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Dr. Baydur is a member of the Division of Pulmonary and Critical Care Medicine, University of Southern California School of Medicine.
Correspondence to: Ahmet Baydur, MD, FCCP, University of Southern California, Keck School of Medicine, 2025 Zonal Ave, GNH 11-900, Los Angeles, CA 90033
Pressures measured at the various boundaries of the respiratory system include the pressure at the airway opening (Paw), alveolar pressure (considered equal to Paw if there is no gas flow and the glottis remains open), and pleural pressure (Ppl). During static and dynamic respiratory maneuvers, it is possible to measure the pressure across the lung (transpulmonary pressure [Ptp]) by measuring the difference between Paw and Ppl. The latter has been measured with needles, trocars, catheters, and most commonly balloons. Only a few direct comparisons of Ppl and esophageal pressure (Pes) have been made.1 These generally show good agreement, except that pressure swings recorded by the balloon technique are larger in the lower third of the esophagus, near the diaphragm. Monitoring total respiratory mechanics (as a reflection of lung mechanics) in patients with acute lung injury or labile airway obstruction (by recording tidal volume and Paw) assumes that the chest wall (ie, rib cage plus abdominal) component remains constant. In fact, this may not be the case in patients with ascites, pregnancy, peritonitis, pleural effusions, or the abdominal compartment syndrome, which result in a reduction of chest wall and, hence, total respiratory compliance. Thus, separately recording Ppl and deriving Ptp from this value allow one to determine if changes in total respiratory compliance are due to changes in lung or chest wall elasticity. In addition, measurement of work of breathing can only be accomplished by recording Ppl (or a reasonable surrogate).
Being able to measure changes in Ppl by taking advantage of other
routes already available, such as central venous or bladder catheters,
can provide a means to measure lung compliance (separate from total
respiratory compliance) in patients receiving mechanical ventilation or
those who have experienced abdominal trauma. Flemale and
colleagues2
discovered that changes in central venous
pressure (
Pcvp) during inspiratory efforts against an occluded
airway closely approximated changes in Pes (Pes). In this issue of
CHEST, Chieveley-Williams and colleagues (see page 533)
compared changes in bladder pressure (Pblad) and Pcvp with
changes of gastric pressure (Pga) and Pes, respectively, in
patients receiving mechanical ventilation and various levels of
inspiratory pressure support. They found that the concordance between
Pes and Pcvp was within ± 10% of unity in 5 of 10 patients,
similar to results reported by Walling and Savege3
and
Flemale et al.2
Divergences between the two pressure
changes could, in part, be explained on the basis of the underlying
diseases and their effects on alveolar gas compression or
decompression,4
5
nonuniform pleural surface pressure
changes, the position of the catheter within the esophagus, cardiogenic
oscillations, and differences between the behavior of fluid-filled
catheter systems and air-filled esophageal systems (a minor
factor).6
While measurements of absolute values of Pes as an estimate of
Ppl are problematic in patients in a supine posture (thought to be due
to the weight of the mediastinal contents on the esophagus), use of the
"occlusion test"7
should avoid this problem; it is
possible to find a spot in the esophagus in which Pes is the same as
Paw swings (Paw) recorded during inspiratory efforts made against a
closed airway. Likewise, Flemale et al,2
using similar
water-filled catheter systems and the occlusion test, showed that in 8
of 10 supine normal volunteers, Pes/Paw was within 10% of unity;
in 3 of their subjects, however, there was much discordance between
Pes and Pcvp (with Pes/Pcvp as high as 176% in 1 subject).
The overall discrepancies were even greater in the study of Walling and
Savege,3
where Pes exceeded Pcvp by as much as 112%
in one subject. These authors did not, however, make use of the
occlusion test to find the proper position of their esophageal
catheter, and they compared air-filled with fluid-filled systems of
different lengths and diameters, so that the frequency response
characteristics were different and could distort the pressure signals.
What about the validity of Pblad? The stomach and bladder, when
partially filled, are both distensible and compressible bags lying
within the abdominal cavity. It might be thought that intra-abdominal
pressure should be transmitted to both viscera equally. Decramer et
al8
showed in dogs, however, that surface pressures on the
abdominal side of the diaphragm may not be uniform. Since
transdiaphragmatic pressure (Pdi) is conventionally determined as the
difference between gastric pressure (Pga) and Pes
(Pdi = Pga - Pes),9
this difference may not be truly
representative of actual Pdi. By the same token, inhomogeneous surface
pressures on the abdominal side of the diaphragm might also contribute
to discordance between Pga and Pblad. Collee et al10
compared only static end-expiratory Pga and bladder pressure (Pblad) in
26 patients who had undergone abdominal surgery. While they found a
mean concordance of within ± 0.2% of unity, there was considerable
variability; in one patient, Pga exceeded Pblad by 63%. Also, their
measurements did not include dynamic respiratory efforts. What is
important is the concordance of not so much the respective static
pressures at zero flow, but their swings during inspiratory efforts
over physiologic tidal ranges. In 5 of their 10 patients,
Chieveley-Williams et al found that the concordance between Pdi and
(Pblad - Pcvp) was within ± 10% of unity. Again, variabilities
among subjects were most likely related to the use of different
catheter systems, as well as to nonuniform abdominal surface pressures.
Interestingly, in patients with fluid-filled abdomens, Pga/Pblad
may approach unity, as pressure swings throughout the abdomen become
more homogeneous.8
Chieveley-Williams et al did not
indicate, however, if any of their five patients with Pga/Pblad
values within ± 10 of unity had abdominal ascites, although one
patient had pancreatitis and another had abdominal sepsis.
The main lesson to be learned from the elegant study of Chieveley-Williams et al is that indwelling central venous and bladder catheters already in place can be used to at least record trends in respiratory effort pressures while monitoring patients who are being weaned off ventilation. Careful attention to uniformity of central venous and bladder catheter systems should help reduce discrepancies in pressure changes between these systems and the more conventionally used esophageal and gastric catheter systems. This would then enable the estimation of lung mechanics and work of breathing by the respiratory muscles and the ventilator in a more convenient manner without resorting to additional catheters. Clearly, more studies comparing these catheter systems in patients with a variety of medical and surgical conditions and in those receiving different modes of ventilation are needed to validate them.
References
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