Secondary Logo

Journal Logo

Lung Recruitment and Positive End-Expiratory Pressure Have Different Effects on CO2 Elimination in Healthy and Sick Lungs

Tusman, Gerardo MD*; Bohm, Stephan H. MD; Suarez-Sipmann, Fernando PhD; Scandurra, Adriana Eng§; Hedenstierna, Göran PhD

doi: 10.1213/ANE.0b013e3181f0c2da
Critical Care, Trauma, and Resuscitation: Research Reports
Free
SDC

BACKGROUND: We studied the effects that the lung recruitment maneuver (RM) and positive end-expiratory pressure (PEEP) have on the elimination of CO2 per breath (VTCO2,br).

METHODS: In 7 healthy and 7 lung-lavaged pigs at constant ventilation, PEEP was increased from 0 to 18 cm H2O and then decreased to 0 in steps of 6 cm H2O every 10 minutes. Cycling RMs with plateau pressure/PEEP of 40/20 (healthy) and 50/25 (lavaged) cm H2O were applied for 2 minutes between 18-PEEP steps. Volumetric capnography, respiratory mechanics, blood gas, and hemodynamic data were recorded.

RESULTS: In healthy lungs before the RM, VTCO2,br was inversely proportional to PEEP decreasing from 4.0 (3.6–4.4) mL (median and interquartile range) at 0-PEEP to 3.1 (2.8–3.4) mL at 18-PEEP (P < 0.05). After the RM, VTCO2,br increased from 3.3 (3–3.6) mL at 18-PEEP to 4.0 (3.5–4.5) mL at 0-PEEP (P < 0.05). In lavaged lungs before the RM, VTCO2,br increased initially from 2.0 (1.7–2.3) mL at 0-PEEP to 2.6 (2.2–3) mL at 12-PEEP (P < 0.05) but then decreased to 2.4 (2–2.8) mL when PEEP was increased further to 18 cm H2O (P < 0.05). After the RM, the highest VTCO2,br of 2.9 (2.1–3.7) mL was observed at 12-PEEP and then decreased to 2.5 (1.9–3.1) mL at 0-PEEP (P < 0.05). VTCO2,br was directly related to changes in lung perfusion, the area of gas exchange, and alveolar ventilation but inversely related to changes in dead space.

CONCLUSIONS: CO2 elimination by the lungs was dependent on PEEP and recruitment and showed major differences between healthy and lavaged lungs.

Published ahead of print August 12, 2010 Supplemental Digital Content is available in the text.

Author affiliations are provided at the end of the article.

Disclosure: The authors report no conflicts of interest.

Reprints will not be available from the author.

Address correspondence to Gerardo Tusman, MD, Department of Anesthesiology, Hospital Privado de Comunidad, Mar del Plata, Argentina. Address e-mail to gtusman@hotmail.com.

Accepted June 22, 2010

Published ahead of print August 12, 2010

The effect of positive end-expiratory pressure (PEEP) on CO2 kinetics has been described. PEEP, at constant ventilation and body metabolism, is related to a decrement in the elimination of CO2 by the lungs because of several factors: (1) a decrement in CO2 transport to the lungs by a decrease in venous return and thus cardiac output (CO),13 (2) a transient decrease in expired tidal volume (VT) caused by the sequential accumulation of air within the lungs right after the increase in PEEP,3,4 (3) a gain in functional residual capacity (FRC) leading to a filling of the lungs with inspiratory gases free of CO2 thereby inducing a transient dilution of alveolar CO2,35 and (4) an increase in airway and alveolar dead space causing a decrease in alveolar ventilation (V[Combining Dot Above]A).6,7

The collapse of healthy anesthetized and acutely injured lungs of patients is well described and the main ventilatory treatment of such collapse conditions is built upon PEEP.811 PEEP and low VT ventilation are parts of a lung-protective ventilatory strategy that aims to minimize the injury caused by tidal recruitment and overdistension.12,13 However, because PEEP has been related to the retention of CO2 within the body,1417 this protective ventilatory strategy could lead to hypercapnia, especially in the context of low VT ventilation.12

We have observed in patients that after a lung recruitment maneuver (RM), a ventilatory intervention aimed at restoring pulmonary aeration, CO2 elimination increased despite the use of high PEEP levels and low VT values.1820 These results contradict the classical understanding of the effects that PEEP seems to have on CO2 kinetics.35 To our knowledge, a systematic analysis of the elimination of CO2 during changes in PEEP combined with a lung RM has not been performed. These ventilatory interventions are likely to show different responses in healthy and sick lungs because of the pathophysiology of acute lung injury resulting from massive lung collapse, lung edema, and tissue inflammation.

Therefore, the aim of this study was to describe such changes in the elimination of CO2 in animals with healthy and surfactant-depleted lungs and to determine whether lung recruitment and PEEP induced retention of CO2 within the blood.

Back to Top | Article Outline

METHODS

After approval by the Animal Research Committee of Uppsala University in Sweden, 14 Swedish mixed country breed pigs (body weight = 24.5 ± 3 kg) were anesthetized with IV ketamine 25 to 50 mg/kg/h, midazolam 90 to 180 μg/kg/h, fentanyl 3 to 6 μg/kg/h, and pancuronium 0.25 to 0.50 mg/kg/h. The trachea was intubated with a 7-mm inner diameter cuffed endotracheal tube and air leaks were identified by incomplete flow-volume loops or changes in the capnograms. The lungs were ventilated with a SERVO-i (Maquet Critical Care, Wayne, NJ) using a volume control mode with a VT of 6 mL/kg, respiratory rate of 30 breaths/min, I:E ratio of 1:2, a fraction of inspired oxygen of 1, and initially without PEEP. Intravenous saline solution was maintained at a fixed rate of 4 mL/kg during the study. Body temperature was maintained by a warm blanket to keep rectal temperature within a range of 37.5°C ± 0.5°C.

Back to Top | Article Outline

CO2 Data

Volumetric capnography was recorded on-line using the NICO capnograph (Respironics, Wallingford, CT). The airway flow and CO2 mainstream sensor were placed at the “Y” piece of the ventilator circuit and delivered data into a custom-made MatLab program (MathWorks, Natick, MA), which constructed volumetric capnograms by a Levenberg-Marquardt fitting method, and all capnography-derived parameters were calculated from this mathematical function.21

The VTCO2,br is the amount of CO2 eliminated in 1 breath obtained by integrating expired airway flow and PCO2 signals.

PETCO2 is the partial pressure of CO2 at the end of expiration and PECO2 is the mixed partial pressure of CO2 in 1 breath. Airway dead space was calculated as the inflection point of the capnogram, which defines the airway-alveolar interface or the limit between VDaw and the alveolar VT (VTalv).21

Dead space to VT ratio (VD/VT) is an index that determines the global inefficiency of ventilation. It was calculated using the Bohr-Enghoff formula22:

The mean value of 10 slopes of phase III (SIII) was calculated as previously described.21SIII is a qualitative and noninvasive marker of the global ventilation-perfusion (V[Combining Dot Above]/Q[Combining Dot Above]) ratio, where low values are related to normal V[Combining Dot Above]/Q[Combining Dot Above] ratios whereas high values are indicators of an increased dispersion of V[Combining Dot Above]/Q[Combining Dot Above].2326

Back to Top | Article Outline

Respiratory Mechanics Data

Respiratory mechanics data were recorded using the flow and pressure sensors of the same NICO capnograph. V[Combining Dot Above]A is the effective portion of ventilation and is defined as the product of VTalv and respiratory rate.

Respiratory system dynamic compliance (Crs) was calculated as ΔVT/ΔPaw. Changes in FRC (ΔFRC) induced by PEEP were calculated by the following formula3:

where VT(0) was the reference exhaled VT and n was the number of breaths with decreased VT [VT(i)] after a PEEP increase or increased VT [VT(i)] after a PEEP decrease, respectively.

Back to Top | Article Outline

Gas Exchange Data

Arterial blood gases were monitored on-line using the multiparameter intraarterial sensor TrendCare (Diametrics Medical Ltd., High Newcombe, UK) inserted into the right carotid artery. Independent arterial and mixed venous blood gas samples were extracted at each protocol step and analyzed within 5 minutes using an ABL 300 (Radiometer, Copenhagen, Denmark).

PaO2, PaCO2, and PVCO2 are the PO2 and CO2 in the arterial and venous blood, respectively. The Pa-ETCO2 is the difference between arterial and end-tidal partial pressure of CO2 representing the area for eliminating CO2 through the lungs where a low difference corresponds to a large area for exchange with a better diffusion of CO2 and vice versa.20 PV-aCO2 is the gradient between venous and arterial CO2. Shunt was calculated using a standard formula.27

Back to Top | Article Outline

Hemodynamic Data

Electrocardiogram and pulse oxymetry were recorded, and a catheter for mean arterial blood pressure measurement was placed in the femoral artery. A 7.5F pulmonary artery catheter CCOmbo (Edwards Lifesciences, Irvine, CA) placed into the right jugular vein provided continuous CO and pulmonary pressures. CO was then subdivided into (1) an ineffective shunting part (COSHUNT), calculated as the product between shunt and CO to get the absolute value in L/min, and (2) an effective pulmonary perfusion part (COEPP) or the portion of the CO that participates in CO2 exchange calculated by subtracting the COSHUNT value from CO. This last parameter was used to represent the effect of pulmonary blood flow on VTCO2,br during the protocol.

Back to Top | Article Outline

Protocol

Animals were randomly assigned to 2 groups: healthy (n = 7) or surfactant-depleted lungs (n = 7). Lung lavages with 35 mL/kg warm isotonic saline solution were performed in the lavaged lung group.28 Lavages were repeated every 5 minutes until PaO2 stabilized between 100 to 150 mm Hg at pure oxygen and PEEP of 8 cm H2O.

The protocol consisted of 3 sequential parts:

  1. An increasing PEEP limb, where PEEP was increased in steps of 6 cm H2O from 0 to 18 cm H2O using a volume control mode of ventilation. These data represent the isolated effect that PEEP would have on the elimination of CO2.
  2. An RM, which consisted of a 2-minute cycling RM in pressure control ventilation using 40/20 cm H2O in healthy lungs29 or 50/25 cm H2O in sick lungs30 for plateau pressure and PEEP, respectively.
  3. A decreasing PEEP limb, as a mere mirror image of part 1 of the protocol where PEEP was decreased from 18 to 0 PEEP in steps of 6 cm H2O. These data represent the cumulative effect that PEEP in combination with a prior RM would have on CO2 elimination.

Each level of PEEP in parts 1 and 3 was maintained for 10 minutes because previous publications35 and our own results from pilot studies showed that >90% of all changes in VTCO2,br caused by PEEP occurred within this timeframe.

Back to Top | Article Outline

Data Analysis

Before starting the protocol, in vitro and in vivo calibrations of devices were performed following the manufacturer's guides. Hemodynamic and on-line blood gas data were stored in a laptop by an acquisition system programmed in LabView (National Instruments, Austin, TX) while CO2 and respiratory data were recorded in another laptop using the dedicated software Aplus (Respironics, Wallingford, CT). Both laptops were synchronized in time. CO2, respiratory mechanics, and hemodynamic data belonging to the last minute of each PEEP step (30 breaths = 30 data points), including the blood gas samples taken at this time, were analyzed.

A descriptive statistical analysis was performed using the MatLab program. Lilliefors test determined a non-Gaussian distribution of the data. Friedman nonparametric test was used to compare the results of the same level of PEEP before with those after RM in a 2-way direction. The same test was used to compare differences between results of consecutive levels of PEEP. Values are expressed as median (interquartile range) and P values <0.05 were considered significant.

Back to Top | Article Outline

RESULTS

All pigs completed the protocol successfully. Absolute values of the main variables belonging to the last minute for each PEEP step are presented in Tables 1 to 3. In general, PEEP applied after lung recruitment improved lung function when compared with PEEP alone in both healthy and lavaged lungs. The recruitment effect was characterized by a gain in ΔFRC, an increase in Crs, and decreases in VD/VT and shunt, paralleled by improvements in gas exchange.

Table 1

Table 1

Table 2

Table 2

Table 3

Table 3

In healthy pigs before recruitment, VTCO2,br decreased from 4.0 (3.6–4.4) mL (0-PEEP) to 3.1 (2.8–3.4) mL (18-PEEP, P < 0.05) as PEEP increased (Fig. 1). Figure 2 shows that the relative changes in the elimination of CO2 with increasing PEEP levels were mainly related to a decrease in the efficacy of ventilation (<V[Combining Dot Above]A) and the decrease in COEPP. The area for eliminating CO2 (Pa-ETCO2) showed a small increase with increasing PEEP levels but with little effect on CO2 elimination. Dead space (VD/VT) and SIII increased proportionally to PEEP (Table 1).

Figure 1

Figure 1

Figure 2

Figure 2

After recruitment, VTCO2,br increased from 3.3 (3–3.6) mL (18-PEEP) to 4.0 (3.5–4.5) mL (0-PEEP, P < 0.05) as PEEP was reduced. This increased CO2 elimination was associated with an increase in V[Combining Dot Above]A and COEPP. Initially, Pa-ETCO2 decreased when going from 18 to 12 cm H2O of PEEP, but progressively increased again when going further down to 0-PEEP (Table 1).

VTCO2,br presented a different behavior in lavaged animals (Figs. 1 and 2). Before recruitment, VTCO2,br initially increased from 2.0 (1.7–2.3) mL (0-PEEP) to 2.6 (2.2–3) mL (12-PEEP) (P < 0.05). This increment in CO2 elimination went along with an increased COEPP and a decreased Pa-ETCO2. VTCO2,br then decreased from 2.6 (2.2–3) mL (12-PEEP) to 2.4 (2–2.8) mL (18-PEEP) (P < 0.05). This time, the impairment of CO2 elimination was associated with a reduced V[Combining Dot Above]A and COEPP despite Pa-ETCO2 showing the lowest value of the increasing limb of PEEP.

After recruitment, the highest VTCO2,br was observed at 12-PEEP (2.9 [2.1–3.7] mL, P < 0.05) which decreased to 2.5 (1.9–3.1) mL at 0-PEEP (P < 0.05). The progressive decrements in the area for CO2 exchange and in COEPP were associated with a lower elimination of CO2 at 0-PEEP. VD/VT and SIII increased with reductions in PEEP (Table 2).

Figure 3A represents the elimination of CO2 over time for a single step change of PEEP from 6 to 12 cm H2O before recruitment. Compared with 6-PEEP, the change in median VTCO2,br was −6% in healthy lungs and +8% in lavaged lungs at 12-PEEP (both P < 0.05). In both healthy and surfactant-depleted animals, VTCO2,br decreased in the first breaths after the PEEP increase with >90% of the effect occurring within 5 minutes at the higher PEEP.

Figure 3

Figure 3

Figure 3

Figure 3

Figure 3B shows the effect of a PEEP change from 6- to 12-PEEP before recruitment on the main variables for 18 consecutive respiratory cycles. The effects were qualitatively similar, but quantitatively different in healthy and in lavaged lungs. VTCO2,br decreased almost to zero in the first breath but recovered within 5 to 6 consecutive breaths in both healthy and lavaged lungs. This change in VTCO2,br was related to a decrease in expired VT right after the PEEP change resulting in an expansion of ΔFRC by approximately 183 mL in healthy and 154 mL in lavaged lungs. As opposed to VTCO2,br, CO was little affected by the change in PEEP.

PVCO2, PaCO2, and PETCO2 are presented in Figure 1 and Tables 1 and 2. In healthy lungs, no clinically significant changes in those variables were observed. In surfactant-depleted lungs, however, the difference between PaCO2 and PETCO2 narrowed significantly but in an inverse relation to the applied PEEP before and after lung recruitment with corresponding changes in pH. Both PVCO2 and PaCO2 decreased with lung recruitment and PEEP.

Back to Top | Article Outline

DISCUSSION

The main findings of this study can be summarized as follows:

  1. Lung recruitment and PEEP have different effects on CO2 elimination in healthy and surfactant-depleted lungs.
  2. At constant metabolism and ventilatory settings, any change in the elimination of CO2 can be explained by a combination of changes in (a) the effectiveness of lung perfusion, (b) the area for CO2 exchange, and (c) the amount of V[Combining Dot Above]A and, thus, in the global V[Combining Dot Above]/Q[Combining Dot Above] relationship of the lungs.
  3. In healthy and lavaged lungs, changes in PEEP altered the elimination of CO2 because of immediate effects on both expired VT values and ΔFRC for 5 to 6 consecutive breaths. Stable new values for VTCO2,br, lung perfusion, area of CO2 exchange, and V[Combining Dot Above]A were reached within 5 minutes.
  4. In lavaged lungs, the efficacy of CO2 elimination was directly related to the recruitment/derecruitment effect. Lung recruitment and PEEP did not retain CO2 in the blood during the study periods.
Back to Top | Article Outline

Effect of PEEP and Lung Recruitment on CO2 Elimination

Breen and Mazumdar3 and Johnson and Breen5 were the first to analyze the effect of PEEP on the non–steady-state CO2 kinetics in healthy lungs. Our main goal was to further their work and to describe the same effect in the context of a lung RM. Thus, to our knowledge, the data presented in the current study are the first to describe the effect of PEEP and lung recruitments on the elimination of CO2 in non–steady-state conditions of healthy and surfactant-depleted lungs.

The elimination of CO2 by the lungs, at constant ventilation and body metabolism, depends on its transport by the blood into the lungs, its diffusion through the alveolar-capillary membrane, and its elimination by the V[Combining Dot Above]A.3,31 Therefore, the final VTCO2,br value measured at the airway opening in response to a PEEP challenge with or without a lung RM is the result of a complex interaction of several factors. Figure 2 and Tables 1 to 3 show that these interactions differ between healthy and lavaged lungs and, sometimes, the influence on CO2 elimination of 1 factor differed from other factors.

Figure 3 shows the change in the elimination of CO2 during an increase in PEEP from 6 to 12 cm H2O without RM. The layout of this figure is similar to the ones presented in the articles by Breen and Mazumdar3 and Johnson and Breen5 to facilitate the reader's comparison of the data. According to the results shown in this figure, changes in VTCO2,br, lung perfusion, CO2 exchange, and V[Combining Dot Above]A after a PEEP challenge vary between healthy and lavaged lungs.

In healthy lungs, 12-PEEP decreased VTCO2,br because of decreased V[Combining Dot Above]A and CO despite a slight improvement in gas exchange (Fig. 3A). More than 90% of the effects on VTCO2,br induced by 12-PEEP occurred within 5 minutes. These results are similar to the findings of Breen and Mazumdar3 observed in healthy dogs and those of Johnson and Breen5 in healthy anesthetized humans. They also found that a PEEP challenge decreased VTCO2,br because of a decrement in V[Combining Dot Above]A and CO, with most of the recovery of VTCO2,br within 10 minutes. Differences in the recovery of VTCO2,br observed between these protocols could be explained by differences in the species studied, differences in the levels of PEEP applied (11 cm H2O in the study by Breen and Mazumdar and 10 cm H2O in the study by Johnson and Breen), or by differences in hemodynamic status and treatments.

In lavaged lungs, VTCO2,br increased until 12-PEEP caused by an increment in the area for CO2 exchange despite decreasing V[Combining Dot Above]A and CO (Fig. 3A). The effects of a partial alveolar recruitment induced by the increasing PEEP levels are supported by concomitant increases in PaO2 and compliance at reduced dead spaces (Table 2). Although CO was reduced by 21%, its COEPP increased by 22% because of the recruitment of shunt areas (Table 3). The final result was a better elimination of CO2 because of an improved V[Combining Dot Above]/Q[Combining Dot Above] ratio as indicated by a decrement in SIII. The different findings in lavaged and healthy lungs point toward differences in the physiological effects that PEEP and recruitment have on normally aerated and on collapsed lungs.

Figure 3B provides a zoomed view of the first breaths after a change in a PEEP step. The decrement in VTCO2,br after an increase in PEEP was caused by the trapped gas within lungs at the onset of the higher PEEP, which diluted alveolar CO2. The opposite results were observed in cases of PEEP reduction. After a PEEP change, a fast recovery in VTCO2,br was found within 5 to 6 consecutive breaths. This finding is similar to the one described by Johnson and Breen5 in anesthetized patients in which the recovery of VTCO2,br after a change of PEEP from 0 to 10 cm H2O took 8 breaths.

Back to Top | Article Outline

Does PEEP and Lung Recruitment Retain CO2 in the Blood?

A protective ventilatory management with low VT and plateau pressures is currently mandatory when treating acutely injured lungs.12,13 Arterial hypercapnia is thus a clinically tolerated negative consequence of an intentional decrease in V[Combining Dot Above]A. This hypercapnic state could become even worse if PEEP, as many authors have postulated, caused CO2 retention in the body.1417

In healthy lungs, VTCO2,br decreased in proportion to PEEP before the recruitment but increased after it. At constant ventilation and metabolism, this decrease in CO2 elimination should lead to retention of CO2 within the body when PEEP is applied without a prior recruitment. However, PVCO2, PaCO2, and thus P[Combining Macron]V-aCO2 were not affected much during the protocol (Table 1 and Figs. 1 and 2), which must be interpreted that CO2 was not retained within the blood, at least during the study period. After recruitment, the elimination of CO2 and global lung physiology improved at PEEP levels down to 12 cm H2O (Table 1 and Figs. 1 and 2) with chances for CO2 retention even lower than before the recruitment.

Our results differ from those of Breen and Mazumdar3 and Johnson and Breen5 who found increased PVCO2 and PaCO2 in healthy lungs at 10 and 11 cm H2O of PEEP, respectively. Differences in the hemodynamic status, protocol time, and experimental models might explain these differences.

In surfactant-depleted lungs, however, results were totally different. PV-aCO2 increased whereas Pa-ETCO2 decreased with positive-pressure ventilation as long as lung collapse was low and overall lung function preserved (Table 2 and Fig. 1). The increased area of gas exchange leading to an augmented diffusion of CO2 across the alveolar-capillary membrane after a lung recruitment can explain this effect and was confirmed by parallel increments in PaO2 and Crs, 2 well-known markers of lung recruitment.32,33 COEPP increased with increasing airway pressures because of the recruitment of previously collapsed capillaries in the atelectatic areas (Table 3). Because VTCO2,br is directly proportional to lung perfusion, this increment in COEPP facilitates the transport of CO2 from the body stores toward the lungs where it is eliminated. Note that the absolute values of PVCO2 and PaCO2 decreased with both lung recruitment and PEEP, thereby confirming that CO2 was not retained within the blood but rather eliminated more efficiently.

In lavaged lungs, the highest recruitment pressures applied in pressure control ventilation resulted in a mean VT of 7.4 mL/kg (221 [202–251] mL). This small and transient increase in minute ventilation could have influenced the elimination of CO2 beyond the actual lung recruitment effect during the descending PEEP steps. However, we believe that the decreased values for PVCO2 and PaCO2 on the descending limb of the PEEP titration were mainly attributable to the recruitment of alveoli because: (1) changes in the area of gas exchange, and not in V[Combining Dot Above]A, had a dominating influence on VTCO2,br (Fig. 2), (2) variables representing the recruitment effect and which are independent of V[Combining Dot Above]A (Crs, SIII, ΔFRC, PaO2, or shunt) improved after lung recruitment, and (3) a transient and marginal increase in minute ventilation for 2 minutes only would not have had a lasting impact on VTCO2,br after a lapse of 10 minutes, the point in time when the blood samples were taken.

Back to Top | Article Outline

Clinical Implications

In contrast to continuous positive airway pressure maneuvers, cycling RMs have the following advantages: (a) they are hemodynamically better tolerated,34 (b) the step-wise and sequential increments in PEEP allow the gained volumes of air to spread progressively instead of abruptly throughout the lung parenchyma,35,36 and (c) they allow real-time monitoring of respiratory variables on a breath-by-breath basis. Today, the way to conduct and optimize RM is a topic of much debate, where the advent of volume-based capnographic monitoring may add important new arguments in favor of such an approach because of the noninvasive and real-time nature of this methodology.

Because CO2 kinetics are context sensitive and highly dependent on the sequence of steps during a cycling RM, in our protocol, the levels of PEEP were not assigned in random order. Had we randomized the protocol steps, we would not have been able to show reproducibly the sequential nature and the time dependence of CO2 elimination. For the same reason, we chose to study the CO2 kinetics during a short lapse of time because we were interested in the CO2 kinetics during the non–steady-state conditions induced by RMs and a PEEP titration process. This is crucial new information, which should contribute to a better understanding of CO2 kinetics, and we hope that it will finally have clinical implications for the monitoring of patients during mechanical ventilation.

Back to Top | Article Outline

Limitations

Surfactant-depleted lungs as used in our experimental study do not adequately represent the complex nature of acute lung injury in real patients, and thus our results should be interpreted with caution.

It is well documented that healthy and sick human lungs have different opening pressures29,30and therefore we chose our recruitment pressures in health and disease assuming that this difference would be true for animals also. To achieve a complete recruitment effect in our surfactant-depleted animals, we decided to use an arbitrary and fixed opening pressure of 50 cm H2O for all animals with sick lungs based on our own previous experience33 because we did not have access to lung imaging by computed tomographic scan to determine an optimal opening pressure individually for each animal. Had we used the same pressure as we did for healthy animals, the risk of having incompletely recruited diseased lungs and thus inconclusive study results would have been high.

Back to Top | Article Outline

CONCLUSIONS

The results of this study show that lung recruitment and PEEP have different effects on the elimination of CO2 in healthy and lavaged lungs. These differences can be explained by a complex interaction between the key factors of lung perfusion, diffusion through the alveolar-capillary membrane, and V[Combining Dot Above]A. Our results suggest that sufficiently high levels of PEEP applied after lung recruitment may help decrease hypercapnia in patients treated with lung-protective ventilation and low VT strategies.

Back to Top | Article Outline

AUTHOR AFFILIATIONS

From the *Department of Anesthesiology, Hospital Privado de Comunidad, Mar del Plata, Argentina; †CSEM Centre Suisse d'Electronique et de Microtechnique SA, Research Centre for Nanomedicine, Landquart, Switzerland; ‡Department of Critical Care Medicine, Fundación Jiménez Díaz-UTE, Madrid, Spain; §Bioengineering Laboratory, Electronic Department, University of Mar del Plata, Mar del Plata, Argentina; and ∥Department of Medical Sciences, Clinical Physiology, University Hospital, Uppsala Sweden.

Back to Top | Article Outline

REFERENCES

1. Qvist J, Pontoppidan H, Wilson RS, Lowenstein E, Laver MB. Hemodynamic response to mechanical ventilation with PEEP: the effect of hypervolemia. Anesthesiology 1975;42:45–55
2. Berglund JE, Haldén E, Jakonson S, Landelius J. Echocardiographic analysis of cardiac function during high PEEP ventilation. Intensive Care Med 1994;20:174–80
3. Breen PH, Mazumdar B. How does positive end-expiratory pressure decrease CO2 elimination from the lung? Respir Physiol 1996;103:233–42
4. Elliott WR, Harris AE, Philip JH. Positive end-expiratory pressure: implications for tidal volume changes in anesthesia machine ventilation. J Clin Monit 1989;5:100–4
5. Johnson JL, Breen PH. How does positive end-expiratory pressure decrease pulmonary CO2 elimination in anesthetized patients? Respir Physiol 1999;118:227–36
6. Hedenstierna G, Lundberg S. Airway compliance during artificial ventilation. Br J Anaesth 1975;47:1277–81
7. Coffey RL, Albert RK, Robertson HT. Mechanisms of physiological dead space response to PEEP after acute oleic acid lung injury. J Appl Physiol 1983;55:1550–7
8. Lundquist H, Hedenstierna G, Strandberg A, Tokics L, Brismar B. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 1995;36:626–32
9. Brismar B, Hedenstierna G, Lundquist H. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985;62:422–8
10. Gattinoni L, Caironi P, Valenza F, Carlesso E. The role of CT-scan studies for the diagnosis and therapy of acute respiratory distress syndrome. Clin Chest Med 2006;27:559–70
11. Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med 2000;342:1334–49
12. The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342:1301–8
13. Amato MBP, Barbas CSV, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, Kairalla RA, Deheinzelin D, Muñoz C, Oliveira R, Takagaki TY, Carvalho CRR. Effect of a protective ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338:347–54
14. Dueck R, Wagner PD, West JB. Effects of positive end-expiratory pressure on gas exchange in dogs with normal and edematous lungs. Anesthesiology 1977;47:359–66
15. Pesenti A, Marcolin R, Prato P, Borelli M, Riboni A, Gattinoni L. Mean airway pressure vs positive end-expiratory pressure during mechanical ventilation. Crit Care Med 1985;13:34–7
16. Isserles SA, Breen PH. Can changes in end-tidal PCO2 measure changes in cardiac output? Anesth Analg 1991;73:808–14
17. Hedenstierna G, White FC, Mazzone R, Wagner PD. Redistribution of pulmonary blood flow in the dog with PEEP ventilation. J Appl Physiol 1979;46:278–87
18. Tusman G, Böhm SH, Suarez-Sipmann F, Turchetto E. Alveolar recruitment improves ventilatory efficiency of the lungs during anesthesia. Can J Anaesth 2004;51:723–7
19. Tusman G, Böhm SH, Suarez-Sipmann F, Maisch S. Lung recruitment improves the efficiency of ventilation and gas exchange during one-lung ventilation anesthesia. Anesth Analg 2004;98:1604–9
20. Tusman G, Suarez-Sipmann F, Böhm SH, Pech T, Reissmann H, Meschino G, Scandurra A, Hedenstierna G. Monitoring dead space during recruitment and PEEP titration in an experimental model. Intensive Care Med 2006;32:1863–71
21. Tusman G, Scandurra A, Böhm SH, Suarez-Sipmann F, Clara F. Model fitting of volumetric capnograms improves calculations of airway dead space and slope of phase III. J Clin Monit Comput 2009;23:197–206
22. Englhoff H. Volumen inefficax. Bemerkungen zur Frage des schädlichen Raumes. Uppsala Läkareforen Forhandl 1938; 44:191–218
23. Harris B, Bailey DL, Chicco P, Bailey EA, Roach PJ, King GG. Objective analysis of whole lung and lobar ventilation/perfusion relationships in pulmonary embolism. Clin Physiol Funct Imaging 2008;28:14–26
24. Blanch LL, Fernandez R, Saura P, Baigorri F, Artigas A. Relationship between expired capnogram and respiratory system resistance in critically ill patients during total ventilatory support. Eur Respir J 1999;13:1048–54
25. Hofbrand BI. The expiratory capnogram: a measure of ventilation-perfusion inequalities. Thorax 1966;21:518–24
26. Strömberg NO, Gustafsson PM. Ventilatory inhomogeneity assessed by nitrogen washout and ventilation-perfusion mismatch by capnography in stable and induced airway obstruction. Pediatr Pulmonol 2000;29:94–102
27. Berggren SM. The oxygen deficit of arterial blood caused by non-ventilated parts of the lungs. Acta Physiol Scand 1942;Suppl 4:4–9
28. Lachmann B, Jonson B, Lindroth M, Robertson B. Modes of artificial ventilation in severe respiratory distress syndrome: lung function and morphology in rabbits after wash-out of alveolar surfactant. Crit Care Med 1982;10:724–32
29. Rothen HU, Sporre B, Englberg G, Wegenius G, Hedenstierna G. Reexpansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993;71:788–95
30. Borges JB, Okamoto VN, Matos GF, Caramez MPR, Arantes PR, Barros F, Souza CE, Victorino JA, Kacmarek RM, Barbas CSV, Carvalho CRR, Amato MBP. Reversibility of lung collapse and hypoxemia in early acute respiratory distress syndrome. Am J Respir Crit Care Med 2006;174:268–78
31. Cherniack NS, Longobardo GS. Oxygen and carbon dioxide gas stores of the body. Physiol Rev 1970;50:196–243
32. Lachmann B. Open up the lung and keep the lung open. Intensive Care Med 1992;18:319–21
33. Suarez-Sipmann F, Böhm SH, Tusman G, Pesch T, Thamm O, Reissmann H, Reske A, Magnusson A, Hedenstierna G. Use of dynamic compliance for open lung positive end-expiratory pressure titration in an experimental study. Crit Care Med 2007;35:214–21
34. Celebi S, Köner O, Menda F, Korkut K, Suzer K, Cakar N. The pulmonary and hemodynamic effects of two different recruitment maneuvers after cardiac surgery. Anesth Analg 2007;104:384–90
35. Hickling KG. Best compliance during a decremental, but not incremental, positive end-expiratory pressure trial is related to open-lung PEEP: a mathematical model of acute respiratory distress syndrome lungs. Am J Respir Crit Care Med 2001;163:69–78
36. Albaiceta GM, Taboada F, Parra D, Luyando LH, Calvo J, Menendez R, Otero J. Tomographic study of the inflection points of the pressure-volume curve in acute lung injury. Am J Respir Crit Care Med 2004;170:1066–72
© 2010 International Anesthesia Research Society