Over recent decades, we have seen many advancements in mechanical ventilation (MV) and respiratory monitoring, some resulting in documented decreases in mortality. Nevertheless, the mortality attributable to acute respiratory distress syndrome (ARDS) and postoperative pulmonary complications remains high. Although invasive, MV is the cornerstone in the treatment of respiratory failure. MV itself can induce lung injury in both ARDS and healthy lungs (ventilator-induced lung injury [VILI]). The main mechanisms of VILI are barotrauma due to high transpulmonary pressure (stress), volutrauma due to alveolar overdistension (strain), atelectrauma due to cyclic opening and collapsed ventilatory units, and biotrauma due to the release of inflammatory cytokines. Many studies have looked at techniques for improving outcomes in patients at risk for VILI, and to date, limiting lung stretch is the most effective strategy identified.
As part of the process of prevention, early detection, and treatment of respiratory failure and pulmonary complications, whether related to the primary disease process or to the potential harmful effects of MV, respiratory monitoring has evolved significantly in several different ways to now hold a central place in modern intensive care practice.
In this review, we highlight various methods of respiratory monitoring in the intensive care unit (ICU), with particular emphasis on implementing protective ventilatory strategies to minimize VILI, with the ultimate goal of improving outcomes.
Invasive and Noninvasive Carbon Dioxide Monitoring
Capnometry is one of the simplest noninvasive tools for indirect assessment of the partial pressure of arterial carbon dioxide (Pa co 2 ) and can provide information about alveolar ventilation, pulmonary perfusion, ventilator disconnection, or tube misplacement. Waveform analysis, with capnography, provides additional information, such as evidence of obstructive airway disease. The characteristic waveform of capnography is composed of three phases. The first phase, which is early expiration, represents the gas flow originated from dead space formed by airways and apparatuses, where CO 2 is virtually absent. Phase II represents the alveolar gas that is progressively emptying from alveoli. Phase III represents CO 2 removed from alveolar gas, the so-called alveolar plateau. The end-tidal CO 2 concentration (P ETCO 2 ) is measured at the highest point in phase III ( Fig. 8-1 ).
An immediate qualitative bedside interpretation of capnography is done by inspecting the slope of phase III, representing ventilation and perfusion heterogeneity. A steeper slope of phase II to phase III is found in patients with severe asthma or in chronic obstructive airway disease and correlates with the severity of obstruction. The different characteristics of capnography are demonstrated in Figure 8-1 .
Measurement of Ventilatory Dead Space
Physiologic dead space (Vd phy ) comprises airway dead space and alveolar dead space. The dead space (Vd) in volumetric capnography can be quantified by plotting CO 2 elimination (V co 2 ) against exhaled tidal volume (V T ). The Vd phy /V T ratio can be calculated by the modified Bohr equation and equals (Pa co 2 –P ETCO 2 )/Pa co 2 , assuming that Pa co 2 is comparable to the alveolar partial pressure of CO 2 (P co 2 ). The alveolar dead space is calculated by subtraction of airway dead space from physiologic dead space. The Douglas bag method is a more accurate but cumbersome technique that requires sampling of exhaled gases in a specific bag. Sinha et al. demonstrated good agreement between dead space measured by volumetric capnography and the Douglas bag method.
Clinical Applications of Dead Space Measurement
Patients with ARDS have an increased alveolar dead space because of closed, injured alveoli: the percentage of alveolar dead space is associated with mortality in ARDS. Positive end-expiratory pressure (PEEP) can both decrease and increase dead space. On the one hand, PEEP induces alveolar recruitment, and this reduces dead space. Conversely, high levels of PEEP may result in alveolar overdistension, compressing adjacent vessels and pulmonary tissue, thereby increasing alveolar dead space. Blanch and colleagues observed that, in patients with respiratory failure who responded to PEEP with alveolar recruitment, a decrease of the Pa co 2 –P ETCO 2 gradient correlated with the PEEP level. Another study, by the same authors, showed good correlation between severity of ARDS with parameters derived from volumetric capnography.
A reduction in pulmonary artery blood flow leads to an increase in alveolar dead space. A normal alveolar dead space fraction increases the negative predictive value of routine d -dimer plasma level in ruling out pulmonary embolism (PE). Alveolar dead space estimated by volumetric capnography showed good diagnostic accuracy in the emergency department, where a rapid exclusion of PE is warranted. The dead space fraction may be useful for monitoring treatment response after thrombolytic therapy in patients with massive PE.
Partial Rebreathing Technique of Carbon Dioxide Measurement
With the use of the indirect Fick principle, cardiac output (CO) is the ratio between V co 2 (the elimination of arterial CO 2 content) and the difference between venous CO 2 content (C V co 2 ) and arterial CO 2 content (C a co 2 ). The partial rebreathing of CO 2 measurement technique is a noninvasive CO monitoring for mechanically ventilated patients that uses this principle. V co 2 is derived from the difference of CO 2 concentration between inspired and expired gas, and this is then used to calculate pulmonary blood flow. Several studies have found a good correlation between CO estimated by NICO and that measured by means of thermodilution methods, but they also found important limitations, especially when the patients have an intrapulmonary shunt or when Pa co 2 is lower than 30 mm Hg.
Transcutaneous Carbon Dioxide Monitoring
The standard method for direct measurement of Pa co 2 is arterial blood gas analysis. However, continuous monitoring requires an invasive procedure that has several technical issues. Likewise, noninvasive measurement such of P ETCO 2 is limited to mechanically ventilated patients. Transcutaneous CO 2 monitoring TC CO 2 is a commercially available alternative that is applicable to nonintubated patients. Three different technologies allow TC CO 2 measurement: direct measurement of CO 2 gas that has diffused through the skin by sensor warming, an electrochemical measurement technique measuring pH from an electrolyte layer in contact with skin, and an optical-only CO 2 technique that uses a principle analogous to pulse oximetry.
The TC CO 2 technique has been used in neonates, patients with sleep disorders, and critical care patients for decades, despite limited accuracy and side effects. Several studies showed the efficacy in monitoring patients with hypercapnic respiratory failure undergoing noninvasive MV.
Gas Exchange Monitoring
Critical care patients often show an increased oxygen demand caused by events such as fever, delirium, shivering, seizures, or systemic inflammatory response.
The most basic approach to gas exchange monitoring is the arterial blood gas analysis, in particular the assessment of Sa o 2 (arterial oxygen saturation); more complete information can be provided by mixed venous blood gas analysis obtained from a pulmonary artery catheter, namely SvO 2 (mixed venous oxygen saturation).
The relationship between the two is described by the formula SvO 2 = Sa o 2 – V o 2 /CO × 1/Hb, where V o 2 is the oxygen consumption, CO is cardiac output, and Hb is the hemoglobin concentration.
Several studies investigated the usefulness of targeting SvO 2 above 70% as a therapeutic goal in high-risk surgical patients and septic shock, showing encouraging results, at the cost of performing an invasive maneuver for the placement of the pulmonary artery catheter.
Saturation of central venous blood, drawn from a central venous catheter, is referred to as ScvO 2 (central venous oxygen saturation) and is considered as a surrogate of SvO 2. It is still debated whether such approximation is acceptable in patients with sepsis because of the uneven contribution of upper body and splanchnic circulation to ScvO 2 . Devices capable of continuously monitoring either ScvO 2 or SvO 2 are becoming widely available, and their cost-effectiveness is under investigation.
Respiratory Mechanics
Respiratory System Compliance, Resistance, and Static Pressure-Volume Curve Analysis
The airway opening pressure (P AO ) is the pressure that overcomes total airway resistance and elastic recoil of the total respiratory system. To measure respiratory system mechanics during MV, one must separate the P AO into two distinct components: the resistive airway pressure (P aw ) and the static or plateau pressure (Pplat). Importantly, for these values to be measured, patients require neuromuscular blockade and volume-controlled ventilation. During constant inspiratory flow, resistive P aw can be measured, as can Pplat, if an inspiratory pause has been set.
Static lung compliance is measured to assess the effect of lung injury on lung parenchyma by various diseases, particularly ARDS. Total respiratory system compliance measurement is a better measure than lung compliance. Total respiratory system compliance is calculated by the ratio of tidal volume to plateau pressure minus total PEEP.
Low respiratory system compliance may result from high Pplat level associated with increased end-expiratory lung volume (EELV) from dynamic hyperinflation consequent of intrinsic PEEP (PEEPi). The end-expiratory occlusion technique can be used to measure PEEPi. However, the limitation of this technique is that it underestimates actual PEEPi in cases of severe narrowing of airways from the equal pressure point, creating upstream and downstream compartments, and it is unreliable when patients are not receiving controlled MV.
High respiratory system resistance may be caused by either bronchospasm or obstruction of the endotracheal tube. The elastic properties of the respiratory system are the result of the complex relationship between the lung elastance and the chest wall elastic recoil. The pressure-volume (PV) curve is useful for understanding alterations in respiratory system mechanics. The standard technique to plot the PV curve is the “supersyringe” method. This involves inflation of a small volume of gas at very low flow rates during measurement and the plotting of the volume-pressure (VP) relationship. Hysteresis is the area between the inflation and deflation limb of the PV curve (PV loop). A greater area is observed in ARDS because of the high alveolar opening pressures. In ARDS, the inspiratory PV curve demonstrates the critical alveolar opening pressure, the alveolar closing pressure, and the recruitability of alveoli. The pressure at which significant alveolar recruitment begins creates a lower inflection point (LIP) on the curve. The exact method to identify the LIP, sometimes known as Pflex, is still debated. Gattinoni et al. proposed Pflex as the pressure at the intersection between the extrapolated lines drawn from the portion of the PV curve at low lung volume (low compliance) and from the steep portion of the PV curve. In ARDS, an MV strategy that included setting PEEP at 2 cm H 2 O above Pflex was shown to be associated with lower mortality compared with a higher stretch approach. The upper inflection point (UIP) indicates the presence of alveolar strain. Therefore, when setting tidal volume and PEEP, physicians should try to avoid the presence of a UIP. This technique is mainly used in research rather than in clinical practice.
Dynamic Pressure–Time and Pressure Volume Curve
Commercially available ventilators are able to display the dynamic pressure curve without interfering with the ventilation. Therefore several parameters may be used as indicators of lung recruitability and overhyperinflation, especially in ARDS. The parameters derived from the airway pressure profile such as the distension index (%E 2 ) or the stress index were recently proposed ( Fig. 8-2 ).
Distension Index (Intratidal Pressure-Volume Loop)
The %E 2 (distension index) is the ratio of the compliance of the last 20% of the dynamic VP curve to the total compliance (C 20 /C). This parameter is derived from multiple linear regression analysis of resistive P aw and flow that included the nonlinearity part of the PV loop. Positive values of %E 2 indicate tidal overdistension, and negative values indicate tidal recruitment. In ARDS, a %E 2 higher than 30% indicates lung overinflation ( Fig. 8-2 ).
Stress Index
The stress index is identified from the shape of the inspiratory pressure–time curve during constant flow in volume-controlled ventilation and is calculated from the midportion of the curve. If downward concavity is present, then the stress index is less than 1 and means tidal recruitment. An upward convexity means that the stress index is greater than 1 and hyperinflation is occurring. The presence of a straight line, where the stress index equals 1, represents normal ventilation ( Fig. 8-2 ).
The use of % E 2 and stress index is controversial in patients with ARDS. During low tidal volume ventilation in injured lungs, the PEEP level providing the lowest lung elastance was erroneously identified as overdistending by the stress index and % E 2 in an experimental study. Furthermore, Formenti and colleagues demonstrated elevation of the stress index despite tidal recruitment without overinflation in a swine model of pleural effusion.
Application of Esophageal Pressure Measurement
Physiologic Background
Stress and distension indices are calculated from the pressure curve and are based on the total respiratory system compliance, which is influenced by the interaction between the lungs and the chest wall. This assumes that the disease process principally affects the lungs, and the chest wall is passive. However, many cases of ARDS derive from extrapulmonary disease (such as sepsis or pancreatitis), whereas other patients have decreased chest wall compliance from increased abdominal pressure, obesity, or pregnancy. This results in higher than normal pleural pressure. The pleural pressure can be indirectly measured with an esophageal balloon catheter. The esophagus is a passive structure adjacent to the pleural space. The pressure at the lower third of the esophagus is comparable to the pleural pressure in the upright position. In addition, with commercially available double balloon catheters, gastric pressure can be measured simultaneously, and its value approximates intra-abdominal pressure (IAP). To test whether the esophageal balloon is placed in the correct position in spontaneous breathing patients, one can use the Baydur technique, and the end-expiratory occlusion maneuver can be applied. When the subjects start to inspire, the fluctuation and ratio of change of both esophageal and airway pressure should be comparable. In passively mechanically ventilated patients, the catheter should be inserted into the stomach and tested by observation of the transient increase in the balloon pressure during abdominal compression. Then the catheter is withdrawn proximally until the point where the cardiac pulsation can be clearly observed. External chest compression can be applied after airway occlusion. A ΔP es /ΔP aw ratio (esophageal pressure/airway pressure ratio) ranging from 0.8 to 1.2 (10% to 20%) is considered to be marker of correct placement.
Applications and Limitations
Transpulmonary pressure is a distending force of the lung, which is the difference between estimated alveolar pressure and pleural pressure. Esophageal pressure is a less accurate surrogate of pleural pressure in the supine position because of the compressive effect of the heart and because P es is the pressure measured only in a mid-lung region. This may be negatively affected by raised IAP and asymmetric lung disease.
Nevertheless, in an ARDS experimental model, with high potential for recruitment, we found good correlations between the variations of invasive pleural pressure measurement and esophageal pressure regardless of the dependent, nondependent, or middle lung regions. In spontaneous breathing patients, esophageal pressure in obese patients tends to be higher than in nonobese patients.
Talmor and colleagues demonstrated the benefit of titrating PEEP using transpulmonary pressure in ARDS. Oxygenation was improved compared with the conventional ARDSNet (ARMA study group) protocol at 72 hours. There was no statistically significant difference in mortality.
Other investigators have proposed the use of a transpulmonary lung approach based on PEEP titration to target an elastance-derived transpulmonary pressure of 26 cm H 2 O (centimeters of water) according to the Gattinoni method. In an experimental ARDS canine model with a stiff chest wall, the transpulmonary pressure based on the lung approach appears to increase lung recruitment without hemodynamic disturbance.
The incidence of intra-abdominal hypertension is high (>30%) in critically ill patients and is associated with elevated mortality. In ARDS with IAP lower than 12 mm Hg, PEEP titration with respiratory mechanics is unaffected by IAP. There is a linear correlation between IAP and chest wall elastance in patients with extrapulmonary ARDS.
In anesthetized, obese patients, increases in body mass index correlate with decreases in lung volume and compliance. Increases in IAP, such as by insufflation, are correlated with a further reduction of chest wall compliance. This may explain why severely obese patients undergoing MV are more prone to having ARDS.
In patients with ARDS, we recommend adjusting the level of PEEP with either IAP or transpulmonary pressure. These measurements are especially important when ARDS develops (1) secondary to extrapulmonary disease, (2) in high-risk postoperative abdominal surgical patients who have abdominal hypertension, and (3) in patients who are obese.
Parameters During Weaning
Work of breathing (WOB) refers to the volume of lung expansion that results from respiratory muscle contraction and is determined by total respiratory system compliance and airway resistance. Monitoring of WOB may be useful for the evaluation of difficult-to-wean patients. In assist-control ventilation, the WOB can be measured with the calculation of the pressure time product (PTP) from P es . This estimates the effort made by the respiratory muscles. The PTP is calculated from the difference between P es during assisted breathing and the elastic recoil pressure of the chest wall during passive ventilation in a similar volume and flow setting. However, P es can be altered by artifacts induced by expiratory muscle contraction. For this problem to be resolved, intragastric pressure should be simultaneously assessed. This allows for calculation of the trans-diaphragmatic pressure, the difference between P es and intragastric pressure.
The rapid shallow breathing index (RSBI) is calculated as the ratio between respiratory rate in minutes −1 and tidal volume in liters. It is a widely used tool to predict weaning success: if the RSBI is less than 100, then the patient is likely to wean. However, in elderly patients older than 70 years, the cutoff value should be raised to 130.
Jubran and colleagues have proposed a new index, the “Pes trend index,” calculated by performing repeated measurements of P es over time. The trend of P es swing during a 9-minute spontaneous breathing trial was used for predicting weaning success, with an area under the receiver operating characteristic curve of 0.94. A high swing of P es during the weaning period resulted in a higher chance of weaning failure. This index showed greater diagnostic accuracy when compared with the RSBI, but it is clearly more complex and invasive.
Airway Occlusion Pressure
The airway occlusion pressure (P 0.1 ) is the measurement of the negative airway pressure within 100 milliseconds (0.1 second) after inspiratory occlusion. P 0.1 is used for estimation of neural inspiratory drive. The P 0.1 is thought to correlate with WOB and predict failure to wean. In patients with chronic obstructive pulmonary disease, a P 0.1 lower than 6 cm H 2 O was associated with successful weaning. In postoperative patients with sepsis, during gradual decrease of pressure support, a P 0.1 higher than 2.9 cm H 2 O was associated with the use of the sternocleidomastoid muscle as an accessory muscle of inspiration. Therefore it may be a useful tool for optimizing the level of pressure support during weaning.
Maximal Inspiratory Pressure
Maximal inspiratory pressure (P Imax ) measurement is a test that reflects inspiratory muscle function, especially the diaphragm. P Imax measurement is performed by occlusion of the proximal end of the endotracheal tube for 25 seconds with a one-way valve that prevents the patient from generating an inspiratory flow. The P Imax is measured at end inspiration, and several studies have shown that a P Imax of less than −20 to −30 cm H 2 O provided high sensitivity, but low specificity, for predicting weaning success.
The combination of P 0.1 and P Imax , the P 0.1 /P Imax ratio, when less than 0.3, has been shown to be a sensitive predictor of weaning failure.
Asynchrony and Waveform Monitoring
Prolonged MV is associated with a high incidence of patient ventilator asynchrony. Although automated detection of asynchrony would be a valuable tool, it has been infrequently studied, and the most commonly used detection method is careful visual inspection of the flow and pressure-time waveform.
Ineffective triggering is the most common cause of asynchrony and usually results from PEEPi. We can detect this by identifying a sudden positive change of flow during the expiratory phase of the flow-time waveform and a negative deflection in the pressure-time waveform ( Fig. 8-3 ).
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