Central Venous and Bladder Pressures During Pressure Support Ventilation
September 1, 2002 3 minutes read
Abstract & Commentary
Synopsis: Respiratory variation in central venous pressure and bladder pressure reflect respiratory muscle effort during reductions in pressure support ventilation.
Source: Chieveley-Williams S, et al. Central venous and bladder pressure reflect transdiaphragmatic pressure during pressure support ventilation. Chest. 2002;121:533-538.
The purpose of this study was to determine whether changes in central venous pressure and bladder pressure reflect changes in esophageal pressure and gastric pressure during reductions of the level of pressure support ventilation. This was a prospective observational study. The study included 10 patients receiving pressure support ventilation through an endotracheal or tracheostomy tube. Central venous pressure was measured from the distal port of a triple-lumen catheter positioned in the superior vena cava. Bladder pressure was measured using the urinary drainage catheter after instilling 50 mL of saline. Esophageal and gastric pressures were measured from air-filled balloons placed into the esophagus and stomach, respectively. Airway pressure and flow were measured from the proximal airway. To minimize the effects of cardiac oscillations on the central venous pressure, the central venous pressure signal was averaged 30 or more breaths. After baseline measurements, the level of pressure support was reduced by 5 cm H2O decrements until the pressure support level was 5 cm H2O. At each level of pressure support, measurements were recorded after 10-20 minutes of equilibration.
Changes in central venous pressure correlated closely (r = 0.95) with changes in esophageal pressure, and changes in bladder pressure correlated closely (r = 0.90) with changes in gastric pressure. When the transdiaphragmatic pressure calculated using esophageal and gastric pressure was compared to that calculated using central venous and bladder pressures as the pressure support level was changed in individual patients, the correlation coefficients varied from 0.95 to 0.99. Chieveley-Williams and colleagues concluded that measurements of respiratory variations in central venous pressure and bladder pressure reflect respiratory muscle effort during reductions in the level of pressure support ventilation.
Comment by Dean R. Hess, PhD, RRT
Pressure, flow, and volume are commonly measured at the proximal airway during mechanical ventilation. During passive ventilation, these measurements, made under dynamic and static conditions, are used to calculate airways resistance and respiratory system compliance. Unless the pleural pressure is measured, however, it is not possible to separate lung and chest wall compliance. Even with a measure of pleural pressure, it is not possible to separate the effects of the rib cage and abdomen unless intra-abdominal pressure is measured. During spontaneous breathing efforts, pressure measurements from the proximal airway are affected little by respiratory muscle effort. For example, airway pressure changes during pressure support ventilation reflect nothing about respiratory muscle effort. Traditionally, air-filled balloons have been placed into the esophagus and stomach to estimate pleural and abdominal pressures, respectively. However, this technology is not commonly available and is seldom used except in research applications in academic centers. It has been known for many years that respiratory variation in central venous pressure reflects changes in pleural pressure.
This study demonstrates that measurements of respiratory variations in central venous pressure and bladder pressure can be used to estimate transdiaphragmatic pressure with reasonable, albeit not perfect, correlation during sequential reductions in the level of pressure support ventilation. Although this was a relatively small study of only 10 patients, it does provide promise for the use of relatively simple measurements of central venous and bladder pressures to quantify respiratory muscle effort during withdrawal of mechanical ventilation. It remains to be determined whether such measurements facilitate the ventilator weaning process.
In my practice, I have used respiratory variation in central venous pressure to titrate reductions in pressure support ventilation. I have reasoned that large negative deflections in central venous pressure during pressure support ventilation reflect an undesirably large load on the respiratory muscles, and I have titrated the level of support accordingly. The results published in this paper support that practice. There are other potential uses for the measurements of respiratory variation in central venous and bladder pressures. These include estimation of chest wall and abdominal compliance in passively ventilated patients, estimation of auto-PEEP in patients with airflow obstruction, and identification of diaphragmatic paralysis. It is interesting that the respiratory variations that make interpretation of central venous pressure problematic may be used to evaluate respiratory function.
Dr. Hess is Assistant Professor of Anesthesia, Harvard Medical School, Assistant Director of Respiratory Care, Massachusetts General Hospital, Cambridge, MA.
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