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A previous volume history should be established prior to pressure- volume (P-V) curve measurement, however the effect of the volume history and the peak inspiratory pressure (PIP) during the P-V measurement has not been explored. Lung injury was created by lavage in nine sheep (25-35 kg). After stabilization, four P-V curves were sequentially obtained with PIP of 40, 50, 60, and 40 cm H2O. Prior to each P-V measurement the PIP delivered for 1 min was the same as during P-V measurement. We compared the lower inflection point (Pflex), upper inflection point (UIP), compliance below Pflex (Cstart), compliance between Pflex and UIP (Cinf), and compliance between UIP and peak pressure (Cend) for the inflation limb, and the point of maximum curvature on the deflation limb (PMC), compliance between peak pressure and PMC (Ctop), and maximum compliance (Cdef) for the deflation limb. In two sheep, Pflex at PIP 40 cm H2O could not be identified but appeared when PIP was raised. Pflex, Cstart, Cend, and Ctop were not affected by the PIP. However, UIP, PMC, Cinf, and Cdef increased as the PIP increased. Volume history and the PIP during P-V curve measurements affect both the inflation and deflation P-V curves.
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INTRODUCTION |
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Keywords: respiratory function tests; adult respiratory distress syndrome; lung compliance; pressure-volume curve; volume history
The pressure-volume (P-V) curve of the respiratory system has been used to identify the limits of mechanical ventilation in acute respiratory distress syndrome (ARDS) and characterize the severity of disease (1). However, controversy exists over the precise meaning of the P-V curve (9). Many have indicated that recruitment occurs at the first point of compliance change on the inflation limb of the P-V curve (lower inflection point, Pflex) (1, 3, 4, 16). However, Hickling demonstrated mathematically that lung recruitment can occur throughout inspiration and that Pflex may simply suggest the P-V relationship where marked recruitment begins (9). Hickling also suggested that the second point of compliance change on the inflation limb of the P-V curve (upper inflection point, UIP) may not represent the pressure where overdistension occurs but simply the point at which the rate of recruitment decreases. Other have suggested, that the deflation limb of the P-V curve may be more important than the inflation limb for identifying the positive end-expiratory pressure (PEEP) that prevents derecruitment (13, 14, 19, 20).
Prior to performing a P-V curve, it is recommended that a volume history be established (15, 21). However, few data exist defining the precise method for establishing the volume history or peak pressure reached during P-V curve measurement in ARDS (21, 24). Some have used the previous approach to the mechanical ventilation (usually peak pressure is < 35 cm H2O) (2, 10) and others the application of several manual "large tidal volume" breaths (18, 20, 24, 25) or the application of several sustained inflations to 35-40 cm H2O (assumed to be total lung capacity) (21). Peak pressure during the P-V curve has been limited to 40-50 cm H2O (4, 10, 17, 18). However, in ARDS lung recruitment occurs at pressures well beyond 40 cm H2O (26, 27). We hypothesized that the peak pressure obtained during the establishment of a volume history and during the performance of the P-V curve affects the shape of the P-V curve. In this study of lung lavaged sheep we compared the effect of three volume histories and peak pressures during the P-V curve measurement on analysis of the P-V curve.
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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Nine female Dorset sheep were studied. After inducing anesthesia by mask, the right jugular vein was cannulated and a pulmonary artery catheter was inserted. Anesthesia was then switched to intravenous, and an endotracheal tube and femoral artery catheter were placed. An infusion of lactated Ringer's Solution was continuously administered and a gastrostomy tube was placed.
Mechanical ventilation was provided with a PB 7200ae ventilator: volume control (VCV), tidal volume (VT) 12 ml/kg, I:E ratio 1:2, fraction of inspired oxygen (FIO2) 1.0, and PEEP 5 cm H2O, throughout the protocol. Respiratory rate (RR) was adjusted to achieve eucapneia. Arterial and pulmonary artery pressure, exhaled CO2, and VT were continuously monitored.
Following instrumentation and a 60-min stabilization period, baseline respiratory and circulatory parameters were obtained (BL). The time course of the study is shown in Figure 1. After the baseline measurements, severe lung injury was produced by bilateral lung lavage. Following stabilization of the lung injury, P-V curve measurements using a 2-L supersyringe at three different volume histories were performed. A total of four inflation and deflation P-V curves were sequentially measured. During the first P-V curve measurement volume was delivered until the pressure increased to 40 cm H2O (PV40), during the second to 50 cm H2O (PV50), during the third to 60 cm H2O (PV60), and during the final curve to 40 cm H2O (PV40-2). Between P-V curves, animals were ventilated (as during initial stabilization) for about 20 min until stabilization, confirmed by continuous blood gas analysis. Post P-V data were obtained 20 min after PV40-2 (Post-PV).
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Prior to each P-V curve a volume history was established by 1 min of ventilation with pressure control (PEEP 5 cm H2O, RR 6 /min, I:E ratio 1:1) at a peak pressure equal to the maximum pressure during the P-V curve measurement (PV40 and PV40-2, peak pressure 40 cm H2O; PV50, peak pressure 50 cm H2O; PV60, peak pressure 60 cm H2O). Following establishment of the volume history the ventilator was disconnected (airway open to atmosphere) for 6 s then the inflation and deflation P-V curve was measured. Volume during the P-V curve measurement was corrected for pressure, temperature, humidity, time, O2 consumption, and CO2 production (28).
Five clinicians trained in P-V curve analysis were asked to independently visually analyze plots of the P-V relationships without knowledge of the origin of the curves. The following parameters (Figure 2) were identified: lower inflection point on the inflation limb (Pflex), upper inflection point on the inflation limb (UIP), point of maximum curvature on the deflation limb (PMC), starting compliance (Cstart), inflation compliance (Cinf), end inspiratory compliance (Cend), deflation compliance (Cdef), and deflation limb top compliance (Ctop) (see on-line data supplement for derivations). If more than three clinicians could not identify a given point (i.e., Pflex, UIP, or PMC), we assumed the curve did not have that point. If Pflex was not identified, Cinf of the particular P-V relationship was assumed to be the same as the compliance of Cstart.
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Data are expressed as mean ± SD. All parameters were compared using an analysis of variance (AVOVA) for repeated measurements or Friedman's ANOVA. A p value < 0.05 was considered significant.
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RESULTS |
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DISCUSSION
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To create a stable lung injury (Pao2 change of less than 10% after 30 min), 2.7 ± 1.1 lavages were required. Respiratory and circulatory parameters at BL, during P-V trials, and Post-PV are listed in Table 1. Peak inspiratory pressure (PIP), plateau pressure (Pplat), and mean airway pressure (Pmean) were increased, and pH, PaO2, SaO2, and arterial blood pressure were decreased significantly by lung lavage. Post-PV data indicate that PaCO2 increased and pH and heart rate (HR) decreased significantly compared with PV40. During the P-V measurements (PV40 to PV40-2), PaCO2 was significantly higher and SaO2 was significantly lower at PV40-2 than PV40 and PV50. The remainder of the respiratory parameters were stable throughout the experiment. There was no significant difference in cardiac output (CO), central venous pressure (CVP), and pulmonary capillary wedge pressure (PCWP). CO was 4.96 ± 1.46, 5.68 ± 2.20, and 5.03 ± 1.53 L/min, CVP was 5 ± 2, 6 ± 2, and 7 ± 1 mm Hg, and PCWP was 8 ± 2, 7 ± 1, and 8 ± 1 mm Hg at BL, PV40, and Post-PV, respectively.
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PIP during P-V curve measurement was 40.7 ± 1.1 (PV40), 51.4 ± 2.5 (PV50), 59.8 ± 4.2 (PV60), and 41.5 ± 2.7 (PV40-2) cm H2O. Representative P-V curves are shown in Figure 3. Table 2 lists the number of sheep at each pressure demonstrating Pflex, UIP, and PMC. Table 3 lists interobserver variability for the five investigators. Mean differences between individual investigator results and the average value for individual points (Pflex, UIP, PMC) and standard deviations for each investigator for all parameters were less than 1 ± 2.0 cm H2O. Two sheep did not demonstrate a Pflex at PV40 or PV40-2, but did demonstrate a Pflex at PV50 and PV60. Only four sheep demonstrated a UIP at PV40 and only one at PV40-2. In the seven sheep that had a complete set of four Pflex values, there was no difference in the value of Pflex among measurements (22.2 ± 2.4, 25.2 ± 3.3, 25.8 ± 3.1, and 24.7 ± 3.1 cm H2O at PV40, PV50, PV60, and PV40-2, respectively, Figure 4). The value of the UIP (n = 7) was larger at PV60 than PV50 (46 ± 2 versus 42 ± 2 cm H2O, respectively). PMC was significantly higher as P-V curve pressure increased (22.2 ± 1.5, 28.2 ± 2.6, 31.4 ± 2.8, and 23.3 ± 1.1 cm H2O at PV40, PV50, PV60, and PV40-2, respectively, Figure 4). There was no difference in Cstart (n = 7) and Ctop among P-V groups (Figure 5). Cinf and Cdef were significantly greater and Cend tended to be lower as P-V curve pressure increased and there were no differences in Cinf and Cdef regardless of P-V curve pressure (Figure 5). There were no significant differences in the P-V curve parameters between PV40 and PV40-2 except that there was a small but significant difference in PMC.
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p < 0.05 versus
PV50, and 
p < 0.05 versus PV40-2.
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DISCUSSION
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The major findings of this study are as follows: (1) The peak pressure of the volume history affected the existence of a Pflex, but not the value of Pflex. (2) Compliance before Pflex (Cstart) was not affected by the peak pressure during establishment of the volume history. (3) The linear portion of the inflation limb of the P-V curve, between Pflex and UIP (Cinf), was affected by the peak pressure of the volume history; the higher the volume history pressure the greater the Cinf. (4) The peak pressure during establishment of the volume history affected the existence of a UIP, and the values of UIP tended to be larger the higher the volume history peak pressure. (5) PMC and Cdef increased as the volume history pressure increased, but Ctop was not affected by the peak pressure. (6) Based on these data, a single P-V curve, especially at a low peak pressure, provides only limited information on lung mechanics.
Effect of Peak Pressure on Pflex and Cstart
CSTAT was not affected by the peak pressure of the volume history. According to Gattinoni and colleagues (18), Cstart is dependent upon lung units open at end expiration. Therefore a stable Cstart implies that the number of open lung units at end-expiration may not be affected by volume history.
Computerized tomography (CT) data from Gattinoni and colleagues (30) and impedance tomography data from Kunst and colleagues (31) suggests that Pflex is affected by superimposed pressure and is primarily a result of a sudden increase in the rate of recruitment of nondependent lung, consistent with the observations that in ARDS, lungs have multiple compartments with different compliance (6, 8, 20). If this is true one would expect volume history and P-V curve pressure to affect Pflex least, as nondependent lung in the supine position would be affected least by superimposed pressure and would be affected most by surface active forces (32).
We could not identify Pflex in some sheep with low pressure volume history but could identify Pflex at higher volume history. Two recent ARDS CT scan studies have shown that the absence of Pflex is associated with lung morphology characterized by a nonhomogeneous distribution of the loss of lung volume (6, 8). Especially in the supine position, greater volume loss is in the dependent as compared to the nondependent lung. Data from Puybasset and colleagues also suggest the existence of several lung compartments with different regional compliances (29). Therefore, our failure to identify a Pflex in some animals reflects the nonhomogeneous distribution of volume loss, the inability of the volume history pressure to overcome the surface active forces, or failure to obtain a sudden increase in the rate of recruitment even though overcoming the opening pressure. There is a possibility that the higher pressure volume history resulted in changes in lung morphology. This is, the nonhomogeneous lung became a relatively homogeneous lung by the higher pressure volume history functioning as a recruitment maneuver.
Effect of Peak Pressure on Cinf
The compliance measured between Pflex and the UIP (Cinf) was greatly affected by the volume history pressure. This finding may be specifically related to the fact that it is easier to inflate a lung with collapsed airways than one with atelectasis (34), and/or that recruitment of lung requires both pressure and time (32). That is, alveoli opened during establishment of the volume history were more easily opened during P-V curve measurement. Koutsoukou and colleagues have suggested that there is some airway collapse during tidal exhalation in ARDS (36), whereas Chelucci and colleagues demonstrated using a biexponential time-flow curve fitting model that the time constant for the slow opening compartments of the lung are > 4 s in injured lungs (37). Neumann and colleagues also demonstrated that the time constant of collapsing alveoli was 20 s in lavage-injured pigs (38). As a result, even after the 6 s of ventilator disconnection following the volume history, functional residual capacity (FRC) including trapped gas volume would be greater than before the volume history. With a greater pressure during the establishment of the volume history more alveoli would open and remain open behind closed or narrowed airways at FRC. Frazer and Weber showed that increasing ventilatory pressure induces more air trapping (39), whereas Van der Kloot and colleagues showed that end-expiratory lung volume was greater when lavage injured dogs were ventilated with larger tidal volumes (27). Thus, in a surfactant-deficient model the pressure required to inflate the lung would decrease while compliance increased as the size and number of recruited lung units increased during the previous volume history. Because we used 100% O2, low PIP, and low PEEP (5 cm H2O) to ventilate between P-V curve measurements (Table 1), all recruited and trapped volumes should have been reabsorbed within the 20-min stabilization period (40, 41).
Effect of Peak Pressure on UIP and Cend
Because recruitment continues as airway pressure is progressively increased and total lung recruitment requires high and sustained airway pressure (26, 27), the existence and magnitude of the UIP would be expected to increase as volume history and P-V curve pressure increased. UIP and Cend were not universally present at PV40 and PV40-2. This is most probably because these pressures were insufficient to maximally recruit the lung. We would agree, based on our data, with Hickling's interpretation of UIP (9). The UIP is not simply a pressure indicating overdistension but a pressure reflective of a decrease in the rate of recruitment that is clearly volume history dependent. The level of Cend could also be affected by the level of ongoing recruitment versus overdistension. Although not significant Cend did tend to decrease at higher P-V curve peak pressure (Figure 5), most probably as a result of greater overdistension of some lung units at PIP of 60 cm H2O versus 50 cm H2O. It may be necessary to obtain P-V curves at various volume history peak and P-V peak pressures to appropriately define lung mechanics. A single curve appears to provide limited data on lung mechanics, especially when performed at low peak pressure.
Effect of Peak Pressure on Deflation Limb
Because Ctop was not affected by the peak pressure of the P-V curve, deflation from each peak pressure to PMC probably does not reflect derecruitment. The elastic recoil of the respiratory system may be the primary factor that defines the rate of pressure volume change between peak pressure and PMC. Below PMC, the rate of derecruitment in our model was the same as the rate of recruitment (Cinf = Cdef). If no additional recruitment occurred, it is doubtful that PMC would continue to increase with increasing pressure. Thus, an increase in PMC indicates additional recruitment at the higher pressure.
Analysis of the P-V curve
As noted in Table 3 there is good agreement among the five investigators analyzing the 36 P-V curves. This is contrary to recently published data indicating a large difference among individuals using a manual method of P-V curve analysis (19, 25). Our data are a result of training and agreement on methodology and definitions as well as practice analysis sessions.
Limitation
First, this study was not performed in patients with ARDS. The lung injury model used in this study was a surfactant depletion model that does differ from human and other animal models of ARDS. Second, the lung injuries in this study model were very severe. We cannot state with assurance that similar findings would occur in a less severe model or if the same injury was maintained over a longer time. Third, we are unable to separate the effects of the pressure obtained during volume history from the pressure obtained during the P-V measurement. That is, we do not know the effect of a volume history of 40 cm H2O on a P-V curve established with a peak pressure of 60 cm H2O or a volume history of 60 cm H2O on a P-V curve established with a peak pressure of 40 cm H2O. Fourth, between the volume history and P-V curve analysis a 6-s discontinuation (the length of the expiratory phase during volume history) from ventilatory support was established. We do not know if our results would have been different if the disconnection period was other than 6 s. In fact, numerous other factors must be evaluated to define the ideal method of P-V curve performance (e.g., volume history mode, PEEP level, inspiratory to expiratory ratio rate). Fifth, we did not measure esophageal pressure and calculate chest wall compliance. Our preliminary data in this model indicated that the thoracic cage did not affect the shape of the P-V curve of the total respiratory system. Finally, we did not randomize the order of peak pressure, because we were concerned that previous higher pressure P-V curve measurements would affect the next lower pressure P-V curve. However, the results of PV40-2 would indicate there was no interaction between measurements.
Conclusion
We have demonstrated that P-V curve methodology affects the shape of the P-V curve. In addition, a single P-V curve, especially if determined at low volume history and peak P-V curve pressure, provides only limited data regarding lung mechanics. However, Pflex and Cstart were not affected by volume history and P-V curve pressure. There needs to be a standard universally accepted approach to performing P-V curves, if data from one center are to be compared with another. Clearly, additional data in animal models identifying the optimal approach to P-V curve determination need to be obtained and the results of these trials compared in humans.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Robert M. Kacmarek, Ph.D., R.R.T., Respiratory Care
Ellison 401, Massachusetts General Hospital, Boston, MA 02114. E-mail: rkacmarek{at}partners.org
(Received in original form January 12, 2001 and accepted in revised form June 26, 2001).
Dr. Takeuchi is partially funded by the Japanese government, Dr. Sedeek is partially funded by Becton Dickinson of Egypt, and Dr. Schettino is partially funded by FAPESP, Brazil.This article has an online data supplement, which is accessible from this issue's table of contents online at www.atsjournals.org
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RESULTS
DISCUSSION
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M. J. Tobin Compliance (COMmunicate PLease wIth Less Abbreviations, Noun Clusters, and Exclusiveness) Am. J. Respir. Crit. Care Med., December 15, 2002; 166(12): 1534 - 1536. [Full Text] [PDF]
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M. J. TOBIN Critical Care Medicine in AJRCCM 2001 Am. J. Respir. Crit. Care Med., March 1, 2002; 165(5): 565 - 583. [Full Text] [PDF]
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