Skip to main content

Clinical review: Respiratory monitoring in the ICU - a consensus of 16


Monitoring plays an important role in the current management of patients with acute respiratory failure but sometimes lacks definition regarding which 'signals' and 'derived variables' should be prioritized as well as specifics related to timing (continuous versus intermittent) and modality (static versus dynamic). Many new techniques of respiratory monitoring have been made available for clinical use recently, but their place is not always well defined. Appropriate use of available monitoring techniques and correct interpretation of the data provided can help improve our understanding of the disease processes involved and the effects of clinical interventions. In this consensus paper, we provide an overview of the important parameters that can and should be monitored in the critically ill patient with respiratory failure and discuss how the data provided can impact on clinical management.


Monitoring plays an important role in the current management of patients with acuterespiratory failure. However, unlike monitoring of other organs and functions,monitoring of respiratory function in the critically ill sometimes lacks definitionregarding which 'signals' and 'derived variables' should be prioritized as well asspecifics related to timing (continuous versus intermittent) and modality (static versusdynamic). In this consensus paper, we summarize current modes of respiratory monitoringand their potential practical applications (Table 1). The amountof text devoted to each modality varies according to perceived familiarity with thetechnique: more text is dedicated to novel strategies and those with newerindications.

Table 1 Summary of the different monitoring techniques

Monitoring systems

1. Gas exchange

Pulse oximetry and transcutaneous carbon dioxide monitoring

Pulse oximetry is widely used in anesthesiology and intensive care and, inintensive care unit (ICU) patients, has a bias of less than 1% and a good tomoderate precision [1]; accuracy decreases in hypoxemia (oxygen saturation as measured bypulse oximetry, or SpO2, of less than 90%). Among the intrinsiclimitations of pulse oximetry are that it is insensitive to changes in arterialpartial pressure of oxygen (PaO2) at high PaO2 levels andcannot distinguish between normal hemoglobin and methemoglobin orcarboxyhemoglobin. Nail polish may affect the measurement by about 2% (not reallyclinically relevant) [2], and pulse oximetry can slightly underestimate arterial oxygensaturation (SaO2) in patients with darkly pig-mented skin [3]. Altered skin perfusion and carboxy-hemoglobin can also lead toinaccurate pulse oximetry readings. The type of probe can make a difference, andaccuracy is usually better for finger than for earlobe probes [4]. False alarms are common, usually because of motion artifacts,particularly in the pediatric population.

Pulse oximetry readings should be used to provide an early warning sign,decreasing the need for blood gas measurements. In a randomized controlled trialin more than 20,000 surgical patients [5], pulse oximetry was not associated with decreased postoperativecomplications or mortality, but 80% of the anesthesiologists felt more secure whena pulse oximeter was used!

Transcutaneous partial pressure of carbon dioxide (PCO2) monitors havealso been developed with probes generally placed on the earlobe. Precision oftranscutaneous PCO2 measurements has improved as technology hasadvanced, and devices have become smaller but still need regular recalibration [6]. Their place in the respiratory monitoring of ICU patients has not yetbeen defined.

Volumetric capnography and dead space calculation

The expiratory capnogram provides qualitative information on the waveform patternsassociated with mechanical ventilation and quantitative estimation of expiredCO2. Capnography tracings show three phases (Figure 1) [7]: phase I contains gas from the apparatus and anatomic dead space(airway), phase II represents increasing CO2 concentration resultingfrom progressive emptying of alveoli, and phase III represents alveolar gas. PhaseIII is often referred to as the plateau and its appearance is relatively flat orhas a small positive slope; the highest point is the end-tidal PCO2 (PetCO2). The almost rectangular shape of the expiredcapnogram depends on the homogeneity of the gas distribution and alveolarventilation. Lung heterogeneity creates regional differences in CO2 concentration, and gas from high V/Q regions first appears in the upperairway during exhalation. This sequential emptying contributes to the rise of thealveolar plateau; the greater the V/Q heterogeneity, the steeper the expiredCO2 slope. Accordingly, the slope of the alveolar plateau has beenshown to correlate with the severity of airflow obstruction [8].

Figure 1
figure 1

The three phases of capnography tracings. Phase I contains gas fromthe apparatus and anatomic dead space (airway), phase II representsincreasing carbon dioxide concentration resulting from progressive emptyingof alveoli, and phase III represents alveolar gas. The highest point ofphase III is the end-tidal partial pressure of carbon dioxide(PetCO2). PaCO2, arterial partial pressure ofcarbon dioxide; PCO2, partial pressure of carbon dioxide.

Physiologic dead space (Vdphys) can be easily calculated from the Enghomodification of the Bohr equation by using arterial partial pressure of carbondioxide (PaCO2) with the assumption that PaCO2 is similar toalveolar PCO2:

V d phys / V T = ( PaC O 2 - P E C O 2 ) / PaC O 2 ,

where VT is the tidal volume and PECO2 is thepartial pressure of CO2 in mixed expired gas and is equal to the meanexpired CO2 fraction multiplied by the difference between theatmospheric pressure and the water vapor pressure. Vdphys is increasedin acute respiratory distress syndrome (ARDS), and a high dead space fractionrepresents an impaired ability to excrete CO2 because of any kind ofV/Q mismatch. Several authors [9, 10] have demonstrated that increased Vdphys values areindependently associated with an increased risk of death in these patients.

Since Vdphys/VT measures the fraction of each tidal breath that iswasted on alveolar dead space (Vdalv) and airway dead space(Vdaw), the Vdaw must be subtracted from Vdphys/VT to obtain the Vdalv/VT [11]. By using the PetCO2 instead of PECO2 in theequation, the Vdalv can be calculated. Equating the alveolar PCO2 to the arterial PaCO2 is, however, valid only in healthy subjects. Inpatients with high right-to-left shunt, PaCO2 is higher than alveolarPCO2 because of the shunted blood with high PvCO2 (partialpressure of carbon dioxide in mixed venous blood). Without correction [12], it must be remembered that a high dead space also includes the shunteffect.

PaCO2 can be grossly estimated by PetCO2. Monitoring PetCO2 can also help to track PaCO2 when changes in PaCO2 are to beavoided (especially in critically ill, neurological patients with normal lungs). Thegradient between PaCO2 and PetCO2 widens in ARDS and correlatesacross the different levels of Vdphys [13]. The difference between PaCO2 and PetCO2 is reduced byusing the maximal values of PetCO2 over time [14].

In patients with sudden pulmonary vascular occlusion due to pulmonary embolism, theresultant V/Q mismatch produces an increase in Vdalv. When volumetriccapnography is used as a bedside technique, the association of a normal D-dimer assayresult plus a normal Vdalv is a highly sensitive screening test to rule outthe diagnosis of pulmonary embolism [15]. Volumetric capnography has also been shown to be an excellent tool formonitoring thrombolytic efficacy in patients with pulmonary embolism [16].

When the application of positive end-expiratory pressure (PEEP) results in global lungrecruitment, physiologic and alveolar dead space decrease [17]; the reverse is true when PEEP application results in lung overdistension [18]. Therefore, volumetric capnography may also be helpful to identifyoverdistension or better alveolar gas diffusion [19].

In summary, volumetric capnography has important potential for monitoring thedifficult-to-ventilate patient. Volumetric capnography needs sophisticated equipment andthis has limited its widespread use.

Blood gases

The PaO2/inspired fraction of oxygen (PaO2/FiO2)ratio is still the most frequently used variable for evaluating the severity of lungfailure and is included in the current definition of acute lung injury/ARDS [20]. The PaO2/FiO2 ratio is often a curvilinear(U-shaped) relationship, being at its lowest for moderate ranges of FiO2,depending on the shunt level, the hemoglobin value, and the arteriovenous differencein O2 content [2123]. For a given PaO2/FiO2 ratio, the higher theFiO2, the poorer the prognosis [24]. In patients with ARDS, the PaO2/FiO2 ratio isdependent on the PEEP level and can be a surrogate, though imperfect, marker ofrecruitment [25]. Hemodynamic status (via the mixed venous oxygen tension, orPvO2) and intracardiac shunt (patent foramen ovale) also influence thePaO2/FiO2 ratio [26]. Despite its limitations, this ratio remains the most commonly used meansof assessing severity of lung disease. The oxygen index ([mean airway pressure ×FiO2 × 100]/PaO2) accounts better for the influence ofventilator pressures on oxygenation value [27].

PaCO2-related variables are tightly correlated to outcome [28] and to lung structural changes [29] sometimes better than oxygen-related variables (such as shunt fraction) [30, 31].

Extravascular lung water

Extravascular lung water (EVLW) is a quantitative measure of pulmonary edema and iscorrelated, in multiple patient populations, to mortality [32]. Normal values are 5 to 7 mL/kg (indexed to predicted body weight), andquantities above 10 mL/kg are associated with adverse clinical outcomes [33].

Indicator dilution techniques for measuring EVLW are available for bedside use incritically ill patients. The single-indicator technique is now well validated andoffers the additional value of simultaneously measuring cardiovascular performance(cardiac output, fluid res-ponsiveness, and filling volumes). Current technology usesan injection of cold saline into the right atrium and assesses transpulmonarythermodilution in the arterial system by using a femoral or brachial catheter.Limitations of the technique include requirements for good indicator mixing withoutloss and for constant blood flow and temperature. EVLW can be assessed only inperfused areas of the lung [34].

EVLW measurements may be used in combination with other cardiovascular and pulmonaryparameters to diagnose pulmonary edema. Complementary information from indicatordilution techniques, such as cardiac filling volumes, helps to differentiate betweenhydrostatic/cardiogenic pulmonary edema and permeability edema [35]. Although repeated measures could be used to assess response tointerventions [35], it is unclear how fast the response time is and whether this techniquecan be used as a tool to guide therapy.

2. Respiratory mechanics

Compliance and resistance

Monitoring airway pressures can provide important information. In flow (volume)-controlled mode, peak airway pressure is determined by both resistance andcompliance - a high peak pressure with a much lower plateau pressure indicates a highresistance related either to the patient (bronchospasm) or to the equipment(small-diameter endotracheal tube [ETT] or narrow or obstructed tubing). Plateaupressure measurement requires a pause at end-insufflation of at least 200 to 500 mswith a quasi-steady pressure. Longer pauses may be required to precisely estimatelung homogeneities or pendelluft phenomena but their clinical role is unclear.Patients must be relaxed during this measurement.

Compliance is easily calculated as the ratio between VT and plateaupressure minus PEEP (Figure 2). Elastance is the reverse ofcompliance (how much pressure we need for a given volume). A low compliance-highelastance reflects mainly a small aerated lung available for ventilation. Highplateau pressure may be related to either low compliance or high end-expiratorypressure (flow limitation or dynamic hyperinflation). Peak airway pressure is verysensitive to changes in respiratory mechanics; performing end-inspiratory andend-expiratory pauses may allow the exact cause of a high peak airway pressure to bedetermined. Compliance is not easily assessed on pressure-predetermined modes,especially when the expiratory phase starts before flow stops. In such cases, anend-inspiratory occlusion test should be performed to assess plateau pressure, evenin time-cycled pressure-limited modes.

Figure 2
figure 2

Analysis of airway pressures and flow during volume-controlled mechanicalventilation. The difference between peak or maximal pressure(Pmax) and plateau pressure (Pplat) defines theresistive pressure, whereas the difference between Pplat andpositive end-expiratory pressure (PEEP) defines the elastic pressure. Analysisof the airway pressure shape during the phase of constant flow inflation(removing initial and final parts) can be used to calculate the stress index(arrow).

Measurements of respiratory mechanics are simple to perform and provide useful andrelevant information for severity assessment and ventilator management. They arereally reliable only in passive conditions of ventilation, in which plateau pressuremonitoring is essential for adequate ventilatory management.

Pressure/volume curves

The study of lung mechanics is particularly helpful in patients with ARDS. Study ofpressure/volume (P/V) curves requires insufflations at very low flow to avoid theinfluence of the resistive components [3638]. The accent has often been placed on identification of the lower (LIP) [39] and upper (UIP) [40] inflection points on the P/V curve, but this approach has limitations.First, identifying the LIP or UIP is sometimes difficult. Second, recruitment takesplace throughout the P/V curve [41, 42], and recruitment and overdistension can occur at the same time. Third,application of an optimal PEEP level should, ideally, be assessed from the expiratoryrather than the inspiratory limb of this relationship.

Interpretation of P/V curves is difficult in the presence of altered chest compliance [43]. Chest wall compliance may be decreased in cases of increased abdominalpressure, thoracic trauma, large pleural effusions, obesity, and so on. Measuringesophageal pressure (surrogate of pleural pressure) allows pressure dissipatedthrough the chest wall to be differentiated from pressure distending the lungs(transpulmonary pressure). In medical patients, the chest wall has little to modestimpact on respiratory pressures [43]; whether this is different in patients with abdominal surgery or obesityneeds further study. Never-theless, the concept remains that ventilating down to toolow a pressure may result in so-called atelectrauma (opening and closing the alveolirepeatedly), and inflating the lungs too much when most of the recruitment hasalready occurred may result in overdistension.

The difference between the inspiratory and expiratory parts of the P/V curve arerelated, in part, to hysteresis [44], which reflects whether PEEP should be increased or not. If the two limbsof the curve are superimposed, increasing PEEP will not help; if there is a largedifference in volume between inspiratory and expiratory portions, PEEP may help(Figure 3). Quantification of recruitment requires multiple P/Vcurves [45], and, although P/V curves are now more frequently available on commercialventilators, the lack of an estimate of recruitment still limits clinical usefulness.The P/V curve technique has thus been used mainly as a research tool.

Figure 3
figure 3

Pressure (horizontal axis)-volume (vertical axis) loop obtained in a sedatedand paralyzed patient with acute respiratory distress syndrome (ARDS) by themeans of a supersyringe with successive small steps of inflation anddeflation. The static pressure volume points are fitted with an S-shapedline with obvious lower and upper inflections (at 10 and 25 cm H2O,respectively). The whole loop shows a marked hysteresis, and there is an upperdeflation inflection at about 20 cm H2O. Paw, airwaypressure.

During constant flow insufflations, a stress index (Figure 2)can be calculated from the shape of the airway pressure-versus-time curve (which isessentially the opposite of the P/V curve since during constant flow time equalsvolume) [46]. If there is downward concavity, compliance improves over time (stressindex of less than 1), reflecting tidal recruitment of collapsed alveoli; if thecurve is straight (stress index of 1), compliance is constant, reflecting ventilationof the normal lung; and if there is upward concavity (stress index of greater than1), it means that compliance is decreasing over time during insufflations, reflectingoverinflation. A stress index of less than 1 may suggest a need to increase PEEP; astress index of greater than 1 may suggest a need to reduce VT [47]. The same limitations described for the P/V curve (that is, recruitmentand overdistension) apply to this kind of analysis. The clinical place andreliability of the stress index are still debated [48].

Diaphragmatic function

Mechanical ventilation has been associated with ventilator-induced diaphragmaticdysfunction [49]. Diaphragmatic function can be altered early and is related to theduration of mechanical ventilation [50]. The trans-diaphragmatic pressure difference (gastric minus esophagealpressure) reflects diaphragmatic function but only in patients who have spontaneousventilatory breaths and who can cooperate. Magnetic phrenic stimulation can be usedto assess diaphragmatic function [51] as a non-invasive method in sedated and non-sedated patients but remains atest of respiratory muscle function rather than a monitoring tool and is used mainlyin research.

Measurements of diaphragmatic electrical activity are now possible and have been usedto drive the ventilator during neurally adjusted ventilatory assist [52]. Although it does not provide absolute values, monitoring diaphragmaticelectrical activity may be of potential interest to detect patient-ventilatorasynchrony.

Pressure and flow monitoring to assess asynchrony

A considerable amount of information can be obtained from pressure and flow timecurve analysis [53]. The airflow trace can reveal the presence of auto-PEEP, when flow doesnot return to zero at the end of expiration (Figure 4).Dyssynchrony can be caused by poor or delayed ventilator triggering or cycling orboth. Excessive levels of pressure support may result in ineffective triggeringbecause they are associated with long inspiratory times and intrinsic PEEP [54], and insufficient assistance (for example, because of a short inspiratorytime during assist/control ventilation) can also result in dyssynchrony.Auto-cycling, which results in excessive assistance and can be due to excessivetriggering sensitivity or leaks, is difficult to detect. It may be revealed byreducing trigger sensitivity during a short series of 'test' breaths. Decreasinglevels of pressure support and increasing expiratory trigger are the most effectivesolutions for ineffective efforts, whereas applying some PEEP may help but does notalways work [55].

Figure 4
figure 4

Example of a flow wave shape typical of expiratory flow limitation andintrinsic positive end-expiratory pressure (PEEP). Qualitative analysisof the expiratory part of the curve provides this information. Exp, expiration;Insp, inspiration.

Recognizing dyssynchrony is important because it can indicate dynamic hyperinflationand may lead to excessive ventilatory assistance [55] and induce delays in weaning from mechanical ventilation [56] and severe sleep disruption [57]. There is no automatic method to detect dyssynchrony. Because of theclinical importance of dyssynchrony, one must learn how to recognize it from traceson the ventilator (this can be relatively easy, at least for gross asynchronies) [56] (Figure 5), and improved bedside training of curvereading is needed. Electromyography can also be of use in determining the presence ofdyssynchrony but is rather complex for clinical use [58].

Figure 5
figure 5

Example of ineffective efforts demonstrated on the esophageal pressureanalysis. These missing efforts can be easily recognized on the airwaypressure trace and the fl ow trace as indicated by the arrows. Id, idem.

Work of breathing

Work of breathing (WOB) represents the integral of the product of volume andpressure. It represents the energy associated with a given VT at a givenpressure (spontaneous, mechanical, or both) [59]. The airway pressure is the pressure of the whole respiratory system(lungs plus chest wall); the transpulmonary pressure is the pressure needed todistend the lung parenchyma (airway pressure minus the pleural pressure); finally,the pleural pressure is the pressure needed to distend the chest wall. In theclinical/physiological setting, esophageal pressure is used as a surrogate forpleural pressure. 'Work' is not the same as 'effort' - effort without volumegeneration will not result in increased WOB. Normal WOB values range between 0.2 and1 J/L.

In paralyzed patients with mechanical ventilation, plots of airway pressure versusVT indicate the total amount of work needed to inflate the respiratorysystem (that is, the work done by the ventilator on the whole respiratory system andthe ETT). This is not the amount of work performed by the respiratory muscles, forwhich esophageal (pleural) pressure measurements are needed. One also needs to knowthe slope of the passive P/V curve of the chest wall (which denotes the relaxation ofthe respiratory muscles). The surface encompassed within the passive P/V curve of thechest wall and the negative esophageal pressure swing during an inspiratory effort isshown in the so-called Campbell diagram [60, 61]. Finally, the two components of work (that is, elastic and resistive) canbe split by joining the zero flow points at the beginning and the end of inspiration(Figure 6). The Campbell diagram allows the true work performedby the respiratory muscles to be estimated under different clinical conditions, evenwhen auto-PEEP is present [60, 61].

Figure 6
figure 6

Campbell diagram with all of its components. The horizontal axis showsthe esophageal pressure (the surrogate of pleural pressure), and the verticalaxis denotes volume above end-expiration. The fitted points to the left of thered line indicate the decrease in esophageal pressure during inspiration, andthe points to the right of the red line indicate the esophageal pressure duringexpiration. The red line joins the points of zero flow at the beginning and theend of inspiration. The continuous black line to the right of the diagramdenotes the chest wall compliance when muscles are relaxed, and the paralleldotted line joining the zero flow point at the beginning of inspiration is usedto account for the presence of intrinsic positive end-expiratory pressure(PEEP) (the horizontal distance between the continuous and the dotted blacklines). The surface to the left of the red line is the resistive component ofwork, and the surface to the right of this red line is the elastic component ofwork, including the elastic component of work due to the presence of intrinsicPEEP (about 3 cm H2O in this example). The elastic work due to theintrinsic PEEP is the surface of the rectangle with base equal to intrinsicPEEP (the horizontal distance between the continuous and the dotted blacklines) and height equal to tidal volume (about 360 mL in the example).Pes, esophageal pressure.

Calculation of WOB may also be useful in under-standing weaning failure. Jubran andcolleagues [62] showed that the esophageal pressure trend during a spontaneous breathingtrial (SBT) complemented the prediction of weaning outcome provided by thefrequency/VT index measured during the first minute of an SBT.Monitoring WOB can also theoretically help in titrating ventilator support. It couldalso be used to evaluate the effects of different ventilatory modes, understand themechanisms of disease (weaning failure, acute asthma, and exacerbations of chronicobstructive pulmonary disease (COPD)), and evaluate the effects of therapeuticinterventions (for example, bronchodilators [63]) and the influence of ventilator performance (triggering, flow delivery,and so on). Because it requires esophageal pressure measurement, this technique hasbeen reserved largely for clinical research. It has potential for clinical use butfew monitors provide bedside calculations.

Occlusion pressure (P0.1)

The occlusion pressure, also referred to as P0.1, reflects the respiratorydrive to breathe and is correlated to WOB for a given patient. Measurements ofP0.1, now automatically provided on ventilators, may be useful toassess the patient's response to titration of ventilator settings (that is, flowrate, PEEP, and so on) and could be used as a surrogate of WOB to help titratepressure support or external PEEP in cases of intrinsic PEEP [60, 64]. A P0.1 of less than 2 cm H2O is considered normal.This measure has been restricted largely to research. However, because the P0.1 is now more widely available in the ICU and is an extremely simple and rapidway to estimate central respiratory drive, its potential clinical role needs to beevaluated.

Pressure-time product

The pressure- time product is the integral of the pressure performed by therespiratory muscles during inspiration or expiration and time or both. Thepressure-time product is an alternative to WOB and has some theoretical and practicaladvantages over WOB calculations. The pressure -time product is associated withoxygen consumption by the respiratory muscles [65] and could be considered a surrogate to quantify the metabolic expense ofrespiratory effort. Since it is independent from the ability of the patient togenerate volume, the pressure-time product is relevant in situations in which thereis a disconnection between effort and volume (for example, during asynchrony) [66]. Normal values for the pressure-time product range between 60 and 150 cmH2O/second per minute [67].

Transpulmonary and esophageal pressure

Transpulmonary pressure is the difference in pressure between the inside (alveoli)and the outside (pleural space) of the lung. Variations in transpulmonary pressureare the true determinant of lung volume variations according to the equation:

Δ Vol = Δ P El,lung × El , lung ,

where PEl,lung is transpulmonary pressure and El,lung is theelastance of the lung.

In static conditions (that is, no flow), the pressure inside the lung can be easilyestimated from Paw (airway pressure), but the pressure outside the lung(that is, the pleural pressure, or Ppl) is not easily measurable and mustbe estimated from the esophageal pressure (Pes): PEl,lung =Paw - Pes.

For any change in lung volume, the higher the elastance of the chest wall(Elcw), the greater the contribution of the Ppl change tothe total Paw change. The chest wall and the lung contribute to the changein airway pressure in proportion to their elastance:

Δ P aw = Δ P El,lung + Δ P es = Δ Vol × El , lung + Δ Vol × E l cw = Δ Vol × ( El , lung + E l cw )

PEl,lung is the real effector of lung volume changes and of potentialventilator-induced lung injury (VILI) and is of major importance in the setting ofmechanical ventilation [68].

Measurement of Pes is not always straightforward, in particular whenabsolute values are used [69], and some clinicians find Pes difficult to use. Chiumello andcolleagues [70] recently explored the concept of specific elastance, which reflects theintrinsic elastic properties of the lung parenchyma and which relates stress(transpulmonary pressure) and strain (change in volume relative to functionalresidual capacity (FRC)). Specific elastance is rather constant among patients withARDS (and even healthy subjects) and thus the measurement of end-expiratory lungvolume (EELV) could allow an effective evaluation of the PEl,lung changecaused by VT; that is, once the strain is measured, it is possible toinfer the stress. The concept that the risk of VILI can be related to the ratiobetween VT and EELV has been suggested by positron emission tomographystudies in patients with ARDS [71].

Specific problems arise from the fact that the ARDS lung is non-homogeneous, and someareas, possibly entire lobes, are not exposed to airway pressure because of collapse,whereas the boundary regions between ventilated and collapsed areas may be exposed tohigh distending pressures, potentially causing VILI. Attention should also be paidwhen applying these concepts to assisted rather than controlled breathing conditions [72]. The pressure developed by the inspiratory muscles and by the diaphragmmay cause negative swings in pleural pressure, bringing the transpulmonary pressureto levels well beyond the VILI threshold. The effects of huge inspiratory effortshave only occasionally been investigated in patients with ARDS [73] but are known to cause lung edema in the experimental animal and inairway-obstructed patients. Decreased pleural pressure has been shown to beassociated with cardiovascular failure during weaning [74], possibly because of increased trans-diaphragmatic pressure and rightheart overload [75].

In clinical practice, transpulmonary pressure estimate poses two problems. First,like WOB and the pressure-time product, it requires correct placement of anesophageal probe. The availability of nasogastric feeding tubes with esophagealballoons should greatly facilitate the use of these techniques. Second, ensuring thevalidity of the absolute value of esophageal pressure in a supine patient forestimating end-inspiratory or end-expiratory transpulmonary pressure values remainsdifficult.

Abdominal pressure

Increased intra-abdominal pressure (IAP) can decrease compliance of the lung andchest wall and increase dead space and shunt fraction (Qs/Qt). Increased IAP reducesthe impact of transpulmonary pressure as the driving force for alveolar opening andprevention of closing. There is some relationship between abdominal and pleuralpressures. IAP can be assessed fairly simply by using a bladder catheter [76], and given that high IAPs can have consequences in terms of diagnosis andmanagement, more regular measurement of IAP is recommended.

3. Lung volumes

Direct measurement of end-expiratory lung volume

ARDS is associated with a marked reduction in lung volume [77]. Monitoring of FRC can provide information to assess pulmonary function.When the closed dilution technique is used, the patient breathes in a fixedconcentration of helium or methane mixed with oxygen and the concentration in theexpired breath can be used to calculate the FRC. This technique is used for researchpurposes. An alternative approach is a washout/washin technique using nitrogen oroxygen. Olegard and colleagues [78] reported that, by changing the FiO2 abruptly by as little as0.1, the FRC could be calculated by using standard gas-monitoring equipment. Theprecision of this method seems acceptable, and the method can be used even in themost severely hypoxemic patients [79, 80].

FRC is sex-, length-, and age-dependent. Ibanez and Raurich [81] showed that FRC decreased by 25% after changing the position from sittingto supine in healthy volunteers. Bikker and colleagues [82] found a reduction of 34% in mechanically ventilated patients with'healthy' lungs and attributed this to the loss of muscle tension with sedation inICU patients. In critically ill patients receiving mechanical ventilation anddifferent levels of PEEP, it is better to speak of EELV [83]. Application of PEEP leads to increased EELV values as a result ofrecruitment or further distention of already ventilated alveoli. To differentiatebetween recruitment and distention, EELV changes can be combined with compliancevalues [82]. From the compliance calculation, one can determine the expected change inEELV for a given change in PEEP. If application of PEEP leads to a higher EELV, thismethod can be used to estimate alveolar recruitment at the bedside [84]. Measurement of EELV has been made available recently for routine use.Although we still have limited experience with this technique, it has considerablepotential, at least in the management of patients with ARDS.

Chest ultrasonography and computed tomography

Chest ultrasonography can be useful at the bedside for early identification of edemaas well as other abnormalities like pneumothorax or pleural effusion [85, 86]. However, this technique requires training. Recently, it was shown thatlung ultrasonography can be used to estimate alveolar reaeration in patients treatedfor ventilator-associated pneumonia [87] and to estimate PEEP-induced lung recruitment [88]. This is a relatively new but promising and non-invasive technique thatcould have important clinical applications in the ICU.

Computed tomography (CT) scanning can be useful to identify ongoing pathology. CTimages can be used to compute average lung density and quantitate the respectiveamounts of air and tissue, but this approach is currently restricted to research [42, 89]. CT could potentially have roles in guiding protective mechanicalventilation in ARDS and in appropriately setting VT and PEEP [90]. The major limitations are the need to transfer the patient to the CTscanner and the complex processing needed for analysis.

Electrical bioimpedance tomography

In electrical bioimpedance tomography (EIT), a current is applied via 16 electrodespositioned around the thorax. A scan of the impedance to flow in a slice of thethorax reflects changes in aeration but gives no information on EELV and measuresonly relative impedance without providing absolute values. Images can be subdividedinto several regions and can be used to monitor regional ventilation. EIT can be usedto show whether a recruitment maneuver has been successful and document the effectsof positioning and of PEEP application [91, 92].

The caudal thoracic level above the diaphragm is of particular importance becauseatelectasis due to mechanical ventilation can be expected at this level. Variousstudies have described ventilation distribution change maps to evaluate lung collapseor overdistension [9395]. Costa and colleagues [93] introduced an algorithm for estimating recruitable alveolar collapse byusing EIT. Bikker and colleagues [94] clearly visualized improvement or loss of ventilation in dependent andnon-dependent parts of the lung by using EIT measurements in ICU patients. When EITwas used at multiple levels in mechanically ventilated patients, ventilationdistribution was shown to shift from the dorsal to ventral region but also from thecaudal to cranial level during a decremental PEEP trial [95].

The increase in airway pressure during normal inspiration is followed by a continuousredistribution of gas from non-dependent to dependent regions. Thus, during theinitial phase of inspiration, most of the inspiratory gas goes to the non-dependentlung, and during the last parts of inspiration, the most dependent parts receive theinspiratory flow, especially in patients with a positive response to a recruitmentmaneuver. This technique may thus represent a means of identifying responders andnon-responders to recruitment during normal tidal ventilation, enabling one to avoidexposing non-responders to high-pressure recruitment maneuvers. Additional clinicalwork is now needed to delineate the place of EIT in the ICU as a qualitative tool tovisualize ventilation distribution or as a quantitative technique to estimate theeffects of interventions.

4. Cardiopulmonary interactions

Hemodynamic monitoring

The use of hemodynamic monitoring in the unstable critically ill patient was reviewedrecently [96]. Hemo-dynamic monitoring is particularly helpful during difficult weaningprocesses to separate cardiac from pulmonary aspects of failed weaning. The heart maynot be able to meet the increased oxygen demand during weaning and then cardiacfilling pressures generally increase and the mixed venous oxygen saturation(SvO2) (or central venous oxygen saturation) decreases. SvO2 is a rather non-specific but sensitive kind of monitoring, as its changesreflect a change in one or more of the major homeostatic systems (respiration,circulation, and energy demand). During the weaning process, a reduction in SvO2 may be expected as spontaneous breathing represents a form of exercise, but adecrease in SvO2 may reflect the inability of the heart to face theincreased oxygen demand, especially if arterial hypertension is present [97].

Echocardiographic evaluation may be helpful in acute respiratory failure, simply toidentify a dilated right ventricle (RV) or RV failure, which may necessitate adecrease in PEEP or VT (or both) to reduce RV afterload. Measurement ofpulmonary artery pressure can also be reliably obtained by Doppler measurements [98]. Echo-graphy can be particularly helpful just before a suspected difficultSBT and sometimes during the SBT. Patients at risk of weaning failure were identifiedas having decreased ejection fraction and increased filling pressures before SBT [99]. Echo can help to estimate pulmonary artery occlusion pressure elevationduring SBT. The limitations of echocardiography are that it requires some trainingand is time-consuming, but it is an increasingly useful tool for cardiorespiratorymonitoring in the ICU.

Cardiac biomarkers, like B-type natriuretic protein (BNP) or N-terminal prohormone ofBNP (NT-proBNP), may be useful for diagnosing heart dysfunction but also formonitoring purposes, especially during weaning from mechanical ventilation [100, 101].

5. Lung inflammation

Bronchoalveolar lavage studies

Bronchoalveolar lavage (BAL) can be used to assess hemorrhage and measureneutrophils, eosinophils, hyaline membranes, lipid inclusion, and cancer cells(although this requires a careful cytologic examination of the alveolar fluidsampled). BAL fibrocyte levels are elevated in ARDS and related to outcome, andlevels higher than 6% were observed in non-survivors [102]. BAL fluid analysis may also help to identify patients who may respond tosteroids. Many studies have shown higher levels of inflammatory mediators (cytokinesand so on) in BAL fluid of non-survivors than survivors of ARDS. Measuring cytokinesor phosphorylation products may help to identify VILI, but there is a highsignal-to-noise ratio at present. Among the limitations of BAL fluid analysis arethat it needs an endoscope and requires some training, and there is no standardizedtechnique (depends on the volume instilled and amount of fluid returned). A potentialcomplication is hypoxemia. Detailed BAL analysis is suitable for bacteriologicalpurposes, but detailed cytological or biomarker assessment is often reserved forclinical trials.

Respiratory monitoring in specific situations

Respiratory monitoring in acute respiratory distress syndrome

As already mentioned, assessment of the severity of ARDS should include not onlyoxygenation but also dead space estimate and lung mechanics. Monitoring of plateaupressure, as a reflection of the maximal alveolar pressure, is essential.Potentially important tools for the most severe patients include esophagealpressure and lung volume measurements. P/V curves with assessment ofrecruitability could also be potentially useful. EVLW estimates may help indifferential diagnosis.

Respiratory monitoring in chronic obstructive pulmonary disease/asthma

In the initial phase of mechanical ventilation, a detailed assessment ofrespiratory mechanics, including plateau pressure and auto-PEEP, is essential tocharacterize the patient. When patients are switched to triggered breaths,detection of asynchrony is very useful in titrating ventilator assistance.

Respiratory monitoring in non-invasive ventilation

Respiratory monitoring in patients receiving non-invasive ventilation (NIV) shouldstart with a full clinical assessment: dyspnea, respiratory muscle function,com-fort, mental alertness, and gastric distention are important signs. Theseclinical indicators should then be combined with additional objective variablesfor a full evaluation of respiratory status. Pulse oximetry is essential but doesnot provide information about PCO2. Expired CO2 can bemeasured (from the mask or helmet), but leaks often make these measurementsunreliable. Transcutaneous capnometry offers a continuous and non-invasive methodof monitoring alveolar ventilation [103]. Arterial blood gases remain important in assessing the response totherapy.

Patient-ventilator asynchrony occurs in almost one half of patients and may berelated largely to leaks [104]. Clinical evaluation (tachypnea, accessory muscle activity, agitation,and lack of cooperation) or waveform analysis can be useful in assessing thepresence of patient-ventilator dyssynchrony. Electromyography tracings arecumbersome, but airway pressures and flows can be used to monitor patient effortsand identify 'autotriggering', premature cycling, or ineffective triggering [105]. Inspired and expired VT values can help to identify airleaks.

In the hypoxemic patient, respiratory monitoring should also help to identify whento intubate the trachea (not too late!). Shock, including measurement of bloodlactate levels, should also be looked for since the presence of acute circulatoryfailure is an exclusion criterion for NIV [106].

Respiratory monitoring in the neurological patient

Neurological dysfunction is one of the most frequent reasons for initiatingmechanical ventilation [107]. Out-comes of critically ill neurological patients are driven mainly bythe underlying neurological pathology [108, 109], and the influence of extracerebral organ dysfunction and ventilatorymanagement on outcomes in this group of patients is not well established [110].

In mechanically ventilated neurological patients, no consensus has been reachedabout optimal VT, PEEP, PaO2, or PaCO2 levels [111], largely because these patients have been universally excluded fromrandomized trials of lung-protective ventilation because of concerns aboutpotential intracranial pressure (ICP) increases due to hypercapnia or increasedthoracic pressures. More-over, owing to persistently decreased levels ofconsciousness, typical weaning and liberation techniques used in medical-surgicalICU patients may not apply to this group [109, 112]. Finally, tracheostomy is commonly implemented as part of themanagement of these neurological patients, but the technique of choice and timingare controversial [109].

Pulmonary hyperventilation rapidly reduces ICP by reducing cerebral blood flow(CBF). The effect on ICP is not sustained, whereas CBF may remain low, raisingrisks of ischemia [113, 114]; hyperventilation should, therefore, be avoided during the first 24hours after injury, when CBF is often already low [115]. The CBF level at which irreversible ischemia occurs has not beenclearly established, but ischemic cell change has been demonstrated followingtraumatic brain injury and is likely to occur when CBF decreases to less than 15to 20 mL/100 g per minute. Hyperventilation should, therefore, be used only forshort-term management of raised ICP and only in patients with life-threateningintracranial hypertension [115, 116]. If hyperventilation is used, jugular venous oxygen saturation(SjO2) or brain tissue oxygen tension (PbrO2) monitoringshould be used to evaluate oxygen delivery where possible [115]. The ideal value for PaCO2 is one that keeps ICP to lessthan 20 mm Hg and cerebral extraction of oxygen (CEO2) to between 24%and 42% to avoid brain ischemia.

Moderate levels of PEEP (for example, less than 15 cm H2O) can besafely used in patients with cerebral lesions, mainly in those with low pulmonarycompliance [117]. Hence, although care should be taken when applying PEEP in patientswith neurological injury, it should not be withheld if needed to maintain adequateoxygenation [114].

Multimodal brain monitoring, including brain tissue oxygen tension, CBFmeasurement, and intracerebral microdialysis (with measurement of lactate,pyruvate, glutamate, glycerol, and inflammatory mediators), may be useful tooptimize mechanical ventilation in patients with severe brain injury [118].

Conclusions and perspectives

Although most of the clinical interventions applied to the respiratory system of thecritically ill are relatively simple, they are often misused, largely as a result of apoor understanding of the physiology underlying a specific intervention or of itsconsequences on the pathophysiology of respiratory disease or both. We need to encourageincreased training in these techniques guided by a better knowledge of underlyingmechanisms and appropriate use and correct interpretation of the data provided byavailable monitoring techniques.

Importantly, two key concepts can be highlighted:

  1. 1.

    Multiple variables need to be integrated: Many critically ill patients with respiratory failure have complex pathologies, and the respiratory failure is part of a broader multiple organ failure. Management will, therefore, require the consideration of monitored data from several different systems. This is one reason why it is difficult to develop protocols for the use of mechanical ventilation.

  2. 2.

    Monitoring of solitary static values provides limited information; evaluation of dynamic changes in variables over time is more important.

The future is likely to see advances in neuro-ventilatory coupling to limit theoccurrence and adverse effects of patient-ventilator asynchrony. Biomarker panels willbe developed to determine the risk of ARDS and VILI and to guide therapy. Chestultrasonography and other, less invasive techniques will also be used more as theybecome more readily available at the bedside and training is improved.



acute respiratory distress syndrome


bronchoalveolar lavage


B-typenatriuretic protein


cerebral blood flow


carbon dioxide


chronic obstructive pulmonary disease


computed tomography


end-expiratorylung volume


electrical bioimpedance tomography


elastance of the chest wall


elastance of the lung


endotracheal tube


extravascular lung water


inspiredfraction of oxygen


functional residual capacity


intra-abdominal pressure


intracranial pressure


intensive care unit


lower inflection point


non-invasive ventilation


occlusion pressure


arterial partial pressure of carbon dioxide


arterial partial pressureof oxygen


airway pressure


partial pressure of carbondioxide


partial pressure of carbon dioxide in mixedexpired gas


positive end-expiratory pressure


esophageal pressure


end-tidal partialpressure of carbon dioxide


pleural pressure




right ventricle


spontaneous breathing trial


mixed venous oxygensaturation


upper inflection point


alveolar dead space


airway dead space


physiologic dead space


ventilator-induced lung injury


tidal volume


work of breathing.


  1. Van de Louw A, Cracco C, Cerf C, Harf A, Duvaldestin P, Lemaire F, Brochard L: Accuracy of pulse oximetry in the intensive care unit. Intensive Care Med. 2001, 27: 1606-1613. 10.1007/s001340101064.

    CAS  PubMed  Google Scholar 

  2. Hinkelbein J, Genzwuerker HV, Sogl R, Fiedler F: Effect of nail polish on oxygen saturation determined by pulse oximetry incritically ill patients. Resuscitation. 2007, 72: 82-91. 10.1016/j.resuscitation.2006.06.024.

    PubMed  Google Scholar 

  3. Feiner JR, Severinghaus JW, Bickler PE: Dark skin decreases the accuracy of pulse oximeters at low oxygen saturation: theeffects of oximeter probe type and gender. Anesth Analg. 2007, 105: S18-23. 10.1213/01.ane.0000285988.35174.d9. tables,

    PubMed  Google Scholar 

  4. Jensen LA, Onyskiw JE, Prasad NG: Meta-analysis of arterial oxygen saturation monitoring by pulse oximetry inadults. Heart Lung. 1998, 27: 387-408. 10.1016/S0147-9563(98)90086-3.

    CAS  PubMed  Google Scholar 

  5. Moller JT, Johannessen NW, Espersen K, Ravlo O, Pedersen BD, Jensen PF, Rasmussen NH, Rasmussen LS, Pedersen T, Cooper JB: Randomized evaluation of pulse oximetry in 20,802 patients: II. Perioperativeevents and postoperative complications. Anesthesiology. 1993, 78: 445-453. 10.1097/00000542-199303000-00007.

    CAS  PubMed  Google Scholar 

  6. Eberhard P: The design, use, and results of transcutaneous carbon dioxide analysis: currentand future directions. Anesth Analg. 2007, 105: S48-S52. 10.1213/01.ane.0000278642.16117.f8.

    PubMed  Google Scholar 

  7. Romero PV, Lucangelo U, Lopez AJ, Fernandez R, Blanch L: Physiologically based indices of volumetric capnography in patients receivingmechanical ventilation. Eur Respir J. 1997, 10: 1309-1315. 10.1183/09031936.97.10061309.

    CAS  PubMed  Google Scholar 

  8. You B, Peslin R, Duvivier C, Vu VD, Grilliat JP: Expiratory capnography in asthma: evaluation of various shape indices. Eur Respir J. 1994, 7: 318-323. 10.1183/09031936.94.07020318.

    CAS  PubMed  Google Scholar 

  9. Lucangelo U, Bernabe F, Vatua S, Degrassi G, Villagra A, Fernandez R, Romero PV, Saura P, Borelli M, Blanch L: Prognostic value of different dead space indices in mechanically ventilatedpatients with acute lung injury and ARDS. Chest. 2008, 133: 62-71. 10.1378/chest.07-0935.

    PubMed  Google Scholar 

  10. Raurich JM, Vilar M, Colomar A, Ibanez J, Ayestaran I, Perez-Barcena J, Llompart-Pou JA: Prognostic value of the pulmonary dead-space fraction during the early andintermediate phases of acute respiratory distress syndrome. Respir Care. 2010, 55: 282-287.

    PubMed  Google Scholar 

  11. Lucangelo U, Blanch L: Dead space. Intensive Care Med. 2004, 30: 576-579. 10.1007/s00134-004-2194-8.

    CAS  PubMed  Google Scholar 

  12. Kuwabara S, Duncalf D: Effect of anatomic shunt on physiologic deadspace-to-tidal volume ratio--a newequation. Anesthesiology. 1969, 31: 575-577. 10.1097/00000542-196912000-00012.

    CAS  PubMed  Google Scholar 

  13. McSwain SD, Hamel DS, Smith PB, Gentile MA, Srinivasan S, Meliones JN, Cheifetz IM: End-tidal and arterial carbon dioxide measurements correlate across all levels ofphysiologic dead space. Respir Care. 2010, 55: 288-293.

    PubMed Central  PubMed  Google Scholar 

  14. Galia F, Brimioulle S, Bonnier F, Vandenbergen N, Dojat M, Vincent JL, Brochard LJ: Use of maximum end-tidal CO(2) values to improve end-tidal CO(2) monitoringaccuracy. Respir Care. 2011, 56: 278-283. 10.4187/respcare.00837.

    PubMed  Google Scholar 

  15. Kline JA, Israel EG, Michelson EA, O'Neil BJ, Plewa MC, Portelli DC: Diagnostic accuracy of a bedside D-dimer assay and alveolar dead-space measurementfor rapid exclusion of pulmonary embolism: a multicenter study. JAMA. 2001, 285: 761-768. 10.1001/jama.285.6.761.

    CAS  PubMed  Google Scholar 

  16. Verschuren F, Heinonen E, Clause D, Roeseler J, Thys F, Meert P, Marion E, El Gariani A, Col J, Reynaert M, Liistro G: Volumetric capnography as a bedside monitoring of thrombolysis in major pulmonaryembolism. Intensive Care Med. 2004, 30: 2129-2132. 10.1007/s00134-004-2444-9.

    PubMed  Google Scholar 

  17. Tusman G, Suarez-Sipmann F, Bohm SH, Pech T, Reissmann H, Meschino G, Scandurra A, Hedenstierna G: Monitoring dead space during recruitment and PEEP titration in an experimentalmodel. Intensive Care Med. 2006, 32: 1863-1871. 10.1007/s00134-006-0371-7.

    PubMed  Google Scholar 

  18. Beydon L, Uttman L, Rawal R, Jonson B: Effects of positive end-expiratory pressure on dead space and its partitions inacute lung injury. Intensive Care Med. 2002, 28: 1239-1245. 10.1007/s00134-002-1419-y.

    CAS  PubMed  Google Scholar 

  19. Aboab J, Niklason L, Uttman L, Kouatchet A, Brochard L, Jonson B: CO2 elimination at varying inspiratory pause in acute lung injury. Clin Physiol Funct Imaging. 2007, 27: 2-6. 10.1111/j.1475-097X.2007.00699.x.

    CAS  PubMed  Google Scholar 

  20. Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, Lamy M, Legall JR, Morris A, Spragg R: The American-European Consensus Conference on ARDS. Definitions, mechanisms,relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994, 149: 818-824. 10.1164/ajrccm.149.3.7509706.

    CAS  PubMed  Google Scholar 

  21. Aboab J, Louis B, Jonson B, Brochard L: Relation between PaO2/FIO2 ratio and FIO2: a mathematical description. Intensive Care Med. 2006, 32: 1494-1497. 10.1007/s00134-006-0337-9.

    PubMed  Google Scholar 

  22. Gowda MS, Klocke RA: Variability of indices of hypoxemia in adult respiratory distress syndrome. Crit Care Med. 1997, 25: 41-45. 10.1097/00003246-199701000-00010.

    CAS  PubMed  Google Scholar 

  23. Whiteley JP, Gavaghan DJ, Hahn CE: Variation of venous admixture, SF6 shunt, PaO2, and the PaO2/FIO2 ratio withFIO2. Br J Anaesth. 2002, 88: 771-778. 10.1093/bja/88.6.771.

    CAS  PubMed  Google Scholar 

  24. Britos M, Smoot E, Liu KD, Thompson BT, Checkley W, Brower RG: The value of positive end-expiratory pressure and FiO2 criteria in the definitionof the acute respiratory distress syndrome. Crit Care Med. 2011, 39: 2025-2030. 10.1097/CCM.0b013e31821cb774.

    PubMed Central  CAS  PubMed  Google Scholar 

  25. Di Marco F, Devaquet J, Lyazidi A, Galia F, da Costa NP, Fumagalli R, Brochard L: Positive end-expiratory pressure-induced functional recruitment in patients withacute respiratory distress syndrome. Crit Care Med. 2010, 38: 127-132. 10.1097/CCM.0b013e3181b4a7e7.

    PubMed  Google Scholar 

  26. Mekontso Dessap A, Boissier F, Leon R, Carreira S, Campo FR, Lemaire F, Brochard L: Prevalence and prognosis of shunting across patent foramen ovale during acuterespiratory distress syndrome. Crit Care Med. 2010, 38: 1786-1792. 10.1097/CCM.0b013e3181eaa9c8.

    PubMed  Google Scholar 

  27. Willson DF, Thomas NJ, Markovitz BP, Bauman LA, DiCarlo JV, Pon S, Jacobs BR, Jefferson LS, Conaway MR, Egan EA: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury: arandomized controlled trial. JAMA. 2005, 293: 470-476. 10.1001/jama.293.4.470.

    CAS  PubMed  Google Scholar 

  28. Nuckton TJ, Alonso JA, Kallet RH, Daniel BM, Pittet JF, Eisner MD, Matthay MA: Pulmonary dead-space fraction as a risk factor for death in the acute respiratorydistress syndrome. N Engl J Med. 2002, 346: 1281-1286. 10.1056/NEJMoa012835.

    PubMed  Google Scholar 

  29. Gattinoni L, Bombino M, Pelosi P, Lissoni A, Pesenti A, Fumagalli R, Tagliabue M: Lung structure and function in different stages of severe adult respiratorydistress syndrome. JAMA. 1994, 271: 1772-1779. 10.1001/jama.1994.03510460064035.

    CAS  PubMed  Google Scholar 

  30. Doyle RL, Szafl arski N, Modin GW, Wiener-Kronish JP, Matthay MA: Identification of patients with acute lung injury. Predictors of mortality. Am J Respir Crit Care Med. 1995, 152: 1818-1824. 10.1164/ajrccm.152.6.8520742.

    CAS  PubMed  Google Scholar 

  31. Monchi M, Bellenfant F, Cariou A, Joly LM, Thebert D, Laurent I, Dhainaut JF, Brunet F: Early predictive factors of survival in the acute respiratory distress syndrome. Amultivariate analysis. Am J Respir Crit Care Med. 1998, 158: 1076-1081. 10.1164/ajrccm.158.4.9802009.

    CAS  PubMed  Google Scholar 

  32. Sakka SG, Klein M, Reinhart K, Meier-Hellmann A: Prognostic value of extravascular lung water in critically ill patients. Chest. 2002, 122: 2080-2086. 10.1378/chest.122.6.2080.

    PubMed  Google Scholar 

  33. Lange NR, Schuster DP: The measurement of lung water. Crit Care. 1999, 3: R19-R24. 10.1186/cc342.

    PubMed Central  PubMed  Google Scholar 

  34. Brown LM, Liu KD, Matthay MA: Measurement of extravascular lung water using the single indicator method inpatients: research and potential clinical value. Am J Physiol Lung Cell Mol Physiol. 2009, 297: L547-L558. 10.1152/ajplung.00127.2009.

    PubMed Central  CAS  PubMed  Google Scholar 

  35. Monnet X, Anguel N, Osman D, Hamzaoui O, Richard C, Teboul JL: Assessing pulmonary permeability by transpulmonary thermodilution allowsdifferentiation of hydrostatic pulmonary edema from ALI/ARDS. Intensive Care Med. 2007, 33: 448-453. 10.1007/s00134-006-0498-6.

    PubMed  Google Scholar 

  36. Jonson B, Richard JC, Straus C, Mancebo J, Lemaire F, Brochard L: Pressure-volume curves and compliance in acute lung injury: evidence ofrecruitment above the lower inflection point. Am J Respir Crit Care Med. 1999, 159: 1172-1178. 10.1164/ajrccm.159.4.9801088.

    CAS  PubMed  Google Scholar 

  37. Richard JC, Brochard L, Vandelet P, Breton L, Maggiore SM, Jonson B, Clabault K, Leroy J, Bonmarchand G: Respective effects of end-expiratory and end-inspiratory pressures on alveolarrecruitment in acute lung injury. Crit Care Med. 2003, 31: 89-92. 10.1097/00003246-200301000-00014.

    PubMed  Google Scholar 

  38. Lu Q, Vieira SR, Richecoeur J, Puybasset L, Kalfon P, Coriat P, Rouby JJ: A simple automated method for measuring pressure-volume curves during mechanicalventilation. Am J Respir Crit Care Med. 1999, 159: 275-282. 10.1164/ajrccm.159.1.9802082.

    CAS  PubMed  Google Scholar 

  39. Matamis D, Lemaire F, Harf A, Brun-Buisson C, Ansquer JC, Atlan G: Total respiratory pressure-volume curves in the adult respiratory distresssyndrome. Chest. 1984, 86: 58-66. 10.1378/chest.86.1.58.

    CAS  PubMed  Google Scholar 

  40. Roupie E, Dambrosio M, Servillo G, Mentec H, el Atrous S, Beydon L, Brun-Buisson C, Lemaire F, Brochard L: Titration of tidal volume and induced hypercapnia in acute respiratory distresssyndrome. Am J Respir Crit Care Med. 1995, 152: 121-128. 10.1164/ajrccm.152.1.7599810.

    CAS  PubMed  Google Scholar 

  41. Crotti S, Mascheroni D, Caironi P, Pelosi P, Ronzoni G, Mondino M, Marini JJ, Gattinoni L: Recruitment and derecruitment during acute respiratory failure: a clinicalstudy. Am J Respir Crit Care Med. 2001, 164: 131-140. 10.1164/ajrccm.164.1.2007011.

    CAS  PubMed  Google Scholar 

  42. Pelosi P, Goldner M, McKibben A, Adams A, Eccher G, Caironi P, Losappio S, Gattinoni L, Marini JJ: Recruitment and derecruitment during acute respiratory failure: an experimentalstudy. Am J Respir Crit Care Med. 2001, 164: 122-130. 10.1164/ajrccm.164.1.2007010.

    CAS  PubMed  Google Scholar 

  43. Owens RL, Hess DR, Malhotra A, Venegas JG, Harris RS: Effect of the chest wall on pressure-volume curve analysis of acute respiratorydistress syndrome lungs. Crit Care Med. 2008, 36: 2980-2985. 10.1097/CCM.0b013e318186afcb.

    PubMed  Google Scholar 

  44. Demory D, Arnal JM, Wysocki M, Donati S, Granier I, Corno G, Durand-Gasselin J: Recruitability of the lung estimated by the pressure volume curve hysteresis inARDS patients. Intensive Care Med. 2008, 34: 2019-2025. 10.1007/s00134-008-1167-8.

    PubMed  Google Scholar 

  45. Maggiore SM, Jonson B, Richard JC, Jaber S, Lemaire F, Brochard L: Alveolar derecruitment at decremental positive end-expiratory pressure levels inacute lung injury: comparison with the lower inflection point, oxygenation, andcompliance. Am J Respir Crit Care Med. 2001, 164: 795-801. 10.1164/ajrccm.164.5.2006071.

    CAS  PubMed  Google Scholar 

  46. Grasso S, Terragni P, Mascia L, Fanelli V, Quintel M, Herrmann P, Hedenstierna G, Slutsky AS, Ranieri VM: Airway pressure-time curve profile (stress index) detects tidalrecruitment/hyperinflation in experimental acute lung injury. Crit Care Med. 2004, 32: 1018-1027. 10.1097/01.CCM.0000120059.94009.AD.

    PubMed  Google Scholar 

  47. Grasso S, Stripoli T, De Michele M, Bruno F, Moschetta M, Angelelli G, Munno I, Ruggiero V, Anaclerio R, Cafarelli A, Driessen B, Fiore T: ARDSnet ventilatory protocol and alveolar hyperinflation: role of positiveend-expiratory pressure. Am J Respir Crit Care Med. 2007, 176: 761-767. 10.1164/rccm.200702-193OC.

    PubMed  Google Scholar 

  48. Formenti P, Graf J, Santos A, Gard KE, Faltesek K, Adams AB, Dries DJ, Marini JJ: Non-pulmonary factors strongly influence the stress index. Intensive Care Med. 2011, 37: 594-600. 10.1007/s00134-011-2133-4.

    PubMed  Google Scholar 

  49. Jaber S, Jung B, Matecki S, Petrof BJ: Clinical review: Ventilator-induced diaphragmatic dysfunction - human studiesconfirm animal model findings!. Crit Care. 2011, 15: 206-10.1186/cc10023.

    PubMed Central  PubMed  Google Scholar 

  50. Jaber S, Petrof BJ, Jung B, Chanques G, Berthet JP, Rabuel C, Bouyabrine H, Courouble P, Koechlin-Ramonatxo C, Sebbane M, Similowski T, Scheuermann V, Mebazaa A, Capdevila X, Mornet D, Mercier J, Lacampagne A, Philips A, Matecki S: Rapidly progressive diaphragmatic weakness and injury during mechanicalventilation in humans. Am J Respir Crit Care Med. 2011, 183: 364-371. 10.1164/rccm.201004-0670OC.

    CAS  PubMed  Google Scholar 

  51. Polkey MI, Duguet A, Luo Y, Hughes PD, Hart N, Hamnegard CH, Green M, Similowski T, Moxham J: Anterior magnetic phrenic nerve stimulation: laboratory and clinicalevaluation. Intensive Care Med. 2000, 26: 1065-1075. 10.1007/s001340051319.

    CAS  PubMed  Google Scholar 

  52. Sinderby C: Neurally adjusted ventilatory assist (NAVA). Minerva Anestesiol. 2002, 68: 378-380.

    CAS  PubMed  Google Scholar 

  53. Georgopoulos D, Prinianakis G, Kondili E: Bedside waveforms interpretation as a tool to identify patient-ventilatorasynchronies. Intensive Care Med. 2006, 32: 34-47. 10.1007/s00134-005-2828-5.

    PubMed  Google Scholar 

  54. Leung P, Jubran A, Tobin MJ: Comparison of assisted ventilator modes on triggering, patient effort, anddyspnea. Am J Respir Crit Care Med. 1997, 155: 1940-1948. 10.1164/ajrccm.155.6.9196100.

    CAS  PubMed  Google Scholar 

  55. Thille AW, Cabello B, Galia F, Lyazidi A, Brochard L: Reduction of patient-ventilator asynchrony by reducing tidal volume duringpressure-support ventilation. Intensive Care Med. 2008, 34: 1477-1486. 10.1007/s00134-008-1121-9.

    PubMed  Google Scholar 

  56. Thille AW, Rodriguez P, Cabello B, Lellouche F, Brochard L: Patient-ventilator asynchrony during assisted mechanical ventilation. Intensive Care Med. 2006, 32: 1515-1522. 10.1007/s00134-006-0301-8.

    PubMed  Google Scholar 

  57. Parthasarathy S, Tobin MJ: Effect of ventilator mode on sleep quality in critically ill patients. Am J Respir Crit Care Med. 2002, 166: 1423-1429. 10.1164/rccm.200209-999OC.

    PubMed  Google Scholar 

  58. Tassaux D, Gainnier M, Battisti A, Jolliet P: Impact of expiratory trigger setting on delayed cycling and inspiratory muscleworkload. Am J Respir Crit Care Med. 2005, 172: 1283-1289. 10.1164/rccm.200407-880OC.

    PubMed  Google Scholar 

  59. Cabello B, Mancebo J: Work of breathing. Intensive Care Med. 2006, 32: 1311-1314. 10.1007/s00134-006-0278-3.

    PubMed  Google Scholar 

  60. Mancebo J, Albaladejo P, Touchard D, Bak E, Subirana M, Lemaire F, Harf A, Brochard L: Airway occlusion pressure to titrate positive end-expiratory pressure in patientswith dynamic hyperinflation. Anesthesiology. 2000, 93: 81-90. 10.1097/00000542-200007000-00016.

    CAS  PubMed  Google Scholar 

  61. Vassilakopoulos T: Understanding wasted/ineffective efforts in mechanically ventilated COPD patientsusing the Campbell diagram. Intensive Care Med. 2008, 34: 1336-1339. 10.1007/s00134-008-1095-7.

    PubMed  Google Scholar 

  62. Jubran A, Grant BJ, Laghi F, Parthasarathy S, Tobin MJ: Weaning prediction: esophageal pressure monitoring complements readinesstesting. Am J Respir Crit Care Med. 2005, 171: 1252-1259. 10.1164/rccm.200503-356OC.

    PubMed  Google Scholar 

  63. Mancebo J, Amaro P, Lorino H, Lemaire F, Harf A, Brochard L: Effects of albuterol inhalation on the work of breathing during weaning frommechanical ventilation. Am Rev Respir Dis. 1991, 144: 95-100. 10.1164/ajrccm/144.1.95.

    CAS  PubMed  Google Scholar 

  64. Alberti A, Gallo F, Fongaro A, Valenti S, Rossi A: P0.1 is a useful parameter in setting the level of pressure supportventilation. Intensive Care Med. 1995, 21: 547-553. 10.1007/BF01700158.

    CAS  PubMed  Google Scholar 

  65. Field S, Sanci S, Grassino A: Respiratory muscle oxygen consumption estimated by the diaphragm pressure-timeindex. J Appl Physiol. 1984, 57: 44-51.

    CAS  PubMed  Google Scholar 

  66. Nava S, Bruschi C, Fracchia C, Braschi A, Rubini F: Patient-ventilator interaction and inspiratory effort during pressure supportventilation in patients with different pathologies. Eur Respir J. 1997, 10: 177-183. 10.1183/09031936.97.10010177.

    CAS  PubMed  Google Scholar 

  67. Sassoon CS, Light RW, Lodia R, Sieck GC, Mahutte CK: Pressure-time product during continuous positive airway pressure, pressure supportventilation, and T-piece during weaning from mechanical ventilation. Am Rev Respir Dis. 1991, 143: 469-475. 10.1164/ajrccm/143.3.469.

    CAS  PubMed  Google Scholar 

  68. Talmor D, Sarge T, Malhotra A, O'Donnell CR, Ritz R, Lisbon A, Novack V, Loring SH: Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008, 359: 2095-2104. 10.1056/NEJMoa0708638.

    PubMed Central  CAS  PubMed  Google Scholar 

  69. Vieillard-Baron A, Jardin F: Esophageal pressure in acute lung injury. N Engl J Med. 2009, 360: 832-

    CAS  PubMed  Google Scholar 

  70. Chiumello D, Carlesso E, Cadringher P, Caironi P, Valenza F, Polli F, Tallarini F, Cozzi P, Cressoni M, Colombo A, Marini JJ, Gattinoni L: Lung stress and strain during mechanical ventilation for acute respiratorydistress syndrome. Am J Respir Crit Care Med. 2008, 178: 346-355. 10.1164/rccm.200710-1589OC.

    PubMed  Google Scholar 

  71. Bellani G, Guerra L, Musch G, Zanella A, Patroniti N, Mauri T, Messa C, Pesenti A: Lung regional metabolic activity and gas volume changes induced by tidalventilation in patients with acute lung injury. Am J Respir Crit Care Med. 2011, 183: 1193-1199. 10.1164/rccm.201008-1318OC.

    PubMed Central  PubMed  Google Scholar 

  72. Marini JJ: Spontaneously regulated versus controlled ventilation of acute lung injury/acuterespiratory distress syndrome. Curr Opin Crit Care. 2011, 17: 24-29. 10.1097/MCC.0b013e328342726e.

    PubMed  Google Scholar 

  73. Kallet RH, Alonso JA, Luce JM, Matthay MA: Exacerbation of acute pulmonary edema during assistaed mechanical ventilationusing a low tidal volume, lung protective strategy. Chest. 1999, 116: 1826-1832. 10.1378/chest.116.6.1826.

    CAS  PubMed  Google Scholar 

  74. Lemaire F, Teboul JL, Cinotti L, Giotto G, Abrouk F, Steg G, Macquin-Mavier I, Zapol WM: Acute left ventricular dysfunction during unsuccessful weaning from mechanicalventilation. Anesthesiology. 1988, 69: 171-179. 10.1097/00000542-198808000-00004.

    CAS  PubMed  Google Scholar 

  75. Permutt S: Circulatory effects of weaning from mechanical ventilation: the importance oftransdiaphragmatic pressure. Anesthesiology. 1988, 69: 157-160. 10.1097/00000542-198808000-00002.

    CAS  PubMed  Google Scholar 

  76. Malbrain ML, Chiumello D, Pelosi P, Wilmer A, Brienza N, Malcangi V, Bihari D, Innes R, Cohen J, Singer P, Japiassu A, Kurtop E, De Keulenaer BL, Daelemans R, Del Turco M, Cosimini P, Ranieri M, Jacquet L, Laterre PF, Gattinoni L: Prevalence of intra-abdominal hypertension in critically ill patients: amulticentre epidemiological study. Intensive Care Med. 2004, 30: 822-829. 10.1007/s00134-004-2169-9.

    PubMed  Google Scholar 

  77. Falke KJ, Pontoppidan H, Kumar A, Leith DE, Geffin B, Laver MB: Ventilation with end-expiratory pressure in acute lung disease. J Clin Invest. 1972, 51: 2315-2323. 10.1172/JCI107042.

    PubMed Central  CAS  PubMed  Google Scholar 

  78. Olegard C, Sondergaard S, Houltz E, Lundin S, Stenqvist O: Estimation of functional residual capacity at the bedside using standardmonitoring equipment: a modified nitrogen washout/washin technique requiring asmall change of the inspired oxygen fraction. Anesth Analg. 2005, 101: 206-212. 10.1213/01.ANE.0000165823.90368.55.

    PubMed  Google Scholar 

  79. Chiumello D, Cressoni M, Chierichetti M, Tallarini F, Botticelli M, Berto V, Mietto C, Gattinoni L: Nitrogen washout/washin, helium dilution and computed tomography in the assessmentof end expiratory lung volume. Crit Care. 2008, 12: R150-10.1186/cc7139.

    PubMed Central  PubMed  Google Scholar 

  80. Patroniti N, Saini M, Zanella A, Weismann D, Isgro S, Bellani G, Foti G, Pesenti A: Measurement of end-expiratory lung volume by oxygen washin-washout in controlledand assisted mechanically ventilated patients. Intensive Care Med. 2008, 34: 2235-2240. 10.1007/s00134-008-1218-1.

    CAS  PubMed  Google Scholar 

  81. Ibanez J, Raurich JM: Normal values of functional residual capacity in the sitting and supinepositions. Intensive Care Med. 1982, 8: 173-177. 10.1007/BF01725734.

    CAS  PubMed  Google Scholar 

  82. Bikker IG, van Bommel J, Reis Miranda D, Bakker J, Gommers D: End-expiratory lung volume during mechanical ventilation: a comparison withreference values and the effect of positive end-expiratory pressure in intensivecare unit patients with different lung conditions. Crit Care. 2008, 12: R145-10.1186/cc7125.

    PubMed Central  PubMed  Google Scholar 

  83. Reis Miranda D, Gommers D: Precise use of medical terminology. Crit Care Med. 2006, 34: 1854-1855.

    Google Scholar 

  84. Dellamonica J, Lerolle N, Sargentini C, Beduneau G, Di Marco F, Mercat A, Richard JC, Diehl JL, Mancebo J, Rouby JJ, Lu Q, Bernardin G, Brochard L: PEEP-induced changes in lung volume in acute respiratory distress syndrome. Twomethods to estimate alveolar recruitment. Intensive Care Med. 2011, 37: 1595-1604. 10.1007/s00134-011-2333-y.

    CAS  PubMed  Google Scholar 

  85. Remerand F, Dellamonica J, Mao Z, Ferrari F, Bouhemad B, Jianxin Y, Arbelot C, Lu Q, Ichai C, Rouby JJ: Multiplane ultrasound approach to quantify pleural effusion at the bedside. Intensive Care Med. 2010, 36: 656-664. 10.1007/s00134-010-1769-9.

    PubMed  Google Scholar 

  86. Reissig A, Copetti R, Kroegel C: Current role of emergency ultrasound of the chest. Crit Care Med. 2011, 39: 839-845. 10.1097/CCM.0b013e318206d6b8.

    PubMed  Google Scholar 

  87. Bouhemad B, Liu ZH, Arbelot C, Zhang M, Ferarri F, Le Guen M, Girard M, Lu Q, Rouby JJ: Ultrasound assessment of antibiotic-induced pulmonary reaeration inventilator-associated pneumonia. Crit Care Med. 2010, 38: 84-92. 10.1097/CCM.0b013e3181b08cdb.

    PubMed  Google Scholar 

  88. Bouhemad B, Brisson H, Le-Guen M, Arbelot C, Lu Q, Rouby JJ: Bedside ultrasound assessment of positive end-expiratory pressure-induced lungrecruitment. Am J Respir Crit Care Med. 2011, 183: 341-347. 10.1164/rccm.201003-0369OC.

    PubMed  Google Scholar 

  89. Puybasset L, Cluzel P, Chao N, Slutsky AS, Coriat P, Rouby JJ: A computed tomography scan assessment of regional lung volume in acute lunginjury. The CT Scan ARDS Study Group. Am J Respir Crit Care Med. 1998, 158: 1644-1655. 10.1164/ajrccm.158.5.9802003.

    CAS  PubMed  Google Scholar 

  90. Pelosi P, Rocco PR, de Abreu MG: Use of computed tomography scanning to guide lung recruitment and adjustpositive-end expiratory pressure. Curr Opin Crit Care. 2011, 17: 268-274. 10.1097/MCC.0b013e328344ddbc.

    PubMed  Google Scholar 

  91. Lindgren S, Odenstedt H, Olegard C, Sondergaard S, Lundin S, Stenqvist O: Regional lung derecruitment after endotracheal suction during volume-orpressure-controlled ventilation: a study using electric impedance tomography. Intensive Care Med. 2007, 33: 172-180. 10.1007/s00134-006-0425-x.

    PubMed  Google Scholar 

  92. Fagerberg A, Stenqvist O, Aneman A: Electrical impedance tomography applied to assess matching of pulmonaryventilation and perfusion in a porcine experimental model. Crit Care. 2009, 13: R34-10.1186/cc7741.

    PubMed Central  PubMed  Google Scholar 

  93. Costa EL, Borges JB, Melo A, Suarez-Sipmann F, Toufen C, Bohm SH, Amato MB: Bedside estimation of recruitable alveolar collapse and hyperdistension byelectrical impedance tomography. Intensive Care Med. 2009, 35: 1132-1137. 10.1007/s00134-009-1447-y.

    PubMed  Google Scholar 

  94. Bikker IG, Leonhardt S, Reis MD, Bakker J, Gommers D: Bedside measurement of changes in lung impedance to monitor alveolar ventilationin dependent and non-dependent parts by electrical impedance tomography during apositive end-expiratory pressure trial in mechanically ventilated intensive careunit patients. Crit Care. 2010, 14: R100-10.1186/cc9036.

    PubMed Central  PubMed  Google Scholar 

  95. Bikker IG, Preis C, Egal M, Bakker J, Gommers D: Electrical impedance tomography measured at two thoracic levels can visualize theventilation distribution changes at the bedside during a decremental positiveend-expiratory pressure (PEEP) trial. Crit Care. 2011, 15: R193-10.1186/cc10354.

    PubMed Central  PubMed  Google Scholar 

  96. Vincent JL, Rhodes A, Perel A, Martin CS, Rocca GD, Vallet B, Pinsky MR, Hofer CK, Teboul JL, de Boode WP, Walley KR, Maggiorini M, Singer M: Update on hemodynamic monitoring: a consensus of 16. Crit Care. 2011, 15: 229-10.1186/cc10291.

    PubMed Central  PubMed  Google Scholar 

  97. Jubran A, Mathru M, Dries D, Tobin MJ: Continuous recordings of mixed venous oxygen saturation during weaning frommechanical ventilation and the ramifications thereof. Am J Respir Crit Care Med. 1998, 158: 1763-1769. 10.1164/ajrccm.158.6.9804056.

    CAS  PubMed  Google Scholar 

  98. Bouhemad B, Ferrari F, Leleu K, Arbelot C, Lu Q, Rouby JJ: Echocardiographic Doppler estimation of pulmonary artery pressure in criticallyill patients with severe hypoxemia. Anesthesiology. 2008, 108: 55-62. 10.1097/01.anes.0000296067.02462.34.

    PubMed  Google Scholar 

  99. Caille V, Amiel JB, Charron C, Belliard G, Vieillard-Baron A, Vignon P: Echocardiography: a help in the weaning process. Crit Care. 2010, 14: R120-10.1186/cc9076.

    PubMed Central  PubMed  Google Scholar 

  100. Mekontso-Dessap A, de Prost N, Girou E, Braconnier F, Lemaire F, Brun-Buisson C, Brochard L: B-type natriuretic peptide and weaning from mechanical ventilation. Intensive Care Med. 2006, 32: 1529-1536. 10.1007/s00134-006-0339-7.

    CAS  PubMed  Google Scholar 

  101. Grasso S, Leone A, De Michele M, Anaclerio R, Cafarelli A, Ancona G, Stripoli T, Bruno F, Pugliese P, Dambrosio M, Dalfi no L, Di Serio F, Fiore T: Use of N-terminal pro-brain natriuretic peptide to detect acute cardiacdysfunction during weaning failure in difficult-to-wean patients with chronicobstructive pulmonary disease. Crit Care Med. 2007, 35: 96-105. 10.1097/01.CCM.0000250391.89780.64.

    CAS  PubMed  Google Scholar 

  102. Quesnel C, Piednoir P, Gelly J, Nardelli L, Lecon V, Lasocki S, Bouadma L, Philip I, Elbim C, Mentre F, Crestani B, Dehoux M: Alveolar fibrocyte percentage is an independent predictor of poor outcome inpatients with acute lung injury. Crit Care Med. 2012, 40: 21-28. 10.1097/CCM.0b013e31822d718b.

    PubMed  Google Scholar 

  103. Storre JH, Steurer B, Kabitz HJ, Dreher M, Windisch W: Transcutaneous PCO2 monitoring during initiation of noninvasive ventilation. Chest. 2007, 132: 1810-1816. 10.1378/chest.07-1173.

    PubMed  Google Scholar 

  104. Vignaux L, Vargas F, Roeseler J, Tassaux D, Thille AW, Kossowsky MP, Brochard L, Jolliet P: Patient-ventilator asynchrony during non-invasive ventilation for acuterespiratory failure: a multicenter study. Intensive Care Med. 2009, 35: 840-846. 10.1007/s00134-009-1416-5.

    PubMed  Google Scholar 

  105. Unroe M, MacIntyre N: Evolving approaches to assessing and monitoring patient-ventilatorinteractions. Curr Opin Crit Care. 2010, 16: 261-268. 10.1097/MCC.0b013e328338661e.

    PubMed  Google Scholar 

  106. Antonelli M, Conti G, Moro ML, Esquinas A, Gonzalez-Diaz G, Confalonieri M, Pelaia P, Principi T, Gregoretti C, Beltrame F, Pennisi MA, Arcangeli A, Proietti R, Passariello M, Meduri GU: Predictors of failure of noninvasive positive pressure ventilation in patientswith acute hypoxemic respiratory failure: a multi-center study. Intensive Care Med. 2001, 27: 1718-1728. 10.1007/s00134-001-1114-4.

    CAS  PubMed  Google Scholar 

  107. Pelosi P, Ferguson ND, Frutos-Vivar F, Anzueto A, Putensen C, Raymondos K, Apezteguia C, Desmery P, Hurtado J, Abroug F, Elizalde J, Tomicic V, Cakar N, Gonzalez M, Arabi Y, Moreno R, Esteban A: Management and outcome of mechanically ventilated neurologic patients. Crit Care Med. 2011, 39: 1482-1492. 10.1097/CCM.0b013e31821209a8.

    PubMed  Google Scholar 

  108. Minardi J, Crocco TJ: Management of traumatic brain injury: first link in chain of survival. Mt Sinai J Med. 2009, 76: 138-144. 10.1002/msj.20105.

    PubMed  Google Scholar 

  109. Esteban A, Anzueto A, Frutos F, Alia I, Brochard L, Stewart TE, Benito S, Epstein SK, Apezteguia C, Nightingale P, Arroliga AC, Tobin MJ: Characteristics and outcomes in adult patients receiving mechanical ventilation: a28-day international study. JAMA. 2002, 287: 345-355. 10.1001/jama.287.3.345.

    PubMed  Google Scholar 

  110. Zygun DA, Kortbeek JB, Fick GH, Laupland KB, Doig CJ: Non-neurologic organ dysfunction in severe traumatic brain injury. Crit Care Med. 2005, 33: 654-660. 10.1097/01.CCM.0000155911.01844.54.

    PubMed  Google Scholar 

  111. Lowe GJ, Ferguson ND: Lung-protective ventilation in neurosurgical patients. Curr Opin Crit Care. 2006, 12: 3-7. 10.1097/01.ccx.0000198055.29600.4b.

    PubMed  Google Scholar 

  112. Namen AM, Ely EW, Tatter SB, Case LD, Lucia MA, Smith A, Landry S, Wilson JA, Glazier SS, Branch CL, Kelly DL, Bowton DL, Haponik EF: Predictors of successful extubation in neurosurgical patients. Am J Respir Crit Care Med. 2001, 163: 658-664. 10.1164/ajrccm.163.3.2003060.

    CAS  PubMed  Google Scholar 

  113. Steiner LA, Balestreri M, Johnston AJ, Czosnyka M, Coles JP, Chatfi eld DA, Smielewski P, Pickard JD, Menon DK: Sustained moderate reductions in arterial CO2 after brain trauma time-course ofcerebral blood flow velocity and intracranial pressure. Intensive Care Med. 2004, 30: 2180-2187. 10.1007/s00134-004-2463-6.

    PubMed  Google Scholar 

  114. Deem S: Management of acute brain injury and associated respiratory issues. Respir Care. 2006, 51: 357-367.

    PubMed  Google Scholar 

  115. Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW: Guidelines for the management of severe traumatic brain injury. XIV.Hyperventilation. J Neurotrauma. 2007, 24 (Suppl 1): S87-S90.

    PubMed  Google Scholar 

  116. Stocchetti N, Maas AI, Chieregato A, van der Plas AA: Hyperventilation in head injury: a review. Chest. 2005, 127: 1812-1827. 10.1378/chest.127.5.1812.

    PubMed  Google Scholar 

  117. Caricato A, Conti G, Della CF, Mancino A, Santilli F, Sandroni C, Proietti R, Antonelli M: Effects of PEEP on the intracranial system of patients with head injury andsubarachnoid hemorrhage: the role of respiratory system compliance. J Trauma. 2005, 58: 571-576. 10.1097/01.TA.0000152806.19198.DB.

    PubMed  Google Scholar 

  118. Young N, Rhodes JK, Mascia L, Andrews PJ: Ventilatory strategies for patients with acute brain injury. Curr Opin Crit Care. 2010, 16: 45-52. 10.1097/MCC.0b013e32833546fa.

    PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Jean-Louis Vincent.

Additional information

Competing interests

Over the last five years, L Brochard's laboratory has received research grants forspecific research projects from the following companies: Dräger (SmartCare;Lübeck, Germany), Maquet (NAVA; Rastatt, Germany), Covidien (PAV+; Dublin,Ireland), General Electric Company (FRC; Fairfield, CT, USA), Fisher & Paykel(Optiflow; Auckland, New Zealand), and Philips Respironics (NIV; Murrysville, PA, USA).GSM and FJB serve on the medical advisory board for Pulsion Medical Systems (Munich,Germany). L Blanch holds €1,001 to €5,000 in stock ownership in Better CareS.L., a spinoff of Corporació Sanitària Parc Taulí (Sabadell, Spain). JMhas received research grants from Covidien and General Electric Company. J-CR hasreceived research grants from Dräger, Covidien, and General Electric Company. DG isa member of the critical care medical advisory board of GE Healthcare (Madison, WI, USA)and has received speaking fees from Dräger and GE Healthcare. AV-B has receivedresearch grants from General Electric Company and Maquet. The research laboratory of SJhas received research grants from Dräger Medical France and Maquet France (Ardon,France). OS has received lecture fees and travel expenses from Dräger Medical andGE Healthcare and has received payment for a patent application from DrägerMedical. The other authors declare that they have no competing interests.

Authors’ original submitted files for images

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Brochard, L., Martin, G.S., Blanch, L. et al. Clinical review: Respiratory monitoring in the ICU - a consensus of 16. Crit Care 16, 219 (2012).

Download citation

  • Published:

  • DOI:


  • Right Ventricle
  • Acute Respiratory Distress Syndrome
  • Dead Space
  • Transpulmonary Pressure
  • Esophageal Pressure