Supporting oxygenation and ventilation are two of the most common interventions in intensive care; in 2007–2008, approximately 41% of patients in Australian and New Zealand ICUs received invasive mechanical ventilation and 8% received non-invasive ventilation (NIV).¹ The technology available for supporting oxygenation and ventilation is complex, ranging from simple interventions, such as nasal cannulae through to invasive mechanical ventilation and extracorporeal support. Additionally, the meaning of ventilator terminology is often unclear and terms may be used interchangeably. Critical care nurses must have a strong knowledge of the underlying principles of oxygenation and ventilation that will facilitate an understanding of respiratory support devices, associated monitoring priorities and risks.

Oxygen Therapy

Oxygen is required for aerobic cellular metabolism and ultimately for human survival, with some cells, such as those in the brain, being more sensitive to hypoxia than others. Refer to Chapter 13 for discussion of oxygen delivery and consumption, the oxyhaemoglobin dissociation curve, hypoxaemia and tissue hypoxia; this material provides rationales for clinical decisions regarding the administration of oxygen therapy or ventilation strategies. Oxygen therapy should be considered for patients with a significant reduction in arterial oxygen levels, irrespective of diagnosis and especially if the patient is drowsy or unconscious.

Indications

Indications for oxygen therapy include:

• cardiac and respiratory arrest

• type I respiratory failure

• type II respiratory failure

• chest pain, cardiac failure, myocardial infarction

• low blood pressure, cardiac output

• increased metabolic demands

• carbon monoxide poisoning

Complications

Administration of oxygen, regardless of the delivery device, has potential adverse effects. High concentrations of oxygen cause nitrogen washout, resulting in absorption atelectasis.

Hypoventilation and CO₂ Narcosis

High-dose oxygen therapy may lead to hypoventilation, worsening hypercapnia and CO₂ narcosis due to inhibition of the hypoxic drive in a small proportion of patients with chronic obstructive pulmonary disease (COPD). These patients require close monitoring of PaCO₂ levels when oxygen therapy is instituted or increased. Although COPD patients frequently may have a lower baseline SpO₂ (88–94% compared to 96–100% in patients with no lung pathology), treatment of hypoxia is still essential, and oxygen should not be withheld or withdrawn while hypoxia remains, even if hypercapnia worsens.^2,³

Practice tip

Oxygen should not be withheld or withdrawn while hypoxia remains, even if hypercapnia worsens.

Oxygen Toxicity

Administration of high concentrations of oxygen may lead to oxygen toxicity; symptoms include non-productive cough, substernal pain, reduced lung compliance, interstitial oedema, and pulmonary capillary haemorrhage. These symptoms may be mistakenly attributed to the underlying illness, especially in a sedated and ventilated patient. Many of the symptoms abate once the percentage or fraction of inspired oxygen (FiO₂) is reduced, although irreversible pulmonary fibrosis may occur (see Box 15.1). The concentration and duration of oxygen exposure that induces oxygen toxicity varies between patients;⁴ the lowest possible FiO₂ should therefore be used to achieve the target PaO₂ or SpO₂.

Oxygen Administration Devices

Initial management of hypoxia in a spontaneously-breathing patient with an intact airway is low-flow oxygen via nasal cannulae (up to 6 L/min) or face mask (up to 15 L/min). Although oxygen devices have traditionally had FiO₂ ascribed to specific flow rates, the FiO₂ delivered to the alveoli is influenced by:

• patient factors: inspiratory flow rate, respiratory rate, tidal volume, respiratory pause

• oxygen device factors: oxygen flow rate, volume of mask/reservoir, air vent size, tightness of fit

Normal inspiratory flow in a healthy adult ranges between 25 and 35 L/min. Patients with respiratory failure tend to increase their flow demand from 50 up to 300 L/min. Patients in respiratory distress are characterised by high respiratory rates and low tidal volumes ^4,⁵ that can significantly decrease the FiO₂ available via an oxygen delivery device, depending on the type in use.

All oxygen delivery devices use some type of reservoir to support oxygen delivery and prevent CO₂ rebreathing. In the case of a face mask, the reservoir is the mask; for nasal cannulae it is the patient’s pharynx. Patients with high inspiratory flow and tidal volume will deplete the reservoir faster than it can be replenished, resulting in air entrainment and dilution of the oxygen concentration.

Variable Flow Devices

A range of low or variable flow oxygen delivery devices are available to meet a patient’s physiological needs. These devices range from nasal cannulae and oxygen masks with different features, through to bag–mask ventilation.

Low-flow Nasal Cannulae

Traditional low-flow nasal cannulae sit at the external nares and deliver 3–4 L/min of oxygen. Higher flows may cause discomfort and damage from the drying effect on respiratory mucosa. They are generally well-tolerated by the patient. Increased flow demand with respiratory distress dilutes the oxygen, reducing the FiO₂ to the alveoli. Mouth-breathing and talking can also render nasal cannulae ineffective.

High-flow Nasal Cannulae

High-flow nasal cannulae (HFNC) have slightly larger prongs that facilitate oxygen flow of up to 60 L/min leading to less air entrainment effect than with other oxygen delivery systems.^5,⁶ HFNC generate low levels of end-expiratory pressure and can therefore reduce tachypnoea and work of breathing.^7,⁸ The high gas flow may flush CO₂ from the anatomical dead space preventing CO₂ rebreathing and thereby decreasing PaCO₂, although this is not well supported by the literature.^9,¹⁰ These systems are also generally well-tolerated by the patient, but must be used with heated humidification to avoid drying the respiratory mucosa.⁸ HFNC are now used more frequently in clinical practice to avoid more invasive therapies but there is limited high-quality evidence on their use in adults.

Practice tip

Patients using any type of nasal cannulae should avoid mouth-breathing and talking to minimise diluting oxygen delivery to the lungs.

Practice tip

Transparent face masks are recommended for bag–mask ventilation as they allow immediate recognition if a patient vomits.

Airway Support

The most common cause of partial airway obstruction in an unconscious patient is loss of oropharyngeal muscle tone, particularly of the tongue. This may be alleviated by tilting their head slightly back and lifting the chin, or thrusting the jaw forward. The head-tilt/chin-lift manoeuvre is not used if cervical spine injury is suspected.¹⁵ The jaw-thrust manoeuvre may require two hands to maintain.¹⁶ If more prolonged support is required, an oro- or nasopharyngeal airway can be used that may also facilitate bag–mask ventilation.

Oro- and Nasopharyngeal Airways

The Guedel oropharyngeal airway is available in various sizes (a medium-sized adult requires a size 4). The airway is inserted into the patient’s mouth past the teeth, with the end facing up into the hard palate, then rotated 180 degrees, taking care to bring the tongue forward and not push it back. Oropharyngeal airways are poorly tolerated in conscious patients and may cause gagging and vomiting.¹⁴

A nasopharyngeal airway (see Figure 15.1) is inserted through the nares into the oropharynx; it can be difficult to insert and require generous lubrication to minimise trauma. This type of airway should not be used for patients with a suspected head injury. As well as opening the airway, suction catheters can be passed to facilitate secretion clearance. Once inserted these airways are better tolerated than an oropharyngeal airway.

FIGURE 15.1 Nasopharyngeal airways.²⁷²

Laryngeal Mask Airway and Its Intubation

The classic laryngeal mask airway (cLMA) (see Figure 15.2) is positioned blindly into the pharynx to form a low-pressure seal against the laryngeal inlet. It is easier and quicker to insert than an endotracheal tube, and is particularly useful for operators with limited airway skills; the cLMA does not carry the same potentially fatal complications such as oesophageal intubation although the risk of aspiration remains.¹⁷

FIGURE 15.2 Laryngeal mask airways.²⁷²

Mechanical ventilation can be delivered with low-airway pressures (less than 20 cmH₂O) via a cLMA. This device is widely used in elective general anaesthesia,¹⁵ and can be used in critical care as an alternative to bag–mask ventilation¹⁷ or endotracheal intubation when initial attempts at intubation have failed.¹⁸ The ‘intubating’ LMA is most commonly used when a difficult intubation is anticipated or encountered. This device has a handle and is more rigid, wider and curved than the cLMA, enabling passage of a purpose-made endotracheal tube.¹⁷

Combitube

The combitube is more widely used in North America for emergency situations than in Australia and the UK.¹⁵ It is a dual-lumen, dual-cuff oesophageal-tracheal airway that enables ventilation if inserted into either the oesophagus or trachea. Inexperienced operators may find a combitube more difficult to insert correctly than a cLMA.¹⁹ Complications may occur in up to 40% of patients and include aspiration pneumonitis, pneumothorax, airway injuries and bleeding, oesophageal laceration and perforation and mediastinitis.²⁰

Intubation

Endotracheal intubation is the ‘gold standard’ for airway support, providing airway protection in the presence of an airway oedema, absent gag, cough or swallow reflex. Intubation facilitates delivery of mechanical ventilation and pulmonary secretion clearance.¹⁶

Endotracheal Tubes

Endotracheal tubes (ETT) are available with internal diameters ranging from 2–10 mm (common adult sizes are 7–9 mm), and are up to 30 cm long. A longitudinal radio-opaque line allows visualisation of tube placement on a chest X-Ray. Markings at 1 cm intervals indicate the length from the distal end. Tubes are available with and without a distal cuff. Adults typically require a cuffed ETT to seal their trachea, facilitating positive pressure ventilation and preventing aspiration of oropharyngeal contents. Cuffs come in a range of profiles and volumes, but are commonly high-volume, low-pressure (see Figure 15.3).

FIGURE 15.3 Endotracheal tube.²⁷²

Endotracheal tubes may be reinforced with a wire coil embedded within the plastic for the entire length of the tube to prevent kinking and occlusion. These tubes are more commonly used in the operating room.²¹ The wire coils can however be irreversibly compressed by a strong bite that occludes the airway. Reinforced tubes also increase the risk of tracheal damage and therefore should be replaced with a standard endotracheal tube on arrival in the ICU. Most endotracheal tubes have a ‘Murphy eye’, an oval-shaped hole in the side of the tube between the cuff and the end of the tube that provides a patent aperture if the distal opening is occluded.²²

Preparation for Intubation

Adequate preparation of the patient, equipment and environment, as well as strong knowledge of emergency procedures is important to ensure safe and efficient intubation. Up to 50% of patients undergoing endotracheal intubation in ICU will experience a complication; 28% will have a serious complication, including hypoxaemia, circulatory collapse, cardiac arrhythmia, cardiac arrest, oesophageal intubation, aspiration and death.²³

Patient Preparation

If appropriate, and time permits, explain the procedure to the patient and family. Prepare the patient with:

• reliable intravenous access established to allow rapid fluid and drug administration

• accurate blood pressure monitoring (preferably intra-arterial)

• continuous oxygen saturation and ECG monitoring

• nasogastric tube (if in situ) should be aspirated and placed on free drainage

• positioned supine in the ‘sniff’ position

Procedure

The patient is preoxygenated to minimise desaturation during apnoea and laryngoscopy, commonly via bag and mask, although other methods such as non-invasive ventilation have been suggested.²⁴ Intubation in ICU is usually performed via laryngoscopy with insertion of an oral ETT. Intubation may be performed using a fibreoptic bronchoscope when difficulty is encountered, or for nasal intubation.

Oral vs Nasal Intubation

Oral intubation is preferred unless there are specific indications for nasal intubation. Oral intubation is easier to perform and allows use of a larger diameter tube. While nasal intubation provides better splinting for the ETT and facilitates oral hygiene, it can damage nasal structures, is contraindicated in skull fractures and increases the risk of maxillary sinusitis and ventilator-associated pneumonia.²⁵

Cricoid Pressure

Cricoid pressure (Sellick manoeuvre) was introduced in the 1960s to prevent aspiration of gastric contents during intubation. The oesophagus lies behind and in line with the trachea. The cricoid cartilage, situated below the thyroid prominence, is a closed tracheal ring which, when compressed, closes the oesophagus while the trachea remains open. Cricoid pressure is performed by placing your thumb on one side of the patient’s trachea, middle finger on the other side and index finger directly on the cricoid.²⁶ Although widely used over the last 50 years, its efficacy is being questioned as technique is frequently poor,²⁷ and there is wide anatomical variation in the exact orientation of the oesophagus in relation to the trachea.²⁸

Backwards, Upwards, Rightward Pressure Manoeuvre

The backwards, upwards, rightward pressure (BURP) manoeuvre on the thyroid cartilage was introduced in the mid-1990s to improve visualisation during difficult laryngoscopy. The patient’s jaw is thrust forward, so their head is in the ‘sniffing’ position. Place your thumb and third finger on either side of the thyroid cartilage and index finger on top. Pressure is applied in the sequence backwards (towards the spine), upwards (towards the head), rightward (towards the patient’s right side). This is easier to perform following administration of muscle relaxants.^29,³⁰

Cuff Management

Endotracheal and tracheostomy tube cuffs prevent airway contamination by pharyngeal secretions and gastric contents and loss of tidal volume during mechanical ventilation. The cuff does not secure the tube in the trachea. Cuff inflation pressures should be maintained at 20–30 cmH₂O.^31,³² Cuff inflation pressures ≤20 cmH₂O (15 mmHg) are associated with an increased risk of aspiration and a 2.5-fold increase in ventilator-associated pneumonia (VAP).³³ Conversely, tracheal wall damage may occur if cuff pressure exceeds the capillary perfusion pressure in the trachea (27–40 cmH₂O/20–30 mmHg).

There are four methods described for assessing cuff inflation:

1. minimal occluding volume (MOV)

2. minimal leak test (MLT)

3. cuff pressure measurement (CPM)

4. palpation.

In Australia and New Zealand, CPM is the most common form of cuff pressure assessment,³⁴ in contrast to the UK³⁵ and North America³⁶ where CPM is used infrequently. Cuff pressure varies with head and body position, tube position and airway pressures.³⁷ The optimum frequency of cuff pressure monitoring is unclear; at a minimum it should be done post-intubation, on arrival in ICU and once per nursing shift. A persistent cuff leak or pressures of ≥30 cmH₂O (22 mmHg) to generate a seal should be reviewed and referred to medical staff.

If performing MOV and MLT, aspiration should be prevented by semi-recumbent positioning, suctioning at the back of the mouth (as far back as tolerated), aspiration of the nasogastric tube and discontinuation of feeds before cuff deflation.

Practice tip

If the pilot tube for the ETT is accidentally cut, cannulate the tubing with a 23- or 24-gauge needle to reinflate the cuff and clamp the tubing. If using a clamp with serrations, place gauze between the tube and the clamps to avoid further damage to the pilot tube.

Endotracheal Tube Fixation

The purpose of ETT fixation is to maintain the tube in the correct position, prevent unintended extubation and facilitate mechanical ventilation while maintaining skin integrity and oral hygiene.³⁸ ETT fixation methods include:

• tying cotton tape around the tube, then around the patient’s neck

• taping the tube to the patient’s face using medical adhesive tape

• commercial tubeholders of varying designs.

There is no evidence supporting a preferred method ³⁹ with each having specific strengths and weaknesses. Two nurses are required to prevent ETT dislodgement during fixation. Although there is also no evidence to recommend a preferred frequency, ETT fixation is generally changed at least daily, to allow assessment of the underlying skin with particular attention to the tops of the ears and corners of the mouth and to facilitate oral hygiene.³⁸ The ETT position in the mouth is alternated at this time.

Practice tip

Adhesive devices may become dislodged as facial hair grows under them.

Confirmation of Tube Position

The correct position of the ETT distal end is 3–5 cm above the carina. A lip level of 20 cm for women and 22 cm for men should prevent endobronchial intubation, with the proximal end fixed at either the centre or the side of the mouth.⁴⁰ Confirmation of the ETT position is required immediately following intubation and at regular intervals thereafter as movement of the tube can occur.

Chest auscultation is the traditional method to confirm ETT position. Observation of chest expansion is, however, unreliable, as the chest may appear to rise with oesophageal intubation. Conversely the chest may not rise with a correctly positioned tube if the patient is obese or has a rigid chest wall. Patients with left main bronchus intubation may exhibit bilateral breath sounds.⁴¹ End-tidal CO₂ monitoring is the ‘gold standard’ method for confirming ETT placement. Disposable devices that change colour in the presence of CO₂ are inexpensive and easy to use, but may be inaccurate during cardiopulmonary resuscitation, or if contaminated. Capnography is the most reliable technique to identify ETT placement in both arrest and non-arrest situations.¹⁸ Continuous end-tidal CO₂ monitoring during intubation is recommended as a minimum standard by the College of Intensive Care Medicine of Australia and New Zealand.⁴²

Practice tip

Always ensure there is someone who is skilled at intubation immediately available when extubating a patient.

Tracheostomy

Tracheostomy may be required for upper airway obstruction, although it is most commonly performed for ICU patients who require prolonged mechanical ventilation. The advantages of tracheostomy over endotracheal intubation include decreased risk of laryngeal damage and subglottic stenosis, reduced airway resistance and deadspace which decreases the work of breathing and therefore supports weaning,⁴³ and improved patient tolerance enabling reduction of sedation. The optimum time to perform tracheostomy remains contentious, and is often influenced by a patient’s diagnosis.⁴⁴

Procedure

Tracheostomy can be performed using a surgical technique (ST) or percutaneous dilatational technique (PDT). PDT is contraindicated in patients with anatomical anomalies of the neck and serious bleeding disorders, and should be undertaken with caution in patients who are obese, have a cervical spine injury, coagulopathy, difficult airway or require high levels of ventilatory support.⁴⁵ PDT is more commonly performed than ST in Australian and New Zealand ICUs.⁴⁵

A variety of tracheostomy tubes are available that facilitate secretion clearance, communication and differing patient anatomy. Inner cannulas (re-usable or disposable) prevent secretion build up on the tracheostomy tube, while fenestrated and talking tracheostomies facilitate communication, as do Passe Muir valves used with the cuff deflated.

Tracheostomy Care

The aim of tracheostomy care is to keep the site free of infection, and prevent tube blockage or dislodgement. The site is cleaned with normal saline and fixation devices changed at least 12-hourly with two nurses to safely perform tape changes.⁴⁶ Velcro tapes are easier to change and more comfortable than cotton tape.⁴⁷ Lint-free or superabsorbent foam dressings may be placed under the flange to absorb secretions. Adequate humidification and suctioning will usually prevent tube obstruction (see later in this chapter). The use of inner cannulae has obviated the need for frequent tracheostomy tube changes. Single lumen (no inner cannula) tracheostomy tubes should be changed every 7–10 days.⁴⁶

Complications of Endotracheal Intubation and Tracheostomy

Tube blockage, tube dislodgement and aspiration are major complications. Partial ETT or tracheostomy tube dislodgement can cause greater harm than complete removal because of delays in diagnosis and resultant aspiration or worsening gas exchange. Tube dislodgement is most likely to occur when turning the patient, if the patient is agitated or when nursing staff are distracted or on breaks.⁴⁸ While physical restraint may be considered to prevent tube dislodgement, multiple studies noted patients were restrained at the time of self-extubation or device removal.⁴⁹^–⁵⁴ Effective levels of analgesia and sedation is therefore most appropriate in minimising the risk of self-extubation.

Complications during and immediately after endotracheal intubation and tracheostomy include cardiovascular compromise, bleeding, injury to the tracheal wall, damage to the vocal cords, pneumothorax, pneumomediastinum and subcutaneous emphysema. Late complications of tracheostomy include tracheal stenosis, tracheomalacia and tracheo-oesophageal fistula and infection. As noted earlier, damage to the trachea is exacerbated by high cuff pressures.⁵⁵ PDT results in fewer wound infections, decreased incidence of bleeding and reduced mortality compared to ST.⁵⁶

Tracheal Suction

Patients with an ETT or tracheostomy tube require tracheal suction to remove pulmonary secretions that can lead to atelectasis or airway obstruction and impair gas exchange.⁵⁷ Suction should be performed as clinically indicated, with assessment of visible or audible secretions, rising inspiratory pressure, decreasing V_T or increased work of breathing.⁵⁸ A sawtooth pattern on the flow-volume waveform may also indicate the need for suction (discussed later in this chapter).⁵⁹

Preoxygenation using a FiO₂ of 1 for 60 seconds prior to performing suction minimises hypoxia and the potential for cardiac arrhythmias. Manual hyperinflation is discouraged due to the risk of barotrauma and lack of benefit. Similarly, installation of saline is not supported due to increased risk of flushing pathogens into distal lung regions.⁶⁰

Methods

The three methods of suctioning are:

• open suction: a suction catheter is passed under aseptic technique directly into the ETT/tracheostomy after disconnection from the ventilator circuit. Disadvantages include loss of PEEP resulting in loss of alveolar recruitment and increased risk of transmission of infective organisms. A surgical mask and protective eyewear should be worn.⁶¹

• semi-closed suction: a suction catheter is passed through a swivel connector with a self-sealing rubber flange.

• closed suction: in-line system is attached between the ETT/tracheostomy tube and the ventilator circuit where the suction catheter is contained in an integrated plastic sleeve. Alveolar derecruitment occurs to a lesser degree than with open suction.

There is no difference between techniques in relation to development of ventilator-associated pneumonia (VAP) and quantity of secretions removed.

The diameter of the suction catheter should not be greater than half the diameter of the airway, using the formula: suction catheter size [Fr] = (ET tube size [mm] − 1) × 2. The suction catheter should be inserted to the carina, then withdrawn 2 cm before suction is applied to prevent damage to the carina. Suction should only last 15 seconds, using continuous, rather than intermittent, suction. Use of ETTs or tracheostomy tubes with integrated subglottic suction ports may assist in preventing VAP, especially when performed with other prevention strategies such as semirecumbant positioning and good cuff seal management.

Adverse Effects

Adverse effects of suction can include hypoxaemia, introduction of infective organisms, tracheal trauma, bradycardia, hypertension and increased intracranial pressure. Tracheal suctioning causes discomfort, and should therefore be performed only when clinically indicated, such as audible presence of secretions and desaturation.⁵⁸

Extubation

Following successful weaning from mechanical ventilation (see later in this chapter), assessment of the patient prior to extubation should include adequate gas exchange, respiratory rate and work of breathing on minimal support for prolonged periods, respiratory muscle strength, the ability to cough and clear secretions spontaneously and a stable haemodynamic status and mental status.⁶² Serious post-extubation complications of laryngospasm and stridor cannot be reliably predicted,⁶³ so the ease/grade of intubation should be considered prior to extubation and provision made for immediate re-intubation.⁶⁴

Mechanical Ventilation

As stated in the introduction, 41% of patients in Australian and New Zealand ICUs received invasive mechanical ventilation and 8% received non-invasive ventilation (NIV) in 2007–08.¹ The median duration of invasive mechanical ventilation for these patients was 2.5 days. In the most recent international study of mechanical-ventilation practices, reporting data from 4968 patients in 349 ICUs and 23 countries found the median duration of ventilation to be 4 days (interquartile range 2–8 days).⁶⁵ In this patient cohort the three most common reasons for mechanical ventilation were postoperative respiratory failure, coma and pneumonia. This international report did not include data from Australia and New Zealand. A study describing ventilation and weaning practices of 55 ICUs in Australia and New Zealand in 2005 reported a similar profile for the most common indications for mechanical ventilation.⁶⁶

Principles of Mechanical Ventilation

Mechanical ventilation describes the application of positive or negative pressure breaths using non-invasive or invasive techniques. Indications for initiation of mechanical ventilation are discussed below. Table 15.1 lists the patient parameters typically observed in acute and chronic respiratory failure that may be influential in the decision to ventilate. During positive pressure ventilation, the type of ventilation used most commonly in critical care, the ventilator delivers a flow of gas into the lungs during inspiration using a pneumatic system. Expiration is passive.

TABLE 15.1 Physiological indications suggesting the need for mechanical ventilation

The Equation of Motion

The equation of motion for the respiratory system is a mathematical model that relates pressure volume and flow during the delivery of a breath, with the pressure required to deliver a volume of gas to the lungs determined by the elastic and resistive properties of the respiratory system ⁶⁷ (see Table 15.2).

TABLE 15.2 Equation of motion

Equation: P_T (P_airway + P_muscle) = V_T/Cr + V_T/T_I × R + PEEP_T
Abbreviations:	P_T = total pressure: the sum of the pressure in the proximal airway and the pressure generated by the respiratory muscles V_T = tidal volume Cr = compliance T_I = inspiratory time R = resistance PEEP_T = total positive end expiratory pressure: alveolar pressure at the end of expiration and is the sum of PEEP applied by the ventilator and any intrinsic (auto) PEEP.

Notes:

V_T/Cr: describes the elastic properties the respiratory system

V_T/T_I: reflects flow in the system

V_T/T_I × R: resistance of the respiratory system.

Compliance and Elastance

Compliance refers to the ease with which lung units distend. Elastance is the tendency of the lung units to return to their original form once stretched. Compliance is defined as the change in volume that occurs due to a change in pressure.

Lung tissue and the surrounding thoracic structures contribute to respiratory compliance. Normal compliance for a mechanically ventilated patient ranges from 35–50 mL/cmH₂O.⁶⁸

Resistance

Resistance refers to the forces that oppose airflow. Resistance in the airways is affected by the diameter and length of the airways, including the artificial airway, the gas flow rate and the density and viscosity of the inspired gas. During mechanical ventilation, bronchospasm, airway oedema, endotracheal tube lumen size, increased secretions, and inappropriate setting of flow rates can influence airway resistance. Normal resistance for intubated patients is 6 cmH₂O/(L/sec).⁶⁸

Ventilator Circuits

Delivery of mechanical ventilation requires a ventilator circuit to transport gas flow to the patient. To prevent condensation from cooling of warm humidified gas, inspired gas is heated via a wire inside the wall of the circuit in either the inspiratory limb alone or both the inspiratory and expiratory limbs.⁶⁹ Historically ventilator circuits were changed frequently (48–72 hours) to decrease the risk of VAP.⁷⁰ Current guidelines for prevention of VAP found evidence that the frequency of ventilator circuit changes had no relationship to the incidence of VAP and therefore recommended routine circuit changes were not necessary and circuits should only be changed when soiled or damaged.⁷¹

Humidification

Humidification techniques warm and moisten gas to facilitate cilia action and mucus removal as well as to prevent drying and irritation of respiratory mucosa and solidification of secretions. During endotracheal intubation and mechanical ventilation, the normal humidification processes of the nasopharynx are bypassed. This, in combination with the use of dry medical gas at high flow rates, means alternative methods of humidification are required. The best conditions for mucosal health and function over prolonged periods are when inspired gas is warmed to core body temperature and is fully saturated with water.⁷²

Absolute and Relative Humidity

Absolute humidity refers to the amount of water vapour in a given volume of gas at a given temperature. Absolute humidity rises with increasing temperature; during mechanical ventilation gas is heated to increase the amount of water vapour it will hold. Relative humidity is expressed as a percentage, and is the actual amount of water vapour in a gas compared to the maximum amount this gas can hold (ratio of absolute to maximal humidity). Ideal humidification is achieved when:

1. the inspired gas delivered into the trachea is at 37°C with a water content of 30–43 g/m³ (relative humidity is 100% at 37°C in the bronchi)

2. the set temperature remains constant without fluctuation

3. humidification and temperature are unaffected by a large or differing types of gas flow

4. the device is simple to use

5. the humidifier can be used with spontaneously breathing and ventilated patients

6. safety alarms prevent overheating, overhydration and electrocution

7. the resistance, compliance and dead space characteristics do not adversely affect spontaneous breathing modes

8. the sterility of the inspired gas is not compromised.⁷³

Humidification is applied using either a heat–moisture exchanger (HME) or a heated water bath reservoir device in combination with a heated ventilator circuit.

Heat–moisture Exchanger

Heat–moisture exchangers conserve heat and moisture during expiration, and enable inspired gas to be heated and humidified. Two types of HMEs exist: hygroscopic and hydrophobic. Hygroscopic HMEs absorb moisture onto a chemically impregnated foam or paper material and have been shown to be more effective than hydrophobic HMEs.⁷⁴ HMEs are placed distally to the circuit Y-piece in line with the endotracheal tube and increase dead space by an amount equal to their internal volume.⁷⁵ HMEs should be changed every 24 hours or when soiled with secretions and are usually reserved for short term humidification.

Heated Humidification

Generally, heated humidification (HH) is used for patients requiring greater than 24 hours of mechanical ventilation. Various models of heater bases and circuits are on the market and we recommend their use in accordance with manufacturer instructions. A recent systematic review and meta-analysis reported no overall effect on artificial airway occlusion, mortality, pneumonia, or respiratory complications when HMEs were compared to HHs, although it noted that PaCO₂ and minute ventilation were increased and body temperature was lower with the use of HMEs.⁷⁶

Non-Invasive Ventilation

Non-invasive ventilation (NIV) is an umbrella term describing the delivery of mechanical ventilation without the use of an invasive airway, via an interface such as an oronasal, nasal, or full face mask or helmet. NIV techniques include both negative and positive pressure ventilation, although in critical care positive pressure ventilation is primarily used.

Terminology

Positive pressure NIV can be further categorised as non-invasive positive pressure ventilation (NIPPV) or continuous positive airway pressure (CPAP). NIPPV is the provision of inspiratory pressure support (also referred to as inspiratory positive airway pressure [IPAP]) usually in combination with positive end expiratory pressure (PEEP) (also referred to as expiratory positive airway pressure [EPAP]). CPAP does not actively assist inspiration but provides a constant positive airway pressure throughout inspiration and expiration.⁷⁷

The terms Biphasic (or bilevel) positive airway pressure (BiPAP®) and non-invasive pressure support ventilation (NIPSV) are also used to refer to NIPPV.⁷⁸ The acronym BiPAP® is registered to Respironics (Murrayville, PA), a company that produces a number of non-invasive ventilators including the BIPAP Vision, a NIV ventilator commonly used in the ICU. The acronym NIPSV is primarily used in European descriptions of NIPPV.

Practice tip

When other members of the ICU team use the term BiPAP/BIPAP, clarify if they are referring to non-invasive or invasive ventilation.

Physiological Benefits

The efficacy of NIV in patients with acute respiratory failure is, at least in part, related to avoidance of inspiratory muscle fatigue through the addition of inspiratory positive pressure thus reducing inspiratory muscle work.⁷⁹ Application of positive pressure during inspiration increases transpulmonary pressure, inflates the lungs, augments alveolar ventilation and unloads the inspiratory muscles.⁸⁰ Augmentation of alveolar ventilation, demonstrated by an increase in tidal volume, increases CO₂ elimination and reverses acidaemia. High levels of inspiratory pressure may also relieve dyspnoea.⁸¹

The main physiological benefit in patients with congestive heart failure (CHF) is attributed to the increase in functional residual capacity associated with the use of PEEP that reopens collapsed alveoli and improves oxygenation.⁸² Increased intrathoracic pressure associated with the application of positive pressure also may improve cardiac performance by reducing myocardial work and oxygen consumption through reductions to ventricular preload and left ventricular afterload.⁸²^–⁸⁴ NIV also preserves the ability to speak, swallow, cough and clear secretions, and decreases risks associated with endotracheal intubation.⁸⁵

Indications for NIV

The success of NIV treatment is dependent on appropriate patient selection.⁸⁶ Table 15.3 outlines indications and contraindications to NIV.

TABLE 15.3 Indications and contraindications for non-invasive ventilation ⁷⁷

Indications
Bedside observations	Increased dyspnoea: moderate to severeTachypnoea: >24 breaths per min [obstructive] >30 breaths per min [restrictive] Signs of increased work of breathing, accessory muscle use and abdominal paradox
Gas exchange	Acute or acute-on-chronic ventilatory failure (best indication), PaCO₂ >45 mm Hg, pH <7.35 Hypoxaemia (use with caution), PaO₂/FIO₂ ratio <200
Contraindications
Absolute	Respiratory arrest Unable to fit mask
Relative	Medically unstable: hypotensive shock, uncontrolled cardiac ischaemia or arrhythmia, uncontrolled upper gastrointestinal bleeding Agitated, uncooperative Unable to protect airway Swallowing impairment Excessive secretions not managed by secretion clearance techniques Multiple (i.e. two or more) organ failure Recent upper airway or upper gastrointestinal surgery

PaCO₂: partial pressure of carbon dioxide in arterial blood; PaO₂: partial pressure of oxygen in arterial blood; PaO₂/FIO₂: ratio of partial pressure of oxygen in arterial blood to fraction of inspired oxygen.

Acute Respiratory Failure

Evidence supporting the role of NIV in patients with hypoxaemic respiratory failure is limited and conflicting.⁸² For patients with community-acquired pneumonia, NIV has been shown to reduce intubation rates, ICU length of stay and 2-month mortality but only in the subgroup of patients with COPD.⁸⁷ Pneumonia also has been identified as a risk factor for NIV failure.⁸⁸

Acute Exacerbation of COPD and CHF

Strong evidence exists to support the use of NIV for patients with acute exacerbation of chronic obstructive pulmonary disease (COPD) and congestive heart failure (CHF). Three meta-analyses have shown a reduction in intubation rates, hospital length of stay and mortality for COPD patients managed with NIPPV compared to standard medical treatment.⁸⁹^–⁹¹ COPD patients most likely to respond favourably to NIPPV include those with an unimpaired level of consciousness, moderate acidaemia, a respiratory rate of <30 breaths/minute and who demonstrate an improvement in respiratory parameters within two hours of commencing NIV.^79,⁹²

Early use of NIV in combination with standard therapy for patients with CHF has also been shown to reduce intubation rates and mortality when compared to standard therapy alone.⁹³^–⁹⁵ A recent meta-analysis found CPAP reduced hospital mortality whereas NIPPV did not have an effect on mortality.⁹⁴ Both NIV modes were shown in this meta-analysis to reduce the need for intubation. An early study comparing NIPPV to CPAP in patients with CHF reported a higher incidence of myocardial infarction.⁹⁶ Based on this finding, practice guidelines from the British Thoracic Society recommend NIPPV should only be used for patients with CHF when CPAP has been unsuccessful.⁹⁷ More recently several studies have found no difference in myocardial infarction rates when comparing the two modes.⁹⁸^–¹⁰¹ A recent large multicentre randomised controlled trial found NIV delivered by either CPAP or NIPPV resulted in symptomatic improvements, but failed to demonstrate a mortality benefit.¹⁰² Practice surveys indicate CPAP may be the preferred method of NIV for patients with CHF in Australia and internationally.^103,¹⁰⁴

NIV in Weaning

NIV may be used as an adjunct to weaning to reduce the duration of invasive ventilation and associated complications.¹⁰⁵ Patients are extubated directly to NIV and then weaned to standard oxygen therapy. This use of NIV differs from its role in preventing reintubation in patients that develop, or who are at high risk of, postextubation respiratory failure.¹⁰⁶ A recent systematic review and meta-analysis of 12 trials of NIV as a weaning adjunct found reductions in mortality, ICU and hospital lengths of stay, duration of ventilation and rates of VAP.¹⁰⁷ Conversely the largest study of NIV use in postextubation respiratory failure reported worsened survival rates hypothesised as a result of delayed reintubation.¹⁰⁸ A subsequent meta-analysis suggested NIV may have a role in preventing the development of respiratory failure postextubation for those at risk, but should be used with caution once respiratory failure has developed and should not delay the decision to reintubate.¹⁰⁶

Other Indications

Other indications for NIV include:

• asthma ¹⁰⁹

• neuromuscular disorders (e.g. muscular dystrophy, amyotrophic lateral sclerosis)

• severe obstructive sleep apnoea

• palliation.

Interfaces and Settings

NIV requires an interface that connects the patient to either a ventilator, portable compressor or flow generator with a CPAP valve. The selection of an appropriate interface can influence NIV success or failure. Oronasal masks cover both the mouth and nose and are the preferred mask type for the management of acute respiratory failure.¹¹⁰ Nasal masks enable speech, eating and drinking, and therefore are used more frequently for long-term NIV use. An oronasal mask enables delivery of higher ventilation pressures with less leak and greater comfort for the patient.¹¹¹ Other interfaces include full-face masks¹¹¹ that seal around the perimeter of the face and cover the eyes as well as the nose and mouth, nasal pillows, mouthpieces that are placed between the patient’s lips, and helmets that cover the whole head and consist of a transparent plastic hood attached to a soft neck collar.^112,¹¹³ These alternative interfaces may increase patient tolerance by reducing pressure ulceration, air leaks and patient discomfort.¹¹⁴

Initiation and Monitoring Priorities

Successful initiation of NIV is dependent on patient acceptance and tolerance. Patient acceptance of NIV may be aided by a brief explanation of the procedure and its benefits. Strategies to enhance patient tolerance include: use of an interface that fits the patient’s facial features, commencing with low pressure levels, holding the mask gently in position prior to securing with the straps/headgear, and ensuring straps prevent major leaks but are not so tight they increase discomfort. Once NIV is commenced, the patient should be monitored for respiratory and haemodynamic stability, response to NIV treatment, ongoing tolerance, and presence of air leaks (Table 15.4). Arterial blood gas analysis should be performed at baseline and within the first one to two hours of commencement.⁹⁷ During the initiation and stabilisation period, patients should be monitored using a nurse-to-patient ratio of 1 : 1 with ongoing coaching to promote NIV tolerance throughout the early stabilisation period.

TABLE 15.4 Monitoring priorities for non-invasive ventilation ¹⁰⁴

Priority	Assessment
Patient comfort	Restlessness Mask tolerance Anxiety level Dyspnoea score Pain score

Conscious level Glasgow coma score Work of breathing

Chest wall motion

Accessory muscle activation

Respiratory rate

Gas exchange parameters

Continuous SpO₂

Arterial blood gas analysis

(Baseline and 1–2 hourly subsequently)

Patient colour

Haemodynamic status

Continuous heart rate

Intermittent blood pressure

Ventilator parameters

Air leak around mask

Adequacy of pressure support (V_T, pH, PaCO₂)

Adequacy peak end expiratory pressure (SpO₂, PaO₂)

SpO₂: saturation of peripheral oxygen; V_T: tidal volume; PaCO₂: partial pressure of carbon dioxide in arterial blood; PaO₂: partial pressure of oxygen in arterial blood.

Practice tip

NIV tolerance may be promoted with a simple explanation of the therapy, reassurance and constant monitoring for your patient. During initiation, allow them to take short breaks from the mask if they are in discomfort or experiencing claustrophobia.

Potential Complications

Masks need to be tight-fitting to reduce air leaks; however, this contributes to pressure ulceration on the bridge of the nose or above the ears (due to mask straps/headgear). Air leaks may cause conjunctival irritation and the high flow of dry medical gas results in nasal congestion, oral or nasal dryness and insufflation of air into the stomach. Claustrophobia associated with the NIV interface may also lead to agitation reducing the efficacy of NIV treatment due to poor coordination of respiratory cycling between the patient and NIV unit.⁷⁹ More serious, yet infrequent, complications include aspiration pneumonia, haemodynamic compromise associated with increased intrathoracic pressures and pneumothorax.⁸⁰

Detecting NIV Failure

Failure to respond to NIV within 1–2 hours of commencement is demonstrated by unchanged or worsening gas exchange, as well as ongoing or new onset of rapid shallow breathing and increased haemodynamic instability.¹¹¹ A decreased level of consciousness may be indicative of imminent respiratory arrest.

Invasive Mechanical Ventilation

Critically ill patients with persistent respiratory insufficiency (hypoxaemia and/or hypercapnia), due to drugs, disease or other conditions, may require intubation and mechanical ventilation to support oxygenation and ventilatory demands.^115,¹¹⁶ Clinical criteria for intubation and ventilation should be based on individual patient assessment and patient response to measures aimed at reversing hypoxaemia.

Mechanical Ventilators

Contemporary ventilators use sophisticated microprocessor controls with sensitive detection, response and control of pressure and gas flow characteristics. These mechanical ventilators are more sensitive to patient ventilatory demands, enabling improved patient–ventilator synchrony during both inspiratory and expiratory breath phases. Parameters commonly manipulated during mechanical ventilation are detailed in Table 15.5. Parameters often observed and documented are discussed below.

TABLE 15.5 Set ventilator parameters

Parameter	Description
Fraction of inspired oxygen (FiO₂)	The fraction of inspired oxygen delivered on inspiration to the patient.
Tidal volume (V_T)	Volume (mL) of each breath.
Set breath rate (f)	The clinician determined set rate of breaths delivered by the ventilator (bpm).
Inspiratory trigger or sensitivity	Mechanism by which the ventilator senses the patient’s inspiratory effort. May be measured in terms of a change in pressure or flow.
Inspiratory pressure (P_insp, P_high)	Clinician determined pressure that is targeted during inspiration.
Inspiratory time (T_insp)	The duration of inspiration (sec).
Inspiratory : expiratory ratio (I : E)	The ratio of the inspiratory time to expiratory time.
Flow (V)	The speed gas travels during inspiration. (L/min).
Pressure support (PS)	The flow of gas that augments a patient’s spontaneously initiated breath to a clinician-determined pressure (cmH₂O).
Positive end-expiratory pressure (PEEP)	Application of airway pressure above atmospheric pressure at the end of expiration (cmH₂O).
Rise time	Time to achieve maximal flow at the onset of inspiration for pressure-targeted breaths.
Expiratory sensitivity	During a spontaneous breath, the ventilator cycles from inspiration to expiration once flow has decelerated to percentage of initial peak flow.
Minute volume (VE)	Generally not set directly but is determined by V_T and f settings. Tidal volume multiplied by the respiratory rate over one minute (L/min).
Airway pressure (P_aw)	The pressure measured in cmH₂O by the ventilator in the proximal airway.
Plateau pressure (P_plat)	The pressure, measured in cmH₂O, applied to the small airways and alveoli. P_plat is not set but can be measured by performing an inspiratory hold manoevre.

Fraction of Inspired Oxygen

The fraction of inspired oxygen (FiO₂) is expressed as a decimal, between 0.21 and 1, when supplemental oxygen is applied. Room air has an oxygen content of 0.21 (21%). Ventilation is commonly commenced on a high FiO₂ setting, but as noted earlier, consideration is given to the risks of oxygen toxicity which include disruption to the alveolar-capillary membrane and fibrosis of the alveolar wall.¹¹⁹

Tidal Volume

Tidal volume (V_T) is the volume, measured in mL, of each breath. The V_T is calculated using the patient’s ideal body weight using height and gender-specific tables ¹²⁰ to achieve 6–8 mL/kg (see Table 15.6). Strong evidence indicates a mortality benefit for using 6 mL/kg in patients with acute respiratory distress syndrome (ARDS).¹²¹ Some evidence also indicates 6 mL/kg as a target for patients without ARDS or acute lung injury (ALI).^122,¹²³ While further studies are required, clinicians should consider aiming for 6–8 mL/kg in all ventilated patients.

TABLE 15.6 ARDSnet tables for predicted body weight for females and males

Respiratory Rate

Mandatory frequency or respiratory rate (f, RR) is set with consideration of the patient’s own respiratory effort, anticipated ventilatory requirements and the effect on the I : E ratio. Use of high doses of sedation with or without neuromuscular blockade requires setting a mandatory rate that facilitates adequate gas exchange and meets oxygenation requirements. A lower frequency can be set for a patient able to breathe spontaneously in modes such as synchronised intermittent mandatory ventilation (SIMV) and assist control (A/C) (see below) to enable spontaneous triggering. Physiologically normal respiratory rates are 12–20 breaths per minute. Patients with hypoxaemic respiratory failure generally breathe 20–30 breaths per minute.¹²⁴

Triggering of Inspiration

Depending on the mode of ventilation, breaths are triggered by the ventilator or patient in various sequences. A breath may be triggered by the ventilator in response to time in modes with clinician-determined set frequency such as CMV, and in A/C and SIMV in the absence of spontaneous effort. Patient triggering requires the ventilator to sense the patient’s inspiratory effort. Most modern generation ventilators now use flow triggering, as evidence indicates that flow triggering may be more responsive to patient effort than pressure triggering.¹²⁵ Pressure triggering requires the patient to create a negative pressure within the ventilator circuit for long enough to enable the ventilator to sense the effort and commence flow of gas. Flow triggering requires a predetermined flow of gas, usually 5–10 L/min, referred to as the bias (or base) flow, that travels continuously through the ventilator circuit. When the patient makes an inspiratory effort, they divert flow that is sensed by the ventilator. If the flow diversion reaches a clinician-determined set value, a breath is initiated.¹²⁶ The flow trigger is usually set at 1–3 L/min (1 L/min represents less patient effort and 3 L/min represents greater patient effort). Despite advances in ventilator technology, various studies continue to identify missed patient triggers that contribute to patient–ventilator asynchrony.¹²⁷ Conversely, ‘auto-triggering’ is triggering by the ventilator in the absence of spontaneous inspiratory effort.

Inspiratory Time and Inspiratory : expiratory Ratio

The total time available for each mandatory breath is determined by the set frequency. The total breath time comprises the inspiratory and expiratory time which can be expressed as a ratio (I : E). In normal spontaneous breathing, expiratory time is approximately twice as long as the inspiratory time (1 : 2 ratio). Gas flow also influences inspiratory time, with higher gas flows resulting in decreased time to achieve the target V_T. The I : E ratio can be manipulated to create an inverse relationship (1 : 1, 2 : 1, 4 : 1) with the goal of increased mean airway pressure resulting in alveolar recruitment and improved oxygenation. Inverse ratios are more frequently applied with pressure control ventilation as application in volume control can result in increased risk of barotrauma due to peak and plateau airway pressure variation.¹²⁸

Inspiratory Flow and Flow Pattern

The flow rate refers to the speed of gas and is measured in litres per minute (L/min). Generally, inspiratory flow is delivered at speeds of 30–60 L/min. Higher flow rates cause gas to become more turbulent and result in increased peak airway pressures. Lower flow rates result in laminar flow, an increased inspiratory time, improved distribution of gas, and lower peak airway pressures.¹²⁹ The flow of inspiratory gas can be delivered in three styles: constant or square wave, decelerating ramp and sinusoidal pattern (see Figure 15.4). In a constant flow pattern, the peak flow is achieved at the beginning of inspiration and is held constant throughout the inspiratory phase. This may result in higher peak airway pressures. Using a decelerating ramp, the gas flow is highest at the beginning of inspiration and tapers throughout the inspiratory phase. Sinusoidal gas flow resembles spontaneous ventilation.

FIGURE 15.4 Standard mechanical ventilator flow-wave patterns.¹²⁹

Pressure Support

When triggered by the patient, the ventilator delivers flow to achieve the clinician-determined set pressure support. The flow is variable, depending on the patient demand. The V_T achieved with pressure support is dependent on chest and lung compliance as well as airway and ventilator resistance. Pressure support is generally set at 5–20 cmH₂O. Increasing the level of pressure support will result in increased V_T, and improvements in gas exchange if compliance and resistance remain constant.

Positive End Expiratory Pressure

Positive end expiratory pressure (PEEP) is the pressure applied at the end of the expiratory cycle to prevent alveolar collapse. PEEP increases residual lung volume thereby recruiting collapsed alveoli, improving V/Q match and enhancing movement of fluid out of the alveoli.^130,¹³¹ PEEP was originally introduced by Ashbaugh and colleagues¹³² in the 1960s as a technique for treating refractory hypoxaemia in patients with ARDS. Animal studies suggest ventilator-associated lung injury (VALI) may be prevented using PEEP by recruiting atelectic alveoli and bronchioles and preventing cyclic opening and closing of alveoli.¹³³^–¹³⁶ PEEP may be beneficial, however, only if the lung has sufficient potential for recruitment which occurs in collapsed, as opposed to consolidated, lung.¹³⁰ The setting of optimal PEEP remains controversial. Low PEEP levels have been shown to be associated with higher mortality for ARDS patients in a number of studies.¹³⁷^–¹⁴⁰ Two recently published randomised, controlled trials comparing low tidal volume ventilation and conventional PEEP to low tidal volume ventilation and high PEEP, with and without additional recruitment manoeuvres (40 cmH₂O applied for 40 sec),^141,¹⁴² did not demonstrate a difference in hospital¹⁴¹ or 28-day¹⁴² mortality.

Rise Time

The rise time controls how quickly the ventilator reaches the clinician-determined inspiratory pressure (P_insp for mandatory breaths and pressure support for spontaneous breaths). Reducing the rise time results in a higher peak flow as the ventilator aims to achieve the inspiratory pressure within a shortened time frame. Reduced rise times may be desired in patients with airflow limitation.

Expiratory Sensitivity

Expiratory sensitivity describes the percentage of decay in peak flow reached during the inspiratory phase that signals the ventilator to cycle to expiration for spontaneous breaths. In some ventilator models this is predetermined at 25%, whilst other ventilator models allow clinician selection. Premature termination of a breath will increase inspiratory muscle workload whereas delayed breath termination increases expiratory muscle load.¹⁴³

Peak Airway Pressure

Airway pressures vary across the respiratory cycle, and are measured by the ventilator’s airway pressure gauge. A number of pressures are identifiable (e.g. peak inspiratory, end-expiratory). The airway pressure (P_aw) is an important parameter in assessing respiratory compliance and patient–ventilator synchrony, and will vary depending on V_T, RR, ventilator flow pattern, dynamic compliance and airway resistance. In pressure-targeted modes the peak inspiratory pressure is equivalent to the P_insp. In volume-targeted modes the peak inspiratory pressure is determined by the set V_T and patient compliance and resistance.

Practice tip

The P_insp setting reflects a different value on different ventilators. P_insp equals total pressure including PEEP on some ventilators and inspiratory pressure above PEEP on others. Use the pressure–time scalar to confirm.

Ventilator Modes

The mode of ventilation describes inspiratory phase variables; how the ventilator controls pressure, volume, and flow during a breath; as well as describing how breaths are sequenced. All breaths have trigger, limit and cycle inspiratory phase variables.¹⁴⁴ Each breath is triggered (started) either by the patient or by the ventilator. During inspiration, the breath is limited to a set target of pressure, volume, or flow. This target cannot be exceeded during each breath. At the end of inspiration, the cycling variable determines the end of the inspiratory phase. Again this variable may be pressure, flow, volume, or time. Gas delivery during each breath is described by the control variable. There are five control variables: pressure, volume, flow, time and dual control (such as used in the mode pressure regulated volume control [PRVC]). Breath sequencing refers to the sequence of mandatory and spontaneous breath. A spontaneous breath is one during which inspiration is both started (triggered) and stopped (cycled) by the patient. Spontaneous breaths may be assisted, as with pressure support, or unassisted. Mandatory breaths are either triggered or cycled by the ventilator.¹⁴⁵ A complete mode description should include: (1) the control variable; (2) the breath sequence; and (3) the targeting scheme (limit variable).

Pressure Control vs Volume Control

Traditionally, clinicians have favoured volume control due to the ability to regulate minute ventilation (VE) and carbon dioxide (CO₂) elimination with straightforward manipulation of ventilation.¹⁴⁶ Volume control provides consistent tidal volume delivery, independent of the patient’s lung mechanics. A disadvantage of volume control, however, is the lack of control over peak airway pressure that changes in response to altered compliance and resistance. Elevated peak airway pressures may cause alveolar overdistension, barotrauma and haemodynamic effects such as reduced venous return, cardiac output, hypotension and thus decreased organ perfusion.¹⁴⁷ Clinicians need to carefully monitor ventilation to avoid injurious pressures. In volume control the peak airway pressure is achieved at the end of inspiration, and only for a short duration, therefore distribution of gas may not be optimised and shearing stress can occur.¹⁴⁸

Pressure control allows ventilator control over the peak inspiratory pressure and inspiratory time. Clinicians are required to monitor minute ventilation and gas exchange due to the lack of a guaranteed tidal volume and possible changes in respiratory compliance and resistance. The variable and decelerating inspiratory gas flow pattern of pressure control enables rapid alveolar filling and more even gas distribution compared to the constant flow pattern that may be used with volume control. This decelerating flow pattern results in improved gas exchange, decreased work of breathing and prevention of overdistension in healthy alveoli.¹⁴⁹^–¹⁵² During pressure control, the set inspiratory pressure is achieved at the beginning of the inspiratory cycle and maintained for the set inspiratory time. This promotes recruitment of alveoli with high opening pressures and long time-constants.

Commonly Employed Modes of Ventilators

Contemporary ventilators now provide a range of modes to facilitate mechanical ventilation. Modes of mechanical ventilation are described in Table 15.7.

TABLE 15.7 Ventilator modes

Mode	Descriptor	Clinical implications
Controlled mechanical ventilation (CMV)	All breaths are mandatory, no patient triggering is enabled. Also called volume controlled ventilation (volume targeted) (VCV) and pressure controlled ventilation (pressure targeted) (PCV)	Patients with respiratory effort require sedation and neuromuscular blockade.Potential for respiratory muscle atrophy due to disuse.
Assist-control (A/C)	Breaths may be either machine or patient triggered but all are cycled by the ventilator. Assist control may be delivered as volume (AC-VC) or pressure (AC-PC) targeted.	Activation of the diaphragm with patient triggering.Potential for respiratory alkalosis If tachypnoea develops.
Synchronised intermittent mandatory ventilation (IMV)	Mandatory breaths are delivered using a set rate and volume (SIMV-VC) or pressure (SIMV-PC). Mandatory breaths are synchronised with patient triggers within a timing window. Between mandatory breaths the patient can breathe spontaneously.	Reduced need for sedation.Activation of the diaphragm with patient triggering.
Pressure support ventilation (PSV)	All breaths are patient triggered and cycled. Pressure applied by the ventilator during inspiration (pressure support) augments patient effort.	Reduced need for sedation.Facilitates ventilator weaning.Level of PS can be adjusted to achieve desired V_T.Sustains respiratory muscle tone and decreases WOB.
Continuous positive airway pressure (CPAP)	All breaths are patient triggered and cycled. Positive pressure is applied throughout inspiratory and expiratory phases of the respiratory cycle.	Requires intact respiratory drive and patient ability to maintain adequate tidal volumes.
Volume support (VS)	Spontaneous mode with clinician preset target tidal volume delivery achieved with the lowest inspiratory pressure.	Requires intact respiratory drive
Pressure-regulated volume control (PRVC)	Mandatory rate and target tidal volume are set, and the ventilator then delivers the breaths using the lowest achievable pressure.	Dual control of volume and pressure enables guarantee of volume and pressure
Airway pressure release ventilation (APRV)	Ventilator cycles between 2 preset pressure levels for defined time periods. I : E ratio is inverse often with a prolonged Inspiratory time (4 sec) and shortened expiratory time (0.8 sec). Patient can breathe spontaneously at both pressure levels	Reduced need for sedation.Activation of the diaphragm with patient triggering.Promotes alveolar recruitment. Considered a rescue mode in ALI/ARDS when used with extreme inverse ratio.
Biphasic positive airway pressure (BiPAP/ BILEVEL/Bivent)	As with APRV, the ventilator cycles between 2 preset pressure levels for defined time periods and the patient can breathe spontaneously at both pressure levels. The inspiratory time is generally shorter than, or the same length, as the expiratory time.	Reduced need for sedation.Activation of the diaphragm with patient triggering.Promotes alveolar recruitment.
Mandatory minute ventilation (MMV)	The patient’s spontaneous minute ventilation is monitored by the ventilator. When the minute ventilation falls below the clinician determined target, the ventilator increases the mandatory rate or size of tidal volumes to regain the desired minute ventilation.	Guarantees minute ventilation for patients with fluctuating respiratory drive and muscle innervation such as patients awakening from anaesthesia and those with Guillain–Barré.
Proportional assist ventilation (PAV)²⁶⁹	Delivers positive pressure throughout inspiration in proportion to patient generated effort, and dependent on the set levels of flow assist (offsets resistance) and volume assist (offsets elastance).²⁶⁸	Requires intact respiratory drive.Patients with high respiratory drive as the ventilator may overassist and continue to apply support when the patient has stopped inspiration.²⁶⁹
Proportional assist ventilation (PAV+™)	Clinician only sets a percentage of work for the ventilator. The ventilator assesses total work of breathing by randomly measuring compliance and resistance every 4–10 breaths.	Requires intact respiratory drive.Decreases work of breathing and improves patient ventilator synchrony.Potential for use as a weaning mode.
Adaptive support ventilation (ASV)	Automatic adaptation of respiratory rate and pressure levels based on a clinician-set desired percentage of minute ventilation.²⁷⁰	Automatically sets all ventilator settings except PEEP and FiO₂.Potential for use as a weaning mode.
Volume assured pressure support (VAPS)	The ventilator switches from pressure control to volume control, or pressure support to volume control during inspiration.	Enables maintenance of a preset minimum V_T and reduces work of breathing.

Controlled Mandatory Ventilation

Controlled mandatory ventilation (CMV) is a mandatory mode, and is the original and most basic mode of ventilation.¹⁵³ CMV delivers all breaths at a clinician-determined set frequency (rate) and the patient’s spontaneous effort is not acknowledged by the ventilator.⁶⁸ CMV may also be called volume-controlled ventilation (VCV) or pressure-controlled ventilation (PCV) depending on the target (volume or pressure) variable. VCV requires clinician selection of the frequency, PEEP, FiO₂, tidal volume, flow waveform, peak inspiratory flow and either the inspiratory time or I : E ratio. PCV requires clinician selection of rate, PEEP, FiO₂, inspiratory pressure, as opposed to tidal volume, and inspiratory time or I : E ratio depending on the ventilator type. Peak inspiratory flow and the flow waveform are manipulated by the ventilator, to achieve the clinician-selected inspiratory pressure within the set inspiratory time. The inability to breathe spontaneously during CMV contributes to diaphragm muscle dysfunction and atrophy which may result in difficulty weaning from the ventilator.¹⁵⁴

Synchronised Intermittent Mandatory Ventilation

Synchronised intermittent mandatory ventilation (SIMV) delivers breaths at a set frequency (rate), and can be either pressure- or volume-targeted. Setting of the ventilator is similar to setting VCV or PCV. The availability of patient triggering with SIMV facilitates provision of gas flow in recognition of a patient’s spontaneous effort. SIMV uses a timing window to deliver mandatory breaths in synchrony with patient inspiratory effort.¹¹⁶ Additional spontaneous breaths occurring outside of the timing window may be assisted with pressure support to augment the patient’s spontaneous effort to a pre-set pressure level.

Assist Control

In assist control (A/C,) the patient can trigger the ventilator, however, unlike SIMV, every patient-initiated breath is assisted to the same clinician-determined tidal volume (A/C [VC]) or inspiratory pressure (A/C [PC]). All breaths are cycled by the ventilator irrespective of being patient- or ventilator-triggered. In the absence of spontaneous breathing, A/C resembles CMV.

Pressure Support Ventilation

Pressure support ventilation (PSV) is a spontaneous mode of ventilation in which the patient initiates and cycles all breaths, with support of the patient’s inspiratory effort by the ventilator using rapid acceleration of flow to achieve a preset level of inspiratory pressure. Unlike CMV, SIMV or A/C, there is no setting of ventilator breaths in this mode. PSV is usually employed with positive end expiratory pressure (PEEP) which maintains partial inflation of alveoli during the expiratory phase to promote alveolar recruitment and oxygenation.

Continuous Positive Airway Pressure

Continuous positive airway pressure (CPAP) is one set baseline positive pressure applied throughout the inspiratory and expiratory phase. In this spontaneous breathing mode, unlike PSV, no additional positive pressure is provided to the patient during inspiration. Due to nomenclature used on some ventilator models, PSV is frequently misrepresented as CPAP.

Pressure-regulated Volume Control

Pressure-regulated volume control, available on the Servo 300 and Servo I (Maquet, Solna, Sweden), uses a ‘learning period’ to establish a patient’s compliance that guides regulation of pressure/volume. During the learning period, four test breaths of increasing pressure are delivered. The ventilator regulates inspiratory pressure based on the pressure/volume calculation of the previous breath and the clinician-determined target tidal volume. To maintain the target tidal volume during ongoing ventilation, the ventilator continues to adapt the inspiratory pressure in response to changing compliance and resistance.

Airway Pressure Release Ventilation and Biphasic Positive Airway Pressure

Airway pressure release ventilation (APRV) and biphasic positive airway pressure (BiPAP) are ventilator modes that allow unrestricted spontaneous breathing independent of ventilator cycling, using an active expiratory valve that allows patients to exhale even in the inspiratory phase.^147,^148,^155,¹⁵⁶ Both modes are pressure-limited and time-cycled. In the absence of spontaneous breathing, these modes resemble conventional pressure limited, time-cycled ventilation.¹⁵⁷ In North America the acronym BiPAP® is registered to Respironics non-invasive ventilators (Murrayville, PA). Therefore ventilator companies have developed brand names such as BiLevel (Puritan Bennett, Pleasanton, CA, GE Healthcare, Madison, WI) Bivent (Maquet, Solna, Sweden), DuoPaP (Hamilton Medical, Rhäzüns, Switzerland), PCV+ (Dräger Medical, Lübeck, Germany) or BiPhasic (Viasys, Conshocken, PA) to describe essentially equivalent modes. Ambiguity exists in the criteria that distinguish APRV and BiPAP. When applied with the same I : E ratio, no difference exists between the two modes. APRV as opposed to BiPAP, however, is more frequently described with an extreme inverse ratio and advocated as a method to improve oxygenation in refractory hypoxemia.¹⁵⁸

Automatic Tube Compensation

Automatic tube compensation (ATC) is active during spontaneous breaths and compensates for the work of breathing associated with artificial airway tube resistance via closed-loop control of continuously calculated tracheal pressure.^159,¹⁶⁰ During spontaneous inspiration, a pressure gradient exists between the proximal and distal ends of the artificial airway due to resistance created by the tube. A reduced pressure at the proximal end of the tube means a patient needs to produce a greater inspiratory force (greater negative pressure) to generate an adequate tidal volume.¹⁶¹ Higher flow rates generate larger pressure gradients and greater resistance. ATC requires the airway type and size to be entered into the ventilator program as well as the percentage of automatic tube compensation (ATC) to be applied. It appears to have most use in reducing the work of breathing for patients with high respiratory drive who require high inspiratory flow.¹⁶²

Neurally-adjusted Ventilatory Assist

Neurally-adjusted ventilatory assist (NAVA) is available on the Servo-I ventilator (Maquet, Solna, Sweden) and uses the electrical activity of the diaphragm to control patient–ventilator interaction.¹⁶³ Electrical activity of the diaphragm, measured using an oesophageal catheter, should result in optimal patient–ventilator synchrony as it represents the endpoint of neural output from the respiratory centres and thus is the earliest signal of patient inspiratory trigger and expiratory cycling. Pressure delivered to the airways (P_aw) is proportional to inspiratory diaphragmatic electrical activity using a clinician determined proportionality factor set on the ventilator.¹⁶⁴ NAVA provides breath-by-breath assist in synchrony with, and in proportion to, respiratory demand.¹⁶⁵ Although clinical data on NAVA is currently limited,^164,¹⁶⁶^–¹⁶⁸ this mode shows promise for improving patient–ventilator synchrony.

Ventilator Graphics

Analysis of ventilator graphics provide clinicians with the ability to assess patient–ventilator interaction, appropriateness of ventilator settings and lung function.

Scalars: Pressure/time, Flow/time, Volume/time

Many mechanical ventilators now offer integrated graphic displays as waveforms that plot one of three parameters, pressure, flow or volume, on the vertical (y) axis against time, measured in seconds, on the horizontal (x) axis referred to as scalars. Examination of scalars can assist with assessment of patient–ventilator synchrony, patient triggering, appropriateness of inspiratory/expiratory times, presence of gas trapping, appropriateness and adequacy of flow, lung compliance and airway resistance and circuit leaks.^169,¹⁷⁰

Pressure vs time scalar

The morphology of this waveform depends on the breath target (volume or pressure) and the breath type (mandatory or spontaneous).¹⁷¹ Pressure–time waveforms reflect airway pressure (P_aw) during inspiration and expiration and can be used to evaluate peak, plateau and end inspiratory pressures as well as inspiratory and expiratory times and appropriateness of flow (see Figure 15.5). Pressure–time scalars vary in appearance depending on the control variable (volume vs pressure). In volume-control breaths, the inspiratory waveform continues to rise until peak airway pressure is achieved at the end of inspiration. In pressure control breaths, the inspiratory waveform reaches its peak at the beginning of inspiration and remains at this elevation until cycling to expiration. Spontaneous triggering of ventilation can be identified by examination of the pressure–time scalar at the beginning of inspiration. A small negative deflection indicates patient effort. When pressure-triggering is used, a breath is triggered when the pressure drops below baseline. The depth of the deflection is proportional to patient effort required to trigger inspiration. A flow-triggered breath occurs when the flow rises above baseline, although this is frequently accompanied by a small negative deflection in the pressure-time scalar. Patient inspiratory attempts that fail to trigger the ventilator can also be identified as negative deflections in the pressure waveform without corresponding responses from the ventilator.¹⁷² Appropriateness of flow can be detected from the pressure–time scalar. If the flow is set too high or the rise time too short this can be seen as a sharp peak in the waveform. Conversely if flow is inadequate or the rise time too long, the incline of the inspiratory portion of the pressure waveform may be dampened.¹⁶⁹

FIGURE 15.5 Airway pressure vs time.

(Courtesy Drägerwerk AG & Co., KGaA.)

Flow vs time scalar

The flow–time scalar presents the inspiratory phase above the horizontal axis and the expiratory phase below (see Figure 15.6). The shape of the inspiratory flow waveform is influenced by the selection of flow pattern (constant, decelerating, sinusoidal) in volume-control breaths or the variable and decelerating flow waveform associated with pressure-control breaths. The inspiratory flow waveform of spontaneous breaths, those triggered and cycled by the patient, is influenced by the presence or absence of pressure support and the expiratory sensitivity.¹⁶⁹

FIGURE 15.6 Pressure, flow, volume vs time.

(Courtesy Drägerwerk AG & Co., KGaA.)

Evaluation of the expiratory limb of the flow-time scalar assists with detection of gas trapping as well as the patient’s response to bronchodilators. In the absence of gas trapping, the expiratory limb drops sharply below baseline then gradually returns to zero before the next breath. Failure to return to baseline indicates gas trapping whereby the gas inspired is not totally expired. Gas trapping results in development of intrinsic or ‘auto-PEEP’. This can adversely affect a patient’s haemodynamic status and cause patient–ventilator asynchrony.¹⁷³ Gas trapping may occur in patients with airflow limitation such as those with COPD and asthma. Consequences of gas trapping include dynamic hyperinflation, reduced respiratory compliance and respiratory muscle fatigue.¹⁷⁴ Evaluation of the expiratory flow waveform also enables evaluation of the effects of bronchodilator therapy as, if efficacious, improvements should be seen in the return to baseline of the expiratory flow waveform (see Figure 15.7).^173,¹⁷⁵ Patient–ventilator asynchrony can be detected in the flow waveform as abrupt decreases in expiratory flow in the expiratory limb and abrupt increases in flow in the inspiratory limb of the flow waveform.¹⁷²

FIGURE 15.7 Gas trapping.²⁷¹

Volume vs time scalar

The volume waveform originates from the functional residual capacity (baseline), rises as inspiratory flow is delivered to reach the maximum inspiratory tidal volume, then returns to baseline during expiration. The volume waveform is useful in troubleshooting circuit leaks (see Figure 15.8) as it will fail to return to baseline if a leak in the circuit–patient interface is present.

FIGURE 15.8 Tidal volume vs time, with and without leak.

Loops: Pressure/volume, Flow/volume

Most contemporary critical care ventilators allow for monitoring of pressure, flow and volume parameters integrated into graphic loops enabling measurement of airway resistance, chest wall and lung compliance.

Pressure–volume loops

The two parameters, P_aw and V_T are plotted against each other, with P_aw on the x axis. For mandatory breaths, the loop is drawn counter clockwise (see Figure 15.9). Spontaneous (triggered and cycled) breaths are drawn in a clockwise fashion. At the beginning of inspiration, the P_aw starts to rise with little change in V_T. As P_aw continues to rise, the V_T increases exponentially as alveoli are recruited, resulting in a marked increase in the slope of the inspiratory limb. This point represents alveolar recruitment and is referred to as the lower inflection point, and may be used to guide PEEP selection.^176,¹⁷⁷ The inspiratory limb continues until peak inspiratory pressure and maximal V_T are achieved. The bend in the inspiratory limb towards the end of inspiration is referred to as the upper inflection point, and denotes the point at which small volume increases produce large pressure increases indicating lung overdistension.¹⁷⁶ The expiratory limb represents lung derecruitment and is also useful in guiding PEEP selection.^178,¹⁷⁹

FIGURE 15.9 Pressure-volume loop.

(Courtesy Drägerwerk AG & Co., KGaA.)

For patient-triggered mandatory breaths, the initial part of the loop occurs to the left of the y axis and flows in a clockwise fashion, reflecting patient effort. The loop then shifts to the right of the y axis and moves in a counter- clockwise fashion as the ventilator assumes the work of breathing.⁶⁸ P–V loops reflect dynamic compliance between the lungs and the ventilator circuit. Decreased compliance requires greater pressure to achieve V_T and is reflected in a flattened P–V loop.¹⁸⁰ The area between the loops represents the resistance to inspiration and expiration, known as hysteresis. As resistance increases, less V_T is delivered resulting in a shorter and wider loop; conversely, as resistance decreases, a longer, wider loop is generated (see Figure 15.10).¹⁸¹

FIGURE 15.10 Pressure–volume loop representing resistance changes.¹²⁹

Flow–volume loops

Flow–volume loops recorded during positive pressure ventilation depict inspiration above the baseline and expiration below it. These loops are useful in determining response to bronchodilators and examining changes in airway resistance.

Management of Refractory HypoxAemia

Refractory hypoxaemia may require strategies in addition to conventional lung-protective mechanical ventilation.¹²¹ These include recruitment manoeuvres, high frequency oscillatory ventilation, extracorporeal membrane oxygenation and nitric oxide.

Recruitment Manoeuvres

Recruitment manoeuvres (RMs) refer to brief application of high levels of PEEP to raise the transpulmonary pressure to levels higher than achieved during tidal ventilation with the goals of opening collapsed alveoli, recruiting slow opening alveoli, preventing alveolar derecruitment, and reducing shearing stress.¹⁸²^–¹⁸⁴ The most common RM is elevation of PEEP to achieve a peak pressure of 40 cmH₂O for a sustained period of 40 sec, although studies report peak pressure elevations ranging from 25–50 cmH₂O for durations ranging from 20–40 sec.¹⁸⁵ The best method in terms of pressure, duration and frequency have yet to be determined.¹⁸⁶ Recruitment manoeuvres in humans have not produced consistent results in clinical studies,^184,¹⁸⁷ with a recent systematic review demonstrating no mortality benefit despite transient increases in oxygenation.¹⁸⁵ Effective recruitment may be difficult to assess with the potential for either overdistension of alveoli or failure to recruit.¹⁴⁰ Once the recruitment manoeuvre is terminated, derecruitment may occur rapidly. Serious adverse effects have been noted during the use of RMs due to increased intrathoracic and intrapulmonary pressures resulting in reductions in venous return and cardiac output, and cardiac arrest and increased risk of barotrauma.^184,¹⁸⁸

High Frequency Oscillatory Ventilation

High frequency oscillatory ventilation (HFOV) requires a specialised ventilator and manipulation of four variables: mean airway pressure (cmH₂O), frequency (Hz), inspiratory time, and amplitude (or power [ΔP]).¹⁸⁹ Alveolar overdistension is limited through the use of sub-deadspace tidal volumes whereas cyclic collapse of alveoli is prevented by maintenance of high end-expiratory lung pressures.^190,¹⁹¹ High frequency (between 3 and 15 Hz) oscillations at extremely fast rates (300–420 breaths/min) create pressure waves enabling CO₂ elimination.^133,¹⁹² Oxygenation is facilitated through application of a constant mean airway pressure via the bias flow (rate of fresh gas).^192,¹⁹³ In adults, recommendations for the initiation of HFOV state mean airway pressure should be set 5 cmH₂O above the peak airway pressure achieved with conventional ventilation.¹⁹⁴ The recommended frequency range is 3–10 Hz with 5 Hz conventionally used to initiate HFOV. Inspiratory time is set at 33% and the amplitude setting is determined by adequate CO₂ elimination.¹³³ Increased CO₂ elimination is achieved by lowering the frequency and increasing the amplitude.

Until recently, HFOV was considered a rescue mode for adult patients with acute respiratory distress syndrome (ARDS) experiencing refractory hypoxaemia and failing conventional ventilation.^195,¹⁹⁶ HFOV has been evaluated in patients in early-onset ARDS and has been found to improve oxygenation and to be well tolerated.¹⁹⁷ While further studies are required, these data suggest HFOV can be implemented in early ARDS.

Extracorporeal Membrane Oxygenation

Extracorporeal membrane oxygenation (ECMO) improves total body oxygenation using an external (extracorporeal) oxygenator, while allowing intrinsic recovery of lung pathophysiology. Indications for ECMO include acute severe cardiac or respiratory failure such as severe ARDS and refractory shock.¹⁹⁸ Bleeding as a complication of anticoagulation is a major risk of ECMO, with cerebral bleeds being the most catastrophic.¹⁹⁹ Another serious complication is limb ischaemia when the femoral artery is used.

ECMO consists of three key components:

1. a blood pump (either a simple roller or centrifugal force pump)

2. a membrane oxygenator (bubble, membrane or hollow fibre)

3. a countercurrent heat exchanger, where the blood is exposed to warmed water circulating within metal tubes.

In addition, essential safety features include bubble detectors that detect gas in the arterial line and shut the pump off; arterial line filters between the heat exchanger and arterial cannula, to trap air thrombi and emboli; pressure monitors placed before and after the oxygenator, that measure the pressure within the circuit and detect rising circuit pressures commonly caused by thrombus or circuit or cannulae occlusion; and continuous venous oxygen saturation and temperature monitoring. On commencement of ECMO the circuit is primed with fresh blood. The acid–base balance and blood gas of the primer is adjusted to ensure that the pH is within the normal range (7.35–7.45) and PaO₂ is adequate. ECMO can be delivered via veno-arterial access which requires cannulation of an artery. This method bypasses the pulmonary circulation while providing cardiac support to the systemic circulation and achieves a higher PaO₂ with lower perfusion rates. The alternative is veno-venous access, used for patients in respiratory failure with adequate cardiac function as there is no support of systemic circulation. Perfusion rates are higher, the mixed venous PO₂ is elevated and the PaO₂ is lower.¹⁹⁹

Nitric Oxide

Nitric oxide (NO) is an endothelial smooth muscle relaxant. Inhaled NO is effective in the dilation of pulmonary arteries resulting in reduced pulmonary shunting and reduced right ventricular afterload due to reduced pulmonary artery tone. Pulmonary shunting refers to failure of uptake of alveolar gas by the pulmonary vascular bed due to vascular constriction or interstitial oedema. Inhaled NO has a role in the management of pulmonary hypertension and was previously thought to have a role in management of refractory hypoxaemia for patients with ARDS. However, the most recent systematic review and meta-analysis of NO in ARDS comprising 14 RCTs and 1303 participants reported no effect on overall mortality despite a statistically significant improvement in oxygenation in the first 24 hours, and some risk of renal impairment among adults.²⁰⁰

Positioning

Regular repositioning of critically ill patients is essential for lung recruitment, prevention of atelectasis and maintenance of skin integrity (see Chapter 6).

Head of Bed Elevation

Supine positioning has been associated with aspiration of abnormally-colonised oropharyngeal and gastric contents ²⁰¹^–²⁰³ and increased incidence of VAP compared to a semirecumbent position, defined as backrest elevation at 45 degrees.²⁰⁴ Guidelines and care bundles for the prevention of VAP recommend semirecumbent positioning for all mechanically-ventilated patients.^71,^205,²⁰⁶ A more recent trial has however questioned the feasibility of 45 degree semirecumbent positioning as this backrest elevation was only achieved for 15% of study observations.²⁰⁷ There was also no differences in VAP incidence between the supine and semirecumbent group. Contraindications to backrest elevation include:

• suspected or existing spinal injury

• intracranial hypertension (for 45 degree elevation)

• unstable pelvic fractures

• prone positioning

• haemodynamic support devices (IABP, LVAD, ECMO)

• femoral catheterisation for continuous renal replacement therapy

• large abdominal wounds

• following femoral sheath removal.

As some degree of semirecumbent position is preferable to supine positioning, patients with suspected or existing spinal injury, pelvic fractures or being managed with prone positioning can have the head elevated by tilting the whole bed. Patients with femoral cannulation and large abdominal wounds can usually achieve 25–30 degree positioning.

Clinical practice audits conducted internationally and in Australia and New Zealand indicate that compliance with a 45 degree semirecumbent position rarely occurs, even when taking into consideration contraindications.²⁰⁸^–²¹² Similarly, interventions to improve compliance failed to demonstrate adherence to the 45 degree backrest position that can be sustained by the patient over time.^213,²¹⁴ Due to uncertainty over compliance with 45 degree semirecumbency in the original trial conducted by Drakulovic,²⁰⁴ and the lack of difference in VAP rates despite difficulty achieving compliance with semirecumbency in the van Niewenhoven study,²⁰⁷ new studies are required to confirm the equivalence or lack of inferiority of lower degrees of backrest elevation to the strict 45 degree semirecumbent position.

Practice tip

Backrest elevation is difficult to estimate accurately. Use an objective measurement device such as an inclinometer or protractor.

Lateral Positioning

Patients with unilateral lung disease experience a mismatch of ventilation to perfusion if the consolidated (pneumonic) or atelectic lung is placed in the dependent position.²¹⁵ Continuous lateral rotational therapy is a positioning therapy advocated for the prevention and management of respiratory complications associated with immobility.²¹⁶ The most recently reported multicentre randomised controlled trial found a significant reduction in VAP and shorter durations of ventilation and ICU stay.²¹⁷ Continuous lateral rotation therapy requires a special bed system enabling rotation of the upper part of the body to a maximum angle of 90 degrees.

Prone Positioning

Prone positioning has been shown to improve oxygenation and intrapulmonary shunt fraction when compared with rotational turning during the first 72 hours of ALI ²¹⁸ and in patients with multiorgan failure.²¹⁹ Prone positioning may also decrease the risk of VAP due to improved bronchial secretion drainage, limitation of colonisation of distal lung, decreased atelectasis and increased alveolar recruitment but may increase spread of pathogens in the lung and may increase the risk of aspiration.²²⁰^–²²³

Prone positioning results in changes to the distribution of ventilation and pulmonary blood flow. Pleural pressures are lower in non-dependent regions and higher in dependent regions due to gravitational forces, the weight of the overlying lung and mismatch between the local physical structures of the lung and chest wall.²²⁴ The weight of the overlying lung increases in ARDS due to parenchymal oedema and fluid within the alveoli.²²⁵ This gradient in pleural pressures means transpulmonary pressure is higher in non-dependent lung regions, compared to dependent regions.²²⁵ Perfusion also increases from previously nondependent to dependent lung regions resulting in optimal matching of ventilation and perfusion to promote gas exchange.

Pleural pressure in the dependent dorsal regions in the supine position can result in airway closure, atelectasis and hypoxaemia.²²⁴ The difference in pleural pressures from non-dependent and dependent lung regions is greater in the supine compared to the prone position. In the supine position, the heart and abdominal contents also compress lung bases and decrease FRC, whereas in prone positioning, the weight of these structures are lifted from the lung.

The benefits of prone positioning continue to be debated. Although oxygenation improves in 70–80% of patients turned from supine to prone,²²⁶ a mortality benefit has not been shown in all trials. The most recent systematic review and meta-analysis²²⁷ confirms a reduction in mortality in patients with severe baseline hypoxaemia (PaO₂/FiO₂ ratio <100 mmHg), but reported this benefit was not present in patients with less-severe hypoxaemia. Other benefits of prone positioning demonstrated were improved oxygenation and decreased rates of VAP. Adverse events related to prone positioning were increased risk of decubitus ulcer formation, endotracheal obstruction and accidental line or tube dislodgement.

Implementing prone positioning requires forward planning to ensure eye care and protection, mouth care, wound dressings, and tracheal suction are attended to before positioning the patient prone. Intravenous lines, electrocardiogram leads, urinary catheter drainage, chest drains and ostomy bags need to be secured and repositioned appropriately once the patient is positioned.²²⁸ Prone positioning can be achieved by manual handling of the patient, requiring up to five staff, although commercial devices are available that facilitate the turning and positioning of the patient.²²⁸

Weaning From the Ventilator

Weaning traditionally occurs via clinician-directed adjustments to the level of support provided by the ventilator, culminating in a spontaneous breathing trial comprising either low level pressure support or a T piece trial.

Current Recommendations

No ventilation strategy is more lung-protective than the timely and appropriate discontinuation of mechanical ventilation. Weaning refers to the transition from ventilatory support to spontaneous breathing.²²⁹ Evidence based consensus guidelines published for weaning in 2001¹¹⁶ and 2007²³⁰ emphasise the importance of preventing unnecessary delays in the weaning process, early recognition of a patient’s ability for spontaneous breathing and the use of a systematic method to identify the potential for extubation.

Weaning Predictors

Clinician judgement regarding prediction of weaning readiness is known to be imperfect, with unnecessary prolongation of ventilation ²³¹ or high rates of reintubation as resultant consequences, both of which are associated with adverse outcomes.^232,²³³ An evidence based review evaluating over 50 objective physiological measurements for determining readiness for weaning and extubation found most had only a modest relationship with weaning outcome; no single factor or combination of factors demonstrating superior accuracy.²³⁴ Of all predictors studied, the respiratory frequency to tidal volume ratio (f/V_T) appears to be most accurate.²³⁵ However inclusion of the f/V_T as part of a weaning protocol was found in one randomised study to increase, as opposed to decrease, the duration of weaning.²³⁶ At present, consensus guidelines²³⁰ do not recommend routine inclusion of weaning predictors.

Weaning Methods

Various studies have attempted to identify the best weaning method. Two of the most frequently-cited studies have produced conflicting results. Brochard and colleagues ²³⁷ compared PSV, T piece trial and SIMV, and concluded that PSV reduced the duration of mechanical ventilation compared with the other methods. Esteban and colleagues²³⁸ compared PSV, T piece trials, CPAP and progressive reduction of SIMV support, and found a once-daily T piece trial led to extubation three times more quickly than SIMV and nearly twice as quickly as PSV. Failure to produce consistent results favouring a single weaning style suggests it is not the mode that is important but rather the application of a systematic process.²³⁹

Spontaneous breathing trials

Spontaneous breathing trials (SBTs) incorporate a focused assessment of a patient’s capacity to breathe prior to extubation ²⁴⁰ and are recommended as the major diagnostic test to determine extubation readiness.²³⁰ SBTs can be conducted using either a T piece or low levels of pressure support²⁴¹ and should need to last only 30 minutes.²⁴² This method of weaning is uncommon in the ANZ setting, in contrast to international findings.^65,⁶⁶

Protocols

Implementation of various organisational strategies such as weaning teams and non-physician-led weaning protocols may assist in the timely recognition of weaning and extubation readiness.²⁴³^–²⁴⁷ Recently, coupling of a sedation and weaning protocol was found to result in a three-day reduction in the duration of ventilation compared to standard care in four North American hospitals.²⁴⁸ A recent systematic review and meta-analysis of 11 weaning protocol trials including 1971 patients demonstrated a reduction in the duration of mechanical ventilation.²⁴⁹ However, the authors cautioned that the effect of weaning protocols may vary according to the ICU organisational characteristics such as an intensivist-led ICU model, high levels of physician staffing, structured ward rounds, collaborative discussion and more frequent medical review; all characteristics reported for ICUs in Australia and New Zealand.^250,²⁵¹

Automated weaning

Automated computerised systems potentially enable more efficient weaning by providing improved adaptation of ventilatory support through continuous monitoring and real-time intervention.²⁵² One such system, SmartCare™/PS, monitors three respiratory parameters, frequency, V_T and end-tidal carbon dioxide (ETCO₂) concentration, every two or five minutes and periodically adapts pressure support (PS).^252,²⁵³ SmartCare/PS establishes a respiratory status diagnosis, based on evaluation of the three parameters, and may either decrease or increase PS, or leave it unchanged to maintain the patient in a defined ‘respiratory zone of comfort’.^254,²⁵⁵ Once SmartCare/PS has successfully minimised the level of PS, a one-hour observation period occurs. For patients who remain within the respiratory zone of comfort throughout the observation period, SmartCare/PS recommends to ‘consider separation’, indicating the patient’s respiratory status now suggests the patient will tolerate extubation.

SmartCare/PS substantially reduced the duration of ventilation and ICU length of stay when compared to physician-controlled weaning using local guidelines in five European ICUs.²⁵⁶ These effects were not confirmed when the SmartCare/PS system was compared to weaning managed by experienced critical care nurses in a single Australian setting.²⁵⁷

The difficult-to-wean patient

International reports indicate patients that require mechanical ventilation for ≥21 days account for less than 10% of all mechanically-ventilated patients, but occupy 40% of ICU bed days and accrue 50% of ICU costs.^258,²⁵⁹ A recommendation from the National Association for Medical Direction of Respiratory Care (NAMDRC) states that prolonged mechanical ventilation should be defined as ‘≥21 consecutive days of ventilation required for ≥6 hours per day’.²³⁰ Prolonged weaning has been defined as greater than 7 days of weaning after the first SBT or more than three SBTs.²³⁰ Little evidence defines the optimal method for managing the difficult-to-wean patient. One trial found no difference in weaning duration or success when comparing tracheostomy trials to low-level pressure support in patients with COPD experiencing weaning difficulty.²⁶⁰ These patients are most likely to benefit from an individualised and structured approach to weaning using progressive lengthening of tracheostomy trials with supportive ventilation in between in combination with early physical therapy.

Practice tip

Tachypnoea and decreased tidal volumes during weaning are clear indicators that a patient is not ready for extubation.

Complications of Mechanical Ventilation

Physiological complications associated with mechanical ventilation include ventilator-associated lung injury (VALI) and nosocomial infection (VAP).^116,¹²² VALI occurs through alveolar over-distension and cyclic opening and closing of alveoli resulting in diffuse alveolar damage, increased permeability, pulmonary oedema, cell contraction and cytokine production.^122,^130,^136,²⁶¹^–²⁶³ VAP substantially increases the duration of ICU stay and is associated with an attributable mortality of 5.8–8.5%.²⁶⁴^–²⁶⁶ Additional complications associated with mechanical ventilation are listed in Table 15.8. Complications can occur due to inappropriate application of mechanical ventilation. This may result in extra-alveolar gas causing pneumothoraces or subcutaneous emphysema due to high peak inspiratory pressures, and alveolar stretch and oedema formation as the result of large tidal volumes.⁶⁸

TABLE 15.8 Complications of mechanical ventilation

Item	Complication
Barotrauma	• pneumothorax • pneumomediastinum • pneumopericardium • pulmonary interstitial emphysema • subcutaneous emphysema

Volutrauma Shearing stress, endothelial and epithelial cell injury, fluid retention and pulmonary oedema, perivascular and alveolar haemorrhage, alveolar rupture Biotrauma Activation of systemic and local inflammatory mechanisms Ventilation/perfusion mismatch Alveolar distension causes compression of the adjacent pulmonary capillaries resulting in dead space ventilation ↓ cardiac ouput Resulting in hypotension, ↓ cerebral perfusion pressure (CPP), ↓ renal and hepatic blood flow ↑ right ventricular afterload Due to ↑ intrathoracic pressureMay result in ↓ left ventricular compliance and preload ↓ urine output Due to ↓ glomerular filtration rate, ↑ sodium reabsorption and activation of the renin-angiotensin-aldosterone system Fluid retention Due to above renal factors as well as ↑ antidiuretic hormone and ↓ atrial natriuretic peptide Impaired hepatic function Due to ↑ pressure in the portal vein, ↓ portal venous blood flow, ↓ hepatic vein blood flow ↑ intracranial pressure Due to ↓ cerebral venous outflow Oxygen toxicity Alterations to lung parenchyma similar to those found in ARDS Pulmonary emboli and deep vein thrombosis Due to immobility Ileus, diarrhoea Due to alterations in gastric motility Gastrointestinal haemorrhage Gastritis and ulceration may occur due to stress, anxiety and critical illness ICU-acquired weakness Neuropathies and myopathies develop in association with critical illness, corticosteroids and neuromuscular blockade Psychological issues Delirium, anxiety, depression, agitation and post-traumatic stress disorder may be experienced by critically ill ventilated patients in the acute and recovery phases