How does positive end-expiratory pressure decrease pulmonary CO2 elimination in anesthetized patients?

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Abstract

In anesthetized, mechanically ventilated patients, 10 cm H2O positive end-expiratory pressure (PEEP10) immediately decreased the CO2 volume exhaled per breath (VCO2,br) by 96%, as exhaled tidal volume (Vt) decreased to expand functional residual capacity during the first 8 breaths after PEEP10 began. Then, the sustained decrease in VCO2,br for over 10 min was due to the 19% decrease in cardiac output (t, decreased CO2 delivery from tissues to lung) and to the decrease in alveolar ventilation (a). In turn, decreased a resulted from decreased Vt (loss of inspired volume into the compressible volume of the ventilating circuit) and possibly from increased physiological dead space, due to the potential for new high alveolar ventilation-to-perfusion (a/) lung regions. VCO2,br increased and recovered to baseline by 20 min of PEEP10 ventilation because t increased to augment the CO2 delivery to the lung and alveolar PCO2 increased (increased mixed venous PCO2 and tissue CO2 retention) to increase VCO2,br while alveolar Vt remained depressed. End-tidal PCO2 (PetCO2) progressively increased during PEEP10 and did not detect the decrease in VCO2,br during PEEP10 ventilation because PetCO2 does not account for exhaled volume.

Introduction

In a previous study of non-steady state CO2 kinetics in anesthetized, open-thorax dogs (Breen and Mazumdar, 1996), CO2 volume exhaled per breath (VCO2,br) decreased by 54% after 1 min of positive end-expiratory pressure (PEEP) (11 cm H2O). Three major mechanisms explained the decrease in VCO2,br during PEEP. First, expired tidal volume (Vt) decreased at onset of PEEP (as thoracic gas volume increased), which decreased VCO2,br. Second, alveolar PCO2 (PaCO2) decreased during PEEP, which decreased VCO2,br. The decrease in PaCO2 resulted from the decrease in venous return and CO2 delivery to the lung, in turn due to the increased central venous pressure during PEEP. Note that the dilution of functional residual capacity (FRC) with fresh gas at onset of PEEP, which decreased PaCO2, was offset by the decreased VCO2,br due to decreased exhaled Vt, which increased PaCO2. Third, wasted ventilation decreased VCO2,br. During PEEP, increased physiological dead space (Vdphy) resulted from an increase in anatomical dead space (Vdana) and appearance of new high alveolar ventilation-to-perfusion (a/) lung units.

Other authors describe adverse effects of PEEP during steady state which could decrease VCO2,br, including decreased delivered Vt (Elliot et al., 1989), generation of high a/ lung units (Dueck et al., 1977, Coffey et al., 1983, Nieman et al., 1988), increased dead space (Suter et al., 1975, Coffey et al., 1983, Vigil and Clevenger, 1996) with CO2 retention (Dueck et al., 1977, Pesenti et al., 1985, Tokics et al., 1987), and decreased cardiac output (t) (Berglund et al., 1994, Huemer et al., 1994, Dambrosio et al., 1996).

Since PEEP is a common intervention used by anesthesiologists in the operating room, we sought to investigate how PEEP affects the non-steady state elimination of CO2 in patients under anesthesia. It was hypothesized that the application of PEEP in mechanically ventilated patients would decrease VCO2,br, similar to the experimental study (Breen and Mazumdar, 1996). However, in patients, the intact thorax could blunt the increase in FRC and Vdana and the intact pleural pressure gradient could limit the generation of high a/ lung units. During clinical anesthesia, CO2 kinetics monitoring is generally restricted to measurement of end-tidal PCO2 (PetCO2), which may not reflect VCO2,br because PetCO2 does not contain exhaled volume information.

To test these hypotheses, serial breath-by-breath measurements of VCO2,br were conducted in anesthetized patients for 20 min after applying 10 cm H2O PEEP during mechanical ventilation. t was measured non-invasively using a new esophageal Doppler cardiac output monitor, which allowed t measurements in this study on healthy patients without the risks of pulmonary artery catheterization. Simultaneous measurements of other cardio-respiratory variables facilitated the elucidation of mechanisms underlying the non-steady state effects of PEEP on VCO2,br.

Section snippets

General preparations

After the Institutional Review Board approval, informed consent was obtained from five adult patients (Table 1) to conduct this study in the period after induction of general anesthesia and before the scheduled surgery began. After placement of ASA standard monitors and pre-oxygenation, patients were induced with intravenous sodium thiopental or propofol and maintained with isoflurane. Muscle relaxation was achieved with succinylcholine at induction followed by non-depolarizing neuromuscular

Results

The breath-by-breath changes for about 20 respiratory cycles after the application of PEEP10 are depicted in Fig. 2. Compared to baseline, VCO2,br (Panel A) decreased by 96% at the first breath, with significant recovery by about breath 8. These changes in VCO2,br were mirrored by VtE (Panel E) which decreased by 912 ml to 265±69 ml by the first breath after PEEP10. Consequently, FRC (Panel G) increased by 779±228 ml with the first inspiration after PEEP10; the total increase in FRC was

Discussion

These are first clinical data, to the authors’ knowledge, of non-steady state breath-by-breath changes in CO2 kinetics after application of PEEP. In anesthetized, mechanically ventilated patients, the application of 10 cm H2O positive end-expiratory pressure (PEEP10) results in an immediate 96% decrease in the CO2 volume exhaled per breath (VCO2,br) by the first exhalation. Thereafter, VCO2,br increased with each breath, but recovered to the baseline value only by 20 min of PEEP10. How does

Acknowledgements

This work was supported by the National Heart, Lung, and Blood Institute Grant HL-42637. We thank Bradley Jacobsen for expert technical assistance and Deltex Medical for provision of the esophageal Doppler cardiac output monitor.

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