Airway Management and Oxygen Therapy Flashcards

A patient under deep sedation develops paradoxical breathing with a see-saw pattern (chest rises as abdomen falls). Which airway complication is most likely occurring?

Answer: Complete upper airway obstruction with continued respiratory effort

Paradoxical (see-saw) breathing — where the chest and abdomen move in opposite directions — is the hallmark of complete upper airway obstruction with preserved respiratory drive. The diaphragm contracts and descends (causing abdominal rise), but because the upper airway is obstructed, the chest wall is sucked inward rather than expanding. Central apnea would show no effort at all; bronchospasm is a lower airway issue producing expiratory wheeze; laryngospasm more typically causes stridor.

During nasal hood oxygen delivery at 6 L/min, a 70 kg adult patient's end-tidal CO₂ climbs from 38 to 52 mmHg over 8 minutes without any change in respiratory rate. What is the most appropriate next action?

Answer: Reduce the sedation infusion rate and stimulate the patient verbally

A rising EtCO₂ without a change in respiratory rate indicates hypoventilation (smaller tidal volumes) rather than airway obstruction — the patient is breathing too shallowly, causing CO₂ retention. The cause is excessive sedation depth, so the correct response is to decrease the sedative agent and provide verbal stimulation. Increasing O₂ flow treats hypoxia, not hypoventilation. A non-rebreather mask does not address CO₂ elimination. A jaw thrust addresses mechanical obstruction, which is not the primary problem here since rate is unchanged.

A dental anesthesia assistant is monitoring a patient receiving IV moderate sedation. SpO₂ drops from 98% to 88% over 30 seconds. After repositioning the airway and applying 100% O₂ via mask, SpO₂ recovers to 96% within 60 seconds, then drops again to 90% when mask is briefly removed. This pattern most likely represents:

Answer: A low functional residual capacity with rapid oxygen desaturation kinetics

Rapid desaturation that responds quickly to supplemental O₂ but recurs when O₂ is removed is characteristic of a patient with low functional residual capacity (FRC) — common in obese patients, those with restrictive lung disease, or when sedation causes loss of muscle tone. Low FRC means minimal oxygen reserve; these patients desaturate quickly during apnea. Methemoglobinemia causes a plateau SpO₂ around 85% regardless of O₂. Pulmonary edema and intracardiac shunts would not respond so briskly and completely to mask O₂.

When performing bag-valve-mask (BVM) ventilation on an apneic sedated patient, the anesthesia assistant notices the chest does not rise despite an apparently good mask seal. The MOST likely cause and correction is:

Answer: Tongue or soft-tissue obstruction; reposition with head-tilt chin-lift and reassess

In a sedated patient, the most common reason BVM ventilation fails despite an adequate mask seal is soft-tissue upper airway obstruction — the tongue and pharyngeal muscles relax onto the posterior pharynx. The immediate corrective action is repositioning (head-tilt chin-lift or jaw thrust) to lift the tongue off the posterior wall. Pneumothorax is rare acutely and presents with other signs. Auto-PEEP causes air-trapping on exhalation, not failure to ventilate initially. Esophageal intubation would only apply if an endotracheal tube were in place.

A patient with a known history of obstructive sleep apnea (OSA) and a Mallampati Class IV airway is scheduled for a dental procedure under moderate IV sedation. Which pre-oxygenation strategy provides the greatest margin of safe apnea time before desaturation?

Answer: Three minutes of tidal volume breathing through a 100% non-rebreather mask at 15 L/min

Three minutes of tidal breathing through a 100% non-rebreather mask at 15 L/min is the standard pre-oxygenation technique that maximally denitrogenates the FRC, replacing N₂ with O₂ and extending the safe apnea window. While 8 vital-capacity breaths can also effectively pre-oxygenate in 60 seconds, this requires full patient cooperation and effort, which is often impractical pre-sedation. HFNC during the procedure provides apneic oxygenation but does not pre-oxygenate the FRC. A nasal cannula at 4 L/min does not deliver sufficient FiO₂ to fully denitrogenate.

During administration of nitrous oxide/oxygen analgesia, a patient reports tingling in the fingers, carpopedal spasm (hands in a claw-like posture), and dizziness. Nitrous concentration is 40% and has been running for 6 minutes. What is the PRIMARY cause of these symptoms?

Answer: Hypocapnia secondary to hyperventilation induced by anxiety or over-breathing during delivery

Carpopedal spasm (tetany) and perioral/finger tingling are classic signs of hypocapnia (low CO₂), caused by hyperventilation. An anxious patient breathing rapidly and deeply through the nasal hood will blow off CO₂, causing respiratory alkalosis and subsequent ionized hypocalcemia, which drives neuromuscular excitability and carpopedal spasm. At 40% N₂O the oxygen fraction (60%) is well above safe minimums, ruling out hypoxia. Nitrous oxide does not directly block neuromuscular transmission. Vasovagal syncope would cause bradycardia and hypotension rather than tetany.