Mechanical ventilation

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Chapter 27 Mechanical ventilation

Mechanical ventilation for acute respiratory failure (ARF) is now a routine aspect of patient management in the intensive care unit (ICU). The 1952 Copenhagen polio epidemic introduced the notion of organised areas (ICU) for the provision of positive-pressure ventilation,1 which was usually applied through a tracheostomy that had been inserted to allow suction of secretions. However, methods of ventilatory assistance without intubation had proliferated prior to the polio epidemic (both negative-pressure chest wall devices and positive-pressure face mask devices), and current trends are to an increased use of non-invasive ventilation (NIV) in patients with respiratory failure.2

Almost all of the ventilatory modes that are conventionally applied during intubated ventilation (IV) can be applied non-invasively; however, IV remains the primary mode of respiratory assistance in critically ill patients. There are also an increasing number of patients receiving chronic ventilatory assistance but, since the majority of these use chronic NIV, this chapter is primarily directed at intubated mechanical ventilation for both ARF and acute-on-chronic respiratory failure.

A PHYSIOLOGICAL APPROACH

During normal spontaneous breathing, contraction of the respiratory muscles overcomes both the elastic recoil and resistance of the respiratory system (lung and chest wall). A fall in regional pleural pressure results in alveolar inflation as gas is forced in under the resultant pressure gradient. Expiration is usually passive but the expiratory muscles may assist the elastic recoil of the respiratory system.

The work (W) performed by the respiratory muscles (Wmus) can be measured from the relationship between pressure (P) and volume (V), and partitioned into elastic (Wel) and resistive (Wres) work:

Equation 1 image

Inertial work is negligible, and usually ignored. Further, Equation (1) does not explicitly describe the elastic work required to initiate inspiration when intrinsic positive end-expiratory pressure (PEEPi) is present.

Because volume is constant in Equation (1), it can be simplified to:

Equation 2 image

It follows that, during positive-pressure ventilatory assistance, where PaO is the ventilatory pressure applied at the airway:

Equation 3 image

and that when the work is solely applied by the ventilator with no respiratory muscle contraction (controlled mechanical ventilation (CMV)):

Equation 4 image

This nomenclature allows physiologic discussion of the different ventilatory modes, from controlled ventilation to spontaneous, unassisted ventilation, and introduces the equation of motion, which is used in the estimation of respiratory mechanics:

Equation 5 image

where Ers is the respiratory system (lung and chest wall) elastance (the inverse of compliance), Rrs is the respiratory system resistance, image is the gas flow rate and Po is the total PEEP (the sum of extrinsic PEEP [PEEPe] and PEEPi). PEEPi imposes a threshold load – additional elastic work – as inspiratory muscle contraction must occur without image until Pao falls below atmospheric pressure (see section on patient–ventilator interaction, below).

MODES OF VENTILATION

CONTROLLED MECHANICAL VENTILATION

The simplest form of positive-pressure breath occurs in a relaxed subject, and the ventilator provides a constant gas flow during inspiration. The volume delivered will depend upon the inspiratory time (Ti), and Pao during inspiration will reflect Ers and Rrs (Figure 27.1). Expiration is a passive, and usually exponential, decline in volume to the relaxation volume of the respiratory system, equal to the functional residual capacity (FRC).

CMV is the most basic form of mechanical ventilation; however, it is an extremely useful baseline, and is still commonly used. A preset minute ventilation is made up from a fixed respiratory rate (f) and tidal volume (VT). Provided that there are not large variations in alveolar dead space, this maintains a preset alveolar ventilation (VA) and CO2 clearance. Consequently, CMV is useful in conditions where there is alveolar hypoventilation (e.g. respiratory muscle weakness), when PaCO2 needs to be maintained in a fixed range (e.g. raised intracranial pressure) or when the work of breathing must be minimised (e.g. severe cardiorespiratory failure). Because CMV may not match respiratory drive, and spontaneous, supported or assisted breaths are not possible during CMV, sedation, and sometimes muscle paralysis, may be needed. CMV is usually combined with PEEPe, which can recruit collapsed lung and reduce intrapulmonary shunt. The components are discussed below.

TIDAL VOLUME (vT)

Although traditional CMV VT has been 12–15 ml/kg, this may result in excessive lung stretch, particularly in patients with acute lung injury (ALI), leading to ventilator-induced (VILI) – also described as ventilator-associated – lung injury (VALI).3 The basis for this larger VT can be traced back to progressive atelectasis and intrapulmonary shunt, when physiologic VT was used during general anaesthesia. This could be reversed by larger VT ventilation or intermittent sigh breaths.4 In patients with ALI, VT of 6 ml/kg versus 12 ml/kg predicted body weight (i.e. often 4–5 ml/kg versus 9–10 ml/kg true weight) reduced mortality from 40% to 31%.5 Consequently, lower VT should be strongly considered during CMV, and other forms of ventilatory assistance in patients with ALI. However, greater levels of PEEP are usually required; similar data are not available for other respiratory diseases. Indeed, although the reduction in VT is particularly applicable to ALI, excessive lung stretch will be less likely in other patient cohorts that are able to ventilate a greater proportion of the lung (see Chapter 29).

INSPIRATORY FLOW PATTERN

The simplest form of CMV uses a constant inspiratory flow (image), and in combination with Ti, a preset volume is delivered. This is also called volume-controlled ventilation (VCV), and some ventilators use VT and Ti to set image. Alternative image patterns that are commonly available with VCV include a ramped descending flow pattern and a sine pattern. When a time-preset inspiratory pressure is delivered, this is termed pressure-controlled ventilation (PCV).

There are no convincing outcome data differentiating these different modes of CMV and PCV. Although the peak airway pressure (Ppk) is lower with PCV than constant-flow CMV, the alveolar distending pressure, which is usually inferred from the plateau pressure (Pplat), is no different provided that Ti and VT are the same.7 During PCV, Pres is dissipated during inspiration so Ppk and Pplat are equal, and during CMV, Pres accounts for the difference between Ppk and Pplat (Figure 27.2). Similarly, different CMVI patterns will alter Ppk without changing Pplat or mean airway pressure (Pmean) when Ti and VT are constant. In ARDS patients, comparing VCV and PCV, there is no difference in haemodynamics, oxygenation, recruited lung volume or distribution of regional ventilation;7,8 however, PCV may dissipate viscoelastic strain earlier.8 However, high image may cause or exacerbate VILI,9 which may explain why some animal models have found PCV to be injurious compared to VCV, as PCV inherently has a high early image.

image

Figure 27.2 Actual pressure–time data from a patient with acute lung injury ventilated with volume-controlled ventilation (panel A), and then with pressure-controlled ventilation (panel B); tidal volume, I:E ratio and respiratory rate are constant. The airway pressure (Paw, bold line) has been broken down to its components, Pel and Pres (see Figure 27.1). Although there is no inspiratory pause, there is marked similarity between panel A and Figure 27.1, with the inspiratory difference between Paw and Pel due to a constant Pres. In panel B, the decelerating inspiratory flow pattern seen with pressure-controlled ventilation results in dissipation of Pres by end-inspiration. Consequently, during pressure-controlled ventilation PawPplat obtained during volume-controlled ventilation. In other words, for the same ventilator settings there is no difference in the elastic distending pressure.

Pressure-regulated volume control (PRVC) is a form of CMV where the VT is preset, and achieved at a minimum pressure using a decelerating flow pattern.

POSITIVE END-EXPIRATORY PRESSURE

PEEP is an elevation in the end-expiratory pressure upon which all forms of mechanical ventilation may be imposed. When PEEP is maintained throughout the respiratory cycle in a spontaneously breathing subject, the term ‘constant positive airway pressure’ (CPAP) is used. The primary role of PEEP is to maintain recruitment of collapsed lung, increase FRC and minimise intrapulmonary shunt. PEEP may also improve oxygenation by redistributing lung water from the alveolus to the interstitium, and although there is no direct effect of PEEP to reduce extravascular lung water, this may occur in patients with left ventricular failure due to a reduction in venous return and left ventricular afterload. Further, inadequate PEEP may contribute to VILI by promoting tidal opening and closing of alveoli.3 PEEP levels of 5–15 cmH2O are commonly used, and levels up to 25 cmH2O may be required in patients with severe ARDS. Although a large multicentre study found no benefit of higher PEEP levels when VT was 6 ml/kg,12 individual titration may need to be considered.

PEEP titration in ARDS is complex (see Chapter 29), and should aim to improve oxygenation and minimise VILI. Since PEEP reduces venous return, cardiac output and O2 delivery may fall despite an improvement in PaO2; indeed, this concept has been used to optimise PEEP in ARF.13 However, in addition to recruitment, increasing PEEP may lead to overinflation of non-dependent alveoli which are already aerated at end-expiration.14,15 This will be less likely if alveolar distending pressure is kept < 30–35 cmH2O, or the change in driving pressure is < 2 cmH2O when VT is constant.16

PEEPe is applied by placing a resistance in the expiratory circuit (Figure 27.3), with most ventilators using a solenoid valve. Independent of the technique, a threshold resistor is preferred since it offers minimal resistance to flow once its opening P is reached. This will minimise expiratory work, and avoid barotrauma during coughing or straining.

PEEPi is an elevation in the static recoil pressure of the respiratory system at end-expiration. PEEPi arises due to an inadequate Te, usually in the setting of severe airflow obstruction. However, it may be a desired endpoint during IRV. The sum of PEEPe and PEEPi is the total PEEP (PEEPtot). The distribution of PEEPi is likely to be less uniform than an equivalent PEEPe, and this may not have the same physiological effects. When patients with severe airflow obstruction are triggering ventilation, PEEPe less than PEEPi may be applied to reduce elastic work (see section on patient–ventilator interaction, below).

SIGH

Many ventilators have the ability to deliver a breath intermittently at least twice VT. Sighs may reduce atelectasis, in part through release of pulmonary surfactant,17 resulting in recruitment and improved oxygenation in ARDS.18 However, if sighs or recruitment manoeuvres are used, care must be taken to avoid recurrent excessive lung stretch.

ASSIST-CONTROL VENTILATION (ACV)

During ACV, in addition to the set f, patient effort can trigger a standard CMV breath (Figure 27.4). This allows greater patient comfort; however, there may be little reduction in respiratory work compared to an unassisted breath at low image, because the respiratory muscles continue to contract through much of the breath.19 The equivalent PCV breath is termed pressure assist-control ventilation (PACV). Differences between triggering modes will be discussed below, in the section on patient–ventilator interaction.