Leif Uttman

Effects of inspiratory pause on CO2 elimination and arterial PCO2 in acute lung injury

A high respiratory rate associated with the use of small tidal volumes, recommended for acute lung injury (ALI), shortens time for gas diffusion in the alveoli. This may decrease CO(2) elimination. We hypothesized that a postinspiratory pause could enhance CO(2) elimination and reduce Pa(CO(2)) by reducing dead space in ALI. In 15 mechanically ventilated patients with ALI and hypercapnia, a 20% postinspiratory pause (Tp20) was applied during a period of 30 min between two ventilation periods without postinspiratory pause (Tp0). Other parameters were kept unchanged. The single breath test for CO(2) was recorded every 5 min to measure tidal CO(2) elimination (VtCO(2)), airway dead space (V(Daw)), and slope of the alveolar plateau. Pa(O(2)), Pa(CO(2)), and physiological and alveolar dead space (V(Dphys), V(Dalv)) were determined at the end of each 30-min period. The postinspiratory pause, 0.7 +/- 0.2 s, induced on average <0.5 cmH(2)O of intrinsic positive end-expiratory pressure (PEEP). During Tp20, VtCO(2) increased immediately by 28 +/- 10% (14 +/- 5 ml per breath compared with 11 +/- 4 for Tp0) and then decreased without reaching the initial value within 30 min. The addition of a postinspiratory pause significantly decreased V(Daw) by 14% and V(Dphys) by 11% with no change in V(Dalv). During Tp20, the slope of the alveolar plateau initially fell to 65 +/- 10% of baseline value and continued to decrease. Tp20 induced a 10 +/- 3% decrease in Pa(CO(2)) at 30 min (from 55 +/- 10 to 49 +/- 9 mmHg, P < 0.001) with no significant variation in Pa(O(2)). Postinspiratory pause has a significant influence on CO(2) elimination when small tidal volumes are used during mechanical ventilation for ALI.

A prolonged postinspiratory pause enhances CO2 elimination by reducing airway dead space.

Background: CO2 elimination per breath (VCO2,T) depends primarily on tidal volume (VT). The time course of flow during inspiration influences distribution and diffusive mixing of VT and is therefore a secondary factor determining gas exchange. To study the effect of a postinspiratory pause we defined ‘mean distribution time’ (MDT) as the mean time given to inspired gas for distribution and diffusive mixing within the lungs. The objective was to quantify changes in airway dead space (VDaw), slope of the alveolar plateau (SLOPE) and VCO2,T as a function of MDT in healthy pigs.

CO2 elimination at varying inspiratory pause in acute lung injury

Previous studies have indicated that, during mechanical ventilation, an inspiratory pause enhances gas exchange. This has been attributed to prolonged time during which fresh gas of the tidal volume is present in the respiratory zone and is available for distribution in the lung periphery. The mean distribution time of inspired gas (MDT) is the mean time during which fractions of fresh gas are present in the respiratory zone. All ventilators allow setting of pause time, TP, which is a determinant of MDT. The objective of the present study was to test in patients the hypothesis that the volume of CO2 eliminated per breath, VTCO2, is correlated to the logarithm of MDT as previously found in animal models. Eleven patients with acute lung injury were studied. When TP increased from 0% to 30%, MDT increased fourfold. A change of TP from 10% to 0% reduced VTCO2 by 14%, while a change to 30% increased VTCO2 by 19%. The relationship between VTCO2 and MDT was in accordance with the logarithmic hypothesis. The change in VTCO2 reflected to equal extent changes in airway dead space and alveolar PCO2 read from the alveolar plateau of the single breath test for CO2. By varying TP, effects are observed on VTCO2, airway dead space and alveolar PCO2. These effects depend on perfusion, gas distribution and diffusion in the lung periphery, which need to be further elucidated.

Computer-aided ventilator resetting is feasible on the basis of a physiological profile.

Background:  Ventilator resetting is frequently needed to adjust tidal volume, pressure and gas exchange. The system comprising lungs and ventilator is so complex that a trial and error strategy is often applied. Comprehensive characterization of lung physiology is feasible by monitoring. The hypothesis that the effect of ventilator resetting could be predicted by computer simulation based on a physiological profile was tested in healthy pigs.

Protective ventilation in experimental acute respiratory distress syndrome after ventilator-induced lung injury: a randomized controlled trial

BACKGROUND Low tidal volume (V(T)), PEEP, and low plateau pressure (P(PLAT)) are lung protective during acute respiratory distress syndrome (ARDS). This study tested the hypothesis that the aspiration of dead space (ASPIDS) together with computer simulation can help maintain gas exchange at these settings, thus promoting protection of the lungs. METHODS ARDS was induced in pigs using surfactant perturbation plus an injurious ventilation strategy. One group then underwent 24 h protective ventilation, while control groups were ventilated using a conventional ventilation strategy at either high or low pressure. Pressure-volume curves (P(el)/V), blood gases, and haemodynamics were studied at 0, 4, 8, 16, and 24 h after the induction of ARDS and lung histology was evaluated. RESULTS The P(el)/V curves showed improvements in the protective strategy group and deterioration in both control groups. In the protective group, when respiratory rate (RR) was ≈ 60 bpm, better oxygenation and reduced shunt were found. Histological damage was significantly more severe in the high-pressure group. There were no differences in venous oxygen saturation and pulmonary vascular resistance between the groups. CONCLUSIONS The protective ventilation strategy of adequate pH or PaCO2 with minimal V(T), and high/safe P(PLAT) resulting in high PEEP was based on the avoidance of known lung-damaging phenomena. The approach is based upon the optimization of V(T), RR, PEEP, I/E, and dead space. This study does not lend itself to conclusions about the independent role of each of these features. However, dead space reduction is fundamental for achieving minimal V(T) at high RR. Classical physiology is applicable at high RR. Computer simulation optimizes ventilation and limiting of dead space using ASPIDS. Inspiratory P(el)/V curves recorded from PEEP or, even better, expiratory P(el)/V curves allow monitoring in ARDS.

Dead space and CO2 elimination related to pattern of inspiratory gas delivery in ARDS patients

IntroductionThe inspiratory flow pattern influences CO2 elimination by affecting the time the tidal volume remains resident in alveoli. This time is expressed in terms of mean distribution time (MDT), which is the time available for distribution and diffusion of inspired tidal gas within resident alveolar gas. In healthy and sick pigs, abrupt cessation of inspiratory flow (that is, high end-inspiratory flow (EIF)), enhances CO2 elimination. The objective was to test the hypothesis that effects of inspiratory gas delivery pattern on CO2 exchange can be comprehensively described from the effects of MDT and EIF in patients with acute respiratory distress syndrome (ARDS).MethodsIn a medical intensive care unit of a university hospital, ARDS patients were studied during sequences of breaths with varying inspiratory flow patterns. Patients were ventilated with a computer-controlled ventilator allowing single breaths to be modified with respect to durations of inspiratory flow and postinspiratory pause (TP), as well as the shape of the inspiratory flow wave. From the single-breath test for CO2, the volume of CO2 eliminated by each tidal breath was derived.ResultsA long MDT, caused primarily by a long TP, led to importantly enhanced CO2 elimination. So did a high EIF. Effects of MDT and EIF were comprehensively described with a simple equation. Typically, an efficient and a less-efficient pattern of inspiration could result in ± 10% variation of CO2 elimination, and in individuals, up to 35%.ConclusionsIn ARDS, CO2 elimination is importantly enhanced by an inspiratory flow pattern with long MDT and high EIF. An optimal inspiratory pattern allows a reduction of tidal volume and may be part of lung-protective ventilation.

Computer simulation allows goal-oriented mechanical ventilation in acute respiratory distress syndrome

IntroductionTo prevent further lung damage in patients with acute respiratory distress syndrome (ARDS), it is important to avoid overdistension and cyclic opening and closing of atelectatic alveoli. Previous studies have demonstrated protective effects of using low tidal volume (VT), moderate positive end-expiratory pressure and low airway pressure. Aspiration of dead space (ASPIDS) allows a reduction in VT by eliminating dead space in the tracheal tube and tubing. We hypothesized that, by applying goal-orientated ventilation based on iterative computer simulation, VT can be reduced at high respiratory rate and much further reduced during ASPIDS without compromising gas exchange or causing high airway pressure.MethodsARDS was induced in eight pigs by surfactant perturbation and ventilator-induced lung injury. Ventilator resetting guided by computer simulation was then performed, aiming at minimal VT, plateau pressure 30 cmH2O and isocapnia, first by only increasing respiratory rate and then by using ASPIDS as well.ResultsVT decreased from 7.2 ± 0.5 ml/kg to 6.6 ± 0.5 ml/kg as respiratory rate increased from 40 to 64 ± 6 breaths/min, and to 4.0 ± 0.4 ml/kg when ASPIDS was used at 80 ± 6 breaths/min. Measured values of arterial carbon dioxide tension were close to predicted values. Without ASPIDS, total positive end-expiratory pressure and plateau pressure were slightly higher than predicted, and with ASPIDS they were lower than predicted.ConclusionIn principle, computer simulation may be used in goal-oriented ventilation in ARDS. Further studies are needed to investigate potential benefits and limitations over extended study periods.

Multiple pressure-volume loops recorded with sinusoidal low flow in a porcine acute respiratory distress syndrome model.

Objectives:  To develop a method for automatic recording of multiple dynamic elastic pressure–volume (Pel/V) loops. To analyse the relationship between multiple dynamic Pel/V loops and static Pel/V loops in a porcine model of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). To test the hypothesis that increasing lung collapse and re‐expansion with decreasing positive end expiratory pressure (PEEP) can be characterized by hysteresis of the Pel/V loops.

Re-inspiration of CO2 from ventilator circuit: effects of circuit flushing and aspiration of dead space up to high respiratory rate

IntroductionDead space negatively influences carbon dioxide (CO2) elimination, particularly at high respiratory rates (RR) used at low tidal volume ventilation in acute respiratory distress syndrome (ARDS). Aspiration of dead space (ASPIDS), a known method for dead space reduction, comprises two mechanisms activated during late expiration: aspiration of gas from the tip of the tracheal tube and gas injection through the inspiratory line - circuit flushing. The objective was to study the efficiency of circuit flushing alone and of ASPIDS at wide combinations of RR and tidal volume (VT) in anaesthetized pigs. The hypothesis was tested that circuit flushing and ASPIDS are particularly efficient at high RR.MethodsIn Part 1 of the study, RR and VT were, with a computer-controlled ventilator, modified for one breath at a time without changing minute ventilation. Proximal dead space in a y-piece and ventilator tubing (VDaw, prox) was measured. In part two, changes in CO2 partial pressure (PaCO2) during prolonged periods of circuit flushing and ASPIDS were studied at RR 20, 40 and 60 minutes-1.ResultsIn Part 1, VDaw, prox was 7.6 ± 0.5% of VT at RR 10 minutes-1 and 16 ± 2.5% at RR 60 minutes-1. In Part 2, circuit flushing reduced PaCO2 by 20% at RR 40 minutes-1 and by 26% at RR 60 minutes-1. ASPIDS reduced PaCO2 by 33% at RR 40 minutes-1 and by 41% at RR 60 minutes-1.ConclusionsAt high RR, re-breathing of CO2 from the y-piece and tubing becomes important. Circuit flushing and ASPIDS, which significantly reduce tubing dead space and PaCO2, merit further clinical studies.

Efficient gas exchange with low tidal volume ventilation in acute respiratory distress syndrome

The immediate and ultimate objectives of mechanical ventilation in the acute respiratory distress syndrome (ARDS) are to maintain gas exchange, ensure survival and allow the patient to regain a high quality of life. To achieve these goals, ventilation must be adequate and ventilator-induced lung injury minimal. A trade-off between the immediate and ultimate goals is required in order to secure adequate gas exchange with respect to CO2 and O2, and this can be achieved with lung-protective ventilation (LPV). LPV is achieved with low tidal volume ventilation, an adequate positive end-expiratory pressure (PEEP) and a limited plateau pressure. These features tend to compromise gas exchange. Dead space is large in ARDS. In this review, methods to enhance gas exchange, even at low tidal volume, by decreasing the huge dead space in ARDS are discussed. Optimizing the ventilator setting involves combining the best values for respiratory rate, minute ventilation and tidal volume, PEEP, the flow or pressure pattern o...