A nurse is preparing to administer pain medication to a postoperative client who had a total knee replacement and reports pain as 5 on a scale of 0 to 10. Which of the following PRN medications should the nurse plan to administer?

A) Give diphenhydramine IM: Diphenhydramine is an antihistamine that can help alleviate allergic symptoms such as itching, hives, and mild allergic reactions. However, in the case of an anaphylactic reaction, which is a severe and potentially life-threatening allergic reaction, diphenhydramine alone may not be sufficient. While it can be administered as an adjunctive therapy, it is not the primary intervention for anaphylaxis. Therefore, giving diphenhydramine IM should not be the next action after stopping the medication infusion.

B) Elevate the client's legs and feet: Elevating the client's legs and feet is a supportive measure that can help improve venous return to the heart and mitigate symptoms of hypotension. However, in the context of an anaphylactic reaction, the priority is to address airway compromise and cardiovascular collapse, as these are life-threatening complications. Elevating the legs and feet may be considered after administering epinephrine and ensuring stabilization of the client's airway, breathing, and circulation.

C) Replace the infusion with 0.9% sodium chloride: While stopping the infusion of the offending medication is essential in managing an anaphylactic reaction, replacing it with 0.9% sodium chloride solution alone does not address the systemic effects of anaphylaxis. The priority is to administer medications such as epinephrine to reverse the allergic response and stabilize the client's condition. Therefore, replacing the infusion with 0.9% sodium chloride should not be the next action after stopping the medication infusion.

D) Administer epinephrine IM: Epinephrine is the first-line treatment for anaphylaxis due to its rapid onset of action and ability to reverse bronchoconstriction, vasodilation, and increased vascular permeability associated with the allergic reaction. Administering epinephrine IM helps counteract the severe manifestations of anaphylaxis, including respiratory distress and hypotension. Therefore, it is the most appropriate next action after stopping the medication infusion and assessing the client's respiratory status.

D) Oxycodone causes central nervous system depression: Oxycodone is an opioid analgesic that acts centrally on the central nervous system (CNS) to relieve pain. One of the most significant side effects of opioids like oxycodone is respiratory depression, which occurs due to the suppression of the CNS, particularly in the brainstem respiratory centers. The brainstem regulates respiratory rate and rhythm, and when opioids depress these centers, it can lead to decreased respiratory drive, resulting in a decrease in respiratory rate. A respiratory rate of 8/min is significantly below the normal range, indicating respiratory depression caused by oxycodone.

A) Oxycodone inhibits prostaglandin synthesis: Oxycodone does not directly inhibit prostaglandin synthesis. Prostaglandins are lipid compounds with various physiological effects, including inflammation and pain modulation. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, inhibit prostaglandin synthesis by blocking cyclooxygenase enzymes. However, oxycodone primarily acts on opioid receptors in the CNS to relieve pain, rather than through prostaglandin inhibition.

B) Oxycodone promotes vasodilation of cranial arteries: While opioids can cause peripheral vasodilation, particularly in large doses, the primary mechanism of action of oxycodone is not through the promotion of vasodilation of cranial arteries. Vasodilation may occur as a side effect of opioid use, but it is not the primary cause of respiratory depression associated with oxycodone.

C) Oxycodone blocks the sodium channel suspending nerve conduction: This statement describes the mechanism of action of local anesthetics, such as lidocaine, which block sodium channels to inhibit nerve conduction. However, oxycodone is not a sodium channel blocker. Its analgesic effects result from binding to opioid receptors in the CNS, particularly mu-opioid receptors, rather than blocking sodium channels. Therefore, this option is not the pathophysiology for the respiratory rate of 8/min observed in the client receiving oxycodone.