Derecruitment volume assessment derived from pressure–impedance curves with electrical impedance tomography in experimental acute lung injury

Abstract

Objective

To investigate the accuracy of derecruitment volume (V_DER) assessed by pressure–impedance (P-I) curves derived from electrical impedance tomography (EIT).

Methods

Six pigs with acute lung injury received decremental positive end-expiratory pressure (PEEP) from 15 to 0 in steps of 5 cmH₂O. At the end of each PEEP level, the pressure–volume (P-V) curves were plotted using the low constant flow method and release maneuvers to calculate the V_DER between the PEEP of setting levels and 0 cmH₂O (V_DER-PV). The V_DER derived from P-I curves that were recorded simultaneously using EIT was the difference in impedance at the same pressure multiplied by the ratio of tidal volume and corresponding tidal impedance (V_DER-PI). The regional P-I curves obtained by EIT were used to estimate V_DER in the dependent and nondependent lung.

Results

The global lung V_DER-PV and V_DER-PI showed close correlations (r = 0.948, P<0.001); the mean difference was 48 mL with limits of agreement of −133 to 229 mL. Lung derecruitment extended into the whole process of decremental PEEP levels but was unevenly distributed in different lung regions.

Conclusions

P-I curves derived from EIT can assess V_DER and provide a promising method to estimate regional lung derecruitment at the bedside.

Keywords

Acute lung injury lung volume electric impedance positive end-expiratory pressure pressure-volume curve lung derecruitment

Introduction

The positive end-expiratory pressure (PEEP) plays an important role in supporting patients with acute respiratory distress syndrome (ARDS) who are on mechanical ventilation because it contributes to the recruitment of atelectatic alveoli and improves oxygenation.¹ However, several large randomized controlled trials failed to demonstrate that patients could benefit from high PEEP levels.^2–4 Not identifying the patients’ response to PEEP possibly led to these contradictory results.⁵ The optimal PEEP level should induce lung recruitment to decrease lung stress and strain.⁶ However, if PEEP levels only act on aerated lung areas, it may mainly result in overdistension and increase the risk of ventilator-induced lung injury.⁷ Therefore, it is of paramount importance to assess lung recruitment continuously at the bedside to determine the optimal PEEP levels for different individuals.

Pressure–volume (P-V) curves provide a quantitative method to assess recruitment or derecruitment volumes at the bedside.^8–10 However, the change in end expiratory lung volume (ΔEELV) induced by PEEP is required to plot multiple P-V curves, which can only be measured by a specific ventilator or the release maneuver at the bedsides.^9,10 Moreover, only the global lung information is provided. Electrical impedance tomography (EIT) is a radiation-free and real-time tool to monitor the change in global and regional impedance in the lungs at the bedside.¹¹ Previous studies have shown that changes in lung volume are closely correlated with changes in impedance as measured by EIT.^12–18 Previous studies found a correlation between recruitment volumes that were measured by EIT and the reference method, but they were both based on a simplified method, which was the difference between the actual and minimal predicted lung volume change induced by PEEP.^19,20 Although the simplified method is convenient for clinical application, recruitment volume that is assessed by the simplified method was significantly lower than that assessed by multiple P-V curves.²¹

In this study, a lung injury model was induced in the pig by the bronchoalveolar instillation of hydrochloride. Low constant flow inflations were performed at decremental PEEP levels. Lung derecruitment volume (V_DER) was measured using pressure–impedance (P-I) curves that were derived from EIT (expressed as V_DER-PI), and they were then compared with that measured using the P-V curve method (expressed as V_DER-PV). We hypothesized that EIT could assess global lung V_DER accurately and that this would have great value in regional V_DER assessments at the bedside.

Materials and methods

This animal study was approved by the Ethics Committee for Experimental Studies at Beijing Neurosurgical Institute, Beijing, China (No. 201803002). All animal procedures were conducted in accordance with the recommendations of the Guide for the Care and Use of Laboratory Animals from the National Institutes of Health.

Animal preparation

The study was performed on six healthy female Bama pigs (weight, 42 [range, 40 to 44] kg; age, 12 [range, 11 to 14] months; in the diestrous cycle). The animals were anesthetized with intramuscular ketamine (10 mg/kg) and xylazine (1 mg/kg) injections, and they were placed in the supine position on a thermocontrolled operation table. Rectal temperature was maintained at approximately 37°C. Femoral venous catheterization was performed for fluid and drug administration, and femoral arterial catheterization was used for invasive blood pressure monitoring and blood gas analysis sampling. A tube with an 8-mm inner diameter (Smiths Medical International Ltd., Kent, UK) was placed by tracheostomy. Mechanical ventilation was set at a tidal volume of 6 to 8 mL/kg of body weight, a respiratory rate (RR) of 16 to 20 breaths/minute was used to keep the arterial partial pressure of carbon dioxide (PaCO₂) within 35 to 45 mmHg, and a PEEP of 5 cmH₂O and an inspired oxygen fraction (FiO₂) of 0.5 (Evita Infinity V500™, Dräger, Germany) were used. The pulse oxygen saturation and partial pressure of end-tidal carbon dioxide (P_ETCO2) were monitored continuously (BeneView T5, Mindray, Shenzhen, China). An additional heated pneumotachograph (Vitalograph. Inc., Lenexa, KS, USA) was positioned between the Y piece and the tracheostomy tube to monitor the gas flow. During the study, propofol (1 to 2 mg/kg/hour), fentanyl (5 μg/kg/hour), and rocuronium bromide (0.25 to 0.5 mg/kg/hour) were infused continuously to minimize suffering and abolish inspiratory effort.

Study protocol

After the initial preparation, the acute lung injury model was induced by instillation of hydrochloric acid (4 mL/kg) into the tracheostomy tube. The successful criteria were an arterial partial pressure of oxygen (PaO₂) of less than 100 mmHg at FiO₂ 0.5 and a PEEP of 5 cmH₂O after 30 minutes.²² The study protocol is shown in Figure 1.

Figure 1.

Illustration of the protocol with the example of positive end-expiratory pressure (PEEP) decreasing from 15 cmH₂O to 10 cmH₂O. The upper panel represents the flow waveform and the lower panel represents the airway pressure waveform over time. The recruitment maneuver was performed with pressure control ventilation to standardize the lung volume before changing the PEEP, which was set as an inspiratory pressure of 25 cmH₂O above PEEP. PEEP was set at 25 cmH₂O, RR at 10 breaths/minute, and the inspiratory-to-expiratory ratio was set at 1:1 for 2 minutes. Then the pigs were ventilated using volume-control ventilation for 10 minutes, and a low constant flow pressure–volume (P-V) curve was performed automatically by the P-V loop tool that was integrated into the ventilator. The pressure was increased from the corresponding PEEP level until the airway pressure was up to 35 cmH₂O (above PEEP) at a constant flow of 6 L/minute. Then mechanical ventilation resumed the previous settings for 10 minutes, and end inspiratory and expiratory occlusion (EIO and EEO) for 5 s were performed consecutively, following a release maneuver by disconnecting the animals from the ventilator during expiratory occlusion. When the flow returned to zero, the animal was reconnected to the ventilator and the recruitment maneuver was performed again. The PEEP was then decreased at a step of 5 cmH₂O.

During the study, PEEP was set from 15 to 0, at decremental steps of 5 cmH₂O, and the other ventilator settings remained unchanged. The recruitment maneuver was performed with pressure control ventilation before setting each PEEP level to standardize the lung volume, using a PEEP of 25 cmH₂O, a peak pressure of 50 cmH₂O, an RR of 10 breaths/minute, and an inspiratory to expiratory ratio of 1:1 for 2 minutes. At each PEEP level, the ventilation was stabilized for 10 minutes, after which a low constant flow inflation (6 L/minute) was performed automatically using the P-V loop tool that was integrated in the ventilator. The inflation was stopped when the airway pressure exceeded 35 cmH₂O over the corresponding PEEP. After completing the P-V curve maneuver, mechanical ventilation was restored to the previous settings for 10 minutes, and then blood gases (PaO₂ and PaCO₂), P_ETCO2, alveolar dead space fraction, and hemodynamics (heart rate and mean arterial pressure) were collected.²² End-inspiratory and end-expiratory occlusion were performed for 5 s to obtain the values that were used to calculate the compliance of the respiratory system (Crs). Then, the release maneuver was performed by disconnecting the animals from the ventilator during end-expiratory occlusion to obtain the PEEP volume resulting from PEEP withdrawal by the pneumotachograph monitor. Finally, PEEP was adjusted to the lower level, and the procedure was repeated as described above (Figure 1).

EIT measurements and analysis

EIT monitoring (PulmoVista 500; Dräger Medical GmbH, Lübeck, Germany) was performed throughout the procedure by placing a dedicated belt with 16 electrodes just below the axilla and one reference electrocardiogram electrode at the right lower extremity. EIT was connected to the ventilator (Evita Infinity V500™, Dräger, Germany) to collect serial flow, volume, airway pressure, and impedance measurements synchronously. The data were continuously recorded at 40 Hz and were downloaded and analyzed off-line using dedicated software (Dräger EIT Data Analysis Tool 6.3, Lübeck, Germany). The lung images were divided horizontally into two equal sizes from ventral to dorsal, as the nondependent lung region and the dependent lung region.²³ The last 1 minute of stable breaths during zero PEEP (ZEEP) was used as the baseline, and changes in lung impedance were reconstructed.²⁴ At the end of each PEEP level, the average values of the following data over 1 minute were calculated, as follows:

The regional distribution of the tidal ventilation in the nondependent lung region and dependent lung region were calculated as the change of region impedance divided by the change of total tidal impedance, expressed as Vt%_Non-dep and Vt%_Dep.¹⁹

The regional Crs for the nondependent lung region and the dependent lung region were calculated as the global Crs multiplied by the percentage of tidal volume in each region, expressed as Crs_Non-dep and Crs_Dep.¹⁹

The global and regional ΔEELV induced by PEEP were calculated as the change of end-expiratory impedance between the selected PEEP level and ZEEP, multiplied by the ratio of V_T (in mL) and the change of global tidal impedance (in absolute units) at the baseline.²²

The global ΔEELV induced by PEEP minus the product of Crs measured at ZEEP and the change of PEEP (ΔPEEP) was defined as V_DER based on the previously reported simplified method, based on the minimal predicted lung volume (expressed as V_DER-MPV) in the following equation: V_DER-MPV =ΔEELV − ΔPEEP × Crs.¹⁹

V_DER measured by P-V curves at a low constant flow inflation

The expired gas volume during the release maneuver was defined as the PEEP volume, which was measured by integrating the monitored flow wave using the pneumotachograph. During low constant flow at each PEEP level, the corresponding PEEP volume was added to each volume as the vertical axis, and airway pressure was represented on the horizontal axis. The four P-V curves at different PEEP levels and ZEEP were placed on the same Figure, in accordance with the pervious method.⁸ V_DER-PV between the selected PEEP level and ZEEP was the difference in lung volume at the same airway pressure of 20 cmH₂O, which was expressed as V_DER-PV in 5 to 0, 10 to 0, and 15 to 0 cmH₂O (Figure 2).²⁵

Figure 2.

The derecruitment volume (V_DER) measured by pressure–volume (P-V) curves and pressure–impedance (P-I) curves. (a) Shows the example of V_DER that was assessed with P-V curves (V_DER-PV). The P-V curves at different positive end-expiratory pressure (PEEP) levels (0, 5, 10, or 15 cmH₂O) were plotted on the same Figure. The V_DER-PV between given PEEP level and ZEEP was the difference in lung volume at the same airway pressure of 20 cmH₂O. (b) Shows the V_DER assessed with P-I curves (V_DER-PI) in the same animal. When the last 1 minute of stable breaths for ZEEP was selected as the reference (c), the change of impedance against reference values by EIT was obtained directly. P-I curves at different PEEP levels were plotted directly on the same graph (b). The difference of impedance between the given PEEP levels and ZEEP at the same airway pressure of 20 cmH₂O was defined as derecruitment impedance, which can be converted to V_DER-PI by multiplying the ratio of tidal volume and tidal impedance variation at ZEEP (c).

V_DER measured by P-I curves derived from EIT during low constant flow inflation

When we selected the last 1 minute of stable breaths at ZEEP as the reference, the impedance obtained directly by EIT at other PEEP levels represented the change in values compared with the reference values. We plotted the impedance of the total lung region against the airway pressure data at different PEEP levels as P-I curves. The difference in impedance between the set PEEP level and ZEEP at the same airway pressure of 20 cmH₂O was defined as derecruitment impedance, and it was converted to V_DER-PI by multiplying the ratio of tidal impedance variation and tidal volume within the reference period (Figure 2).²⁴ Additionally, the regional P-I curves in the nondependent and dependent lung region were also plotted to measure regional V_DER-PI using the same method, and we further calculated the difference in V_DER-PI between two adjacent PEEP levels as the ΔV_DER-PI between PEEP 15 to 10 cmH₂O, 10 to 5 cmH₂O, and 5 to 0 cmH₂O.²⁵

Statistical analysis

The sample size was calculated using the sampling correlation coefficient test in MedCalc (MedCalc Software, Ostend, Belgium). We considered the correlation coefficient between changes in impedance and volume on the P-V curve to be 0.97 with a type I error rate of 0.01 and type II error rate of 0.20 based on a previous study.¹⁴ Thus, the minimum required sample size was 6.

Categorical variables are reported as numbers and percentages. Continuous data are reported as the median and interquartile range (IQR). Agreement between V_DER-PV and V_DER-PI, the PEEP volume measured by the release maneuver, and the ΔEELV measured by EIT were tested using the Bland and Altman analysis.²⁶ Bias and standard deviation of the mean bias were calculated. Upper and lower limits of agreement were defined as bias ± 1.96 standard deviation (SD) of the mean bias. The correlations were analyzed using the Spearman coefficient (r). The differences in variables across different PEEP were assessed using Friedman’s nonparametric test. Post hoc pairwise comparisons were performed using the Wilcoxon test. Analyses were conducted using SPSS version 20.0 (IBM Corp., Armonk, NY, USA). P < 0.05 was considered to be statistically significant.

Results

The main characteristics of the animals are shown in the Table 1. The acute lung injury modeling successfully induced oxygenation (PaO2/FiO2) less than 200 (151 [IQR, 137–159]).

Table 1.

Baseline characteristics of pigs after ALI.

Variables	N = 6
Weight (kg)	42 (40,44)
Age (month)	12 (11,14)
Tidal volume (mL)	300 (300,315)
Respiratory Rate (breaths/minute)	20 (18.5,20)
PaO₂/FiO₂	151 (137,159)
PaCO₂ (mmHg)	46 (41,51)
P_ETCO₂ (mmHg)	32 (29,36.5)
Dead Space%	32 (28,33)
Crs (mL/cmH₂O)	35 (31, 43)
HR (beats/minute)	53 (47,72)
MAP (mmHg)	89 (72,95)

The data shown as the median (IQR).

ALI, acute lung injury; PaO₂, partial pressure of oxygen in arterial blood; FiO₂, inspired oxygen fraction; PaCO₂, partial pressure of carbon dioxide in arterial blood; P_ETCO₂, partial pressure of end-tidal carbon dioxide; Crs, compliance of respiratory system; HR, heart rate; MAP, mean arterial pressure; IQR, interquartile range.

Agreement of V_DER assessed by P-I and P-V curves

The calculated V_DER-PI had a close correlation with V_DER-PV (r = 0.948, P < 0.001); the bias (the lower and upper limits of agreement) was 48 (−133 to 229) mL (Figure 3a and 3b). ΔEELV that was measured by the EIT and the PEEP volume (the integral of flow during the release maneuver) also showed a significant correlation (r = 0.986, P < 0.001); the bias was 87 (−65 to 241) mL (Figure 3c and 3d). During low constant flow inflation, the increase in impedance was closely correlated with the increase in volume, and the correlation coefficient of regression increased from 0.973 to > 0.999.

Figure 3.

(a, b) Show the V_DER-PI that was correlated significantly with V_DER-PV (r = 0.948, P < 0.001, a), and the bias (lower and upper limits of agreement) was 48 (−133 to 229) mL (b). (c, d) Shows that ΔEELV measured by EIT had a close correlation with PEEP volume (r = 0.986, P < 0.001, c), and the bias between ΔEELV and PEEP volume was 87 (−65 to 241) mL (d).

The bias (lower and upper limits of agreement) between V_DER-MPV and V_DER-PV was −65 (−275 to 145) mL, and the correlation coefficient was 0.928 (P < 0.001).

Difference of ΔV_DER-PI in different lung regions

Figure 4 shows the change in global and regional ΔV_DER _- _PI in different regions. Although lung derecruitment occurred at different PEEP levels, it was unevenly distributed between the nondependent and dependent lung regions. In the nondependent region, values of ΔV_DER _- _PI between 15 and 10 cmH₂O had a decreasing tendency when compared with between 10 and 5 cmH₂O and between 5 and 0 cmH₂O. However, in the dependent region, values of ΔV_DER _- _PI between 15 and 10 cmH₂O were higher than those between 5 and 0 cmH₂O (P = 0.028) (Figure 4). The Vt%_Dep showed a close correlation with decreasing PEEP (P < 0.001) levels, indicating that the dependent lung region needed a higher PEEP to keep the lung open and improve ventilation. Additionally, the Crs of the dependent lung region decreased significantly as PEEP decreased (P = 0.003), whereas the Crs of the global and nondependent lung regions were maximized at a PEEP of 10 cmH₂O and decreased at a PEEP of 15 cmH₂O.

Figure 4.

Regional derecruitment volume (ΔV_DRE-PI) between the two adjacent PEEP levels in different lung regions. In the dependent region (triangles), ΔV_DRE-PI between PEEP 15 to 10 cmH₂O and PEEP 10 to 5 cmH₂O was higher than that within PEEP 5 to 0 cmH₂O (P = 0.028). However, in the global and non-dependent lung region (circle and square), ΔV_DRE-PI between PEEP 15 to 10 cmH₂O showed a decreasing tendency compared with PEEP 10 to 5 cmH₂O and 5 to 0 cmH₂O. The ΔV_DRE-PI across different PEEPs were analyzed using Friedman’s nonparametric test. Post hoc pairwise comparisons were performed using the Wilcoxon test. P < 0.05 was considered to be statistically significant. The * represents P < 0.05 vs. ΔV_DRE-PI between PEEP 5 to 0 cmH₂O.

The increased PEEP contributed to improved oxygenation (P = 0.001) and decreased dead space (P = 0.001). There was no obvious fluctuation of heart rate or mean arterial pressure while changing PEEP levels (Table 2).

Table 2.

Gas exchange, hemodynamics, and ventilation data.

	PEEP (cmH₂O)				P
	0	5	10	15	P
PaO₂/FiO₂	118 (103,129)	151 (137,180)*	232 (198,300),*	245 (207,296),*	0.001
Dead space (%)	39 (38,50)	35 (28,37)*	26 (24,29),*	26 (24,30),*	0.001
Vt%_Non-dep (%)	88 (83,89)	85 (77,88)	77 (69,83)*	69 (65,72),*	0.000
Vt%_Dep (%)	12 (11,17)	15 (13,24)	24 (18,30),*	32 (27,36),*	0.000
Crs_Global (mL/cmH₂O)	25 (22,29)	35 (31,43)*	42 (31,57)*	34 (31,42),*	0.007
Crs_Non-dep (mL/cmH₂O)	21 (18,25)	29 (25,33)*	34 (26,40)*	24 (24,27)***	0.003
Crs_Dep (mL/cmH₂O)	3 (2,5)	6 (4,9)*	8 (7,15),*	10 (8,15),,**	0.003
HR (beats/minute)	48 (46,73)	48 (45,71)	67 (49,80)	74 (60,90)	N.S.
MAP (mmHg)	89 (86,93)	90 (81,94)	82 (72,91)	77 (70,89)	N.S.

Data are shown as median (IQR).

The data were analyzed using a repeated-measures ANOVA and p < 0.05 represented a statistically significant difference.

*, **, *** represent p < 0.05 vs. the PEEP of 0, 5, and 10, respectively.

PEEP, positive end-expiratory pressure; PaO₂, partial pressure of oxygen in arterial blood; FiO₂, inspired oxygen fraction; Vt%_Non-dep, the distribution of tidal ventilation in the non-dependent lung region; Vt%_Dep, the distribution of tidal ventilation in the non-dependent lung region; Crs_Global, compliance of the entire (global) respiratory system; Crs_Non-dep, compliance of non-dependent lung region; Crs_Dep, compliance of dependent lung region; HR, heart rate; MAP, mean arterial pressure; IQR, interquartile range; ANOVA, analysis of variance; N.S., not significant.

Discussion

In this study, we compared the V_DER-PI that was derived from EIT with V_DER-PV in a lung-injured animal model. The main finding was that V_DER-PI was well-correlated with V_DER-PV. Thus, it is a reliable method to assess regional V_DER with EIT at the bedside.

For ARDS patients, PEEP is helpful to re-inflate nonaerated alveoli and keep them open, but PEEP can also result in hyperinflation of aerated alveoli. Defining the best method by which to set optimal PEEP levels remains challenging in routine clinical practice. Optimal PEEP levels were expected to induce recruitment of collapsed alveoli to decrease lung stress and strain and improve the ventilation-to-perfusion ratio. Therefore, measurement of lung recruitment volume that was induced by PEEP is important to guide the PEEP settings. Computed tomography is the gold standard for the assessing the global and regional PEEP-induced alveolar recruitment,^8,27 but it exposes patients to radiation and cannot be performed routinely or repeated easily. Multiple P-V curves have shown that they can be used to assess recruitment or derecruitment volumes quantitatively at the bedside.⁸ However, plotting P-V curves requires further measurement of ΔEELV that is induced by PEEP with the help of specific ventilators or the release maneuver.^8,9 Therefore, it is still rather complex and can even be harmful for patients when the ventilator is disconnected. Additionally, only global information about the lung is available using the P-V curves method.

EIT has been used in respiratory measurement based on how the degree of impedance varies with volume.^12–18 In the present study, we performed low constant flow inflations at different PEEP levels under EIT monitoring and introduced a new method to estimate V_DER using multiple P-I curves that were derived from EIT. We found that the V_DER-PI were closely correlated with V_DER-PV, although they were slightly overestimated. Additionally, ΔEELV that was assessed by EIT also showed a close correlation with PEEP volume as measured by pneumotachograph during PEEP release; this result showed an overestimation in the same manner. The presence of airway closure was excluded by closely observing the shape of P-V curves, to rule out cases of incomplete expiration.²⁸ However, the derecruitment process over time (10 minutes) during ventilation at ZEEP was ignored because the pneumotachograph measured expired volume at exactly the moment of PEEP withdrawal, which might explain why ΔEELV derived from EIT was higher than the PEEP volume that was measured by the pneumotachograph. In the previous study, researchers also found that the PEEP volume that was measured using a pneumotachograph was lower than that calculated by CT because of additional time-dependent derecruitment, which further caused V_DER-PV to be lower than measurements that were derived from CT.⁸ Consistent with these results, the slightly higher estimations of V_DER-PI compared with V_DER-PV means that V_DER-PI more closely approaches the “true” values. Additionally, the change in impedance as measured by EIT was closely correlated with the change in volume; this was validated in our study and is consistent with the results of previous studies.^12–18 This supports the concept that the P-I curves are a promising method of accurately measuring V_DER at the bedside.

EIT makes it possible to visualize regional ventilation.¹⁰ It is feasible to evaluate regional derecruitment with the regional P-I curves, as described in previous studies.^{12,13,18,29–32} In this study, we calculated ΔV_DER-PI that was induced by adjacent PEEP in nondependent and dependent lung regions by the regional P-I curves. The results have shown that the different lung regions have different responses to PEEP. For the nondependent lung region, the ΔV_DER-PI is prominent when PEEP is set at 5 to 0 cmH₂O and 10 to 5 cmH₂O and has a decreasing tendency as PEEP decreases from 15 to 10 cmH₂O, which probably suggests that the number of collapsed lung units in the nondependent lung region have decreased when PEEP levels are at 15 cmH₂O; further increasing PEEP might induce regional overdistension and worsen respiratory mechanics. Conversely, high PEEP levels could drive more air into the dependent lung region and thereby improve gas distribution and respiratory mechanics. Decreasing PEEP from 15 to 10 and 5 cmH₂O leads to significant decruitment. The previous studies also showed that reginal P-I curves in the dependent lung region were different from global and non-dependent lung region P-I curves, which had higher values of a lower inflection point indicating that higher pressure was needed to open atelectatic alveoli.^{12,13,18,29–32} In our study, considering the optimization of ΔV_DER-PI distribution between the two distinct regions, 10 cmH₂O may represent the optimal PEEP level to maximize open alveoli and minimize alveoli overdistension. Although the regional P-I curves could provide more detailed information, the best way to determine the optimal PEEP levels based on regional recruitment volume was to balance overdistention and collapse, but this requires further investigation.

EIT has several advantages over the other two methods (CT scan and P-V curves) for exact V_DER measurements. EIT, unlike CT, is free from radiation and could be performed routinely and repeated easily at the bedside.¹¹ In contrast to P-V curves, P-I curves derived from EIT inherently include the information about ΔEELV. EIT could also acquire regional information about lung derecruitment. Although two previous studies have introduced a method by which to assess recruitment volumes quantitatively using EIT based on the theory of the minimal predicted lung volume (i.e., calculating the difference between the ΔEELV as measured by EIT and the product of Crs and ΔPEEP), the reference methods also selected the simplified minimal predicted lung volume method, and ΔEELV was measured using the helium dilution technique or the integral of flow waveform during release maneuvers.^19,20 The weakness of the simplified minimal predicted lung method is that it is based on the assumption that lung compliance will remain constant regardless of PEEP adjustment, but many studies, including our own, have shown that PEEP had an obvious effect on lung compliance.²¹ The previous study also found that recruitment volume that is assessed using this simplified method was correlated but significantly lower than the recruitment volume that was assessed by P-V curves.²¹ Similarly, in our study, we also obtained V_DER that was assessed by EIT based on the simplified minimal predicted lung method, as V_DER-MPV, and we found that V_DER-MPV underestimated the recruitment volume compared with V_DER-PV with a relatively large difference; the bias (the lower and upper limits of agreement) was −65 (−275 to 145) mL. Although the MPV method is simpler to use in clinical practice, the V_DER assessed by the P-I curves was relatively more accurate.

There are several limitations in our study. First, we set up an experimental acute lung injury model using hydrochloric acid. This allowed for a relatively steady model, but we did not observe any examples of lung injury that resulted from different etiologies (such as saline surfactant wash-out or oleic acid injection). Second, we measured the V_DER with the P-V curves as the reference instead of performing the “gold standard,” (i.e., CT method), but a previous study showed that there was a good correlation between values that were measured by CT and P-V curves.⁹ Third, EIT imaging is related to the EIT belt position, and only approximately 50% of the lung area is covered.

Conclusions

P-I curves that are derived from EIT can be used to assess global and regional lung V_DER during low constant flow at the bedside. Further studies are required to explore the potential to balance the regional V_DER distribution with personalized PEEP settings.

Footnotes

Declaration of conflicting interest

The authors declare that there is no conflict of interest.

Funding

Funding was received from the National Natural Science Foundation of China (No: 81871582). The sponsor had no role in the study design, data collection, data analysis, data interpretation, or writing of the report.

ORCID iDs

Guang-Qiang Chen

Yu-Mei Wang

Jian-Xin Zhou

References

Briel

Meade

Mercat

, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA 2010; 303: 865–873. DOI: 10.1001/jama.2010.218.

Mercat

Richard

Vielle

, et al. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299: 646–655. DOI: 10.1001/jama.299.6.646.

Writing Group for the Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial I, Cavalcanti

Suzumura

, et al. Effect of lung recruitment and titrated positive end-expiratory pressure (PEEP) vs low PEEP on mortality in patients with acute respiratory distress syndrome: a randomized clinical trial. JAMA 2017; 318: 1335–1345. DOI: 10.1001/jama.2017.14171.

Sahetya

Brower

RG.

Lung recruitment and titrated PEEP in moderate to severe ARDS: is the door closing on the open lung?

JAMA 2017; 318: 1327–1329. DOI: 10.1001/jama.2017.13695.

Gattinoni

Caironi

Cressoni

, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med 2006; 354: 1775–1786. DOI: 10.1056/NEJMoa052052.

Chiumello

Cressoni

Carlesso

, et al. Bedside selection of positive end-expiratory pressure in mild, moderate, and severe acute respiratory distress syndrome. Crit Care Med 2014; 42: 252–264. DOI: 10.1097/CCM.0b013e3182a6384f.

Ranieri

Eissa

Corbeil

, et al. Effects of positive end-expiratory pressure on alveolar recruitment and gas exchange in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 1991; 144: 544–551. DOI: 10.1164/ajrccm/144.3_Pt_1.544.

Rouby

JJ.

Measurement of pressure-volume curves in patients on mechanical ventilation. Methods and significance. Minerva Anestesiol 2000; 66: 367–375.

Constantin

Nieszkowska

, et al. Measurement of alveolar derecruitment in patients with acute lung injury: computerized tomography versus pressure-volume curve. Crit Care 2006; 10: R95. DOI: 10.1186/cc4956.

10.

Richard

Maggiore

Jonson

, et al. Influence of tidal volume on alveolar recruitment. Respective role of PEEP and a recruitment maneuver. Am J Respir Crit Care Med 2001; 163: 1609–1613. DOI: 10.1164/ajrccm.163.7.2004215.

11.

Walsh

Smallwood

CD.

Electrical impedance tomography during mechanical ventilation.

Respir Care 2016; 61: 1417–1124. DOI: 10.4187/respcare.04914.

12.

Kunst

Bohm

Vazquez De Anda

, et al. Regional pressure volume curves by electrical impedance tomography in a model of acute lung injury. Crit Care Med 2000; 28: 178–183. DOI: 10.1097/00003246-200001000-00029.

13.

Hinz

Moerer

Neumann

, et al. Regional pulmonary pressure volume curves in mechanically ventilated patients with acute respiratory failure measured by electrical impedance tomography. Acta Anaesthesiol Scand 2006; 50: 331–339. DOI: 10.1111/j.1399-6576.2006.00958.x.

14.

Van Genderingen

Van Vught

Jansen

JR.

Estimation of regional lung volume changes by electrical impedance pressures tomography during a pressure-volume maneuver.

Intensive Care Med 2003; 29: 233–240. DOI: 10.1007/s00134-002-1586-x.

15.

Marquis

Coulombe

Costa

, et al. Electrical impedance tomography's correlation to lung volume is not influenced by anthropometric parameters. J Clin Monit Comput 2006; 20: 201–207. DOI: 10.1007/s10877-006-9021-4.

16.

Adler

Amyot

Guardo

, et al. Monitoring changes in lung air and liquid volumes with electrical impedance tomography. J Appl Physiol (Bethesda, Md: 1985) 1997; 83: 1762–1767. DOI: 10.1152/jappl.1997.83.5.1762.

17.

Frerichs

Hinz

Herrmann

, et al. Detection of local lung air content by electrical impedance tomography compared with electron beam CT. J Appl Physiol (Bethesda, Md: 1985) 2002; 93: 660–666. DOI: 10.1152/japplphysiol.00081.2002.

18.

Beda

Carvalho

, et al. Mapping regional differences of local pressure-volume curves with electrical impedance tomography. Crit Care Med 2017; 45: 679–686. DOI: 10.1097/CCM.0000000000002233.

19.

Mauri

Eronia

Turrini

, et al. Bedside assessment of the effects of positive end-expiratory pressure on lung inflation and recruitment by the helium dilution technique and electrical impedance tomography. Intensive Care Med 2016; 42: 1576–1587. DOI: 10.1007/s00134-016-4467-4.

20.

Wang

Sun

Zhou

, et al. Use of electrical impedance tomography (EIT) to estimate global and regional lung recruitment volume (V_REC) induced by positive end-expiratory pressure (PEEP): an experiment in pigs with lung injury. Med Sci Monit 2020; 26: e922609. DOI: 10.12659/MSM.922609.

21.

Chiumello

Marino

Brioni

, et al. Lung recruitment assessed by respiratory mechanics and computed tomography in patients with acute respiratory distress syndrome. What is the relationship? Am J Respir Crit Care Med 2016; 193: 1254–1263. DOI: 10.1164/rccm.201507-1413OC.

22.

Wrigge

Zinserling

Muders

, et al. Electrical impedance tomography compared with thoracic computed tomography during a slow inflation maneuver in experimental models of lung injury. Crit Care Med 2008; 36: 903–909. DOI: 10.1097/ccm.0b013e3181652edd.

23.

Anderson

Breen

PH.

Carbon dioxide kinetics and capnography during critical care.

Crit Care 2000; 4: 207–215. DOI: 10.1186/cc696.

24.

Bikker

Leonhardt

Bakker

, et al. Lung volume calculated from electrical impedance tomography in ICU patients at different PEEP levels. Intensive Care Med 2009; 35: 1362–1367. DOI: 10.1007/s00134-009-1512-6.

25.

Maggiore

Jonson

Richard

, et al. Alveolar derecruitment at decremental positive end-expiratory pressure levels in acute lung injury: comparison with the lower inflection point, oxygenation, and compliance. Am J Respir Crit Care Med 2001; 164: 795–801. DOI: 10.1164/ajrccm.164.5.2006071.

26.

Bland

Altman

DG.

Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986; 1: 307–310. DOI: 10.1016/s0140-6736(86)90837-8.

27.

Rouby

Puybasset

Nieszkowska

, et al. Acute respiratory distress syndrome: lessons from computed tomography of the whole lung. Crit Care Med 2003; 31: S285–S295. DOI: 10.1097/01.CCM.0000057905.74813.BC.

28.

Sun

Chen

Zhou

, et al. Airway closure could be confirmed by electrical impedance tomography. Am J Respir Crit Care Med 2018; 197: 138–141. DOI: 10.1164/rccm.201706-1155LE.

29.

Scaramuzzo

Spadaro

Waldmann

, et al. Heterogeneity of regional inflection points from pressure-volume curves assessed by electrical impedance tomography. Crit Care 2019; 23: 119. DOI: 10.1186/s13054-019-2417-6.

30.

Grychtol

Wolf

Arnold

JH.

Differences in regional pulmonary pressure-impedance curves before and after lung injury assessed with a novel algorithm.

Physiol Meas 2019; 30: S137–S148. DOI: 10.1088/0967-3334/30/6/S09

31.

Frerichs

Dargaville

Rimensberger

PC.

Regional respiratory inflation and deflation pressure-volume curves determined by electrical impedance tomography.

Physiol Meas 2013; 34: 567–577. DOI: 10.1088/0967-3334/34/6/567.

32.

Becher

Rostalski

Kott

, et al. Global and regional assessment of sustained inflation pressure-volume curves in patients with acute respiratory distress syndrome. Physiol Meas 2017; 38: 1132–1144. DOI: 10.1088/1361-6579/aa6923.

Derecruitment volume assessment derived from pressure–impedance curves with electrical impedance tomography in experimental acute lung injury

Abstract

Objective

Methods

Results

Conclusions

Keywords

Introduction

Materials and methods

Animal preparation

Study protocol

EIT measurements and analysis

VDER measured by P-V curves at a low constant flow inflation

VDER measured by P-I curves derived from EIT during low constant flow inflation

Statistical analysis

Results

Agreement of VDER assessed by P-I and P-V curves

Difference of ΔVDER-PI in different lung regions

Discussion

Conclusions

Footnotes

Declaration of conflicting interest

Funding

ORCID iDs

References

V_DER measured by P-V curves at a low constant flow inflation

V_DER measured by P-I curves derived from EIT during low constant flow inflation

Agreement of V_DER assessed by P-I and P-V curves

Difference of ΔV_DER-PI in different lung regions