How Accurately Can Clinicians Identify the Lower Inflection Point?
ABSTRACT & COMMENTARY
The "lung-protective" ventilatory strategy currently in vogue for managing acute respiratory distress syndrome (ARDS) is based on maintaining tidal ventilation above the lower inflection point (Pflex) on the static pressure-volume curve. However, in this study estimates of Pflex from the same data curves by six different clinicians varied by 4-9 cm H2O for a given curve.
As data supporting the existence of ventilator-induced lung injury accumulate from both animal and human studies, clinicians are changing the way they manage patients with ARDS. The currently advocated "lung-protective strategy" for ventilatory management includes the use of tidal volumes of 5-7 mL/kg, the avoidance of alveolar (i.e., end-inflation static) pressures exceeding 35 cm H2O, permissive hypercapnia, and the use of enough positive end-expiratory pressure (PEEP) to keep tidal ventilation above the lower inflection point (Pflex) on the static pressure-volume (P-V) curve (See Figure). Because Pflex is thought to represent alveolar and airway opening, ventilating the lung at pressures and volumes above this point is intended to avoid lung injury from the shear stresses created by cyclically opening and closing these structures.
In order to apply it in an individual patient, this strategy assumes that Pflex can be identified clinically on the P-V curve. O’Keefe and colleagues at Harborview Medical Center in Seattle sought to determine whether this was the case by constructing P-V curves in critically ill patients and having six clinicians attempt independently to identify Pflex in each case. The eight patients included in the study were all in the surgical-trauma ICU, and each had a known risk factor for developing ARDS. Their mean PaO2/FIO2 ratio was 152 torr (range, 80-320 torr), and their ARDS risk factors included sepsis (4 patients), multiple long-bone fractures (2), pulmonary contusions (2), and multiple transfusions (2). All were studied within 24 hours of onset of the risk factor.
O’Keefe et al constructed the P-V curves by gradually inflating the patients’ lungs manually using a 3L calibration syringe, while simultaneously recording pressures and volumes on a commercial inline computerized respiratory monitoring system. All patients were pharmacologically paralyzed at the time of the measurements. PEEP was discontinued for 5 minutes, and measurements at 50-mL tidal volume increments were made until 15 mL/kg was delivered or static pressure reached 60 mm Hg. Three inflation procedures were done in each patient within 10 minutes, and the data were plotted onto a single curve. Direct printouts of the P-V curves were then presented to five intensivists and one respiratory therapist, who independently determined Pflex visually from the curves.
Estimated mean Pflex in these eight critically ill surgical patients ranged from 9.5-20.8 cm H2O, with standard deviations of 1.3-3.4 cm H2O. No individual clinician systematically determined Pflex to be significantly higher or lower than the other clinicians, but the estimated Pflex values varied substantially, with an interindividual range for each patient of 4-9 cm H2O. O’Keefe et al conclude that estimation of Pflex by this technique is imprecise and potentially of little use in selecting minimum PEEP levels in individual patients. (O’Keefe GE, et al. J Trauma 1998;44[6]:1064-1068.)
COMMENT BY DAVID J. PIERSON, MD
Although current understanding of ventilator-induced lung injury supports the concept that PEEP should be set above Pflex in patients with acute lung injury, the present study casts doubt as to whether this can be done meaningfully in individual patients. I have taken informal "show-of-hands" polls of physicians and respiratory therapists attending several conferences on ARDS management, and my impression is that the majority of clinicians do not actually construct P-V curves on their patients. Such curves are not currently used routinely in patient management at the institution where this study was performed.
I think there are three reasons for this. First, the P-V curves used in lectures and to illustrate data in published papers tend to look like the hypothetical curve in the figure. However, curves from actual patients are often less smooth, and it is usually a judgment call as to where the slope begins to increase. Even the strongest advocates of performing individual P-V curves report a certain percentage of patients in whom a distinct Pflex cannot be identified. Second, construction of P-V curves by the technique described in this study is cumbersome and fairly labor-intensive. Admittedly, attempts are being made to speed and simplify the process, but such streamlined techniques are not currently available to the clinician. Finally, to construct a reproducible P-V curve in the ICU requires that the patient be completely motionless, which for practical purposes means pharmacologically paralyzed. While short-term use of muscle relaxants is necessary for certain procedures and may be justifiable for the purpose discussed here, there are numerous compelling reasons for avoiding their use in critically ill patients whenever possible.
Most studies on patients with medical illnesses predisposing to ARDS have determined Pflex to be in the range of 8-10 cm H2O. Accordingly, it makes sense to use at least about 10 cm H2O of PEEP in such patients when ARDS develops. I think it is clinically acceptable to make this assumption, rather than attempting to construct P-V curves in all patients, when managing ARDS according to the current "lung-protective" strategy. It is important to realize, however, that different patient groups may have different requirements for PEEP, fluid support, and other aspects of management, as illustrated by the considerably higher mean Pflex values determined in the critically ill surgical-trauma patients included in this study.
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