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 (W_mus) can be measured from the relationship between pressure (P) and volume (V), and partitioned into elastic (W_el) and resistive (W_res) work:

Equation 1

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 (PEEP_i) is present.

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

Equation 2

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

Equation 3

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

Equation 4

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

where E_rs is the respiratory system (lung and chest wall) elastance (the inverse of compliance), R_rs is the respiratory system resistance, is the gas flow rate and P_o is the total PEEP (the sum of extrinsic PEEP [PEEP_e] and PEEP_i). PEEP_i imposes a threshold load – additional elastic work – as inspiratory muscle contraction must occur without until P_ao 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 (T_i), and P_ao during inspiration will reflect E_rs and R_rs (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).

Figure 27.1 Schematic diagram of a volume-controlled breath with constant inspiratory flow. A period of no inspiratory gas flow has been interposed before expiration (pause) to illustrate dissipation of lung resistance as airways resistance (fall from P_pk to P₁) and tissue resistance (fall from P₁ to P₂). The inspiratory pressure due to the elastic properties of the respiratory system is illustrated as the filled area (P_el), and the lung resistive pressure is labelled as P_res. See text for more detail.

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 (V_T). Provided that there are not large variations in alveolar dead space, this maintains a preset alveolar ventilation (V_A) 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 PEEP_e, which can recruit collapsed lung and reduce intrapulmonary shunt. The components are discussed below.

TIDAL VOLUME (v_T)

Although traditional CMV V_T 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 V_T can be traced back to progressive atelectasis and intrapulmonary shunt, when physiologic V_T was used during general anaesthesia. This could be reversed by larger V_T ventilation or intermittent sigh breaths.⁴ In patients with ALI, V_T 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 V_T 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 V_T 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).

RESPIRATORY RATE (f)

The desired minute ventilation can be selected from the product of V_T and f. Common CMV rates are 10–20 breaths/min in adults. Sufficient expiratory time (T_e) must be allowed to minimise dynamic hyperinflation and PEEP_i. Although high f (up to 35 breaths/min) were allowed in the Acute Respiratory Distress Syndrome (ARDS) Network protocol, and the low-V_T, low-mortality group had a mean f of ∼30 breaths/min,⁵ laboratory data suggest a possible additive role of high f in VILI.⁶

INSPIRATORY FLOW PATTERN

The simplest form of CMV uses a constant inspiratory flow (), and in combination with T_i, a preset volume is delivered. This is also called volume-controlled ventilation (VCV), and some ventilators use V_T and T_i to set . Alternative 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 (P_pk) is lower with PCV than constant-flow CMV, the alveolar distending pressure, which is usually inferred from the plateau pressure (P_plat), is no different provided that T_i and V_T are the same.⁷ During PCV, P_res is dissipated during inspiration so P_pk and P_plat are equal, and during CMV, P_res accounts for the difference between P_pk and P_plat (Figure 27.2). Similarly, different CMV_I patterns will alter P_pk without changing P_plat or mean airway pressure (P_mean) when T_i and V_T 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 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 .

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 (P_aw, bold line) has been broken down to its components, P_el and P_res (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 P_aw and P_el due to a constant P_res. In panel B, the decelerating inspiratory flow pattern seen with pressure-controlled ventilation results in dissipation of P_res by end-inspiration. Consequently, during pressure-controlled ventilation P_aw ≈ P_plat 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 V_T is preset, and achieved at a minimum pressure using a decelerating flow pattern.

INSPIRATORY PAUSE

An end-inspiratory pause allows examination of the decay in P_pk, and measurement of P_plat. If T_i and V are maintained constant there is no improvement in oxygenation, and a more rapid will be needed. This may alter the distribution of ventilation. Theoretically, an end-inspiratory pause will allow a 32% dissipation of the total energy loss within the respiratory system,¹⁰ which may significantly reduce the forces driving expiration, and this could exacerbate gas trapping in patients with severe airflow limitation.

INSPIRATORY TIME, EXPIRATORY TIME, I:E RATIO

The combination of V_T and inspiratory will determine T_i, which in combination with f sets T_e. A typical T_i is 0.8–1.2 s; with a V_T of 500 ml and inspiratory of 0.5 l/s, the T_i is 1.0 s. During spontaneous ventilation, the distribution of ventilation at low is determined by regional E, and at high inspiratory by regional R, leading to greater ventilation of non-dependent lung. In patients with severe airflow limitation high inspiratory flow rates may be used in order to prolong T_e and minimise dynamic hyperinflation.¹¹

The I:E ratio is usually set at or below 1:2 to allow an adequate T_e for passive expiration. During inverse-ratio ventilation (IRV), the I:E ratio is greater than 1:1. The putative benefits of a prolonged T_i include recruitment of long time-constant alveoli, and a short T_e results in gas trapping and PEEP_i. Early reports of clinical benefit did not control for PEEP_i, and when total PEEP, f and V_T are constant,^7,8 pressure control (PC) IRV tends to reduce PaCO₂ but does not improve oxygenation, may have deleterious haemodynamic effects and may exaggerate regional overinflation.⁸

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 V_T 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 V_T is constant.¹⁶

PEEP_e 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.

Figure 27.3 Positive end-expiratory pressure values.

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

FRACTIONAL INSPIRED OXYGEN CONCENTRATION (FIO₂)

Adequate arterial oxygen saturation is achieved through a combination of minute ventilation, PEEP and FiO₂ adjustment. Even patients with normal respiratory systems usually need an FiO₂ > 0.21, due to ventilation–perfusion mismatch secondary to positive-pressure ventilation. In patients with ARF it is common to start with an FiO₂ of 1 and titrate down as PEEP and minute ventilation are adjusted. Because high FiO₂s are damaging to the lung, and nitrogen washout may exacerbate atelectasis, it is reasonable to aim at an FiO₂ ≤ 0.6.

SIGH

Many ventilators have the ability to deliver a breath intermittently at least twice V_T. 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 , 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.

Figure 27.4 Schematic representation of airway pressure versus time for a variety of forms of ventilatory assistance. SV, spontaneous ventilation; CPAP, continuous positive airway pressure; PEEP, positive end-expiratory pressure; CMV, controlled mechanical ventilation; IMV, intermittent mandatory ventilation; PSV, pressure support ventilation; IRV, inverse-ratio ventilation; APRV, airway pressure release ventilation.

INDICATIONS AND OBJECTIVES OF MECHANICAL VENTILATION³⁰

Institution of mechanical ventilation is a clinical decision; it can only be supported by parameters such as blood gases or measures of respiratory muscle function. Even then, the decision to choose IV over NIV will be influenced by numerous factors, including the likely course of the ARF and its response to treatment. Often there will be an indication for intubation (Table 27.1) and mechanical ventilation; however, if intubation is required to overcome upper-airway obstruction, no ventilatory assistance may be needed despite the increase in respiratory work imposed by the endotracheal or tracheostomy tube.¹⁸Once the decision has been made to proceed to ventilatory support the choice of mode should be based on a physiological approach, local expertise and simplicity.

Table 27.1 Indications and objectives of intubated mechanical ventilation

Patients who are likely to need ventilatory assistance (e.g. acute severe asthma) should be considered for early ICU admission since this will allow faster responses and avoid cardiorespiratory arrest. Specific issues and methods of ventilatory assistance are dealt with in Chapters 29, 31 and 33. In patients with traumatic brain injury IV is commonly required to protect the airway and control ICP; similarly, patients with severe pancreatitis or serious abdominal infection may need prolonged IV to maintain an adequate FRC, reduce work of breathing, protect their airway and allow suctioning of secretions.

COMPLICATIONS OF MECHANICAL VENTILATION (Table 27.2)²⁶

Although mechanical ventilation may be vital, it also introduces numerous potential complications. Monitoring includes a high nurse-to-patient ratio (usually 1:1), ventilator alarms and pulse oximetry. Capnography is recommended to confirm endotracheal tube placement, and may be used to monitor the adequacy of V_A;however, expired CO₂ is strongly influenced by factors that alter alveolar dead space, such as cardiac output. Intermittent blood gases, PEEP_i, airway pressures in volume-preset modes and V_T in pressure-preset modes should be recorded. Individual patients may benefit from more extensive monitoring of their respiratory mechanics or tissue oxygenation.

Table 27.2 Complications of intubation and mechanical ventilation

The patient’s airway (i.e. patency, presence of leaks and nature and amount of secretions), breathing (i.e. rate, volume, oxygenation) and circulation (i.e. pulse, blood pressure and urine output) must be monitored. Ventilatory and circuit alarms should be adjusted to monitor an appropriate range of V,P and temperature. This should alert adjacent staff to changes in P and/or V that may be caused by an occluded endotracheal tube, tension pneumothorax or circuit disconnection. These alarms may be temporarily disabled while the cause is detected, but never permanently disabled. Sudden difficulties with high P during volume-preset ventilation or oxygenation must initiate an immediate search for the cause. This should start with the patency of the airway, followed by a structured approach to both the circuit and ventilator, and to factors altering the E and R of the lung and chest wall such as bronchospasm, secretions, pneumothorax and asynchronous breathing. In addition to careful clinical examination an urgent chest radiograph and bronchoscopy may be required.

Mechanical ventilation is also associated with a marked increase in the incidence of nosocomial pneumonia due to a reduction in the natural defence of the respiratory tract, and this represents an important advantage offered by NIV. In patients successfully managed with NIV, Girou and colleagues reported a reduction in the incidence of nosocomial pneumonia, associated with improved survival, compared to IV.³³ Erect versus semirecumbent posture³⁴ also reduces the incidence of ventilator-associated pneumonia.

Although lung overdistension may result in alveolar rupture leading to pulmonary interstitial air, pneumomediastinum or pneumothorax, it may also lead to diffuse alveolar damage similar to that found in ALI and ARDS. Both are termed VILI, and V_T reduction leads to a marked decrease in ALI mortality, due to a reduction in multiple-organ dysfunction.⁵ There are also laboratory data suggesting that inadequate PEEP with tidal recruitment and derecruitment of alveoli leads to VILI; however, this has not been proven in a clinical trial. Finally, patient–ventilator asynchrony may result in wasted respiratory work, impaired gas exchange and respiratory distress (see below).

Positive-pressure ventilation elevates intrathoracic pressure, which reduces venous return, right ventricular preload and cardiac output. The impact is reduced by hypervolaemia and partial ventilatory support, where patient effort and a reduction in pleural pressure augment venous return. Secondary effects include a reduction in regional organ blood flow leading to fluid retention by the kidney, and possibly impaired hepatic function. This latter effect is only seen at high levels of PEEP where an increase in resistance to venous return and a reduction in cardiac output may combine to reduce hepatic blood flow.

Sleep disturbance, and agitation and discomfort are common in mechanically ventilated patients. These effects may be reduced with sedation until weaning is planned; however, it is important not to prolong mechanical ventilation due to excessive use of sedatives, which may also depress blood pressure and spontaneous respiratory effort. Finally, complex neuropsychological sequelae have been described in recovering ARDS patients.^35,36 These do not appear to reflect the severity of the acute illness since ARDS patients have a poorer quality of life than patients with a similar severity of illness without ARDS.³⁷ However, they do correlate with their duration of hypoxaemia. Clearly, this is an important issue that needs further research.

WITHDRAWAL (WEANING) FROM MECHANICAL VENTILATION

Once the underlying process necessitating mechanical ventilation has started to resolve, withdrawal of ventilatory support should be considered; increased duration of ventilation leads to a progressive rise in complications such as ventilator-associated pneumonia. However, other important parameters that must be considered include the neuromuscular state of the patient (ability to initiate a spontaneous breath), adequacy of oxygenation (typically low requirements for PEEP (5–8 cmH₂O) and FiO₂ < 0.4–0.5) and cardiovascular stability.³⁸ Once a patient is considered suitable to wean, a secondary question is whether an artificial airway is still required for airway protection or suction of secretions. Many patients can rapidly make the transition from mechanical ventilation to extubation, but ∼20% of patients fail weaning despite meeting clinical criteria.²¹ Advanced age, prolonged mechanical ventilation and chronic obstructive pulmonary disease all increase the likelihood that weaning will be difficult.²¹

Weaning failure is usually associated with an increase in respiratory drive and respiratory rate and a fall in V_T which contributes to hypercapnoea;³⁹ about 10% of patients fail due to central respiratory depression. Various indices such as maximal inspiratory pressure (MIP), minute ventilation (V_E), f,V_Tf/V_T ratio and the compliance, respiratory rate, oxygenation, maximum inspiratory pressure (CROP) index have been investigated as predictors of weaning failure (Table 27.3). They are rarely used alone and careful clinical assessment is often adequate, yielding a reintubation rate as low as 3%,⁴⁰ and none of these indices assess airway function following extubation. Although the typical threshold value for the rapid shallow-breathing index (f/V_T ratio) is > 105, a large recent multicentre study reported progressive increase in risk as this increased with a threshold of 57; in addition apositive fluid balance immediately prior to extubation was a significant risk factor for reintubation.⁴¹ Consequently, weaning indices should not necessarily delay extubation or a weaning trial. However, they may quantitate important issues in the general clinical assessment, and may be directly relevant for a given patient. For example, frequent small V_T, an inadequate vital capacity (less than 8–12 ml/kg), large minute ventilation (= 15 l/min), depressed respiratory drive and reduced respiratory muscle strength (MIP = –15 cmH₂O) or drive should be strongly factored into deciding whether a patient is ready to undergo a trial of weaning safely.

Table 27.3 Sample of measurements that have been used to predict successful outcome from weaning in critically ill patients*

MIP, maximal inspiratory pressure; CROP, compliance, respiratory rate, oxygenation, maximum inspiratory pressure.

* See reference 38 for further detail.

† Although threshold values are often used, the data are not dichotonous. For example, as the f/V_T ratio increases, so does the rate of reintubation.⁴¹

# CROP index = (C_dyn × MIP × [PaO₂/PAO₂]/f).²¹

Direct comparisons between T-piece trials, PSV and SIMV as weaning techniques have been performed in patients previously failing a 2-hour trial of spontaneous breathing. In the study by Brochard and colleagues,⁴² PSV led to fewer failures and a shorter weaning period. In contrast, Esteban and coworkers⁴³ found that a once-daily trial of spontaneous breathing resulted in the shortest duration of mechanical ventilation; however, a relatively high proportion of patients required reintubation (22.6%). Viewed together these studies suggest that weaning was slower with SIMV,¹⁹ although SIMV with PSV was not studied, and that either PSV or a T-piece trial is the preferred method for weaning. Since low levels of PSV can help compensate for the additional work of breathing attributable to the endotracheal tube and circuit, some clinicians use low levels of PSV (5–7 cmH₂O) during weaning or during a spontaneous breathing trial. However, the work of breathing following extubation is usually higher than expected, probably due to upper-airway oedema and dysfunction, so that work is similar to that during a T-piece trial.²¹

Reintubation is associated with a 7–11-fold increased risk of hospital death.¹⁹ A number of factors may account for this, including selection of previously unaccounted-for severity of illness as the mortality rate associated with reintubation is much higher in patients whose primary diagnosis was respiratory failure. In addition, complications which may (pneumonia, heart failure) or may not be attributable to extubation contribute to this poor outcome. Hence, an important goal during mechanical ventilation will be to proceed to early and expeditious extubation with a low reintubation rate.

PATIENT–VENTILATOR INTERACTION

This is an extremely important issue in patients with either partial ventilatory support, or those breathing spontaneously through the ventilator. Dyssynchrony can lead to agitation, diaphoresis, tachycardia, hypertension and weaning failure or a failure of NIV. Once this pattern is identified it is crucial that airway complications (partial obstruction, displacement) or a major change in the clinical state (e.g. pneumothorax, acute pulmonary oedema) are excluded before considering problems with patient–ventilator interaction. For simplicity this will be subdivided into: (1) triggering of inspiration; (2) inspiration; and (3) cessation of inspiration; however, difficulties at each of these phases will lead to changes in respiratory drive and effort that may be expressed throughout the respiratory cycle. Importantly, major problems with patient–ventilator dyssynchrony can be identified by carefully observing respiratory effort and ventilator cycling at the bedside and this may be assisted by observing P,V and waveforms displayed by the ventilator.

TRIGGERING OF INSPIRATION

1 PEEP_i is an important hindrance to the triggering of inspiration in patients with severe airflow limitation, since their inspiratory muscles must first reduce P_ao below ambient pressure.⁴⁴ Consequently P_mus must exceed PEEP_i prior to triggering an assisted breath either by reducing airway pressure (pressure trigger) or by reducing circuit flow (flow trigger). This inspiratory threshold load may be up to 40% of the total inspiratory work in ARF with dynamic hyperinflation, and commonly results in ineffective triggering. Triggering can be markedly improved and respiratory work reduced by low levels of CPAP^37,45 – commonly 80–90% of dynamic PEEP_i.⁴⁶

2 A fall in P_ao has been the most common form of triggering. Pressure is usually sensed at the expiratory block of the ventilator. Sensing at the Y-piece is not superiorsince there is a similar delay in sensing as the transducer is usually sited in the ventilator. Flow triggering senses a fall in continuous circuit flow, and was introduced as a method of reducing inspiratory work. However, there has been a marked improvement of both pressure and flow triggering in modern ventilators, with the trigger time delay falling from ∼400 to ∼100 ms, and a similar improvement in the maximum fall in airway pressure.⁴⁷ Attempts to improve the trigger function by oversetting the pressure sensitivity (> –0.5 cmH₂O) may lead to autocycling, which may also occur with overset flow triggering. This is due to the P and effects of cardiac oscillations, hiccups, circuit rainout or mask leak with NIV, and has been reported as a cause of apparent respiratory effort in brain-dead patients.⁴⁸ Flow triggering reduces the risk of autocycling at a given trigger sensitivity, and reduces respiratory effort a small amount compared to pressure triggering; however, it does not alter the frequency of ineffective efforts,⁴⁹ or patient effort following triggering.⁴⁰

INSPIRATION

Once inspiration is triggered or sensed by the ventilator, is determined by P,T_i or . For example, during PSV ventilation a target P is held until expiration is sensed, and during ACV is held for a set T_i. During ACV there may be continued inspiratory effort, and since inspiratory is fixed, this will be reflected by a scalloping of the P_ao–T graph if is inadequate. Again this may be illustrated using the equation of motion:

Equation 6

P_mus will reflect the difference between P_ao due to E,R and P_o and the observed P_ao. In contrast, during P-cycled ventilation (PACV), greater patient effort is rewarded, and inspiratory work is lower than during equivalent ACV.⁵⁰

Modern ventilators allow adjustment of inspiratory and pattern, and the rate of rise of P_ao. Low inspiratory rates during ACV result in significant inspiratory work, but this may be markedly reduced by increasing inspiratory to 65 l/min.⁵¹ However, these issues are quite complex, and f increases (probably due to a lower respiratory tract reflex) as increases,⁵² reducing T_e, which may contribute to dynamic hyperinflation in patients with severe airflow obstruction. During PSV and PACV, many ventilators allow adjustment of the rate of rise of P to its target. A steeper P ramp leads to earlier attainment of the P target, greater early rates and reduction of inspiratory drive and work.^53,54

CESSATION OF INSPIRATION

During PSV, an increase in airways resistance will result in a delayed fall in . Since this is the trigger for cycling to expiration, the ventilator may continue to provide while the patient desires to exhale. This commonly leads to recruitment of expiratory muscles, detected both clinically and as a transient rise in the end-inspiratory P_ao.⁵⁵ Some modern ventilators allow control of the fall in that is sensed as end-inspiration. High levels of PSV (≥ 20 cmH₂O), weak respiratory muscles and mask leak with NIV are other common causes of dyssynchrony at the termination of inspiration. In this last group, PACV, which is time-cycled, allows improved patient–ventilator synchrony at end-inspiration compared to PSV.⁵⁶