Airway Management and Oxygen Therapy Flashcards

A patient receiving intravenous sedation in the dental chair develops laryngospasm. After repositioning the jaw and providing positive pressure ventilation with 100% oxygen, the spasm does not break. What is the next appropriate pharmacological intervention?

Answer: Succinylcholine 0.1–0.2 mg/kg IV (subparalytic dose)

When laryngospasm does not resolve with jaw thrust and positive-pressure O₂, a subparalytic ('defasciculating') dose of succinylcholine (0.1–0.2 mg/kg IV) can break the spasm without producing full neuromuscular blockade. Atropine addresses bradycardia/secretions but does not relieve laryngospasm. Flumazenil reverses benzodiazepines but cannot relax laryngeal muscles. A full 1 mg epinephrine IV push is cardiac arrest dosing and not indicated here.

During office-based sedation, a patient's pulse oximeter reads 94% SpO₂ but the waveform is dampened and the perfusion index is 0.3%. The patient appears comfortable and has normal capnography. What is the MOST likely explanation for the low SpO₂ reading?

Answer: Peripheral vasoconstriction causing a poor-quality pulse oximetry signal

A dampened waveform and very low perfusion index (<1%) indicate the probe is not reliably detecting pulsatile flow — most commonly due to peripheral vasoconstriction (cold extremities, vasopressors, or motion artifact). Normal capnography makes true hypoventilation-driven desaturation less likely. Methemoglobinemia drives SpO₂ readings toward 85%, not 94%. CO₂ retention does not mask hypoxia on the oximeter. The correct action is to relocate the probe (forehead, earlobe) and reinterpret.

A 68-year-old patient with severe COPD (FEV₁ 38% predicted) is receiving moderate sedation. You are titrating supplemental O₂ via nasal cannula. Which target SpO₂ range is MOST appropriate to avoid suppressing his hypoxic respiratory drive while preventing dangerous hypoxemia?

Answer: 88–92% — sufficient to prevent tissue hypoxia while preserving drive

In patients with severe COPD who may rely on hypoxic drive (particularly those with chronic hypercapnia), targeting SpO₂ of 88–92% balances adequate tissue oxygenation against the risk of suppressing ventilatory effort. Targeting 99–100% with uncontrolled O₂ flow can blunt the hypoxic stimulus and cause CO₂ retention (the Haldane effect also shifts the CO₂ dissociation curve). Targeting 85–87% risks cellular hypoxia. Standard 95–98% targets are appropriate for healthy patients but excessive for severe COPD with hypercapnic risk.

End-tidal CO₂ (EtCO₂) monitoring via nasal cannula capnography shows a sudden loss of waveform (flatline) in a sedated patient who still has a palpable pulse and appears to be moving air. What is the MOST likely cause?

Answer: Mouth breathing causing expired gas to bypass the nasal sampling port

Nasal cannula capnography samples expired gas from the nares. If the patient transitions to mouth breathing (common in sedated patients with nasal congestion or airway obstruction), CO₂-laden exhalate bypasses the sampling port entirely, producing a flatline waveform despite ongoing ventilation. A palpable pulse and visible chest movement confirm this is not cardiac or respiratory arrest. Bronchospasm typically prolongs the expiratory phase and produces a 'shark fin' waveform, not a flat one. Always correlate EtCO₂ loss with clinical assessment before intervening.

A dental patient requires general anesthesia with a laryngeal mask airway (LMA). The anesthetist selects a size 4 LMA and inflates the cuff to the recommended maximum of 60 cmH₂O. During positive pressure ventilation, a significant leak is noted. The MOST appropriate next step is:

Answer: Deflate and reinsert the LMA, verifying correct size and positioning before re-inflating

LMA cuff pressures above 60 cmH₂O significantly increase the risk of pharyngeal mucosal ischemia and nerve injury without reliably improving seal. The correct response to a persistent leak at maximum recommended pressure is to deflate the cuff and reassess position and size — the device may be malpositioned (folded epiglottis, lateral rotation) or the wrong size for the patient's airway. Exceeding 60 cmH₂O is contraindicated. Immediate ETT conversion is premature before correcting positioning. Compensating with higher tidal volumes risks gastric insufflation.

During office sedation, a patient develops stridor with paradoxical chest wall movement (chest retracts on inhalation, abdomen protrudes). SpO₂ is 87% and falling. After opening the airway with a head-tilt/chin-lift, which supplemental oxygen delivery device provides the HIGHEST fraction of inspired oxygen (FiO₂) in this patient who is still making respiratory effort?

Answer: Non-rebreather mask at 15 L/min (FiO₂ ~95–100%)

A non-rebreather mask (NRM) with a reservoir bag and one-way valves, at a flow rate of 10–15 L/min sufficient to keep the reservoir inflated, delivers the highest FiO₂ (~95–100%) of any device that does not require a sealed circuit or intubation. A simple face mask at 8 L/min only achieves 40–60% because room air entrainment through the side ports is high. A nasal cannula at 6 L/min achieves roughly 44% FiO₂. A Venturi mask provides a precise but fixed lower concentration (24–60%) and is designed for COPD titration, not emergency oxygenation.