Free CPAN Exam Flashcards

Phase I is intensive recovery immediately after anesthesia, focused on airway, ventilation, hemodynamic stabilization, and emergence. Phase II prepares the stabilized patient for discharge home or to an inpatient unit. CPAN validates Phase I competency; recovery is a physiologic continuum, not a fixed clock-based interval.

Airway and effective ventilation before any lower-priority intervention. Confirm a patent airway, adequate respiratory effort, and gas exchange first, then assess circulation, neurologic status, pain, and temperature. A normal single vital sign does not override a deteriorating airway.

On supplemental oxygen, SpO2 can stay falsely reassuring while ventilation is already failing because the oxygen reservoir delays desaturation. Capnography, respiratory rate and depth, chest movement, airway sounds, and mental status detect hypoventilation earlier than SpO2 alone.

Most post-anesthesia obstruction is from posterior tongue collapse and loss of pharyngeal tone. Initial actions: reposition (head tilt/jaw thrust), suction visible secretions, insert an oral or nasal airway adjunct, apply oxygen, and assist ventilation if needed. Escalate if it does not resolve quickly.

Sustained reflex glottic closure presenting as stridor, retractions, paradoxical chest movement, or silent (complete) obstruction. Call for help, apply jaw thrust and positive-pressure oxygen, remove airway stimulation, suction secretions, and prepare for medication support per protocol. Untreated laryngospasm leads to hypoxemia rapidly.

Develops when a patient generates forceful inspiration against an obstructed airway (often after laryngospasm). The patient may briefly improve after obstruction relief, then develop hypoxemia, frothy sputum, crackles, and distress. Treat with oxygenation and positive-pressure support; it is a delayed, deceptive presentation.

Capnography (end-tidal CO2) reflects ventilation and detects hypoventilation, apnea, and rising CO2 in near real time. Pulse oximetry reflects oxygenation, which can stay normal on supplemental oxygen even while the patient is not ventilating. They measure different problems and are not interchangeable.

Look for weak or absent cough, low tidal volume, shallow breathing, drooping eyelids or diplopia, inability to sustain a 5-second head lift, weak hand grip, snoring/pharyngeal collapse, and anxiety with poor movement despite being awake. Any of these means the airway is not yet safely protected.

The ability to lift and hold the head for about 5 seconds is a practical bedside indicator of adequate neuromuscular recovery and pharyngeal strength. Inability to sustain a head lift is a weakness clue and is NOT a discharge-ready finding, even if the patient appears awake.

Sugammadex encapsulates aminosteroid nondepolarizing blockers (rocuronium, vecuronium) and reverses even deep blockade rapidly. Neostigmine, an acetylcholinesterase inhibitor usually paired with an anticholinergic, indirectly reverses moderate nondepolarizing blockade. Neither agent eliminates the need for continued monitoring for recurrent weakness.

Neostigmine increases acetylcholine everywhere, causing muscarinic effects such as bradycardia, salivation, and bronchospasm. It is co-administered with an anticholinergic (glycopyrrolate or atropine) to block those muscarinic effects while still reversing neuromuscular blockade at the junction.

A depolarizing blocker with rapid onset and short duration. Risks the PACU nurse must recognize: hyperkalemia in susceptible patients, bradycardia, postoperative myalgias, raised intraocular/intragastric pressure concerns, and being a malignant hyperthermia trigger. CPAN tests recognizing the consequence, not dose calculation.

Paralysis is not sleep. Neuromuscular blockers produce skeletal muscle paralysis with no analgesia, no amnesia, and no unconsciousness. A weak patient may still be in pain or aware, so sedation and pain must be assessed separately from motor recovery.

Naloxone reverses opioid-induced respiratory depression. Abrupt reversal can cause severe pain, sympathetic surge, hypertension, nausea/vomiting, and rarely pulmonary edema, plus withdrawal in opioid-dependent patients. Critically, naloxone can wear off before the opioid does, so monitoring must continue after the patient improves.

Flumazenil reverses benzodiazepine sedation but may precipitate seizures in benzodiazepine-dependent patients or mixed overdose. It does NOT reverse opioid respiratory depression, residual neuromuscular blockade, inhalational anesthetic effect, hypoglycemia, or stroke. Re-sedation can occur as it wears off.

Produces rapid, smooth hypnosis with quick offset. PACU concerns are airway obstruction, apnea, and hypotension from vasodilation and reduced cardiac output. Hypotension after propofol-based anesthesia should still be evaluated against bleeding and hypovolemia rather than assumed to be only drug effect.

An alpha-2 agonist providing sedation and analgesia with comparatively little respiratory depression. The trade-off is bradycardia, hypotension, and sometimes delayed wakefulness. It is useful for opioid-sparing sedation but still requires hemodynamic surveillance.

Provides analgesia and dissociation with relative preservation of airway reflexes and respiration at analgesic doses. Watch for emergence reactions (vivid dreams, agitation), increased secretions, and sympathetic stimulation causing hypertension and tachycardia.

Inhalational agents are eliminated mainly through the lungs, so emergence depends on ventilation. They contribute to PONV, shivering, and slow awakening with hypoventilation, and they are malignant hyperthermia triggers. Adequate ventilation speeds clearance and recovery.

A hypermetabolic crisis after exposure to volatile anesthetics or succinylcholine in susceptible patients. Hyperthermia is often LATE — do not wait for fever. Earlier signs: unexplained rising end-tidal CO2, tachycardia, masseter or generalized rigidity, acidosis, hyperkalemia, dysrhythmias, and cola-colored urine.

Activate the MH crisis response immediately: call for help, notify anesthesia and surgeon, get the MH cart, give high-flow 100% oxygen and hyperventilation as directed, and prepare dantrolene (the specific antidote). Support cooling when indicated and monitor for acidosis, hyperkalemia, renal injury, and coagulopathy.

May follow regional blocks, infiltration, or local anesthetic infusions. Early neurologic signs: circumoral numbness, metallic taste, tinnitus, dizziness, agitation, confusion, tremor, or seizure. Progression brings cardiovascular toxicity — hypotension, conduction delay, ventricular dysrhythmias, or arrest.

Stop the local anesthetic source, call for anesthesia help, protect airway and oxygenation, treat seizures per orders, and prepare 20% lipid (intralipid) emulsion per the facility LAST protocol. Act fast — neurologic symptoms can progress to cardiovascular collapse quickly.

Risk rises with depressed airway reflexes, vomiting, ileus, obesity, pregnancy, emergency surgery, and opioids. Signs: emesis, coughing, wheeze, hypoxemia. Position to protect the airway, suction the mouth/pharynx, apply oxygen, assess lung sounds and SpO2, and escalate for persistent hypoxemia, crackles, fever, or distress.

An expanding neck hematoma is an airway emergency, not a wound issue. Signs: increasing neck swelling, pressure, voice change, or stridor after neck surgery. Prepare for airway management and summon the surgeon and anesthesia immediately; the priority is securing the airway before it occludes.

Postoperative agitation has many causes: hypoxia, hypercarbia, pain, bladder distention, hypoglycemia, residual anesthetic, and emergence delirium. Rule out physiologic causes — especially hypoxia and hypoventilation — before attributing agitation to emergence delirium. Sedating an agitated, hypoxic patient is dangerous.

Tachycardia, falling blood pressure (often a late sign), narrowing pulse pressure, cool clammy skin, restlessness, low urine output, and increasing drainage or a high-blood-loss surgical history. Treat trend changes and bright-red bleeding as active hemorrhage until proven otherwise and escalate early.

Neuraxial blockade causes sympathetic blockade (vasodilation), producing hypotension; a high block can also block cardiac accelerator fibers, causing bradycardia. Management per orders typically includes fluids, positioning, vasopressors, and oxygen. Monitor block level — an ascending block threatens respiration.

An ascending neuraxial block causing progressive hypotension, bradycardia, dyspnea, hand/arm numbness, difficulty speaking, and ultimately apnea and loss of consciousness. This is a respiratory and hemodynamic emergency requiring airway/ventilatory support, circulatory support, and immediate anesthesia escalation.

Track sensory level and motor return against the expected block distribution. Document return of sensation, movement, and proprioception before mobilizing. A persistently numb or weak limb is a fall and injury risk; severe pain despite a block can signal block failure or a complication, not adequate analgesia.

Classic for compartment syndrome, especially after extremity trauma or surgery. This is not a routine analgesia situation — perform an urgent neurovascular check and notify the provider immediately. Treating it as ordinary postoperative pain delays a limb-threatening diagnosis.

Interpret the rating with procedure, baseline opioid use, sedation level, respiratory rate and depth, blood pressure, and complication clues. Before giving more opioid, verify airway and ventilation. A somnolent, hypoventilating patient with high pain needs ventilatory support and a revised plan — not automatic dose escalation.

Combining mechanisms (acetaminophen, NSAIDs when appropriate, regional/local techniques, ice, positioning, and titrated opioids) reduces opioid burden. Cautions: NSAIDs in bleeding, renal impairment, or ulcer history; acetaminophen dose limits in liver disease or heavy alcohol use. Match the adjunct to the patient.

Rising sedation precedes opioid-induced respiratory depression, so a sedation scale is a key safety screen during titration. Increasing sedation with a falling SpO2 trend or rising end-tidal CO2 is more urgent than a single in-range vital sign and should halt further opioid until reassessed.

Postoperative nausea and vomiting is a comfort issue that can also threaten the airway, wounds, and hemodynamics. Protect the airway first: position laterally or turn the head when appropriate, suction, withhold oral intake until safe, and assess for aspiration. Then give ordered antiemetics and support hydration.

Persistent vomiting with abdominal distention, blood in emesis, hypotension, severe headache, or new neurologic changes is not ordinary PONV. Connect the symptom to the procedure and anesthetic history and evaluate for bleeding, ileus, raised intracranial pressure, or a transfusion reaction before treating it as nausea.

Core temperature below about 36 C delays drug metabolism, worsens coagulopathy, increases wound complications, and triggers shivering. Use forced-air warming, warm blankets, warmed IV fluids if ordered, and continued temperature monitoring. Hypothermia also slows emergence and prolongs PACU stay.

Shivering sharply increases oxygen consumption and cardiac workload. In patients with coronary disease, anemia, limited pulmonary reserve, or major blood loss, this added demand can precipitate ischemia or hypoxemia. Active warming and ordered measures reduce shivering and its metabolic cost.

Hyperthermia urgency depends on timing and associated findings: warming overshoot, infection, transfusion reaction, thyroid storm, serotonin syndrome, or malignant hyperthermia. A rapidly rising temperature with rigidity, tachycardia, and rising CO2 after trigger exposure is an MH emergency, not a routine fever.

Signs include fever, chills, back or flank pain, hypotension, and dark urine. STOP the transfusion immediately, keep the line open with normal saline using new tubing, and notify the provider and blood bank. Stopping the product comes before further workup because continued infusion worsens hemolysis.

Oliguria may reflect hypovolemia, renal hypoperfusion, catheter obstruction or kinking, urinary retention (especially after neuraxial anesthesia or opioids), or medication/endocrine effects. Assess catheter patency and volume status before assuming intrinsic renal injury, and trend output against vital signs.

Causes include renal impairment, succinylcholine in susceptible patients, crush/tissue injury, and acidosis. ECG progression: peaked T waves, widening QRS, then arrhythmia. It is a key consequence to recognize in malignant hyperthermia and in succinylcholine reactions; report and escalate promptly.

A standardized PACU discharge-readiness tool scoring five parameters 0-2 each (max 10): Activity (voluntary movement), Respiration, Circulation (blood pressure relative to baseline), Consciousness, and Oxygen saturation. The Modified Aldrete replaces color with SpO2. It structures readiness assessment but does not replace clinical judgment.

A commonly used target is a score of 9-10, with each parameter trending toward baseline and no offsetting instability. Discharge readiness rests on objective physiologic criteria and safe support — not on time elapsed in PACU or the patient's wish to leave. Confirm facility-specific criteria.

Safe ambulatory discharge requires a responsible adult escort, a transportation plan, clear activity and medication instructions, and defined warning signs/escalation triggers. A patient cannot drive after anesthesia or sedation. Missing escort or instructions delays discharge regardless of physiologic readiness.

Teach-back has the patient or caregiver demonstrate or restate instructions, verifying what they can actually do after anesthesia-related sedation, anxiety, or limited health literacy. A yes/no question ("Do you understand?") only confirms agreement, not comprehension, and is weaker for discharge teaching.

SBAR (Situation, Background, Assessment, Recommendation) structures the anesthesia-to-PACU and PACU-to-unit handoff: anesthetic course, airway events, medications, fluids/blood loss, lines, drains, orders, allergies, and unresolved concerns. The nurse must clarify or escalate an unsafe or incomplete handoff before accepting routine transfer responsibility.

In pregnant patients (typically beyond mid-pregnancy), the supine position lets the gravid uterus compress the aorta and vena cava, reducing venous return and causing hypotension. Apply left uterine displacement or lateral tilt, and coordinate fetal and obstetric communication as ordered.

OSA patients are highly sensitive to opioids, sedatives, and residual anesthesia, with elevated risk of airway obstruction and hypoventilation. Use opioid-sparing analgesia, careful positioning, continuous oximetry, and extended monitoring before discharge. Apnea can occur during apparently quiet sleep, not only when stimulated.

Chart objective, timely findings: assessments, interventions, patient responses, and team notifications, including trends and escalation timing. An incident report supports system safety improvement and is NOT part of the medical record — never reference it in the chart and never let it substitute for clinical documentation.