Open Access

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

  • Laurent Brochard1, 16,
  • Greg S Martin2,
  • Lluis Blanch3, 17,
  • Paolo Pelosi4,
  • F Javier Belda5,
  • Amal Jubran6,
  • Luciano Gattinoni7,
  • Jordi Mancebo8,
  • V Marco Ranieri9,
  • Jean-Christophe M Richard1,
  • Diederik Gommers10,
  • Antoine Vieillard-Baron11,
  • Antonio Pesenti12,
  • Samir Jaber13,
  • Ola Stenqvist14 and
  • Jean-Louis Vincent15Email author
Critical Care201216:219

DOI: 10.1186/cc11146

Published: 26 April 2012

Abstract

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.

Introduction

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 technique

Continuous versus intermittent

Specific situations

Potential usefulness

Limitations

Pulse oximetry

Continuous

All patients receiving MV

Detection of hypoxemia

 

Ventilator pressures

Continuous

All patients receiving volume-controlled modes

 

Less reliable when patient is breathing actively

Ventilator traces

Continuous

All patients receiving MV

 

Clinicians need to learn how to read traces (no automatic detection)

Respiratory mechanics

Intermittent

Passive patients

ARDS, COPD

Less reliable when patient is awake

Pressure/volume curves

Intermittent

Passive patients

ARDS

Complex and need sedation and relatively homogeneous lungs

Work of breathing, pressure-time product

Intermittent

Respiratory distress, ventilator setting, weaning

Research

No automated measurement; needs esophageal pressure

Extravascular lung water

Intermittent

Pulmonary edema

Diagnosis of pulmonary edema

Complex and needs invasive devices

Lung volumes

Intermittent

ARDS

Could help to define risks of ventilation and assess recruitment

Need a passive patient

Electric impedance tomography

Continuous

ARDS

Could help to visualize regional ventilation

Needs a specific tool

Hemodynamic monitoring

Continuous or intermittent

Patients who have hemodynamic impairment and who are receiving MV

Helps to understand hypoxemia and its consequences

More or less invasive

Volumetric capnography

Continuous

ARDS

 

Complex analysis

Esophageal and transpulmonary pressure

Continuous or intermittent

ARDS

Could help to titrate ventilator pressures

Complex interpretation and difficult placement

Diaphragmatic electromyography

Continuous

Patients receiving assisted ventilation

 

Needs specific catheter, no absolute value

ARDS, acute respiratory distress syndrome; COPD, chronic obstructive pulmonarydisease; MV, mechanical ventilation.

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].
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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.
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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.
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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].
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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].
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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].
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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.

Abbreviations

ARDS: 

acute respiratory distress syndrome

BAL: 

bronchoalveolar lavage

BNP: 

B-typenatriuretic protein

CBF: 

cerebral blood flow

CO2

carbon dioxide

COPD: 

chronic obstructive pulmonary disease

CT: 

computed tomography

EELV: 

end-expiratorylung volume

EIT: 

electrical bioimpedance tomography

Elcw

elastance of the chest wall

Ellung

elastance of the lung

ETT: 

endotracheal tube

EVLW: 

extravascular lung water

FiO2

inspiredfraction of oxygen

FRC: 

functional residual capacity

IAP: 

intra-abdominal pressure

ICP: 

intracranial pressure

ICU: 

intensive care unit

LIP: 

lower inflection point

NIV: 

non-invasive ventilation

P0.1

occlusion pressure

PaCO2

arterial partial pressure of carbon dioxide

PaO2

arterial partial pressureof oxygen

Paw

airway pressure

PCO2

partial pressure of carbondioxide

PECO2

partial pressure of carbon dioxide in mixedexpired gas

PEEP: 

positive end-expiratory pressure

Pes

esophageal pressure

PetCO2

end-tidal partialpressure of carbon dioxide

Ppl

pleural pressure

P/V: 

pressure/volume

RV: 

right ventricle

SBT: 

spontaneous breathing trial

SvO2

mixed venous oxygensaturation

UIP: 

upper inflection point

Vdalv

alveolar dead space

Vdaw

airway dead space

Vdphys

physiologic dead space

VILI: 

ventilator-induced lung injury

VT

tidal volume

WOB: 

work of breathing.

Declarations

Authors’ Affiliations

(1)
Department of Intensive Care, Hôpitaux Universitaires de Genève
(2)
Division of Pulmonary, Allergy and Critical Care, Emory University School of Medicine, Grady Memorial Hospital
(3)
Critical Care Center, Corporacio Sanitaria Universitària Parc Tauli, Universitat Autònoma de Barcelona
(4)
Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, San Martino Hospital
(5)
Department of Anesthesia and Surgical Critical Care, Hospital Clínico Universitario
(6)
Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. VA Hospital
(7)
Dipartimento di Anestesiologia, Terapia Intensive e Scienze Dermatologiche, and Dipartimento do Anestesia, Rianimazione (Intensive e Subintensiva) e Terapia del Dolore, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Università degli Studi di Milano
(8)
Servicio Medicina Intensiva, Hospital de la Santa Creu i Sant Pau
(9)
Department of Anesthesia and Intensive Care Medicine, University of Turin, S. Giovanni Battista, Molinette Hospital
(10)
Adult Intensive Care, Erasmus MC
(11)
Intensive Care Unit, Section Thorax - Vascular disease - Abdomen - Metabolism, CHU Ambroise Paré
(12)
Anesthesia and Intensive Care, University of Milan-Bicocca
(13)
Department of Critical Care Medicine and Anesthesiology, Saint Eloi University Hospital and Montpellier School of Medicine
(14)
Department of Anesthesiology and Intensive Care, Sahlgrenska University Hospital
(15)
Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles
(16)
Université de Genève
(17)
CIBER Enfermedades Respiratorias

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