24 Mechanical ventilation

Mechanical ventilation is used to assist or replace spontaneous respiration. Gas flow can be generated by negative pressure techniques, but it is positive pressure ventilation that is the most efficacious in intensive care. There are numerous pulmonary and extrapulmonary indications for mechanical ventilation, and it is the underlying pathology that will determine the duration of ventilation required. Ventilation modes can broadly be classified as volume- or pressure-controlled, but modern ventilators combine the characteristics of both in order to complement the diverse requirements of individual patients. To avoid confusion, it is important to appreciate that there is no international consensus on the classification of ventilation modes. Ventilator manufacturers can use terms that are similar to those used by others that describe very different modes or have completely different names for similar modes. It is well established that ventilation in itself can cause or exacerbate lung injury, so the evidence-based lung-protective strategies should be adhered to. The term acute lung injury has been abolished, whilst a new definition and classification for the acute respiratory distress syndrome has been defined.

Mechanical ventilation is a machine-driven method of assisting or replacing spontaneous breathing. In order for gas to flow into the lungs, a pressure difference between the atmosphere and the alveoli is required. In spontaneous respiration, the respiratory muscles expand the chest wall, generating negative intrapleural pressure that draws air in. Mechanical ventilation is classified into negative pressure ventilation (NPV) and positive pressure ventilation (PPV).

In PPV, gas flow is achieved by applying positive pressure at the upper airway, either externally through a face mask (as described in Chapter 25) on NIV or internally through a tracheal tube. NPV requires the use of a rigid external chest wall device, such as the cuirass, a modern version of the iron lung, which generates negative pressure inside the shell that helps to expand the chest wall. NPV is rarely used in intensive care because of its many practical limitations; thus, the ventilation modes described in this chapter refer to PPV only.

Mechanical ventilation is indicated for any cause of hypoxaemic and/or hypercapnic respiratory failure (type I and/or type II, respectively), where the airway is compromised, in non-respiratory disorders where oxygen delivery (see Box 24.1) is impaired and shock ensues, and post-operatively for ‘warming, weaning, and waking’, e.g. following cardiac surgery (see Table 24.1).

This section provides a brief overview of the respiratory physiology relevant to mechanical ventilation, to define and place in context terms that are used subsequently in this chapter. (See also Chapter 15.)

The respiratory system is composed of the upper and lower respiratory tracts. The nose, mouth, pharynx, and larynx form the upper respiratory tract which accounts for two-thirds of the resistance to airflow. The lower respiratory tract is subdivided, according to Weibel’s classification [1], into 23 generations.

Each lung is partitioned by connective tissue into ten bronchopulmonary segments, each with its own artery, vein, and bronchus. The pulmonary arteries feed the respiratory units, but the bronchi receive their blood supply directly from the aorta. A rich network of lymphatics drains fluid from the interstitium into the thoracic duct. Nerve supply comes from the sympathetic and vagal plexuses.

Alveoli are the fundamental units of gas exchange. An adult has 300 million alveoli, giving a total surface area in excess of 50 m². Pulmonary capillaries line the alveoli in densely packed sheets to match this large area of ventilated lung. Gas exchange occurs between the alveolar–capillary membrane which is 0.3 microns thick in healthy lung tissue. The rate of oxygen diffusion depends on the oxygen partial pressure gradient between the alveolus and pulmonary capillary (PA-PaO₂) gradient and the thickness of the endothelium between them.

The PA-PaO₂ gradient is largely determined by the FiO₂, however, alveolar PaCO₂ will also affect PaO₂. The sum of the partial pressures of all the alveolar gases cannot exceed the atmospheric pressure; therefore, the higher the PaCO₂, the lower the PaO₂ will be. Oxygen diffusion will be impeded by any accumulation of fluid between the alveolar–capillary membrane (pulmonary oedema) and other material such as collagen (pulmonary fibrosis).

Oxygenation is also affected by the contact time between the RBCs and alveoli, which is inversely related to the cardiac output. Cooperative bonding of oxygen by Hb allows the alveolar and RBC oxygen tensions to equilibrate by the time the RBCs have traversed one-third of the capillary. This only takes a quarter of a second, so a very high cardiac output can contribute to desaturation if the contact time is less than this.

CO₂ diffuses rapidly from pulmonary capillaries into the alveoli, down its concentration gradient; therefore, elimination relies on alveolar ventilation. The tidal volume needs to match the CO₂ production which is 200 mL/min in an average70 kg man and accounts for the physiological and equipment dead space. Increasing minute ventilation enhances CO₂ clearance as long as the tidal volume exceeds the total dead space in conventional mechanical ventilation (as described in Ventilation modes section).

Ventilation (V) needs to match perfusion (Q) in order to optimize gas exchange (V/Q = 1). Dead space (V/Q >1) describes areas that are ventilated but not perfused, whereas a shunt (V/Q <1) refers to areas of the lung that are perfused but not ventilated or the dilution of arterial blood with venous blood. V/Q mismatch represents a spectrum, with dead space at one end and shunt at the other. Anatomical dead space is the part of the respiratory tract that does not take part in gas exchange, from the mouth and nose down to the 16th generation of bronchioles. This is normally 2–3 mL/kg and is generally taken to be approximately 150 mL. Anatomical shunt is the dilution of arterial blood by deoxygenated blood from the bronchial veins that drain into the LA and the endocardium of the LV that drains into the left heart chambers via the Thebesian veins. This right-to-left shunt only causes a slight drop in PaO₂. In pathological shunting, increasing the FiO₂ does not fully reverse the hypoxia; the supplementary oxygen increases dissolved oxygen which has a minor role in oxygen delivery. Hb passing through the ventilated areas becomes fully saturated early and cannot compensate for the deoxygenated Hb with which it subsequently mixes. Hypoxic pulmonary vasoconstriction (HPV) diverts blood away from underventilated areas, thereby providing physiological compensation to minimize the effects of V/Q mismatching.

Even in normal, healthy lungs, alveolar V/Q varies from the apex to base. This arises as a result of a natural gradient in intrapleural pressure, which gradually increases vertically, regardless of the patient’s position. The lung is divided into three functional zones (West zones) [2] to illustrate this process (see Figure 24.1). A lower intrapleural pressure at the apex allows the alveoli to distend; therefore, the alveolar pressure is highest and perfusion is reduced. The alveolar dead space (DA) is normally negligible, but, if alveolar pressure is increased significantly with PPV or PEEP or the capillary artery pressure is reduced due to hypovolaemia or shock, the DA will increase.

At the lung bases, the pulmonary capillary pressure is higher and the alveoli have smaller volumes. The physiological dead space is the sum of the anatomical and alveolar dead space. Pathological causes of increased dead space and shunt are listed in Table 24.2.

The thoracic cage, formed of ribs and intercostal muscles, along with the diaphragm, represents the chest wall. The thoracic cage has a tendency to spring outwards, whereas the lungs, being elastic, tend to collapse; these opposing forces generate a negative intrapleural pressure. Inspiration occurs mainly through diaphragmatic contraction and augments the negative intrapleural pressure. This decrease in TPP (alveolar minus pleural) draws air in. The volume of gas that remains in the lungs at the end of normal expiration and holds the lung open is the functional residual capacity (FRC) and represents a point of equilibrium between the opposing recoil of the lungs and thoracic cage. Lung volumes vary with age, gender, and height; in an adult, the tidal volume is approximately 7 mL/kg (500 mL) and the FRC is 2500 mL.

The ease with which the lungs inflate in response to a change in TPP is the lung compliance. The more distended alveoli at the lung apex and the more collapsed alveoli at the base have a lower compliance, compared to those in the mid zones. Surfactant has a crucial role in maximizing lung compliance by reducing the surface tension within the alveoli. Pressure in the alveoli is related to tension and radius: PA = 2 T/r. In the absence of surfactant, alveoli with the smallest radii would have the greatest pressure and therefore would tend to collapse and empty into larger alveoli.

Total respiratory compliance combines lung and chest wall compliance; any alveolar or interstitial infiltrate, such as pulmonary oedema or fibrosis, will decrease lung compliance, whereas chest wall compliance is increased by conditions such as oedema and obesity. At FRC, the respiratory compliance is optimal; the lung sits on the steepest part of the P/V curve; subsequently, a small change in pressure results in the largest change in volume (see Figure 24.2).

Note that, during spontaneous respiration, the basal alveoli sit on a more favourable part of the P/V curve and therefore are more compliant than the apical alveoli. Greater expansion of these alveoli gives preferential ventilation to the lung bases, matching the greater basal blood flow. In situations where the FRC is reduced (supine position, mechanical ventilation), the lungs shift down the P/V curve and compliance, and the distribution of ventilation changes and will be greater at the apices, thereby increasing the V/Q mismatch and contributing to the basal collapse seen commonly in ventilated patients.

Gas flow into the lungs is proportional to pressure change but inversely related to airways resistance. In the larger airways (generations 1–5), the flow is predominantly turbulent and accounts for higher resistance, whereas resistance in the more distal airways is lower due to laminar flow. High-velocity flow increases turbulence, and therefore airways resistance. During deep inspiration, flow rates as high as 60 L/min can be reached. The energy required to overcome airways resistance and elastance (reciprocal of compliance) amounts to the work of breathing.

Ventilation modes are classified according to: (1) the type of breath delivered in terms of cycling (phase variables), and (2) how the gas flow is driven (control variables).

The terminology used to describe ventilator breaths revolves around the two phases of the natural respiratory cycle: inspiration and expiration. Like normal respiration, ventilators provide active inspiration and passive expiration. The inspiratory time (TI) and expiratory time (TE) represent the duration of inspiration and expiration, respectively, while the transition from one phase to another is known as cycling. Inspiratory cycling marks the beginning of inspiration, and expiratory cycling marks the beginning of expiration. These four variables are referred to as the phase variables, as they can be manipulated to suit the patient’s respiratory mechanics and gas exchange requirements.

The inspiratory phase itself can have two components: an active or flow phase, followed by a pause. Inspiration is said to have ended at the end of the flow phase, whereas the inspiratory phase ends after the pause.

The cycle time is the sum of TI and TE, expressed in seconds, and the RR or frequency is the number of cycles per minute. The usual ratio of TI to TE is 1:2. These variables are interconnected so that setting any two parameters determines the third.

An intubated patient who is breathing spontaneously controls every aspect of the breathing cycle; CPAP is usually delivered to keep the alveoli open, but the breath is not supported.

If the ventilator determines both inspiratory and expiratory cycling, so that the patient has no control over ventilation, the mode is described as mandatory. This is the mode used intraoperatively, as patients are often paralysed or their respiratory drive is abolished by deep anaesthesia. Terms that describe this mode are intermittent positive pressure ventilation (IPPV), continuous mandatory ventilation (CMV), or, if the patient is allowed to take other breaths in between, intermittent mandatory ventilation (IMV).

When a patient takes breaths during ventilation on a mandatory mode, the ventilator may allow the patient to draw in gas, in which case these breaths are accommodated. If not, the circuit pressure falls, and the ventilator alarm sounds.

Unlike in theatre, on ICUs, the sedation dose used is the lowest that will keep the patient comfortable. It is preferable to allow the patient to make some respiratory effort to minimize respiratory muscle weakness and facilitate weaning off the ventilator. If the patient’s respiratory effort determines the inspiratory cycling, then the breath is said to be triggered, and the ventilator is on a demand, assist, or support mode.

A hybrid mode is a combination of mandatory and triggered ventilation. Synchronized intermittent mandatory ventilation (SIMV) is a hybrid mode where mandatory breaths are set at a certain frequency. If the patient makes an inspiratory effort, this triggers the ventilator to give a breath, instead of the mandatory breath (this breath will have the same control characteristics as the mandatory breath in terms of pressure or volume). This will not happen every time an inspiratory effort is made, but only when that inspiratory effort falls within a ‘trigger window’ (see Figure 24.4) in the time interval before the mandatory breath was due. Inspiratory effort outside this trigger window may be accommodated or supported with different control variables than the mandatory breath.

When inspiratory cycling depends completely on triggering, an apnoea interval is employed so that, if the patient stops breathing for a set period of time, the ventilator alarm sounds and it changes to a mandatory mode.

Phase variable are summarized in Table 24.3.

The control variables that determine how gas flow is delivered by the ventilator are pressure and volume, and those that determine inspiratory and expiratory cycling are flow and time.

In volume-controlled ventilation (VCV), a target tidal volume is set on the ventilator. Flow is constant for a fixed time period. Inspiration and expiration are determined by the time allocated for each respiratory cycle (frequency) and the TI:TE ratio. Ventilation is said to be time-cycled. The ventilator will deliver the tidal volume to the patient, and the pressure generated will be determined by the patient’s compliance (see Figure 24.5). Larger tidal volumes or a shorter TI produce higher peak pressures. The consistency of minute volume with VCV results in more predictable CO₂ elimination. Theoretical disadvantages of VCV include a risk of barotrauma (see Ventilator-associated lung injury section) and increased incidence of patient–ventilator asynchrony.

With pressure-controlled ventilation (PCV), the inflating pressure is set on the ventilator, and the breath is delivered using a decelerating flow pattern. Initially, both airway pressure and flow rise briskly to a peak; the pressure is maintained at this level for the remainder of inspiration, whereas flow decreases exponentially (see Figure 24.6). The tidal volume delivered depends on the patient’s compliance and airway resistance. Cycling is flow-dependent, and expiration occurs when flow drops below a predetermined level which is usually 25% of the peak flow. Patient comfort is improved, because an increase in the inspiratory effort is matched with an increase in the gas flow; however, changes in compliance will increase or decrease the tidal volume proportionately and risk volutrauma (see Ventilator-associated lung injury section).

While each mode of ventilation has theoretical advantages and disadvantages, clinical trials have failed to show any difference in complication rates, length of ICCU stay, or mortality. The above descriptions of VCV and PCV are simplified schemes to illustrate the basic principles behind the control variables. Modern ventilators have sophisticated sensors and controls that allow multiple ventilation parameters to be adjusted in order to fine-tune the breath characteristics. The beneficial features of VCV and PCV can be combined.

In dual modes, the variable that drives the gas flow is labelled as ‘control’ while the limiting variable is labelled ‘limit’ or ‘target’ or ‘regulated’, e.g. pressure-regulated volume control (PRVC). In this mode, the desired volume and a pressure limit are set.

The full tidal volume will only be delivered so long as the pressure remains below the pressure limit. If the pressure limit is reached, then the ventilator cycles to expiration and sounds an alarm. An additional feature of modern ventilators is the automatic (auto) mode which can sense the patient’s respiratory effort and switch between mandatory and triggered modes accordingly. The ventilator responds to a gradual change in the patient’s compliance by increasing or decreasing the pressure support given in small increments. Theoretically, these multifaceted ventilation modes, such as the adaptive support ventilation (ASV) or the proportional assist ventilation (PAV), will encourage weaning as the patient improves and shorten the duration of mechanical ventilation.

A recent Cochrane review [3] compared the effects of weaning patients using an automated weaning protocol with clinician-led weaning protocols. In the automated weaning mode, the ventilator is able to measure selected respiratory variables, adapt output to individual patient needs using predetermined algorithms, and automatically conduct spontaneous breathing trials when predetermined thresholds are met. The study combined data from ten trials involving 654 patients and found automated weaning protocols significantly decreased weaning time to successful extubation and reduced ICU stay. The review suggested that these results were achieved without any increase in adverse effects (e.g. reintubation) but suggested that further studies are needed to confirm this.

There are several dual ventilation modes which can be pressure-controlled and volume-targeted or, as described earlier, volume-controlled and pressure-limited. They can be mandatory or triggered, or hybrids of these phase variables. Confusion occurs because of the numerous combinations of control and phase variables. There is no universally agreed classification or terminology for ventilation modes; manufacturers have different names for similar ventilation modes or may use the same name to describe very different modes.

Asynchrony, also known as ‘fighting the ventilator’, arises out of mismatching of the patient’s intrinsic respiratory rhythm and the ventilator settings. The patient’s inspiratory drive, timing, and respiratory mechanics influence the interaction with the ventilator (see Table 24.4). If the ventilator does not accommodate or trigger when a patient tries to inspire, considerable discomfort will be felt. Equally, if the patient’s peak inspiratory flow rate is not matched by the ventilator’s, flow restriction will occur. This problem tends to occur with VCV with a constant flow rate. The patient will respond by making a greater inspiratory effort, which generates a large negative pressure in the airway. In PCV, the pressure rise time, support level, and flow threshold for expiratory cycling affect patient–ventilator asynchrony. Patients with high airway resistance require a higher flow threshold for expiratory cycling than the preset 25%, and those with poor compliance may need a lower threshold.

A number of techniques attempting to reduce ventilator asynchrony have been trialled, notably pressure-assisted ventilation (PAV) (see above) and neurally adjusted ventilator assists (NAVAs). These techniques provide an assistive pressure that is proportional to the patient’s own respiratory effort, based on either elastic and resistive components of the respiratory system (PAV) or the electrical activity of the diaphragm measured using a probe (NAVA). Although numerous small-scale clinical trials have been performed that suggest fewer asynchrony events with PAV [4] and NAVA [5], there are no large-scale randomized controlled trials that show any benefit in outcome-relevant endpoints, and so the exact role of these techniques is yet to be fully determined.

It is by understanding the patient’s mechanics that complementary ventilator modes and settings can be established. In difficult cases, the patient’s respiratory drive can be abolished by deepening of sedation or muscle paralysis as a temporary solution.

Mechanical ventilation itself is associated with lung damage—ventilator-associated lung injury (VALI).

Four mechanisms underlie VALI: volutrauma, atelectrauma, barotraumas, and biotrauma.

Overdistension of alveoli leads to direct damage to the alveolar–capillary membrane as a result of excessive wall stress (ratio of alveolar wall tension to thickness). This leads to a rapid increase in permeability, with leakage of protein-rich fluid into the alveoli and interstitium. The action of surfactant is severely impaired, leading to alveolar collapse and a reduction in lung compliance. The increase in extravascular lung water occurs more readily in animal models with established lung injury. Animal studies have also clearly demonstrated that this form of pulmonary oedema is directly related to the high volumes and not the increase in pressure that is usually associated with the delivery of a high tidal volume.

It is the repeated cyclical opening and closing of small airways and alveoli that occur with ventilation at low lung volumes. Ventilation associated with supine positioning and a reduced FRC, particularly in the absence of PEEP, results in an atelectatic (collapsed) lung where the air–liquid interface is more proximal at the terminal conducting bronchioles instead of in the alveoli. The high shearing forces required to open these airways are associated with surfactant depletion and physical disruption of the alveolar epithelium.

The use of excessive pressures leads to epithelial damage and air leakage, causing pneumothoraces, subcutaneous emphysema, or, less commonly pneumomediastinum or pneumopericardium. Studies suggest that high TPPs are more relevant than airway pressure per se; however, it is not easy to measure TPPs clinically, so plateau and mean pressures are used as surrogate markers.

The release of pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF-α) and interleukin 1 (IL-1) and interleukin 6 (IL-6), contributes to lung injury, and they enter the systemic circulation to cause systemic inflammation and MODS.

Lung-protective ventilation is a trio of low tidal volumes, low plateau pressures, and the application of PEEP.

PEEP is synonymous with CPAP but applies to the continuous airway pressure applied during ventilation with a mandatory or assisted mode. It maintains the small airways and alveoli open and helps to return the FRC towards the normal physiological range. Preventing derecruitment reduces atelectrauma and allows adequate oxygenation to be achieved using lower tidal volumes. PEEP therefore reduces shearing stress and cytokine release and curtails surfactant depletion.

Chest CT imaging of patients with ARDS showed a more homogenous distribution of tidal volume at PEEP of 20 cmH₂O than at lower levels of 0, 5, 10, and 15. There is no easy method of establishing optimal PEEP for each individual patient. Some studies suggest that the patient’s P/V curve should be used to determine the lower inflection point (see Figure 24.7) and set PEEP slightly above that level, but this is time-consuming and is subject to considerable observer variability. In reality, the level of PEEP used is based on clinical judgement, depending on the patient’s body habitus, and underlying pathology, with the aim to minimize the FiO₂, and is usually no more than 10 cmH₂O, except in patients with ARDS. Clinical trials have failed to show a mortality benefit between low or high PEEP [6], although there may be a reduction in ventilator days which was greatest in those with more severe lung oedema.

It has been clearly established that ventilation with traditional tidal volumes of 10–15 mL/kg is harmful, particularly in patients with pre-existing lung injury. These high tidal volumes often lead to high peak and plateau pressures and significantly increase the risk of both volutrauma and barotrauma. A number of early small studies using lower tidal volumes did not consistently demonstrate any benefit. However, a landmark study by the ARDS network compared a traditional ventilation strategy with tidal volumes of 12 mL/kg and plateau pressures of up to 50 cmH₂O, with a protective strategy using tidal volumes of 6 mL/kg and plateau pressures <30 cmH₂O. PEEP was set according to the FiO₂ and ranged from 4 to 15 cmH₂O. The PEEP and FiO₂ required to maintain oxygenation in the lower tidal volume group was significantly higher. This large multicentre trial was stopped early, because interim analysis showed a significantly lower mortality in the protective strategy group. The number of ventilator-free days and non-pulmonary organ failure was also lower in this group.

Most of the initial studies of protective ventilation strategies involved patients with established lung injury; however, large tidal volumes have also been associated with ALI within 5 days of mechanical ventilation in other patient groups without ALI. A recent trial in adults at intermediate to high risk of pulmonary complications after major abdominal surgery compared a lung-protective strategy with tidal volumes of 6–8 mL/kg, PEEP 6–8 cmH₂O, and recruitment manoeuvres repeated every 30 min versus tidal volumes of 10–12 mL/kg and neither PEEP nor recruitment. The result was a statistically significant reduction in pulmonary and extrapulmonary complications, reduced need for NIV, and shorter hospital length of stay. A meta-analysis of 20 articles with nearly 3000 participants without ARDS also concluded that ventilation with low tidal volumes was associated with better clinical outcomes [7, 8].

It is accepted that lung-protective strategies improve mortality and hospital length of stay in patients with ARDS and ALI. A Cochrane review of six trials supports this; however, the mortality benefit was lost if plateau pressures were <31 cmH₂O in the control group [9, 10].

The use of low tidal volumes often leads to hypercapnia and acidosis. Current consensus suggests allowing the pH to drop to 7.2, which should be treated with sodium bicarbonate if it drops further. However, it is unclear whether the correction of acidaemia is helpful or harmful. Mechanically ventilated patient with ARDS tend to tolerate very high CO₂ and low blood pH without any adverse sequelae; however, a population of cardiac patients may behave very differently.

CO₂ causes PH, vasodilation, reduction in SVR, and tachycardia, resulting in an increase in cardiac output. These effects are transient and do not cause myocardial depression in patients without cardiac disease. Hypercapnia increases both end-diastolic and end-systolic volume and can impair LV contractility, particularly in conjunction with acidaemia. The vasodilation which normally increases coronary blood flow can decrease the perfusion of ischaemic areas. Profound hypercapnia is therefore not recommended in the ischaemic or failing heart, arrhythmias, and active CAD. Non-cardiac contraindications for hypercapnia include cerebral oedema, such as that following cardiac arrest, seizures, mass lesions, or GI bleeds.

Hyperoxia increases the production of oxygen-derived free radicals and causes neutrophil recruitment and the release of inflammatory mediators. Surfactant production is impaired, and pulmonary interstitial oedema occurs, followed by fibrosis. An increase in intrapulmonary shunting occurs as a result of the collapse of unstable alveolar units. High FiO₂ should therefore be avoided, if possible, to minimize this risk of dose-related cellular toxicity and reabsorption atelectasis. There is no evidence-based threshold for FiO₂; recommendations are to take aggressive measures to reduce FiO₂ below 0.65, but limiting airway pressure takes precedence. Lower SaO₂ and PaO₂ should be accepted, unless contraindicated.

Recruitment refers to the reinflation of atelectatic lung to decrease intrapulmonary shunting and improve oxygenation. The principle is to apply sustained high airway, and therefore TPP, to open up the collapsed airways and alveoli. CPAP at 10 cmH₂O above plateau pressure is applied for 30–60 s. An alternative protocol is to increase CPAP in a stepwise fashion, in increments of 5 cmH₂O for 40 s up to 20 cmH₂O above plateau pressure. Recruitment manoeuvres can be employed by hand, using a separate circuit (usually Mapleson C circuit) or through the ventilator if it has an inspiratory hold function. Caution is required, because a high CPAP reduces venous return, and cardiac output, and blood pressure inevitably drop and can precipitate a period of cardiovascular instability in susceptible patients.

Increasing TI, in relation to TE, so that the I:E ratio is >1 can provide more uniform inflation of alveoli with varying time constants. This can be achieved by increasing the TI during PCV or by adding an inspiratory pause during VCV (modern ventilators simply allow the I:E to be altered and will adjust the mode settings accordingly). Prolonging TI can maintain the tidal volume and mean airway pressure at lower peak alveolar pressure and reduces dead space. Reduced TE can lead to air trapping, barotrauma, cardiovascular instability, and hypercapnia.

Lung perfusion that favours dependent areas in the supine position becomes more uniformly distributed in the prone position. The normal ventral to dorsal TPP gradient is reversed, resulting in more homogenous ventilation. Patients with any form of ALI exhibit an exaggerated TPP gradient and are more susceptible to atelectasis. Proning significantly improves V/Q matching and improves oxygenation in the majority of patients. The process of turning a patient to the prone position requires much staff input and risks cardiovascular instability as well as the dislodgement of tracheal tubes, lines, and chest drains. The main complications are pressure sores and facial and periorbital oedema. Prone ventilation is usually reserved for those with the most severe impairment in oxygenation. Previous studies failed to show a significant mortality benefit, until the recent PROSEVA study which showed a significant reduction in 28-day mortality in patients with severe ARDS who were prone for at least 16 hours duration. The incidence of complications were similar in the groups, except for the incidence of cardiac arrest which was higher in the supine group [11].

Several contraindications exist, including patients with unstable cardiac rhythms requiring defibrillation or CPR and those with abdominal or thoracic wounds at risk of dehiscence.

This alternative to conventional ventilation uses sustained lung inflation set as mean airway pressure and extremely high respiratory frequencies of 4–5 Hz (300 breaths/min). An oscillating diaphragm produces a sinusoidal airflow pattern whereby both inspiration and expiration are active. The amplitude required for airflow is proportional to the patient’s compliance. Tidal volumes generated are very small, typically less than the anatomical dead space; therefore, gas transport does not occur by the usual physiological process. A combination of seven potential mechanisms accounts for alveolar ventilation, including augmented diffusion, turbulence, and coaxial flow patterns. Minute volume is maintained, and hypercapnia does not necessarily occur.

High-frequency oscillatory ventilation (HFOV) improves V/Q mismatch and increases mean airway pressure, thereby improving oxygenation. The lungs are held open, and tidal volumes are minimized; however, breath stacking can occur, causing barotrauma. In theory, this is the ultimate in protective ventilation, but this is not supported by clinical trials. A recent meta-analysis in patients with moderate to severe ARDS failed to demonstrate any benefit for HFVO over conventional ventilation [12]. The OSCAR study with nearly 800 patients did not show any difference in terms of mortality, length of stay, or any other measured variables such as pressor use. However, OSCILLATE showed a higher mortality as well as higher usage of midazolam and neuromuscular blockers in the HFOV group [13, 14].

Airway pressure release ventilation (APRV) or BiVent (depending on the manufacturer) is an applied continuous positive pressure mode of ventilation with interval release of positive pressure, causing lung ventilation. Originally described in 1987 [15], APRV allows spontaneous respiration, while maintaining high (or expanded) lung volumes, allowing high alveolar recruitment to maintain oxygenation. It has been suggested that this mode of ventilation may be of benefit for patients with acute lung injury, ARDS, and atelectasis after major surgery [16–19]. The advantages of APRV/BiVent are lower mean airway pressures to maintain ventilation, lower minute ventilation, reduced dead space ventilation, and a reduction in adverse effects to the cardio-vascular system [20]. Furthermore, by allowing the patient to breathe spontaneously, it reduces the sedation requirement and eliminates the use of muscle relaxants. To date, however, no major studies have demonstrated a reduction in mortality or outcomes.

When a patient desaturates, particularly if this occurs rapidly or unexpectedly, there is a sequence of events that should ensue to exclude some common causes. These should only take a few minutes and are not a substitute for a full respiratory examination and appropriate investigations:

How to initiate lung-protective ventilation in ARDS, based on the ARMA trial protocol, is as follows:

Mechanical ventilation is an important component of the management of many post-operative and critically ill patients. Positive pressure techniques are used in most cases, but there is a role for NPV, e.g. on the paediatric cardiac ICU following complex surgery for congenital heart disease. A basic comprehension of respiratory physiology and mechanics is essential in order to understand mechanical ventilation. There are numerous ventilation modes, and terminology is inconsistent; nevertheless, these can be simplified by classification into their basic elements of phase and control variables. Ventilation itself can induce or exacerbate pre-existing lung injury and lead to multiple organ dysfunction; recommendations for lung-protective ventilation therefore aim to minimize this effect. In view of this and improvements in technology, in recent years, there has been a resurgence of interest in extracorporeal support in adults for both oxygenation and CO₂ removal.