Evidence Lacking for Volume-Controlled Ventilation in Critical Care

Aaron B. Holley, MD


March 24, 2017

Volume Controlled Ventilation Does Not Prevent Injurious Inflation During Spontaneous Effort

Yoshida T, Nakahashi S, Nakamura MA, et al
Am J Respir Crit Care Med. 2017 Feb 17. [Epub ahead of print]


The ARDSNet trial of limited tidal volume (TV) has dictated ventilator settings for almost two decades.[1] The premise is fairly simple: If TVs are controlled and plateau pressure is less than 30 cm H2O, the lung won't be injured by positive inspiratory pressures. It's a parsimonious concept that generally holds true, and unlike other critical care interventions associated with a mortality reduction, it's stood the test of time.

As with any simple model describing a complex system, however, it's limited. TVs don't account for regional variations in lung injury,[2,3] and plateau pressure doesn't estimate transpulmonary pressure (PL).[4] Esophogeal manometry can estimate PL,[5] but it's much less accurate when the lung is injured and no longer fluid.

Yoshida and colleagues documented the physiologic behavior of the injured lung. In so doing, it reminds us that it takes more than low TVs to protect the respiratory system.

The Study

The authors studied animal models and a patient case using electrical impedance tomography. They inserted two separate pressure catheters in the animals; the first was esophageal, and the second intrapleural. The animals were subjected to multiple conditions: (1) healthy vs diseased lung; (2) pressure vs volume-control mode; and (3) spontaneous breathing vs paralysis. Results between conditions and catheters were compared to describe lung behavior.

When the lung was healthy, the two catheters provided similar measurements irrespective of mode or spontaneous effort. When the lung was injured, differences occurred that were affected by presence of spontaneous effort but not by mode. When animals initiated breaths, PL was twice as high according to the intrapleural vs the esophageal catheter. When animals were paralyzed, the opposite occurred: PL was higher via the esophageal catheter.

Electrical impedance tomography in diseased lungs (animal or human) showed evidence of volume shift from nondependent to dependent areas of the lung (pendelluft) during spontaneous breaths. Ventilator mode had no effect on pendelluft.


The authors have modeled pendelluft in the past,[2] and regional variations in pleural pressure are well described in the diseased lung. They have proven that low TVs don't prevent large regional pressure swings.

What does this mean at the bedside? In a recent review, Yoshida and colleagues advocated using airway pressure-release ventilation (APRV) to limit regional lung injury.[6] The logic is that positive-pressure breaths aren't synchronized with spontaneous effort, so you get the benefit of dependent recruitment without excessive PL swings.

Although they don't mention APRV by name in the current study, the authors imply support in their discussion. They highlight the potential for injury when synchronizing machine with patient breaths, and note that high positive end-expiratory pressure and maximal recruitment will optimize fluid vs solid lung behavior (thus distributing positive and negative pressure changes evenly across the lung). As they note in their review, though, APRV isn't associated with improvements in clinical outcomes.[6,7] We don't know whether the animal and physiology models translate to actual patient care, and therefore we still don't know whether APRV is the right choice for our critical care patients.


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