Table of Contents  

Masri: Lung recruitment tools

Gas flow (F)

The cornerstone of ventilation is gas flow through tubular conductors (the bronchial tree) and spherical containers (the alveoli). Gas flow has to overcome two types of forces – the resistance of tubular passages of the bronchial tree, which is the airway resistance, and the recoil forces of the lung and chest wall, which is the respiratory system compliance – and then be evenly distributed among the alveoli.

Flow is defined as the quantity of a fluid, i.e. a gas or liquid, passing a point in a unit of time, as in equation 1 from Davis and Kenny (p. 11).1

(1)
F = Q / t

where F is the mean flow, Q is the quantity (mass, volume) and t is the time.

During normal quiet inspiration, gas flow becomes turbulent at the level of the larynx and trachea; this is because air flow is rapid at the beginning of the respiratory cycle. Laminar flow is chiefly confined to the bronchi and smaller airways, despite a progressive reduction in the airway diameter; this because the air flow through the smaller airways is slower because of an increase in the total cross-sectional area of the airways as branching occurs.13 So gas flow during normal inspiration decelerates to ensure laminar flow. All modern ventilator machines have this decelerating flow pattern to simulate the normal inspiratory cycle and ensure laminar flow. Laminar flow ensures three elements important for healthy ventilation: first, homogeneous gas distribution through the bronchial tree; second, reduced airway resistance; and, as a result, third, less effort required for breathing in the event of spontaneous breathing, or lower driving pressure in the case of positive pressure ventilation.2 In contrast, turbulent flow increases airway resistance and the effort required for breathing and has unpredictable gas distribution and uneven flow so that eddies occur.1,2 Changes between laminar and turbulent flow depend on the gas specification (density and viscosity) and velocity of the gas, which in turn depends on the volume flow and thus on the diameter of the tubing and airway.1 Laminar flow may change to turbulent flow if a constriction is encountered, or a sharp angle or branching that results in an increase in the gas velocity that exceeds a critical value, Reynolds’ number,1,3 such as an undetected sharp bend in the endotracheal tube in the pharynx, bronchial secretions in the airways or some degree of bronchospasm. Airway constriction has a significant effect when it happens immediately before branching of the airway owing to the Coandă effect. This happens where a narrow tube enters a ‘Y’ junction of wider bore and, because most the flow is one side, air is not distributed evenly between the two outlets but flows through only one limb of the ‘Y’.1 A high flow volume can convert laminar flow to turbulent flow as the critical velocity is exceeded, as during tachypnoea while weaning off mechanical ventilation or using high tidal volume (VT) in volume-controlled ventilation in a patient with low lung compliance. In laminar flow, there is a linear relationship such that flow is directly proportional to pressure, as shown by the Hagen–Poiseuille equation1,2 for laminar flow, but in turbulent flow, multiplying the pressure by 4 (equation 4) results in only doubling of the flow.1,2,4

(2)
Q ˙ = π P d 4 128 η l

This is the Hagen–Poiseuille equation, where Q ˙ is the flow through the tube, P is the pressure across the tube, d is the diameter of the tube, l is the length of the tube and η is the viscosity of the fluid.

This equation can be rearranged to show how the pressure drop across a tube depends on various factors:

(3)
P = 128 η l Q ˙ π d 4
(4)
Q ˙ P

The pressure gradient (ΔP) during turbulent flow increases much more than the volume or flow (ΔV); therefore. airway resistance (R) increases more and is higher than the resistance for the same laminar flow, as in equation 5 from Miller (p. 586).2 This explains how laminar flow reduces the effort required for breathing and the patient can achieve a better flow with less effort:

(5)
R = Δ P / Δ V

Halving the diameter of the tube [endotracheal tube (ETT) or bronchospasm] reduces laminar flow to one-sixteenth the original value and increases the pressure gradient to 16 times the original value (equation 3); consequently, a slight reduction in the diameter of an ETT can have an appreciable effect on resistance and therefore on flow.1,4 For this reason, the ETT should have the largest possible internal diameter. Because flow distribution is better, airway resistance is lower and less effort is required for breathing, laminar flow is the ideal flow for better lung recruitment during mechanical ventilation and, most importantly, during weaning from mechanical ventilation. By comparison, we can say that turbulent flow is anti-recruitment flow and should be avoided by preventing the predisposing factors.

Quantity (Q) and time (t)

According to equation 1, flow and volume (quantity) are linked together by an essential, effective and determining factor during ventilation, which is the time. Flow is the rate of change in volume per unit of time. The quantity is affected by all factors affecting flow and pressure, as shown by the Hagen–Poiseuille equation (equation 2) for laminar flow.

Alveolar filling is dependent on compliance, airway resistance and time. Mathematically, this can be explained by the time constant equation from Morgan et al. (p. 553):3

(6)
T = CT × R

where T is the time constant, CT is lung and chest wall compliance and R is airway resistance.

T = ( 0.1 l / cmH 2 O ) × ( 2.0 cmH 2 O / l / s ) = 0.2 s

The time constant is the time required to complete 63% of an exponentially changing function, such as inflation of the alveoli (2T = 87%, 3T = 95% and 4T = 98% of the function). A normal lung needs 4T, i.e. 0.8 seconds, to be properly inflated. The compliance of individual alveoli differs from the top to the bottom of the lung: the compliance increases from top to bottom and the resistance of individual airways will vary widely depending on their length and calibre. Accordingly, in a certain period of time, the lung is unevenly ventilated, with a variety of alveolar time constants throughout the lung. Alveolar filling occurs in an exponential manner, and the degree of filling obviously depends the duration of the inspiration. When inspiratory time is unlimited, the final alveolar inspiratory volume depends only on compliance. When there is an increase in the airway resistance (as in asthma or chronic obstructive pulmonary disease) or compliance (as in the dependent part of the normal lung), the time constant will increase, i.e. the time needed for proper lung inflation also increases. Regions of lower compliance (as in emphysema or restrictive pulmonary disease) have a shorter time constant and will be filled by air earlier.2 Adjusting the inspiratory time during mechanical ventilation is crucial in the diseased lung because of the significant difference in the time constant between healthy alveoli and alveoli that are mildly or severely diseased. Because gas usually flows to less resistant alveoli first before continuing to more compliant regions,5 if the inspiratory time is insufficient, as may occur during tachypnoea or when respiratory rate is high, e.g during mechanical ventilation, some lung regions will become overdistended and others will become atelectatic with increased intrapulmonary shunting and induced barotrauma. Rapid, shallow breathing creates uneven gas distribution as a result of a short inspiratory time and high velocity flow, both of which encourage turbulent flow, and tidal volume will be distributed in the apical region of the lung first because of its shorter time constant and lower compliance. Prolonged inspiratory time has several physiological effects. It may enable additional alveoli to be recruited (avoiding injury due to traumatic, sudden inflation of the alveoli by recruitment manoeuvres), increase gas mixing time and improve ventilation–perfusion matching.5

Lung volumes

Lung volumes affect the dynamics of the lung and usually have a significant effect on the flow, airway resistance, lung compliance, ventilation–perfusion ratio and recruitment. All determinants of maximal flow during expiration are usually dependent on lung volume. As expiration continues, lung volume decreases, airways narrow, resistance increases and the flow rate progressively decreases.2 Lung compliance increases with increased lung volume as long as hyperinflation is avoided, in accordance with equation 7:

(7)
CT ( l / cmH 2 O ) = Δ V ( l ) / Δ P ( cmH 2 O )

where CT is total lung compliance, ΔV lung volume and ΔP the pressure gradient.

Functional residual capacity and closing volume or closing capacity

Functional residual capacity (FRC) has a significant role in maintaining the structure and function of the lung. FRC, by definition, is the volume of lung that exists at the end of a normal exhalation after a normal tidal volume when there is no muscle activity, no gas flow and the alveolar pressure (PA) is equal to the ambient pressure in the mouth.2 Closing volume (CV) or closing capacity (CC) is the volume of the lung at which small intrathoracic airways start to close during expiration.3 CV is normally lower than tidal respiration,2 being between tidal volume and residual volume,3 and the potential for the airway to start closing increases with the volume of the lung at the end of expiration, i.e. FRC approaches the residual volume (Figure 1).2 The relationship between FRC and CV is more important than either FRC or CV alone. In normal circumstances, the CV of the lung is less than tidal volume and no airways are closed at any time during tidal respiration, i.e. FRC > CV, and anything that decreases the FRC relative to CC converts normal lung regions to low-ventilation/-perfusion areas or shunts and atelectasis.2 In patients with normal lungs, airway closure may still occur even if exhalation is not forced, provided residual volume (RV) is approached closely enough, as in an elderly person.2 Airway closure occurs first in the dependent lung regions, which constitute the FRC, because the distending transpulmonary pressure in the dependent regions is less and the pleural pressure is more positive.2,3 Active or forced expiration usually increases the pleural pressure far above atmospheric pressure, and at a high gas flow rates, during active expiration, the drop in pressure down the air passages is also steeper, both of which mechanisms encourage early airway closure.2

FIGURE 1

The relation between functional residual capacity and closing volume.

9-2-5-fig1.jpg

Tachypnoea and active expiration, frequently seen during weaning from mechanical ventilation and after extubation, are major factors predisposing to derecruitment of the lung owing to the short inspiratory time in addition to positive pleural pressure and a drop in airway pressure. The patency of small intrathoracic airways distal to the 11th generation, which do not have cartilage, i.e. the bronchioles, is a function of lung volume and can be maintained by the tethering effect of the elastic recoil in the lung parenchyma.2,3 In some lung diseases, such as emphysema, bronchitis, asthma and pulmonary interstitial oedema, as a result of of distortion of the lung tissue, airway closure occurs at milder active expiration, lower gas flow rates and higher lung volumes.2 In intubated and mechanically ventilated patients in the intensive care unit (ICU), the dependent region constitutes a larger proportion of the lung, which puts the patient at high risk of having an early and significant airway closure for many reasons: first, a supine position or 30–45° head-up tilt causes the abdominal contents to exert additional pressure on the diaphragm;3 second, interstitial pulmonary oedema and increased interstitial fluid pressure due to fluid overload and the effect of gravity in an immobile patient creates peribronchial positive pressure;2 and, third, there is a relatively positive pleural pressure in the dependent regions of the lung2 and pleural effusion from different aetiologies. All these factors will reduce the lung volume, at the expense of FRC, reduce the transpulmonary distending pressure owing to positive pleural pressure and positive interstitial fluid pressure and result in lung regions with early airway closure, a low ventilation–perfusion ratio and atelectasis (Figure 2).

FIGURE 2

A computerized tomography scan of the chest of a patient intubated in the ICU showing atelectasis and pleural effusions in the dependent lung regions.

9-2-5-fig2.jpg

This short review explains the importance of the relationships between FRC and CV in maintaining normal lung structure and proper respiratory function in patients in the ICU. Maintaining normal FRC is an essential step in recruitment and protecting the lung from derecruitment.

Positive end-expiratory pressure and the pressure–volume curve

Positive end-expiratory pressure (PEEP) has two major beneficial pulmonary effects: it increases FRC and the redistribution of pulmonary extravascular water. By increasing the volume of patent alveoli with a low ventilation–perfusion ratio and recruiting atelectatic alveoli, PEEP can increase the lung volume, increase the FRC and thus maintain a normal relationship between FRC and CV, i.e. FRC > CV, and improve lung compliance. PEEP maintains positive pressure inside the airways and prevents early airway closure, and this is very important in patients in whom the structural integrity of the lung tissue is damaged, e.g. by emphysema, bronchitis and bronchial asthma; as a result, the recoil force of the lung tissue is reduced and patency of the bronchioles cannot be maintained.2 PEEP plays an important role in strategies designed to protect the lung from ventilator-induced lung injury (VILI). Atelectrauma, one of the major predisposing factors for lung injury during mechanical ventilation, occurs when the patient loses FRC or when FRC is less than CV, as is usual in patients in the ICU. This situation can be corrected and managed by the proper use of PEEP.2,3,68 Patients in this category (FRC < CV) are at higher risk of VILI, unless treated correctly with PEEP: first, atelectrauma may occur and go unnoticed as the arterial blood gases (ABG) are normal most of the time (because high tidal volume during mechanical ventilation keeps the alveoli open during the inspiratory phase but atelectatic at end-expiration); second, a high tidal volume exposes the lung to volutrauma. PEEP, by preventing and/or recruiting atelectatic lung regions, can maintain the lung structure and protects against VILI.912 Analysis of the pressure–volume (P/V) curve of the respiratory system is the basis for lung protection. The shape of the P/V curve gives information about the extension and the homogeneity of lung injury, indicating the possibility of lung recruitment.13 Lung ventilation below the lower inflection point (LIP) and above the upper inflection point (UIP) could generate end-expiratory collapse and end-inspiratory overdistension, both of which are associated with the occurrence and/or progression of lung injury. Setting the PEEP above LIP and the plateau pressure below UIP is therefore recommended in order to protect the lung from further injury.1315 A lung-protective ventilation strategy, as recommended by the National Institutes of Health (NIH) National Heart, Lung and Blood Institute (NHLBI) Acute Respiratory Distress Syndrome (ARDS) clinical network, aims to protect the lung from volutrauma and atelectrauma by using a low tidal volume (6 ml/kg), a moderate to high level of PEEP, maintaining plateau pressure ≤ 30 cmH2O, partial pressure of arterial oxygen (PaO2) 55–80 mmHg or peripheral capillary oxygen saturation (SpO2) 88–95%, and maintaining arterial pH within normal limits (Figure 3).1618 Clinical studies comparing this lung-protective approach with a conventional ventilation strategy demonstrated the beneficial effects of individualized ventilator settings based on the effect of the P/V curve on mortality and the progression of pulmonary and systemic inflammation.1720

FIGURE 3

NIH NHLBI ARDS clinical network: summary of the mechanical ventilation protocol (available from www.ardsnet.org/tools.shtml).

9-2-5-fig3.jpg

The inspiratory P/V curve above the FRC in patients with acute lung injury (ALI) has a sigmoidal shape, with a LIP corresponding to the pressure and volume required to initiate recruitment of collapsed alveoli, an intermediate linear part whose steepness varies depending on lung compliance and a UIP corresponding to the pressure/end-inspiratory volume at which alveolar overdistension occurs.20,21 The P/V curve has been used to individualize PEEP settings and as an indicator of lung recruitability, as will be discussed later. Jonson and Svantesson22 suggested that a marked LIP may be due to the simultaneous reopening of many alveoli with similar threshold opening pressures, as happens in homogeneously diseased lungs. In contrast, when the lung injury is heterogeneous, as in ARDS, alveolar units with different threshold opening pressures coexist, and the LIP may be insignificant or absent. In patients with atelectatic lower lobes coexisting with aerated upper lobes, the P/V curve is characterized by a moderate decrease in slope due to decreased lung compliance and a low or non-existent LIP.7,23,24 Therefore, the presence of LIP on the respiratory system P/V curve may simply indicate a homogeneously diseased lung and the need for lung recruitment.9,23 The compliance of the intermediate, linear, part of the P/V curve gives an indication of lung recruitability.25 The higher compliance at zero end-expiratory pressure (ZEEP) reflects the progressive reopening of alveolar units collapsed at the end of expiration – the steeper intermediate section of the P/V curve – while, when the lung is fully recruited with PEEP, the intermediate section flattens and compliance is lower.26

Optimum PEEP

Optimum PEEP2,3 should provide the greatest benefits and least adverse effects:

  • improve ventilation–perfusion ratio (reduce intrapulmonary shunt);

  • increase FRC and lung compliance;

  • achieve PaO2 > 60 mmHg with fraction of inspired oxygen (FiO2) < 0.5;

  • avoid increasing pulmonary dead space (avoid alveolar distension);

  • avoid cardiovascular side-effects and maintain cardiac output.

Generally:

  • A PEEP of 5–10 cmH2O in an intubated patient without identifiable pulmonary pathology is considered physiological PEEP.

  • A PEEP ≤ 10 cmH2O is responsible for increasing the volume of patent alveoli.

  • A PEEP ≥ 10 cmH2O is generally responsible for alveolar recruitment.

  • The increase in alveolar volume reaches a plateau at 15 cmH2O.

  • At a PEEP > 15 cmH2O, the alveolar pressure increases without a measurable increase in alveolar diameter (beginning of side-effects).

  • The only generally accepted indication for a PEEP of 15 cmH2O or greater is ALI and ARDS.

How to optimize ventilator settings for positive end-expiratory pressure

All the studies on optimizing the ventilator settings in patients with ALI and ARDS have followed a lung-protective ventilation strategy. The optimal PEEP is still controversial and there are different methods of adjusting PEEP.

Based on the FiO2/positive end-expiratory pressure table

This uses the incremental FiO2/PEEP combination (Table 1) recommended by the NIH NHLBI ARDS clinical network to achieve the oxygenation goal.

TABLE 1

NIH NHLI ARDS clinical network: recommended FiO2/PEEP combinations (available from www.ardsnet.org/tools.shtml)

Lower PEEP/higher FiO2
FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 18–24
Higher PEEP/lower FiO2
FiO2 0.3 0.3 0.3 0.3 0.3 0.4 0.4 0.5 0.5 0.5–0.8 0.8 0.9 1.0 1.0
PEEP 5 8 10 12 14 14 16 16 18 20 22 22 22 24

Here we have to mention that, according to the NIH NHLBI ARDS clinical network, clinical outcome is similar whether lower or higher PEEP levels are used.27

Decremental positive end-expiratory pressure trials after recruitment manoeuvres with guidance on PaO2 and lung compliance

After baseline ventilation, Suh et al.28 performed a recruitment manoeuvre and PEEP was increased to 20 cmH2O or the highest PEEP guaranteeing a minimal tidal volume of 5 ml/kg. Then PEEP was decreased every 20 minutes in 2 cm decrements. The ‘optimal’ PEEP was defined as the lowest PEEP attainable without causing a significant drop (> 10%) in PaO2. Suh et al.28 found that the PaO2FiO2 ratio increased from 154.8 ± 63.3 mmHg at baseline to 290.00 ± 96.4 mmHg at the highest PEEP and to 302.7 ± 94.2 mmHg at ‘optimal’ PEEP. Static compliance was also significantly higher at ‘optimal’ PEEP (27.2 ± 10.4 ml/cmH2O) than at the highest PEEP (22.3 ± 7.7 ml/cmH2O) (P< 0.05). Suter et al.29 also found that optimum PEEP coincides with best lung compliance. Decreased compliance at the highest PEEP might indicate recruitment of some parts of the lung and distension or overdistension, if high PEEP resulted in a decrease in PaO2, in other parts.28,29 Greater compliance above the LIP in the P/V curve traced from ZEEP indicates greater improvements in lung recruitment with increasing PEEP and a highly recruitable lung.9,2628

Based on the pressure–volume curve: (quasi) static approaches or dynamic approaches

Alveolar reinflation occurs along the whole inspiratory limb of the P/V curve, which can, therefore, be considered a recruitment curve. The LIP indicates the beginning of alveolar opening and does not indicate the PEEP needed to prevent alveolar collapse. Alveolar closure occurs over a wide range of pressures along the expiratory limb of the P/V curve and LIP is a poor predictor of alveolar closure and is of limited value for determining the PEEP level required to prevent alveolar collapse. The UIP, classically seen as the beginning of overdistension, may also indicate the end of recruitment.13,26,30,31 While the inspiratory limb of the P/V curve is appropriate for studying the process of recruitment and protecting the lung from overdistension, derecruitment follows a different pattern and is related to the expiratory limb of the P/V curve. Crotti et al.,32 in patients, and Pelosi et al.,33 in an animal model, found that derecruitment is a continuous process occurring along the entire expiratory P/V curve, with no relationship with LIP, which is compatible with the results of Maggior et al.26 This may be relevant for PEEP selection, as PEEP is an expiratory and not an inspiratory phenomenon.17 Guillermo et al.30 found that PEEP adjusted at the point of maximum curvature of the deflation limb of the P/V curve was related to an improvement in oxygenation, an increase in normally aerated lung volumes, a decrease in non-aerated lung volumes and greater alveolar stability. There was also an increase in the partial pressure of arterial carbon dioxide (PaCO2), airway pressures and hyperaerated lung volume.

Positive end-expiratory pressure guided by oesophageal pressure

The idea was that mechanical ventilation should provide sufficient transpulmonary distending pressure to maintain oxygenation while minimizing repeated alveolar collapse or overdistension. Tamlor and colleagues34 described a randomized trial of mechanical ventilation strategy in which PEEP was adjusted according to the end-expiratory transpulmonary pressure. Transpulmonary pressure was measured as the difference between the airway pressure and the pleural pressure; pleural pressure was estimated from oesophageal pressure by inserting a special balloon catheter into the oesophagus. PEEP was then adjusted to produce an estimated transpulmonary pressure at end-expiration of 0–10 cmH2O, according to a sliding scale based on PaO2 and FiO2. Tidal volume was calculated to be 6 ml/kg predicted body weight, and limited to keep transpulmonary pressure at less than 25 cmH2O, the physiological value at end-inspiration. Tamlor et al.34 found that a ventilation strategy using oesophageal pressure to estimate transpulmonary pressure significantly improved oxygenation in the oesophageal pressure-guided group: the PaO2/FiO2 ratio was 88 mmHg higher than in the control group, respiratory system compliance was significantly improved and higher than in the control group, PEEP was also significantly higher than in the control group and the plateau airway pressure at end-inspiration was higher than in the control group but the transpulmonary pressure never exceeded 24 cmH2O and did not differ from that in the control group. The Tamlor study was criticized by Gusmao et al.35 because 39% of the patients in Tamlor’s study had extrapulmonary ARDS, and because of the difference in the lung and chest wall elasticity between pulmonary and extrapulmonary ARDS. Gusmao et al.35 believe that measuring oesophageal pressure to set the PEEP will not benefit patients with pulmonary ARDS.

Based on a chest computerized tomography scan or radiograph

Using chest radiography or computerized tomography (CT) in conjunction with the P/V curve and changes in gas exchange may aid the correct use of PEEP and avoid the complication of lung overdistension. Patients with ARDS normally have aerated lung regions coexisting with oedematous and atelectatic areas at ZEEP.36 The extension of non-aerated territories and the regional distribution of the loss of aeration have a major influence on the P/V curve, as mentioned earlier, and, accordingly, the level of PEEP to be used. The potential benefit of keeping the diseased lung fully open during tidal ventilation has to be balanced against the well-established risk arising from lung overinflation.7,37,38 PEEP should be individualized and the physician should evaluate the lung morphology pattern by considering chest radiographs or CT scans to choose the correct level of PEEP to avoid lung overinflation. In patients with atelectatic lower lobes coexisting with aerated upper lobes or patients whose loss of aeration has a focal distribution, high PEEP levels result in overinflation of aerated parts of the lungs, whereas lower lobes and non-aerated regions are only partially recruited.24 So the concept of ‘keeping the lung fully open during tidal ventilation’ cannot be applied to patients with focal loss of aeration without reintroducing the risk of VILI; in this situation PEEP should be limited to relatively low levels (10–12 cmH2O).7,24 In patients with ARDS without any normally aerated lung regions and diffuse bilateral hyperdensities at ZEEP, the risk of overinflation appears to be minimal even for high PEEP.24,36 The highest PEEP consistent with the administration of tidal volume providing enough CO2 elimination without reaching a plateau pressure greater than the UIP should be administered.18 The concept of keeping the lung fully open during tidal ventilation can be applied to these patients without introducing a risk of VILI and PEEP up to 20–25 cmH2O can be used.7

Adjusting positive end-expiratory pressure using electrical impedance tomography

Electrical impedance tomography (EIT) is a non-invasive, radiation-free bedside imaging technique that allows monitoring of electrical impedance within the thoracic cavity in a two-dimensional and cross-sectional plane in order to assess regional ventilation.39,40 Physiological and pathophysiological changes in the lung can be observed from the EIT images in real time at the bedside.39 Assessment of lung behaviour using EIT has the potential to tailor respiratory therapy, adjustment of tidal volumes, airway pressure, PEEP and the indication for lung recruitment.40 Titration of PEEP to avoid atelectasis and regional overdistension could be supported by EIT.4042 The influences of PEEP on regional ventilation during ARDS have been demonstrated by EIT.40,4345 Measurement of regional ventilation by EIT has been compared successfully and validated with standard methods: advanced spirometry, pathology, scintigraphy, single-photon emission CT, and dynamic and static CT.40

Recruitment manoeuvres

Recruitment manoeuvres can be accomplished by raising the transpulmonary pressure periodically and briefly to a higher level than that achieved during tidal ventilation. Recruitment manoeuvres can help in recruiting atelectatic lung regions.18,4648 The most common recruitment manoeuvres used are as follows:

  1. The maximum recruitment strategy (MRS) consists of two phases – a recruitment phase to calculate opening pressures (incremental steps under pressure-controlled ventilation up to a maximum inspiratory pressure of 60 cmH2O, at a constant driving-pressure of 15 cmH2O above PEEP) and a PEEP titration phase (decremental PEEP steps from 25 to 10 cmH2O) used to estimate the minimum PEEP to keep the lungs open.4951 MRS allows significant and long-lasting improvement in lung function.5052

  2. Sustained pulmonary inflation (SI)47,49,51 with a positive pressure of 40 cmH2O for 40 seconds, and the end manoeuvre PEEP set to 5–10 cmH2O. SI is the most popular recruitment manoeuvre and has a major impact on haemodynamics and has been shown to worsen lung damage and inflammation in experimental lung injury.51,53

  3. Prolonged recruitment manoeuvre (PRM) in which the inspiratory pressure is progressively increased every 2 minutes in steps of 5 cmH2O from 15 cmH2O to 25 cmH2O above a fixed PEEP of 15 cmH2O. The end-manoeuvre PEEP is set to 5 or 10 cmH2O. PRM improves lung function, with less damage to alveolar epithelium, resulting in reduced pulmonary injury.49,54

Clinical and experimental studies have been conducted to identify the durability of the beneficial effects of recruitment manoeuvres and when and how to perform these manoeuvres, early or late in the course of ARDS and with high or low PEEP, and which categories of patients will benefit from these manoeuvres. Gattinoni et al.55 found that the percentage of potentially recruitable lung is extremely variable in the population and strongly associated with the response to PEEP. Three prospective randomized clinical trials did not show decreased mortality with lung-protective mechanical ventilation with alveolar recruitment and application of higher PEEP levels, but higher levels of oxygenation, and improvements in relevant secondary endpoints, such as less need for rescue therapies and more ventilator-free days, were achieved.51,5658 Recruitment manoeuvres did not induce greater and more sustained improvement in SpO2 and FiO2/PEEP, and respiratory system compliance did not increase further after recruitment manoeuvres when using high PEEP during ventilation in patients with ALI and ARDS.46 Greater recruitment manoeuvre effects on arterial oxygenation and static respiratory compliance occurred while ventilating patients with ALI and ARDS with lower levels of PEEP.46,59 This may be because the higher PEEP levels achieved greater levels of recruitment than those usually achieved with traditional PEEP levels.46 Recruitment manoeuvres were successful in improving oxygenation and recruiting most of the collapsed lung tissue in early and severe ARDS and was unsuccessful and potentially haemodynamically harmful in late ARDS.50,60 Recruitment manoeuvres were effective when ventilating the patient with a low tidal volume because low tidal volume promotes progressive derecruitment, and maintaining adequate post-recruitment manoeuvre levels of PEEP is crucial in avoiding derecruitment.49,6062 Thille et al.63 found that alveolar recruitment was similar in pulmonary and extrapulmonary ARDS and that PEEP should not be determined based on the cause of ARDS. Gattinoni et al.64 found a better response to PEEP in extrapulmonary than in pulmonary ARDS, and that extrapulmonary ARDS has greater potential for recruitment than pulmonary ARDS. The potential for recruitment was more than 50% of the lung in experimental extrapulmonary ARDS,33,62 whereas the potential for recruitment was only 6% in a clinical study on pulmonary ARDS.32,62 Significant recruitment manoeuvre effects on oxygenation at 1 hour were observed in another study in which 16/20 patients had pulmonary ALI, but only when lower PEEP levels and neuromuscular relaxants were used.46 The use of muscle relaxants during the recruitment manoeuvre was recommended by the American–European Consensus Conference on ARDS part 2.15 Lim et al.59 found that recruitment manoeuvres had a longer-lasting effect on oxygenation and lung compliance when using muscle relaxants with proper sedation. Spieth et al.51 stated that routine use of recruitment manoeuvres is not recommended, but higher PEEP levels are indicated. Recruitment manoeuvres are not without risks, and attention is required when performing them to allow early detection and management of possible complications such as hypotension, low SpO2 and barotrauma.46 Other complications are stress injury of more compliant lung units, redistribution of blood flow and increasing intrapulmonary shunt due to alveolar overdistension.65

References

1. 

Davis PD, Kenny GNC. Basic Physics and Measurement in Anaesthesia, 5th edn. London: Butterworth-Heinemann; 2003.

2. 

Miller RD. Anesthesia, 4th edn. New York: Churchill Livingstone; 1994.

3. 

Morgan GE Jr, Mikhail MS, Murray MJ. Clinical Anesthesiology, 4th edn. USA: McGraw-Hill; 2006.

4. 

Al-Shaikh B, Stacey S. Essentials of Anaesthetic Equipment, 3rd edn. Philadelphia: Churchill Livingstone; 2007.

5. 

MacIntyre NR. Principles of mechanical ventilatory support. Adult Multiprofessional Critical Care Review Course 2005: 203–8.

6. 

Putensen C, Baun M, Hormann C. Selecting ventilator settings according to variables derived from the quasi-static pressure/volume relationship in patients with acute lung injury. Anesth Analg 1993; 77:436–47. http://dx.doi.org/10.1213/00000539-199309000-00004

7. 

Rouby JJ, Lu Q, Goldstein I. selecting the right level of positive end-expiratory pressure in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2002; 165:1182–6. http://dx.doi.org/10.1164/ajrccm.165.8.2105122

8. 

Malo J, Wood LD. How does positive end-expiratory pressure reduces intrapulmonary shunt in canine pulmonary edema? J Appl Physiol 1984; 57:1002–10.

9. 

Maggiore SM, Brochard L. Pressure–volume curve in the critically ill. Curr Opin Crit Care 2000; 6:1–10. http://dx.doi.org/10.1097/00075198-200002000-00001

10. 

Muscedere JG, Mullen JBM, Gari K, Slutsky AS. Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994; 149:1327–34. http://dx.doi.org/10.1164/ajrccm.149.5.8173774

11. 

Slutsky AS, Tremblay LN. Multiple system organ failure: is mechanical ventilation a contributing factor? Am J Respir Crit Care Med 1998; 157:1721–5. http://dx.doi.org/10.1164/ajrccm.157.6.9709092

12. 

Chiumello D, Pristine G, Slutsky AS. Mechanical ventilation affects local and systemic cytokines in an animal model of acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 160:109–16. http://dx.doi.org/10.1164/ajrccm.160.1.9803046

13. 

Maggiore SM, Richard J-C, Brochard L. What has been learnt from P/V curves in patients with acute lung injury/acute respiratory distress syndrome? Eur Respir J 2003; 22(Suppl. 42):22–6. http://dx.doi.org/10.1183/09031936.03.00004204

14. 

Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema: respective effects of high airway pressure, high tidal volume and positive end-expiratory pressure. Am Rev Respir Dis 1988; 137:1159–64. http://dx.doi.org/10.1164/ajrccm/137.5.1159

15. 

Artigas A, Bernard GB, Carlet J, et al. The American European Consensus conference on ARDS, part 2. Ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling. Am J Respir Crit Care Med 1998; 157:1332–47. http://dx.doi.org/10.1164/ajrccm.157.4.ats2-98

16. 

The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301–8. http://dx.doi.org/10.1056/NEJM200005043421801

17. 

Kallet RH. Evidence-based management of acute lung injury and acute respiratory distress syndrome. Respir Care 2004; 49:793–809.

18. 

Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective–ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338:347–54. http://dx.doi.org/10.1056/NEJM199802053380602

19. 

Ranieri VM, Suter PM, Totorella C, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA 1999; 282:54–61. http://dx.doi.org/10.1001/jama.282.1.54

20. 

Terragni PP, Rosboch GL, Lisi A, Viale AG, Ranieri VM. How respiratory system mechanics may help in minimizing ventilator-induced lung injury in ARDS patients. Eur Respir J 2003; 22(Suppl. 42):15–21. http://dx.doi.org/10.1183/09031936.03.00420303

21. 

Pelosi P, Gattinoni L. Respiratory mechanics in ARDS: a siren for physicians? Intensive Care Med 2000; 26:653–6. http://dx.doi.org/10.1007/s001340051227

22. 

Jonson B, Svantesson C. Elastic pressure–volume curves: what information do they convey? Thorax 1999; 54:82–7. http://dx.doi.org/10.1136/thx.54.1.82

23. 

Vieira SR, Puybasset L, Lu Q, et al. A scanographic assessement of pulmonary morphology in acute lung injury. Significance of the lower inflection point detected on the lung pressure-volume curve. Am J Respir Crit Care Med 1999; 159:1612–23. http://dx.doi.org/10.1164/ajrccm.159.5.9805112

24. 

Rouby JJ, Puybasset L, Cluzel P, Richecoeur J, Lu Q, Grenier P. Regional distribution of gas and tissue in acute respiratory distress syndrome. II. Physiological correlations and definition of an ARDS severity. Intensive Care Med 2000; 26:1046–56. http://dx.doi.org/10.1007/s001340051317

25. 

Maggiore S, Jonson B, Richard J-C, Jaber S, Lemaire F, Brochard L. Alveolar derecruitment at decremental positive end-expiratory pressure level in acute lung injury. Comparison with the lower inflection point, oxygenation and compliance. Am J Respir Crit Care Med 2001; 164:795–801. http://dx.doi.org/10.1164/ajrccm.164.5.2006071

26. 

Jonson B, Richard JC, Straus C, Mancebo J, Lemaire F, Brochard L. Pressure-volume curves and compliance in acute lung injury. Evidence of recruitment above the lower inflection point. Am J Respir Crit Care Med 1999; 159:1172–8. http://dx.doi.org/10.1164/ajrccm.159.4.9801088

27. 

Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with acute respiratory distress syndrome. N Engl J Med 2004; 351:327–36. http://dx.doi.org/10.1056/NEJMoa032193

28. 

Suh GY, Yoon JY, Park SJ, et al. A practical protocol for titrating Optimal PEEP in acute lung injury: recruitment maneuver and PEEP decrement. J Korean Med Sci 2003; 18:349–45. http://dx.doi.org/10.3346/jkms.2003.18.3.349

29. 

Suter PM, Barrie H, Isenberg MD. Optimum End-Expiratory airway pressure in patients with acute pulmonary failure. N Engl J Med 1975; 292:284–9. http://dx.doi.org/10.1056/NEJM197502062920604

30. 

Guillermo MA, Luis HL, Diego P, et al. Inspiratory vs. expiratory pressure–volume curves to set end-expiratory pressure in acute lung injury. Intensive Care Med 2005; 31:1370–78. http://dx.doi.org/10.1007/s00134-005-2746-6

31. 

Hickling KG. The pressure-volume curve is greatly modified by recruitment. A mathematical model of ARDS lungs. Am J Respir Crit Care Med 1998; 158:194–202. http://dx.doi.org/10.1164/ajrccm.158.1.9708049

32. 

Crotti S, Mascheroni D, Caironi P, et al. Recruitment and derecruitment during acute respiratory distress failure. A clinical study. Am J Respir Crit Care Med 2001; 164:131–40. http://dx.doi.org/10.1164/ajrccm.164.1.2007011

33. 

Pelosi P, Goldner M, McKibben A, et al. Recruitment and derecruitment during acute respiratory failure: an experimental study. Am J Respir Crit Care Med 2001; 164:122–30. http://dx.doi.org/10.1164/ajrccm.164.1.2007010

34. 

Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008; 359:2095–104. http://dx.doi.org/10.1056/NEJMoa0708638

35. 

Gusmao D, Tanner AC, Teles JM. Correspondence. Esophageal pressure in acute lung injury. N Engl J Med 2009; 8:831–3.

36. 

Puybasset L, Gluzel P, Gusman P, Grenier P, Preteux F, Rouby JJ. Regional distribution of gas and tissue in acute respiratory distress syndrome – part 1: consequences on lung morphology. Intensive Care Med 2000; 26:847–63.

37. 

Goldstein I, Bughalo MT, Marquette CH, Lenaour G, Lu Q, Rouby JJ; Experimental ICV Study Group. Mechanical ventilation-induced air-space enlargement during experimental pneumonia in piglets. Am J Respir Crit Care Med 2001; 163:958–64. http://dx.doi.org/10.1164/ajrccm.163.4.2006072

38. 

Rouby JJ, Lherm T, Martin de Lassale E, et al. Histologic aspects of pulmonary barotrauma in critically ill patients with acute respiratory failure. Intensive Care Med 1993; 19:383–9. http://dx.doi.org/10.1007/BF01724877

39. 

Pomprapa A, Schwaiberger D, Pickerodt PH, Tjarks O, Lachmann B, Leonhardt S. Automatic protective ventilation using the ARDSNet protocol with the additional monitoring of electrical impedance tomography. Crit Care 2014; 18:R128. http://dx.doi.org/10.1186/cc13937

40. 

Bodenstein M, David M, Markstaller K. Principles of electrical impedance tomography and its clinical application. Crit Care Med 2009; 37:713–24. http://dx.doi.org/10.1097/CCM.0b013e3181958d2f

41. 

Dueck R. Alveolar recruitment versus hyperinflation: a balancing act. Curr Opin Anaesthesiol 2006; 19:650–54. http://dx.doi.org/10.1097/ACO.0b013e328011015d

42. 

Hinz J, Gehoff A, Moerer O, et al. Regional filling characteristics in the lungs in mechanically ventilated patients with acute lung injury. Eur J Anaesthesiol 2007; 24:414–24. http://dx.doi.org/10.1017/S0265021506001517

43. 

Kunst PW, de Vries PM, Postmus PE, Bakker J. Evaluation of electrical impedance tomography in the measurement of PEEP-induced changes in lung volume. Chest 1999; 115:1102–6. http://dx.doi.org/10.1378/chest.115.4.1102

44. 

Hinz J, Morer O, Neumann P, Dudykerych T, Hellige G, Quintel M. Effect of positive end-expiratory pressure on regional ventilation in patients with acute lung injury evaluated by electrical impedance tomography. Eur J Anaesthesiol 2005; 22:817–25. http://dx.doi.org/10.1017/S0265021505001377

45. 

Barbas CS, de Matos GF, Pincelli PM, et al. Mechanical ventilation in acute respiratory failure: recruitment and high positive end-expiratory pressure are necessary. Curr Opin Crit Care 2005; 11:18–28. http://dx.doi.org/10.1097/00075198-200502000-00004

46. 

Brower RG, Morris A, MacIntyre N, et al. Effects of recruitment maneuvers in patients with acute lung injury and acute respiratory distress syndrome ventilated with high positive end-expiratory pressure. Crit Care Med 2003; 31:2592–7. http://dx.doi.org/10.1097/01.CCM.0000090001.91640.45

47. 

Lapinsky SE, Aubin M, Mehta S. Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure. Intensive Care Med 1999; 25:1297–301. http://dx.doi.org/10.1007/s001340051061

48. 

Rimensberger PC, Cox PN, Frndova H, Bryan AC. The open lung during small tidal volume ventilation: concepts of recruitment and “optimal positive end-expiratory pressure”. Crit Care Med 1999; 27:1946–52. http://dx.doi.org/10.1097/00003246-199909000-00038

49. 

Das A, Cole O, Chikhani M, et al. Evaluation of lung recruitment maneuvers in acute respiratory distress syndrome using computer simulation. Crit Care 2015; 19:8. http://dx.doi.org/10.1186/s13054-014-0723-6

50. 

de Matos GF, Stanzani F, Passos RH, et al. How large is the lung recruitability in early acute respiratory distress syndrome: a prospective case series of patients monitored by computed tomography. Crit Care 2012; 16:R4. http://dx.doi.org/10.1186/cc10602

51. 

Spieth PM, de Abreu MG. Lung recruitment in ARDS: we are still confused but on a higher PEEP level. Crit Care 2012; 16:108.

52. 

Borges JB, Okamoto VN, Matos GFJ, et al. Reversibility of lung collapse and hypoxemia in early acute respiratory distress syndrome. Am J Respir Crit Care 2006; 174:268–78. http://dx.doi.org/10.1164/rccm.200506-976OC

53. 

Silva PL, Cruz FF, Fujisaki LC, et al. Hypervolemia induces and potentiates lung damage after recruitment maneuver in model of sepsis–induced acute lung injury. Crit Care 2010; 14:R114. http://dx.doi.org/10.1186/cc9063

54. 

Rzezinski AF, Oliveira GP, Santiago VR, et al. Prolonged recruitment maneuver improves lung function with less ultrastructural damage in experimental mild acute lung injury. Respir Physiol Neurobiol 2009; 169:271–81. http://dx.doi.org/10.1016/j.resp.2009.10.002

55. 

Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med 2006; 354:1775–86. http://dx.doi.org/10.1056/NEJMoa052052

56. 

Mercat A, Richard JM, Vielle B, et al. Positive end-expiratory setting in adult with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299:646–55. http://dx.doi.org/10.1001/jama.299.6.646

57. 

Meade MO, Cook DJ, Guyatt GH, et al. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299:637–45. http://dx.doi.org/10.1001/jama.299.6.637

58. 

Briel M, Mead M, Mercat A, et al. Higher versus lower positive end-expiratory pressures in patients with the acute lung injury and acute respiratory distress syndrome. Systematic review and Meta-analysis. JAMA 2010; 303:865–73. http://dx.doi.org/10.1001/jama.2010.218

59. 

Lim CM, Koh Y, Pak W, et al. Mechanistic scheme and effect of “distended sigh” as a recruitment maneuver in patients with acute respiratory distress syndrome. Crit Care Med 2001; 29:1255–60. http://dx.doi.org/10.1097/00003246-200106000-00037

60. 

Grasso S, Mascia L, Turco MD, et al. Effects of recruitment maneuvers in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology 2002; 96:795–802. http://dx.doi.org/10.1097/00000542-200204000-00005

61. 

Richard JC, Maggiore SM, Jonson B, Mancebo J, Lemaire F, Brochard L. Influence of tidal volume on alveolar recruitment. Am J Respir Crit Care Med 2001; 163:1609–13. http://dx.doi.org/10.1164/ajrccm.163.7.2004215

62. 

Lim CM, Jung H, Koh Y, et al. Effect of alveolar recruitment maneuver in early acute respiratory distress syndrome according to antiderecruitment strategy, etiological category of diffuse lung injury, and body position of the patient. Crit Care Med 2003; 31:411–18. http://dx.doi.org/10.1097/01.CCM.0000048631.88155.39

63. 

Thille AW, Richard JC, Maggiore SM, Ranieri VM, Brochard L. Alveolar recruitment in pulmonary and extrapulmonary acute respiratory distress syndrome. Anesthesiology 2007; 106:212–17. http://dx.doi.org/10.1097/00000542-200702000-00007

64. 

Gattinoni L, Pelosi P, Suter PM, Pedota A, Vercesi P, Lissoni A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med 1998; 158:3–11. http://dx.doi.org/10.1164/ajrccm.158.1.9708031

65. 

Villagra A, Ochagavia A, Vatua S, et al. Recruitment maneuvers during lung protective ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med 2002; 165:165–70. http://dx.doi.org/10.1164/ajrccm.165.2.2104092




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