American Journal of Respiratory and Critical Care Medicine Vol 165. pp. 1271-1274, (2002)
© 2002 American Thoracic Society
ARDSNet Lower Tidal Volume Ventilatory Strategy May Generate Intrinsic Positive End-Expiratory Pressure in Patients with Acute Respiratory Distress Syndrome
Gabriella de Durante,
Monica del Turco,
Laura Rustichini,
Patrizia Cosimini,
Francesco Giunta,
Leonard D. Hudson,
Arthur S. Slutsky and
V. Marco Ranieri
Dipartimento di Chirurgia-Terapia Intensiva, Cattedre di Anestesiologia e Rianimazione, Ospedale S. Chiara, Università di Pisa, Pisa, Italy; Division of Pulmonary and Critical Care Medicine, Harborview Medical Center, University of Washington, Seattle, Washington; and Department of Critical Care Medicine, St. Michael's Hospital, Interdepartmental Division of Critical Care Medicine, Respiratory Division, Department of Medicine, University of Toronto, Ontario, Canada
Correspondence and requests for reprints should be addressed to V. Marco Ranieri, Dipartimento di discipline Medico-Chirurgiche, Sezione di Anestesiologia e Rianimazione, Ospedale S. Giovanni Battista, Università di Torino, Corso Dogliotti 14, 10126 Torino, Italy. E-mail: mranieri{at}teseo.it
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ABSTRACT
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The ARDSNet trial revealed that the use of a smaller tidal volume (VT) reduced mortality by 22%. However, three earlier studies that lowered VT did not find a decrease in mortality. We tested the hypothesis that the increased respiratory rate used in the ARDSNet lower VT strategy might have led to intrinsic positive end-expiratory pressure (PEEPi), raising total PEEP (PEEPtotal). Ten patients with acute respiratory distress syndrome (ARDS) were ventilated using the ARDSNet lower VT protocol. Respiratory rate was then reduced (10–15 breaths/minute) to obtain a VT of 12 ml/kg (ARDSNet traditional VT). PEEP on the ventilator (PEEPnominal: 10.1 ± 0.7 cm H2O), FIO2 (0.7 ± 0.1), and minute ventilation (VE: 12.4 ± 1.7 L/minute) were set using the ARDSNet protocol and maintained constant during the two ventilatory strategies. Values of airway pressure at end-expiration of a regular breath (PEEPexternal) and 3–5 seconds after the onset of an end-expiratory occlusion (PEEPtotal) were measured. PEEPi was calculated by subtracting PEEPexternal from PEEPtotal. PEEPtotal and PEEPi were, respectively, 16.3 ± 2.9 and 5.8 ± 3.0 cm H2O during the lower VT strategy and 11.7 ± 0.9 and 1.4 ± 1.0 cm H2O during the traditional VT strategy (p < 0.01). The reduced mortality observed with the ARDSNet strategy may have been due to the protective effect of a higher PEEPtotal.
Key Words: ARDS • protective ventilatory strategy • PEEP • intrinsic PEEP
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INTRODUCTION
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A large number of animal studies have demonstrated that alveolar overdistension may induce lung injury manifest as increased alveolar–capillary permeability and increased levels of inflammatory mediators (1, 2). The recent multicenter randomized controlled trial conducted by the ARDSNet investigators highlighted the clinical importance of these studies by demonstrating a 22% reduction in mortality in the 6 ml/kg, "low stretch" group (3). Although these results are exciting, the mechanism of the decreased mortality is uncertain, especially given that three earlier clinical studies that had minimized end-inspiratory stretch did not find a decrease in mortality (4–6).
Mechanical ventilation can also worsen lung injury by the stresses produced by repetitive alveolar recruitment–derecruitment (2). Two randomized clinical trials showed that a protective ventilatory strategy that minimized both alveolar overdistension (by using low tidal volume [VT]) and repetitive alveolar recruitment–derecruitment (by using high positive end-expiratory pressure [PEEP]) decreased pulmonary and systemic cytokines (7) and decreased mortality in patients with acute respiratory distress syndrome (ARDS) (8). In the ARDSNet study, similar levels of PEEP (8–12 cm H2O) were applied to both the 6 and 12 ml/kg groups and a respiratory rate (RR) up to a maximal of 35 breaths/minute was used to provide a minute ventilation (VE) that minimized hypercapnia and respiratory acidosis (3). Under these circumstances, the shortening of the expiratory time consequent to the higher respiratory rate in the 6 ml/kg VT group may have generated substantial intrinsic PEEP (PEEPi) leading to an unrecognized increase in total PEEP (PEEPtotal) (9, 10), thereby minimizing alveolar recruitment–derecruitment.
In the present investigation, we used the end-expiratory occlusion technique during respiratory muscle paralysis to measure PEEPtotal during the two ARDSNet ventilatory strategies. We tested the hypothesis that the ventilator settings used in the ARDSNet protective ventilatory strategy could have caused substantial PEEPi and an increase in PEEPtotal.
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METHODS
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The study included 10 consecutive patients with ARDS enrolled within 36 hours of admission into the intensive care units (ICUs) of the Santa Chiara Hospital (University of Pisa). Inclusion criteria were diagnosis of ARDS and age more than 18 years (3). Exclusion criteria were pregnancy, increased intracranial pressure, obesity (weight  1 kg per cm of height), chronic obstructive pulmonary disease, and/or presence of chest tubes. The institutional review board approved the protocol, and informed consent was obtained from the patient or next of kin. Patients were studied in the supine position, and were sedated (diazepam, 0.1–0.2 mg/kg and fentanyl, 2–3 µg/kg) and paralyzed (vecuronium, 4–8 mg). A physician not involved in the research study was always present for patient care.
Patients were ventilated in the volume control mode according to the ARDSNet lower VT strategy (3). VT was set at 6 ml/kg predicted body weight (PBW). The ARDSNet table was used to set on the ventilator PEEP (PEEPnominal) and FIO2 to obtain a SaO2 of 90–95% and/or a PaO2 of 60–80 mm Hg (3). Respiratory rate was set to obtain a VE that kept arterial pH between 7.30 and 7.45, but was not allowed to exceed 35 breaths/minute (3). VT was then increased to 12 ml/kg PBW (ARDSNet traditional VT strategy); RR was decreased to obtain the same VE as during the 6 ml/kg strategy. PEEPnominal was maintained constant during the two ventilatory strategies (3). Inspiratory time (Ti) on the ventilator (900C; Siemens-Elema, Berlin, Germany) was set at 33% of the respiratory duty cycle (Ttot).
Flow, airway pressure (Paw), and volume were measured (pneumotachograph and differential pressure transducers) and collected on a computer. Values of Paw at end-expiration of a regular breath (PEEPexternal) and 3–5 seconds after the onset of an end-expiratory occlusion (PEEPtotal), and of an end-inspiratory occlusion (Pplateau) were measured during the lower VT strategy, and 20–30 minutes after ventilation with the traditional VT strategy (Figure 1) . Values of total inspiratory resistance (Rtot) were calculated. The increase in functional residual capacity ( FRC) with the two ventilatory strategies was estimated as the difference between end-expiratory lung volume and the volume at the elastic equilibrium point of the respiratory system (Vr). Vr was assessed by reducing respiratory rate to the lowest value while removing PEEP and giving sufficient time (10–15 seconds) to fully exhale (11). To check that Vr had been reached, the expiratory tubing of the ventilator was occluded at the end of the prolonged expiration: if after the occlusion there was no increase in Paw, Vr had been reached. Measurements were obtained during application of the PEEPnominal value resulting from application of the ARDSNet protocol, and after 2–3 minutes of ventilation with PEEPnominal equal to zero (zero end-expiratory pressure: ZEEP). PEEPi was calculated by subtracting PEEPexternal from PEEPtotal (11).
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Figure 1. Physiologic variables in a representative patient receiving mechanical ventilation according to the ARDSNet traditional VT (A) and the ARDSNet lower VT (B) ventilatory strategies: (top) flow; (middle) airway pressure (Paw); and (bottom) volume. VT = tidal volume; EELV = end-expiratory lung volume; Vr = volume at the elastic equilibrium point of the respiratory system; FRC = increase in functional residual capacity; PEEP = positive end-expiratory pressure; PEEPnominal = value of PEEP set on the ventilator; PEEPexternal = value of PEEP measured on Paw at the end of expiration of a regular breath; PEEPtotal = value of PEEP measured on Paw at the end of a 3–5-second end-expiratory occlusion.
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Data are expressed as mean ± standard deviation (SD). Values obtained with the two ventilatory strategies were compared using analysis of variance (ANOVA) for repeated measures followed by Tukey–Kramer test. Differences were considered statistically significant at p < 0.05.
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RESULTS
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Breathing pattern during the lower VT and traditional VT strategies are shown in Table 1. The reduction in RR consequent to the application of the traditional VT strategy lengthened Ti (1.25 ± 0.08 versus 0.60 ± 0.03 seconds; p < 0.001) and Te (2.51 ± 0.16 versus 1.20 ± 0.06 seconds; p < 0.001).
Figure 1 shows the physiologic variables in one representative patient. PEEPnominal was 9 cm H2O during both ventilatory strategies and PEEPexternal was 9.1 and 10.0 cm H2O during the lower VT and the traditional VT strategies, respectively. During the lower VT strategy, PEEPtotal was 13.2 cm H2O, and when PEEP was reduced to zero, PEEPtotal was 3.6; during the traditional VT strategy, PEEPtotal was 11.1 cm H2O, and decreased to 1.5 cm H2O with a PEEPnominal of zero. As a consequence, the increase in FRC was 1.06 and 0.60 during the lower VT and 0.71 and 0.06 L during the conventional VT strategy, with a PEEPnominal of 9 cm H2O and ZEEP, respectively.
When the ventilator was set with PEEPnominal equal to zero, a slightly positive end-expiratory pressure was found (0.4 ± 0.4 and 0.8 ± 0.5 cm H2O during the lower VT and the traditional VT strategies, respectively); PEEPtotal and FRC were 5.1 ± 2.1 cm H2O and 0.71 ± 0.20 L, and 1.2 ± 0.5 and 0.09 ± 0.05 L during the lower VT and the traditional VT strategies, respectively (p < 0.01).
Values of the physiologic variables with the two ARDSNet ventilatory strategies are shown in Table 2
. PEEPi ranged between 2.1 and 10.0 cm H2O during the lower VT and between 0.1 and 2.6 cm H2O during the traditional VT strategy (p < 0.001). PEEPtotal during the lower VT strategy correlated significantly with Rtot (R2= 0.79; p = 0.0005) and Pplateau (R2 = 0.61; p = 0.007). The higher values of PEEPtotal were observed in patients who had higher values of Rtot and lower values of Pplateau.
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DISCUSSION
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Several studies have demonstrated that mechanical ventilation can worsen pre-existing lung injury or produce acute lung injury de novo in previously normal lungs (1, 2). The presence of shear forces during mechanical ventilation may explain such deleterious effects. In a nonuniformly expanded lung, tidal recruitment of collapsed regions surrounded by open alveoli (2) and/or overdistension of normal alveoli (1) may generate mechanical stresses. Repetitive alveolar recruitment–derecruitment may be prevented by the use of higher levels of PEEP (2); alveolar overdistension may be prevented by the use of low inflating volumes/pressures (1). The recent multicenter randomized controlled trial conducted by the ARDSNet investigators demonstrated that a lung protective ventilatory strategy designed to minimize only alveolar overdistension by using a VT of 6 ml/kg PBW significantly decreased mortality by 22%, compared with a control ventilatory strategy using a VT of 12 ml/kg PBW (3). To minimize the respiratory acidosis in the ARDSNet study, investigators used higher respiratory rates up to a maximum of 35 breaths/minute. The present study shows that the lower VT protocol can be associated with substantial PEEPi, associated with increased PEEPtotal, which may have minimized the ventilator-induced lung injury due to tidal recruitment–derecruitment of collapsed regions. These data may partially explain the difference in mortality between the ARDSNet trial (3) and previous studies (4–6) that did not use such high respiratory rates to limit the respiratory acidosis induced by the low VT strategy.
In the present study, PEEPi was calculated as follows: PEEPi = PEEPtotal – PEEPexternal. Reliability of such fractionation may not be valid under condition of flow limitation, which Koutsoukou and coworkers have shown can occur in patients with ARDS (12). Using the analogy waterfall/airflow limitation (13, 14) and rearranging the equation above: PEEPtotal = PEEPi + PEEPexternal. It appears that in the presence of the waterfall/airflow limitation PEEPtotal will be equal to PEEPi (i.e., to the pressure upstream of the waterfall/airflow limitation) as long as PEEPexternal (i.e., the pressure downstream from the waterfall/airflow limitation) does not exceed PEEPi. On the contrary, in the absence of the waterfall/airflow limitation, the increase in downstream pressure (PEEPexternal) will increase PEEPtotal at any given level of upstream pressure (PEEPi). Our data show that the lower VT strategy generated 3–9 cm H2O of PEEPi with values of PEEPnominal equal to zero; the application of PEEPexternal raised PEEPtotal by an amount roughly equivalent to the value of PEEPi. Although indirect, these data suggest that patients included in the present investigation were not flow-limited. Further studies are required to investigate the role of expiratory flow limitation during protective ventilatory strategy.
The magnitude of increase in FRC (FRC) and PEEPi are determined by the elastic recoil pressure at end-inspiration of the proceeding inflation, the total flow resistance, and the expiratory duration (11–14). It has been reasoned that PEEPi during the lower VT strategy should not occur because: (1) VE, which is believed to be the major determinant of PEEPi (15), was similar in the low and high VT group (9); and (2) a high RR is unlikely to cause PEEPi in ARDS because the lungs are stiff (10). Our data demonstrate that even if VE is identical for the two ventilatory strategies of the ARDSNet trial, a substantial PEEPi may develop in the lower VT group due to the relatively high resistance, low elastic recoil pressure, and the short expiratory time.
Our results are in accord with preliminary data from Lee and coworkers (16) and Aboab and coworkers (17). Lee and coworkers retrospectively reviewed the records of patients enrolled in the ARDSNet trial at Harborview Medical Center. They found that the lower VT strategy was associated with a PEEPi of 2 cm H2O or more only in patients ventilated with a RR greater than 24 breaths/minute (18). In the study by Lee and colleagues, only 50% of the patients were ventilated with such respiratory rates. Consistent with the data of Lee and coworkers, we found that when RR values of 25–35 breaths/minute were used to obtain the endpoints of the lower VT strategy, PEEPtotal was 2–10 cm H2O higher than the PEEPtotal measured during the conventional VT strategy. These data suggest that the low VT strategy may be associated with a significant PEEPi only when values of RR close to the limit of 35 breaths/minute are used.
In the ARDSNet study, RR in the 6 ml/kg group was 29 ± 7 breaths/minute on Day 1. In our study, a RR ranging between 32 and 35 breaths/minute was required in all patients to obtain a pH of 7.3–7.45. Of the patients included in the present study, five had sepsis and eight had a body temperature higher than 38° C. Both sepsis and fever may have increased CO2 production, thus explaining why all our patients required RR close to the high limit (35 breaths/minute) of the lower VT strategy.
Randomization of the ARDSNet ventilatory strategies was not performed. This study was designed to examine the effects of the two ARDSNet ventilatory strategies on PEEPi and changes in FRC. Katz and coworkers showed that in patients with ARDS, changes in FRC consequent to different ventilator settings occur within 3–5 breaths (18). In the present investigation, measurements of PEEPtotal and of FRC were taken after a prolonged period of ventilation with the lower VT strategy and then repeated after 20–30 minutes of traditional VT ventilation. Under these circumstances, our measurements should reflect the level of PEEPtotal and the corresponding increase in FRC developed by the two ARDSNet ventilatory strategies during "steady-state" conditions, and the lack of randomization should not have influenced our results.
In conclusion, our findings suggest that patients with ARDS ventilated at relatively high RRs develop greater PEEPi than when ventilated at lower rates, even for the same VE. This mechanism may produce decreased lung injury secondary to recruitment–derecruitment, and hence provides a plausible explanation for some of the decreased mortality observed in the ARDSNet trial in the 6 ml/kg group.
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FOOTNOTES
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Supported by Consiglio Nazionale delle Ricerche, grant 98.00934.CT04 and MURST Fondo 60%, 2001.
Received in original form May 11, 2001;
accepted in final form March 1, 2002
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ABSTRACT
INTRODUCTION