, increasing the inspired oxygen fraction is not helpful except for the case of CO poisoning, where high inspired oxygen (e.g., 100% oxygen at ambient barometric pressure or placement of the subject into a hyperbaric chamber) competes with CO binding at the heme site (recall Haldane's first law)." - https://www.ncbi.nlm.nih.gov/books/NBK54113/
Also, to eliminate the other options:
Hypoventillation would have an increased pCO2 and decreased pO2.
High altitude wuold have low PO2, low pCO2 (Hyperevntillation)
V/Q mismatch would also have a low pO2 and high pCO2, since gases are exchanging.
Hyperventillation would have a normal PO2 and low PCO2