AS11.1-6 | Oxygen Therapy and Airway Management Foundations — Graded Quiz

The NRM reservoir bag must remain at least one-third full throughout the respiratory cycle. If the bag collapses completely, the patient is entraining room air through the exhalation ports, diluting the FiO₂ significantly. Increasing the flow rate (typically to 12–15 L/min) maintains the bag and ensures high FiO₂ delivery.

The NRM reservoir bag must remain at least one-third full during inspiration. Complete bag collapse means entrainment of room air and loss of high FiO₂ delivery. Recommended flow for NRM is 12–15 L/min to keep the bag inflated and maximise FiO₂ (~60–90%).

Reducing flow worsens the problem. A Venturi mask would lower the FiO₂ and is not appropriate for a post-arrest patient who needs maximum oxygen. Removing the one-way valve destroys the NRM's function, allowing exhaled air to re-enter the bag. A collapsing bag is a failure signal, not a sign of adequate breathing.

In some COPD patients, high FiO₂ can cause hypercapnia through multiple mechanisms (reduced hypoxic pulmonary vasoconstriction, Haldane effect, and suppression of hypoxic drive). The ABG shows acute-on-chronic respiratory acidosis with metabolic compensation (elevated HCO₃⁻), consistent with CO₂ retention from over-oxygenation.

Over-oxygenation in COPD can precipitate or worsen CO₂ retention. The SpO₂ target in COPD is 88–92%. A titrated approach using a 24–28% Venturi mask is the safest strategy. High HCO₃⁻ with low pH and high PaCO₂ = acute-on-chronic respiratory acidosis.

The SpO₂ is 95% — oxygenation is already excessive for a COPD target. Pneumothorax requires clinical signs not described here. The elevated HCO₃⁻ reflects chronic compensation (type 2 respiratory failure baseline) and the low pH confirms respiratory acidosis, not metabolic alkalosis.

Current adult BLS guidelines specify: compression rate 100–120/min, depth 5–6 cm, 30:2 ratio (both single and two-rescuer adult), minimise interruptions. Shockable rhythms are VF and pulseless VT — not PEA or asystole, which are non-shockable.

Adult CPR: compressions at 100–120/min, depth 5–6 cm, ratio 30:2 (single or two rescuers), minimise pauses. Shockable rhythms = VF and pulseless VT only. PEA and asystole are non-shockable — continue CPR without shock for these rhythms.

>120/min rates can reduce filling time and cardiac output. The 15:2 ratio is for paediatric two-rescuer CPR, not adult. PEA and asystole are non-shockable rhythms. 3-second ventilations are excessive; breaths should take approximately 1 second each.

The NPA lies outside the oropharynx, so it does not stimulate the gag reflex like an OPA does. This makes it the preferred adjunct in semi-conscious patients who would not tolerate an OPA. Minor nasal trauma or mild bleeding is a relative — not absolute — contraindication; the absolute contraindication is suspected base-of-skull fracture.

The NPA is preferred over OPA in semi-conscious patients because it lies in the nasopharynx and does not stimulate the oropharyngeal gag reflex. The absolute contraindication to NPA is suspected basal skull fracture (CSF rhinorrhoea, periorbital bruising, Battle's sign). Minor nasal bleeding or trauma is a relative contraindication only.

Airway adjuncts do not themselves deliver oxygen — they maintain airway patency. The NPA does not provide a more secure or larger airway than the OPA; neither is a definitive airway. Any nasal bleeding is not an absolute contraindication (base-of-skull fracture is).

For a Cormack-Lehane grade III view, external laryngeal manipulation (BURP) and/or use of a gum-elastic bougie are the appropriate first-line manoeuvres to facilitate intubation. The SpO₂ is still good, so there is time for a structured optimisation attempt before escalating.

Cormack-Lehane grade III view (epiglottis only) can often be overcome with BURP manoeuvre (external thyroid cartilage pressure), optimal head position, or a gum-elastic bougie. Escalating to surgical airway is reserved for 'cannot intubate, cannot oxygenate' situations after multiple failed attempts with optimal technique.

Blind intubation risks oesophageal intubation. Cricothyrotomy is a rescue technique for 'cannot intubate, cannot oxygenate' — it is premature here. Advancing the blade too far risks laryngeal or dental trauma. Waking the patient is an option if multiple attempts fail — not after the first difficulty.

A flat capnograph (ETCO₂ = 0) combined with epigastric breath sounds and falling SpO₂ is diagnostic of oesophageal intubation. The tube must be removed immediately, the patient mask-ventilated with 100% oxygen, and intubation reattempted after re-oxygenation.

A flat capnograph waveform (ETCO₂ = 0) after intubation means the tube is in the oesophagus or there is no cardiac output. Combined with epigastric breath sounds and falling SpO₂, the diagnosis is oesophageal intubation. Remove the tube immediately and re-oxygenate. Continuous waveform capnography is the gold standard for confirming tracheal intubation.

Mainstem bronchus intubation would show decreased breath sounds on one side but would still have a normal capnograph waveform. Waiting for CXR is dangerous when SpO₂ is falling; the capnograph is highly reliable. Laryngospasm occurs with an intact airway — not after tube placement.

PEEP (positive end-expiratory pressure) works by maintaining positive airway pressure at end-expiration, preventing alveolar collapse. In ARDS, widespread alveolar flooding and collapse leads to V/Q mismatch and shunt. PEEP recruits these units, increases functional residual capacity (FRC), and improves oxygenation.

PEEP is the primary ventilator knob for improving oxygenation in ARDS. It recruits collapsed alveoli, increases FRC, and reduces intrapulmonary shunt. CO₂ clearance is controlled by minute ventilation (RR × TV). Excessive PEEP can cause haemodynamic compromise by reducing venous return.

PEEP primarily addresses oxygenation, not CO₂ clearance (which is controlled by minute ventilation). PEEP does not reduce airway resistance. Higher PEEP actually increases mean airway pressure; while it can reduce tidal overdistension injury, it does not inherently lower peak airway pressure and can itself cause barotrauma if set too high.

HFNC delivers heated, humidified gas at flow rates up to 60 L/min (FiO₂ 0.21–1.0). At these flows it matches or exceeds peak inspiratory demand, reducing entrainment of room air. It also generates a small CPAP-like effect (2–5 cmH₂O), reduces work of breathing, and improves mucociliary clearance via humidification.

HFNC at 40–60 L/min matches peak inspiratory flow, delivers up to 100% FiO₂, provides humidified gas that improves comfort and mucociliary function, and generates 2–5 cmH₂O CPAP effect that reduces work of breathing. It is an important bridge between conventional oxygen therapy and invasive ventilation in acute hypoxaemic respiratory failure.

HFNC delivers FiO₂ up to 1.0 (100%), higher than NRM (~60–90%). Unlike a Venturi mask, HFNC's FiO₂ is not fixed with the same precision — it varies slightly with breathing pattern, though at high flows this effect is minimised. Eliminating monitoring is never appropriate for high-dependency patients.

The Venturi mask was chosen because it delivers a controlled, measurable FiO₂. Nasal cannula FiO₂ is variable and dependent on the patient's breathing pattern. While the SpO₂ appears acceptable now, you lose the ability to reliably titrate oxygen and to detect early changes — particularly relevant in asthma where respiratory pattern is labile.

Fixed-performance devices (Venturi mask) should be used when precise, reproducible FiO₂ is clinically important — e.g., in patients where subtle desaturation or over-oxygenation would alter management. The Venturi mask allows reliable titration and comparison across serial observations, unlike variable-performance devices.

A nasal cannula at 4 L/min delivers approximately 36–40% FiO₂ — not dramatically lower than 35%. The concern is not immediate oxygenation but rather the loss of precision and monitoring reliability during a dynamic illness. Nasal cannulas are not contraindicated in asthma; patient-device mismatch may worsen compliance and reduce safety.

Plateau pressure >30 cmH₂O indicates alveolar overdistension and risk of barotrauma/volutrauma (ventilator-induced lung injury). The priority is to reduce tidal volume — decrease by 1 mL/kg IBW increments until plateau pressure falls below 30 cmH₂O. Minute ventilation can be compensated by increasing RR after the VT reduction.

Plateau pressure reflects alveolar distending pressure. A plateau pressure >30 cmH₂O signals alveolar overdistension. The intervention is to reduce tidal volume (typically to 6 mL/kg IBW). RR may need to increase to maintain CO₂ clearance. This is the cornerstone of lung-protective ventilation.

Increasing PEEP would raise mean airway pressure further and worsen overdistension. Increasing FiO₂ addresses oxygenation, not airway pressure. Increasing RR without reducing TV fails to address the fundamental problem of elevated plateau pressure from excessive tidal volume.