Increasing Respiratory Rate to Improve PaCO2 in Patients with ALI and ARDS
October 1, 2002 6 minutes read
Abstract & Commentary
Synopsis: In patients with ALI or ARDS, use of a higher respiratory rate did not increase CO2 clearance and resulted in the generation of dynamic hyperinflation and adverse hemodynamic effects.
Source: Vieillard-Baron A, et al. Increasing respiratory rate to improve CO2 clearance during mechanical ventilation is not a panacea in acute respiratory failure. Crit Care Med. 2002;30:1407-1412.
The ardsnet lung-protective ventilation strategy for managing acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) calls for an increase in respiratory rate (to a maximum of 35 breaths/min) in an attempt to normalize PaCO2 when a low tidal volume strategy is used. The purpose of this study was to determine the effects of this increased respiratory rate on PaCO2, auto-PEEP, and right ventricular function. The study included 14 patients meeting the definition for ALI or ARDS. Patients were sedated and paralyzed for the study. The ventilator was set for volume-controlled continuous mandatory ventilation. Tidal volume was set at 8 mL/kg and I:E was set at 1:2. Plateau pressure was maintained at £ 25 cm H2O. PEEP was set to a level that counterbalanced auto-PEEP. Respiratory rates of 15 breaths/min and 30 breaths/min were compared without changing the inspiratory flow, tidal volume, or PEEP settings. Respiratory and echocardiographic measurements were made at each respiratory rate setting.
Compared to the lower respiratory rate, the higher rate setting did not significantly decrease the PaCO2 (47 ± 8 mm Hg with the high rate and 51 ± 7 mm Hg with the low rate). Alveolar dead space was significantly higher with the high rate (0.21 ± 0.08) compared to the low rate (0.14 ± 0.06). The high respiratory rate resulted in significant auto-PEEP (6.4 ± 2.7 cm H2O). With the higher respiratory rate, right ventricular outflow impedance was increased, resulting in a significant decrease in cardiac output (2.9 ± 0.6 L/min/m2 for the high rate compared to 3.3 ± 0.7 L/min/m2 for the low rate).
Comment by Dean R. Hess, PhD, RRT
Few would debate that the ARDSnet results1 provide compelling evidence for the mechanical ventilation of patients with ALI and ARDS. Using a strategy that targeted a tidal volume of 6 mL/kg of predicted body weight and an end-inspiratory plateau pressure £ 30 cm H2O, an absolute reduction in mortality of almost 10% was reported. This produces a number-needed-to-treat of 10, meaning that 1 life will be saved for every 10 patients in whom this volume and pressure limitation strategy is used. With such compelling evidence, I have been amazed at the number of arguments that have been proposed to avoid adoption of this strategy.
Some have argued that volume-controlled ventilation is the wrong mode and some have argued that the PEEP level used in the ARDSnet study was too low. Others have argued for strategies such as prone positioning and recruitment maneuvers (strategies for which there is no evidence of a survival benefit). Another attack on the ARDSnet strategy, and the one put forward in this study, is that the high respiratory rate is bad; that it will produce auto-PEEP and dangerous effects associated with such.2 This is an easy target, as auto-PEEP was not reported in the ARDSnet study. In the present study, auto-PEEP increased with the higher respiratory rate and this was associated with an increased dead space and adverse hemodynamic effects.
I have difficulty knowing how to apply these findings to my practice. I advocate strict adherence to the ARDSnet protocol (the only way to compare results in my patients to ARDSnet is to implement that strategy verbatim). ARDSnet calls for measuring the height of the patient, calculating predicted body weight (PBW) based upon that height, and targeting a tidal volume of 6 mL/kg PBW. In this study, the technique used to determine body weight is not stated and a tidal volume of 8 mL/kg was used. Accordingly, the tidal volume in this study may have been substantially greater than that used in ARDSnet, which may have contributed to the amount of auto-PEEP and hemodynamic effects. Vieillard-Baron and associates also did not set PEEP according to the ARDSnet strategy, which may have affected the amount of dead space.
Perhaps the greatest limitation of this study is that the inspiratory time was unchanged when the rate was increased. Thus the I:E was 1:2 at a rate of 15 breaths/min, but 1:1 at a rate of 30 breaths/min. In practice, most clinicians would decrease the inspiratory time when the rate is increased—particularly if auto-PEEP occurs. In practice, auto-PEEP is measured and the I:E adjusted if such is present. This was a short-term physiologic study. Accordingly, we do not know if the "adverse" physiologic effects reported are associated with any effect—good or bad—on ultimate patient outcomes.
Even if auto-PEEP occurs when the ARDSnet ventilation strategy is used, it does not eliminate the very important point that this ventilation strategy is associated with a survival benefit. If I am the unfortunate patient with ALI or ARDS, I’ll happily accept a little auto-PEEP to improve my chance of survival. n
References
1. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342(18):1301-1308.
2. de Durante G, et al. ARDSNet lower tidal volume ventilatory strategy may generate intrinsic positive end-expiratory pressure in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. 2002;165(9):1271-1274.
Comment by David J. Pierson, MD
ALI and ARDS are 2 variants of a syndrome of acute generalized lung injury that follows or accompanies a variety of severe pulmonary and nonpulmonary disorders. ALI and ARDS have the same diagnostic criteria except for the severity of oxygenation impairment, as measured by the relationship between arterial PO2 and inspired oxygen concentration (PaO2/FIO2). There are 4 components in the diagnosis:
1. Bilateral opacities on chest radiograph;
2. Pulmonary artery wedge pressure < 18 mm Hg (or, in the absence of a PA catheter, no clinical evidence of left atrial hypertension);
3. Hypoxemia: PaO2/FIO2 < 300 mm Hg = ALI PaO2/FIO2 < 200 mm Hg = ARDS
4. An appropriate clinical setting (acute illness; presence of a recognized risk factor or at least no other likely explanation for findings).
There is no "primary" (eg, directly therapeutic) treatment for ARDS. Anecdotal reports and clinical trials of a variety of agents aimed at preventing or counteracting the effects of the presumed mediators of lung injury have all been unconvincing or negative. There is also no evidence that achieving "better" oxygenation (ie, a higher PaO2/FIO2) improves outcomes. Management is therefore supportive, with the main aims of providing adequate tissue oxygenation, support of vital organ function, and the prevention of further lung damage and other complications.
The practical implementation of mechanical ventilation according to the ARDS Network protocol (http://hedwig.mgh.Harvard.edu/ardsnet) is nicely discussed by Kallet and associates in a recent review1 This protocol uses volume-targeted, assist-control ventilation because this mode makes the goals of limiting both static inflation pressure and delivered tidal volume easier to achieve. It uses tidal volume (corrected for ventilator circuit compression volume) based on PBW, calculated as follows:
Male: PBW in kg = 50 + 2.3 (height in inches - 60)
Female: PBW in kg = 45.5 + 2.3 (height in inches - 60)
As mentioned above by Dr. Hess, there is a great deal of debate about the ARDSnet protocol among leading intensivists. Some clinicians, after embracing pressure control ventilation because of its lower peak airway pressure and (still largely theoretical) other advantages over volume-targeted ventilation, have had a hard time with the idea of returning to "old fashioned" assist-control. I have little doubt that using pressure control to achieve the primary objectives of the ARDSnet protocol—tidal volume no more than 6 mL/kg and plateau pressure no more than 30 cm H2O—would be as effective in improving outcomes. The trick is in actually achieving these goals consistently, and making sure that the tidal volume does not exceed 6 mL/kg as the patient’s respiratory system compliance varies. There is also strong belief among some clinicians that PEEP should be used differently than stipulated by the ARDSnet protocol. At present, clinically relevant proof of this is lacking, and the second phase of the ARDS Network study (still unpublished) did not demonstrate a convincing difference in outcomes with a higher-PEEP, lower-FIO2 approach as compared to the use of lower PEEP and higher FIO2.
Reference
1. Kallet RH, et al. Implementation of a low tidal volume ventilation protocol for patients with acute lung injury or acute respiratory distress syndrome. Respir Care. 2001;46(10):1024-1037.
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