0
Editorials: POINT/COUNTERPOINT EDITORIALS |

Counterpoint: Is Pressure Assist-Control Preferred Over Volume Assist-Control Mode for Lung Protective Ventilation in Patients With ARDS? NoPressure Control Is Not Preferred for Ventilation FREE TO VIEW

Neil MacIntyre, MD, FCCP
Author and Funding Information

From the Duke University Medical Center.

Correspondence to: Neil MacIntyre, MD, FCCP, Duke University Medical Center, Durham, NC 27710; e-mail: neil.macintyre@duke.edu


Financial/nonfinancial disclosures: The author has reported to CHEST the following conflict of interest: Dr MacIntyre has served as a consultant to CareFusion of Yorba Linda, California, since 1985.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(2):290-292. doi:10.1378/chest.11-1052
Text Size: A A A
Published online

On most modern mechanical ventilators, the gas delivery algorithm is generally one of two types: flow/volume targeting (volume assist-control ventilation [VACV]) or pressure targeting with time or flow cycling (pressure assist-control ventilation [PACV] or pressure support ventilation). With flow/volume targeting, the clinician sets an inspiratory flow along with a volume cycling criteria. Airway pressure is, thus, the dependent variable (ie, varying according to lung mechanics and effort). With pressure targeting, the clinician sets an inspiratory pressure target along with either time or flow cycling criteria. Flow and volume are now the dependent variables (ie, varying with lung mechanics and effort). Changes in compliance, resistance, or patient effort will change airway pressure (but not flow) with flow/volume targeting. In contrast, similar changes in compliance, resistance, or effort will cause a change of flow and tidal volume (Vt) (but not airway pressure) with pressure targeting.

An important clinical question is whether the different breath delivery algorithms of newer pressure-targeted modes provide advantages over the more traditional flow/volume-targeted breath. This question generally revolves around two key issues. First, which approach best limits Vt and end-inspiratory stretch to prevent ventilator-induced lung injury (VILI)? Second, which approach best synchronizes with patient breathing efforts to minimize sedation needs? Proponents of pressure targeting usually argue that: (1) pressure settings can be provided (either manually or in a feedback fashion) that maintain safe Vts and guarantee an upper pressure limit, and (2) the variable flow feature of pressure targeting will synchronize with patient inspiratory effort better than fixed flow breaths and, thus (at least theoretically) reduce sedation needs. Proponents of flow/volume targeting would counter: (1) flow/volume targeting guarantees a safe Vt at all times, and (2) the putative synchrony advantages of pressure targeting are overblown. Dr Marini1 has articulated the pressure-targeting argument in the Point segment of the Point/Counterpoint Editorials in this issue of CHEST. It is now time to look at the argument for flow/volume targeting in more detail.

As noted, the clinician-set Vt is guaranteed with a flow/volume-targeted breath. So how important is this? The evidence is strong that limiting tidal stretch is as important (if not more important) as limiting maximal stretch in reducing VILI.2,3 Tschumperlin et al4 observed in alveolar cell tissue cultures that the lethal effects of overstretch could be mitigated by smaller tidal stretch. Mascheroni et al5 showed in normal sheep that 3 days of excessive tidal breathing caused significant lung injury even though the end-inspiratory transpulmonary pressures were only modestly elevated and well below physiologic maximums. Dreyfuss et al,6 in a series of animal experiments, convincingly demonstrated that it was end-inspiratory lung volume, not end-inspiratory lung pressure, that produced injury.

All of these observations culminated in the design of the ARDS Network ventilator management trial, in which Vt was clinician controlled along with a secondary peak/plateau pressure limitation.7 The results of this trial convincingly showed the importance of limiting volumes and pressures to minimize VILI. Moreover, in secondary analysis of data, Hager et al8 showed a beneficial effect of Vt reduction from 12 mL/kg to 6 mL/kg ideal body weight (IBW) regardless of plateau pressure before Vt reduction. The analysis of these data coupled with their review of other clinical studies and animal experiments led these investigators to conclude that there was no “safe” plateau pressure below which the benefit of Vt reduction disappears. These findings support a strategy in which control of Vt should take precedence over control of inspiratory pressure.

So why not simply use pressure-targeting modes and set the pressure to deliver the desired Vt? Although attractive conceptually, the reality is that Vts will vary in most patients receiving pressure-targeted breaths as respiratory system mechanics change and/or patient effort fluctuates. Indeed, Kallet et al9 found that with PACV Vts “markedly” exceeded the Vt target of 6 mL/kg IBW in 40% of patients with acute lung injury/ARDS—twice the rate observed with VACV. Interestingly, the volume-feedback mode, pressure-regulated volume control ventilation, yielded similar results to PACV, with 40% of patients still having low Vt violations. Taken together, these data argue that if Vt control is considered important, the flow/volume targeted breath makes considerable sense.

At the end of the day, there are very few studies that directly compare flow/volume-targeted and pressure-targeted strategies for lung-protective ventilation in ARDS, and most have confounding issues. The most extensive study was performed by Meade et al,10 who compared these approaches in a large international multicenter randomized controlled trial. In both arms of this trial, a Vt target of 6 mL/kg IBW was used, and outcomes were found to be similar (28-day mortality in VACV vs PACV was 32.3% vs 28.4%, respectively, [P = .2], and barotraumas were 9.1% vs 11.2%, [P = .33]). Unfortunately, different positive end-expiratory pressure/Fio2 strategies were used in the two arms, confounding the comparison.

Advocates of flow/volume targeting point to another potential advantage in providing lung protection: There is considerable evidence that clinicians have not reliably applied low Vt ventilation.11 Indeed, Rubenfeld et al12 identified “unwillingness to relinquish ventilator control” as a primary barrier to initiating lung-protective ventilation in a survey of ICU respiratory therapists and nurses. When a written protocol focused on Vt settings was used, however, compliance with low Vt strategies was found by these investigators to be improved.13 This is important because successful implementation of new treatment algorithms requires simplicity and familiarity. Explicitly setting Vt, rather than setting airway pressure and repeatedly measuring Vt, is certainly simpler and, thus, seems intuitively advantageous in achieving widespread adoption.

The other point that proponents of flow/volume targeting argue is that the pressure limiting and synchrony features of pressure targeting are overblown and unnecessary. With flow/volume targeting, pressure limits/alarms can always be set to assure that an end-inspiratory pressure limit is not exceeded. Regarding patient-ventilator synchrony, there is literature showing that the variable flow of pressure targeting might be easier to synchronize with patient efforts than fixed flow breaths.14 Results in clinical trials, however, are not always supportive of this notion. Chiumello et al15 showed in patients with acute respiratory failure that when the peak inspiratory flow of VACV was adjusted properly to support a given Vt, there were no differences in work of breathing and inspiratory pressure against a closed shutter after 100 milliseconds compared with PACV. Kallet et al9 also showed in a group of patients with acute lung injury receiving small Vts that PACV had similar patient work reductions to those obtained with carefully titrated VACV. Taken together, these studies suggest that if pertinent mechanical parameters (eg, peak flow, Vt) are adjusted properly by skilled clinicians, flow/volume targeting can produce patient-ventilator synchrony similar to pressure targeting in most (if not all) patients.

There are other potential advantages to flow/volume-targeted modes. For example, under circumstances in which patient drive is reduced/absent (eg, sleep, sedatives, neuromuscular blockers, and so forth) and/or respiratory system mechanics worsen, a fixed Vt assures continuation of a desired level of support. Indeed, flow/volume targeting would seem to be an ideal choice to assure adequate ventilation in patients with potential for respiratory mechanical variability, breathing pattern unreliability, or both to breathe spontaneously at an adequate level.

Recently, another use for a fixed flow breath was introduced. Ranieri et al16 described the concept of a “stress index” to assess respiratory system mechanics and thereby help guide the positive end-expiratory pressure and Vt setting. This stress index requires a clinician-controlled constant flow Vt. If there is no appreciable recruitment or overdistention occurring during this type of breath, the airway pressure profile should be a smooth, straight, diagonal line. In contrast, if recruitment occurs at the beginning of the breath, the airway pressure curve is convex downward; if overdistention occurs at the end of the breath, the airway pressure curve is concave upward. Whether this concept will translate into more lung-protective ventilator settings remains to be demonstrated.

References

Marini JJ. Point: is pressure assist-control preferred over volume assist-control mode for lung protective ventilation in patients with ARD? Yes. Chest. 2011;1402:286-290. [CrossRef] [PubMed]
 
Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from the bench to the bedside. Intensive Care Med. 2006;321:24-33. [CrossRef] [PubMed]
 
Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med. 1998;1571:294-323. [PubMed]
 
Tschumperlin DJ, Oswari J, Margulies AS. Deformation-induced injury of alveolar epithelial cells. Effect of frequency, duration, and amplitude. Am J Respir Crit Care Med. 2000;1622 pt 1:357-362. [PubMed]
 
Mascheroni D, Kolobow T, Fumagalli R, Moretti MP, Chen V, Buckhold D. Acute respiratory failure following pharmacologically induced hyperventilation: an experimental animal study. Intensive Care Med. 1988;151:8-14. [CrossRef] [PubMed]
 
Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis. 1988;1375:1159-1164. [PubMed]
 
The Acute Respiratory Distress Syndrome NetworkThe Acute Respiratory Distress Syndrome Network Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;34218:1301-1308. [CrossRef] [PubMed]
 
Hager DN, Krishnan JA, Hayden DL, Brower RG. ARDS Clinical Trials Network ARDS Clinical Trials Network Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. Am J Respir Crit Care Med. 2005;17210:1241-1245. [CrossRef] [PubMed]
 
Kallet RH, Campbell AR, Dicker RA, Katz JA, Mackersie RC. Work of breathing during lung-protective ventilation in patients with acute lung injury and acute respiratory distress syndrome: a comparison between volume and pressure-regulated breathing modes. Respir Care. 2005;5012:1623-1631. [PubMed]
 
Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators Lung Open Ventilation Study Investigators Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;2996:637-645. [CrossRef] [PubMed]
 
Young MP, Manning HL, Wilson DL, et al. Ventilation of patients with acute lung injury and acute respiratory distress syndrome: has new evidence changed clinical practice? Crit Care Med. 2004;326:1260-1265. [CrossRef] [PubMed]
 
Rubenfeld GD, Cooper C, Carter G, Thompson BT, Hudson LD. Barriers to providing lung-protective ventilation to patients with acute lung injury. Crit Care Med. 2004;326:1289-1293. [CrossRef] [PubMed]
 
Umoh NJ, Fan E, Mendez-Tellez PA, et al. Patient and intensive care unit organizational factors associated with low tidal volume ventilation in acute lung injury. Crit Care Med. 2008;365:1463-1468. [CrossRef] [PubMed]
 
MacIntyre NR, McConnell R, Cheng KC, Sane A. Patient-ventilator flow dyssynchrony: flow-limited versus pressure-limited breaths. Crit Care Med. 1997;2510:1671-1677. [CrossRef] [PubMed]
 
Chiumello D, Pelosi P, Calvi E, Bigatello LM, Gattinoni L. Different modes of assisted ventilation in patients with acute respiratory failure. Eur Respir J. 2002;204:925-933. [CrossRef] [PubMed]
 
Ranieri VM, Zhang H, Mascia L, et al. Pressure-time curve predicts minimally injurious ventilatory strategy in an isolated rat lung model. Anesthesiology. 2000;935:1320-1328. [CrossRef] [PubMed]
 

Figures

Tables

References

Marini JJ. Point: is pressure assist-control preferred over volume assist-control mode for lung protective ventilation in patients with ARD? Yes. Chest. 2011;1402:286-290. [CrossRef] [PubMed]
 
Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from the bench to the bedside. Intensive Care Med. 2006;321:24-33. [CrossRef] [PubMed]
 
Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med. 1998;1571:294-323. [PubMed]
 
Tschumperlin DJ, Oswari J, Margulies AS. Deformation-induced injury of alveolar epithelial cells. Effect of frequency, duration, and amplitude. Am J Respir Crit Care Med. 2000;1622 pt 1:357-362. [PubMed]
 
Mascheroni D, Kolobow T, Fumagalli R, Moretti MP, Chen V, Buckhold D. Acute respiratory failure following pharmacologically induced hyperventilation: an experimental animal study. Intensive Care Med. 1988;151:8-14. [CrossRef] [PubMed]
 
Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis. 1988;1375:1159-1164. [PubMed]
 
The Acute Respiratory Distress Syndrome NetworkThe Acute Respiratory Distress Syndrome Network Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;34218:1301-1308. [CrossRef] [PubMed]
 
Hager DN, Krishnan JA, Hayden DL, Brower RG. ARDS Clinical Trials Network ARDS Clinical Trials Network Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. Am J Respir Crit Care Med. 2005;17210:1241-1245. [CrossRef] [PubMed]
 
Kallet RH, Campbell AR, Dicker RA, Katz JA, Mackersie RC. Work of breathing during lung-protective ventilation in patients with acute lung injury and acute respiratory distress syndrome: a comparison between volume and pressure-regulated breathing modes. Respir Care. 2005;5012:1623-1631. [PubMed]
 
Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators Lung Open Ventilation Study Investigators Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;2996:637-645. [CrossRef] [PubMed]
 
Young MP, Manning HL, Wilson DL, et al. Ventilation of patients with acute lung injury and acute respiratory distress syndrome: has new evidence changed clinical practice? Crit Care Med. 2004;326:1260-1265. [CrossRef] [PubMed]
 
Rubenfeld GD, Cooper C, Carter G, Thompson BT, Hudson LD. Barriers to providing lung-protective ventilation to patients with acute lung injury. Crit Care Med. 2004;326:1289-1293. [CrossRef] [PubMed]
 
Umoh NJ, Fan E, Mendez-Tellez PA, et al. Patient and intensive care unit organizational factors associated with low tidal volume ventilation in acute lung injury. Crit Care Med. 2008;365:1463-1468. [CrossRef] [PubMed]
 
MacIntyre NR, McConnell R, Cheng KC, Sane A. Patient-ventilator flow dyssynchrony: flow-limited versus pressure-limited breaths. Crit Care Med. 1997;2510:1671-1677. [CrossRef] [PubMed]
 
Chiumello D, Pelosi P, Calvi E, Bigatello LM, Gattinoni L. Different modes of assisted ventilation in patients with acute respiratory failure. Eur Respir J. 2002;204:925-933. [CrossRef] [PubMed]
 
Ranieri VM, Zhang H, Mascia L, et al. Pressure-time curve predicts minimally injurious ventilatory strategy in an isolated rat lung model. Anesthesiology. 2000;935:1320-1328. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543