Ventilation strategies for front of neck airway rescue: an in silico study

Abstract

Background: During induction of general anaesthesia a 'cannot intubate, cannot oxygenate' (CICO) situation can arise, leading to severe hypoxaemia. Evidence is scarce to guide ventilation strategies for small-bore emergency front of neck airways that ensure effective oxygenation without risking lung damage and cardiovascular depression.

Methods: Fifty virtual subjects were configured using a high-fidelity computational model of the cardiovascular and pulmonary systems. Each subject breathed 100% oxygen for 3 min and then became apnoeic, with an obstructed upper airway. When arterial haemoglobin oxygen saturation reached 40%, front of neck airway access was simulated with various configurations. We examined the effect of several ventilation strategies on re-oxygenation, pulmonary pressures, cardiovascular function, and oxygen delivery.

Results: Re-oxygenation was achieved in all ventilation strategies. Smaller airway configurations led to dynamic hyperinflation for a wide range of ventilation strategies. This effect was absent in airways with larger internal diameter (≥3 mm). Intrapulmonary pressures increased quickly to supra-physiological values with the smallest airways, resulting in pronounced cardio-circulatory depression (cardiac output <3 L min^-1 and mean arterial pressure <60 mm Hg), impeding oxygen delivery (<600 ml min^-1). Limiting tidal volume (≤200 ml) and ventilatory frequency (≤8 bpm) for smaller diameter cannulas reduced dynamic hyperinflation and gas trapping, preventing cardiovascular depression.

Conclusions: Dynamic hyperinflation can be demonstrated for a wide range of front of neck airway cannulae when the upper airway is obstructed. When using small-bore cannulae in a CICO situation, ventilation strategies should be chosen that prevent gas trapping to prevent severe adverse events including cardio-circulatory depression.

Keywords: airway management; airway obstruction; apnoea; cannot intubate; cannot oxygenate; front of neck airway; oxygenation simulation.

Fig. 1

Airway pressures calculated over the cohort of 50 in silico subjects. Mean values are shown for end-expiratory lung pressure, end-inspiratory lung pressure and ventilator pressure (bottom panels) for airway configurations A (inner diameter 1.8 mm, length 6.3 cm), B (inner diameter 2.0 mm, length 7.5 cm), and C (inner diameter 3.0 mm, length 5.8 cm). Standard deviations have not been reported for graphical reasons and because they were not significant. Levels of pressures were represented with different colour coding; blue represented ‘safe’ pressures (<30 cm H₂O), purple represents pressures 30–60 cm H₂O, and green represented high pressures (>60 cm H₂O). These thresholds have been chosen because of clinical consideration and studies showing a proportional relationship between driving pressures and potential patient harm in other patient cohorts where a plateau pressure >30 cm H₂O might be acceptable under certain conditions.

Fig. 2

Time taken to achieve arterial haemoglobin oxygen saturation (SaO₂) of 95% in the small-bore airway configurations (A, B, and C) during all patterns of tidal ventilation studied. Vf, ventilatory frequency (bpm); Vt, tidal volume (ml).

Fig. 3

Time-course of lung volumes, Pao₂ and SaO₂, during pre-oxygenation, apnoea, and airway opening with different provisions of tidal ventilation in a representative subject; right panel: tidal volume 20 ml and ventilatory frequency 4 bpm; middle panel: tidal volume 200 ml and ventilatory frequency 8 bpm; left panel: tidal volume 500 ml and ventilatory frequency 20 bpm.

Fig. 4

End-inspiratory lung pressure, end-expiratory lung pressure and ventilator pressure for various airway lengths and diameters, with tidal volume 100 ml and ventilatory frequency 8 bpm. Blue areas: pressure <30 cm H₂O; purple areas: pressures 30–60 cm H₂O and green areas: pressures >60 cm H₂O.

Fig. 5

Arterial oxygen delivery (DO₂), cardiac output (CO), and mean arterial pressure (MAP) in the small-bore configurations (A, B, and C) at the end of tidal ventilation provision. Before opening of the obstructed airway (at the end of apnoea), DO₂, CO, and MAP were 227.2 (22.9) ml min⁻¹, 2.7 (0.1) L min⁻¹, and 57.2 (2.7) mm Hg, respectively. Vf, ventilatory frequency (bpm); Vt, tidal volume (ml).

Fig. 5

Arterial oxygen delivery (DO₂), cardiac output (CO), and mean arterial pressure (MAP) in the small-bore configurations (A, B, and C) at the end of tidal ventilation provision. Before opening of the obstructed airway (at the end of apnoea), DO₂, CO, and MAP were 227.2 (22.9) ml min⁻¹, 2.7 (0.1) L min⁻¹, and 57.2 (2.7) mm Hg, respectively. Vf, ventilatory frequency (bpm); Vt, tidal volume (ml).

Fig. 6

Arterial partial pressure of oxygen (Pao₂) and carbon dioxide (Paco₂) calculated in the small-bore configurations (A, B, and C) at the end of tidal ventilation provision. Before opening of the obstructed airway (at end of apnoea), Pao₂ and Paco₂ were 3.8 (0.1) kPa and 11.1 (1) kPa, respectively. Vf, ventilatory frequency (bpm); Vt, tidal volume (ml).