In the #FOAMed world there is a lot of talk about airway management – about difficult airways, algorithms, vortex, apneic oxygenation techniques and much more.

In a recent paper in the Western Journal of Emergency Medicine, Mosier et. al. talk about the “physiologically difficult airway” – a very good and nicely written perspective on airway management in the critical patient (full paper available for free here). It expands on topics already mentioned by (who else?) Scott Weingard a few years back.

Essentially, the authors say that a difficult airway not only consists of appreciating anatomical abnormalities but also identifying those conditions that create a high risk for patients to go into cardiac arrest because of airway management. Then they give recommendations how to deal with those situations.

The four “high risk airway management scenarios” they mention are:

  • Hypoxia
  • Hypotension
  • Severe Metabolic Acidosis
  • Right ventricular failure

The recommendations from their paper are (all cited from Mosier et. al. The Physiologically Difficult Airway. Western Journal of Emergency Medicine 2015), I’m highlighting especially interesting parts.


1. Preoxygenation and apneic oxygenation should be performed in all critically ill patients. Despite mixed data, apneic oxygenation is a low-risk intervention that may provide signi cant bene t in prolonging the safe apneic period. If a HFNC system is not available, a wide-bore nasal cannula or standard nasal prongs should be used to augment preoxygenation and provide apneic oxygenation.
2. In patients with shunt physiology due to atelectasis or alveolar  lling from pneumonia, ARDS or pulmonary edema, NIPPV can improve alveolar recruitment and oxygenation. In select patients, supraglottic airways may be considered when higher pressures are needed or a mask seal with NIPPV cannot be achieved. One must balance this potential bene t of a supraglottic airway with the risk of aspiration or upper airway injury. Nasal continuous positive airway pressure with a nasal mask may be useful to maintain alveolar recruitment during intubation in patients at high risk.
3. For patients who cannot tolerate the NIPPV mask (e.g. delirium), analgesia, anxiolysis, or DSI may be considered to optimize preoxygenation. If procedural sedation for preoxygenation is performed, one must be prepared to intubate at the onset of DSI, even with ketamine, due risk of cardiac arrest, laryngospasm and apnea, which have all been reported with ketamine.


1. Patients with conditions that reduce venous return are particularly susceptible to hypotension and patients at risk are suggested by pre-intubation hypotension or an elevated shock index >0.8. These patients should be hemodynamically optimized prior to intubation. This includes aggressive volume resuscitation if the patient is likely to be a volume responder. Hemodynamically stable induction agents should be used when possible.
2. For patients unresponsive to volume resuscitation, a norepinephrine infusion should be initiated.
3. If pre-intubation resuscitation is not feasible due to impending cardiopulmonary arrest in patients with shock, peripherally administered vasopressor boluses can be prepared quickly at the bedside and may maintain blood pressure during intubation and resuscitation. This intervention has not been studied in critically ill adults; however, diluted epinephrine (given as 10-50mcg boluses with a concentration of 1-10mcg/ mL) may be preferred due to its inotropic effect.
4. For patients without shock who have a transient drop in blood pressure after intubation due to the vasodilatory effects of induction agents or transition to positive pressure ventilation, diluted phenylephrine (given as 50- 200mcg boluses with a concentration of 100mcg/mL) may be useful.

Severe metabolic acidosis:

1. Intubation should be avoided, if possible, in patients with severe metabolic acidosis who have a minute ventilation requirement not likely to be met by the mechanical ventilator, despite a low pH. A short trial of NIPPV may adequately support the respiratory work of breathing until correction of the underlying metabolic acidosis can occur and will provide an estimate of the patient’s intrinsic minute ventilation by measuring the patient’s respiratory rate and tidal volume delivered with each breath.
2. If intubation is necessary, maintaining spontaneous respiration becomes the critical action both during intubation and with mechanical ventilation. This will allow the patient to maintain their own high minute ventilation and includes using sedative agents that are less likely to reduce the patient’s respiratory drive. Rapid sequence intubation should be avoided if possible, and if one is deemed necessary, a short-acting neuromuscular blocker such as succinylcholine should be used.
3. After intubation, we recommend choosing a ventilator mode that allows the patient to set and maintain their own minute ventilation in order to best maintain their respiratory compensation. A pressure-targeted ventilator mode such as pressure support ventilation or pressure control mode will allow the patient to set the rate and tidal volume received. Special care should be taken to monitor for air trapping given the high rates and tidal volumes reached as well as monitor for respiratory muscle fatigue, which will result in a loss of compensation.

Right heart failure

1. Bedside echocardiographic assessment of RV function should be performed to assess RV dysfunction versus RV failure. If the patient has some contractile reserve (RV dysfunction), cautious  uid resuscitation should be performed.
2. Preoxygenation is essential despite the dififculties resulting from intracardiac shunt and ventilation-perfusion (V/Q) mismatch, which commonly occur in right heart failure.
3. Apneic oxygenation should be performed given the potential for benefit. INO (intranasal nitric oxide) at low concentrations (<30ppm), delivered in-line continuously through the nasal cannula, can augment oxygenation by improving V/Q matching in the hypoxemic patient but may worsen V/Q mismatch at higher concentrations. In the RV failure patient without hypoxemia, 30-80ppm of iNO delivered
through the nasal cannula, or inhaled epoprostenol during preoxygenation and apneic oxygenation can reduce pulmonary vascular resistance.
4. Induction agents should be considered carefully. Hemodynamically neutral sedatives such as etomidate should be used for induction. Intravenous fentanyl premedication may be useful to blunt the hypertensive response to laryngoscopy.
5. Continuous norepinephrine infusion should be started prior to induction in hypotensive patients with the goal of increasing mean arterial pressure higher than pulmonary artery pressure, which can be determined by bedside echocardiography. For patients without hypotension, norepinephrine should be primed and “in-line” in the event of post intubation or sedative induced hypotension.
6. The goals of mechanical ventilation include maintenance of a low mean airway pressure and avoidance of hypoxemia, atelectasis, and hypercapnea, which increase RV afterload.
I highly recommend reading the whole paper, the different scenarios are very nicely explained and worked up.
What do you think about it? Do you concur with the recommendations?

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