Atelectasis, an important cause of impaired gas exchange during general anesthesia, may be eliminated by a vital capacity maneuver. However, it is not clear whether such a maneuver will have a sustained effect. The aim of this study was to determine the impact of gas composition on reappearance of atelectasis and impairment of gas exchange after a vital capacity maneuver.
A consecutive sample of 12 adults with healthy lungs who were scheduled for elective surgery were studied. Thirty minutes after induction of anesthesia with fentanyl and propofol, the lungs were hyperinflated manually up to an airway pressure of 40 cmH2O. FIO2 was either kept at 0.4 (group 1, n = 6) or changed to 1.0 (group 2, n = 6) during the recruitment maneuver. Atelectasis was assessed by computed tomography. The amount of dense areas was measured at end-expiration in a transverse plane at the base of the lungs. The ventilation-perfusion distributions (VA/Q) were estimated with the multiple inert gas elimination technique. The static compliance of the total respiratory system (Crs) was measured with the flow interruption technique.
In group 1 (FIO2 = 0.4), the recruitment maneuver virtually eliminated atelectasis for at least 40 min, reduced shunt (VA/Q < 0.005), and increased at the same time the relative perfusion to poorly ventilated lung units (0.005 < VA/Q < 0.1; mean values are given). The arterial oxygen tension (PaO2) increased from 137 mmHg (18.3 kPa) to 163 mmHg (21.7 kPa; before and 40 min after recruitment, respectively; P = 0.028). In contrast to these findings, atelectasis recurred within 5 min after recruitment in group 2 (FIO2 = 1.0). Comparing the values before and 40 min after recruitment, all parameters of VA/Q were unchanged. In both groups, Crs increased from 57.1/55.0 ml.cmH2O-1 (group 1/group 2) before to 70.1/67.4 ml.cmH2O-1 after the recruitment maneuver. Crs showed a slow decrease thereafter (40 min after recruitment: 61.4/60.0 ml.cmH2O-1), with no difference between the two groups.
The composition of inspiratory gas plays an important role in the recurrence of collapse of previously reexpanded atelectatic lung tissue during general anesthesia in patients with healthy lungs. The reason for the instability of these lung units remains to be established. The change in the amount of atelectasis and shunt appears to be independent of the change in the compliance of the respiratory system.
Key words: Anesthesia, general. Lung: atelectasis; compliance; gas exchange. Measurement techniques: computed tomography; multiple inert gas elimination. Ventilation, mechanical: ventilation perfusion ratio.
GENERAL anesthesia regularly impairs gas exchange, and despite preventive measures such as an increase of the inspired oxygen fraction, this often results in a decreased oxygenation of blood. [1,2]The formation of atelectasis with subsequent pulmonary shunt has been shown to be an important factor for the derangement of gas exchange. [3-5]However, atelectasis may be reexpanded and virtually eliminated by hyperinflation of the lungs. [6-8]We demonstrated that such a recruitment maneuver may result in a sustained effect on atelectasis, a decrease of pulmonary shunt, and a slightly improved oxygenation for at least 40 min. In that investigation, air was used for the recruitment maneuver, the lungs of all patients were ventilated with 40% Oxygen2in nitrogen, and there was an increase in the perfusion to units with low ventilation-perfusion ratios (V with dot A/Q with dot) after the recruitment.
It has been shown that lung units with low V with dot A/Q with dot may be prone to collapse, particularly if high inspiratory concentrations of oxygen or other gases with a high solubility in blood are used. On the other hand, a single deep breath may result in release of surfactant, [11,12]thus contributing to an improved alveolar stability and preventing lung collapse. We therefore tested the effect of low or high inspired oxygen concentration (FIO20.4 or 1.0, balance nitrogen) on the reappearance of atelectasis, gas exchange, and compliance of the respiratory system after a vital capacity maneuver during general anesthesia.
Materials and Methods
Twelve consecutive patients scheduled for neurosurgical procedures or general surgery were included in the study (Table 1). Another four patients refused to participate in the study, i.e., the refusal rate was 25%. As judged by patient history and clinical examination, no patient had a cardiac or pulmonary disease. There were two smokers.
The study was approved by the Ethics Committee of the University Hospital of Uppsala, and informed consent was obtained from each patient. The estimation of the sample size (n = 12) was based on previous studies, [5,8]detect a difference of 50% in the amount of atelectasis, at a P value of 0.05 and a power of 90%, between the two groups 40 min after reexpansion of atelectasis. .
On request, the patients received 0.04-0.08 mg *symbol* kg sup -1 cetobemidon (Ketogan, an opioid) intramuscularly as premedication. Before anesthesia, 0.5 mg atropine was given intravenously. Anesthesia was induced with 1-2 micro gram *symbol* kg sup -1 fentanyl and 2 mg *symbol* kg sup -1 propofol intravenously, followed by a continuous infusion of 4-8 mg *symbol* kg sup -1 *symbol* h sup -1 propofol. During the induction, the lungs were manually ventilated via a face mask, using 100% Oxygen2. To facilitate orotracheal intubation, the patients received 0.1 mg *symbol* kg sup -1 pancuronium, and additional doses of 1-2 mg were given when needed. The lungs were mechanically ventilated (Servo Ventilator 900C, Siemens) at a rate of 10 breaths/min with 40% Oxygen2in nitrogen during the following phase of the study (Figure 1). No positive end-expiratory pressure was used. The minute ventilation was adjusted to maintain an end-tidal carbon dioxide concentration of approximately 4% (carbon dioxide analyzer Eliza, Engstrom).
The patients were assigned randomly (sealed envelopes) to two different groups. In group I, FIO2was kept at 0.4, whereas in group 2, FIO2was switched to 1.0 during the recruitment maneuver (see below).
Three sets of measurements were performed (details are given below and in Figure 1): an estimation of atelectasis by computed tomography (CT) of the lungs, an estimation of the ventilation perfusion relationship (V with dot A/Q with dot) with the multiple inert gas elimination technique (MIGET), and an estimation of the compliance of the total respiratory system (Crs) with the flow interruption technique. In the awake state, the measurements included CT of the lungs and the estimation of V with dot A/Q with dot. After 20 min of stable anesthesia, the CT scans and the V with dot A/Q with dot measurements were repeated, and the Crswas measured (= "anesthesia, baseline"). This was followed by the recruitment maneuver (see below). The CT, V with dot A/Q with dot and Crsmeasurements were repeated until 40 min after the recruitment (Figure 1). Finally, the patient was moved to the operating theater.
To reexpand atelectasis, a recruitment maneuver was performed as described previously. Using a super syringe, the lungs were inflated with air three times up to an airway pressure (Paw) of 30 cmH2O (Figure 1). For the final inflation to a Pawof 40 cmH2O, either air (group 1) or 100% Oxygen2(group 2) was used, and in group 2, FIO2was changed to 1.0 on the ventilator for the succeeding study period. Each inflation was held for 15 s, and between each inflation, the lungs were ventilated for 1-2 min with the baseline settings of the ventilator. During the recruitment maneuver, the airway pressure was measured with a manometer (BOC, Ohmeda) attached to the endotracheal tube.
Computed Tomography of the Lungs
Atelectasis was studied by CT (Somatom plus, Siemens). The subjects were in the supine position with arms above the head. A frontal scout view covering the chest was obtained at end-expiration, awake, and after induction of anesthesia. For each subsequent analysis, a CT scan in the transverse plane was performed at end-expiration, 1 cm above the top of the right diaphragm. An additional scan at the level of the hilum and at the apex of the lungs was taken after induction of anesthesia, immediately after the recruitment maneuver and 40 min thereafter. The scan time was 1 s at 255 mAs and 137 kV. The slice thickness was 8 mm, and a matrix of 512 x 512 was used, resulting in a pixel (picture element) of approximately 1.5 x 1.5 min. The total x-ray exposure for each patient was 3mSv (Millisievert; total average exposition in Sweden 5 mSv per year).
To identify atelectasis, a magnified image (approximately 3x) was made of the dorsal portion of the CT scan of both the right and the left lungs. The dorsal border between the thoracic wall and the dense areas was drawn manually, whereas the ventral border between inflated lung tissue and atelectasis was identified by the region-of-interest (ROI) program. The atelectatic area, including all pixels with density values between -100 and +100 Hounsfield units (HU), was calculated by the computer. As an example, lung tissue with a density value of -100 HU represents a lung unit with 10% gas and 90% tissue. The amount of atelectasis was expressed in absolute values (cm2) and as percent of the total intrathoracic area (including the mediastinum). For details, see references 3 and 16.
To evaluate possible changes in regional lung volume in nondependent parts of the lungs, vessels that could be seen on consecutive scans were identified, and the angles between these vessels were measured. For this purpose, the CT scans were transferred to an image analysis software package (BioScan OPTIMAS, Edmonds, WA). This program allows the simultaneous analysis of several CT scans and the measurement of angles between lines (an example is given in Figure 2).
Ventilation Perfusion Ratios and Blood Gas Analysis
The ventilation-perfusion ratios (V with dot A/Q with dot) were assessed with the multiple inert gas elimination technique. Isotonic saline with a mixture of six inert gases (sulphur hexafluoride, ethane, cyclopropane, enflurane, diethyl ether, and acetone) was infused continuously into a peripheral vein. Under steady-state conditions, arterial blood and mixed expired gas samples were collected in duplicate for subsequent analysis by gas chromatography (Hewlet Packard Gas Chromatograph 5880A and 5890). Oxygen uptake (VO2) and carbon dioxide elimination (VCO2) were estimated with the Douglas-bag technique, thus collecting expired gas and measuring the concentrations of mixed expired oxygen and carbon dioxide (Beckman OM-14 and Leybold-Heraeus). During anesthesia, only VCO2was measured directly, whereas VO2was calculated assuming the same respiratory quotient as measured awake. The cardiac output was estimated as 20*VO2, assuming an arteriovenous oxygen difference of 50 ml *symbol* l sup -1 blood and expressing VO2in ml *symbol* min sup -1. The mixed venous inert gas concentrations were computed from the arterial and mixed expired values using mass balance principles. By mathematical analysis of the inert gas data, each V with dot A/Q with dot distribution was recovered in a 50-compartment model, and the result with the best fit of data (smallest remaining sum of squares, RSS) of each pair of duplicate samples was used for further statistical analysis. Intrapulmonary shunt (QS/QT) was defined as the fraction of total blood flow perfusing lung units with V with dot A/Q with dot < 0.005, and low V with dot A/Q with dot was defined as the fraction of total blood perfusion to lung units with 0.005 < V with dot A/Q with dot < 0.1. logSDQ, the standard deviation of the logarithmic distribution of perfusion, was calculated as a measure of the dispersion of blood flow distribution. logSDV is the standard deviation of the logarithmic distribution of ventilation. RSS for all measurements was on the average 2.0 and exceeded 6.0 in only two measurements, thus fulfilling the criteria as established by Wagner and West. .
In two patients (one from each group), a thorough analysis of V with dot A/Q with dot was performed by so-called Monte Carlo simulation and by linear programming, as described previously. Thus, the inert gas data were analyzed taking into account both the experimental error of inert gas measurement and the uncertainty, inherent to the determination of V with dot A/Q with dot distributions by the multiple inert gas elimination technique.
Blood gas measurements were performed by standard technique (ABL-2, Radiometer).
Compliance of the Respiratory System
Estimations of static compliance of the respiratory system (C sub rs) were obtained using the technique of flow interruption. Pressure and flow were measured in the ventilator on the inspiratory side and fed into a computer for on-line signal processing (Macintosh IIFx, with LabView 2, National Instruments). The mean value of two "inspiratory hold" maneuvers (2 s hold) was used for each point. Crswas calculated as tidal volume (VT) divided by end-inspiratory pressure minus end-expiratory pressure. Thus, Crsreflects the elastic behaviour of the lungs and the chest wall over the tidal volume range.
Where not stated otherwise, mean values and standard deviations are presented. In addition, for major variables, 95% confidence intervals (95% CI) are given. To compare variables at different times within groups, we used the Friedman two-way ANOVA and the Wilcoxon's signed-rank test. To compare data between the two group, the Mann-Whitney U test was used. Spearman's rank correlation coefficient was used to analyze relationships between variables. For all calculations, the SYSTAT computer software package (SYSTAT, Evanston, IL) was used.
Baseline Awake and after Induction of Anesthesia
The CT scans in the awake patients displayed no abnormalities. All patients experienced atelectasis after induction of anesthesia, with an overall mean area of 8.0 plus/minus 8.2 cm2(group 1 10.0 plus/minus 7.1 cm2, group 2 6.1 plus/minus 9.3 cm2). Figure 3shows an example in two patients, Table 1shows details of the data, and Figure 4gives a summary.
The ventilation-perfusion measurements are summarized below and in Table 2. In the awake condition, a shunt (V with dot A/Q with dot < 0.005) was found in only one patient (2.5% of cardiac output [CO]), the same patient also had a considerable amount of low V with dot A/Q with dot (14.2% CO). On the average, low V with dot A/Q with dot (0.005 < V with dot A/Q with dot < 0.1) was 3.1 plus/minus 4.2% CO. Pa sub O2, measured while breathing air, exceeded 75 mmHg (10.0 kPa) in 11 of 12 patients (mean 98 plus/minus 22 mmHg [13.0 plus/minus 2.9 kPa]), and mean PaCO2was 39.0 plus/minus 5.3 mmHg (5.2 plus/minus 0.7 kPa). The patient with the rather marked derangement of V with dot A/Q with dot and the low PaO2was well premeditated and fell asleep during the measurement of V with dot A/Q with dot "awake." Furthermore, he was obese and had the second highest body mass index (patient 8 in Table 1).
After induction of anesthesia the pulmonary shunt was increased to 6.5 plus/minus 5.2%, low V with dot A/Q with dot increased to 5.3 plus/minus 3.3%, PaO2was 150 plus/minus 55 mmHg (20.0 plus/minus 7.4 kPa) at an FIO2of 0.4, and PaCO2was 33.7 plus/minus 2.3 mmHg (4.5 plus/minus 0.3 kPa). The estimated mean cardiac output, used to calculate the V with dot A/Q with dot distributions, was 4.4 plus/minus 1.0 l *symbol* min sup -1 in the awake subjects and 3.5 plus/minus 0.81 l *symbol* min sup -1 after induction of anesthesia.
After Recruitment Maneuver
The recruitment maneuvers caused no clinically important adverse effects.
Immediately after recruitment, atelectasis was virtually eliminated in both groups (0.0 plus/minus 0.1 and 0.1 plus/minus 0.2 cm sup 2 in groups 1 and 2, respectively). In group 1 (FIO2= 0.4), there was a slow increase in the amount of atelectasis, which reached about one-sixth of the initial area of atelectasis 40 min after the recruitment (after 5 min 0.2 plus/minus 0.2 cm2; after 40 min 1.6 plus/minus 2.1 cm2, 95% CI 0 to 3.8 cm2, P = 0.028 vs. anesthesia baseline). In group 2 (FIO2= 1.0), the amount of atelectasis was increased to a value close to prerecruitment 5 min after the recruitment maneuver (5.3 plus/minus 8.7 cm2, 95% CI 0 to 16.5 cm2, no significant difference vs. anesthesia baseline), and there was a further slow increase during the rest of the study period (after 40 min 7.9 plus/minus 9.7 cm2, no significant difference vs. anesthesia baseline). See Figure 3for an example in two patients and Figure 4for a summary of the data. The mean intrathoracic area, expressed as percentage of the intrathoracic area in the awake subject, showed only small, insignificant changes from anesthesia baseline to 0 and 40 min after recruitment both in group 1 (91.3 plus/minus 5.6%/94.5 plus/minus 4.9%/92.0 plus/minus 5.2%) and in group 2. (90.5 plus/minus 10.4%/92.0 plus/minus 9.3%/90.8 plus/minus 9.7%).
Pulmonary vessels, suitable for measurements of angles, could be identified on subsequent CT scans of four patients in group 1 and of all six patients in group 2. Between anesthesia baseline and the first measurement immediately after the recruitment, there was a decrease of the intervascular angle in all but two patients (P = 0.013), the mean decrease being 12 plus/minus 7%/11 plus/minus 10% (group 1/2). As compared to the value before recruitment, the mean angles remained decreased in group 1 by 9 plus/minus 6% and 11 plus/minus 10% at 5 and 40 min after the recruitment, respectively. In group 2, the respective values were 5 plus/minus 7% and 3 plus/minus 10% (no significant difference vs. prerecruitment); thus there was a gradual increase of the intravascular angle toward the prerecruitment value.
In group 1, shunt decreased from 7.2 plus/minus 5.2% CO at anesthesia baseline to 1.3 plus/minus 2.2 and 2.3 plus/minus 2.6% CO 20 and 40 min after the recruitment maneuver (P = 0.028 and 0.028, if compared to anesthesia baseline), respectively. Low V with dot A/Q with dot increased from 6.7 plus/minus 2.1% CO to 11.0 plus/minus 3.5 and 8.0 plus/minus 3.7% CO (P = 0.028 and 0.3, if compared to anesthesia baseline). In group 2, there was no significant change in any of the measured parameters of the ventilation-perfusion distribution. At 40 min after the recruitment, shunt was 6.4 plus/minus 6.6%, and low VA/Q was 3.3 plus/minus 2.5% CO. Further details of the V with dot A/Q with dot measurements are given in Table 2. There was a correlation between the amount of atelectasis and shunt before the recruitment (group 1 r = 0.91, group 2 r = 0.99) and 40 min after recruitment (group 1 r = 0.69, group 2 r = 0.83), In group 1, PaO2measured at an FIOsub 2 of 0.4, increased from 137 mmHg (18.3 kPa) after induction of anesthesia to 163 mmHg (21.7 kPa) 40 min after the recruitment maneuver (Table 2). In group 2, the change in FIO2from 0.4 to 1.0 per se has an influence on PaO2.
The V with dot A/Q with dot data at 20 min after the recruitment were analyzed in more detail in two arbitrarily chosen patients, one from each group. In both, low V with dot A/Q with dot was significantly different from zero. Shunt, however, was not different from zero in patient 5 (group 1, with no or minor atelectasis 20 min after the recruitment: largest possible shunt of 2,500 calculations 4% CO), whereas it was different from zero in patient 9 (group 2, with reappearance of atelectasis 20 min after the recruitment; smallest possible shunt of 2,500 calculations 6% CO). Furthermore, there was a significant difference between shunt and low V with dot A/Q with dot in patient 5 and a significant difference between the shunt of patient 5 and that of patient 9. An increase or a decrease of the estimated CO by plus/minus 25% did not alter the statistical outcome. Thus, in these patients, it was possible to detect shunt and low V with dot A/Q with dot and to separate them from each other.
The time course of Crsshowed no difference between the two groups (Figure 4). In both groups, Crswas increased by the recruitment maneuver (70.1 plus/minus 27.5/ 67.4 plus/minus 21.2 ml *symbol* cmH2O sup -1 in group 1/2, P = 0.028 vs. anesthesia baseline in both groups). Forty minutes after the recruitment, Crswas still higher than after induction of anesthesia (group 1 61.4 plus/minus 19.6 ml *symbol* cmH2O sup -1, group 2 60.0 plus/minus 20.2 ml *symbol* cmH2O sup -1, P = 0.028 vs. anesthesia baseline in both groups). The change in Crsby the recruitment maneuver was not related to the amount of atelectasis immediately before the recruitment (Figure 5). There also was no correlation between compliance and shunt or low V with dot A/Q with dot awake or after induction of anesthesia nor between compliance and atelectasis, shunt or low V with dot A/Q with dot.
This study confirms that reexpansion of atelectasis during general anesthesia in patients with healthy lungs may have a sustained effect with respect to atelectasis, shunt, and PaO2, if the lungs are ventilated with 40% Oxygen2in nitrogen. If 100% Oxygen sub 2 is used, however, lung collapse reappears within a few minutes, and as compared to prerecruitment, the ventilation-perfusion relationship is essentially unchanged after the recruitment. This time course of atelectasis suggests that gas resorption plays an important role in the recurrence of collapse in previously reexpanded atelectatic lung tissue. Such lung regions appear to be unstable, and the mechanisms that keep a lung unit open possibly are overcome by the forces caused by gas absorption.
The amount of atelectasis was estimated by CT. Methodologic details concerning the analysis of dense regions in dependent parts of the lungs have been discussed in detail elsewhere. [3,16]Atelectasis that appears after induction of general anesthesia is located mostly in dependent, basal parts of the lung. To avoid excessive exposure to radiation, we decided to perform only one CT scan per condition under investigation. At three occasions, an additional scan at the level of the hilum and the apex of the lungs was taken. As in previous investigations, [3,8]the amount of atelectasis at these additional levels was always smaller as compared to the CT scan close to the dome of the diaphragm. With respect to the time course of atelectasis, the analysis of these additional scans provided no further information and therefore is not presented in this paper.
The ventilation-perfusion distribution in the lungs was analyzed with the multiple inert gas elimination technique. This method is based on the elimination and retention of a number (usually six) of "inert" gases. To calculate these parameters, the measurement of cardiac output and the concentrations of the "inert" gases in mixed expired air, mixed venous blood, and arterial blood is necessary. Some of these parameters thus necessitate the use of a pulmonary artery catheter. However, a simplified methodology can be applied, requiring measurements in arterial (or venous) blood and in mixed expired air only. We decided to use this latter technique as it was not considered justifiable to apply the more invasive procedure of pulmonary artery catheterization to the subjects eligible for this study. Thus, mixed venous "inert" gas concentrations were computed using mass balance principles, and cardiac output was estimated from the oxygen consumption. This approximation of cardiac output is imprecise, but it has been shown that indexes of V with dot A/Q with dot mismatch (e.g., logSDQ and logSDV) remain essentially unaffected by such uncertainties. Errors in cardiac output measurements, however, may be transmitted to other parameters of V with dot A/Q with dot, including shunt, low V with dot A/Q with dot, and mean V with dot A/Q with dot. Thus, a quantitative estimation of these parameters is less reliable. However, if cardiac output is constant during the study period, relative changes in shunt and low V with dot A/Q with dot can be estimated. This may be seen from the formula used to calculate mixed venous partial pressures (Pv) of an "inert" gas from the arterial partial pressure (Pa) and the partial pressure in mixed expired gas (PE) : Pv = Pa + ((PE * VE)/lambda * QT)), where lambda blood gas partition coefficient, VE: minute ventilation, and QT: cardiac output.
With VE, QT, and lambda unchanged, changes in Pa and PE will transmit directly to changes in PV. Variations in shunt and low V with dot A/Q with dot during unchanged anesthesia therefore will not merely reflect errors in measurement but may be interpreted as changes of shunt or low V with dot A/Q with dot. Because oxygen uptake did not vary during anesthesia in those cases in which repeated measurements were made, we assume that CO was more or less constant during the study. Moreover, an analysis of the data of our investigation showed that a variation of cardiac output by 25% will result in a rather modest variation of shunt and low V with dot A/Q with dot by about 20% of the measured values.
Finally, Monte Carlo simulation and linear programming showed that low V with dot A/Q with dot could be separated from shunt and that the V with dot A/Q with dot distribution in patient 5 of group 1 (no or minor atelectasis 20 min after the recruitment) was significantly different from that in patient 9 of group 2 (with atelectasis 20 min after the recruitment). This lends support to our conclusion that the reappearance of atelectasis after a recruitment maneuver affects the V with dot A/Q with dot distribution.
Mechanism of Atelectasis Formation
The findings of this study are in accordance with previous investigations with respect to atelectasis and ventilation-perfusion relationship (V with dot A/Q with dot) before and after induction of general anesthesia with mechanical ventilation. [4,5]Furthermore, the changes in the amount of atelectasis and V with dot A/Q with dot after the recruitment maneuver in the patients ventilated with a FIO2of 0.4, yielded results similar to a recently performed study. The very fast reappearance of densities in the group ventilated with 100% Oxygen2after the recruitment maneuver, however, deserves further discussion.
That resorption of gas may play a role in the formation of atelectasis during anesthesia has been discussed on theoretical grounds [10,25,26]and in a number of experimental and clinical studies, [25,27,28]although it was not possible to demonstrate lung collapse on conventional x-ray. The role of this mechanism for the formation of atelectasis during general anesthesia remained unclear until now. In the current investigation, the fast reappearance of atelectasis in the group ventilated with 100% Oxygen2suggests that gas resorption is a major factor for a renewed collapse of previously reopened lung tissue.
Collapse by gas resorption may be present in a lung unit if there is a total stop of gas flow to this unit (thus resulting in trapped gas) or if the expired ventilation of this lung unit falls to zero (critical V with dot A1/Q with dot10). In the current study, the amount of atelectasis and shunt was reduced by the recruitment maneuver, the amount of lung units with low V with dot A/Q with dot increased at the same time. Therefore, the amount of units with a critical V with dot A1/Q with dot probably increased, too. It may be assumed that units with a low V with dot A/Q with dot are the ones that were collapsed and caused shunt before the recruitment. Therefore, they are located in dependent parts of the lungs. As the preinspiratory lung volume in supine subjects is markedly smaller in dependent than in nondependent parts of the lungs, the gas used for an inflation up to vital capacity will be distributed predominantly to dependent lung units, too. Thus, if 100% Oxygen2is used for this maneuver, the concentration of oxygen will increase mostly in such lung units.
To summarize, a recruitment maneuver with oxygen results in all increase of lung units with low V with dot A/Q with dot, prone to fast collapse because of increased oxygen content within such units. In a computer model of absorption atelectasis, the time to collapse in a lung unit filled with 100% Oxygen2and excluded from ventilation has been estimated to be about 8 min. This collapse may be faster if a mixture of nitrous oxide and oxygen is used. [25,26]According to the same study, this time will be about 3 h if a lung unit was filled with 30% Oxygen2in nitrogen before exclusion from ventilation. Whether a decreased function of surfactant, as suggested during general anesthesia, or other, yet unknown factors play an additional role for instability of lung units remains to be shown.
Further evidence that this atelectasis is caused by resorption of gas is suggested by the results of our measurements of initravascular angles in nondependent parts of the lungs. These angles were decreased by the recruitment maneuver, and they increased again thereafter. This indicates that competition for space may cause a compression of nondependent parts of the lungs when dependent parts are expanded and an expansion of nondependent parts when dependent parts of the lungs collapse. In two other studies, it was found that lung units in the immediate vicinity of atelectatic tissue were well aerated or even hyperinflated, [32,33]thus fitting with an interdependence between adjacent lung units.
The compliance of the respiratory system (Crs) did not show the same course as atelectasis. In both groups, Crswas increased and atelectasis was decreased by the recruitment maneuver, but thereafter Crsdecreased similarly in both groups, whereas the behavior of atelectasis was different between groups 1 and 2. Furthermore, there appears to be no close relationship between the amount of atelectasis and the relative change in Crsbefore and immediately after the recruitment maneuver (Figure 5). For example, there were subjects showing an increase in Crsby one-third and having almost no atelectasis. On the other hand, the subject with the second largest amount of atelectasis had only a small increase in Crswith the recruitment maneuver, despite the fact that the atelectasis was eliminated.
These findings indicate that atelectasis is not the only cause of decreased compliance. [34-36]Other mechanisms that may be involved are changes in thoracic configuration (although we did not see any significant change in the transverse thoracic area in the present study), changes in the micromechanics of acinus or alveolar walls, and an altered function of surfactant. It has been shown that a single stretch of alveolar type II cells may be followed by a stimulation of surfactant secretion that is sustained for up to 30 min. This time scale is fairly similar to that of the behavior of compliance in the current investigation. The compliance measurement was made over the tidal volume range, which makes it sensitive to the presence of poorly ventilated lung regions. Regions with low V with dot A/Q with dot were more common in group 1 (with little atelectasis) than in group 2, and they may have balanced the effect of atelectasis on compliance.
In conclusion, atelectasis as found during general anesthesia in patients with healthy lungs may be reexpanded by deep inflations of the lungs, but resorption of gas plays an important role in the recurrence of collapse in such lung units. Therefore, gas exchange may be improved only by a recruitment maneuver, if the lungs are ventilated with a gas mixture containing a poorly resorbed gas such as nitrogen. The change in the amount of atelectasis and shunt appears to be independent of the change in total compliance of the respiratory system. The reason for the instability of lung units, leading to atelectasis with induction of anesthesia, remains to be established.
The authors appreciate the assistance of Malin Lundin, laboratory technician, and Marianne Almgren and Lena Haglund, x-ray technicians. The authors thank Peter D. Wagner, Department of Medicine, University of California, San Diego, San Diego, California, for his help in the detailed analysis of V with dot A/Q with dot, and Johan Bring, Department of Statistics, Uppsala University, for statistical advice.