What lab result would the nurse anticipate for a patient with metabolic acidosis?

A. Antihistamines and expectorants:Antihistamines are primarily used for allergic rhinitis and may excessively dry out the sinuses, potentially worsening a headache. Expectorants help thin bronchial secretions but are not the primary treatment for sinus-related nasal congestion. This combination does not directly address the inflammatory pain of a sinus headache.

B. Antibiotics and antivirals:These agents target specific pathogens and do not provide immediate relief for the mechanical symptoms of congestion or pain. Antibiotics are only appropriate if a bacterial etiology is confirmed, and antivirals are rarely used for standard sinusitis. They lack the analgesic properties required to manage an acute headache.

C. Antitussives and mucolytics:Antitussives are used to suppress a non-productive cough and have no role in relieving sinus pressure or headaches. Mucolytics thin mucus but do not provide the vasoconstriction needed to reduce nasal passage edema. This combination fails to address the vascular and inflammatory components of the patient's manifestations.

D. Decongestants and analgesics:Decongestants like pseudoephedrine cause vasoconstriction of the nasal mucosa to reduce edema and improve drainage. Analgesics such as ibuprofen or acetaminophen target the inflammatory pathways responsible for the headache and localized facial pain. Together, they provide the most comprehensive symptomatic relief for sinusitis.

A. Increase the patient's IV fluid rate:Accelerating fluid administration does not address the primary issue of impaired gas exchange or pulmonary ventilation. In fact, excessive fluids could exacerbate low oxygen levels if the patient is developing pulmonary edema. This intervention is irrelevant to resolving acute desaturation.

B. Reassure the patient and continue to monitor:A saturation level of 88% represents significant hypoxemia that requires immediate active intervention to prevent tissue hypoxia. Passive monitoring while a patient is in respiratory distress allows for further physiological decline. Clinical action must prioritize correcting the oxygen deficit over observation.

C. Notify the anesthesiologist immediately:While communication with the surgical team is necessary, the nurse must first stabilize the patient's immediate physiological threat. Delaying life-saving oxygen therapy to place a phone call can lead to avoidable complications. Assessment and immediate intervention must precede notification in emergency situations.

D. Administer supplemental oxygen via nasal cannula:Increasing the fraction of inspired oxygen is the priority action to correct acute hypoxemia. This intervention immediately supports cellular oxygenation and reduces the workload of the heart and lungs. It is the standard initial nursing response for postoperative respiratory depression.