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(Chest. 2002;121:533-538.)
© 2002 American College of Chest Physicians

Central Venous and Bladder Pressure Reflect Transdiaphragmatic Pressure During Pressure Support Ventilation*

Sarah Chieveley-Williams, MD; Lila Dinner, MD; Anna Puddicombe, RGN; Debbie Field, Msc; A. T. Lovell, MD and John C. Goldstone, MD

* From the Department of Anesthesia, University College London Medical School, London, UK.

Correspondence to: John C. Goldstone, MD, Center for Anesthesia, Room 103, First Floor Crosspiece, Middlesex Hospital, Mortimer St, London W1N 8AA, UK; e-mail: j.goldstone{at}ucl.ac.uk


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To determine whether the change in bladder pressure (Pblad) and central venous pressure (Pcvp) may reflect the changes in esophageal pressure (Pes) and gastric pressure (Pgas) when inspiratory pressure support (IPS) is altered.

Design: Prospective clinical study.

Setting: The ICUs of a teaching hospital.

Patients: Ten patients currently receiving IPS ventilation via a tracheostomy or an endotracheal tube who already had bladder and central venous catheters in situ.

Measurements and results: Airway pressure, Pes, Pgas, Pcvp, Pblad, and flow were measured at the original IPS setting. IPS then was reduced by 5-cm H2O increments until IPS was zero or was at the minimum pressure that could be tolerated by each patient. At each level of IPS, pressures and flow were measured at steady-state breathing. The maximum pressure difference for each pressure during inspiration was calculated. We found that the {Delta}Pblad correlated closely with the {Delta}Pgas (r = 0.904) and that the {Delta}Pes correlated with the {Delta}Pcvp (r = 0.951). When the {Delta}Pcvp - {Delta}Pblad was compared with the transdiaphragmatic pressure for each patient as the IPS was altered, the correlation coefficients varied from 0.952 to 0.999.

Conclusion: Although absolute values for the {Delta}Pcvp during mechanical ventilation do not always reflect the {Delta}Pes, useful information can be obtained from this route. In individual patients, the two sites of measurement followed each other when IPS was changed, enabling a bedside assessment of the response to reducing respiratory support.

Key Words: central venous pressure • esophageal pressure • mechanical ventilation • monitoring of respiratory muscle function • transdiaphragmatic pressure


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Although respiratory muscle function and strength are important, monitoring of the diaphragm is invasive and is performed infrequently in critically ill patients. During inspiration, the diaphragm descends, raising intra-abdominal pressure and reducing intrathoracic pressure. To quantify diaphragmatic strength, the pressure difference across the diaphragm is measured from the addition of gastric pressure (Pgas) and esophageal pressure and termed transdiaphragmatic pressure (Pdi). While Pes and Pgas are the standard methods of measuring Pdi, pressure changes during respiration are transmitted to other structures in the mediastinum and abdomen.

Flemale and co workers1 measured central venous pressure (Pcvp) and Pes in healthy volunteers during inspiratory efforts against a closed airway. They concluded that measurements of Pcvp reflect pleural pressure (Ppl) changes and found that the ratio of the {Delta}Pcvp to the {Delta}Pes was close to unity. The use of intravesical pressure as a measure of intra-abdominal pressure has been investigated by other research groups,2 3 4 who have validated it against Pes and abdominal pressure. Intravesical pressure was shown to be an accurate reflection of both directly measured intra-abdominal pressure and intragastric pressure.

During inspiratory pressure support (IPS) ventilation, the respiratory muscles contract and initiate ventilation. When IPS is maximal, little effort is required, and when IPS is reduced, respiratory muscle effort is increased. We have studied patients receiving IPS to test whether Pcvp and bladder pressure (Pblad) reflect Pes and Pgas, and to investigate whether useful information can be obtained from the {Delta}Pblad - {Delta}Pcvp. Furthermore, we have investigated whether the {Delta}Pblad - {Delta}Pcvp can monitor changes when IPS is altered.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Prior to the study, written informed consent was obtained from the patient for a protocol that had been approved previously by the institutional review committee. Ten patients were enrolled into the study, comprising 6 male and 4 female patients. All patients were recovering from critical illnesses and were then being weaned from mechanical ventilation, which entailed daily assessments during periods of breathing through a simple circuit. Table 1 provides a summary of the demographic information for the patients.


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  		Table 1. Demographic Details for All Subjects*

 
At the time of the study, all patients were breathing spontaneously with IPS ventilation via a cuffed oral endotracheal tube or a cuffed tracheostomy. All patients had both a bladder catheter and a central venous catheter in situ as part of their medical care. The central venous catheter entered either the internal jugular or subclavian vein with the distal end located radiographically in the superior vena cava.

Measurements
Airway pressure (Paw), Pes, Pcvp, Pgas, and Pblad, as well as inspiratory flow at the airway, were measured for each patient. Airflow was measured with a heated pneumotachograph (Hans Rudolph; Kansas City, MO), and air volume was obtained from the integrated flow signal.

Pes and Pgas were measured using 10-cm air-filled balloon catheters (P.K. Morgan; Kent, UK) that were passed transnasally into the patient under local anesthesia. Two milliliters of air was injected into the gastric balloon, and 0.5 mL of air were passed into the esophageal balloon. The correct placement of the esophageal catheter was confirmed according to the method described by Baydur et al.5 Each catheter was connected to a differential pressure transducer (Medex Medical; Lancashire, UK).

Pcvp was measured from the distal port of a triple-lumen central venous catheter (Arrow; London, UK) connected to a differential pressure transducer (Medex Medical) that was filled with a 0.9% saline solution. The Pblad was measured by draining the bladder and instilling 50 mL sterile 0.9% saline solution to ensure a fluid-filled system, as described by Collee et al.2 A 21-gauge needle was inserted through the catheter sampling membrane, and the Pblad was transduced using a 0.9% saline solution-filled differential pressure transducer (Medex Medical).

Pressure and flow were calibrated prior to each study using a water manometer and an air flowmeter (Platon; London, UK). All measurements were recorded on a microprocessor system (Macintosh; Apple; Cupertino, CA). The signals were recorded at 100 Hz, were stored, and were analyzed using virtual instruments developed within a software package (MacLab, version 3.6.1; ADIntruments; East Sussex, UK).

Protocol
Before commencing recordings, the patient was made comfortable in a semi-recumbent position of approximately 45o, and secretions were cleared from the airway to prevent coughing during data collection.

A 1-min recording of all data was made at the original level of IPS. The level of IPS then was reduced by 5-cm H2O decrements, and 1-min recordings were made at each level of IPS until the patient was breathing with only 5 cm H2O positive end-expiratory pressure. At each level of IPS, recordings were made after 10 to 20 min to allow a period of equilibration. During the protocol, each patient was observed for signs of respiratory distress (ie, high respiratory rate, fall in oxygen saturation, or cardiac arrhythmia). If these conditions developed, the study would be terminated and the patient would be returned to the original level of ventilatory support.

Statistical Analysis
Prior to analysis, the Pcvp signal was averaged because the cardiac component of the Pcvp added noise to the respiratory waveforms.

We used the onset of inspiration, which was defined as the first negative deflection in the flow signal, to act as a trigger for a software signal averager. Because the heart rate is independent of the respiratory rate, the effect of averaging >= 30 breaths together is that the respiratory signal is reinforced while the cardiac signal is reduced.

The maximal changes in Pgas, Pblad, Pes, and Pcvp during inspiration (between the points of zero flow) at each level of pressure support were measured. Pdi (ie, the {Delta}Pgas - {Delta}Pes) and the {Delta}Pblad - {Delta}Pcvp then were calculated for each patient at each level of IPS.

Pdi and {Delta}Pblad - {Delta}Pcvp were compared using the method described by Bland and Altman6 and were correlated for each individual at varying levels of pressure support. The results are presented as the mean difference ± SD for both methods of measurement.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
During the study protocol, no patient developed signs of severe respiratory distress. Table 2 shows the changes in values for Pes, Pcvp, Pgas, and Pblad for each patient at the minimum level of pressure support tolerated, together with the ratio of the {Delta}Pes to the {Delta}Pcvp and the {Delta}Pgas to the {Delta}Pblad. The {Delta}Pes/{Delta}Pcvp ratio varied between 0.8 and 2.1 and the {Delta}Pgas/{Delta}Pblad ratio varied between 0.6 and 1.3 at the minimum level of pressure support .


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  		Table 2. Comparison Between {Delta}Pes/{Delta}Pcvp Ratio and {Delta}Pgas/{Delta}Pblad Ratio at Minimum Tolerated IPS

 
As pressure support was reduced, we calculated the slope of the {Delta}Pes to the {Delta}Pcvp for each patient. The mean slope of the {Delta}Pes to the {Delta}Pcvp was 1.1, ranging from 0.8 to 1.8 for individual patients. The correlation coefficient for each patient varied from 0.775 to 0.998. A Bland-Altman plot of the {Delta}Pes and the {Delta}Pcvp shows that the mean difference between the measurements is -1.0 cm H2 0 (SD, 4.1 cm H2O) and that the limits of agreement range from 7.1 to -9.1 cm H2O.

Pgas and Pblad changes also were compared as ventilatory support was reduced. The slope of the line of the {Delta}Pblad to the {Delta}Pgas varied from 0.4 to 1.3 for individual patients. The correlation coefficient of the {Delta}Pblad to the {Delta}Pgas during IPS reduction for each patient varied from 0.877 to 0.987. When compared as a Bland-Altman plot, the mean difference between the {Delta}Pgas and the {Delta}Pblad was -0.4 cm H2O (SD, 0.9 cm H2O).

Table 3 shows Pdi (ie, {Delta}Pgas - {Delta}Pes) and {Delta}Pblad - {Delta}Pcvp, together with the Pdi/{Delta}Pblad - {Delta}Pcvp ratio for each patient at the minimum level of IPS tolerated. Figure 1 shows Pdi and {Delta}Pblad - {Delta}Pcvp plotted for each patient as pressure support was varied. The slope of the line of Pdi to {Delta}Pblad - {Delta}Pcvp was 1.05 for the entire group, varying from 0.4 to 1.1 for individual patients. However, in all patients the relationship between Pdi and {Delta}Pblad - {Delta}Pcvp was linear, with correlation coefficients varying from 0.906 to 0.999 for each individual (Table 4 ). When Pdi and {Delta}Pblad - {Delta}Pcvp were compared using a Bland-Altman plot, the mean difference between the two measurements was -0.2 cm H2O (SD, 4.0 cm H2O), giving limits of agreement from -8.2 to 7.8 cm H2O.


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  		Table 3. Pdi and {Delta}Pblad - {Delta}Pcvp for All Subjects at Minimum Tolerated IPS

 


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  		Figure 1. The relationship between Pdi and {Delta}Pblad - {Delta}Pcvp for 10 patients. IPS was increased from the minimum tolerated to the maximum. The results from each patient are represented by a single line. Correlation coefficient (r) values range from 0.906 to 0.999 for individual patients.

 

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  		Table 4. Correlation Coefficient and Slope of Ratio of Pdi to {Delta}Pblad - {Delta}Pcvp for Each Subject as IPS Was Varied

 
Figure 2 shows how Pdi and {Delta}Pblad - {Delta}Pcvp, the values for which were normalized as the percent change from baseline values at the lowest levels of IPS, varied for each patient as IPS was changed. Except at very low levels of pressure support, Pdi, when measured by both methods, was reduced as ventilatory support increased, and in all cases {Delta}Pblad - {Delta}Pcvp mirrored the changes induced in Pdi.



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  		Figure 2. The percentage change in Pdi and {Delta}Pblad - {Delta}Pcvp with changing IPS for each patient.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In the present study, changes in Pcvp are easily detected during mechanical ventilation and vary from a positive deflection when the respiratory muscles are completely inactive to pronounced negative swings during large inspiratory efforts. In all cases during this study, the negative deflections were greatest at the lowest levels of pressure support and increased in size as pressure support was reduced. The {Delta}Pcvp reflected the {Delta}Pes, and when the data are normalized the agreement is striking.

This finding may be useful at the bedside, as many patients receiving pressure support have continuous Pcvp monitoring, and it is easy to detect the impact of reducing pressure support in these patients. For example, when IPS was reduced in patient 7, the pressure swing increased fivefold, indicating a substantial increase in respiratory muscle effort. Pdi increased simultaneously from 7.8 to 32.8 cm H2O. Furthermore, the pattern of minimal respiratory effort can be detected either when the {Delta}Pcvp is positive or minimally negative. In these cases, pressure support can be reduced and the response noted.

The agreement between the two sites of measuring transpleural pressure was in some cases not accurate enough to use the two measurements interchangeably. While all the patients with high or low pressure swings could be identified from the {Delta}Pcvp, subtle differences could not be detected in all cases.

There are several reasons that might contribute to the lack of concordance between the measurements of the {Delta}Pes and the {Delta}Pcvp. First, Pcvp was measured with a fluid-filled catheter system in comparison to the air-filled esophageal catheter system. While it is accepted that fluid-filled systems have better frequency responses than air-filled systems, Asher and colleagues7 did not demonstrate large differences when air-filled and fluid-filled systems were compared. This, therefore, would account for only very minor differences between Pes and Pcvp.

The relative positions of the esophageal and central venous catheters may be of more significance. Milic-Emili and coworkers8 compared Pes and Paw at a variety of catheter positions within the esophagus. When close to the diaphragm, Pes reflected transpulmonary pressure accurately. As the catheter was withdrawn, there was a greater variability between Pes and Paw. The position of our esophageal catheters was confirmed by the method described by Baydur et al5 and was in the middle third of the esophagus. In every case, the central venous catheter tip was more cephalad than the esophageal balloon, and this may account for some of the lack of concordance between the two measurements. However, such an effect, if constant, would still allow valuable trend data to be obtained from the Pcvp within an individual.

In the patients who demonstrated the extremes of the {Delta}Pes/{Delta}Pcvp ratio, their underlying pathologies may have contributed to the discrepancy between the two measurements. In both adults and neonates,9 10 Pes is augmented at high lung volumes by the effect of excess gas decompression, resulting in Pes overestimating Ppl. In subject 8, who had COPD, the {Delta}Pes/{Delta}Pcvp ratio was 2.14. It is probable that this patient had significant air-trapping and a raised functional residual capacity. Therefore, Pes may be augmented, increasing the {Delta}Pes/{Delta}Pcvp ratio during dynamic breathing. Conversely, in patients with consolidated or wet lungs (and therefore reduced lung volumes), Pes may be an underestimate of Ppl. The resultant {Delta}Pes/{Delta}Pcvp ratio may be less than unity, as demonstrated by subjects 9 and 10, who had ratios of 0.78 and 0.71, respectively. These two effects may be cancelled by dual pathology. For example, subject 1 had COPD and had undergone a laparotomy, with the first condition increasing lung volume and the latter decreasing it. The resultant {Delta}Pes/{Delta}Pcvp ratio was 1.01.

While the absolute {Delta}Pes might not equal the {Delta}Pcvp in every case, trends in {Delta}Pcvp can be compared usefully with {Delta}Pes, as indicated by the correlation coefficient of the {Delta}Pes/{Delta}Pcvp ratio when IPS is adjusted.

In 1965, Comroe11 suggested that an intrathoracic vein with its thin wall is capable of transmitting intrapleural pressure and might therefore be an acceptable alternative to the esophagus for transpulmonary pressure measurement. Flemale et al1 studied healthy adults using three identical fluid-filled systems to record mouth pressure, Pes, and Pcvp. They found that in most instances valid measurements of Ppl could be obtained from Pes or Pcvp. An x-y plot of the {Delta}Pes/{Delta}Pcvp ratio fell close to the line of identity.

Walling and Savege12 suggested that Pcvp was more reliable than Pes in reflecting a change in Ppl in the anesthetized supine patient. Pes was found to be marginally greater than Pcvp, a finding confirmed in our study by most patients. They hypothesized that this was due to the weight of the mediastinal contents on the esophagus in the supine position. However, in their study, as in ours, dissimilar catheter systems were used, the central venous catheter system being fluid-filled and the esophageal system being air-filled.

We tested the frequency response of the fluid-filled Pcvp system in vitro prior to the study and found it to be satisfactory at 13.5 Hz compared to 15 Hz for the air-filled system. However, the patients studied had central venous lines that had been in situ for several days, and it is possible that the frequency response characteristics of the system were altered by thrombus, drug crystals in the line, or the catheter lying next to the vessel wall.

Removing the cardiac waveform from the Pcvp trace was straightforward using time synchronization, with clear waves related to inspiration visible on all traces. Although there was greater overall variability between Pgas and Pblad values in our study, this had only a minor effect during the calculation of Pdi since intrathoracic pressure changes made a much greater contribution to the end result. The study by Collee et al2 used identical fluid-filled systems for both the stomach and bladder. Their results were similar to ours, with Pgas changes being approximately 2.5 cm H2O above or below intravesical pressure.

In conclusion, Pblad and Pcvp provided reflections of respiratory muscle effort when pressure support was reduced. We suggest that the change in Pcvp might be used as a guide to diaphragmatic contraction during IPS reduction, thus providing a rapid assessment when an esophageal balloon catheter is not in situ. The {Delta}Pblad/{Delta}Pcvp ratio may be a useful additional assessment and warrants further investigation during the ventilation-weaning process.


   Footnotes
 
Abbreviations: IPS = inspiratory pressure support; Paw = airway pressure; Pblad = bladder pressure; Pcvp = central venous pressure; Pdi = transdiaphragmatic pressure; Pes = esophageal pressure; Pgas = gastric pressure; Ppl = pleural pressure

Received for publication February 23, 2000. Accepted for publication June 6, 2001.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Flemale, A, Gillard, C, Dierckx, J (1988) Comparison of central venous, oesophageal and mouth occlusion pressure with water-filled catheters for estimating pleural pressure changes in healthy adults. Eur Respir J 1,51-57[Abstract]
  2. Collee, G, Lomax, D, Ferguson, C, et al (1993) Bedside measurement of intra-abdominal pressure via an indwelling naso-gastric tube: clinical validation of the technique. Intensive Care Med 19,478-480[CrossRef][ISI][Medline]
  3. Iberti, T, Lieber, C, Benjamin, E (1989) Determination of intra-abdominal pressure using a transurethral bladder catheter: clinical validation of the technique. Anesthesiology 70,47-50[ISI][Medline]
  4. Sugrue, M, Buist, M, Lee, A, et al (1994) Intra-abdominal pressure measurement using a modified nasogastric tube: validation of a new technique. Intensive Care Med 208,588-590
  5. Baydur, A, Behrakis, P, Zin, W, et al (1982) A simple method for assessing the validity of the esophageal balloon technique. Am Rev Respir Dis 126,788-791[ISI][Medline]
  6. Bland, J, Altman, D (1986) Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1,307-310[CrossRef][ISI][Medline]
  7. Asher, M, Coates, A, Collinge, J, et al (1982) Measurement of pleural pressure in neonates. J Appl Physiol 52,491-494[Abstract/Free Full Text]
  8. Milic-Emili, J, Mead, J, Turner, J (1964) Topography of esophageal pressure as a function of posture in man. J Appl Physiol 19,212-216[Abstract/Free Full Text]
  9. Beardsmore, C, Stocks, J, Silverman, M (1983) Esophageal pressure in infants at elevated lung volumes and positive airway pressure. J Appl Physiol 55,377-382[Abstract/Free Full Text]
  10. Baydur, A, Eun-Jong, C, Sassoon, C (1987) Validation of esophageal balloon technique at different lung volumes and postures. J Appl Physiol 62,315-321[Abstract/Free Full Text]
  11. Comroe, J (1965) Physiology of respiration. Year Book Medical Publishers Chicago, IL.
  12. Walling, P, Savege, T (1976) A comparison of oesophageal and central venous pressures in the measurement of transpulmonary pressure change. Br J Anaesth 48,475-479[Abstract/Free Full Text]



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