ABPANC CPANFree Certified Post Anesthesia Nurse practice test

Correct answer: B. Administer sugammadex 2 mg/kg IV and continue monitoring

A TOF ratio below 0.9 and a head-lift under 5 seconds indicate clinically significant residual neuromuscular blockade (RNMB). Sugammadex at 2 mg/kg IV is the appropriate dose for moderate residual block (TOF count ≥2) and rapidly encapsulates rocuronium, providing complete, reliable reversal. Neostigmine cannot be safely re-dosed after prior administration (ceiling effect, risk of cholinergic excess) and is not reliable at low TOF ratios when used with steroidal NMBAs. Supplemental oxygen alone does not address the underlying pharmacologic cause. Dismissing the finding risks progressive hypoxemia and airway compromise.

Correct answer: B. Post-dural puncture headache from cerebrospinal fluid leak

Post-dural puncture headache (PDPH) classically presents as a positional, bilateral frontocervical headache that is significantly worse in the upright position and relieved by lying flat, resulting from CSF leakage through the dural puncture site and subsequent intracranial hypotension. Epidural hematoma presents with back pain and progressive neurological deficits rather than positional headache. Migraine is not characteristically postural. Hypertensive encephalopathy produces headache regardless of position and is associated with markedly elevated blood pressure and potential neurological changes.

Correct answer: B. Stage II (Excitement/Delirium)

Stage II anesthesia (the excitement or delirium stage) is characterized by loss of consciousness with accompanying agitation, combativeness, irregular breathing, and reflex activity including breath-holding or vomiting risk; the patient cannot follow commands. This stage is encountered during both induction and emergence as anesthetic depth passes through light planes. Stage I involves analgesia with intact consciousness. Stage III is surgical anesthesia with loss of reflexes and purposeful movement. Stage IV represents life-threatening medullary depression with cardiovascular and respiratory collapse.

Correct answer: B. Administer naloxone 0.04 mg IV and titrate to effect

The clinical picture — somnolence, respiratory rate of 6/min, and SpO2 of 88% in an obese patient with OSA after significant intraoperative opioid use — is consistent with opioid-induced respiratory depression. Naloxone titrated in small incremental doses (0.04 mg IV) reverses opioid-mediated CNS and respiratory depression while minimizing precipitous reversal that can cause acute pain crisis or neurogenic pulmonary edema. CPAP supports oxygenation but does not address the underlying pharmacologic cause. Lateral positioning is an adjunct but insufficient alone. Flumazenil reverses benzodiazepines, not opioids; no benzodiazepine was documented in this case.

Correct answer: B. Propofol is associated with a lower incidence of postoperative nausea and vomiting

Propofol has well-documented antiemetic properties at sub-hypnotic plasma concentrations and TIVA with propofol is associated with a significantly lower incidence of postoperative nausea and vomiting (PONV) compared to volatile inhalation agents such as isoflurane, sevoflurane, and desflurane; this is a major advantage for PACU management and patient comfort. Propofol has no intrinsic analgesic activity and does not reduce opioid requirements. It produces rapid awakening — not prolonged sedation — due to its short context-sensitive half-life. Propofol has no neuromuscular blocking properties.

Correct answer: B. Naloxone and flumazenil

Midazolam is a benzodiazepine reversed by flumazenil, and fentanyl is an opioid reversed by naloxone; both agents contribute to the observed sedation and respiratory depression in this MAC case with no reversal given. Sugammadex and neostigmine are neuromuscular blockade reversal agents and are not relevant because no neuromuscular blocking agent was documented. The appropriate pharmacologic reversal strategy targets both contributing agents — naloxone for fentanyl and flumazenil for midazolam — while the nurse monitors for re-sedation given that flumazenil's duration (approximately 45–90 minutes) may be shorter than midazolam's clinical effect.

Correct answer: B. Notify the anesthesiologist immediately and assess for signs of spinal hematoma or epidural complication

Persistent unilateral motor and sensory deficits three hours after spinal anesthesia that deviate from expected bilateral symmetric regression warrant urgent anesthesiologist notification and assessment for neurologic complications, including spinal hematoma, which can present with unilateral or asymmetric neurological findings and requires emergent MRI and neurosurgical consultation if suspected. While minor asymmetry in block resolution can occur, unilateral absence of motor function and sensation at three hours is outside expected recovery parameters and must not be dismissed. Ephedrine treats hypotension, not neural blockade, and warm compresses have no effect on local anesthetic clearance.

Correct answer: B. Emergence delirium associated with sevoflurane

Emergence delirium (ED) is a well-recognized complication of sevoflurane (and desflurane) anesthesia in pediatric patients, characterized by inconsolable agitation, dissociation, thrashing, and failure to recognize parents despite physiologically stable oxygenation and ventilation — it is not pain-driven. Sevoflurane is the most common volatile agent associated with pediatric ED, with reported incidences ranging from 10–80% depending on assessment criteria and population. Opioid-induced hyperalgesia involves paradoxical pain sensitization, not dissociative agitation. Malignant hyperthermia presents with hyperthermia, rigidity, tachycardia, and metabolic acidosis. Postoperative cognitive dysfunction is a delayed phenomenon primarily observed in adults, not acute agitation in children.

Correct answer: B. Pseudocholinesterase is responsible for metabolizing succinylcholine in the plasma; its deficiency prolongs the drug's duration of action

Succinylcholine is normally hydrolyzed rapidly in the plasma by pseudocholinesterase (butyrylcholinesterase); individuals with genetic variants causing decreased pseudocholinesterase activity cannot metabolize the drug efficiently, resulting in prolonged depolarizing blockade that may last hours instead of minutes. Succinylcholine is not renally eliminated — plasma hydrolysis is the primary clearance mechanism. Pseudocholinesterase deficiency does not cause receptor upregulation or pharmacodynamic changes in potency. Succinylcholine does not convert to a non-depolarizing agent; it remains a depolarizing agent throughout.

Correct answer: B. Bradycardia and excessive secretions

Neostigmine is a non-selective acetylcholinesterase inhibitor that potentiates acetylcholine at both nicotinic (neuromuscular) and muscarinic (autonomic) receptors. Unopposed muscarinic stimulation causes bradycardia, bronchospasm, increased secretions, and gastrointestinal hypermotility. Glycopyrrolate (an anticholinergic) is co-administered to block these muscarinic effects, but if its dose is inadequate or it wears off before neostigmine, bradycardia and excessive secretions may emerge. Tachycardia and hypertension are not muscarinic effects of neostigmine. Dry mouth and urinary retention are anticholinergic side effects reflecting excessive glycopyrrolate activity. Skeletal muscle weakness reflects residual nicotinic neuromuscular blockade, not inadequate muscarinic coverage.