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.

Local tissue perfusion and diffusion

Cellular hypoxia results if there is impairment of perfusion to local tissues. Oedema associated with medical illness or local injury increases the diffusion distance between blood and cell, thus mandating a higher PaO₂to ensure adequate tissue oxygen delivery.

Tissue utilization of oxygen

Increased oxygen flux is required if:

• Tissue demands for oxygen are higher than normal, or

• Tissue utilization of oxygen is impaired.

Elevation of cardiac output increases oxygen flux in these circumstances, but frequently this too is significantly impaired by the disease state.

Tissue demands for oxygen increase by 7% for each degree Celsius elevation in body temperature, and considerably greater increases in demand occur in seizures, sepsis, severe dyspnoea, restlessness and shivering.²

Tissue extraction of oxygen is impaired in sepsis, and by poisons such as carbon monoxide or cyanide. In all cases, oxygen therapy must be combined with general measures such as reduction of fever and specific treatment of the primary disease process.

Definitions

Variable-performance oxygen delivery systems

These systems deliver a variable F_IO₂ to the patient that is altered by the inspiratory flow rate, the minute volume of the patient, and the physical characteristics of the delivery system.

Fixed-performance oxygen delivery systems

These systems deliver a specified F_IO₂ to the patient that is not altered by changes in ventilatory pattern, volume or inspiratory flow rate.

One hundred per cent (100%) oxygen systems

This is a subgroup of fixed-performance systems wherein 100% oxygen is delivered to the patient.

General principles

In most Australasian emergency departments the oxygen source consists of a wall-mounted flowmeter capable of delivering oxygen up to 15 L/min. Most available oxygen delivery systems connect to this apparatus. The 15 L/min flow rate limits the delivery of high F_IO₂ to adults for the following reasons:

• A quietly breathing adult has a peak inspiratory flow rate (PIFR) of approximately 30–40 L/min, which exceeds the oxygen supply. Hence a free flowing system such as a Hudson mask must entrain air into the system in order to match the patient’s PIFR, with a resultant reduction in F_IO₂to a maximum of 0.6.³

• A quietly breathing adult has a respiratory minute volume of 4–8 L; in a child this value is approximately 150 mL/kg. Oxygen is stored during expiration by incorporating a reservoir into the circuit for use during inspiration, with a considerable improvement in the economy of oxygen use. This system is limited by the patient’s minute volume. If the minute volume exceeds 15 L there is a danger of the patient asphyxiating due to insufficient gas supply, or if safety valves allow air into the system, the F_IO₂ falls.

Multiple-port oxygen supply outlets can overcome the above limitations of inspiratory flow rate and minute volume. The use of ‘Y’ connectors and ‘T’ pieces enable 30, 45 or 60 L per minute to be delivered to the patient to achieve an F_IO₂ of very nearly 1.0. Extra source oxygen flow may cause variable-performance systems such as the Hudson mask to become fixed-performance systems. Hence the terms ‘variable performance’ and ‘fixed performance’ are loosely applied and are largely dependent on whether or not the flow of gas delivered to the patient is sufficient to match their ventilatory requirements.

A fine example of this is in paediatric oxygen delivery. A high F_IO₂ can be delivered using a standard 15 L/min oxygen source because the child’s ventilatory requirements are smaller in proportion to the available oxygen supply.

The oxygen delivery systems available for use in emergency medicine are broadly summarized in Table 2.2.1. They can be further subdivided according to economy of oxygen use and whether or not the system can be used to ventilate the patient manually. Figures depicting the various systems have been published elsewhere.³

Variable performance systems

The F_IO₂ delivered by these systems is summarized in Table 2.2.2. Options available for use in emergency medicine include:

• Nasal cannulae

• Face masks with air inlets

• T pieces and Y connectors.

Table 2.2.2 Variable-performance oxygen delivery systems

Apparatus	Oxygen flow (L/min)	Oxygen concentration (%)
Nasal catheters	1–4	24–40
Semi-rigid mask	6–15	35–60
Semi-rigid mask + double O₂ supply	15–30	Up to 80
Semi-rigid mask + reservoir bag	12–15	60–90

Nasal cannulae

The system must be used at flow rates 4 L/min or less to avoid painful drying of the nasal mucosa, although a flow rate of 2 L/min or less is insufficient to create a nasopharyngeal reservoir during the expiration pause, for inspiration with the next breath.

The inspired oxygen concentration is a function of the patient’s inspiratory flow rate, and is usually in the vicinity of 22–28%. At flow rates of 2–4 L/min the nasopharynx acts as a partial reservoir during the expiratory pause, resulting in an increased F_IO₂. The delivered F_IO₂ is then influenced by the pattern of breathing (mouth or nose) and the positioning of the nasal cannula.⁴

Nasal cannulae provide a higher F_IO₂ in paediatric patients and nose breathers. They are less effective in dyspnoeic patients because of the greater amounts of air inspired through the mouth. They are frequently used in patients with stable COPD because of the absence of dead space that prevents CO₂ rebreathing. However, fluctuations in F_IO₂ make nasal cannulae less than ideal in the management of patients who rely on hypoxic respiratory drive, and they are second choice after Venturi masks in the emergency management of these patients. Advantages for home therapy include the ability to eat and drink, less noise than masks, and economy of oxygen use.

Face masks (e.g. Hudson, Edinburgh, Medishield)

A small reservoir of oxygen is provided by these masks, but this has little effect on F_IO₂. The small increase in dead space created by the mask necessitates a flow rate greater than 6 L/min to prevent rebreathing of CO₂. Two factors influence the F_IO₂ provided by this system:

1 The patient’s inspiratory flow rate

2 The source oxygen supply flow rate.

At flow rates of 6–14 L/min, the delivered F_IO₂ varies from 0.35 to 0.6. This will be less in a dyspnoeic patient because of the higher inspiratory flow rate, and greater in a child because the converse applies. If the PIFR increases, greater amounts of air will be entrained into the mask, diluting the oxygen. During expiration, the exhaled gas and excess oxygen are vented through the side perforations.

Attaching a reservoir bag to this mask improves the economy of oxygen use by storing this vented gas during the expiratory phase. This increases the delivered F_IO_2, but this may be at the expense of increased CO₂ rebreathing. Commercially available reservoir bags have a volume of 750 mL to 1 L, which is inadequate for a dyspnoeic patient. The author recommends a minimum flow rate of 12 L/min to avoid CO₂ retention.

Using a source oxygen supply of 15 L/min, the maximum F_IO₂ delivered via a Hudson mask to a quietly breathing adult is 0.6.³ By attaching another source of oxygen using a ‘T’ piece or ‘Y’ connector, the resultant flow rate of 30 L/min can deliver an F_IO₂ up to 0.8. With even greater flow rates the mask may be converted into a fixed-performance system delivering an F_IO₂ of almost 1.0. Then the ability to deliver 100% oxygen is limited by the mask’s ‘fit’.

The Medishield mask is stated to be more efficient than the Hudson because dead space is reduced by bringing the oxygen supply closer to the mouth, allowing more effective entrainment during inspiration. An F_IO₂ of 0.75 may be obtained with a gas flow rate of 15 L/min.

T pieces and Y connectors

The term ‘T piece’ has been used to describe a number of different oxygen delivery systems, including the ‘T piece’ for supplying humidified oxygen to patients with a tracheostomy, and the ‘Ayre’s T piece’ which is the Mapleson E circuit. The use of ‘T pieces’ or ‘Y connectors’ in emergency medicine is to supplement an existing oxygen supply with:

• extra oxygen

• nebulized medication

• humidification.

The disadvantage of the system is that several oxygen ports are necessary, which is untidy and may restrict the patient’s mobility. There is loss of economy of oxygen use because of higher flow rates. T pieces allow a higher F_IO₂ to be delivered to severely dyspnoeic patients.

Fixed-performance systems

Two systems are available for use in emergency departments:

1 High-flow Venturi masks

2 Oxygen blenders.

High-flow Venturi mask

Oxygen flow through a Venturi system results in air entrainment with delivery of a fixed concentration of oxygen to the patient. The masks deliver F_IO₂ values from 0.24, 0.28, 0.35, 0.40 and 0.50 to 0.60, using different colour-coded adaptors, or by varying the position of a dial on the mask. Many studies have assessed their accuracy.⁵^–⁸ It is generally considered that the patient receives the stated F_IO₂ provided the total flow rate exceeds 60 L/min or is 30% higher than the patient’s PIFR.^9,¹⁰ As the patient’s PIFR increases, the system’s performance becomes variable.

In supplying an F_IO₂ of 0.24 using 6 L/min flow rate, the total flow rate delivered to the patient is 120 L/min. This falls to 30 L/min total flow for F_IO₂ = 0.6 using 15 L/min oxygen supply.³ This is just equal to the PIFR of a quietly breathing adult, and unlikely to be sufficient to provide consistent performance in delivery of the stated F_IO₂. In severe dyspnoea these masks may not deliver the stated F_IO₂.⁶ Increasing the oxygen flow rate above the manufacturer’s recommendations will increase the total gas flow to the mask, while maintaining the stipulated F_IO₂.⁸ At very high flow rates, however, turbulence is likely to reduce the performance of the system.

Venturi masks provide the best means of managing patients with chronic obstructive airways disease in the ED, because they provide a predictable F_IO₂ and the air entrained is more humid than fresh oxygen (see below). The entrained gas mixture can be further heated and humidified to assist with sputum clearance. High gas flows minimize rebreathing of CO₂ and claustrophobia, but cause problems with sleeping due to noise.

Oxygen blenders

Air is blended with oxygen from a number of inlet ports to supply a fixed F_IO₂ to the patient. It is a high-flow system, and fine-tuning of F_IO₂ from 0.21 to 1.0 is possible. The resultant mixture can then be channelled to the patient through systems such as continuous positive airways pressure, or humidifiers. Lack of portability and high cost are disadvantages. Oxygen blenders are best suited to the resuscitation room and critical-care settings.

100% oxygen delivery systems

These systems vary in their economy of oxygen use, and are summarized in Table 2.2.3. The least economical is the free-flowing system, because it can only deliver 100% oxygen if the flow rate exceeds the patient’s PIFR. Incorporating a reservoir and unidirectional valves into the circuit enables greater economy of oxygen use by storing oxygen during expiration ready for the inspiratory phase.

Table 2.2.3 Classification of 100% oxygen systems

Devices incorporating a reservoir into the circuit are capable of delivering 100% oxygen only when the total oxygen flow equals or exceeds the patient’s respiratory minute volume (RMV), plus there are no leaks in the system. The reservoir volume must exceed the patient’s tidal volume, otherwise storage of oxygen is inefficient, fresh gas loss occurs when the reservoir is full, and there is the risk of asphyxia during inspiration.

A demand valve system delivers precisely the patient’s minute volume without the added bulk and problems of a reservoir. It is able to cope with changes in RMV provided fresh gas flow always exceeds the patient’s PIFR. Closed-circuit systems are the most economical in oxygen consumption. Carbon dioxide is absorbed by soda lime, and low-flow fresh oxygen replaces that consumed during metabolism, which is approximately 250–1000 mL/min, which is considerably less than the patient’s minute volume.

Classification

One hundred per cent oxygen-delivery systems available for use in emergency medicine are summarized in Table 2.2.3.

Free-flowing circuits

In order to provide 100% oxygen using a free-flowing system, flow rates in excess of the patient’s PIFR are required. This necessitates the use of multiple oxygen ports. The system may not deliver 100% oxygen, is wasteful of oxygen and may be untidy, restricting patient mobility for investigations. Sophisticated free-flowing systems using oxygen blenders and humidification are available, but restrict the ability to move the patient.

Soft reservoir circuits

These are non-rebreathing systems incorporating unidirectional valves to channel fresh oxygen to the patient and exhaled gas to the atmosphere. With one oxygen supply port the system delivers 100% oxygen, provided the patient’s minute volume is less than 15 L/min. Two oxygen supply ports enable delivery of up to 30 L/min. Fresh gas flow is titrated to the patient’s minute volume by watching the reservoir bag. This should be fully distended at the start of inspiration, and more than one-third full when inspiration is complete.

The reservoir bag has a minimum volume of 3 L, and for optimal performance the patient’s tidal volume should not exceed 2 L. A soft silicone mask is strapped to the head to ensure a firm but comfortable fit without leaks. The system cannot be used to ventilate patients manually, and may be hazardous if the patient has an impaired conscious state owing to the risk of aspiration if they vomit, and asphyxiation if there is a fall in fresh gas flow or a sudden rise in minute volume. Complications can be avoided with careful clinical vigilance, and the use of safety valves to entrain air if the oxygen supply ceases.

Self-refilling, non-rebreathing resuscitators (Air viva and Laerdal systems)

Most Australasian emergency departments possess at least one type of these self-refilling systems. They can be used to ventilate patients manually as well as allowing spontaneous ventilation. The Laerdal system has three sizes for adults, children and infants, whereas the Air viva system has one size for adults only (Table 2.2.4).

Table 2.2.4 Self-refilling, non-rebreathing resuscitators

	Self-refilling bag volume (mL)	Reservoir bag volume
Air viva	1700	2300
Laerdal (Adult)	1600	2600
Laerdal (Child)	500	2600
Laerdal (Infant)	240	600

Advantages

• Self-inflation and hence the ability to ventilate patients with air if oxygen supply is exhausted.

• Low resistance unidirectional valves prevent rebreathing of CO₂.

• Use in spontaneously ventilating patients and for manual ventilation.

• Provided fresh gas flow exceeds minute volume and the reservoir bag is attached, the system is capable of delivering F_IO₂ = 1.0. Without the reservoir bag, a maximum F_IO₂ of 0.6 is obtainable.

• A safety valve entrains air into the system to prevent asphyxiation if there is a sudden rise in minute volume, but this is at the expense of F_IO₂.

• Over-pressure valves are incorporated into the Laerdal paediatric and infant apparatus to prevent barotrauma in these patients.

• The addition of positive end-expiratory pressure (PEEP) to the system is possible by attaching a PEEP valve to the expiratory limb. Close apposition of the mask to the face, or endotracheal intubation, is required for this to be effective.

Disadvantages

• A reduction in F_IO₂ occurs when minute volume exceeds fresh gas flow. Dual oxygen supply ports can minimize this problem, especially in very dyspnoeic patients.

• The unit is bulky, and disconnections sometimes occur.

• There is less ‘feel’ during manual ventilation than with soft bag circuits, and inflation of the stomach is more likely during bag/mask ventilation, especially if there is airway obstruction or reduced pulmonary compliance.

Oxygen-powered resuscitators

Examples of this type of system include the Oxy viva, Laerdal, and DAN demand valve systems. High-pressure oxygen is fed to a demand valve which delivers high-flow oxygen to the patient. The system can be used in spontaneously breathing patients, and for manual ventilation by depressing a manual override button. Spontaneously ventilating patients initiate an oxygen flow of up to 120 L/min by generating a negative pressure of 0.3 kPa (2.25 mmHg) at the start of inspiration. Fresh gas flow is delivered at a pressure of up to 5.3 kPa (40 mmHg).

Advantages

• Portability, as it is easy to attach to an oxygen cylinder and take to the field. There are no bulky reservoir bags attached.

• Economy of oxygen use, as the patient’s minute volume is precisely delivered at sufficient flow rates to match the PIFR. Provided there are no leaks, the system delivers F_IO₂= 1.0.

Disadvantages

• Increased work of breathing for spontaneous ventilation because negative pressure must be generated to initiate oxygen flow.

• The system cannot function when fresh gas supply is exhausted.

• During manual ventilation it is almost impossible to judge ventilatory volume except by observing the patient’s chest. The safety over-pressure valve may not prevent barotrauma, especially in children. Lack of ‘feel’ during manual ventilation may lead to over-inflation of the stomach if there is airway obstruction or reduced pulmonary compliance.

Mapleson circuits

A detailed description of these circuits has already been published.¹¹ Partial rebreathing of gases occurs with all of the circuits, and CO₂ retention can be avoided if fresh gas flow exceeds minute volume by a ratio of 2–2.5:1.

Mapleson circuits are still used in some emergency departments. The most commonly used versions are the Mapleson B and the Mapleson F, which are covered under paediatric considerations. Mapleson A, C, D and E circuits will not be discussed further.

Advantages of the Mapleson B circuit

• Use for both spontaneous and manual ventilation. Its performance is similar in both circumstances.

• The soft bag has excellent ‘feel’ for manual ventilation, and it is easy to monitor spontaneous ventilation by observing the filling and emptying of the reservoir bag.

Disadvantages

• Carbon dioxide build-up with lower oxygen flow rates. This can be avoided with higher flow rates, or by intermittently purging the reservoir bag.

• The system cannot function without a fresh gas supply.

• It may be difficult to use when ventilating patients manually using a mask.

• The valve assembly may occasionally ‘stick’.

Closed-circuit systems

An example is the MD Oxyresuscitator. The circuit is the same as the Boyle’s anaesthetic circle system. A soda lime canister absorbs exhaled CO₂, and a low-flow oxygen supply replaces oxygen consumed by metabolism at approximately 0.5–2 L/min. Considerable economy of oxygen use is thus achieved by rebreathing from the circuit.

Advantages

• Economy of oxygen use. More than 6 hours of oxygen can be provided by a ‘C’ sized oxygen cylinder at 1 L/min. This markedly exceeds the endurance of the cylinder using other systems.

• It can be used for spontaneous or manual ventilation. A soft reservoir bag provides excellent ‘feel’ for ventilation.

• The pressure on the system is controlled by the operator during manual ventilation. This minimizes gastric distension.

• It is portable and can easily be taken to the field.

Disadvantages

• The circuit ceases to function when fresh gas flow is exhausted.

• Exhaled nitrogen from the patient’s early breaths may enter the circuit and reduce F_IO₂ below 1.0. This can be prevented by intermittent purging of the reservoir.

• CO₂ may accumulate if the soda lime canister is old or stops functioning.

• Incorrect packing of the soda lime canister may result in inhalation of soda lime dust (this is extremely rare).

• The reservoir bag is remote from the patient mask and the system may be cumbersome to operate.

Helium and oxygen mixtures

Over the last decade there has been interest in adding helium to oxygen (maximum 30% oxygen, also known as ‘Heliox’). Heliox has a lower density than air and the potential to reduce airway resistance and hence the work of breathing, when treating disease processes such as COPD and asthma.

Helium (He₂, MW = 4) is much lighter than nitrogen and therefore significantly lowers the density of the gas mix when combined with oxygen in the range of F_IO₂ = 0.2–0.4. This advantage is lost when F_IO₂ > 0.4. Despite lower density, the viscosity of Heliox is not significantly lower than that of air. Its main theoretical advantage is if there is turbulent gas flow that is density dependent. This may occur with COPD, where there is a combination of small and medium airways disease. Early studies also suggested that Heliox may enhance nebulizer particles in the lung; however, greater flow rates may be required to drive the nebulizer.¹² Despite the potential advantages, the clinical evidence for use in COPD is not strong.

Two Cochrane reviews of the topic concluded that there is insufficient evidence to support the routine use of Heliox to treat COPD exacerbations, or exacerbations of asthma.^13,¹⁴ However, the review of adults and children with asthma did conclude that Heliox may improve pulmonary function when there is more severe obstruction. Most of the studies of Heliox for asthma have assessed it as a driver of nebulizer therapy, rather than for continuous administration. Of the two studies of Heliox therapy for COPD assessed in the Cochrane review, only one study included acutely decompensated patients in the ED.¹⁵ This study failed to show a benefit from Heliox when it was used to drive nebulized β-agonist therapy. There is a need for further randomized studies using Heliox in asthma and COPD, both continuously and as a driver for nebulizer therapy, with hard endpoints such as physiological parameters, response to nebulized β agonists, need for non-invasive ventilation or intubation, and admission rates.

Measurement of oxygenation

Clinical assessment of oxygenation is unreliable, and the time-honoured sign of cyanosis varies with the level of haemoglobin, skin pigmentation, perfusion and external light.^1,^16,¹⁷ Arterial blood gases and pulse oximetry provide an objective measurement of oxygenation and enable precise titration of oxygen therapy to the clinical situation.

Pulse oximetry

Pulse oximetry has become the most frequently used indicator of oxygenation in emergency medicine, as it is non-invasive.^18,¹⁹ It is colloquially known as the ‘fifth vital sign’, and provides continuous real-time assessment of a patient’s oxygenation and response to therapy. It has a proven role in emergency medicine and is an excellent clinical tool, provided the limitations are understood. The principles behind pulse oximetry have been described elsewhere.^20,²¹

A detailed knowledge of the haemoglobin–oxygen dissociation curve is required to interpret pulse oximetry, as well as the factors that influence readings obtained by this equipment. These factors are summarized in Table 2.2.5.

Table 2.2.5 Factors that influence pulse oximetry readings ^16,^17,^20,²¹

Factor	Cause
Signal interference	High-intensity external light source
	Diathermy
	Shivering/movement of digit
Reduced light transmission	Dark coloured nail polish
	Dirt
	(NB: melanin pigment/jaundice have no effect)
Reduction in plethysmographic volume	Peripheral vasoconstriction (shock, hypothermia)
Inaccurate readings due to abnormal haemoglobin	COHb causes over-estimation as is not distinguished from O₂Hb
	Methaemoglobin > 10% causes oximeter to read 85% saturation, regardless of O₂ saturation
	Profound anaemia – insufficient haemoglobin for accurate signal
Falsely low readings	Intravenous dyes with absorption spectra near 660 nm, e.g. methylene blue
	Stagnation of blood flow

Paediatric considerations in oxygen therapy

The general principles of oxygen therapy and its indications apply equally well for children as for adults, but there are a number of important differences in relation to body size, psychology and oxygen toxicity.

Body size

Children are smaller than adults both anatomically and physiologically, so that any increases in equipment dead space will significantly increase CO₂ retention. Children are less able to tolerate increased resistance to ventilation, particularly if negative pressure must be generated to open valves in the apparatus.

Peak inspiratory flow rate and respiratory minute volume are lower; hence a given oxygen supply flow rate will produce a higher F_IO₂ in a child than in an adult. A Hudson mask at 8 L/min may supply a F_IO₂ of 0.8 in a young child.² Reservoir bags are not required to deliver F_IO₂ values near 1.0 to children weighing less than 15 kg because available supply flow rates (maximum 15 L/min) exceed the child’s PIFR.

Appropriately sized equipment is essential: many sizes of oxygen masks, oximeter probes, laryngoscopes and endotracheal tubes must be available to manage children of different ages, as serious barotrauma may result from the use of excessive volume during manual ventilation. Resuscitator bags are available with paediatric-sized reservoirs. The Laerdal system has both paediatric and infant sizes. These units also have a pressure relief valve designed to prevent barotrauma. Pressure rapidly rises as the child’s lung reaches full inflation.

A smaller Mapleson circuit, the Jackson-Rees (Mapleson F) circuit, is available to ventilate children. It can be used for both spontaneous and manual ventilation. Rebreathing of carbon dioxide does not occur provided fresh gas flow is 2–3 times minute volume, and the bag is separated from the patient by a tube of internal volume greater than the patient’s tidal volume. The overall relationship between fresh gas flow, minute volume and PaCO₂ is complex.¹¹ The principal advantages over the Laerdal system are that the operator can observe bag movement in spontaneous respiration, and has a better ‘feel’ for airway obstruction in manual ventilation. However, considerable skill and experience are required to use the system safely.

Psychological considerations

Gaining the trust and confidence of an ill child is an art learnt with experience. They frequently respond with fear when oxygen therapy is administered, so it is helpful to obtain assistance by asking their parents to nurse the child during treatment. A tight-fitting mask is less important in a child because source flow rate more closely approximates PIFR. Parents may assist by holding the oxygen mask close to the child’s face, or by directing high-flow oxygen straight at the child’s mouth using a tube only. A cupped hand with the oxygen tube held between middle and ring fingers can serve as a surrogate oxygen ‘mask’.

Oxygen toxicity

Prolonged administration of oxygen at F_IO₂ > 0.6 for longer than 24 hours may be toxic to infants. This toxicity may not become apparent during their acute stay in the emergency department, but the oxygen dose received there contributes to the cumulative toxicity. Appropriate monitoring using pulse oximetry ensures administration of the correct dose and minimizes the risk of toxicity. However, supplemental oxygen should never be withheld because of fear of toxicity.

Transfer of patients on oxygen therapy

Supplemental oxygen therapy is a vital part of transporting the ill patient, and is especially important for air travel, where lower ambient P_IO₂ may exacerbate hypoxia already present as a result of the patient’s disease process. The partial pressures of oxygen at various altitudes have been summarized elsewhere.²² Patients with decompression illness or arterial gas embolism should not be transported at cabin pressures lower than 101.3 kPa (1 atmosphere absolute, ATA) because lower ambient pressure exacerbates their disease process by increasing bubble size. A number of factors must be considered for successful oxygen therapy during transport of a patient.²³

Knowledge of the oxygen delivery apparatus and its maximum rate of delivery is essential for estimating transport oxygen requirements. These estimates must take into account current oxygen consumption, duration of transport (including delays), oxygen required in the event of deterioration, and a safety factor of at least 50%.

The sizes of oxygen cylinders available in Australasia, their filling pressures and approximate endurances are summarized in Table 2.2.6. The most economical circuit for prolonged transport with F_IO₂ = 1.0 is a closed circuit with a CO₂ absorber, and the least economical is a free-flowing circuit.

Table 2.2.6 Oxygen cylinder sizes for patient transport

Monitoring during transport should be of the same standard as that initiated in the emergency department. Pulse oximetry is an essential tool to detect hypoxia during transport, and should include audible and visual alarms. Oxygen therapy can be titrated against SaO₂, and this is particularly important in air travel, where P_IO₂ varies with ascent and descent. All the usual clinical parameters must also be monitored.

Oxygen therapy in specific circumstances

Asthma

Hypoxia in asthma results from ventilation–perfusion mismatch created by bronchospasm, secretions, and airway inflammation and oedema. Supplemental oxygen should be titrated to provide a SaO₂ >90% (preferably 94%), and must be continued during the interval between doses of inhaled bronchodilators.

Initial management should include a Hudson mask at 8 L/min flow rate. SaO₂ should be monitored continuously by pulse oximetry. The oxygen dose should be rapidly increased up to 100% if the patient remains hypoxic. Bronchodilator therapy should be administered proportionate to the severity of the attack, using oxygen to drive the nebulizer. Oxygen should not be withheld or administered in low doses because of fear of respiratory depression. Hypercapnia is an indication of extreme airway obstruction, and its presence mandates aggressive therapy and/or mechanical ventilation.

Mechanical ventilation in asthma

Mechanical ventilation requires an F_IO₂ = 1.0, high inspiratory flow rate (100 L/min), low tidal volume (6–8 mL/kg), a prolonged I:E ratio of at least 1:3 and a low ventilation rate (6–10 breaths/min or less), to reduce the risks of progressive dynamic hyperinflation and the development of auto-PEEP (iPEEP) reducing venous return and hence preload, and of barotrauma with the development of a pneumothorax. Permissive hypercapnia is accepted with mechanical ventilation.

Occasionally patients with asthma become hypoxic during nebulizer therapy because the oxygen flow rates driving the nebulizer (6–8 L/min) are lower than the flow rate required to maintain SaO₂ > 90%. In these circumstances, extra oxygen may be supplied to maintain SaO₂ via a T piece or Y connector during the nebulizer therapy.

Chronic obstructive pulmonary disease

Most patients with chronic obstructive pulmonary disease (COPD) possess a degree of acute respiratory failure that has caused their emergency presentation. This may be due to infection, bronchospasm, retention of secretions, coexistent left ventricular failure, worsening right heart failure, pulmonary embolism, pneumothorax or sedation. Clues to the degree of severity and chronicity of the COPD may be obtained from the patient’s history, past clinical records, emergency department blood gases and the response to initial oxygen therapy.

Clinical indicators of patients at risk of CO₂ retention include a housebound patient, FEV₁<1 L, polycythaemia, a warm vasodilated periphery and cor pulmonale. In the acutely unwell patient, treatment may be required before the history can be obtained.

COPD groups

In terms of management, patients with COPD fall into two groups, although this classification is still a source of debate.²⁴^–⁶

• Patients with a normal ventilatory response to CO₂ (‘can’t breathe’ is the most common). Gas exchange and air flow into the lungs are impaired, but ventilatory drive is normal.

• Patients with impaired ventilatory response to CO₂ (‘won’t breathe’ is less common). Ventilation does not increase in response to hypercapnia and acidosis.

There is an overlap between the advanced stages of illness. The aims of oxygen therapy are targeted to produce an SaO₂ of 88–90%, and to identify the second group of patients so that the oxygen dose can be titrated to achieve an acceptable clinical response, without excessive elevation of PaCO₂. Serial arterial blood gas analysis is an essential tool in the management of these patients.

The majority will have a normal ventilatory response to CO₂. Hypercapnia indicates that ventilatory failure is developing, and there may be a danger of respiratory arrest if the patient’s disease is severe and progressive. This may also result from uncontrolled oxygen therapy and failure to monitor the patient’s clinical status and arterial blood gases. Any patient with impaired consciousness due to respiratory failure should be manually ventilated while they are being clinically assessed and treated.

Controlled titration of oxygen dose in COPD

One of the foundations of successful management of the cooperative patient with COPD is controlled titration of oxygen dose. Variable-performance oxygen masks do not have a role in the emergency management of COPD. It is reasonable to use a consistent initial approach to oxygen therapy for conscious patients with advanced COPD because at the time of presentation their ventilatory response to CO₂ is unknown. In most patients the administration of 24–28% oxygen by Venturi mask will improve their oxygenation, with a target SaO₂ of about 88–92%.²⁷

Below 90% saturation the Hb–O₂ dissociation curve is steep, and unless a pulmonary shunt is present even these small increments in oxygen will make a positive difference.¹ The patient’s response to initial oxygen therapy (F_IO₂ = 0.24–0.28) will direct further oxygen dose changes and identify any patients not already known to be suffering chronic hypercapnia. A repeat ABG sample should be taken after 10 minutes of breathing F_IO₂ = 0.24–0.28. The PaCO₂ may rise slightly because of the ‘Haldane effect’.^1,²⁵ If this rise is excessive (>1–1.3 kPa [8–10 mmHg]), it is consistent with an impaired ventilatory response to CO₂. The F_IO₂ should then be adjusted downwards in steps to achieve a satisfactory pulse oximetry reading that is compatible with acceptable CO₂ levels.

Arterial blood gas sampling in COPD

Arterial blood gas (ABG) samples taken during the initial assessment of these patients (breathing air or controlled oxygen) will assist management. If the bicarbonate level is >30 mmol/L or is elevated by more than 4 mmol/L for each 1.3 kPa (10 mmHg) rise in PaCO₂ above normal (5.3 kPa, 40 mmHg), this provides strong evidence of chronic hypercapnia, provided there is no other cause of metabolic alkalosis.²⁸

Management considerations in COPD

Patients with a normal ventilatory response to CO₂ will not exhibit a significant elevation of PaCO₂ in response to oxygen therapy. If hypoxaemia persists and the PaCO₂ remains stable, then the oxygen dose may be increased incrementally until the desired oxygen saturation is achieved. A lower than normal SaO₂ (~88%) and PaO₂ (~56 mmHg) may be acceptable provided the patient remains conscious and cooperative.

Non-invasive positive-pressure ventilation is indicated if the patient remains hypoxic, or becomes progressively more hypoxic and the elevation of PaCO₂ persists or worsens, or their conscious state deteriorates.²⁷ Intubation and ventilation may be required, but this should be regarded as a last resort. Supplemental oxygen should never be abruptly withdrawn from patients with COPD because a catastrophic fall in PaO₂ will occur. All reductions in controlled oxygen dose should be in a stepwise manner.

In the majority of cases an acceptable balance between PaO₂ and PaCO₂ can be achieved, whereas both hypoxia and hypercarbia are reversed by specific therapy. Treating the cause of the ventilatory failure is a high priority and is covered in other chapters.

A pilot study ²⁹ showed that the administration of bronchodilators using oxygen-driven nebulizers in the acute management of chronically hypercapnic patients may be safe. Caution is advised, however, because a recent Australian study ³⁰ suggested that COPD is still poorly managed in the emergency department with respect to oxygen dose. Interestingly, the authors of that paper offered only limited practical advice on the titrated use of oxygen in the acute management of COPD, and did not differentiate between COPD patients with an acute elevation of CO₂ and those with chronic elevation.

Complications of oxygen therapy

These can be classified into three categories:

1 Equipment-related complications

2 Carbon-dioxide narcosis

3 Oxygen toxicity.

Equipment-related complications

These are entirely preventable with careful monitoring and many have been dealt with in the discussion of each individual apparatus. Tight-fitting masks may cause asphyxia if there is insufficient oxygen reservoir or flow, and aspiration of vomitus may occur if the patient has depressed airway reflexes. Use of appropriate oxygen flow rates with rebreathing circuits prevents CO₂ accumulation.

During mechanical ventilation barotrauma can be prevented by the use of appropriate volumes and pressures, although it may be difficult to avoid when there is reduced lung compliance, as in the moribund asthmatic. Knowledge of potential equipment complications enables prompt intervention should they arise. When investigating a sudden deterioration in the patient’s condition, a thorough check of the equipment in use is mandatory.

Carbon-dioxide narcosis

This can be prevented by controlled oxygen therapy titrating the F_IO₂ against SaO₂, arterial blood gases and conscious state (see above). Unconscious patients should be intubated and manually ventilated using high F_IO₂, preferably 100% oxygen. Patients with deteriorating conscious state and respiration due to CO₂ narcosis need to be vigorously stimulated and encouraged to breathe, whilst F_IO₂ is reduced in a stepwise manner. Oxygen should never be suddenly withdrawn, because this precipitates severe hypoxia. Reversible causes of respiratory failure should be treated, and non-invasive ventilation instituted.^27,³⁰

Oxygen toxicity

Oxygen is toxic in high doses and this is a function of P_IO₂ and duration of exposure. The toxicity is thought to occur by the formation of free radicals and toxic lipid peroxides, inhibition of enzyme systems, and direct toxic effects on cerebral metabolism.³¹ Toxicity is mainly restricted to the respiratory system and central nervous system (CNS), although it may affect other regions such as the eye. Premature infants develop retrolental fibroplasia after prolonged exposure to high F_IO₂. CNS oxygen toxicity manifested by neuromuscular irritability and seizures (Paul Bert effect) is restricted to hyperbaric exposures.

Pulmonary oxygen toxicity (Lorraine–Smith effect) is of the greatest relevance to emergency medicine, although exposures of 0.6–1 ATA for more than 24 hours are required to produce it.³¹ Acute changes such as pulmonary oedema, haemorrhage and proteinaceous exudates are reversible on withdrawal of oxygen. Longer durations of high P_IO₂ may lead to permanent pulmonary fibrosis and emphysema. Physicians should be alert to acute symptoms of cough, dyspnoea and retrosternal pain, although these are non-specific symptoms of oxygen toxicity. A progressive reduction in vital capacity may be demonstrated. As with all drugs, oxygen dose should be monitored and carefully titrated against SaO₂ and clinical effect. However, oxygen therapy should never be withheld acutely because of fear of toxicity.

Special delivery systems

Oxygen humidification

This may be desirable when prolonged use (>6 hours) of supplemental oxygen is required, as oxygen is totally dry, possessing no water vapour. Humidification is particularly necessary in patients ventilated with an endotracheal tube because the natural humidification that occurs in the nose, mouth and nasopharynx is bypassed. Patients with COPD and retained secretions benefit from humidification.

Additional heat is required to provide effective humidification by vaporization of water. Various systems are available to humidify inspired gas, and ideally they should be able to deliver inspired gas to the trachea at 32–36 °C with low resistance and at greater than 90% humidity. These devices should be simple to use, and able to maintain temperature and humidity at varying gas flows and F_IO₂. There should also be safety alarms monitoring temperature and humidity.²⁸

Humidification of warmed inspired gas also enables heat transfer to hypothermic patients, and is essential in treating the pulmonary complications of near drowning. Dry oxygen will exacerbate hypothermia. The Fischer and Paykel apparatus provides more effective humidification by using a heating coil with a large surface area for contact with inspired gas.

Continuous positive airways pressure

This topic has been reviewed in detail in the literature.³² Continuous positive airways pressure (CPAP) has a role in the management of pulmonary oedema, pneumonia, bronchiolitis, respiratory tract burns and acute respiratory failure.³³^–⁷ Benefit to the patient is achieved as a result of increasing functional residual capacity and reduced pulmonary compliance. Hypoxaemia is reversed by reduction in intrapulmonary shunting, and the work of breathing is reduced.³²

Circuit designs for CPAP

Circuit designs usually consist of a reservoir based on the Mapleson D circuit, or a high-flow turbine system.³³ Humidification can be added to the system, and is considered essential for long-term use (>6 hours). Use of an oxygen blender enables variable F_IO₂ to be administered. CPAP has a proven role in the emergency department in the acute management of cardiogenic pulmonary oedema. Reduced requirements for endotracheal intubation have been demonstrated when CPAP is used for severely ill patients.³³ Complications of CPAP include aspiration and pulmonary barotrauma. It may elevate intracranial pressure, and precipitate hypotension by reducing venous return to the thorax.

Hyperbaric oxygen treatment

Hyperbaric oxygen (HBO) treatment consists of administering oxygen at pressures greater than 1 ATA, usually in the range of 2.0–2.8 ATA. This requires a hyperbaric chamber that is pressurized with air while the patient breathes F_IO₂ = 1.0 from various delivery systems for periods of 2–7 hours. The high P_IO₂ results in PaO₂ of up to 267 kPa (2000 mmHg) if 2.8 ATA treatment pressure is used. This is beneficial, as there is increased dissolved oxygen in the plasma (up to 300 mL oxygen may be carried to the periphery each minute in the dissolved form), which maintains oxygen flux even if haemoglobin is non-functional, for instance in carbon monoxide poisoning. Increased P_IO₂ enables more rapid elimination of toxic gases from the body, for example carbon monoxide or H₂S.

Uses of hyperbaric oxygen

The increased PO₂ also creates a greater driving pressure of oxygen into ischaemic tissues in problem wounds, and reduces swelling by vasoconstriction in crush injuries. HBO treatment has a number of benefits in treating gas embolism and decompression illness (DCI). It provides extra oxygen to tissues rendered ischaemic by nitrogen bubbles, and the increased pressure reduces bubble size and enhances nitrogen removal from the body. HBO treatment is also of benefit in anaerobic infections by being bacteriostatic to anaerobes, inhibiting clostridial α toxin, and stimulating host defences via granulocyte function. Recognized indications for acute referral to a hyperbaric facility for HBO treatment are summarized in Table 2.2.7 ³¹ (see also Chapter 28.3).

Table 2.2.7 Indications for acute treatment with hyperbaric oxygen ³¹

Decompression illness

Air or gas embolism

Carbon monoxide poisoning

Gas gangrene and anaerobic fasciitis

Necrotizing soft tissue infections

Acute crush injury with compartment syndrome

Acutely compromised skin flaps or grafts, due to injury or post surgery

References

1 West JB. Respiratory physiology – the essentials, 6th edn. Baltimore: Lippincott, Williams & Wilkins, 1999.

2 Oh TE, Duncan AW. Oxygen therapy. Medical Journal of Australia. 1988;149:141-146.

3 Smart DR, Mark PD. Oxygen therapy in emergency medicine. Part 1. Physiology and delivery systems. Emergency Medicine (Fremantle). 1992;4:163-178.

4 Bethune DW, Collins JM. An evaluation of oxygen therapy equipment. Thorax. 1967;22:221-225.

5 Campbell EJM. A method of controlled oxygen administration which reduces the risk of carbon dioxide retention. Lancet. 1960;2:10-11.

6 Hill SL, Barnes PK, Hollway T, Tennant R. Fixed performance oxygen masks: an evaluation. British Medical Journal. 1984;288:1261-1263.

7 Fracchia G, Torda TA. Performance of Venturi oxygen delivery devices. Anaesthesia and Intensive Care. 1980;8:426-430.

8 Friedman SA, Weber B, Briscoe WA, et al. Oxygen therapy. Evaluation of various air-entraining masks. Journal of the American Medical Association. 1974;228:474-478.

9 Goldstein RS, Young J, Rebuck AS. Effect of breathing pattern on oxygen concentration received from standard face masks. Lancet. 1982;27:1188-1190.

10 Woolner DF, Larkin J. An analysis of the performance of a variable Venturi-type oxygen mask. Anaesthesia and Intensive Care. 1980;8:44-51.

11 Dorsch JA, Dorsch SE. The breathing system. II. The Mapleson systems. In Dorsch JA, Dorsch SE, editors: Understanding anaesthesia equipment. Construction, care and complications, 2nd edn, Baltimore: Williams & Wilkins, 1984.

12 Hess DR. Heliox and non-invasive positive-pressure ventilations: a role for Heliox in exacerbations of chronic obstructive pulmonary disease? Respiratory Care. 1999;51:640-650.

13 Rodrigo G, Pollack C, Rodrigo C, et al. Heliox for nonintubated acute asthma patients. Cochrane Database of Systematic Reviews. (Issue 4):2006. Art No.: CD002884. DOI: 10.1002/14651858. CD002884.pub2

14 Rodrigo G, Pollack C, Rodrigo C, et al. Heliox for treatment of exacerbations of chronic pulmonary disease. Cochrane Database of Systematic Reviews. (Issue 1):2007. Art No.: CD003571. DOI: 10.1002/14651858. CD003571

15 deBoisblanc BP, DeBleiux P, Resweber S, et al. Randomized trial of the use of heliox as a driving gas for updraft nebulization of bronchodilators in the emergency treatment of acute exacerbations of chronic obstructive pulmonary disease. Critical Care Medicine. 2000;28:3177-3180.

16 Morgan-Hughes JO. Lighting and cyanosis. British Journal of Anaesthesia. 1968;40:503-507.

17 Hanning CD. “He looks a little blue down this end”. Monitoring oxygenation during anaesthesia. British Journal of Anaesthesia. 1985;57:359-360.

18 Jones J, Heiselman D, Cannon L, Gradisek R. Continuous emergency department monitoring of arterial saturation in adult patients with respiratory distress. Annals of Emergency Medicine. 1988;17:463-468.

19 Lambert MA, Crinnon J. The role of pulse oximetry in the Accident and Emergency Department. Archives of Emergency Medicine. 1989;6:211-215.

20 Adams AP. Capnography and pulse oximetry. In: Atkinson RS, Adams AP, editors. Recent advances in anaesthesia and analgesia. Edinburgh: Churchill Livingstone; 1989:155-175.

21 Phillips GD, Runciman WB, Ilsley AH. Monitoring in Emergency Medicine. Resuscitation. 1989;18:21-35.

22 Hackett PH, Roach RC, Sutton JR. High altitude medicine. In: Auerbach PS, Geehr EC, editors. Management of wilderness and environmental emergencies. 2nd edn. Missouri: CV Mosby; 1989:1-34.

23 Saunders CE. Aeromedical transport. In: Auerbach PS, Geehr EC, editors. Management of wilderness and environmental emergencies. 2nd edn. Missouri: CV Mosby; 1989:359-388.

24 Stradling JR. Hypercapnia during oxygen therapy in airways obstruction: a reappraisal. Thorax. 1986;41:897-902.

25 Aubier M, Murciano D, Milic-Emili J, et al. Effects of the administration of oxygen on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. American Review of Respiratory Disease. 1980;122:747-754.

26 Sassoon CSH, Hassell KT, Mahutte CK. Hyperoxic induced hypercapnia in stable chronic obstructive pulmonary disease. American Review of Respiratory Disease. 1987;135:907-911.

27 McKenzie DK, Frith PA, Burdon JGW, et al. The COPDX Plan: Australian and New Zealand Guidelines for the management of chronic obstructive pulmonary disease 2003. Medical Journal of Australia. 2003;178:S1-S39.

28 Bersten A, Soni M. Oh’s intensive care manual, 5th edn. Oxford: Butterworth–Heinemann, 2003.

29 Cameron P, Coleridge J, Epstein J, Teichtahl H. The safety of oxygen driven nebulisers in patients with chronic hypoxaemia and hypercapnia. Emergency Medicine (Fremantle). 1992;4:159-162.

30 Joosten SA, Xiaoning Bu, Smallwood D, et al. The effects of oxygen therapy in patients presenting to an emergency department with exacerbation of chronic obstructive pulmonary disease. Medical Journal of Australia. 2007;186:235-238.

31 Feldmeier JJ. Indications and results. In The Hyperbaric Oxygen Therapy Committee Report. Kensington: Maryland USA Undersea and Hyperbaric Medicine Society; 2003.

32 Duncan AW, Oh TE, Hillman DR. PEEP and CPAP. Anaesthesia and Intensive Care. 1986;14:236-250.

33 Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe cardiogenic pulmonary oedema with continuous positive airway pressure delivered by face mask. New England Journal of Medicine. 1991;325:1825-1830.

34 Taylor GJ, Brenner W, Summer WR. Severe viral pneumonia in young adults. Therapy with continuous airway pressure. Chest. 1976;69:722-728.

35 Beasley JM, Jones SEF. Continuous positive airways pressure in bronchiolitis. British Medical Journal. 1981;283:1506-1508.

36 Venus B, Matsuda T, Copiozo JB, et al. Prophylactic intubation and continuous positive airways pressure in the management of inhalation injury in burn victims. Critical Care Medicine. 1981;9:519-523.

37 Katz JA, Marks JD. Inspiratory work with and without continuous positive airway pressure in patients with acute respiratory failure. Anaesthesiology. 1985;63:598-607.

2.3 Haemodynamic monitoring

Liz Steel, Craig Hore

Essentials

1 Haemodynamic monitoring involves observation of the complex physiology of blood flow with the aim of providing data that can be used to improve patient management and outcomes.

2 Numerous methods are available that should be considered in a stepwise fashion, from simple clinical assessment to highly technical, invasive procedures such as the pulmonary artery catheter.

3 Effective use of haemodynamic monitoring devices requires a good understanding of cardiovascular physiology.

4 Currently there is a move away from simple blood pressure measurements towards targeting end-organ perfusion and the adequacy of cardiac output.

5 Use of all monitoring technology in the emergency department needs to take into consideration the time associated with its introduction, the skill levels needed and the clinical benefits that may be provided.

6 No monitoring modality improves outcome unless it is linked to a treatment protocol.

7 The pulmonary artery catheter was for many years considered the ‘gold standard’ of haemodynamic monitoring, but current evidence suggests no improvements in patient outcome. It should therefore not be used in the emergency department.

8 Less invasive devices have been developed in recent years. Their role in the emergency department is yet to be fully elucidated.

9 Further developments will probably result in greater use of less invasive methods for haemodynamic monitoring and an increased ability to monitor at a microcirculation and/or cellular level, with better correlation between observed events and final diagnosis.

Introduction

Haemodynamics is concerned with the physiology of blood flow and the forces involved within the circulation.¹Haemodynamic monitoring involves studying this complex physiology using various forms of technology to understand these forces and put them into a clinical context that can be used to direct therapy.² The utility of basic monitoring is universally accepted. However, the maxim that ‘not everything that counts can be counted and not everything that can be counted counts’ (Albert Einstein, 1879–1955) should be borne in mind.³ This is particularly salient in the emergency department (ED), where the pressure of work and the diversity of patients do not allow the unlimited use of complex and expensive monitoring systems.

This chapter provides an outline of current approaches to the various technologies available for haemodynamic monitoring and their applicability in the ED. Many methods are available which should be thought of in a stepwise progression from simple clinical assessment to invasive, highly technical methods and sophisticated devices.

Historical background

As recently as 100 years ago, only temperature, pulse and respirations were measured and used to manage patients. The technology for auscultatory blood pressure measurement was available, but did not come into regular use until the 1920s.

Intensive care as a medical/nursing specialty evolved in tandem with the electronic revolution of the 1960s.⁴ At the same time, increasingly sophisticated haemodynamic and laboratory techniques vastly improved diagnosis, and provided a way to further evaluate therapy. Despite these major advances in the ability to monitor multiple physiological variables, there is little evidence to suggest that they have resulted in tangible improvements in patient outcome.⁵

The practical use of any monitoring device must be appropriate to the individual clinical environment. Thus, it may be reasonable to insert a pulmonary artery catheter in the intensive care unit (ICU) where the necessary time can be taken, yet impractical and potentially unsafe in a busy ED.² Another consideration is that haemodynamic monitoring should only be used when the clinical outcome can be influenced and potentially improved. Once irreversible cellular damage has occurred, current evidence suggests that no benefit will occur no matter how far therapy is maximized.⁶ Further, haemodynamic monitoring may not improve patient outcome unless linked to a clinical protocol or ‘goal-directed therapy’.^7- Improvements in morbidity and mortality have been shown when such protocols are utilized.^6,^10,¹¹

Clinicians should only introduce monitoring equipment that will have a direct influence on their choice of therapy, as the use of invasive monitoring carries potential risks of harm to the patient. The injudicious use of physiologically based treatment protocols has been shown to cause harm and lead to worse outcomes.¹² All monitored variables must be evaluated and applied in a manner proven to lead to benefit, in terms of both the diagnosis and the management.¹³

Overview of cardiovascular physiology

It is beyond the scope of this chapter to go into a detailed discussion of cardiovascular physiology, but one possible reason that haemodynamic monitoring has not been associated with improvements in outcome is an inability to understand and manipulate patients’ physiology effectively.

The circulatory model

Haemodynamic data are traditionally considered in the context of a circulatory model. This model varies, but usually consists of a non-pulsatile pump, and a hydraulic circuit with discrete sites of flow resistance, alongside the Frank–Starling mechanism with its concepts of preload, contractility and afterload.¹⁴

Cardiac output

Cardiac output (CO) is the volume of blood pumped by the heart per unit of time, usually expressed in litres per minute (L/min).¹⁵ The heart operates as a pump and ejects a bolus of blood known as the stroke volume (SV) with each cardiac cycle. CO is the product of SV and heart rate (HR).

A complex set of interrelated physiological variables determines the magnitude of CO, including the volume of blood in the heart (preload), the downstream resistance to the ejection of this blood (afterload) and the contractility of the heart muscle.¹⁶ However, it is the metabolic requirements of the body that are the most potent determinant of cardiac output.⁴

The regulation of CO is therefore complex. A single measurement represents the interaction of many interacting physiological processes. Basal CO is related to body size and varies from 4 to 7 L/min in adults.¹⁶ The value can be divided by the body surface area to enable comparison between patients with different body sizes, giving the cardiac index (CI).

Although CO can be measured, this does not mean it should be done routinely. Indeed, misuse of CO data may worsen outcomes.¹⁸ The International Consensus Conference on Haemodynamic Monitoring in Shock (2007)¹⁷ suggested that monitoring of CO is only of value if it guides therapies to improve outcome.

Cardiac index (CI)

CI measurement scores over simple blood pressure recording as it describes the total volume of blood flow in the circulation per unit of time, and hence serves as an indicator of oxygen delivery to the tissues. The CI is also useful for understanding and manipulating the pump activity of the heart.

Role of haemodynamic monitoring in the emergency department

The role of haemodynamic monitoring in the ED is even less well defined. Given the plethora of devices but the lack of a ‘gold standard’, there are insufficient data to recommend any one method over another.¹⁷

Recent advances in the management of sepsis include haemodynamic optimization with early goal-directed therapy (EGDT) during the pre-intensive care period, especially in the ED.¹⁹ The Surviving Sepsis Campaign guidelines published in 2004²⁰ emphasized that resuscitation of a patient with severe sepsis should begin as soon as the diagnosis is made, and should not be delayed until ICU admission. The use of such an approach based on strict treatment protocols has been shown to reduce morbidity and mortality⁶ (see Chapter 2.5).

Although widely accepted, the application of this strategy in clinical practice is far from common. Obstacles include a lack of skills to perform the initial procedures, and difficulties in providing the required higher level of care due to ED overcrowding.¹⁹ However, with a potential stay in the ED of >24 hours,²¹ and approximately 15% of critical care being provided in this setting,²² it is necessary to address this issue in education terms and by improved use of available haemodynamic monitoring. This will improve the recognition of therapeutic opportunities in the ED that may be missed.¹⁹

Clinical assessment

Current guidelines on haemodynamic monitoring recommend frequent measurement of blood pressure and physical examination variables, including signs of hypoperfusion such as reduced urine output and abnormal mental status.¹⁷ Clinical examination is ‘low risk’ yet may yield much important information, but the sensitivity and specificity are low, even when individual elements are interpreted in isolation. Also, clinical assessment of the circulatory state can be misleading.²³

Clinical assessment still has an important role in the initial assessment of a critically ill patient,²⁴ particularly as the use of some invasive methods leads to poorer outcomes.¹³

Paradoxically, the development of haemodynamic measuring devices was driven by the poor ability to assess the critically ill patient clinically, ^25,²⁶ yet those patients managed simply by clinical assessment may do better than those managed with invasive, complex devices.¹³

Clinical markers of cardiac output

The underlying issue may not be what a patient’s CO is, but rather whether this CO is effective for that particular patient.²⁷ Trends are more important than specific, single-point values in guiding therapy. An effective CO should need no compensation, and therefore a patient should have warm toes simultaneously with a normal blood pressure and heart rate.^28,²⁹ One of the advantages of clinical endpoints is that they remain the same whatever the phase of the illness.²⁷

Clinical endpoints that are important in the management of septic shock were set out by the American College of Critical Care Medicine (ACCM) in 1999,³⁰ and again in 2007 by an International Consensus Conference.¹⁷ These are essentially markers of perfusion and include skin temperature, urine output and cerebral function.

Physiological measurements and clinical endpoints should be viewed as complementary. Physiological measurements combined with clinical examination may provide a numeric target for a management strategy.²⁷ Measurements also provide a universal language for information exchange.

Sound clinical evaluation in the ED in terms of markers of effective CO aid the early diagnosis and implementation of EGDT.¹⁹ Abnormal findings also suggest the need for more invasive haemodynamic monitoring, and the need to involve the ICU team early in the patient’s management.

Blood pressure monitoring

The pressure under which blood flows is related to the force generated by the heart and the resistance to flow in the arteries.³² Measurement of mean arterial pressure (MAP) is a more reliable measure of blood pressure than either the systolic or diastolic pressures. It is least dependent on the site or method of measurement, least affected by measurement damping, and it determines the actual tissue blood flow.¹⁴

Traditionally, low blood pressure was used to reflect shock and haemodynamic instability. This approach is being challenged as more reliance is placed on concepts of global tissue hypoxia, and the measurement of CO and its adequacy.¹⁹

Non-invasive blood pressure measurement

Non-invasive blood pressure (NIBP) measurements using a sphygmomanometer and palpation were first proposed in the late 1800s before Korotkoff introduced the auscultatory method in 1905.³² Originally, routine blood pressure measurements were not a regular part of clinical patient assessment. Today, non-invasive or indirect blood pressure measurement is the most common method used in the initial assessment of cardiovascular status.³¹ Although there are significant differences between direct (i.e. invasive) and indirect measurements,³³ non-invasive measurements should rightly form part of every patient’s assessment and management in the ED.¹⁷

Non-invasive blood pressure devices

Non-invasive measurement techniques use blood flow within a limb to measure pressure. Automated oscillometric devices are now the standard, with manual methods (using either palpation or auscultation) becoming increasingly obsolete in clinical ED practice.

The cuff width should be about 40% of the mid-circumference of the limb. Failure to use the appropriate size of cuff leads to inaccurate and misleading measurements. The cuff is inflated until all oscillations in cuff pressure cease, then the occluding pressure is gradually reduced and proprietary algorithms compute mean, systolic and diastolic pressures.

The 95% confidence limits in the normotensive range are ±15 mmHg, but in states of hypotension and hypertension oscillometry tends to respectively over- and underestimate the pressures.¹⁴ Complications are unusual, although repeated measurements could cause skin bruising, oedema and even ulceration.

Invasive blood pressure measurement

Arterial cannulation allows continuous blood pressure measurement, beat-to-beat waveform display and repeated blood sampling.¹⁴ A cannula inserted into an artery is connected via fluid-filled, non-compliant tubing <1 m in length to a linearly responsive pressure transducer. The system is then zeroed with reference to the phlebostatic axis (the midaxillary line in the fourth intercostal space). Modern transducers are precalibrated, and therefore no further calibration is needed.³⁴

Sites and safety of arterial cannulation

The most common site for cannulation is the radial artery,³⁵ as this is easy to access during placement and subsequent manipulations, the wrist has a dual arterial supply,³¹ and there is a low complication rate.³⁵^–⁸ Temporary occlusion of the artery may occur, and in a small number of cases this may be permanent.³⁵ Other complications include haematoma formation,³⁹ bleeding,⁴⁰ cellulitis,⁴¹ and those associated with the catheter itself.⁴² Alternative arterial cannulation sites are femoral, axillary and brachial, but all have similar complications. Arterial cannulation is a safe procedure if the optimal site for insertion is selected carefully for each patient.³⁵ The preference in the ED is for the radial and femoral sites.

Use of invasive blood pressure monitoring

Invasive blood pressure monitoring should be used in all haemodynamically unstable patients and when vasopressor or vasodilator therapy is used.¹⁷ Relying on external NIBP monitoring to guide therapy and diagnosis does not provide sufficient diagnostic data, especially in sepsis.⁶ Additional methods of haemodynamic monitoring may be considered in these patients, with early involvement of the intensive care department.

The remainder of this chapter discusses some of the supplementary methods available to assess various physiological measures considered important to guide the management of haemodynamically unstable patients.

Other non-invasive monitoring methods for cardiac output

The ideal device has yet to be developed for the non-invasive measurement of CO and other related variables in the ED setting. Devices that are available do not compare reliably with invasive methods, and are not suited to all patient cohorts and/or may be too elaborate or time-consuming for a busy ED.

Ultrasonic cardiac output monitor (USCOM)

This device was developed in Australia and introduced for clinical use in 2001. It provides non-invasive transcutaneous measurement of CO based on continuous-wave Doppler ultrasound.⁴³ An ultrasound transducer is used to obtain a Doppler flow profile (velocity–time graph) from either the aortic (suprasternal notch) or the pulmonary (left of sternum, below the second intercostal space) window. The transducer is manipulated to obtain the best flow profile and audible feedback. CO is calculated from the product of the velocity–time integral (vti) and the cross-sectional area of the target valve.⁴⁴

The device appears to perform well in terms of the time taken to become a competent operator, and the reproducibility of its readings.^45,⁴⁶ It appears to be a rapid and safe measure of CO and may assist in the prompt starting of EGDT by emergency physicians, even during a medical retrieval out of hospital.⁴⁷ The correlation of USCOM with standard measures of CO, such as by thermodilution using a pulmonary artery catheter, has been reported as good.⁴³ Some concerns were raised that reliability is affected by patient pathology and the severity of their illness.⁴⁶

More work is needed to clearly define the utility of USCOM in the ED. The device can be used as part of the overall clinical assessment, but probably should not be used in isolation. It may be best for looking at responses to treatment and diagnosis, such as changes in CO associated with a fluid bolus.

Oesophageal Doppler

Measurement of CO using various Doppler-based techniques has been extensively studied.⁴⁸ The main difficulties are an inability to obtain acceptable flow signals with the transthoracic approach, and problems in the measurement of the cross-sectional area using flow.⁴⁹ The transoesophageal approach has been found to be more reliable than the transthoracic.⁵⁰

The oesophageal Doppler device requires minimal training, and volume challenge protocols may be developed so that nursing staff can use them at the bedside.¹⁴ However, this technique is not well tolerated in awake patients⁴³ and thus has limited application in the ED.

Echocardiography

Echocardiography may be used to determine left ventricular size, thickness and performance.⁵² Recently, it has also been reported to accurately identify patients who require fluids.⁵³ The use of echocardiography has increased as the technology has improved, and as the utility of non-invasive techniques has become more accepted. There is a move towards training for the majority of intensive care specialists in this technique, and there is no reason why ED physicians should not also learn. Effective treatment decisions can be based on what is seen on the screen, and in subsequent assessment of left ventricular function.⁵¹

The major criticisms regarding the use of echocardiography for haemodynamic monitoring is that it cannot be done continuously.⁵¹ Other problems include the lack of skilled operators and the need to reassess variables after changes to patient management regimens. Thus, although promising, the usefulness of echocardiography for haemodynamic monitoring in the ED is uncertain at present.

Invasive devices

Central venous pressure monitoring

Central venous access was first performed in Germany in the late 1920s,⁵⁴ but it was not until the 1950s, with the work of Brannon⁵⁵ and Zimmerman,⁵⁶ that the utility of the process was really appreciated. This ultimately led to the development of cardiac angiography, central blood oxygenation determination and pressure recordings.⁵⁷ The technique, management and clinical relevance of continuous central venous pressure (CVP) monitoring were first described in 1962.⁵⁸ This first step in bedside invasive cardiac monitoring allowed direct determination of right heart function and assessment of intravascular volume status.

However, correlation with left heart function was found to be unpredictable and unreliable in the critically ill.⁵⁷ Hence the physiological meaning of the values obtained and their role in patient management are not clear. Problems may result from errors in measurement and failure to correctly understand the physiology involved.⁵⁹

Central venous access is obtained in the ED by inserting a catheter into a peripheral or central vein. Central venous access is defined by the position of the catheter tip: to be central the tip should be positioned at the junction of the proximal superior vena cava and right atrium.⁶⁰

There is no ideal insertion site. Selection depends on the experience of the operator, and patient factors such as body habitus, injuries sustained and coagulation profile.⁵⁷ The main routes used are the internal jugular, subclavian and femoral veins.¹⁴

Indications for central venous access

Indications for the establishment of central access include fluid and electrolyte replacement; drug therapy where peripheral use is contraindicated, such as vasopressor; monitoring of the CVP to guide management; sampling of central venous blood to monitor central venous oxygen saturation; venous access for insertion of a pulmonary artery catheter or transvenous pacemaker; and a lack of an accessible peripheral vein.

Complications related to insertion can be divided into early and late. The most relevant early complications in the ED setting include pneumothorax, haemothorax, dysrhythmias and injury to surrounding structures, including arterial puncture, and nerve and tracheal injury. Late complications include catheter-related sepsis, superior vena cava erosion with cardiac tamponade, and thrombosis.¹⁴

The CVP is often used as a marker of preload and is considered an estimate of right atrial pressure (RAP).² The normal CVP in the spontaneously breathing supine patient is 0–5 mmHg, whereas 10 mmHg is considered an upper limit of normal in those being mechanically ventilated.¹⁴ The CVP also correlates with left ventricular end-diastolic pressure (LVEDP) in a patient with normal heart and lungs. However, in disease states this relationship is frequently abnormal.⁵⁷ Thus the CVP is only a rough guide to right ventricular preload, with emphasis on dynamic changes rather than absolute values.^2,¹⁴

The Rivers’ study

The Rivers’ study ⁶ demonstrated that in cases of septic shock, early aggressive resuscitation guided by CVP, MAP and continuous central venous oxygen saturation (ScvO₂) monitoring reduced 28-day mortality rates from 46.5% to 30.5%. ScvO₂ is measured on blood taken via the central venous catheter and reflects the balance between oxygen delivery and oxygen consumption.¹⁹ Normally oxygen extraction is about 25–30% and a ScvO₂ >65% reflects an optimal balance.^63,⁶⁴ ScvO₂ correlates well with mixed venous saturations (SvO₂) obtained via a pulmonary artery catheter.^65,⁶⁶ Current guidelines recommend instituting goal-directed therapy in septic shock, especially when the ScvO₂ is below 70%.¹⁷ The ScvO₂ has also been shown to be significant in postoperative surgical patients in the ICU, with levels <70% being independently associated with a higher rate of complications⁶¹ and increased length of hospital stay.⁶²

Continuous measurement of ScvO₂ is feasible in the ED setting ⁶⁷ where central venous catheterization is commonly performed, and where the alternative of pulmonary artery insertion is not practical.¹⁹

Pulse contour techniques for cardiac output

The use of pulse contour techniques to obtain a continuous CO by analysis of the arterial waveform dates back over 100 years.² Erlanger and Hooker⁶⁸ first proposed a correlation between stroke volume and changes in arterial pressure, and suggested there was a correlation between CO and the arterial pulse contour. Advances in computer technology have since led to the development of complex algorithms relating the arterial pulse contour and CO.

The appeal of arterial waveform monitoring is that it can now be performed using a minimally invasive technique, with at least four companies currently producing devices that take measurements from an arterial line. The PiCCO system (Pulsion Medical Systems, Munich, Germany) is discussed as one example. However, given the rapid pace of technological development in this area, alternative systems are likely to arise in the near future that may be of particular use in the ED.

PiCCO system of arterial waveform monitoring

The PiCCO system uses pulse contour analysis to provide a continuous display of CO according to a modified version of Wesseling’s algorithm.^69,⁷⁰ The patient requires a central line sited in either the internal jugular, the subclavian or the femoral veins, and an arterial catheter with a thermistor placed in one of the larger arteries, such as the femoral or axillary artery.⁷¹ The femoral site is preferable as it requires only one sterile field for both lines, but does require a 50 cm long venous line.

The PiCCO system combines the pulse contour method for continuous CO measurement and a transpulmonary thermodilution technique to offer complete haemodynamic monitoring.⁷² Transpulmonary thermodilution works on the principle that a known volume of thermal indicator (cold 0.9% NaCl) is injected into a central vein. The injectate rapidly disperses both volumetrically and thermally within the pulmonary and cardiac volumes. This volume of distribution is termed the intrathoracic volume. When the temperature signal reaches the arterial thermistor, a temperature difference is detected and a dissipation curve is generated. The Stewart Hamilton equation is applied to this curve and CO is calculated.

This transpulmonary thermodilution also gives measures of preload in terms of global end-diastolic blood volume (GEDV) as well as intrathoracic blood volume (ITBV).⁷³ The extravascular lung water (EVLW) is also calculated and has been shown to be a sensitive indicator of pulmonary oedema.⁷⁴ The technique of transpulmonary thermodilution has been compared to pulmonary artery thermodilution and confirmed to be as accurate.⁷⁵ Following calibration by thermodilution the PiCCO continually quantifies various parameters.⁷¹

PiCCO parameters quantified

• Pulse-induced contour cardiac output (CO)

• Arterial blood pressure

• Heart rate

• Stroke volume (SV)

• Systemic vascular resistance (SVR)

• Intrathoracic blood volume (ITBV)

• Extravascular lung water (EVLW)

• Cardiac function index (CFI).

The last three parameters are relatively new, and the manufacturer has devised decision trees to guide their use in the clinical setting. The ITBV has been found to be a potentially more reliable and superior indicator of cardiac preload than pulmonary artery wedge pressure (PAWP)⁷⁶ and has also been shown to be helpful in guiding fluid therapy.⁷⁷

EVLW correlates with extravascular thermal volume in the lungs ⁷¹ and with mortality. One study found that patients with an EVLW of up to 8–10 mL/kg had a mortality of 25%, which increased significantly to 75% if the EVLW was >10 mL/kg.⁷⁸ The EVLW may also be used to guide fluid management, especially in those already known to have pulmonary oedema.^79,⁸⁰

The Cardiac Function Index (CFI) aids in evaluation of the contractile state of the heart and hence overall cardiac performance. It is a preload-independent variable and reflects the inotropic state of the heart. The CFI has the potential to become a routine parameter of cardiac performance.⁷¹

The main advantage of the PiCCO system is that it is less invasive than a pulmonary artery catheter, requiring only a central line and an arterial line, which most critically ill patients already have. This in turn leads to fewer complications.⁷⁵ The data collected are also extensive and allow manipulation of haemodynamics using reliable parameters.

There are contraindications to using the PiCCO, for example when access to the femoral artery is restricted, such as in burns. The PiCCO may also give inaccurate thermodilution measurements in the presence of intracardiac shunts, an aortic aneurysm, aortic stenosis, pneumonectomy, and during extracorporeal circulation.⁷¹

The use of the PiCCO system in the ED is plausible. The technique is relatively non-invasive and uses access lines that are already used in the management of the critically ill. The device can both aid diagnosis and provide a monitoring tool for clinical decision making regarding fluid replacement.⁸¹

Pulmonary artery catheter

The pulmonary artery catheter (PAC) or Swan–Ganz catheter has long been considered the ‘gold standard’ method of monitoring the unstable circulation.² Since its introduction in the 1970s, it was assumed that the extra information provided improved patient outcomes. However, various observational studies have now shown that its use does not improve outcome and may even be associated with a worse outcome.¹³ Hence, the use of the PAC without targeting specific endpoints confers no benefit to the patient. Conversely, the insertion of the PAC does not necessarily confer any disadvantage to the patient, except for the time, expertise and skill required to use it competently.⁷^–⁹