1Nuffield Department of Anaesthetics, University of Oxford, Radcliffe Infirmary, Oxford OX2 6HE, UK. 2Service Anesthésie Réanimation, Hopital de la Croix Rousse, 103 Grande-Rue de la Croix, Rousse, F-69317 Lyon Cedex 04, France*Corresponding author
Accepted for publication: April 10, 2000
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Br J Anaesth 2000; 85: 4569
Keywords: ventilation, positive end-expiratory pressure; oxygen, tension
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
Methods and results |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
A prototype intravascular PO2 sensor (IE Sensors, Salt Lake City, Utah, USA) was inserted into the aorta and left to stabilize. This Clark-type amperometric sensor had a 1090% response time of 24 s. Fibre optic pulmonary artery catheters (Opticath Catheter; Abbott Critical Care Systems, Chicago, Illinois, USA) were used to measure mixed venous blood oxygen saturation continuously using the principle of reflectance spectroscopy (Oximetric 3; Abbott Critical Care Systems). Intermittent measurement of blood gases and pH were made using a blood-gas analyser (ABL 330; Radiometer, Copenhagen, Denmark), and the same blood sample was used to measure other blood variables by co-oximetry (OSM 3, Radiometer). Cardiac output, Q·T, was measured by thermodilution (Oximetric 3, Abbott Critical Care Systems). The value of Q·S/Q·T was calculated conventionally using the FIO2, blood gas and saturation data, assuming a respiratory quotient of 0.8.
Correct positioning of the PO2 sensor in the aorta was assessed by observing the blood pressure tracing from the sensors blood sampling port and by a stable mean PaO2. The PO2 sensor was calibrated against drawn heparinized arterial blood using the blood-gas analyser. Inspired and expired oxygen concentrations were measured, at the end of the tracheal tube, using a respiratory Quadrupole mass spectrometer (VG Quadrupoles, Middlewich, UK).
Throughout the study, the mechanically ventilated animals received a constant mean (SD) inspired FIO2 of 0.72 (0.01). Tidal volume and respiratory rate were kept constant during each individual study, but ranged from 0.25 to 0.30 litres and 11 to 13 breaths min1, respectively, between animals to maintain an end-expired carbon dioxide concentration of 4.7 (0.6)% v/v. After surgery, a stabilization period of 12 h was allowed and baseline (prelavage) values were recorded (Table 1). Bronchopulmonary lavage was performed to deplete the lung surfactant, inducing a large pulmonary shunt. The lavage procedure was repeated, typically 1020 times, until PaO2 had decreased from 57 to 10 kPa (Table 1). This procedure produced a typical initial shunt fraction, Q·S/Q·T, of 53% (SD 16%).
|
Results (Table
1 and Fig. 1) are expressed as
mean (SD), and the statistical analysis was by one-way
analysis of variance with repeated measurements. When this analysis showed
significance, post hoc comparisons of the means were made by
Scheffés test. A P value less than 0.05 was
considered as significant. Table 1 shows the overall effect of increasing and
decreasing PEEP on blood gases, oxygen saturation, cardiac output, shunt
fraction and arterial blood pressure. The table also shows the conventional
pulmonary blood-flow shunt fraction calculated at each PEEP level.
Bronchopulmonary lavage reduced the mean (prelavage)
PaO2 by 47 kPa and the mean
PO2 by 2.3 kPa. At the initial low mean PaO2, 9.5 (0.7) kPa, the PaO2 signal began to oscillate about its mean value with an amplitude of 1.2 (0.8) kPa, and both the mean PaO2 and its oscillation amplitude began to increase as PEEP was imposed. Figure 1A shows typical results taken from a single animal study. It must be noted that the PaO2(t) time-varying tracings presented in this figure are not related to each other on the time axis, and no physiological inference can be made from the time-phase differences of these traces. Figure 1B shows the effect of incremental changes on
PaO2 (mean (SD)) for all the studies, as PEEP was firstly increased from 0 to 2 kPa and then decreased from 2 to 0 kPa. Each individual study showed the same effects of PEEP on
PaO2 as those illustrated in Fig. 1, namely that (i) as PEEP was initially increased, both the mean PaO2 and
PaO2 increased; but that (ii)
PaO2 began to decrease after a certain PEEP value was reached, although the mean PaO2 continued to rise. This pattern was reversed as PEEP was reduced back to its baseline (ZEEP) level. In all instances, the PaO2 oscillations followed the ventilator frequency, and appeared to become maximal at the end of inspiration and minimal at the end of expiration. There was also a transport lag between the ventilator inspiratoryexpiratory phases and the PaO2 oscillations.
|
![]() |
Comments |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Both Purves and the Kreuzer group, in the 1960s and 1970s, reported respiratory-induced oscillations in arterial PO2 in animal models.3 4 These were a direct consequence of tidal ventilation fluctuations in alveolar gas oxygen tension, and had the same period as the ventilator setting. An increase in tidal volume or a decrease in ventilation frequency led to an increase in the amplitude of the PaO2 oscillations. These early studies ruled out the possibility that the effects of cyclical variations in arterial pressure, or blood flow, could produce the measured PaO2 fluctuations. In contrast to our own animal ARDS model, these earlier studies investigated these PaO2 oscillations only in the healthy lung.
Our own findings confirm those of previous authors, such as Bergmans report in 19612 of oscillations in arterial oxyhaemoglobin saturation, SaO2, (when haemoglobin was not fully saturated) and, more recently, those of Elwell et al. in 1996,11 which demonstrated that oscillations in arterial saturation occur with the induction of mild hypoxia. The results of Elwell et al. were explained by Lovell et al. in 1997,11 who showed that changes in ventilator settings could alter the SaO2 oscillations. Bergman showed that the amplitude of the SaO2 oscillations diminished as haemoglobin became saturated, but he was not able to measure PaO2 on-line.2 However, on the basis of his SaO2 studies, he hypothesized that the most likely explanation of his results was that pulmonary shunt varied during the respiratory cycle as a result of the lung collapsing during expiration and then reopening during positive-pressure inspiration.
Two problems need to be faced. These are that (i) the PaO2 amplitudes observed in our study were larger than would be expected in healthy lungs; and (ii) current knowledge suggests that PaO2 oscillations on the steep part of the oxyhaemoglobin association/dissociation curve are buffered by the shape of the curve describing the relationship of oxygen content with PO2. Significant PaO2 oscillations in this steep part of the curve could be caused by: (i) the presence of inhomogeneity in the lung ventilationperfusion ratio induced by the pulmonary lavage; (ii) different degrees of atelectasis occurring in the lung during the inspiratory and expiratory phases of the respiratory cycle (the Bergman hypothesis); or (iii) a combination of both mechanisms, as they do not exclude one another.
We consider that, during inspiration, more alveoli are recruited, with a decrease in venous admixture (during inspiration) and consequently an increase in both the mean PaO2 and the PaO2(t) time-varying oscillatory signal. During expiration, these recruited alveoli could collapse and contribute to an increased shunt fraction and, thus, a decrease in mean PaO2. When PEEP was increased sufficiently to induce permanent recruitment during the expiratory phase, the overall PaO2 amplitude would decrease and the mean PaO2 rise. On the other hand, if shunt fraction was constant during both the inspiratory and expiratory phases of respiration (the conventional view of Q·S/Q·T) then the PaO2 oscillations would not appear at all at low mean PaO2 values because of the buffering capacity of oxyhaemoglobin in this region of the dissociation curve.
It now seems clear that PaO2 oscillations occur in the atelectatic lung, and that the application of PEEP not only elevates the mean arterial PaO2 but also affects the magnitude of the PaO2 oscillations superimposed on this mean. The effect of these oscillations in the clinical care setting is not clear.
![]() |
Acknowledgements |
---|
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
2 Bergman NA. Cyclic variations in blood oxygenation with the respiratory cycle. Anaesthesiology 1961; 22: 9008[ISI]
3 Purves MJ. Fluctuations of arterial oxygen tension which have the same period as respiration. Respir Physiol 1966; 1: 28196[ISI][Medline]
4 Folgering H, Smolders FDJ, Kreuzer F. Respiratory oscillations of the arterial PO2 and their effects on the ventilatory controlling systems in the cat. Pflügers Arch 1978; 375: 17
5 Hlastala MP. A model of fluctuating alveolar gas exchange during the respiratory cycle. Respir Physiol 1972; 15: 21432[ISI][Medline]
6 Yokota H, Kreuzer F. Alveolar to arterial transmission of oxygen fluctuations due to respiration in anaesthetised dogs. Pflügers Arch 1973; 340: 291306
7 Lin KH, Cumming G. A model of time-varying gas exchange in the human lung during a respiratory cycle at rest. Respir Physiol 1973; 17: 93112.[ISI][Medline]
8 Williams EM, Hamilton R, Sutton L, Hahn CEW. Measurement of respiratory parameters using inspired oxygen sinusoidal forcing signals. J Appl Physiol 1996; 81: 9981006
9 Arieli R, Van Liew HD. Corrections for the response time and delay of mass spectrometers. J Appl Physiol 1981; 51, 141722
10 Elwell CE, Owen-Reece H, Wyatt JS, Cope M, Reynolds EOR, Delpy DT. Influence of respiration and changes in expiratory pressure on cerebral haemoglobin concentration measured by near infrared spectroscopy. J Cereb Blood Flow Metab 1996; 16, 3537[ISI][Medline]
11 Lovell AT, Owen-Reece H, Elwell CE, Smith M, Goldstone JC. Predicting oscillation in arterial saturation from cardiorespiratory variables. Implications for the measurement of cerebral blood flow with NIRS during anaesthesia. Adv Exp Med Biol 1997; 428: 62938[ISI][Medline]