Patients who present with severe acute pulmonary oedema (APO) should receive CPAP to improve cardiac and pulmonary function while medical therapy with nitrates and diuretics is initiated.² However, the use of bilevel NIV in patients with APO gives no additional benefit and may increase the rate of myocardial infarction. On the other hand, patients who present with an exacerbation of chronic obstructive pulmonary disease (COPD) do benefit from bilevel NIV rather than CPAP alone.³

There is also some evidence to support the use of NIV in patients with respiratory failure due to other common ED conditions, such as community-acquired pneumonia ⁴ or asthma.⁵ Thus it is common ED practice to now administer a trial of NIV in many patients with respiratory failure, prior to instituting ETI and mechanical ventilation. Contraindications to NIV include comatose or combative patients, poor tolerance of a tight-fitting face mask, and the lack of familiarity or lack of trained medical staff to institute and monitor the NIV.

Endotracheal intubation

Endotracheal intubation provides secure, definitive airway management and allows assisted mechanical ventilation. Patients with respiratory failure who are either ineligible for NIV or fail a trial of NIV should receive ETI and mechanical ventilation.

There are additional challenges to emergency endotracheal intubation in the ED compared to elective ETI in the operating theatre. There is often inadequate time for a complete clinical assessment of the upper airway or thorough consultation with the patient and/or family, and details of current medications, previous anaesthetics and allergies may not be available. Also, the status of the cervical spine in patients with an altered conscious state following trauma is unknown, even if initial plain imaging and even CT scanning appear normal.

There are a number of possible techniques for ETI, which are reviewed below. The selection of the appropriate technique depends on physician preference, experience and the clinical setting.

Rapid sequence induction (RSI) intubation

Unless the patient is deeply comatose or in cardiac arrest, upper airway reflexes will be present and ETI will require the use of sedative and neuromuscular blocking drugs to facilitate laryngoscopy and the placement of the endotracheal tube. Rapid sequence induction (RSI) of anaesthesia or rapid sequence intubation (the preferred North American RSI term) involves the simultaneous administration of sedation and a short-acting muscle relaxant in predetermined doses, and is the technique of choice when definitive emergency airway management is required in the ED.

Precautions and relative contraindications

Precautions and relative contraindications to the performance of RSI include patients with upper airway obstruction; distorted facial anatomy; likely difficult or impossible intubation, for example due to micrognathia or an ankylosed neck; and lack of appropriate operator skill or experience. An alternative intubation technique such as awake intubation under local anaesthesia, or an awake surgical airway such as a cricothyroidotomy or even a tracheostomy, may be preferred.

Preparation for RSI

Careful preparation is essential on each and every occasion RSI is required. If time and patient status allow, seek a history of current medications, allergies and time of the last meal. Make a careful examination of the upper airway looking for anatomical features that may predict difficult intubation.

Intubation process

The conscious patient should receive explanation and reassurance. Pre-oxygenate with 100% oxygen to prevent oxygen desaturation during the procedure. Ideally, administer NIV with 100% oxygen for a 3-minute period.⁶ If this is not possible, then breathing through a tight-fitting oxygen mask circuit using 15 L/min oxygen flow is an alternative way to pre-oxygenate the patient. Position the patient in the ‘sniffing the morning air’ position with the neck flexed and the head extended, using a pillow under the head. If the patient has suspected spinal column injury, immobilize the neck in the anatomically neutral position. Ensure there is reliable intravenous access, as well as equipment for suctioning the airway and a tipping trolley.

Monitoring during RSI

Arrange appropriate monitoring, including a continuous ECG trace and pulse oximetry. Measure the blood pressure either non-invasively using an automated monitoring device, or invasively using an intra-arterial cannula. Prepare waveform capnography for end-tidal carbon dioxide (ETCO₂) measurement following RSI.

Drugs used in RSI

The drugs required will depend on physician preference and the clinical situation. Common choices for induction include propofol at 1–2 mg/kg,⁷ a narcotic such as morphine 0.15 mg/kg with a benzodiazepine such as midazolam 0.05–0.1 mg/kg, followed by a rapid-onset depolarizing neuromuscular blocking drug such as suxamethonium 1.5 mg/kg (Table 2.1.1). An alternative when suxamethonium is contraindicated is the rapid acting non-depolarizing drug rocuronium 1 mg/kg. Contraindications to suxamethonium include known allergy, hyperkalaemia or risk of from burns, spinal cord injury or crush injury (not in the acute setting), and a history of malignant hyperthermia (rare).⁸ Details of the indications, dosages and side effects of all the commonly used drugs for RSI intubation are shown in Table 2.1.1.

Table 2.1.1 Common intravenous drugs for rapid sequence induction (RSI) intubation

Preparation of equipment and personnel prior to RSI

All drugs must be drawn up and checked in advance, and the syringes clearly labelled. A spare laryngoscope must be available in case of failure of the first, and the appropriate size of endotracheal tube (ETT) opened, lubricated and the cuff checked. Another ETT (one size smaller) should be immediately available. Finally, an introducer and a gum-elastic or plastic bougie must be ready to hand.

At least two assistants will be required, one to assist the operator with the drugs and equipment, and another to provide cricoid pressure following the induction of sedation and muscle relaxation.⁹ An additional person is required to provide in-line manual immobilization in the case of RSI for the trauma patient with possible spinal column injury. Additional equipment in case of difficult or failed intubation should be readily available, ideally kept together in a ‘Difficult Airway Kit’ containing the items necessary for a failed intubation protocol (Fig. 2.1.1).

Fig. 2.1.1 Algorithm for failed intubation. ICP, intracranial pressure; BVM, bag/valve/mask; LMA, laryngeal mask airway; ILMA, intubating laryngeal mask airway; ODD, oesophageal detector device; ETCO₂, end-tidal carbon dioxide.

Complications of RSI intubation

Hypotension following endotracheal intubation is common and must be addressed promptly. The causes include the vasodilator and/or negative inotropic effects of the sedative drug(s) given, and/or the reduction in preload from positive-pressure ventilation decreasing venous return and cardiac output. Treatment consists of administration of a fluid bolus of 10–20 mL/kg and/or inotrope, depending on the clinical setting. Alternatively, in the setting of bronchospasm hypotension may be due to gas trapping, with dynamic hyperinflation from excessive ventilation and the development of auto-PEEP (positive end-expiratory pressure), or even to a tension pneumothorax occurring after the commencement of positive-pressure ventilation. Hypertension usually indicates inadequate sedation and should be treated with supplemental sedation.

The following additional measures need to be considered during intubation in patients with severe head injury. An assistant must hold the head in the neutral position as there is the possibility of cervical spine instability, which increases the difficulty of visualizing the larynx. Also, laryngoscopy may raise intracranial pressure, although the benefit of pretreatment with lignocaine (lidocaine) 1.5 mg/kg is uncertain.¹² Thiopentone or propofol must be used cautiously in patients with shock, or with severe head injury and possible hypovolaemia, as precipitate and prolonged hypotension may occur. Doses as small as one-tenth of normal may be necessary, e.g thiopentone 0.5 mg/kg or propofol 0.2 mg/kg.

The technique of RSI is not recommended for patients with a grossly abnormal upper airway, and/or impending upper airway obstruction. In this setting, the larynx may not be visualized and ventilation of the apnoeic patient may become impossible, leading to the extreme emergency of the ‘can’t intubate, can’t ventilate’ situation. An initial awake technique, such as using local anaesthesia, or a fibreoptic assisted intubation, should be performed in these patients. Alternatively, an inhalational anaesthetic agent or a short-acting intravenous agent such as propofol is used, as the sedative effects will rapidly reverse and spontaneous respirations resume if intubation and ventilation prove impossible.

The difficult intubation

Endotracheal intubation under direct vision may be easy or difficult, depending on the view of the larynx during laryngoscopy. This view has been classified by Cormack and Lehane ¹³ into grades 1–4.

Cormack and Lehane laryngoscopy view

A Cormack and Lehane grade 1 laryngoscopy shows a clear view of the entire laryngeal aperture. A grade 2 laryngoscopy shows only the posterior part of the larynx visible. In a grade 3 laryngoscopy only the epiglottis is visualized, and in grade 4 only the soft palate is seen. A difficult intubation is defined as a grade 3 or 4 view at laryngoscopy.

Difficult intubation may be anticipated in the presence of pathological facial and upper airway disorders that may be congenital or acquired, such as maxillofacial and airway trauma, airway tumours and abscesses, or cervical spine immobility. There may also be anatomical reasons for a Cormack and Lehane grade 3–4 laryngoscopy, such as micrognathia or microstomia, poor mouth opening and/or a large tongue. A range of clinical tests have been proposed that may predict difficulty in visualization of the larynx, including relative size of the tongue to the pharynx, atlanto-occipital joint mobility, and a thyromental distance <6 cm. However, these are not always clinically useful in the emergency setting.¹⁴

Failed intubation drill

Attempts at blind placement of the ETT down the trachea when the larynx is not visualized are unlikely to be successful, and repeated attempts may result in direct pharyngeal or laryngeal trauma (making the situation even more difficult) and hypoxaemia. In this situation a failed intubation drill must be initiated.¹⁵ A failed intubation algorithm suitable for use in the ED is shown in Figure 2.1.1. Depending on local hospital staffing and resources, an urgent call for assistance from another physician with additional experience should also be made.

Simple initial manoeuvres to improve visualization of the larynx include adding a second pillow to further flex the neck (unless cervical spine injury is suspected), the use of a straight Mackintosh laryngoscope blade, and ‘backward/upward/rightward external pressure’ (BURP) on the thyroid cartilage. A new approach to laryngoscopy using the GlideScope Video Laryngoscope (GVL) (Verathon, Bothell, WA, USA) provides a real-time view of the larynx on a colour monitor, which has been shown in a large case series to convert a Cormack and Lehane grade 3–4 view to a grade 1–2 view 77% of the time.¹⁶ In the absence of a GlideScope, and if the larynx still cannot be visualized, blind placement of a gum-elastic bougie and subsequent insertion of the ETT by railroading it over the bougie should be attempted as the preferred next manoeuvre.¹⁷ Rotating the ETT through 90° in an anticlockwise direction may be helpful if resistance to its passage occurs at the larynx.

If these initial steps are unsuccessful, adequate oxygenation must be maintained using a bag/mask with an oral airway at all times. Alternative equipment suitable for use in the ED should be prepared.¹⁸ A summary of these devices for a failed intubation drill is given below (see Fig. 2.1.1). However, if oxygenation can not be maintained during the attempted use of these devices, immediate cricothyroidotomy is indicated. Make sure additional help has also been summoned.

Laryngeal mask airway

The laryngeal mask airway (LMA) is now used routinely for airway management during elective general anaesthesia. During a failed intubation drill, the LMA may be superior to a bag/mask and oral airway for oxygenation and ventilation.^15,¹⁷ However, the LMA has had a limited role in the ED, for two reasons. First, if pulmonary compliance is low or airway resistance is high, there will be a leak around the cuff of the LMA when peak inspiratory airway pressures exceed 20–30 mmHg. Second, there is the potential risk of aspiration pneumonitis as the airway remains unprotected. The LMA ProSeal (Vitaid Ltd, Toronto, Ontario, Canada) modification of the standard LMA minimizes this risk, and includes a double cuff to improve the seal and a distal drainage tube to provide access for suctioning the upper oesophagus. The LMA may also be used to assist in orotracheal intubation, using either a 6 mm ETT passed blindly through the LMA, or an ETT placed over a fibreoptic bronchoscope which is then passed through the LMA into the trachea.

Intubating laryngeal mask airway

The ‘intubating LMA’ (ILMA) is a modification of the standard LMA that incorporates a rigid, anatomically curved airway tube with handle, and a special modified endotracheal tube and extender specifically made to pass blindly through the ILMA into the trachea. This appears to have a high success rate even with inexperienced operators, both in managing patients with a difficult airway in hospital ¹⁹ and in the pre-hospital setting.²⁰ The ILMA is placed and ventilation commenced, and once oxygenation is assured, the ETT component is passed through the ILMA. Once sited, the ETT cuff is inflated and the position confirmed using capnography and then chest X-rays.

Fibreoptic bronchoscope-assisted intubation

A fibreoptic bronchoscope assists in the intubation of the patient when RSI fails or is contraindicated. In particular, fibreoptic bronchoscope-assisted intubation (FBI) is the technique of choice in suspected traumatic injury to the larynx, and in the obstructed airway, particularly with distorted anatomy such as with an upper airway burn or tumour. The FBI may diagnose the severity of the laryngeal injury or pathology and the possible requirement for surgery. However, it requires considerable training and should only be performed by an experienced operator. Equipment sterilization, maintenance and checking procedures must also be in place (see later).

Intubation procedure

If the patient is awake, apply topical anaesthetic to the nasal passage and upper airway as for blind nasotracheal intubation (BNTI – see later). Initially, introduce a well-lubricated ETT nasally and pass to the posterior pharynx. Then insert the bronchoscope through the ETT to visualize the vocal cords. The suction port of the bronchoscope may be used to clear any secretions, and also to administer further local anaesthesia into the airway. Advance the bronchoscope through the larynx and railroad the ETT over it and down the trachea. Administer further sedation at this time. Ventilate the patient with oxygen following removal of the bronchoscope. If a LMA has been used during a failed intubation drill and is in place to provide ventilation, this may be utilized to guide the bronchoscope (with the ETT already placed over it) into the larynx. Removal of the LMA then requires placement of a gum-elastic bougie; the ETT and LMA are removed, then the ETT is replaced over the bougie.

The use of a fibreoptic bronchoscope in the ED is limited by several factors. The bronchoscope and light source must be immediately available during a failed intubation drill. The technique requires considerable practice for skills maintenance, yet its use is rare in ED practice. The larynx may be difficult to visualize in the presence of blood, vomitus or copious secretions. Finally, the equipment is expensive to purchase and maintain.

Retrograde intubation

When other techniques fail the technique of retrograde intubation may occasionally be used in the ED if time permits.²¹ The cricothyroid membrane is punctured by a needle/cannula and a guide-wire is passed through the cannula, directed cephalad. The wire is then brought out through the mouth using Magill’s forceps. There are a number of techniques used to then guide the ETT over the wire and back into the larynx, such as a proprietary device (Cook, Cook Medical Inc, Bloomington, IN, USA), or the introducer of a Minitrach II kit (Portex Ltd, Hythe, Kent, UK).²² Alternatively, the wire may be passed inside the end of the ETT and then out through the ‘Murphy eye’. Resistance may be felt when the ETT reaches the larynx, and some anticlockwise rotation may be required to facilitate passage into the larynx. When the level of the cricothyroid is reached, the guide-wire is removed and the ETT passed further down the trachea. The technique of retrograde intubation takes time and experience to perform and is usually unsuitable in a critical airway emergency.

Blind nasotracheal intubation

Blind nasotracheal intubation (BNTI) is a technique that is now rarely used in the operating theatre, but may occasionally be useful in the ED, either as the initial technique of choice or as part of a failed intubation drill once spontaneous respirations have resumed. Contraindications include a fractured base of skull or maxillary fracture, a suspected laryngeal injury, coagulopathy or upper airway obstruction.

High-flow oxygen is administered by mask and the nasal passages are inspected to assess patency. The larger nasal passage is prepared with a pledget soaked in local anaesthetic and vasoconstrictor, such as 5 mL lignocaine (lidocaine) 2% with epinephrine 1:100 000. After several minutes the pledget is removed and sterile lubricant applied. Local anaesthetic may also be sprayed into the upper airway, and/or intravenous sedation may be administered if required and clinically appropriate. An ETT one size smaller than the predicted oral size is passed via the nose to the pharynx and advanced slowly towards the larynx, with the operator listening for breath sounds.

The head may need to be flexed, extended or rotated to facilitate entry into the larynx, the ETT rotated clockwise through 90°, and/or a suction catheter used to guide the ETT. When the tube passes into the trachea, louder spontaneous respirations heard from the ETT, or the onset of coughing down the tube, confirm successful placement. However, there are significant complications with BNTI, including epistaxis,²³ injuries to the turbinates, perforation of the posterior pharynx, laryngospasm and injury to the larynx. In addition, an already jeopardized airway may be made worse, leaving the situation impossible to then control.

Cricothyroidotomy

Cricothyroidotomy is an essential skill for all emergency physicians and must be considered immediately in the situation of ‘can’t intubate, can’t ventilate’. There are several possible techniques for emergency cricothyroidotomy.

Techniques for emergency cricothyroidotomy

First, there are proprietary kits that allow a cricothyroidotomy tube to be placed using the Seldinger technique. In this approach, the cricothyroid membrane is punctured with a needle mounted on a syringe; free aspiration of air confirms placement in the airway. A guide-wire is passed through the needle down the trachea. The needle is then removed and a dilator passed along the wire, then a 4.5–6 mm cricothyroidotomy tube is mounted on a guide and passed along the wire and into the trachea. The position of the cricothyroidotomy tube must be carefully checked, as it is easy to misplace it anterior to the trachea. However, if the cricothyroidotomy tube is uncuffed, interpretation of a capnograph waveform can be difficult as much of the exhaled gas may pass into the upper airway, and not through the cricothyroidotomy tube during exhalation, resulting in a false-negative end-tidal CO₂ trace.

Surgical cricothyroidotomy

Alternatively, perform a surgical cricothyroidotomy by making a small vertical incision over the cricothyroid membrane. Use artery forceps for blunt dissection to the cricothyroid membrane, which is incised and the cricothyroid membrane opened horizontally with artery forceps. Pass a size 6 mm cuffed ETT or tracheostomy tube through the opening into the trachea, inflate the cuff and commence bag/valve ventilation. This technique is usually faster to perform than a guide-wire technique, although physicians with limited surgical experience may prefer the Seldinger approach.²⁴

Longer-term placement of a larger tube (>6 mm) through the cricothyroid membrane is unsatisfactory because of the possibility of stricture occurring at the level of the cricoid ring. Therefore, the cricothyroidotomy is converted to either an oral endotracheal intubation or a tracheostomy when it is safe and convenient to do so.

Tracheostomy

Compared with cricothyroidotomy, a surgical tracheostomy is time-consuming and difficult to perform in the ED. Pre-tracheal dissection requires adequate lighting, instruments and diathermy, because the thyroid isthmus may be anterior to the trachea. Distorted anatomy and bleeding make the technique more complex. However, percutaneous dilatational tracheostomy is commonly performed in the ICU, and can be rapidly performed by an experienced operator in the ED, although there is little published experience with this technique outside the ICU. In addition, some techniques use a second operator visualizing correct tube placement via a bronchoscope.

Mechanical ventilation

Once intubation has been achieved, the patient is connected to a mechanical ventilator to provide continued ventilatory support. Because ventilated patients may initially be managed for some time in the ED, it is important that recommendations for optimal mechanical ventilation are implemented in the ED.

Recommendations for optimal mechanical ventilation

A tidal volume of 10 mL/kg and a respiratory rate of 10–14 breaths per minute are considered safe for most patients. However, patients with acute lung injury may have reduced pulmonary compliance and hence elevated peak inspiratory pressures. These patients should receive a ‘protective lung strategy’.²⁵ This involves limiting the tidal volume to 6 mL/kg, with the respiratory rate setting increased to 16–20 breaths per minute to prevent excessive hypercapnia. Deliberate hyperventilation using a respiratory rate of 16–20 breaths per minute may also be indicated to provide hypocapnia in other situations, such as in patients with severe metabolic acidosis, and in patients with raised intracranial pressure, in whom transient hypocapnia of 30–35 mmHg (4.0–4.7 kPa) may temporarily reduce intracranial pressure while other treatments for intracranial hypertension are being implemented.

Conversely, patients with severe airways obstruction such as asthma or COPD should receive a standard tidal volume of 10 mL/kg, but a decreased respiratory rate from 4 to 8 breaths per minute to allow sufficient time for adequate passive exhalation.²⁶ This reduces the risk of pulmonary hyperinflation, with the development of auto-PEEP leading to hypotension, even electromechanical dissociation. Thus when ventilating a critical asthmatic the PaCO₂ level will rise (known as ‘permissive hypercapnia’), with the aim being to initially concentrate only on oxygenation.

Extubation in the emergency department

Increasingly, patients who are intubated ‘in the field’ by paramedics or by a physician in the ED may be considered for planned extubation in the ED, after investigation and treatment have excluded a requirement for admission to the ICU. Examples include patients with a drug overdose, or those requiring brief general anaesthesia for a procedure.

Prediction of successful extubation

Prediction of successful extubation is problematic in the ICU,²⁷ and there are even fewer published data to guide successful elective ED extubation. In general, patients should be awake, able to follow commands and cough, pass a trial of spontaneous breathing with the ventilator set to a continuous positive airways pressure (CPAP) of 5 cmH₂O, with minimal pressure support of 5–10 cmH₂O, and who require only modest supplemental oxygen, that is, < 50% inspired oxygen (FiO₂ < 0.5). Ideally, the stomach should be emptied via an orogastric or nasogastric tube prior to extubation.

Controversies

• Choice of drugs used in RSI intubation, and the role of premedication agents.

• Training and skills maintenance of airway management techniques in the ED.

• The optimal ‘Difficult Airway Kit’.

• Practising the failed intubation drill in the ED, including the role of simulation.

References

1 Hill NS, Brennan J, Garpestad E, Nava S. Noninvasive ventilation in acute respiratory failure. Critical Care Medicine. 2007;35:2402-2407.

2 Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet. 2006;367:1155-1163.

3 Ram FS, Lightowler JV, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Systematic Review. 1, 2004. CD004104

4 Keenan SP, Sinuff T, Cook DJ, et al. Does non-invasive positive pressure ventilation improve outcome in acute hypoxemic respiratory failure? A systematic review. Critical Care Medicine. 2004;32:2516-2523.

5 Ram FS, Wellington S, Rowe B, et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Systematic Review. 3, 2005. CD004360

6 Baillard C, Fosse JP, Sebbane M, et al. Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. American Journal of Respiratory and Critical Care Medicine. 2006;174:171-177.

7 Wilbur K, Zed PJ. Is propofol an optimal agent for procedural sedation and rapid sequence intubation in the emergency department? Canadian Journal of Emergency Medicine. 2001;3:302-310.

8 Sluga M, Ummenhofer W, Studer W, et al. Rocuronium versus succinylcholine for rapid sequence induction of anesthesia and endotracheal intubation: a prospective, randomized trial in emergent cases. Anesthesia and Analgesia. 2005;101:1356-1361.

9 Ellis DY, Harris T, Zideman D. Cricoid. Pressure in emergency department rapid sequence tracheal intubations: a risk-benefit analysis. Annals of Emergency Medicine. 2007;50:653-665.

10 Deiorio NM. Continuous end-tidal carbon dioxide monitoring for confirmation of endotracheal tube placement is neither widely available nor consistently applied by emergency physicians. Emergency Medicine Journal. 2005;22:490-493.

11 Schaller RJ, Huff JS, Zahn A. Comparison of a colorimetric end-tidal CO₂ detector and an esophageal aspiration device for verifying endotracheal tube placement in the prehospital setting: a six-month experience. Prehospital and Disaster Medicine. 1997;12:57-63.

12 Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emergency Medicine Journal. 2001;18:453-457.

13 Cormack RS, Lehane J. Difficult intubation in obstetrics. Anaesthesia. 1984;39:1105-1111.

14 Shiga T, Wajima Z, Inoue T, Sakamoto A. Predicting difficult intubation in apparently normal patients: a meta-analysis of bedside screening test performance. Anesthesiology. 2005;103:429-437.

15 Henderson JJ, Popat MT, Latto IP, et al. Difficult Airway Society. Difficult Airway Society guidelines for management of the unanticipated difficult intubation. Anaesthesia. 2004;59:675-694.

16 Cooper RM, Pacey JA, Bishop MJ, McCluskey SA. Early clinical experience with a new videolaryngoscope (GlideScope) in 728 patients. Canadian Journal of Anaesthesia. 2005;52:191-198.

17 Jabre P, Combes X, Leroux B, et al. Use of gum elastic bougie for prehospital difficult intubation. American Journal of Emergency Medicine. 2005;23:552-555.

18 Bair AE, Filbin MR, Kulkarni RG, et al. The failed intubation attempt in the emergency department: analysis of prevalence, rescue techniques, and personnel. Journal of Emergency Medicine. 2002;23:131-140.

19 Ferson DZ, Rosenblatt WH, Johansen MJ, et al. Use of the intubating LMA-Fastrach in 254 patients with difficult-to-manage airways. Anesthesiology. 2001;95:1175-1181.

20 Timmermann A, Russo SG, Rosenblatt WH, et al. Intubating laryngeal mask airway for difficult out-of-hospital airway management: a prospective evaluation. British Journal of Anaesthesia. 2007;99:286-291.

21 Weksler N, Klein M, Weksler D, et al. Retrograde tracheal intubation: beyond fibreoptic endotracheal intubation. Acta Anaesthesiologica Scandinavica. 2004;48:412-416.

22 Slots P, Vegger PB, Bettger H, et al. Retrograde intubation with a Mini-Trach II kit. Acta Anaesthesiologica Scandinavica. 2003;47:274-277.

23 Piepho T, Thierbach A, Werner C. Nasotracheal intubation: look before you leap. British Journal of Anaesthesia. 2005;94:859-860.

24 Sulaiman L, Tighe SQ, Nelson RA. Surgical vs wire-guided cricothyroidotomy: a randomised crossover study of cuffed and uncuffed tracheal tube insertion. Anaesthesia. 2006;61:565-570.

25 Girard TD, Bernard GR. Mechanical ventilation in ARDS: a state-of-the-art review. Chest. 2007;131:921-929.

26 Shapiro JM. Management of respiratory failure in status asthmaticus. American Journal of Respiratory and Critical Care Medicine. 2002;1:409-416.

27 Meade M, Guyatt G, Cook D, et al. Predicting success in weaning from mechanical ventilation. Chest. 2001;120:400S-4424S.

2.2 Oxygen therapy

David R. Smart

Essentials

1 Oxygen is the most commonly used drug in emergency medicine.

2 Oxygen-delivery systems may be divided into variable performance (delivering a variable concentration of oxygen) and fixed performance (delivering a fixed concentration of oxygen, including systems that deliver 100% oxygen).

3 Controlled-dose oxygen therapy is required when treating patients with chronic obstructive pulmonary disease (COPD), commencing with 24–28%. Response to therapy in these patients should be monitored with arterial blood gases measurements.

4 Oxygen should never be abruptly withdrawn from patients in circumstances of suspected CO₂ narcosis.

5 Fixed-performance systems are essential where precise titration of oxygen dose is required, such as with COPD, or where 100% oxygen is required.

6 In attempting to deliver 100% oxygen, free-flowing circuits are least efficient. A reservoir or demand system improves efficiency, and a closed-circuit delivery system is most efficient.

7 Pulse oximetry provides valuable feedback regarding the appropriateness of oxygen dose provided to individual patients.

Introduction

Oxygen was first discovered by Priestley in 1772 and was first used therapeutically by Beddoes in 1794. It now forms one of the cornerstones of medical therapy.

Oxygen (O₂) constitutes 21% of dry air by volume. It is essential to life. Cellular hypoxia results from a deficiency of oxygen, regardless of aetiology. Hypoxaemia is a state of reduced oxygen carriage in the blood. Hypoxia leads to an anaerobic metabolism that is inefficient, and may lead to death if not corrected. A major priority in acute medical management is correction of hypoxia, hence oxygen is the most frequently administered and important drug in emergency medicine. There are sound physiological reasons for the use of supplemental oxygen in the management of acutely ill and injured patients.

Uses of supplemental oxygen

• To correct defects in the delivery of inspired gas to the lungs. A clear airway is essential.

• Where there is inadequate oxygenation of blood due to defects in pulmonary gas exchange.

• To maximize oxygen saturation of the arterial blood (SaO₂) where there is inadequate oxygen transport by the cardiovascular system.

• To maximize oxygen partial pressure and content in the blood in circumstances of increased or inefficient tissue oxygen demand.

• To provide 100% oxygen where clinically indicated.

• To titrate oxygen dose in patients with impaired ventilatory response to carbon dioxide.

Physiology of oxygen

Oxygen transport chain

Oxygen proceeds from inspired air to the mitochondria via a number of steps known as the oxygen transport chain. These steps include:

1 Ventilation

2 Pulmonary gas exchange

3 Oxygen carriage in the blood

4 Local tissue perfusion

5 Diffusion at tissue level

6 Tissue utilization of oxygen.

Ventilation

The normal partial pressure of inspired air oxygen (P_IO₂) is approximately 20 kPa (150 mmHg) at sea level. If there is a reduction in the fraction of inspired oxygen (F_IO₂), as occurs at altitude, hypoxia results. This is relevant in the transport of patients at 2400 m in commercial ‘pressurized’ aircraft, where ambient cabin pressures of 74.8 kPa (562 mmHg) result in a P_IO₂ of 14.4 kPa (108 mmHg).

Hypoxia can result from inadequate delivery of inspired gas to the lung. The many causes include airway obstruction, respiratory muscle weakness, neurological disorders interfering with respiratory drive (seizures, head injury), disruption to chest mechanics (chest injury), or extrinsic disease interfering with ventilation (intra-abdominal pathology). These processes interfere with the maintenance of an adequate alveolar oxygen partial pressure (P_AO₂), which is approximately 13.7 kPa (103 mmHg) in a healthy individual.

Alveolar gas equation

An approximation of the alveolar gas equation permits rapid calculation of the alveolar oxygen partial pressures:

Pulmonary gas exchange

Oxygen diffuses across the alveoli and into pulmonary capillaries, and carbon dioxide diffuses in the opposite direction. The process is passive, occurring down concentration gradients. Fick’s law summarizes the process of diffusion of gases through tissues:

where = rate of gas (oxygen) transfer, ∝ = proportional to, A = area of tissue, T = tissue thickness, Sol = solubility of the gas, MW = molecular weight, P_A = alveolar partial pressure, and P_pa = pulmonary artery partial pressure.

In healthy patients oxygen passes rapidly from the alveoli to the blood, and after 0.25 seconds pulmonary capillary blood is almost fully saturated with oxygen, resulting in a systemic arterial oxygen partial pressure (P_AO₂) of approximately 13.3 kPa (100 mmHg). The difference between the P_AO₂ and the PaO₂ is known as the alveolar to arterial oxygen gradient (A–a gradient). It is usually small and increases with age.

Expected A–a gradient

The expected A–a gradient when breathing air approximates to: age (years) ÷ 4 + 4. An approximation of the actual value may be calculated as follows:

There is a defect in pulmonary gas exchange if the calculated value exceeds the expected value. The A–a O₂ gradient is increased if there is a barrier to diffusion, such as pulmonary fibrosis or oedema, or a deficit in perfusion such as a pulmonary embolism. An increased A–a gradient also reflects widespread ventilation–perfusion mismatch. In circumstances of impaired diffusion in the lung, raising the F_IO₂ assists oxygen transfer by creating a greater pressure gradient from the alveoli to the pulmonary capillary. The increase in F_IO₂ may not be as helpful when lung perfusion is impaired as a result of increased intrapulmonary shunting.

Oxygen carriage in the blood

Three steps are required to deliver oxygen to the periphery:

1 Uptake of oxygen by haemoglobin (Hb).

2 Generation of a cardiac output to carry the oxygenated haemoglobin to the peripheral tissues.

3 Dissociation of oxygen from haemoglobin to allow diffusion from blood to cell.

The haemoglobin–oxygen (Hb–O₂) dissociation curve

The haemoglobin-oxygen (Hb–O₂) dissociation curve is depicted in Figure 2.2.1, which also summarizes the factors that influence the position of the curve. If the curve is shifted to the left, this favours the affinity of haemoglobin for oxygen. These conditions are encountered when deoxygenated blood returns to the lung. A shift of the curve to the right favours unloading of oxygen and subsequent delivery to the tissues.

Fig. 2.2.1 The haemoglobin–oxygen dissociation curve.

A number of advantages are conferred by the shape of the Hb–O₂ dissociation curve that favour uptake of oxygen in the lung and delivery to the tissues:¹

• A flat upper portion of the curve allows some reserve in the P_AO₂ required to keep the haemoglobin fully saturated; a reduction in P_AO₂ of 20% will have minimal effect on the oxygen loading of Hb.

• The flat upper portion of the curve also ensures that a large difference remains between P_AO₂ and the pulmonary capillary oxygen partial pressure (P_pcO₂), even when much of the haemoglobin has been loaded with oxygen. This pressure difference favours maximal Hb–O₂ loading.

• The lower part of the curve is steeper, which favours offloading of oxygen in peripheral tissues with only small falls in capillary PO₂. This maintains a higher driving pressure of oxygen, facilitating diffusion into cells.

• The right shift of the Hb–O₂ curve in circumstances of increased temperature, fall in pH, increased PCO₂and increased erythrocyte 2,3-DPG assists in further offloading of oxygen, even when the driving pressure has fallen and PO₂ has reached 5.3 kPa (40 mmHg), i.e. venous blood which is still 75% saturated with oxygen.

Oxygen is carried in the blood as dissolved gas and in combination with haemoglobin. At sea level (101.3 kPa), breathing air (F_IO₂ = 0.21), the amount of oxygen dissolved in plasma is very small (0.03 mL oxygen per litre of blood for each 1 mmHg PaO₂). This dissolved component assumes greater significance in a hyperbaric situation, where at 284 kPa and F_IO₂ = 1.0 up to 60 mL oxygen can be carried in the dissolved form per litre of blood.

Haemoglobin carries 1.34–1.39 mL oxygen per gram when fully saturated. Blood with a haemoglobin concentration of 15 g/L carries approximately 200 mL oxygen per litre.

Oxygen flux

The total amount of oxygen delivered to the body per minute is known as oxygen flux.¹

where Hb = haemoglobin concentration g/L; S_aO₂ = arterial oxygen saturation (percentage); PaO₂ = partial pressure of arterial oxygen (mmHg); Q = cardiac output (L/min).

A healthy individual breathing air transports approximately 1000 mL oxygen per minute to the tissues, with a cardiac output of 5 L/min; 30% or 300 mL/min of this oxygen is not available, because at least 2.7 kPa (20 mmHg) driving pressure is required to allow oxygen to enter the mitochondria, and therefore approximately 700 mL/minute are available for use by peripheral tissues. This provides a considerable reserve above the 250 mL/min consumed by a healthy resting adult.

In illness or injury this reserve may be considerably eroded. Factors that reduce oxygen flux include a fall in cardiac output of any aetiology (including shock states), anaemia or a reduction in functional haemoglobin (carbon monoxide poisoning) and a drop in the S_aO₂. These situations are frequently encountered in emergency medicine. Supplemental oxygen is required in addition to specific therapy such as volume replacement, transfusion, and measures to improve cardiac output.