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Literature Review

The Changes in Pulse Pressure Variation or Stroke Volume Variation After a “Tidal Volume Challenge” Reliably Predict Fluid Responsiveness During Low Tidal Volume Ventilation

Myatra S, Prabu N, Divatia JV, Monnet X, Kulkarni AP, Teboul JL. Crit Care Med. 2017;45(3):415-421.

Reviewers: Susan C. Lee, MD1; Sandeep Markan, MD2

  1. Assistant Professor, Division of Trauma Anesthesiology, Ben Taub General Hospital, Baylor College of Medicine, Houston, TX
  2. Associate Professor, Deputy Chief of Anesthesiology, Director of Trauma Anesthesiology, Ben Taub General Hospital, Baylor College of Medicine, Houston, TX

Fluid resuscitation in patients with acute circulatory failure can be life-saving or detrimental. While half of the patients will benefit from fluid administration (fluid responders), the other half will suffer the consequences of fluid overload. Making an informed decision on fluid strategy in these patients is challenging because volume expansion does not always cause an increase in cardiac output. Currently, measured indices such as pulse pressure variation (PPV) and stroke volume variation (SVV) do not reliably predict fluid responsiveness at low tidal volumes (<8 mL/kg). This study hypothesizes that the changes in these 2 indices after transiently increasing the tidal volume from 6 mL/kg to 8 mL/kg consistently reveal the fluid responders.


Twenty adult patients with acute circulatory failure receiving low tidal volume ventilation were included in this study. PPV, SVV, cardiac index, and end-expiratory occlusion test (EEOT) were recorded at a baseline tidal volume 6 mL/kg. A “tidal volume challenge” to 8 mL/kg was then initiated for 1 minute. After the tidal volume was reduced to 6 mL/kg, a fluid bolus was given and cardiac index changes were recorded. If the cardiac index increased more than 15%, patients were identified as fluid responders. Absolute and percent changes between the PPV and SVV at 6 mL/kg, 8 mL/kg, and postfluid bolus also were calculated.


A total of 30 sets of measurements were obtained. At low tidal volumes at 6 mL/kg, fluid responders could not be identified based on PPV and SVV values. After the “tidal volume challenge,” fluid responders showed absolute increases in PPV and SVV, with cutoff values of 3.5% and 2.5%, respectively. Postfluid administration, fluid responders showed an appropriate decrease in the same measurements as well as an increase of 15% in the cardiac index.


Compared to pulse pressure and stroke volume variations obtained at a steady low tidal volume of 6 mL/kg, transiently increasing the tidal volume to 8 mL/kg yielded better measurements in predicting a patient’s responsiveness to fluid.


In recent years, besides the old methods of passive leg raising and fluid challenges, SVV and PVV have been added to the critical care physician’s inventory of tools to determine fluid responsiveness. In this era of lung protective ventilation, we generally use lower tidal volumes. However, in suitable patients, transient applications of higher tidal volumes of 8 mL/kg may be applied to better discern fluid responsiveness in certain patient subgroups. Applying a “tidal volume challenge” is a simple maneuver that can be done by bedside. These are validated in patients who are intubated, under sedation, and do not have exclusionary factors such as arrhythmias, open chest, and right heart failure. Although changes in PPV alone can be used to predict fluid responsiveness without invasive cardiac monitoring, it has its limitations. The authors demonstrate that the combination of SSV and PPV when checked at 2 different tidal volumes may increase the specificity and sensitivity for measuring fluid responsiveness.

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